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946 Cards in this Set

  • Front
  • Back
b
the adrenal cortex secretes:
1) cortisol:
a) a glucocorticoid -- an endogenous steroidal hormone that affects MANY metabolic activities of the body
b) exogenous steroids (made in a lab & given to patients) mimic this glucocorticoid.
2) aldosterone: a mineralocorticoid that "directs" the kidneys to "hold onto" Na+ in the blood (and therefore also "hold onto" water -- H2O generally follows Na+) in exchange for secretion of K+ into the urine.
A. Addison's disease
B. Cushing's
C. Diabetes
D. hypercortisolism
b
hypercortisolism and hyperaldosteronism.
1) hypercortisolism-- higher-than-normal levels of cortisol in body
a) usually called______ when the high levels of cortisol are due to receiving chronic steroid treatment (remember, exogenous steroids are essentially cortisol)
A. Addison's disease
B. Cushing's syndrome
C. Cushing's disease
D. hypercortisolism
?
c
there is pathologic oversecretion of adrenocorticotropic hormone (ACTH) from the pituitary gland
(a) normally ACTH & cortisol balance each other out in a normal negative feedback loop
(b) if pituitary malfunctions, such as when there is a pituitary tumor, the amount of ACTH is abnormally high stimulates adrenal cortex to secrete abnormally high amounts of cortisol
(2) the adrenal cortex itself has a tumor or other malfunction that causes it to hypersecrete cortisol.
2) hyperaldosteronism - oversecretion of aldosterone by adrenal cortex.
A. Addison's disease
B. Cushing's syndrome
C. Cushing's disease
D. hypercortisolism
d
no matter what the original etiology, increased levels of cortisol & aldosterone cause following S&S:
a. pathologically increased glycogenolysis & gluconeogenesis, so patient will often have _____________, which can lead to the development of Type II diabetes mellitus
A. Addison's disease
B. Cushing's syndrome
C. Cushing's disease
D. hyperglycemia
?
a
abnormal breakdown of adipose tissue (lipolysis), resulting in high levels of circulating fat products (hyperlipidemia) and their deposition in certain body areas:
1) trunk ("truncal obesity"); face ("moon face"); and back ("buffalo hump)— this combination is often known as "cushinoid appearance"
2) high levels of LDL & increased risk for atherosclerosis
3) weight gain in general.
A. increase of cortisol & aldosterone
B. Cushing's syndrome
C. increase of cortisol & lipoproteins
D. hypercortisolism
a
1) trunk ("truncal obesity"); face ("moon face"); and back ("buffalo hump)— this combination is often known as "cushinoid appearance"
2) high levels of LDL & increased risk for atherosclerosis
3) weight gain in general.
4) Hyperglycemia
c. abnormally catabolized protein--has negative effects on skin & muscle:
muscle weakness & wasting (thin arms & legs)
2) in children—short stature
3) weakened collagen fibers leads to skin fragilityskin bruises & tears easily; and stretchingpurple striae (stretch marks) often seen where skin has stretched from increased fat deposits
A. increase of cortisol & aldosterone
B. Cushing's syndrome
C. increase of cortisol & lipoproteins
D. hypercortisolism
a
d. increased break down of bone (increased osteoclastic activity) can lead to:
1) hypercalcemia and its S&S's—lethargy, fatigue, etc
2) spillage of calcium into urine (hypercalcinuria) increased risk of renal calculi.
3) osteoporosis & pathological fractures; risk increases even more because in Cushing's there is also reduced calcium absorption in gut.
e. suppression of prostaglandin activity, resulting in:
1) anti-clotting effects --patient may bleed more easily
2) anti-immunocyte effects -- more susceptible to infection
3) decreased protection of stomach lining (due to steroidal inhibition of hospholipase in arachidonic pathway, prostaglandin no longer protects stomach) increased risk of peptic ulcers
4) increased peripheral vasoconstriction HTN
A. increase of cortisol & aldosterone
B. Cushing's syndrome
C. increase of cortisol & lipoproteins
D. hyperaldosteronism
d
S&S
1) increased Na & H20 retention fluid volume overloadweight gain, edema, HTN
2) hypokalemia
g. other miscellaneous problems such as acne and hirsutism (increased hair growth, usually in inappropriate places)
A. increase of cortisol & aldosterone
B. Cushing's syndrome
C. increase of cortisol & lipoproteins
D. hyperaldosteronism
b
dx—draw cortisol levels at different times of the day
6) tx—withdraw or decrease exogenous steroids; fix pituitary or adrenal tumor if that is the problem; give drugs that block aldosterone if necessary.
A. increase of cortisol & aldosterone
B. Cushing's
C. increase of cortisol & lipoproteins
D. hyperaldosteronism
a
cause: most frequent one is autoimmune attack on adrenal gland with resultant destruction of tissue; other possible causes includes pituitary problem (hypopituitarism).
2) sequelae of hypocortisolism: hypoglycemia, which results in fatigue, weakness, apathy, confusion; also anorexia, N, V, D, weight loss
3) sequelae of hypoaldosteronism: increased excretion of Na and H20 by distal tubule into urine low blood volume, dehydration; if bad enough, can have
severe hypotension, called crisis.
4) tx—steroids, aldosterone, high-salt diet (within reason!)
A. Addison's disease
B. Cushing's syndrome
C. Cushing's disease
D. hypercortisolism
b
severe hypotension due to fluid loss
A. increase of cortisol & aldosterone
B. Addisonian crisis
C. increase of cortisol & lipoproteins
D. hyperaldosteronism
c
hyperglycemia & glucosuria, and also (most of the time) long-term problems that are system-wide
2) usually also polyuria & polydipsia, so DM is a DRY disease.
3) 3rd "P" is polyphagia, excess hunger, seen in Type I.
b. diagnosis / monitoring
1) FBS (fasting blood sugar) > 126 on two occasions (norm = 70 to 110)
2) Hgb A1C: the percentage of glucose-carrying Hgb molecules over the lifespan of an RBC; norm around 4%; aim for diabetics—keep it < 7%; high A1C = high average daily blood glucose
A. increase of cortisol & aldosterone
B. Addisonian crisis
C. diabetes mellitus
D. hyperaldosteronism
d
diagnosis / monitoring of DM
a. normal fasting serum glucose = ___________ (glucose level normally rises after meals, but should normalize as insulin "ushers" it into cells)
A. 60-100
B. 50-100
C. 80-120
D. 70-110
c
b. diagnosis / monitoring
1) FBS (fasting blood sugar) > 126 on two occasions (norm = 70 to 110)
2) Hgb A1C: the percentage of glucose-carrying Hgb molecules over the lifespan of an RBC; norm around 4%; aim for diabetics—keep it < 7%; high A1C = high average daily blood glucose
A. increase of cortisol & aldosterone
B. Addisonian crisis
C. diabetes mellitus
D. hyperaldosteronism
a
(used to be called "juvenile onset")-- it is due to a TOTAL lack of insulin secretion from beta cells of pancreas
A. Diabetes Type 1
B. Addisonian crisis
C. Diabetes Type 2
D. hyperaldosteronism
c
(used to be called "adult onset") -- it is caused by:
1) abnormally low insulin production (but there is SOME insulin) and impaired insulin utilization (insulin resistance)
A. Diabetes Type 1
B. Addisonian crisis
C. Diabetes Type 2
D. hyperaldosteronism
a
cause: autoantibodies destroy pancreatic tissue NO INSULIN
2) 2 categories of acute sequelae of no insulin:
hyperglycemia & its untoward effects, including dehydration.
no cellular energy source
3) hyperglycemia & its untoward effects
BS's (blood sugars) of untreated type I diabetic usually run 200 to 300
high BS exceeds renal threshold & glucose "spills" into urine high urine osmolality H2O drawn into urine from tubular cells polyuria & dehydration polydipsia, dry skin, dry mucus membranes, etc.
no cellular energy source
after all glycogen is used up, gluconeogenesis begins fat breaks down first, then muscles (protein)  ketonemia & ketonuria acidosis
patient stays thin & nutritionally deprived despite polyphagia.
if not treated, side effects of gluconeogenesis can lead to DKA (diabetic ketoacidosis)
A. Diabetes Type 1
B. Addisonian crisis
C. Diabetes Type 2
D. hyperaldosteronism
a
ABGs show metabolic acidosis
patient might have acetone breath (ketones are being blown off)
might have Kussmaul respirations to blow off CO2 & bring up pH.
 extreme state patient could become unconscious (from irritating effects of acidosis on brain tissue)—this would be a form of diabetic coma.
5) tx—insulin
A. Diabetes Type 1
B. Addisonian crisis
C. Diabetes Type 2
D. hyperaldosteronism
c
patho begins with increased fat cells in the body, which causes wide spread resistance to insulin
 SOME glucose is getting into the cells from the blood, but some is NOT, so the glucose in the blood increases
 pancreas reacts to this continued hyperglycemia by increasing secretion of insulin hyperinsulinemia
 no matter how much insulin gets secreted, still can only get a small portion of glucose into cells due to their insulin resistance eventually pancreas "poops out"— beta cells "run out of steam" & there is decreased insulin production continued hyperglycemia
A. Diabetes Type 1
B. Addisonian crisis
C. Diabetes Type 2
D. hyperaldosteronism
c
S&S--
 hyperglycemia & glucosuria, like type I, but no DKA or weight loss because there is still SOME glucose getting into cells.
 since this is slow process, sometimes S&S very subtle—mild polydipsia & polyuria, fatigue
 also, BS's can get very high - 400-900—without patient realizing it; this can cause extremely high serum osmolality, polyuria, & dehydration; this acute combination known as HHNK—hyperglycemic, hyperosmolar, nonketotic state
 extreme state patient can become unconscious (usually from brain cell dehydration)—this would be another form of diabetic coma.
3) tx—diet, weight loss, various combinations of meds, including sometimes insulin
A. Diabetes Type 1
B. Diabetes Meillitus
C. Diabetes Type 2
D. hyperaldosteronism
b
1) angiopathy, from toxic effects of glucose molecules on lining of arterial vessels
 microangiopathy—damage to small vessels
o diabetic retinopathyblurred vision, blindness
o kidney arteriolerenal failure
o capillaries of skin easy bruising
 macroangiopathy—damage to medium & large vessels—stroke, CAD, aneurysms, PAD.
A. Diabetes Type 1
B. Diabetes Meillitus
C. Diabetes Type 2
D. hyperaldosteronism
b
2) neuropathy due to angiopathic ischemia to nerves in various tissue (plus direct toxicity of glucose)
o peripheral neuropathy—burning, pain, numbness of legs & feet that can lead to high risk of trauma
o autonomic neuropathy—autonomic nervous system affected--gastroparesis, bladder control problems, "silent MI."
3) phagocytic damage from glucose toxicity high risk of infections (UTIs, yeast infections, non-healing sores)
A. Diabetes Type 1
B. Diabetes Meillitus
C. Diabetes Type 2
D. hyperaldosteronism
d
a cluster of conditions that greatly increases a person's risk for heart disease—type II DM, elevated LDLs & decreased HDL, HTN, abdominal obesity. 25% of people in US have this!!!
A. Hypoglycemia
B. Diabetes Meillitus
C. Cushing's syndrome
D. metabolic syndrome
a
1) etiology-- decreased food intake & other nutritional factors; in case of diabetes, can occur from too much anti-diabetic medication such as insulin 2) S&S—fatigue, shakiness, irritability, sweating—occur from effect of counter-regulatory hormones.
3) tx—orange juice / sugar; IV dextrose; glucagon.
4) extreme state hypoglycemic coma (called insulin shock or insulin coma if due to too much insulin); much more dangerous state than diabetic extreme state.
A. Hypoglycemia
B. Diabetes Meillitus
C. Cushing's syndrome
D. metabolic syndrome
diabetes, dry
diabetes, dry
a
if person can swallow ok, give glucose in form of orange juice, packet of sugar, etc
(follow that by complex carb like cracker)
b. if in danger of not being able to swallow and/or is unconscious, give IV glucose; or can give intramuscularly (IM) or subcutaneously (subQ).
A. Hypoglycemia
B. Diabetes Meillitus
C. Cushing's syndrome
D. metabolic syndrome
b
dry skin, unconscious, possibility of dying, and treat with insuling are related to:
A. Insulin Coma
B. Diabetic Coma
a
diaphoresis, unconscious, seizures, possibility of dying, treat with glucose and glucagon are related to:
A. Insulin Coma
B. Diabetic Coma
c
A patient with Type I diabetes has a pH of 7.32. This is most likely caused from the byproducts of increased:
a. insulin resistance.
b. hyperinsulinism.
c. gluconeogenesis.
d. glucagon.
?
B, E, H, J, K, L
Type I and Type II diabetes usually have in common all the following EXCEPT (choose all that apply):
a. macroangiopathy.
b. polyphagia.
c. neuropathy.
d. risk for dehydration.
e. Kussmaul respirations.
f. high serum osmolality.
g. micrioangiopathy.
h. acetone breath.
i. use of insulin.
j. use of oral anti-hyperglycemic meds.
k. sweaty skin.
l. blood pH < 7.35
?
a
The nurse caring for a woman with Cushing's disease may expect assessment finding of all below EXCEPT:
a. exophthalmus.
b. hirsutism.
c. truncal obesity.
d. high blood pressure.
?
d
A patient presents with S&S of dehydration, weight loss, and a blood glucose of 50. A likely diagnosis is:
a. Cushing's disease.
b. hyperpituitarism.
c. hypothyroidism.
d. Addison's disease.
d
Complaints of polydipsia and polyuria could be linked to all the following disease processes EXCEPT:
a. DM
b. Addison's disease.
c. diabetes insipidus.
d. SIADH.
b
reflux of HCL (hydrochloric acid) and pepsin from the stomach into the esophagus.
b. may be due to a relaxation of the lower esophageal sphincter (LES) and/or delayed emptying of the stomach.
c. may have symptoms of heartburn, epigastric pain, coughing, within 1 hour of eating
d. S&S worsen when lying down, aggravated by ETOH, coffee, and smoking
a. hiatal hernia
b. gastroesophageal reflux disorder GERD
c. gastritis
d. Barrett's esophagus
a
herniation of the stomach through the diaphragm so that it protrudes into the thoracic cavity.
b. pt may experience GERD, epigastric pain, dysphagia, or no S&S at all.
c. tx—may need surgery.
a. hiatal hernia
b. gastroesophageal reflux disorder GERD
c. gastritis
d. Barrett's esophagus
c
a. an inflammation that affects gastric mucosa and can cause erosions (superficial areas of wearing-away of mucosa).
b. S&S include pain or burning over epigastric area, and occasionally bleeding (acute hemorrhagic gastritis).
c. can be acute or chronic:
a. hiatal hernia
b. gastroesophageal reflux disorder GERD
c. gastritis
d. Barrett's esophagus
c
usually results from use of overuse of NSAIDS (suppress protective prostaglandins) or ETOH (direct chemical damage).
b) heals spontaneously once the offending agent is removed.
a. hiatal hernia
b. chronic gastritis
c. acute gastritis
d. peptic ulcer disease (PUD)
b
thought to be autoimmune etiology
b) occurs mainly in the elderly and causes an atrophy of the gastric mucosa.
c) as a result of the atrophy they develop pernicious anemia because of the loss of intrinsic factor.
a. hiatal hernia
b. chronic gastritis
c. acute gastritis
d. peptic ulcer disease (PUD)
d
chronic inflammatory condition of stomach & proximal duodenum in which disturbance of their mucosal lining allows acid to ulcerate the underlying tissue, causing gastric and/ or duodenal ulcers
2. aggressive change factors that can cause mucosal disturbance and/or increase tissue vulnerability to ulceration
a. ASA & other NSAID use; chronic steroid use (decrease synthesis of prostaglandins, which have protective effect on stomach lining)
b. heavy ETOH use
c. cigarette smoking (thought to stimulate HCl secretion & decrease blood flow to tissue in the area)
d. chronic diseases such as chronic gastritis, liver disease, CKD, diabetes, COPDe. severe psychological stress
a. hiatal hernia
b. chronic gastritis
c. acute gastritis
d. peptic ulcer disease (PUD)
d
S&S and treatment
a. sometimes it can be painless; others cause burning epigastric pain 1-3 hours after meals or pain that awakens the person during the night
b. if it begins eroding blood vessels, patient can have GI bleeding of various degrees, depending on size of vessel (to be discussed more in GI bleeding section.)
c. is treated by antacids, H2-blockers (Zantac, Pepcid), PPIs (proton pump inhibitors—Nexium, Prevacid), & eradication of H. pylori with antibiotic regimen.
a. hiatal hernia
b. chronic gastritis
c. acute gastritis
d. peptic ulcer disease (PUD)
d
besides usually having one or more of the above factors, most patients diagnosed with PUD are also positive for an organism called 1) __________ is a bacterium that can be ingested via food, drinking water or other oral/fecal route-- infection more common in same families or in crowded conditions
2) once ingested, can "swim" through HCl, burrow through and disrupt the mucous layer of stomach, & attach to surface epithelial cells & colonize (can survive in HCl!)
3) majority of people infected by do not develop ulcers, but by damaging the mucosa, the organism creates more vulnerability to injury by pepsin & HCl when a person has other risk factors
a. hiatal hernia
b. chronic gastritis
c. acute gastritis
d. H. Pylori
dysplasic, precancer
dysplasic, precancer
a
number 3 killer amongst all cancers
b. almost always arises from a pre-existing benign neoplasm, usually in the form of a polyp (stalk-like growth on the wall of the colon) which becomes malignant.
c. risk factors:
1) age over 50
2) high-fat diet, obesity, sedentary lifestyle
3) smoking & ETOH over-consumption
4) family hx
a. Colorectal cancer
b. chronic gastritis
c. acute gastritis
d. peptic ulcer disease (PUD)
a
S&S, dx, tx
a. few obvious early S&S but most common are:
1) blood in stool, either visible or occult
2) change in bowel habits
b. dx'd most often by colonoscopy
c. tx
1) if confined to a polyp, a simple polypectomy during the colonoscopy will cure it
2) if more widespread, tx will include colectomy (removal of part of colon) & sometimes colostomy (opening created in abdomen for stool); chemothx.
3) best tx—prevention! --high-fiber diet, lifestyle changes.
a. Colorectal cancer
b. Inflammatory bowel disease (IBD)
c. acute gastritis
d. peptic ulcer disease (PUD)
b
is a chronic disorder characterized by inflammation of the lining and walls of the intestines.
b. it includes 2 main types—Crohn's disease & ulcerative colitis
c. common features of both:
1) basic problem is inflammation which causes episodes of bloody diarrhea & abdominal cramps that have patterns of exacerbation & remission, often related to stress
2) no proven primary etiology but possible causes include:
a) infectious agents (bacteria, viruses)
b) links to familial occurrence
c) autoimmune response:
(1) formation of autoantibodies against glycoproteins in walls of the intestines inflammation.
2) sometimes patient has manifestations of systemic autoimmune features as well—arthritis, vasculitis, iritis
a. Colorectal cancer
b. Inflammatory bowel disease (IBD)
c. acute gastritis
d. peptic ulcer disease (PUD)
b
along with inflammation that causes diarrhea & cramps, other potential problems include:
a) intestinal obstruction from chronic inflammation and scarring
c) fistula formation --abnormal channels or tracts that develops in the presence of inflammation and infection)
d) sometimes perforation of intestinal wall & spillage of intestinal contents into abdominal cavity
4) treatment--generally directed at controlling inflammation by giving steroids & other meds; sometimes surgery to remove parts of bowel
a. Colorectal cancer
b. Inflammatory bowel disease (IBD)
c. Crohn's disease
d. ulcerative colitis
c
pattern of intestinal involvement differs from ulcerative colitis:
1) may involve any portion of the GI tract, but in 70 % of cases involve duodenum, ileum, and/or & cecum; 20% of cases involve rest of large intestines
2) ALL layers of bowel are involved—ie, entire wall -- transmural involvement
3) random segments of inflamed tissue are separated by normal tissue ie, has a "patchy" pattern
b. S&Ss—see "common features" above; also, malabsorption, malnutrition, weight loss, since most nutrients are absorbed in small intestines, especially duodenum.
a. Colorectal cancer
b. Inflammatory bowel disease (IBD)
c. Crohn's disease
d. ulcerative colitis
d
1) found only in colon, not small intestines-- severe inflammation and ulcerations begin in the rectum & progress to involve entire colon
2) the involved segments are not separated by normal tissue—ie, areas are confluent, not patchy
3) inflammation and ulcerations are usually not transmural—do not extend beyond submucosa
b. S&Ss-- main differences:
1) dehydration risk more severe in this because colon is usually the site of main water reabsorption by body
2) risk not as high for nutritional deficiency in this
a. intestinal obstruction
b. Inflammatory bowel disease (IBD)
c. Crohn's disease
d. ulcerative colitis
a
an occlusion of either the small or large intestine that can be partial or complete in nature.
b. pathogenesis / S&S: obstruction → sequestration of gas and fluid proximal to the obstruction → abdominal distention (become swollen/stretched)→ causes following S&S:
1) severe, colicky abdominal cramping
2) N &V
3) can have either constipation or, with partial obstruction, sometimes can have diarrhea
a. intestinal obstruction
b. Inflammatory bowel disease (IBD)
c. Crohn's disease
d. ulcerative colitis
b
scar tissue from surgery or from a chronic inflammation such as IBD.
a. intestinal obstruction
b. adhesions
c. hernia
d. ulcerative colitis
c
intestine protrudes through a weakness in the abdominal muscle or through the inguinal ring
c. tumor in the lumen of the intestine
a. intestinal obstruction
b. adhesions
c. hernia
d. intussusception
d
telescoping of one portion of the bowel into the other, causing strangulation of blood supply; more common in infants.
a. volvulus, AKA torsion
b. adhesions
c. hernia
d. intussusception
a
-- twisting of the intestine with occlusion of blood supply.
a. volvulus, AKA torsion
b. paralytic ileus
c. hernia
d. intussusception
b
loss of peristaltic motor activity in the intestine
1) not a physical obstruction, but a functional one, because all peristalsis stops, & fluids, gases, etc, build up, causing distention, constipation, pain, etc
2) associated with immobility, post-anesthesia effects, surgery (especially abdominal), peritonitis, electrolyte imbalances, spinal trauma.
3) prevention—increasing patient mobility as soon as possible.
a. volvulus, AKA torsion
b. paralytic ileus
c. hernia
d. intussusception
c
herniations or saclike outpouchings of mucosa from the muscle layer of the intestine that protrude from the intestine
b. most commonly occur in the sigmoid colon.
a. diverticulosis
b. Appendicitis
c. diverticulum
d. diverticulitis
a
asymptomatic diverticular disease
a. diverticulosis
b. Appendicitis
c. diverticulum
d. diverticulitis
d
inflammation / infection of the diverticula.
a. S&S: pain-- most often LLQ pain; fever; leukocytosis
b. can result in abscess formation, rupture and peritonitis if not treated adequately.
c. tx: increase dietary fiber, avoid certain foods (seeds, nuts); sometimes antibiotics, occasionally surgery is required.
a. diverticulosis
b. Appendicitis
c. diverticulum
d. diverticulitis
b
an inflammation most often caused by fecal matter getting caught in lumen of appendix, inviting infection & inflammation; a slight genetic predisposition
b. the most common surgical emergency of the abdomen; treatment is appendectomy.
2. S&S /complications:
1) epigastric or periumbilical pain that then migrates to become RLQ pain.
2) like many inflammatory problems, pain is exacerbated upon movement (patient wants to hold very still)
3) "rebound" tenderness sometimes present.
b. N/V/D, anorexia.
c. fever, leukocytosis
d. if not acted upon quickly, inflammation can spread to peritoneum (the membranous-like covering of abdominal organs), resulting in peritonitis, a potentially life-threatening condition that can lead to sepsis and other complications.
a. diverticulosis
b. Appendicitis
c. diverticulum
d. diverticulitis
b
pain pattern:
1) epigastric or periumbilical pain that then migrates to become RLQ pain.
2) like many inflammatory problems, pain is exacerbated upon movement (patient wants to hold very still)
3) "rebound" tenderness sometimes present.
b. N/V/D, anorexia.
c. fever, leukocytosis
a. diverticulosis
b. Appendicitis
c. diverticulum
d. diverticulitis
a
acute hemorrhagic gastritis
b. esophageal varices - large torturous veins in the esophagus caused by liver disease that can be easily irritated & caused to bleed
c. peptic ulcers
2. S&S that tell you bleeding is coming from UGI area of gut:
a. hematemesis sudden vomiting of blood
1) visible, or "frank" hematemesis (usually seen with acute problems):
a) bright red, usually indicating very acute problem like esophageal bleeding or erosion of artery related to peptic ulcer or can be "coffee ground" hematemesis—brownish-red with flecks, indicating there is acute bleeding but it has had a little more time to be partially digested in the stomach or duodenum
2) occult bleeding-- vomitus looks normal, but actually has small amt of hidden blood from a slower, perhaps chronic bleeding situation
A. Upper GI
B. Lower GI
a
bleeding from esophagus, stomach, duodenum
A. Upper GI
B. Lower GI
a
deposition of excess bilirubin under skin, mucous membranes, sclera of eyes; types (based on the part of the bilirubin cycle that has been altered)—prehepatic, hepatic, posthepatic
a. jaundice (icterus)
b. prehepatic
c. posthepatic, or obstructive jaundice
d. diverticulitis
c
Autoimmue/systemic. bloody stools/diarrhea,
A. Crohn's
B. Ulcerative colitis
C. both
a
ileum, patchy areas, transmural, weightloss, malnurished, thin
A. Crohn's
B. Ulcerative colitis
C. both
b
rectum, confluent, dehydration, non-transmural
A. Crohn's
B. Ulcerative colitis
C. both
b
most common causes:
a. IBD
b. diverticulitis
c. neoplasms
2. S&S that tell you bleeding is coming from LGI area of gut
a. occult bleeding
1) stool may look normal, but actually has small amt of hidden blood from a slower, chronic bleeding situation such as a cancer or diverticulitis.
2) detected by using hemoccult test
b. frank bleeding--_________________________—red blood mixed with stool (would NOT have melena because digestion occurs in upper GI areas, not lower GI.)
A. Upper GI
B. Lower GI
a
normal physiology of bilirubin
1) bilirubin is the product of RBC break-down
2) there is normally a small amount in the blood, but most is excreted as a waste product:
a) in the stool-- gives stool its normal brownish color.
b) in the urine as urobilinogen.
b. if there is an alteration in the normal bilirubin cycle and it accumulates in the blood, the bilirubin is deposited in various pathological places in the body, manifesting as a yellow-green pigment—this condition is called jaundice, AKA icterus.
c. usual pigmented areas: skin, sclera, under tongue, palate of mouth.
d. causes: can be due to several mechanisms, generally grouped into 3 categories according to the part of the bilirubin cycle that has been altered: prehepatic jaundice, hepatic jaundice, and posthepatic (obstructive) jaundice
a. jaundice (icterus)
b. prehepatic
c. posthepatic, or obstructive jaundice
d. diverticulitis
b
occurs because of increase in unconjugated bilirubin (AKA indirect bilirubin)
b. most common causes are hemolytic conditions:
1) increased unconjugated bili occurs when the rate of hemolysis (the breakdown of RBCs) exceeds the liver's ability to handle the bilirubin load-- SO much unconjugated bilirubin is in the blood that the liver cannot conjugate it all.
2) can result in various forms of hemolytic anemia
a) a hemolytic anemia (decreased RBCs due to excess destruction of them) can occur in many situations; example: certain drugs can cause excess breakdown of RBCs
b) another example is hemolytic anemia of the newborn, known as erythroblastosis fetalis; :
a. jaundice (icterus)
b. prehepatic
c. posthepatic, or obstructive jaundice
d. diverticulitis
b
can happen in the second (or more) pregnancy when mother is Rh neg & fetus is Rh pos (and mom didn't receive Rhogam with previous similar pregnancy)—the baby becomes severely jaundiced as the mother's antibodies to the Rh factor hemolyzes the fetus's RBCs.
(2) pathologic vs physiologic prehepatic jaundice:
(a) the jaundice of erythroblastosis fetalis differs from physiologic jaundice, which commonly occurs to some degree in many newborns
(b) physiologic jaundice is due to the immaturity of the conjugating enzyme glucuronyl transferase.
(c) the treatment is UV light therapy, which helps to convert the unconjugated bilirubin to conjugated.
(d) the baby's glucuronyl transferase usually soon matures & takes over this job.
a. jaundice (icterus)
b. prehepatic
c. posthepatic, or obstructive jaundice
d. diverticulitis
b
1) total serum bili high
2) serum indirect bilirubin (ie, unconjugated bili) —high
3) serum direct bilirubin —normal
a. jaundice (icterus)
b. prehepatic
c. posthepatic, or obstructive jaundice
d. diverticulitis
c
blood test results that reflect posthepatic jaundice:
1) total serum bilirubin—high
2) indirect bilirubin—normal
3) direct bilirubin--—high
a. jaundice (icterus)
b. prehepatic
c. posthepatic, or obstructive jaundice
d. diverticulitis
a
1) total serum bili high or normal
2) serum indirect bilirubin (ie, unconjugated bili) —high
3) serum direct bilirubin —low(because the diseased liver cannot conjugate)
a. hepatic jaundice (icterus)
b. prehepatic
c. posthepatic, or obstructive jaundice
d. diverticulitis
c
occurs because of increase in conjugated bilirubin (AKA direct bilirubin) in the blood.
b. liver converts unconjugated bilirubin to conjugated just fine, but there is a problem with the flow of bilirubin actually making its way to the intestines due to an obstruction and/or inflammation (ex-- cholecystitis, choledocholithiasis, tumor of the area, etc)
c. the conjugated bilirubin, having nowhere else to go, "backs up"-- begins to leak from liver cells back into the circulation jaundice.
d. because of this lack of bilirubin getting to the intestines, a hallmark sign of this is stool that is gray-colored (lack of pigment from bilirubin)
a. hepatic jaundice (icterus)
b. prehepatic
c. posthepatic, or obstructive jaundice
d. diverticulitis
a
occurs because of increase in unconjugated bili
b. if hepatocytes are diseased, such as in hepatitis & cirrhosis, the liver cannot conjugate the unconjugated bilirubin that arrives remains in blood as unconjugated= higher-than-normal level of indirect bilirubin in the blood.
c. in addition since it cannot conjugate bili, the conjugated bili will be LOW.
a. hepatic jaundice (icterus)
b. prehepatic
c. posthepatic, or obstructive jaundice
d. diverticulitis
b
inflammation of the gall bladder—is almost always caused by irritation of stones inside the gall bladder itself (cholelithiasis) and/or in a nearby duct such as the common bile duct (choledocholithiasis)
2. patho cholelithiasis / cholecystitis:
a. the stones are caused by situations in which either:
1) cholesterol increases (cholesterol is normal part of bile)
2) there is less water in the body, such as in dehydration
b. result of above situations is formation of small (2-8mm) to large stones (3-4cm) made of cholesterol & bilirubin precipitant.
c. the chemical irritation of concentrated bile in the gall stones causes swelling of the GB & generalized inflammation in the biliary area
a. hepatic jaundice (icterus)
b. cholecystitis
c. posthepatic, or obstructive jaundice
d. diverticulitis
b
pain in the RUQ & epigastric area
1) often manifested as painful spasms/ contractions of the GB & bile ducts called bilary colic
2) most commonly comes on or worsens after high-fat meal (more fat in intestines = more need for bile to emulsify it secretion of bile puts strain on inflamed GB & causes pain)
b. may also have referred pain to the back, above waistline and especially to R shoulder, R scapula.
c. almost always there is nausea & vomiting
d. if a large stones completely blocks common bile duct, may also cause obstructive jaundice & gray stools
a. hepatic jaundice (icterus)
b. cholecystitis
c. posthepatic, or obstructive jaundice
d. diverticulitis
b
risk factors:
a often associated with obesitymore cholesterol in the bile
b. estrogen reduces synthesis of bile acid & increases liver secretion of cholesterol into bilestones more common in women, especially those on contraceptives or have had multiple pregnancies
c. starvation, rapid weight loss can increase "sludge"—thickened mucoprotein
d. may be strong genetic component
e. classically disease is characterized by the 5 "F's"—female, fat, forty, fertile, fair (statistically more typical in whites)
a. hepatic jaundice (icterus)
b. cholecystitis
c. posthepatic, or obstructive jaundice
d. diverticulitis
b
1) often leukocytosis (from inflammation & sometimes infection)
2) high direct bilirubin levels (an obstructive process)
b. other tests: ultrasound (can detect stones as small as 1-2cm), CAT scan
c. there are several treatments, but if the is inflamed enough, the tx of choice is often to remove it (cholecystectomy)
a. hepatic jaundice (icterus)
b. cholecystitis
c. posthepatic, or obstructive jaundice
d. diverticulitis
c
severe, life-threatening disorder associated w/ escape of pancreatic enzymes into pancreas & surrounding tissues, causing autodigestion and hemorrhage
a. cause:
1) can be due to gallstones, in which the pancreatic duct obstruction and/or biliary reflux is believed to activate enzymes in the pancreatic duct system
2) other main cause is alcohol—exact mechanism unknown, but is known to be potent stimulator of pancreatic secretions
a. hepatic jaundice (icterus)
b. cholecystitis
c. acute pancreatitis
d. diverticulitis
c
S&S
1) pain in epigastric area --abrupt onset of post-prandial or post-alcohol- ingestion epigastric pain that is severe and often radiates to the back
2) jaundice may appear because of biliary obstruction/inflammation
c. diagnosis
1) labs-- serum amylase & lipase will be elevated; may also have leukocytosis
2) abdominal CT (CAT scan).
a. hepatic jaundice (icterus)
b. cholecystitis
c. acute pancreatitis
d. pancreatic cancer
d
a. 4th leading cause of death in US—one of most deadly malignancies; risk of getting increases w/age—most occurs 60 to 80 years
b. cause unknown—smoking & diet high in fat, meat, salt, dehydrated foods, fried foods, refined sugars have been linked as major risk factors; may be certain genetic risk
a. hepatic jaundice (icterus)
b. cholecystitis
c. acute pancreatitis
d. pancreatic cancer
d
similar S&S to pancreatitis, but much more insidious onset
1) pain, jaundice, wt loss
2) because so close to common duct & ampula of Vater, tends to obstruct bile flow, so jaundice is frequently presenting symptom
3) but more often than not, by the time the pt presents with it, has metastasized
d. dx—same as pancreatitis
a. cystic fibrosis
b. cholecystitis
c. acute pancreatitis
d. pancreatic cancer
b
inflammation of the liver
a. overview
1) many causes, including autoimmune problems, microbes, idiopathic.
2) spectrum from very mild & self-limiting to causing cirrhosis and death.
3) S&S vary & may include aching, fatigue, malaise, N,V, D, jaundice.
b viral hepatitis: 3 most common strains: A(HAV) , B (HBV), C (HCV)
a. cystic fibrosis
b. hepatitis
c. acute pancreatitis
d. pancreatic cancer
b
S&S have fairly acute onset (fever, malaise, jaundice); course usually mild with full recovery
b) often transmitted enterally; ex-- tainted food such as oysters c) a vaccine is now available for this, but can also get immunoglobulin shot if you haven't been vaccinated & suspect that you have been exposed
a. cystic fibrosis
b. HAV
c. acute pancreatitis
d. HBV and HCV
d
transmitted parenterally (from "outside" the gut) via IV drug abuse, receiving blood, needlestick of infected patient & sexually
b) insidious onset with potentially devastating destruction of liver cells; can exist without S&S for many years while being passed on to others unknowingly
c) vaccine & immunoglobulin available for HBV, but NOT for HCV
a. cystic fibrosis
b. HAV
c. cirrhosis
d. HBV and HCV
c
defined as end-stage, IRREVERSIBLE disease of liver
1) usually begins with some inflammatory initiation, which eventually leads to most of normal architecture of entire liver being destroyed and replaced with fibrous tissue and abnormal nodules
2) causes normal hepatocyte function to cease and disrupts flow in vascular channels & biliary duct systems
3) SOME damage to liver can be reversed—there is a spectrum—but when cirrhosis is finally diagnosed, have reached irreversible stage
4) how well or badly a patient does depends on how much normal tissue is remaining.
a. cystic fibrosis
b. HAV
c. cirrhosis
d. HBV and HCV
c
1) the major, most common cause is excessive ETOH (alcohol) intake; alcohol's toxic metabolites gradually destroy hepatocytes & they are replaced by fibrotic tissue & fat cells
2) toxic reactions to drugs & chemicals (ex—too much acetaminophen overtaxes liver's ability to metabolize it damaged hepatocytes)
3) viral hepatitis (and other microbes)
4) diseases of the bile ducts such as primary biliary cirrhosis (an autoimmune dz) or secondary biliary cirrhosis from obstruction of bile flow—chronic cholecystitis, etc)
5) genetic disorders
a. cystic fibrosis
b. HAV
c. cirrhosis
d. HBV and HCV
c
a) without ____________ liver cannot perform normal metabolic functions & patient will have some or all of the problems / S&S listed below.
b) nutritional problems due to impaired...
(1) production of bile saltsunable to absorb fat & fat- soluble vitamins—will have many vitamin deficiencies, weight loss
(2) fat & cholesterol metabolism, will have impaired synthesis of lipoproteins & altered cholesterol levels
(3) glycogenolysis & gluconeogenesis, may easily become hypoglycemic
a. cystic fibrosis
b. cirrhosis-portal hypertension
c. cirrhosis-diminished hepatocyte function
d. HBV and HCV
c
protein depletion problems
(1) decreased levels of plasma proteins, which contributes to fluid shift problems such as ascites & generalized edema
(2) decreased levels of clotting factors-- fibrinogen, prothrombin, other factors
(a) this is partially due to inability to create these proteins
(b) result-- will tend to bleed easily & labs reflecting clotting times will be abnormal; ex--PT, PTT will be prolonged
(note: contributing to bleeding problems will be thrombocytopenia from splenomegaly [hypersplenism])
a. cystic fibrosis
b. cirrhosis-portal hypertension
c. cirrhosis-diminished hepatocyte function
d. HBV and HCV
c
problems related to metabolic dysfunction:
1) nutritional problems due to impaired:
• bile salt productionmalabsorption of fats & fat-soluble vitamins
• fat & cholesterol metabolism can't synthesize lipoproteins
• ability to create, store, and catabolize glycogen impaired hypoglycemia
2) protein supply impaired:
• cannot produce albumin & other proteins hypoproteinemia ascites & peripheral edema
• clotting factors are proteins, so they too are decreased; liver also unable to process vitamin K; these two problems lead to bleeding dyscrasias prolonged PT & PTT, easy bleeding.
a. cystic fibrosis
b. cirrhosis-portal hypertension
c. cirrhosis-diminished hepatocyte function
d. HBV and HCV
c
3) metabolism of drugs, hormones, & other substances impaired: cannot break down:
• ammonia to urea (normally proteins are catabolized to ammonia then urea then excreted in urine)increased ammonia levels hepatic encephalopathy (confusion, blurred vision, asterixis, szres, coma)
• sex hormones gynecomastia. hirsutism
• cortisol Cushing's
• aldosteroneretention of fluids edema
• drugs increased effect of many drugs
a. cystic fibrosis
b. cirrhosis-portal hypertension
c. cirrhosis-diminished hepatocyte function
d. HBV and HCV
b
1) ascites—back pressure from venous blood that can't flow through the liver (too stiff & obstructive) fluid backs up into small arteries & capillaries of abdomen increased hydrostatic pressure causes fluid to leak into abdominal tissues swollen abdomen
2) splenomegaly due to back-up pressure that is part of portal HTN hypersplenism develops—stasis of blood in enlarged spleen this sequestration results in breakdown of RBCs, thrombocytes, leukopenia anemia, easy bleeding, increased infection risk
3) varices—enlarged veins from back-up pressure of portal HTN; most common are in esophagus & rectal areas (esophageal varices & hemorrhoids)
4) hepatic encephalopathy— caused from high blood ammonia levels & from shunting of blood around liver; many metabolites don't get the normal liver processing because of this shunting accumulate, go to brain.
e. dx of cirrhosis—labs elevated: bilirubin, AST, ALT, ALP; liver bx
f. tx—quit ETOH; put on low protein diet; give diuretics & IV albumin; good nutrition, protect against infection.
a. cystic fibrosis
b. cirrhosis-portal hypertension
c. cirrhosis-diminished hepatocyte function
d. HBV and HCV
b
A patient with cirrhosis has an RBC count of 2 million, and a low platelet count. These are most likely caused by:
a. cellular hemolysis from pancreatitis.
b. splenomegaly secondary to portal hypertension.
c. esophageal varices secondary to portal stricture.
d. cholecystitis due to malfunctioning lithotripsy.
a
The patient in question 1 also has ascites. In reviewing the patient's lab work, the nurse understands that one likely cause of the ascites is: (normal osmolality is 280-295)
a. serum osmolality of 275 due to decreased serum proteins.
b. serum osmolality of 300 due to increased serum proteins.
c. hypernatremia due to decreased levels of aldosterone.
d. hypernatremia due to increased levels of aldosterone.
c
A jaundiced patient has a higher than normal direct bilirubin. The mechanism most likely responsible for this is ________, and a likely responsible disease process is ____________.
a. prehepatic obstruction; erythroblastosis fetalis
b. increased unconjugated bilirubin; hepatitis.
c. posthepatic obstruction; cholelithiasis.
d. transmural intestinal ulceration; Crohn's disease.
d
The nurse caring for a patient with cirrhosis notices signs and symptoms of encephalopathy such as confusion and asterixis. The cause of these is most likely:
a. increased serum lipase.
b. prolonged PT & PTT.
c. decreased conjugated bilirubin.
d. increased serum ammonia.
b
A patient is having melena stools. This is most likely due to:
a. low level of intrinsic factor in the gut.
b. digested blood from a duodenal ulcer.
c. gastroparesis causing slow emptying.
d. hematemesis from PUD.
b
The patient at most risk for an intestinal obstruction would be one who
a. smokes and consumes large amounts of caffeine.
b. is on prolonged bedrest.
c. is eating a low fiber and high fat diet.
d. has diverticulosis.
d
A patient with ulcerative colitis will have
a. a paralytic ileus.
b. patchy area of inflammation of the jejunum.
c. intestinal polyps.
d. hematochezia
d
All the following are consistent with upper GI problems EXCEPT:
a. GERD.
b. H. pylori.
c. esophageal varices.
d. diverticulitis.
a
A patient with choledocholithiasis is likely to have a _______ because_____.
a. high serum direct bilirubin: obstruction of bile duct results in leakage of conjugated bilirubin into the blood.
b. normal level of conjugated bilirubin; prehepatic breakdown of RBCs is unaffected.
c. low serum direct bilirubin: obstruction of bile duct results in leakage of unconjugated bilirubin into the blood.
d. high level of indirect bilirubin: a stone in the bile duct causes bleeding and hemolysis.
lower, gi, bleed, in, stool
lower, gi, bleed, in, stool
a
the cause is in the esophagus, stomach, duodenum (ex- PUD):
a. hematemesis (blood in vomit): either be occult, frankly bloody, or coffee ground (digested blood)
b. stools: occult blood or melena (tarry black = digested blood) Ex. GERD, H. pylori, esophageal varices
A. upper gi
B. Lower gi
b
- the cause is in the jejunum, ileum, large intestines (ex- IBD)- stools can contain occult blood or be frankly bloody (hematochezia) EX. Diverticulitis, IBD, neooplasms
A. upper gi
B. Lower gi
macrocytic, pernicious, gastritis
macrocytic, pernicious, gastritis
b
lab tests specific for liver:
a) elevated indirect serum bilirubin; sometimes also low direct bilirubin
1) patho of high indirect bili: normal level of unconjugated bili enters liverthe diseased hepatocytes cannot conjugate itremains in blood as unconjugated= higher- than-normal level of indirect bilirubin in the blood.
(2) patho of low direct bili: diseased liver cells cannot conjugate bilirubin low serum direct bili.
b) elevated serum liver enzymes: AST (aspartate aminotransferase), ALT (alanine aminotransferase), and ALP (alkaline phosphatase)—all abnormally increase in the blood when hepatocytes are damaged
a. cystic fibrosis
b. cirrhosis
c. diminished hepatocyte function
d. HBV and HCV
b
2) tx of liver disease
a) enhance nutrition & no alcohol
b) reestablish appropriate fluid balance
(1) give diuretics to mobilize fluid from tissue to blood to urine
(2) sometimes give IV albumin to increase protein in blood so water won't be going out from blood to tissues
c) control ammonia - low protein diet & certain drugs can be given
d) protection—against infection, trauma, overdose of drugs
e) liver transplant
a. cystic fibrosis
b. cirrhosis
c. diminished hepatocyte function
d. HBV and HCV
b
splenomegaly—shunting of blood into splenic vein enlarges spleen
(1) syndrome develops called hypersplenism— stasis of blood in the abnormally large spleen causes RBCs, thrombocytes, and WBCs to undergo more breakdown than usual due to their prolonged time in the spleen
(2) sequelae include anemia, thrombocytopenia, leukopenia S&S of fatigue & SOB, easy bleeding / bruising, and/or increased susceptibility to infection.
e) varices—enlarged, thin-walled veins
(1) can occur in esophagus, rectum (hemorrhoids), & umbilicus area
(2) worst one is esophageal varicescan easily rupture & pt can bleed to death from huge outpouring of blood into esophagus.
a. cystic fibrosis
b. cirrhosis-portal hypertension
c. cirrhosis-diminished hepatocyte function
d. HBV and HCV
tachycardia, hyperkalemia, hypolarization
tachycardia, hyperkalemia, hypolarization
a
—"enlarged prostate" proliferation of prostate glandular tissue that is a common age-related change-- begins at age 40-45 and continues until death; by age 60, 60% of men have an enlarged prostate.
b. S&S
1) as the gland enlarges it can compress the urethra where it passes through the prostate, resulting in varying degrees of obstruction to urinary flow.
2) S/S include urgency, delay in starting urine flow, decrease in flow of urine, urine retention
A. benign prostastic hyperplasia (BPH)
B. prostate cancer
C. testicular cancer
D. dysmenorrhea
a
b. S&S
1) as the gland enlarges it can compress the urethra where it passes through the prostate, resulting in varying degrees of obstruction to urinary flow.
2) S/S include urgency, delay in starting urine flow, decrease in flow of urine, urine retention
A. benign prostastic hyperplasia (BPH)
B. prostate cancer
C. testicular cancer
D. dysmenorrhea
a
diagnosis
1) history of S&S
2) enlarged prostate is felt on digital rectal exam (should be done yearly beginning at age 50).
3) sometimes PSA elevated.
d. treatment
1) certain meds geared towards decreasing size of prostate
2) also surgery to decrease size—TURP (transurethral resection of the prostate); a certain amount of hyperplastic tissue is "resected," meaning "surgically removed."
A. benign prostastic hyperplasia (BPH)
B. prostate cancer
C. testicular cancer
D. dysmenorrhea
b
malignant neoplastic condition of the prostate gland
b. the most common cancer in American males.
c. risk factors include age over 50, family history, a diet high in saturated fat, high testosterone levels (promotes tumor growth).
A. benign prostastic hyperplasia (BPH)
B. prostate cancer
C. testicular cancer
D. dysmenorrhea
b
often dx'd by elevated PSA -prostate-specific antigen
1) tumor marker that is specific to the prostate gland and will be elevated when there is an inflammatory or malignant process of the prostateoccurring.
2) this is measured yearly in men over 50 to screen for prostate cancer.
f. yearly routine screening should be done, starting between age 40-50, with PSA and rectal examination of the prostate.
A. benign prostastic hyperplasia (BPH)
B. prostate cancer
C. testicular cancer
D. dysmenorrhea
c
malignant neoplastic condition of the testicle.
b. occurs most commonly in age range 15-35; higher incidence in males with
unresolved cryptorchidism (undescended testes) because a testis that remains in the abdomen cannot be checked regularly for signs of cancer (_________can be detected early when regular self-exam done)
A. benign prostastic hyperplasia (BPH)
B. prostate cancer
C. testicular cancer
D. dysmenorrhea
d
_______________(undescended testes) associated with testicular cancer
A. benign prostastic hyperplasia (BPH)
B. gyncosims
C. dysmenorrhea
D. cryptorchidism
c
S&S
1) painless testicular mass is the usual presenting sign.
2) may have testicular heaviness or dull ache in the lower abdomen.
d. detection / treatment
1) has a cure rate of 95% when caught early; testicular self-exam should be done monthly, for early detection
2) surgery, radiation, or chemotherapy
A. benign prostastic hyperplasia (BPH)
B. prostate cancer
C. testicular cancer
:D. dysmenorrhea
18:30
d
infection
inflammation, discomfort in penis, sometimes dysuria, occasionally a discharge
A. benign prostastic hyperplasia (BPH)
B. prostatitis
C. testicular cancer
D. urethritis
b
infection
inflammation / infection of prostate— same S&S as above.
c. both most often caused by sexually transmitted infections (STIs) such as Chlamydia & gonorrhea.
A. benign prostastic hyperplasia (BPH)
B. prostatitis
C. GU Infection
D. urethritis
a
d. treatment
1) certain meds geared towards decreasing size
2) also surgery to decrease size—TURP (transurethral resection of the prostate); a certain amount of hyperplastic tissue is "resected," meaning "surgically removed."
A. benign prostastic hyperplasia (BPH)
B. prostatitis
C. GU Infection
D. urethritis
c
general term for menstruation that is more painful, frequent, and/or larger in bleeding volume than is normal.
b) most often cause by hormonal disturbances but variety of other causes.
A. benign prostastic hyperplasia (BPH)
B. endometriosis
C. dysmenorrhea
D. amenorrhea
d
absence of menses due to variety of causes (ex—anorexia, over-exercising); in later life can mean onset of menopause
A. benign prostastic hyperplasia (BPH)
B. endometriosis
C. dysmenorrhea
D. amenorrhea
b
__________presence of functioning endometrium outside the uterus.
1) affects 15% of women of reproductive age and can cause infertility.
2) caused by retrograde menstruation: in addition to being sloughed off with the menstrual blood via cervix & vagina, which is normal, endometrial tissue can abnormally escape into pelvic cavity via fallopian tubes
3) this ecotopic (out of place) endometrium responds to the menstrual hormones by proliferating and bleeding wherever it implants itself, just as if it is still in the uterus.
4) S&S include dyspareunia (pain during intercourse), dysmenorrhea, pelvic pain.
5) treatment usually involves hormonal therapy and/or surgery.
A. ecotopic
B. endometriosis
C. dysmenorrhea
D. amenorrhea
a
this ___________(out of place) endometrium responds to the menstrual hormones by proliferating and bleeding wherever it implants itself, just as if it is still in the uterus.
A. ecotopic
B. endometriosis
C. dysmenorrhea
D. amenorrhea
b
4) S&S include dyspareunia (pain during intercourse), dysmenorrhea, pelvic pain.
5) treatment usually involves hormonal therapy and/or surgery.
A. ecotopic
B. endometriosis
C. ovarian cancer
D. amenorrhea
c
malignant neoplastic condition of the ovaries with unknown etiology.
a. causes the most cancer deaths related to the female reproductive system-- by the time someone is diagnosed the cancer is often advanced and treatment is difficult.
b. early S&S very vague—bloating, mild abdominal discomfort, constipation
1) for this reason, if not found early during yearly pelvic exams often metastasizes before can be diagnosed
2) metastasizes intra-abdominally, causing such symptoms as pain, ascites (especially from liver involvement), dyspepsia, vomiting, alterations in bowel movements.
A. ecotopic
B. endometriosis
C. ovarian cancer
D. amenorrhea
31
a
infections
a. reproductive tract—
1) an infection in a woman's reproductive tract is often called ______
2) most often starts with STI (sexually transmitted infection) such as Chlamydia infecting and inflaming the cervix-- cervicitis (other STIs such as gonorrhea can cause PID too, but Chlamydia is most common)
3) infection often then spreads into uterus (endometritis and/or myometritis), fallopian tubes (salpingitis), and ovaries (oophertis) - salpingo-oopheritis = infection of fallopian tubes AND ovaries
4) S&S—varies according to how severe the infection & spread: a)usually abnormal vaginal discharge present
b) pelvic / abdominal pain usually has pattern of being worse with movement, so patient tends to want to be still
5) sequela—can cause infertility; tx—antibx, pain killers
A. pelvicinflammatory disease (PID)
B. endometriosis
C. ovarian cancer
D. amenorrhea
a
3) infection often then spreads into uterus (endometritis and/or myometritis), fallopian tubes (salpingitis), and ovaries (oophertis) - salpingo-oopheritis = infection of fallopian tubes AND ovaries
4) S&S—varies according to how severe the infection & spread: a)usually abnormal vaginal discharge present
b) pelvic / abdominal pain usually has pattern of being worse with movement, so patient tends to want to be still
5) sequela —can cause infertility; tx—antibx, pain killers
A. pelvicinflammatory disease (PID)
B. urologic infection
C. ovarian cancer
D. amenorrhea
b
can involve just bladder (cystitis) and/or kidneys (pyelonephritis) or entire tract (UTI—urinary tract infection)
2) pathogen can be bacterial, fungal, viral, or parasitic (most common organism of infection is E. coli, usually part of normal intestinal flora)
3) highest risk group—women, due to:
a) proximity of anus and vaginal os ("os" = "opening") to the urethral meatus
b) much shorter urethra = shorter distance from outside to urinary tract
4) S&Ss
a) dysuria --pain on urination, frequency and urgency of urination due to irritation on pressure-sensors of bladder; usually small amount of urine voided at a time.
c) hematuria --from irritation / inflammation of bladder and other linings of urinary tract.
d) pyuria--pus in urine; makes urine cloudy, foul-smelling.
e) abdominal & sometimes back pain at costovertebral angle where kidneys are located (if pyelonephritis), sometimes fever
5) dx'd by S&S, UA (urinalysis), and sometimes urine C&S (culture & sensitivity)
A. pelvicinflammatory disease (PID)
B. urologic infection
C. ovarian cancer
D. amenorrhea
b
Mostly Women
S&Ss
a) dysuria --pain on urination, frequency and urgency of urination due to irritation on pressure-sensors of bladder; usually small amount of urine voided at a time.
c) hematuria --from irritation / inflammation of bladder and other linings of urinary tract.
d) pyuria--pus in urine; makes urine cloudy, foul-smelling.
e) abdominal & sometimes back pain at costovertebral angle where kidneys are located (if pyelonephritis), sometimes fever
5) dx'd by S&S, UA (urinalysis), and sometimes urine C&S (culture & sensitivity)
A. pelvicinflammatory disease (PID)
B. urologic infection
C. STI
D. amenorrhea
c
bacterial infection caused by trachomatis; S&S include:1) urethritis in men—inflammation, discomfort in penis, sometimes dysuria, occasionally a discharge
2) most common cause of PID in women (see S&S of PID)
A. gonorrhea
B. genital herpes
C. chlamydia
D. syphilis
a
1) bacterial infection of the genital tracts of men and women caused by Neisseria
2) women may be asymptomatic, or may have vaginal discharge or bleeding, and/or go on to have full PID
3) men tend to have purulent discharge from the penis and dysuria
A. gonorrhea
B. genital herpes
C. chlamydia
D. syphilis
d
STI caused by spirochete Treponema pallidum
2) if treated during first stage, easily treated with antibx, but can become systemic & evolve into other stages if not treated early.
3) course of the disease:
a) 1st stage-- primary: lesions (chancres) of the skin develop anywhere that the microbe touches mucous membranes or skin (lips, labia, penis)
A. gonorrhea
B. genital herpes
C. chlamydia
D. syphilis
b
caused by simplex virus (HSV), subtype 2 (HSV2)
a) HSV 1 invades lips & surrounding area-- sometimes known as having "cold sores"—can be passed on via kissing, but otherwise not considered an STI.
b) HSV 2 is an STI-- invades genital area & can spread to perineum & anus.
(1) infection appears on skin as painful, red, often crusty-looking crops of lesions
(2) break-out episodes occur sporadically and often depend on stress level.
(3) sometimes there are systemic S&S such as fever and malaise during break-out episodes.
2) patho of HSV2
a) after initial infection has resolved, HSV penetrates local nerve fibers & then travels up to spinal ganglion and lies dormant
b) travels "back down" to genital area or to circumoral area periodically, usually in times of stress, & breaks out on skin again.
3) tx--once a person contracts HSV, it is there for life; antivirals can help control S&S, but can't cure it.
A. gonorrhea
B. genital herpes
C. chlamydia
D. syphilis
b
2) patho of HSV2
a) after initial infection has resolved, HSV penetrates local nerve fibers & then travels up to spinal ganglion and lies dormant
b) travels "back down" to genital area or to circumoral area periodically, usually in times of stress, & breaks out on skin again.
A. gonorrhea
B. genital herpes
C. Obstructive disorder
D. syphilis
c
1) anything that interferes with flow of urine from kidneys to urethral meatus can be classified as obstructive disorder
2) most potentially harmful sequela (if obstruction not removed/treated quickly) is hydronephrosis
A. gonorrhea
B. genital herpes
C. Obstructive disorder
D. syphilis
a
connects kidneys to bladder
A. Ureter
B. Urethra
b
connects bladder to outside
A. Ureter
B. Urethra
d
("water on the kidney") is enlargement of & pressure in renal pelvis & calyces due to pathologic accumulation of fluid
b) it is caused by retrograde ("back-up") urinary flow that can't get past an obstruction in ureters, bladder, and/or urethra
c) within a short time this accumulation of urine can lead to infection & eventual fibrosis (scarring & stiffening of tissue), within the kidney & significant decline in function of nephrons
A. gonorrhea
B. genital herpes
C. Obstructive disorder
D. hydronephrosis
obstructions, tumors, scarring, pelvic, prolapse
specific __________(obstructions) (a couple of these are gender-specific; others can happen in either gender equally)
1) ________(tumors)
2) _________(scarring) (called adhesions) from previous problems (eg, STDs, endometriosis. various surgeries) can cause strictures (ie, pinching, narrowing) of ureter and/or urethra.
3) in females: ___(pelvic) organ pelvic organ ______(prolapse)
a) a prolapse is a "falling-down" or intrusion of an organ due to deterioration of muscle tone holding it in place or other factors
b) best example is uterine prolapse (uterus drops from its normal mooring and puts pressure on bladder, urethra, or other structures—acts as obstruction to urine)
a
Obstructive Disorder (uterus drops from its normal mooring and puts pressure on bladder, urethra, or other structures—acts as obstruction to urine)
A. uterine prolapse
B. genital herpes
C. Kidney stones
D. hydronephrosis
obstructive, males, bph, neurogenic, plegia
_______(Obstructive) Disorder in _____(males): ______(BPH)—urine can't get through a urethra narrowed by large prostate (prostate is the obstruction)
5) ______(neurogenic) problems—para_____(plegia), quadriplegia-- neurogenic bladder dysfunction (bladder loses tone—acts as obstruction to urine flowingforward)
stones, calculus, lith
kidney _____(stones)
a) other terms for stone: ______(calculus) (calculi is plural) or "_____(lith);" applications / examples according to area found:
(1) kidney stones = renal calculi = renal lithiasis= nephrolithiasis
(2) ureteral calculus= ureteral lithiasis = kidney stone in ureter
(3) urethral calculus= urethral lithiasis = kidney stone in urethra
c
Risk Factors
(1) male gender (4 times more likely)
(2) having gout: uric acid accumulation or overproduction
(3) dehydration—not drinking enough water, sweating, etc.
(4) various dietary factors
(5) diseases such as multiple myeloma that cause
hypercalcemia
A. uterine prolapse
B. genital herpes
C. Kidney stones
D. hydronephrosis
c
patho:
(1) as urine is formed in the renal tubules it becomes supersaturated with calcium, uric acid, or other ions which eventually bond together and form a type of crystal these can attract each other and form "stones" in kidney pelvis
(2) iare greater than about 2mm, as they flow into the ureter with urine, they can then get stuck in the ureter  obstruction urine backs up, AKA retrograde urine flow  can cause
hydronephrosis & possible renal failure if obstruction
remains.
d) S&S:
(1) excruciating flank and/or groin pain that comes & goes in spasms—AKA colicky pain
(2) presence of hematuria from stone "raking" the ureteral lining
e) dx is based on clinical presentation, hematuria, and diagnostic tools such as CAT scan.
f) tx
(1) pt usually sent home on pain meds & "push fluids instructions" to try to get stone to pass on its own
(2) if too large to pass, lithotripsy done (sound waves bombard & dissolve the stone) or surgery (if other measures not successful)
A. uterine prolapse
B. genital herpes
C. Kidney stones
D. hydronephrosis
c
d) S&S:
(1) excruciating flank and/or groin pain that comes & goes in spasms—AKA colicky pain
(2) presence of hematuria from stone "raking" the ureteral lining
e) dx is based on clinical presentation, hematuria, and diagnostic tools such as CAT scan.
f) tx
(1) pt usually sent home on pain meds & "push fluids instructions" to try to get stone to pass on its own
(2) if too large to pass, lithotripsy done (sound waves bombard & dissolve the stone) or surgery (if other measures not successful)
A. uterine prolapse
B. genital herpes
C. Kidney stones
D. hydronephrosis
a
~95% water and the other 5% contains urea (AKA urea nitrogen), creatinine, a certain amount of Na, K, PO4, & other solutes (also other substances like hormones, etc.) is the
A. Normal urine
B. Abnormal urine
C. Megatrophy Urine
b
glomerulus
a) as blood enters glomerulus from afferent arteriole, it circulates in the glomerular capillaries, which have basement membranes that serve as a screening, or filtration, tool—
A. Normal urine
B. glomerular membrane
C. Bowman's capsule
D. tubular secretion
d
movement of fluids and solutes from the peritubular capillaries (ie, vascular circulation) to the cells lining the tubular lumen, and from there into the tubular lumen
A. Normal urine
B. glomerular membrane
C. Bowman's capsule
D. tubular secretion
c
GFR is an important concept—when a problem or disorder decreases the GFR, we know that the appropriate amount of water and solutes are not being sent into the urine, thus increasing risk of accumulation of wastes & water in the body.
(3) clinically (in patients you are taking care of as a nurse), decreases in GFR often can be seen as
A. Normal urine
B. increased urine output
C. decreased urine output
D. tubular secretion
d
tubular reabsorption
A. movement of fluids and solutes from the tubular lumen into the cells lining the tubular lumen, and from there into the peritubular capillaries to disengage the vascular circulation
B. movement of fluids and solutes from the tubular lumen into the cells lining the tubular lumen, and from there into the glomerular capillaries to join the vascular circulation
C. movement of fluids and solutes to the tubular lumen into the cells lining the tubular lumen, and from there into the peritubular capillaries to join the vascular circulation
D. movement of fluids and solutes from the tubular lumen into the cells lining the tubular lumen, and from there into the peritubular capillaries to join the vascular circulation
high
If kidneys aren't working properly, person would have _____________(high/low) serum creatinine & urea nitrogen
low
If kidneys aren't working properly, person would have _____________ (high/low) urine creatinine & urea nitrogen.
fluid, deficit, angio, 2, aldosterone, retention, na
_____(fluid) _____(deficit) low fluid sensed by the kidneys renin secreted by the JGA (juxtaglomerular apparatus—area around the glomeruli of each nephrons unit)  ultimately stimulates creation of ______(angio)tensin __(2), which stimulates secretion of ___________(aldosterone) by adrenals aldosterone goes to DCT (distal convoluted tubule)causes __________(retention) of ___(Na)+ into the blood, followed by H2O (in exchange for holding onto Na+, the kidney tubules excrete K+)
fluid, oveload, bnp, anp, heart, excrete
_______(fluid) _______(overload) ____(BNP) & _____(ANP) secreted by ____(heart) & go to renal tubules, which are stimulated to _____(excrete) more water into the urine you will void large amounts of more dilute urine (kidneys have gotten rid of water to help your overloaded state)
kidneys, reg, hco3, h, activate, d, erythropoietin
maintenance of certain metabolic functions; the _______(kidneys):
a. greatly affect acid / base balance by:
1) making & ____(reg)ulating ______(HCO3).
2) deciding how much ___(H)+ (acid gang member) to excrete or hold onto
b. help to promote stable nutrition by minimizing non-appropriate substances such as proteins from entering urine.
c. regulate calcium absorption by _________(activate) vitamin __(d)(you get vitamin D from diet, and from effect of sun on skin cells, but still must be activated by kidneys)
d. regulate BP by increasing or decreasing renin as needed (renin begins RAAS response regulates fluid volume and arterial vasoconstriction & therefore has a part in regulating pressure in the arteries).
e. help promote stable hematological status by:
1) making hormones such as __________(erythropoietin), which helps with RBC birth & growth
2) making sure no RBCs "spill" from blood to urine.
gfr, low, aki, ckd
when a person's ___(GFR) and/or waste product secretion ____(low), even a small amount, we consider that person to be at some point on a spectrum from acute kidney injury _____(AKI) to chronic kidney disease ______(CKD)- ie, the spectrum of renal compromise (concept map below).
a
abrupt (occurs over <48hrs) decrease in urine output (ie, GFR) and/or in serum creatinine, so typical patient has acute oliguria and/or acute jump in serum creatinine.
b. the patient can fully recover or can go on to have some degree of kidney problems, often depending on how quickly the problem is caught & fixed.
A. acute kidney injury (AKI)
B. chronic kidney disease (CKD)
C. anemia
D. pruritis
b
S&S include oliguria and often decreased preload S&S such as dry mucus membranes, poor skin turgor.
2) causative factors of the decreased preload include acutely decreased
arterial flow to the kidneys due to:
a) acute vasoconstriction or trauma to aorta and/or renal arteries
b) hypotension / hypovolemia from hemorrhage, dehydration, etc; and /or an inadequate CO
3) prognosis/tx:
a) treatment includes giving fluids and/or fixing other basic problem such as vasoconstriction / heart problem, etc.
b) if NOT reversed fairly early, patient can go into intrarenal
A. acute kidney injury (AKI)
B. prerenal acute kidney injury (AKI)
C. intrarenal acute kidney injury (AKI)
D. postrenal acute kidney injury (AKI)
d
occurs when there is an acute obstruction that occurs somewhere between kidneys & urethral meatus.
1) examples of causative factors:
a) urethral obstruction such as BPH in a man or
uterine prolapse in a woman.
b) ureteral obstruction such as calculi
2) patho/S&S/prognosis of postrenal AKI (THINK OBSTRUCTION)
a) usually acute oliguria plus S&S of the causal problem, such as pain from a kidney stone
b) prognosis for return to normal renal function is good if the obstruction is "fixed" fairly quickly... but if not:
(1) as with any obstruction in the urinary apparatus,
there is a risk of retrograde flow of urine up into the kidneys.
(2) this urine back flow can result in hydronephrosis & intrarenal
A. acute kidney injury (AKI)
B. prerenal acute kidney injury (AKI)
C. intrarenal acute kidney injury (AKI)
D. postrenal acute kidney injury (AKI)
c
1) something goes wrong IN the kidney tissue, leading to ATN, acute tubular necrosis
2) S&S are oliguria, & high serum creatinine, plus casts in UA, and other renal-specific lab changes
3) if not fixed, can go into CKD
A. acute kidney injury (AKI)
B. prerenal acute kidney injury (AKI)
C. intrarenal acute kidney injury (AKI)
D. postrenal acute kidney injury (AKI)
b
1) something goes wrong with arterial flow BEFORE the kidneys
2) S&S include oliguria, plus fluid volume deficit issues
3) if not fixed, can go into intrarenal AKI
& possibly CKD
A. acute kidney injury (AKI)
B. prerenal acute kidney injury (AKI)
C. intrarenal acute kidney injury (AKI)
D. postrenal acute kidney injury (AKI)
d
1) something goes wrong with urine flow AFTER the kidneys
2) S&S include oliguria and S&S of obstruction
3) if not fixed, can lead to hydronephrosis, then intrarenal AKI & possibly CKD
A. acute kidney injury (AKI)
B. prerenal acute kidney injury (AKI)
C. intrarenal acute kidney injury (AKI)
D. postrenal acute kidney injury (AKI)
b
Fluid volume deficit is only involved in
A. acute tubular necrosis (ATN)
B. prerenal acute kidney injury (AKI)
C. intrarenal acute kidney injury (AKI)
D. postrenal acute kidney injury (AKI)
c
2) the kidneys have acutely diminished function from direct kidney tissue; injury; examples:
a) effect of nephrotoxic drugs; poisons & toxins; renal infections
b) autoimmune situations; example here will be post-streptococcal glomerulonephritis (GN)
(1) most often happens in conjunction with recovery from strep throat; antibody that attacked strep then attacks tissues such as glomeruli of kidneys (and/or valves of heart...remember rheumatic heart disease?)
(2) patho: autoantibody attaches to the glomerular membranes  irritates them, begins inflammatory process neutrophils, macrophages infiltrate area inflammatory mediators are released glomerular
capillaries pathologically vasodilate & leak protein & blood into urine.3) no matter what the initial trigger of intrarenal AKI is, the basic problem becomes ischemia to kidney and death to tubules tubular necrosis - this is called ATN--
A. acute tubular necrosis (ATN)
B. prerenal acute kidney injury (AKI)
C. intrarenal acute kidney injury (AKI)
D. postrenal acute kidney injury (AKI)
a
ischemia eventual necrosis of tubules this leads to dead cells of the tubular lining being sloughed off into the lumen of the tubulecasts formation tubular blockage / sluggish urine flow
(2) when there is tubular blockage, it creates pressure on the Bowman's capsule & glomerular capillaries  reduced GFR oliguria & decreased ability to excrete creatinine.
A. acute tubular necrosis (ATN)
B. prerenal acute kidney injury (AKI)
C. intrarenal acute kidney injury (AKI)
D. postrenal acute kidney injury (AKI)
b
S&S scenario: a patient in the hospital following a drug overdose drops urine output from 35ml/hr to 15 ml/hr within 24 hrs, the nurse suspects AKI, because of:
A. the chronic oliguria, lab work shows serum creatinine is high,
(2)the nurse suspects prerenal AKI, because of: the patient's initial dx (drug overdose), the urinalysis (UA) shows casts
B. the acute oliguria, lab work shows serum creatinine is high,
(2)the nurse suspects intrarenal AKI, because of: the patient's initial dx (drug overdose), the urinalysis (UA) shows casts
C. the acute oliguria, lab work shows serum creatinine is low,(2)the nurse suspects intrarenal AKI, because of: the patient's initial dx (drug overdose), the urinalysis (UA) shows casts
D. the acute oliguria, lab work shows serum creatinine is low,(2)the nurse suspects postrenal AKI, because of: the patient's initial dx (drug overdose), the urinalysis (UA) shows casts
c
cause is usually the narrowing or blockage of arteries supplying brain (carotid or vertebral arteries) or intracranial arteries themselves
1) usually related to atherosclerosis and other processes that damage arterial walls, resulting in same process as plaque formation in coronary arteries
2) patho: diminished perfusion to brain tissuecellular ischemia, injury, and/ or infarction (death)inflammatory processswelling, cerebral edemaincreased ICPfurther decrease in perfusion
3) can be thrombotic in nature and/or embolic
a) thrombotic stroke—occurs from a clot or plaque that blocks off the artery in which it has developed & causes ischemia distally.
b) embolic stroke—when fragments that break from an arterial thrombus (as above) & travel "downstream" until they "get stuck" in a smaller
A. diffuse injury stroke
B. TIA transient ischemic attack
C. ischemic brain attack
D. hemorrhagic brain attack
b
can happen in either thrombotic or embolic situation & causes the same S&S as a fully-evolved stroke, but does not damage brain tissue because it is transient, i.e., temporary— resolves itself quickly
2) by definition, S&S from this type only last <24 hours & have no lasting neurologic deficit (some TIAs last less than 5 minutes)
3) however, it are often a warning that more serious, fully-evolved stroke can occur at later date (without tx, 80% of pts with this have full strokes later!)
A. diffuse injury stroke
B. TIA transient ischemic attack
C. ischemic brain attack
D. hemorrhagic brain attack
c
examples of specific potential thrombotic & embolic events:
a) atrial fibrillation (5-fold increase in risk for stroke) disorganized motion of the left atrium allows some incoming blood to pool & promotes stasis  small clots develop in portion of atria break off travel to brain via carotids lodge in a cerebral arteryischemia / infarct to distal tissue
b) atherosclerosis of carotids common place for thrombi to develop; small clots can break off from these & travel downstream.
c) air emboli (usually iatrogenic—ex, during surgery)
d) clots around mitral or aortic valve prosthesis or vegetation from around infected valve
e) intracranial artery plaque can develop in the circle of Willis; if breaks free can lodges in smaller arteries.
A. diffuse injury stroke
B. TIA transient ischemic attack
C. ischemic brain attack
D. hemorrhagic brain attack
d
_______ is usually caused by the effects of blood that leaks out directly onto brain tissue (in most areas of brain there is normally NO blood directly on brain tissue—is carried in arteries & veins, and when arrives at capillary beds, O2 & nutrients diffuse into tissue cells & CO2 & other wastes diffuse out of cells)
2) ex: an intracerebral aneurysm begins to leak blood onto brain tissue  blood irritates the tissue inflammatory processswelling, cerebral edema increased ICPcellular ischemia, injury, and/ or infarction of the surrounding area.
A. diffuse injury stroke
B. TIA transient ischemic attack
C. ischemic brain attack
D. hemorrhagic brain attack
d
the pressure of hypertension
2) weakened arterial walls from atherosclerosis
3) aneurysms-- pts with intracranial aneurysms can remain asymptomatic for many years, but once leakage of blood and/or rupture begins, usually have intense headache and may suddenly lapse into unconsciousness
4) congenital vascular malformations—deformities in the arteries that predispose them to bleed
5) bleeding into a tumor
6) coagulation disorders (ex—hemophilia, excess coumadin, etc) cause:
A. diffuse injury stroke
B. TIA transient ischemic attack
C. ischemic brain attack
D. hemorrhagic brain attack
a
S&S do not depend on whether the stroke is ischemic or hemorrhagic—can't tell from clinical presentation whether a stroke is one or the other.
2) S&S depend on
A. site
B. cause
C. disease
D. containment
diffuse, injury, symmetric
diffuse, injury, symmetric
b
a) being alert or easily arousable to alertness if asleep ("wakeful" areas of brain are ok)
b) being oriented X 4 (self, time, place, events)
c) following commands appropriately
d) having normal speech (speech centers in brain ok)
e) conversing appropriately (cognition, "mental status" ok)
Are signs of
A. site
B. Normal Level of consciousness (LOC)
C. Abnormal Level of consciousness (LOC)
D. containment
c
not being alert: from being lethargic to inability to awaken the patient at all (coma)
b) not oriented to some or all of self, time, place, events
c) doesn't follow commands
d) speech might be garbled or no speech at all
e) verbal responses / conversational efforts show inappropriate or dysfunctional mental status; examples:
(1) confusion - spectrum of severity
(2) behavioral changes such as withdrawal or aggression
Are signs of
A. site
B. Normal Level of consciousness (LOC)
C. Abnormal Level of consciousness (LOC)
D. containment
d
so if there is a focal lesion related to a CN, expect to have asymmetric findings, with the defect manifesting unilaterally on the same side, ie, the ____________ side, of the lesion
A. pyramidal
B. Normal Level of consciousness (LOC)
C. Abnormal Level of consciousness (LOC)
D. ipsilateral
b
--if there is focal cerebral edema around a CN that enervates the right side of the face, you would expect to see a facial defect on the ________________side.
A. left
B. right
b
if there is focal cerebral edema around a right CN that is supposed to cause the normal reflex of the pupil constricting to light, you would expect to see no constriction in the ___________pupil
A. left
B. right
a
corticospinal tracts-- descending (motor) tracts ("cortico"—cortex of brain); also called _________________________ tracts
(a) bundles of long axons that originate in the cell bodies of certain areas of the motor cortex on either side of the brain.
A. pyramidal
B. Normal Level of consciousness (LOC)
C. Abnormal Level of consciousness (LOC)
D. ipsilateral
b
descending (motor) tracts ("cortico"—cortex of brain); also called pyramidal tracts
A. pyramidal
B. corticospinal tracts
C. spinothalamic tracts
D. ipsilateral
b
anatomically, these axons cross over, or decussate from their point of origin in the cerebral cortex to the opposite side of the body at the junction between the spinal cord and brain stem
A. pyramidal
B. corticospinal tracts
C. spinothalamic tracts
D. ipsilateral
c
ascending (sensory) tracts.
(a) carry sensations of pain, temperature, crude and light touch from body to brain (thalamus) for processing.
(b) the spinothalamic tracts cross over from one side of the body to the other side of the brain similar to corticospinal tracts, but in a different area.
A. pyramidal
B. corticospinal tracts
C. spinothalamic tracts
D. ipsilateral
d
if there is a focal lesion related to corticospinal or spinothalamic tracts in the brain, expect to see _______________ sensorimotor changes i.e stroke on the left side would see motor below the shoulder on the right side
A. symmetric
B. corticospinal tracts
C. spinothalamic tracts
D. asymmetric
a
the pathologic changes will usually be unilateral, on the _________________side of the body because of decussation —ie, abnormal findings on the opposite side of the lesion in the brain.
A. contralateral
B. corticospinal tracts
C. spinothalamic tracts
D. asymmetric
b
ex: a patient with a tumor on the right side of the brain would have decreased strength & sensation of arms and legs on the contralateral, or _______________side of the body.
A. right
B. left
a
Above the shoulder injury response we would see injuries on the
A. same
B. opposite (contralateral)
b
Below the shoulder injury response we would see injuries on the
A. same
B. opposite (contralateral)
c
a "positive babinski" reflex (AKA plantar reflex) means that stroking plantar surface of foot makes big toe flex ("upgoing toe").
b) this is normal until after 2 years old; after that, it is a sign of ____________ dysfunction of some sort.
A. cardiac
B. respiratory
C. neurologic
D. asymmetric
d
ex— a patient stops breathing arteries are carrying deoxygenated blood to the brainthe whole brain becomes hypoxic & edematous IIP
2) S&S are seen equally throughout the body, both above & below shoulders:
a) sensation, muscle tone, movement, & strength would be weaker bilaterally & often fairly symmetrically.
b) reflexes weaker, usually symmetrically, and sometimes there is bilateral positive Babinski's.
A. cardiac injury
B. respiratory injury
C. neurologic injury
D. diffuse injury
d
usually see brain stem abnormalities, all due to cerebral edema & IICP putting pressure on brain stem:
a) diminished LOC : most often with brain stem problems, patient is comatose or in near-coma state (see page 333)
b) if patient is comatose, sometimes can see bizarrely abnormal motor responses to stimuli, such as decerebrate & decorticate posturing (pg 338), reflecting effect of cerebral edema on brain stem nuclei.
c) breathing, heart rate and blood pressure changes due to pressure on the medulla, which controls those autonomic functions; example of breathing pattern changes—Cheyne-Stokes (seen in patients in comatose state who are not on ventilator)
d) protective reflexes such as sneezing, coughing, gagging, & swallowing are diminished or lost
e) a variety of other problems such as mixed degree of cranial nerve problems (remember, the CN's originate in the brain stem) such as HR problems when the vagus nerve (CN X) is affected.
A. cerebellar CVA
B. respiratory injury
C. neurologic injury
D. diffuse injury
a
there are usually problems with coordination and balance:
1) vertigo, nystagmus (rapid eye movement).
2) nausea and vomiting .
3) loss of coordination.
4) falling down.
A. cerebellar CVA
B. cerebral hemispheric
C. neurologic injury
D. diffuse injury
b
general patho: lack of blood flow OR bleeding in an area of the left or right of cerebrum results in swelling & edema  S&S are from three possible sets of deficits:
a) sensorimotor deficits caused by lesion / pressure on CNs in / near the affected area in that location
b) sensorimotor deficits caused by lesion / pressure on corticospinal tracts in / near the affected area in that place
AND/OR
b) deficits based on what "special functions" are controlled by that hemisphere.
2) to best assess how a hemispheric stroke has affected sensorimotor status, divide body into longitudinal halves & then consider each half above the shoulders & then separately below the shoulders
A. cerebellar CVA
B. cerebral hemispheric
C. neurologic injury
D. diffuse injury
c
cerebral hemispheric stroke, sensorimotor assessment above the shoulders (eyes, face, tongue, some shoulder function) :
A. (1) what you are assessing: resting nerves (RN) function— ie, is there a lesion in a RN and/or in the cerebral brain tissue around it?
(2) is the lung equal to the rate, tone, movement, strength? If not, consider that there might be a focal problem with a RN.
B. (1) what you are assessing: cardiac nerves (CN) function— ie, is there a lesion in a CN and/or in the cerebral brain tissue around it?
(2) is the pumping equal to the right side in sensation
C. (1) what you are assessing: cranial nerves (CN) function— ie, is there a lesion in a CN and/or in the cerebral brain tissue around it?
(2) is the left side equal to the right side in sensation, tone, movement, strength? If not, consider that there might be a focal problem with a CN.
D. (1) what you are assessing: cranial nodes (CN) function— ie, is there a lesion in a CN and/or in the cerebral brain tissue around it?
(2) is the right side equal to the right side in sensation, tone, movement, strength? If not, consider that there might be a focal problem with a CN.
?
a
(1) what you are assessing: certain parts of the sensorimotor apparatus — the corticospinal tracts & the spinothalamic tracts-- is there a lesion in one of these tracts and/or in the cerebral brain tissue around it?
(2) is the left side equal to the right side in sensation, tone, movement, strength? If not, consider that there might be a focal lesion and/or edema where a corticospinal tract passes through that cerebral hemisphere.
A. sensorimotor assessment below the shoulders
B. sensorimotor assessment above the shoulders
C. assessing deficits that special / specific to each hemisphere
D. diffuse injury
c
in most people, the left hemisphere controls
(a) many aspects of speech, so patient with left hemispheric CVA might have dysphasia or aphasia— general terms referring to varying degrees of inability to comprehend, integrate, and express language
(b) ability to do math, organize, reason, and analyze, so
these faculties might be impaired with left hemispheric stroke.
(2) in most people, the right hemisphere controls
(a) spatiality—where you are in space, & where things are around you; sometimes people with a right hemispheric lesion develop what is called left-sided neglect- a tendency to completely ignore the environment on the left side. (ex—pt won't perceive that there is anything on the left side of a plate of food or that there is a nurse standing on his left)
(b) also is the seat of insight (including insight to his/her disease), creativity, face recognition, musical ability, etc.
A. sensorimotor assessment below the shoulders
B. sensorimotor assessment above the shoulders
C. assessing deficits that special / specific to each hemisphere
D. diffuse injury
a
hemispheric CVA in most people, the right hemisphere controls
A. spatiality—where you are in space, & where things are around you; sometimes people with a right hemispheric lesion develop what is called left-sided neglect- a tendency to completely ignore the environment on the left side. (ex—pt won't perceive that there is anything on the left side of a plate of food or that there is a nurse standing on his left). Also is the seat of insight (including insight to his/her disease), creativity, face recognition, musical ability, etc.
B. many aspects of speech, so patient with CVA might have dysphasia or aphasia— general terms referring to varying degrees of inability to comprehend, integrate, and express language. Ability to do math, organize, reason, and analyze
b
hemispheric CVA in most people, the left hemisphere controls
A. spatiality—where you are in space, & where things are around you; sometimes people with a right hemispheric lesion develop what is called left-sided neglect- a tendency to completely ignore the environment on the left side. (ex—pt won't perceive that there is anything on the left side of a plate of food or that there is a nurse standing on his left). Also is the seat of insight (including insight to his/her disease), creativity, face recognition, musical ability, etc.
B. many aspects of speech, so patient with CVA might have dysphasia or aphasia— general terms referring to varying degrees of inability to comprehend, integrate, and express language. Ability to do math, organize, reason, and analyze
a
A patient is alert and oriented X 4. He is able to smile to command on the left side of his face, but not on the right, which droops a bit—ie, he definitely has facial asymmetry.
(1) where is the focal lesion—right or left hemisphere?
A. right
B. left
a(spatility)
A patient is alert and oriented X 4. He is looking down on a plate but can't see the left side of it, where is the focal lesion—right or left hemisphere?
A. right
B. left
b
If right hand is in a claw like shape the lesion is on the
A. right
B. left
33
c
diagnosis & treatment of brain attack:(1 hour diagnosis)
D.
a. dx made through history of incident, presenting S&S, CAT scan, MRI
1) public is encouraged to use the "act FAST" scale—
A. Face: Ask the person to smile. Does one side of the face droop? Arms: Ask the person to raise both arms. Does one arm drift downward? Speech: Ask the person to repeat a simple sentence. Are the words slurred? Can he or she correctly repeat the sentence? Transfer: If the answer to any of the above questions is yes, transport is important. Don't call 911 just drive.
B. Face: Ask the person to smile. Does one side of the face droop? Air: Ask the person to breath. Sound: Ask the person can they hear. Can he or she hear correctly? Time: If the answer to any of the above questions is yes, time is important. Immediately, call 911 or go to the nearest hospital emergency room. Brain cells are dying.
C. Face: Ask the person to smile. Does one side of the face droop? Arms: Ask the person to raise both arms. Does one arm drift downward? Speech: Ask the person to repeat a simple sentence. Are the words slurred? Can he or she correctly repeat the sentence? Time: If the answer to any of the above questions is yes, time is important. Immediately, call 911 or go to the nearest hospital emergency room. Brain cells are dying.
d
A hemorrhagic stroke may need
A. correct underlying problem such as atrial fibrillation with drugs, etc, thrombolytic drugs (clot-busters) but must be within 2 hours of start of incident ("with a brain attack, time is brain!"), institution of anticoagulant therapy: at first Heparin, then send home on Coumadin
B. t-pa
C. rest
D. may need surgical intervention for certain types of hemorrhagic strokes
a
ischemic stroke
A. correct underlying problem such as atrial fibrillation with drugs, etc, thrombolytic drugs (clot-busters) but must be within 2 hours of start of incident ("with a brain attack, time is brain!"), institution of anticoagulant therapy: at first Heparin, then send home on Coumadin
B. t-pa
C. rest
D. may need surgical intervention for certain types of hemorrhagic strokes
b
2 types
1) f(FAD)—inheritance-linked - can be early onset or late
2) non-hereditary (AKA sporadic)-- late onset—70% of cases
A. seizures
B. Alzheimer's disease
C. Parkinson's disease
D. multiple sclerosis
b
exact cause unknown, but thought to be due to genetic mutation that improperly encodes a normal protein called amyloid end result is accumulation of abnormal amyloid in brainthe abnormal amyloid forms plaque-like material called senile plaques.
2) also, microtubules of neurons in the brain become distorted and twisted and form a neurofibrillary tangle.
3) the amyloid plaques and the neurofibrillary tangle combine to disrupt normal nerve impulses in the brain.
c. clinical manifestations
1) dementia—a type of forgetfulness that is different from normal absentmindedness; emotional upset, behavioral changes
2) if posterior frontal lobe is involved, there are also motor changes such as rigidity, and postural & gait change
A. seizures
B. Alzheimer's disease
C. Parkinson's disease
D. multiple sclerosis
c
is a basal ganglia dysfunction disease caused by unknown source, but suspected to be genetic, viral, or environmental toxin-induced depletion in dopamine
a) a decrease in dopamine tips the scales of balance towards cholinergic, excitatory activity --not actually more acetylcholine, but more effect.)
b) the result of increased cholinergic
effect gives S&S related to hypertonia (rigidity) & dyskinesia (movement disorder)
A. seizures
B. Alzheimer's disease
C. Parkinson's disease
D. multiple sclerosis
c
S&S
1) any dysfunction of the extrapyramidal system (not just Parkinson's, but with any disease process or drug that disorders function of basal ganglia) results in "parkinsonianisms"—ie, characteristic S&S below
2) hypertonia manifestations include
a) overall rigidity, often noticed in the face—mask-like face
b) "cog-wheel rigidity" of forearm
c) dysarthria (difficulty forming words)
d) dysphagia (difficulty swallowing)
3) dyskinesia manifested as
a) involuntary facial & trunk movements such as "Parkinson's tremor"—a pattern of alternating movements between thumb & forefinger described as "pill-rolling"
b) inability to make appropriate posture adjustment when tipping or falling, so walking takes on typical pattern called "basal ganglion gait" AKA "Parkinsonian gait"—stooped, shuffling posture; decreased arm swing
A. seizures
B. Alzheimer's disease
C. Parkinson's disease
D. multiple sclerosis
c
treatment for _________'s— give medication containing dopamine (L-dopa) and anticholinergic medications (benadryl)
A. seizures
B. Alzheimer's disease
C. Parkinson's disease
D. multiple sclerosis
d
relatively common autoimmune disorder, onset between 20 & 50, with male/female ratio 1:2
b. patho overview: previous viral insult has occurred in genetically susceptible person stimulates abnormal immune response in the CNS person's own T-cells attack a myelin protein in brain neurons
A. seizures
B. Alzheimer's disease
C. Parkinson's disease
D. multiple sclerosis
d
inflammation & injury from T-cell attack degenerates the myelin in multifocal areas—this degeneration is known as demyelination & the areas are called demyelinating lesions, or demyelinating plaques
3) depending on degree of demyelination & inflammation, nerve conduction is sporadically blocked or altered over 20 year period or so, there is often scarring and hardening ("sclerosis") of neuroglia (supporting tissue in brain) & deterioration of axons
4) causes progressive loss of functioning, because when axons become demyelinated, they transmit the nerve impulses 10 times slower than normal myelinated ones
A. seizures
B. Alzheimer's disease
C. Parkinson's disease
D. multiple sclerosis
d
S&S
1) overview
a) generally S&S are variable, individualistic, and usually asymmetric, since plaques are unevenly distributed in brain (can be symmetric, but this would be more uncommon)
b) have periods of remission & exacerbation in an irregular fashion, often related to stressors such as heat, cold, and emotional pressures.
2) typical S&S:
a) parasthesia--unusual sensory sensation such as numbness, shooting pains, etc
b) weakness of certain muscles asymmetrically—one leg affected, or one arm, etc.
c) if cerebellum also affected, can have vertigo, incoordination, & ataxia--staggering gait
d) other possibilities (depending on areas of lesions): dysarthria (difficulty speaking due to actual jaw muscle weakness); double vision, bladder control problems
A. seizures
B. Alzheimer's disease
C. Parkinson's disease
D. multiple sclerosis
b
severe episodic headaches that occur in a typical pattern for each person but usually some elements are common:
1) prodrome (S&S before the headache, including an aura, sometimes),
2) headache itself, which is often unilateral and accompanied by N,V, photophobia (light hurts eyes), phonophobia (sound hurts ears)
3) postdrome—washed out, tired, weak.
A. seizures
B. migraines
C. meningitis
D. myasthenia gravis
b
b. patho:
1) exact cause unknown, but thought to be a disorder of blood flow to brain.
2) those who get migraines seem to have hyperreactivity to certain stressful events or to chemicals (wine, chocolate)
3) first phase of migraine: stress  spasm of arteries at base of brain flow to brain reduced platelets begin to clump, releasing serotonin a powerful vasoconstrictor further constrict ischemia to brain (S&S sometimes similar to ischemic stroke at this point)
4) second phase: body senses this decrease in CPP & dilates intracerebral arteries to compensate prostaglandins are part of that dilatory response & they will cause pain; also, the increased blood flow may cause a throbbing sensation.
c. tx—trigger-avoidance, NSAIDS, serotonin-inhibitors like Immitrex.
A. seizures
B. migraines
C. meningitis
D. myasthenia gravis
a
sudden, explosive, disorderly charge of neurons—sudden, transient alteration in brain function
b. can be due to congenital seizure disorder (epilepsy) or to an acute problem in the brain, such as a head injury or stroke
c. classified as general and partial
1) general (used to be called grand mal seizures)
a) can be precipitated by brain irritation due to cerebral edema
b) S&S: patient is ALWAYS unconscious; movement is tonic-clonic --alternating rigidity & contraction of muscles
2) partial—begin locally and can have varied level of unconsciousness
d. post condition
1) a synonym for convulsion is ictus, and the state of a patient following the end of a seizure is sometimes known as post-ictal
2) the patient is often dazed, confusion, and sometimes combative—the brain's "circuits" are still not back to normal.
A. seizures
B. migraines
C. meningitis
D. myasthenia gravis
a
can be precipitated by brain irritation due to cerebral edema
b) S&S: patient is ALWAYS unconscious; movement is tonic-clonic --alternating rigidity & contraction of muscles
A. general seizures
B. partial seizures
C. status epilepticus
b
begin locally and can have varied level of unconsciousness
A. general seizures
B. partial seizures
C. status epilepticus
c
unremitting, not-responsive to medications
A. general seizures
B. partial seizures
C. status epilepticus
c
overview / patho:
` 1) organisms are spread via sneezing, coughing, sharing utensils, etcmicrobe enters highly vascular nasopharyngeal area & crosses into blood blood system takes it to the meninges via the blood-vessel-rich choroid plexus inflammatory process begins that eventually results in increased vascular permeability and edema.
2) can be caused by many different organisms; most common two are viral & bacterial
A. seizures
B. migraines
C. meningitis
D. myasthenia gravis
b
also known as aseptic meningitis— ie, almost never causes sepsis.
2) same basic spread & entry as other meningitis but much milder S&Ss and clinical course than bacterial
A. bacterial meningitis
B. viral meningitis
a
can be caused by several strains of bacteria
a) the most common are meningococcus & pneumococcus
b) these are more virulent and dangerous than the other & cause a worse clinical picture for the patient
A. bacterial meningitis
B. viral meningitis
c
S&S :
a) S&S related to edema:
(1) S&S of edema of meninges surrounding brain are due to the increased ICP:
(a) photophobia (pain in eyes when exposed to light); also can have blurred vision
(b) headache, irritability, restlessness, decreased LOC
(c) nausea & vomiting
(2) S&S of edema of meninges surrounding spinal cord manifest as signs of meningeal irritation:
(a) neck stiffness, also know as nuchal rigidity
(b) positive Brudzinski's and /or Kernig's signs— maneuvers that demonstrate any kind of meningeal irritation
sometimes petechiae and purpura
A. seizures
B. viral meningitis
C. bacterial meningitis
D. myasthenia gravis
c
, but gold standard is lumbar puncture ("spinal tap") -- specimen of CSF obtained and sent to lab for analysis; CSF will show:
a) high WBC count
b) higher-than-normal protein count because of the presence of bacteria and protein exudates (from inflamed meningeal blood vessels & increased vascular permeability)
c) lower glucose than usual, because bacteria is "eating" the glucose
d) blood (there should be no blood in the CSF normally)
A. seizures
B. migraines
C. meningitis
D. myasthenia gravis
b
Overview
1. main category we will study under is neuromuscular junction disorders
2. normal A&P of neuromuscular junction
a. the synapse between neuron and effector muscle is called the neuromuscular junction (NMJ).
b. correct function of the NMJ involves balance of several events at the synapse that result in movement of muscle:
1) release of adequate amounts of acetylcholine from the neuron
2) its subsequent binding to receptors of the effector muscle cell
3) as part of body's "checks and balance" system, cholinesterase is also released at the synapse to break down any extra acetylcholine that isn't used at the receptor sites (cholinesterase is "the clean-up crew")
3. abnormalities
a. anything that decreases acetylcholine production and/ or reception, and/or anything that increases cholinesterase can cause muscle weakness
b. one of most common neuromuscular junction disorders is myasthenia gravis
A. Central nervous system (CNS) disorders
B. Peripheral nervous system (PNS) disorders
C. meningitis
D. myasthenia gravis
d
chronic autoimmune disease sometimes associated with thymic tumor or other changes in thymus (mechanism for this unclear)
b. antibodies produced by the body's own immune system block, alter, or destroy the receptors for acetylcholine
Symptoms are symptomatic
A. Central nervous system (CNS) disorders
B. Peripheral nervous system (PNS) disorders
C. meningitis
D. myasthenia gravis
d
S&S:
a.one of main signs is progressive muscle weakness with motor activity--
1) this is because with each repeating nerve impulse the amount of acetylcholine released usually declines
2) this is normal in everyone-- healthy people have lots of receptors to "pick up" every last drop of acetylcholine
3) in , autoantibodies destroy many of the receptors, so even a "normal" reduction in acetylcholine quickly results in inability to complete nerve transmission to muscle cells.
b. so, hallmark of is muscle weakness that increases during periods of activity and improves after periods of rest
1) this weakness can include muscles that control eye and eyelid movements, facial expression, chewing, talking, and swallowing, and neck and limb movements
2) if affects breathing, called myasthenia crisis
3. tx—anticholinesterase drugs, steroids; sometimes thymectomy helps
A. Central nervous system (CNS) disorders
B. Peripheral nervous system (PNS) disorders
C. meningitis
D. myasthenia gravis
a
pupillary dilation, usually occurs equally in both pupils upon exposure to less light—ie, the less the light, the more the dilation.
b. results from sympathetic nervous system releasing norepinephrine and stimulating alpha-1 adrenergic receptors on iris.
A. mydriasis
B. miosis
C. diplopia
D. nystagmus
b
pupillary constriction, usually occurs equally in both pupils upon exposure to light
b. results from parasympathetic fibers within cranial nerve III (the oculomotor nerve) releasing acetylcholine, which act on receptors on iris.
c. damage (ischemia, increased pressure, etc) to CNIII will cause the loss or diminishing of pupillary constriction abilities, so that pupil will dilate abnormally & will not respond to light (or respond sluggishly).
1) this is an important sign of a neurologic disorder such as increased cranial pressure.
2) it is usually an ipsilateral sign—"same side"--ie, if there is malfunction in the right eye, the source of the problem is on the right side of the brain and/or cranial nerve.
A. mydriasis
B. miosis
C. diplopia
D. nystagmus
c
double vision; caused by a week ocular muscle, neuromuscular disease, cerebral hemisphere diseases, or thyroid disease.
A. mydriasis
B. miosis
C. diplopia
D. nystagmus
d
rhythmic, involuntary, unilateral or bilateral movement of the eyes.
a. can be horizontal or vertical movement.
b. can be congenital or can be a sign of cerebellum or inner ear dysfunction—associated with vertigo and balance problems.
A. mydriasis
B. papilledema
C. diplopia
D. nystagmus
b
edema and inflammation of the optic nerve where it enters the retina.
b this is caused by the blockage of venous return from the retina mainly because of increased intracranial pressure
c. can't be seen by naked eye—have to assess via ophthalmoscope
A. mydriasis
B. papilledema
C. diplopia
D. nystagmus
a
A person diagnosed with meningitis will be at risk for
a. increased intracranial pressure.
b. decreased cerebral edema.
c. a negative Kernig's sign.
d. motor tract decussation.
b
Upon assessing his patient, a nurse notes right-sided hemiparesis and aphasia which began 2 days ago. He therefore thinks it is most likely that the patient has had
a. basal ganglion issues.
b. a CVA involving the left hemisphere of the brain.
c. a brain attack involving the right hemisphere of the brain.
d. a TIA involving the left hemisphere of the brain.
b
A nurse reviewing the drug list of a Parkinson's patient notes that he is on an anticholinergic drug. The nurse knows that the reason for the patient to be on this drug this is most likely:
a. due to risk for increased environmental allergies.
b. to suppress some of the function of acetylcholine in the brain.
c. stimulation of adrenergic receptors in the eyes.
d. to decrease dopamine levels of the brain.
d
A patient with myasthenia gravis is on a drug to block cholinesterase. This drug is most likely being taken to decrease the
a. amount of acetylcholine in neuromuscular junctions.
b. serotonin secreted by platelets.
c. effect of hypertonia.
d. breakdown of acetylcholine in neuromuscular junctions.
d
A patient complains of vertigo, N, V, and nystagmus. Which of the following would be the most likely diagnosis?
a. brain stem stroke.
b. macular degeneration.
c. brain attack of right hemisphere.
d. cerebellar CVA.
b
S&S of unconsciousness, bilateral decerebrate posturing, and Cheyne-Stokes breathing pattern would be typical of:
a. a focal lesion in the right cerebral hemisphere.
b. diffuse increase in ICP.
c. Alzheimer's.
d. multiple sclerosis.
c
A serotonin-blocking drug will most likely to be given in which situation?
a. "I've had a migraine for hours—the pain is killing me."
b. "Nurse Ratchet, this patient is post-ictal."
c. "I'm having a pre-migraine aura, but it's not bad."
d. "My dad's memory is getting worse and worse."
c
CSF testing on a patient with fever and neck stiffness shows a high protein level. This is most likely due to
a. leakage of protein into the CSF from spinal cord injury.
b. edema from an embolic stroke.
c. the presence of bacteria in the CSF.
d. the presence of amyloid in the CSF.
d
Following an illness, a patient becomes hypocalcemic. Which of the following compensatory mechanisms is likely to occur to increase the calcium in her blood?
a. the pituitary will decrease its secretion of T4.
b. the thyroid will increase secretion of calcitonin.
c. a negative feedback mechanism will decrease secretion of parathyroid hormone.
d. a negative feedback mechanism will increase the secretion of PTH.
b
A person with Graves disease likely has all the following EXCEPT:
a. an autoimmune disease
b. Hashimoto's thyroiditis
c. goiter.
d. a heart rate of 120.
a
Lab work is done on a person with Graves disease . The expected findings would be a ___TSH and a _____T4.
a. low; high
b. high; low
c. normal; high
d. high; normal.
c
Lab work is done on a person with Graves disease . The patientgoes into a crisis state, which is called
a. myxedema coma.
b. tetany.
c. thyroid storm.
d. cretinism.
c
Osteopenia is likely associated with all the following EXCEPT:
a. hypercalcemia.
b. hyperparathyroidism.
c. high levels of calcitonin.
d. increased osteoclastic activity.
b
A patient who just came out of general anesthesia has lab work done. The serum osmo is 165. The nurse taking care of this patient suspects that the _____ is due to _________.
a. hyperosmolality: diabetes insipidus (DI).
b. hypoosmolality: syndrome of inappropriate ADH (SIADH).
c. dry mucus membranes: SIADH.
d. shift of calcium into blood: a state of hypopolarization inside the cells.
b
A patient who just came out of general anesthesia has lab work done. The serum osmo is 165. The nurse iwould expect all the following S&S EXCEPT:
a. signs of cerebral edema such as decreased LOC.
b. signs of cerebral cell dehydration such as headache.
c. generalized edema
d. crackles in the lungs upon auscultation.
a
is also know as hypophysis, located in brain near base of skull
2. known as master gland because it secretes many important hormones that govern other glands (including these that we will talk about in our 2 endocrine lectures):
a. antidiuretic hormone (ADH)
b. thyroid-stimulating hormone (TSH)
A. pituitary gland
B. diabetes insipidus
C. syndrome of inappropriate antidiuretic hormone (SIADH)
D. Hyperthyroidism
b
[undersecretion]
a. nomenclature of : means "to pass too much urine;" means "flavorless" (refers to the fact that the urine has no color because it is very dilute)
b. etiology & mechanisms of DI:
1) renal-related etiology: —"sick" kidneys often have a decreased response of renal tubules to ADH
2) CNS-related etiologies:
a) a lesion such as a pituitary tumor causes the gland to diminish its secretion of ADH
b) acute abnormality in the brain such as head injury or other causes of cerebral edema & IICP in the brain can put pressure on the pituitary gland & cause it to diminish ADH secretion
3) whatever the etiology, without the influence of ADH, you won't "hold onto" water effectively --water will indiscriminately flow from the peritubular capillaries of the kidneys into the tubules and becomes very dilute urine
A. pituitary gland
B. diabetes insipidus
C. syndrome of inappropriate antidiuretic hormone (SIADH)
D. Hyperthyroidism
b
S&S (in this general order):
a) you void huge amounts (polyuria) of dilute urine
b) this makes you thirsty, so you drink water, but it just flows right out no matter how much you drink.
c) this translates eventually to your blood compartment having less water  concentration increaseshigher serum osmolality  since the blood now has a higher osmolality than the next door tissue compartment (all over the body), water will be PULLED INTO the blood compartment (and constantly "peed out") leaving the tissue cells dehydrated & shrunken
d) so you have S&S of dehydration eventually, which include: poor skin turgor& dry mucous membranes; t to b
A. pituitary gland
B. diabetes insipidus
C. syndrome of inappropriate antidiuretic hormone (SIADH)
D. Hyperthyroidism
b
1) ectopically-produced (ectopic = "outside usual") ADH such as from small-cell bronchogenic cancer
2) various drugs that effect the brain, especially general anesthetics(sometimes seen in post-op recovery period).
3) trauma to brain such as brain tumors, head injury, etc. (swelling of brain puts pressure on pituitary gland, but can be in opposite way than DI; in in this there is OVERsecretion of ADH.)
A. pituitary gland
B. diabetes insipidus
C. syndrome of inappropriate antidiuretic hormone (SIADH)
D. Hyperthyroidism
c
characterized by abnormally high levels of ADH: you "hold onto" water
too much by abnormally decreasing urination results in increased vascular fluid volume essentially means that water has been added to the blood = diluted plasma compartment & lower serum osmolality small amounts highly concentrated urine.
2) S&S include
a) decreased urine output (oliguria) because
your body is holding onto water inappropriately in the vascular space
b) since the plasma compartment is so dilute now, which way is water PULLED IN when the blood reaches all the tissues? B to T edema
c) S&S are related to the above fluid overload situation, including peripheral & pulmonary edema.
A. pituitary gland
B. diabetes insipidus
C. syndrome of inappropriate antidiuretic hormone (SIADH)
D. Hyperthyroidism
a
more about T3 & T4 hormones:
a. typically, these are the thyroid hormones that are most often mentioned in thyroid disorders; calcitonin is less talked about.
b. their adequate production is very dependent on iodide uptake from blood -- iodide is consumed in our diet (from seafood and iodized salt)
c. T3 & T4 act on receptor cells of many different organs and affect body's:
A. metabolic rate, caloric requirements, oxygen, growth & development, brain & nervous system functions
B. respiratory rate, caloric requirements, carbon dioxide, growth & development, brain & nervous system functions
C. metabolic rate, caloric requirements, oxygen, growth & development, PNS system functions
D. cardiac rate, caloric requirements, oxygen, shrinkage & development, brain & nervous system functions
d
is the state of having excess T3 & T4 production and release
b. the most common cause-- Graves disease:
1) an autoimmune disorder in which autoantibodies attack/stimulate TSH receptors on the thyroid
2) the autoantibodies do this by "mimicking" TSH results in thyroid secreting more T3 & T4
A. pituitary gland
B. diabetes insipidus
C. syndrome of inappropriate antidiuretic hormone (SIADH)
D. Hyperthyroidism
c
the state of having excess T3 & T4 production and release
b. the most common cause--
A. Hypothyroidism
B. exophthalmus
C. Graves disease
D. Hyperthyroidism
d
lab work (this is also part of diagnosis): serum T4 will be higher than normal range and serum TSH will be lower than normal
b. other features of include is one of "overactive" S&S, due to the processes caused by high levels of T3, T4:
1) pysch/CNS—nervous, irritable, tremors, insomnia, emotionally labile, sometimes psychosis (hallucinations, paranoia)
2) cardiovascular—tachycardia, increased afterload, sometimes HF due to increased heart workload
3) GI—increased appetite, diarrhea
4) hair changes
a) hair follicles are very sensitive to your metabolic state & get "stressed" by too much thyroid hormone—hair thins out or falls out (alopecia).
b) like goiters, alopecia can happen in the other one, too, but cause would be different
A. Hypothyroidism
B. exophthalmus
C. Graves disease
D. Hyperthyroidism
b
(bulging eyes from deposits of excess tissue behind eyes) one of the signs of hyperthyroidism
A. Hypothyroidism
B. exophthalmus
C. Graves disease
D. Hyperthyroidism
d
goiter- an enlargement of the thyroid gland that can sometimes be easily visualized; causes:
a) changes occur because the cells are being pathologically stimulated by autoantibodies to increase their thyroid hormone output ("overdrive" = increased size of cells)
(1) the enlargement is a result of overactive cells
7) other body changes:
a) fatigue & weight loss (due to "overdrive" state using up energy), increased body temp & overall heat-intolerance, skin is usually flushed, warm, and damp from excessive sweating.
3. as with most endocrine disorders, hyperthyroidism has an extreme state; it is called thyrotoxic crisis (AKA thyroid storm)
a. this is a hyperthyroid emergency triggered by some stressor such as infection, trauma, surgery, etc
A. Hypothyroidism
B. exophthalmus
C. Graves disease
D. Hyperthyroidism
d
S & S's:
1) neuro: extreme restlessness & agitation; delirium; seizures; coma.
2) circulatory: severe tachycardia, heart failure, shock
3) other: diaphoresis, hyperthermia (103-105 F)
4. treatment:
a. antithyroid meds that inhibit synthesis of thyroid hormones
b. surgery-- thyroidectomy (usually ~ 90 % removed)
A. Hypothyroidism
B. exophthalmus
C. Graves disease
D. Hyperthyroidism
a
is the state of deficient T3 & T4 production and release
b. is one of most common medical disorders in US -- affects 8% of women & 2% of men over 50.
c. caused by loss of functional thyroid tissue from one or more of the following:
1) congenital defects
2) direct removal of tissue (tumor) or direct destruction of tissue (ex-- radiation)
3) autoimmune thyroiditis, (AKA Hashimoto thyroiditis)
a) autoantibodies actually destroy tissue
b) has insidious onset with thyroid tissue slowly replaced by lymphocytes & scar tissue
A. Hypothyroidism
B. exophthalmus
C. Graves disease
D. Hyperthyroidism
b
because of lack of iodide in diet, thyroid hormone synthesis drops
b) can be especially significant in children: because of pregnant mom not getting enough iodide in diet, baby can have congenital hypothyroidism with stunted mental & physical growth--____________
A. Hypothyroidism
B. cretinism
C. Graves disease
D. Hyperthyroidism
a
S&S
a. lab work (this is also part of diagnosis): serum T4 will be lower than normal range and serum TSH will be higher than normal
b. everything HYPOmetabolic:
1) psych/CNS—confusion, slow speech & thinking, memory loss, depression.
2) circulatory—anemia, bradycardia, decreased CO
3) pulmonary—dyspnea, hypoventilation, CO2 retention
4) GI—decreased appetite, constipation
A. Hypothyroidism
B. cretinism
C. Graves disease
D. Hyperthyroidism
a
hair is dry and brittle, and may fall out (alopecia); this is secondary to not having enough thyroid hormone to support metabolic needs of follicles
6) skin :often patient has myxedema: which is due to changes in the dermis that cause water to get trapped under the skin over a period of time, till patient takes on overall puffy appearance, also skin is very coarse and dry.
7) goiter—the enlargement is caused by two factors:
a) hyperplasia & hypertrophy of the tissue as a compensatory response trying to "desperately" increase thyroid hormone secretion
b)inflammation and eventual scar tissue from autoimmune attack
other body changes:weight gain despite decreased appetite, decreased body temp and cold-intolerance, as with most endocrine disorders, has an extreme state; it is called myxedema crisis (or coma).
a. precipitated by stressor such as infection, drug, exposure to cold, trauma
b.manifested by progression of hypothyroid sluggishness & drowsiness into gradual or sudden impaired consciousness and often hypotension and hypoventilation.
4. tx of hypothyroidism most often is synthetic thyroid hormone -- levothyroxine (Synthroid)
A. Hypothyroidism
B. cretinism
C. Graves disease
D. Hyperthyroidism
c
is secreted by the thyroid gland and enhances movement of calcium from blood into bone.
A. Hypothyroidism
B. cretinism
C. calcitonin
D. PTH
d
_______ is secreted by parathyroid gland & stimulates calcium movement
a) this word means movement of a substance back into the circulation from somewhere else; in this case refers to movement of calcium from bone to circulation & is sometimes referred to as "bone resorption"
b) enhances movement of calcium from bone into bloodstream by ncreasing osteoclastic activity (calcium goes from BONE TO BLOOD)
A. osteoclasts
B. cretinism
C. calcitonin
D. PTH
a
________are cells that migrate along the walls of capillaries found in bones
(2) their job is to break down bone cells to free up calcium, which then can move into bloodstream(calcium goes from BONE TO BLOOD)
A. osteoclasts
B. cretinism
C. calcitonin
D. PTH
a
if there is a state of hypocalcemia, or if calcium is needed in other parts of body, PTH secretion is ________ and calcitonin secretion by thyroid is _________ , resulting in increased osteoclastic activity and bringing up serum calcium levels.
A. increased, suppressed
B. suppressed, increased
a
if there is a state of hypercalcemia, or if more calcium is needed in the bone (e.g., for building more bone matrix), calcitonin secretion by thyroid is _______ , and PTH secretion is _____________, resulting in decreased osteoclastic activity and bringing down serum calcium levels.
A. increased, suppressed
B. suppressed, increased
b
general term meaning pathologically "porous bone."
a. normally there is a perfect balance between calcium going into the bone and being used for bone-building by osteocytes, and osteoclastic activity—bone being broken down to release calcium to the blood (resorption).
b. unfortunately, as a part of the aging process & genetics, resorption will slowly increase due to increased osteoclastic activity—ie, osteoclastic break down of bone & movement of calcium into the blood exceeds the bone formation that is maintained by the osteocytes
A. osteoclasts
B. osteoporosis
C. osteopenia
D. PTH
?
b
happens in both genders as they age, but women are much more likely to have problems, due to two factors:
a) women's bones are significantly less dense than men's to begin with
b) menopausal loss of estrogen
(1) bones have estrogen receptors; when stimulated by estrogen, bone-building & maintenance of density results
(2) during and after menopause there is atrophy of ovaries & therefore less estrogen
(3) less estrogen = less bone building balance is tipped toward osteoclastic activitymore resorption than bone-buildingless density
2) a drop in bone density is often categorized according to severity on a spectrum that includes osteopenia & osteoporosis (bone density is calculated by undergoing a bone density scan)
A. osteoclasts
B. osteoporosis
C. osteopenia
D. PTH
c
the condition of having somewhat less than normal bone density
A. osteoclasts
B. osteoporosis
C. osteopenia
D. PTH
b
bone density that is markedly lower than normal
A. osteoclasts
B. osteoporosis
C. osteopenia
D. PTH
b
Hypercalcemia can cause
A. muscle loss
B. kidney stones
C. stroke
D. necrosis
right, atrium, tricuspid, ventricle, pulmonic, valve, artery, arterioles, capillaries, venules, vein, left, atrium, mitral, ventricle, aortic, aorta
_____(Right) ____(atrium),______(tricuspid) valve, right _______(ventricle), _______(pulmonic) _____(valve), pulmonary _______(artery), pulmonary _____(arterioles), pulmonary _______(capillaries) [gas exchange with alveoli occurs here], pulmonary _______(venules), pulmonary _____(vein), _____(left) _______(atrium), ________(mitral) valve, left ______(ventricle) , _____(aortic) valve, ____(aorta)
a
think of right side of heart as
A. venous deoxygenated
B. arterial oxygenated
C. venous oxygenated
B. arterial deoxygenated
b
think of left side of heart as
A. venous deoxygenated
B. arterial oxygenated
C. venous oxygenated
B. arterial deoxygenated
aorta, legs, pedal, arterioles, capillary, venules, veins, inferior
_____(aorta), major arteries in _____(legs) (ileac, femoral, popliteal), ____(pedal) arteries (D.P. & P.T.), ________(arterioles) of tissue beds of legs and feet, ______(capillary) beds [gas exchange here: O2 from blood to tissue, CO2 from tissue to blood], _____(venules), _____(veins) of feet & legs, _______(inferior) vena cava.
c
______ are thin-walled vessels that take deoxygenated blood from tissue beds all over the body back to the right side of the heart/deoxygenated blood in and towards the heart
A. capillaries
B. arteries
C. veins
D. venules
b
most ______ disorders occur in the _____ and usually have to do with some degree of failure to keep entire amount of blood flowing in its proper direction—that is upward, towards the heart
A. arterial, heart
B. venous, legs
C. venous, heart
D. arterial, legs
d
this flow back to the heart is often called "________ " and also sometimes called "venous drainage of tissues."
A. arterial return
B. drainage tank
C. venous lungs
D. venous return
systole, push, venous, towards, heart, open
during ________(systole), when blood is being pushed into arteries by the heart, the systolic pressure is also helping to _______(push) _______(venous) blood back __________(towards) the ______(heart); vein valves in the legs are ____(OPEN) during this time.
2) during diastole, the leg vein valves CLOSE so that blood doesn't back flow & succumb to gravity.
b
_____—oxygenated blood out and away from heart
A. capillaries
B. arteries
C. veins
D. venules
venous, congestion, peripheral
as a result, some venous blood tends to stay and settle out in the veins of the leg and foot tissues—this is known as _______(venous) congestion (think of ________(CONGESTION) of _______(peripheral) tissues when you think of venous insufficiency).
venous, congestion, gravity, incompetence
factors contributing to ______(venous) ________(congestion) include:
1) _______(gravity) "winning"
a) ex-- simply being on one's feet too long can cause gravity to pull fluid downward into distal leg tissues.
b) unless severe, this is a type of venous congestion that is "within normal experience"—ie, not necessarily a pathologic process
2) valve ______(incompetence)-- when this is the problem, a pathology is involved, and the disorder is called venous insufficiency
b
is most often caused by leg vein valves wearing out and becoming "floppy"—they don't close tightly during diastole, allowing backflow into distal veins of legs & feet (venous congestion)
2) this congestion can be pictured as a pool of non-moving blood in the veins this is called venous stasis and results in increased hydrostatic pressure inside the affected veins.
3) this increased pressure pushes fluid into tissues of legs and feet, causing edema in the affected area
a) the edema causes mild to moderate discomfort, but over time can also cause dry, tight skin, often with brownish discolorations
b) sometimes the area becomes so engorged with edema that the skin cells cannot function properly & the tissue easily breaks down (especially over bony prominences such as heels, ankles, coccyx), causing venous stasis ulcers
A. gravity winning
B. chronic venous insufficiency
C. deep vein thrombosis
D. state of lumen
a
this congestion can be pictured as a pool of non-moving blood in the veins this is called venous stasis and results in increased hydrostatic pressure inside the affected veins.
3) this increased pressure pushes fluid into tissues of legs and feet, causing edema in the affected area
a) the edema causes mild to moderate discomfort, but over time can also cause dry, tight skin, often with brownish discolorations
A. chronic venous insufficiency
B. venous stasis ulcers
C. varicose veins
D. state of lumen
29:11
b
sometimes the area becomes so engorged with edema that the skin cells cannot function properly & the tissue easily breaks down (especially over bony prominences such as heels, ankles, coccyx), causing
A. chronic venous insufficiency
B. venous stasis ulcers
C. varicose veins
D. state of lumen
c
increased hydrostatic pressure can also cause such backflow pressures to surface veins that they can become twisted & distorted- ____________; these are not usually a health hazard but can become painful and cosmetically distressing to your patients.
A. chronic venous insufficiency
B. venous stasis ulcers
C. varicose veins
D. state of lumen
d
contributing factors to development of CVI:
A. aging, inherited predisposition, obesity, sometimes pregnancy (especially multiple), and job-related issues (such as years of standing)AND/OR lack of assistance from musculature, such as when there is good muscle tone due to immobility and/or inactivity
B. aging, inherited predisposition, anorexia , sometimes pregnancy (especially multiple), and job-related issues (such as years of standing)AND/OR lack of assistance from musculature, such as when there is poor muscle tone due to immobility and/or inactivity
C. Young , inherited predisposition, obesity, sometimes pregnancy (especially multiple), and job-related issues (such as years of standing)AND/OR lack of assistance from musculature, such as when there is poor muscle tone due to immobility and/or inactivity
D. aging, inherited predisposition, obesity, sometimes pregnancy (especially multiple), and job-related issues (such as years of standing)AND/OR lack of assistance from musculature, such as when there is poor muscle tone due to immobility and/or inactivity
a
a ______ is a clot that develops on the wall of a vein, most of the time in deep veins (not usually surface veins) of thighs & calves 1) once _____ develops, the vein and entire area around vein can become inflamed & swollen, this is called thrombophlebitis ("thrombo"—blood clot; "phleb" means "having something to do with veins")
S&S
a) local redness, pain, warmth, edema (ie, inflammatory signs), usually seen only unilaterally (in one leg), can be extreme or hardly noticeable, also, may have no S&S at all.
A. Deep Vein Thrombosis (DVT)
B. Chronic Venous Insufficiency (CVI)
C. thrombophlebitis
D. None of the above
c
once DVT develops, the vein and entire area around vein can become inflamed & swollen
2) this is called ____________ ("thrombo"—blood clot; "phleb" means "having something to do with veins")
A. Deep Vein Thrombosis (DVT)
B. Chronic Venous Insufficiency (CVI)
C. thrombophlebitis
D. None of the above
a
S&S
a) local redness, pain, warmth, edema (ie, inflammatory signs), usually seen only unilaterally (in one leg), can be extreme or hardly noticeable, also, may have no S&S at all.
A. Deep Vein Thrombosis (DVT)
B. Chronic Venous Insufficiency (CVI)
C. thrombophlebitis
D. Virchow's triad
d
those at highest risk for DVT:
1) have one or more elements of ____________________; this is the
classic triad of:
a) injury to endothelium of vein
b) stasis of blood flow, this can be from an underlying venous disorder such as CVI and/or, inactivity of the muscles surrounding the veins (more on this further on...)
c) hypercoagulability states
A. Deep Vein Thrombosis (DVT)
B. Chronic Venous Insufficiency (CVI)
C. dehydration
D. Virchow's triad
c
hypercoagulability states
(1) most often hypercoagulability is caused by some degree of _______________________ (if there is less water in the blood, blood is more concentrated, so clotting factors & platelets can "find each other" more easily to cause pathologic clotting)
(2) but can also be due to individual tendencies to clot more easily
-- these tendencies are a type of coagulopathy
A. Deep Vein Thrombosis (DVT)
B. Chronic Venous Insufficiency (CVI)
C. dehydration
D. Virchow's triad
d
summary of situations in which one or more elements of __________ is present; people who:
sit a lot or for long periods ("desk jockeys," airline travelers, couch potatoes), have casts or other immobilizing devices on legs, are bed-ridden or wheelchair-bound, are pregnant, are obese, are on medications such as:, diuretics (can cause dehydration), certain hormone therapy like BCPs (estrogen can increase the levels of certain clotting factors)
g) have pre-existing problems such as circulation issues (eg, CVI) and/or clotting problems and/or recent surgery
A. Deep Vein Thrombosis (DVT)
B. Chronic Venous Insufficiency (CVI)
C. dehydration
D. Virchow's triad
b
possible DANGEROUS sequela of DVT: ______
A. Deep Vein Thrombosis (DVT)
B. pulmonary embolus (PE)
C. dehydration
D. Virchow's triad
embolus, arterioles, 30
pulmonary ________(embolus)
1) if thrombus or part of one breaks free from an existing DVT, it can then become a venous embolus; understanding circulatory flow, here is the usual pattern of travel: DVT of leg IVC RARVPAusually gets stuck in tiny pulmonary __________(arterioles)
2) ____(30)% of people with DVT develop PE
3) S&S - chest pain, SOB, hemoptysis (blood in sputum), shock
b
2) 30% of people with DVT develop this
3) S&S - chest pain, SOB, hemoptysis (blood in sputum), shock
A. Deep Vein Thrombosis (DVT)
B. pulmonary embolus (PE)
C. perfusion
D. Virchow's triad
dvt, moving, hydration, elevate, heparin, aspirin
Treatment for _____(dvt):
encourage mobility—get your patients ________(moving)! Also, devices used on patient's legs to keep strong muscle tone around veins, encourage _______(hydration), ________(elevate) legs / feet it increases venous, be careful of skin breaks—swelling / edema increases risk of skin integrity, compromise, sometimes blood thinners like __________(Heparin) & / or Coumadin or sometimes just ______(aspirin) are used to prevent more clotting
arteries, thick, muscled
________(arteries) are ____(thick)-walled, _______(muscled) vessels that accept oxygenated blood from the heart and circulate it to tissue beds all over the body
the ability of arteries to work efficiently in maintaining flow of oxygenated blood from heart to tissues is greatly determined by the muscle tone of their walls and the state of their lumens.
tone, vasomotor, arterial, flexible, bp
muscle _____(tone) of arterial wall —AKA __________(vasomotor) tone
1) part of _______(arterial) walls are made of muscle cells/fibers which respond to various influences and needs of the body
2) these muscular elements can constrict and dilate the artery as needed, and in general maintain a certain muscle tone to the vessel
3) arteries with a normal, good muscle tone are _______(flexible), compliant, not too constricted, not too dilated—"just right."
4) having a good blood pressure (BP) is often dependent on having this "just right" vasomotor of the arteries
lumen, smooth, patent, free
state of _______(lumen)—healthy lumen lining is ___________(smooth) & _________(patent) (open) - ie, ________(free) ofblockage of any sort, so forward blood flow is smooth, uninterrupted.
vasomotor, lumen, perfusion
the above two components (GOOD ______________(VASOMOTOR) TONE and PATENT ______(LUMEN)) contribute to good __________(perfusion) of distal tissues
c
is process of delivery of oxygen and nutrients via arterial system to tissue beds all over body. delivery
A. Deep Vein Thrombosis (DVT)
B. pulmonary embolus (PE)
C. perfusion
D. Virchow's triad
perfusion, output, arterial
good or bad ______(perfusion) results in good or bad tissue oxygenation & is determined by cardiac ________(output) (discussed later) & other factors such as state of ___________(arterial) vessels (ie, do the arteries have good vasomotor tone & patent lumens?).
perfusion, 110/60, 115/70
S&S that are usually associated with good _________(perfusion) (ie, desired findings upon assessment)
1) DESIRED BP range is ~ _______(110/60) to _________(115/70) ("normal" is under 120/80)
2) NORMAL pulses.
a) "pulses" are the pulsations in the arterial system that occur with every heart contraction
b) they can be palpated ("felt") in several areas; most easily felt are:
(1) the carotid pulses in the neck
(2) the radial pulses in the wrist
(3) the pedal pulses: dorsalis pedis (DP) on top of feet & posterior
tibialis (PT) on inner side (medial), next to malleolus (ankle bone)
pulses, carotid, neck, pedal, top, feet
2) NORMAL _____(pulses).
a) "pulses" are the pulsations in the arterial system that occur with every heart contraction
b) they can be palpated ("felt") in several areas; most easily felt are:
(1) the ______(carotid) pulses in the ___(neck)
(2) the radial pulses in the wrist
(3) the _____(pedal) pulses: dorsalis pedis (DP) on _______(top) of ___(feet) & posterior tibialis (PT) on inner side (medial), next to malleolus (ankle bone)
capillary, refill, arterial, equal, 2
NORMAL _________(capillary) ____(refill)-- AKA "nail blanching"
a) how quickly does your ______(arterial) system refill the empty capillaries?
b) normal: < or ____(equal) to ___(2) seconds (means arterial system efficiently refills the capillaries in <2 sec)
a
because commonality of ALL of them is insufficient amount of O2 getting to distal tissue, ie, ischemia.
b. is almost always due to atherosclerosis a process in which arteries become stiffer (sclerosis) and collect fat (athero) and other unwanted substances in their walls.
A. arterial insufficiency
B. venous insufficiency
C. atherosclerosis
D. arteriosclerosis
c
arterial diseases sometimes known as arterial insufficiency because commonality of ALL of them is insufficient amount of O2 getting to distal tissue, ie, ischemia.
b. arterial insufficiency is almost always due to __________________________, a process in which arteries become stiffer (sclerosis) and collect fat (athero) and other unwanted substances in their walls.
A. arterial insufficiency
B. venous insufficiency
C. atherosclerosis
D. arteriosclerosis
d
chronic disease of arterial system usually related to aging, in which artery walls become thick & hardened (sclerose = to harden); etiology:
1) over time, arterial vessels are increasingly damaged by hypertension (HTN), smoking, diabetes, infection, high blood levels of cholesterol, and/or other factors such as genetics, free radicals, and "plain old aging."
2) as the intima (inner lining) of the arterial walls become microscopically damaged, collagen fibers enter the walls & stiffen them (remember, arteries have thick, usually-elastic muscular walls).
3) this process decreases elasticity and compliance of the arteries (thus pathologically altering vasomotor tone.)
A. arterial insufficiency
B. venous insufficiency
C. atherosclerosis
D. arteriosclerosis
c
fatty deposit)-- hence the name that is most often used for arterial disease—________.
2) not only do collagen fibers collect in arteriosclerotic walls, but so do LDLs—they become "fatty deposits."
3) when these fatty deposits enter the arterial wall, the tissue becomes irritated and inflammatory & coagulatory responses are triggered.
A. plaque
B. compromised perfusion (delivery)
C. atherosclerosis
D. arteriosclerosis
a
the combination of stiff arteries, deposits of fat, and inflammatory and clotting responses ultimately leads to formation of a fibrous capsule with a fatty middle section in the wall of the artery— eventually as it grows, the ________ protrudes into the arterial lumen, thus reducing its patency, and often the decreased patency is enough to reduce blood flow to distal tissues
A. plaque
B. compromised perfusion (delivery)
C. atherosclerosis
D. arteriosclerosis
b
because of narrowed, stiff, atheromatous arteries that often have plaques, the end result of most arterial disorders is ________
A. plaque
B. compromised perfusion (delivery)
C. atherosclerosis
D. arteriosclerosis
arterial, disease, vasomotor, loss, non-patent, lumen
commonalities of ________(arterial) _________(disease) in ALL parts of body:
a) alteration in _______(vasomotor) tone - ____(loss) of flexibility & responsiveness—ie, loss of
"just right" status of muscle wall; instead, there is constant constriction & brittleness.
b) __________(non-patent) ______(lumen), due to build-up of blockage material such as fat &
clots in and along arterial walls.
femoral, arteries, calves
when _____(femoral) _______(arteries) are affected there might be pain in _______(calves), especially when patient walks.
arterial, pale, delayed, heal, less, cardiac, urine
_________(arterial) disorder decreased perfusion &ischemia that are specific to the part of the body affected:
a) periphery (mainly arteries in arms, legs)
(1) pulses: diminished/ absent
(2) delayed capillary refill: >2
(3) skin: _____(pale), cool, sometimes mottled or blue-ish (in people of color, pallor not as obvious-- manifests as duskiness under their normal coloring and paleness of mucous membranes.)
(4) sometimes ________(delayed) healing; ex: low perfusion to skin abrasion to skin doesn't ______(heal) because no O2worsens into ulceration (ischemic skin ulcer)
b) heart—altered function, usually _____(less) _______(cardiac) output
c) brain—altered level of consciousness; stroke (a stroke is what happens when brain doesn't get enough O2 & there is brain tissue damage).
d) kidneys—diminished ____(urine) output.
d
some of risk factors of arterial disease:
a. non-modifiable risk factors:
A. diet / obesity /sedentary lifestyle
B. heavy alcohol consumption
C. smoking
D. family history (athero /hypercholesterolemia.)aging
c
modifiable risk factors of arterial disease
A. vasoconstrictor
B. lipodystrophy
C. smoking, heavy alcohol consumption, diet / obesity /sedentary, both diabetes
D. family history (athero /hypercholesterolemia.)aging
b
a characteristic of DM2 in which there is increased circulating LDLs
A. vasoconstrictor
B. lipodystrophy
C. smoking, heavy alcohol consumption, diet / obesity /sedentary, both diabetes
D. family history (athero /hypercholesterolemia.)aging
a
also, nicotine is a powerful
A. vasoconstrictor
B. lipodystrophy
C. smoking, heavy alcohol consumption, diet / obesity /sedentary, both diabetes
D. vasodilator
a
literally a disease of any arterial vessels outside the heart, but the term is most commonly applied to arterial problems of the legs.
b. like all arterial vessel problems, usually manifests as problems of ischemia due to narrowed, peripheral arteries; specifically the S&S are in the legs.
A. peripheral arterial disease(PAD)
B. intermittent claudication
C. hypertension
D. arterial thromboembolic
b
ischemic pain in muscles of legs which sometimes causes limping (the word "claudication" has its roots in the Latin word "claudicare", which means "to limp")
b) exacerbated with exercise & decreases with rest (hence the term"intermittent" )
S&S of ischemia—feet cool & pale, diminished pulses, cap refill >2 secs, no hair grows on legs, skin shiny, ischemic skin ulcers --when skin is not "fed" enough O2, it becomes more fragile & traumatizes easily, The "p's" of PAD—
pain, paresthesia, pallor, pulselessness, poikilothermia
A. peripheral arterial disease(PAD)
B. intermittent claudication
C. hypertension
D. arterial thromboembolic
d
like venous thrombi, arterial thrombi form where flow is sluggish, and/or where there is narrowing of vessels and/or injuries in vessel walls, but there are a couple of major differences having to do with direction of flow
1) when veins get blocked, flow towards the heart is blocked, leading to a type
of back-flow & tissue congestion distal to the blockage.
2) when arteries get blocked, it's a problem of distal tissue ischemia; examples;
a) if there was narrowing / injury / atherosclerosis at bifurcation of femoral arteries, a thrombus might form; what kinds of changes
would you see to the distal tissue (legs & feet)? The "p's" of PAD—pain, paresthesia, pallor, pulselessness, poikilothermia
b) if part of a thrombus that had formed at that bifurcation broke free and became an embolus, where would it travel to?distal feet
A. peripheral arterial disease(PAD)
B. intermittent claudication
C. hypertension
D. arterial thromboembolic
c
the consistent elevation of systemic arterial blood pressure, measured with sphygmomanometer as "blood pressure (BP)", with normal/ optimal being ~110/70 (or at least <120/80
A. peripheral arterial disease(PAD)
B. intermittent claudication
C. hypertension
D. arterial thromboembolic
32:34
b
90/60
A. peripheral arterial disease(PAD)
B. hypotension
C. hypertension
D. arterial thromboembolic
32:34
c
140/90
A. peripheral arterial disease(PAD)
B. hypotension
C. hypertension
D. arterial thromboembolic
d
— uncommon type of HTN; caused by altered hemodynamics associated with a disease process such as an adrenal tumor, renal problems
A. primary hypertension
B. hypotension
C. hypertension
D. secondary hypertension
a
caused by a complex set of factors; also called essential or idiopathic HTN; 92 to 95% of all hypertensives have, 3rd leading cause of death in the world, high dietary intake of sodium  water retention  higher pressure in circulatory system
A. primary hypertension
B. hypotension
C. hypertension
D. secondary hypertension
primary, htn, atherosclerosis, sympathetic, raas
pathophysiology of _____(primary) _____(HTN)
1) primary HTN is linked to many factors in various combinations, but certain
conditions are usually present to some degree:
a) _____(atherosclerosis) and/or
b) overactivity of _______(sympathetic) nervous system and/or
c) overactivity of ______(RAAS)
sympathetic, psych, epine, intra
Primary HTN
overactivity of ______(sympathetic) nervous system
a) for poorly understood reasons, the sympathetic nervous system
becomes chronically overactive.
b) this overactivity can be due to:
(1) overt or subtle, sustained, _______(psych)ological and/or physical stressors ("fight or flight")
AND / OR
(2) genetic predisposition
c) patho:
(1) _____(epine)phrine is consistently "over-released" by _______(intra)cardiac sympathetic nerve fibers à "over-stimulates" beta receptors of heart muscle to "over-increase" HR & contractility (the vigorousness of heart contraction)
(2) the increase in HR & contractility = greater cardiac output & ejection pressure= pathologically larger volume of blood and driving pressure in peripheral arteriesà over time, will cause sustained increase in BP
over, raas, kick, need, overactive
________(over)activity of ______(RAAS) (renin-angiotensin-aldosterone-system) a) NORMALLY, RAAS is a compensatory system that is usually activated when there is a DROP in BP, and the result is vasoconstriction & increased blood volume to increase BP.
b) for poorly understood reasons, instead of being stimulated to "____(kick) in" appropriately when the body _____(need)s it, the RAAS becomes
chronically _______(overactive) thus blood volume & pressure is chronically high.
overactivity, raas, sympathetic, decrease, lumena, intima, increase, inflammation
sequela of these two states of __________________(overactivity) __________(raas), ____________(sympathetic):
a) chronic higher pressures against the blood vessels stimulate arterial smooth muscle to "shore up" against the extra pressure by building up their strength via hypertrophy & hyperplasia à ___________(decrease)s size of arterial ___________(lumenà) increases HTN even more --vicious circle
b) also, bombardment of increased pressure eventually damages ________(intima) (innermost layer) of arteries & arteriolesà inflammatory release of histamine, leukotrienes, prostaglandinsà increases swelling & permeability of intimal endothelial cells _________(increase) _________(inflammation)
htn, neuro, strokes, retina, infarct, protein, urine, heart, attacks
____(htn) most often affects the arterial vasculature of 3 primary systems:
a) ___________(neuro)logical system; some examples:
(1) brain: ______(strokes)—loss of function of parts of brain, in this case would be due to ischemia from the narrowed arterial vessels and high pressures.
(2) eyes: narrowing of the tiny arterioles in the _______(retina), resulting in ischemia & _______(infarct) of parts of retina & often vision changes
b) renal system--the high pressures & damage to renal arteries can eventually cause spilling of blood and/or _________(protein) into _____(urine) (hematuria, proteinuria) and eventually cause renal failure
c) cardiovascular system: increased workload on heart as it tries to eject blood against narrowed, stiff arteries & higher BP can causemultiple types of heart problems, including _______(heart) ________(attacks)
c
a localized dilatation or outpouching of arterial vessel wall
1) atherosclerosis & usually HTN weaken arterial walls, eventually creating bulges in certain areas
2) minute injuries to intimal lining accumulate & allow blood to seep from lumen into layers of arterial muscle and tissue, increasing size of aneurysm and danger of rupture.
A. HTN
B. Deep vein thrombosis
C. aneurysms
D. peripheral arterial disease
aneurysms, brain, weakness, side
areas of typical ___________(aneurysms):
1) _________(brain): if leaks or ruptures, can cause S&S of stroke—_________(weakness) on one _______(side) of body and/or change in level of consciousness and/or sudden horrific headache—many possible S&S
2) aorta: particularly susceptible to aneurysms due to constant stress on vessel wall, especially from the higher pressures of HTN; S&S of aortic aneurysm:
a) if gradually develops & stays small (FYI..."small" means<5cm),
may not have any S&S
b) abdominal aortic aneurysm (AAA)—often found by routine physical exam of the abdomen--a pulsatile mass palpated; sometimes abdominal and/or back pain
c) thoracic aortic aneurysm—usually found accidentally by xray; if any S&S, usually resemble heart attack--chest and/or\
back pain.
aneurysms, aorta, small, 5cm, abdomen, thoracic, accident, xray
areas of typical ________(aneurysms):
1) brain: if leaks or ruptures, can cause S&S of stroke—weakness on one side of body and/or change in level of consciousness and/or sudden horrific headache—many possible S&S
2) ______(aorta): particularly susceptible to aneurysms due to constant stress on vessel wall, especially from the higher pressures of HTN; S&S of aortic aneurysm:
a) if gradually develops & stays_____________(small)(FYI..."small" means<____(5cm)),
may not have any S&S
b) abdominal aortic aneurysm (AAA)—often found by routine physical exam of the ___________(abdomen)--a pulsatile mass palpated; sometimes abdominal and/or back pain
c) _________(thoracic) aortic aneurysm—usually found ___________(accident)ally by ____(xray); if any S&S, usually resemble heart attack--chest and/or\
back pain.
treatment, arterial, stress, smoking, hdl, omega, high
_______(Treatment), nursing implications, of __________(arterial) problems
1. prevention / treatment of HTN, atherosclerosis, and generally any kind of arterial disorder (including coronary artery disease—CAD—which we will discuss in next
section) includes non-medicinal approaches such as to:
?
a. manage _______(stress), stop ____________(smoking), moderate alcohol.
b. keep on nutritious diet with salt in moderation & good management of fat
intake: keep LDL's low; keep ________(HDL)'s & ________(omega)-3 fats __________(high)
?
hdl, high, protein, low, cholesterol, greater, 40, exercise
_______(HDL) is ______(high)-density lipoprotein—______(high) level of _______(protein), _____(low) level of _______(cholesterol).
b) serves as a type of scavenger, "picking up" excess cholesterol from blood vessels & delivering it to liver for processing
c) HDL should be AT LEAST_______(greater) > ___(40) mg/dl
d) best way to raise HDL = ________(exercise); also niacin sometimes.
for, sympathetic, beta-blockers, raas, ace, clots, coumadin
____(for) medicinal approaches (linked to patho):
a. to combat overactivity of ________(sympathetic) nervous system: sometimes ____________(beta-blockers) are given.
b. to combat vasoconstrictive overactivity of ______(RAAS): sometimes _____(ACE) inhibitors (ACEI) are given.
c. to decrease chance of pathologic ______(clots)" sometimes blood "thinners" like aspirin, __________(Coumadin) & Heparin are given.
not, elevate, arterial, harder, flow, ischemia
______(not) it be helpful to _______(elevate) feet (like in venous disease) in someone with peripheral __________(arterial) problem, It would be ____(harder) for arterial ____(flow) to _____(ischemia) areas
a
HR faster than normal, called _______( greater 100beats/min); some possible causes:
A. tachycardia
B. bradycardia
C. dysrhythmia
D. none of the above
a
respiratory rate" (RR) and "normal" is ~ _______breaths per minute
A. 12-20
B. 10-15
C. 21-25
D. 26-30
b
slower than normal, called _________( less 60 beats/min);
A. tachycardia
B. bradycardia
C. dysrhythmia (arrhythmia)
D. none of the above
bradycardia, vagus, acetyl, decrease, hr, ischemia, right
slower than normal, called ___________(bradycardia) (less 60 beats/min); neurohormonal influences of the parasympathetic nervous system (PNS)
a) PNS governs "slower" processes (digestion, urination, etc)
b) related to the heart, the _______(vagus) nerve secretes ______(acetyl)cholineà ______(decrease)s ___(HR)
2) certain electrolyte changes such as hypokalemia causes hyper polarization.
3) _______(ischemia) from a __________(right) coronary artery (RCA) narrowing or blockage—the RCA "feeds" the SA node & AV node in most people.)
4) other situations such as "glitches" in SA node & AV node regulation;
c
rhythm pattern can become irregular instead of normal sinus rhythm
A. tachycardia
B. bradycardia
C. dysrhythmia (arrhythmia)
D. none of the above
dysrhythmia, ischemic, infarcted, electrolyte, age, atrial, ventricular
called _________(dysrhythmia) (or arrhythmia);
a) causes include:
(1) ________(ischemic) or ____________(infarcted) tissue interferes with normal impulse conduction
(2) __________(electrolyte) imbalances, especially related to K+ (hypo & hyper)
(3) ______(age)-related wear & tear of conduction system
b) there are many, many types of dysrhythmias; we will concentrate on _____(atrial) fibrillation & ________(ventricular) fibrillation
atrial, fibrillation, quiver, elderly, 3, long, hypoxic, hf
_____________(atrial) ________(fibrillation)—"Afib" (example of atrial dysrhythmia)
a) a chaotic series of electrical impulses in the atria that cause them to _____(quiver) ineffectively instead of contracting smoothly.
b) fairly common amongst _______(elderly), due to heart disease or simple aging—___(3)% of adult population has chronic atrial fib
c) can occur during acutely ischemic situations but most often begins when myocardium has to endure ___(long)-term ______(hypoxic) strain or a chronic problem such as heart failure ___(HF)
afib, small, significant, decrease, co, no, kick
____(afib) ______(small) but sometimes __________(significant) ________(decrease) in ____(CO); etiology:
(1) usually atria have a small coordinated contraction at the end of diastole—this is called "atrial kick"— helps propel more blood into ventricles before they contract.
(2) when the atria quiver instead of contracting effectively, this can diminish CO to varying degrees because there is ______(no) atrial ____(kick)
?
afib, pooling, arterial, thrombi, emboli, stroke, venous, emboli, lungs
______(afib) _______(pooling) of blood in atria; etiology & sequelae:
(1) if the atria muscles are quivering instead of delivering blood to the ventricles in a coordinated fashion, some blood will remain in the atria & form static pools ("sludge-like")—perfect conditions for thrombi & emboli formation
(2) ________(arterial) ________(thrombi) form in the left atrium & if they get "loose" and become _______(emboli) to brain arteries, patient can have a ______(stroke) (S&S-- weakness on one side of body, confusion, etc, due to ischemia in brain).
(3) ____________(venous) thrombi form in the right atrium & if they get "loose" and become _______(emboli) to _______(lungs), it's called having a pulmonary embolus (S&S-- SOB, hemoptysis, chest pain, shock)
vfib, chaotic, deadly, no, co, death
ventricular fibrillation—"____(Vfib)" (example of ventricular dysrhythmia)
a) a ________(chaotic) series of electrical impulses in the ventricles that cause them to quiver ineffectively instead of contracting smoothly.
b) Vfib is the most __________(deadly) dysrhythmia because results in _______(no) ____(CO) at all; S&S of no CO?_____(death)
stroke, volume, contract, changes, negative
______(stroke) _______(volume) (SV) changes that may pathologically affect CO:
a. ___________(contract)ility ________(changes) that are pathologic would be __________(negative) inotropic changes;
examples:
venous, increased, preload, volume
______(venous) preload changes that can be pathologic
1) ________(increased) ___________(preload) usually = increased blood ________(volume); pathologically this would equate to fluid volume overload & would increase workload on a sick heart.
2) decreased preload usually = decreased blood volume; pathologically this would equate to fluid volume deficit & would eventually decrease CO & BP.
increased, afterload, rv, athero, pulmonary, bronchitis
pathologically ____________(increased) ______________(afterload) makes it harder) for the ventricles) to eject) blood into the receiving arteries:
a) for _____(RV): _____(athero)sclerosis of _____________(pulmonary) artery & branches; lung disorders such as chronic ___________(bronchitis).
b) for LV: atherosclerosis of aorta & systemic arteries; peripheral arterial vasoconstriction; HTN; pathologically high
blood volume
increased, afterload, lv, athero, htn, volume
pathologically ___________(increased) ________(afterload) makes it harder for the ventricles to eject blood into the receiving arteries:
a) for RV: atherosclerosis of pulmonary artery & branches; lung disorders such as chronic bronchitis.
b) for ____(LV): ______(athero)sclerosis of aorta & systemic arteries; peripheral arterial vasoconstriction; ______(HTN); pathologically high
blood _______(volume)
decreased, afterload, lv, vasodilation, shock, anaphylaxis
pathologically ________(decreased) _______(afterload) for the _____(LV) is usually related to massive peripheral arterial ____________(vasodilation), which can result in _____(shock) states. (examples of massive vasodilation that we have seen: septic shock and _____(anaphylaxis)
d
a disorder in which the coronary arteries are narrowed and/or
occluded
A. aneurysms
B. Chronic venous insufficiency (CVI)
C. HF
D. Coronary artery disease (CAD)
cad, elevated, homocysteine, crp,
risk factors and causes of ______(CAD) are HTN & all the same risk factors associated with HTN & atherosclerosis.
3) in addition, risk of getting CAD:
a) increases with ________(elevated) serum levels of __________(homocysteine), an amino acid that can contribute to atherosclerosis via oxidative damage, similar to free radicals (some people are more prone to having higher homocysteine levels than others)
b) has been correlated with an elevated serum C-reactive protein c-reactive protein —______(CRP) is linked to the inflammatory process of plaque formation in the coronary arteries (if you have coronary atherosclerosis, your CRP will likely be elevated.)
cad, plaque, athero, inflam, negative, inotropic, infarction
patho of ______(CAD)
1) as with arterial vascular problems in other parts of the body, ischemia is the primary problem in CAD- coronary vessels are narrowed and occluded by ______(plaque)s, due to the _______(athero)sclerotic / ____(inflam)matory processes.
2) ischemia to cardiac cells is a _________(negative) ________(inotropic) influence on the heart & can lead to decreased cardiac output.
3) if not reversed, ischemia leads to cellular death (necrosis); tissue necrosis in the heart caused by ischemia is known as myocardial ________(infarction)—this is of course an even worse negative inotropic influence.
spectrum, ischemia, mild, reversed, max, infarction
_______(spectrum) of _________(ischemia):
a) various cells in the cardiac tissue can be affected to different degrees and may all be in different stages of O2 deprivation
b) therefore, important to think of the above processes and ability to reverse them as a spectrum:
____________(Mild) ischemia Effect on cells minimal & can be ___________(reversed) by restoring oxygenation. _______(Max)imal ischemia, _________(Infarction) (irreversible)
a
a painful constriction or tightness; in this case it is short for angina pectoris (AKA "chest pain") and refers to ischemic pain in the heart muscle.
A. angina
B. HTN
C. HF
D. Coronary artery disease (CAD)
angina, tightness, 3, 5, exercise, increase, pain
characteristics of classic ______(angina)
a) usually patient often will describe it as _________(tightness), heaviness ("elephant sitting on me"); sometimes burning, indigestion-like; will sometimes place clenched fist over sternum
b) intensity varies according to how much ischemia; ex: "3/10" - significant ischemia..."8-10/10" - full MI.
c) once it comes on, usual duration is ___(3) to ____(5) minutes, and then may go away on its own (though sometimes nitroglycerin is needed to relieve it)
d) as with most ischemic pain, is often exacerbated by _______(exercise) _____(increase) ____(pain)(increased cardiac output needs = increased oxygen needed that can't get to tissue) and lessened by rest.
angina, buildup, lactic, stretching, myocardium, afferent
pathophysiology of _____(angina) perception:
a) ______(buildup) of _____(lactic) acid and abnormal ______(stretching) of ischemic ________(myocardium) irritate myocardial nerve fibers
b) the _______(afferent) sensory nerve fibers in the area transmit the pain impulses to areas of the spinal tract that include C3 to T4
c) the variety of nerve root areas is part of what causes the variation in pain patterns that each individual has & also explains why some patients may have radiation of pain into classic areas such as left arm, jaw, & back
cad, asymptomatic, stable, acs
classifications of _____(CAD) states:
1) CAD status of a person is based on degree of coronary occlusion and ischemia, which is usually reflected in severity of S&S
2) a person with CAD can:
a) be _________(asymptomatic)
OR
b) if they become symptomatic, they belong to one of two categories: ____(stable) or acute coronary syndrome *(acs)
stable, angina, cad, predictable, well-controlled, meds
______(stable) _____(angina)
a. main characteristic of this category of _____(CAD)—pain pattern is very _______(predictable) and ___________(well-controlled) by lifestyle changes, ______(meds), etc.; ex-- "I always feel tightness in the center of my chest when I walk for too long, and it always goes away when I take one NTG"
angina, slowly, ateriogenesis, better, collateral, circulation, better, stable
patho of stable _______(angina)
1) the blockage that causes the angina has developed ______(slowly) and there are no dramatic changes to it.
2) when there is a slow development of plaque in a coronary artery, the steady but small and subtle ischemia to tissues stimulates a compensatory response called ______________(arteriogenesis)
3) the end result of this is the establishment of ______(better) ________(collateral) _________(circulation) composed of new branches of the
coronaries that develop and can "feed" tissue beyond an occluded or nearly-occluded vessel
4) the _______(better) the collateral circulation, the more ______(stable) the CAD.
treat, stable, angina, maximize, patency, nitro, aspirin
________(treat)ment of _____(stable) ______(angina)
1) anything that helps to:
a) ________(maximize) coronary _______(patency) & therefore increase perfusion to myocardium
b) decrease workload of the heart
2) the above accomplished by including treatments such as
a) ________(nitro)glycerin (NTG) under tongue prn (as needed), and/or daily as a patch or an extended release pill à dilates blood vessels so they can bring more oxygen to myocardium
b) ______(aspirin)—acts as anti-inflammatory (remember what an important role inflammation plays in plaque formation!) and decreases platelet adhesion (less clotting = less chance of worsening plaque).
acs, several, flow, blocking, clot, arterial, embolus, plaque
acute coronary syndrome _______(ACS):
a. this is when one of _________(several) possible coronary-artery-____(flow)-________(blocking) situations occurs:
1) sudden _____(clot) development.
2) an ________(arterial) _______(embolus) flows into a narrowed coronary artery
3) an existing _______(plaque) ruptures & its contents fill up the lumen.
b. ACS is manifested as one of two subcategories:
either unstable angina or myocardial infarction (MI):
unstable, angina, worse, nitro, not, work, ekg, shows, blockage
______(unstable) ________(angina)-- when someone with stable angina develops a change for the _____(worse) (usually sudden) in their pattern of S&S
a) usually indicates worsening or change in existing coronary plaques that leads to worsening of ischemia
b) S&S usually include:
(1) a substantial change in pain, such as a patient who usually gets rid of pain with one ___(nitro) ___(not) ______(work) suddenly can make it only marginally better with 3 NTG tabs
(2) ___(EKG) usually ____(shows) acute ischemic changes_____(blockage)
c) patient usually ends up admitted to the hospital, where treatment is still geared towards maximizing coronary patency & perfusion to myocardium and decreasing workload of the heart with acute interventions such as IV NTG, IV morphine, possibly angioplasty, heart surgery, etc.
unstable, angina, ekg, acute, treat, patency, perfusion, iv, surgery
______(unstable) ________(angina)-- when someone with stable angina develops a change for the worse) (usually sudden) in their pattern of S&S
(2) ______(EKG) usually shows ___(acute) ischemic changes
c) patient usually ends up admitted to the hospital, where _______(treat)ment is still geared towards maximizing coronary ________(patency) & ________(perfusion) to myocardium and decreasing workload of the heart with acute interventions such as IV NTG, ____(IV) morphine, possibly angioplasty, heart ______(surgery), etc.
mi, necrosis, severe, pain, ck, troponin, clot-busting
myocardial infarction___(mi)
a) an infarction is when some myocardial cells are starting to undergo _______(necrosis)
b) ***note: though some of the cells have become necrosed, which is irreversible, if the patient is very early into the infarcting process, and interventions are successful, tissue damage can be minimized by preventing more cells from undergoing necrosis --i.e., degree of infarction is part of a spectrum—goal is to stop the infarction early on!
c) S&S usually include
(1) ________(severe), unrelenting ______(pain), with other S&Ss according to artery that is blocked
(2) EKG changes reflecting ischemia & certain degree of necrosis
d) dx based on history & S&Ss and include certain lab test findings that show increases in:
(1) non-specific enzymes that are released by most injured and dying cells, such as creatine kinase __(CK)
(2) specific substance only released by injured and dying myocardial cells--________(troponin). (the higher the serum titer, the more extensive the damage)
e) tx is similar to unstable angina, but even more emergent; also may need _______(clot-busting) drugs.
acs, tachy, brady, dysrhythmia, fatigue, mental, hypo, dyspnea, >2, oliguria
miscellaneous S&S that often occur in ____(ACS) in addition to (or even instead of angina
1) central nervous system (CNS) reaction to pain- N&V, large amount of sweating (diaphresis)
2) variations in HR & rhythm
a) ______(tachy)cardia (from epinephrine -- "fight or flight")
b) _________(brady)cardia (especially if the RCA is blocked SA node would get ischemic & be impaired in generating impulses)
c) ___________(dysrhythmia)s
3) in general with ACS, the worse the ischemia, the worse all the S&S above, and the worse the effect on contractility & CO & therefore on perfusion; S&S of low CO & perfusion:
a) _______(fatigue), weakness
b) ________(mental) status change, deterioration of responsiveness
c) ____(hypo)tension
d) _____(dyspnea)
e) prolonged capillary refill _____(>2) seconds)
f) low) urine) output _______(oliguria)
hypertrophy, cardiomegaly, compensatory, point, continue, hf
________(hypertrophy) leading to ___________(cardiomegaly) (enlarged heart) - increase in size of cells over time due to cells "working harder" to compensate for less oxygen
is an effective _________________(compensatory) mechanism UP TO A _______(POINT)
b) however, if there ____________(continue) to be ischemic stressors and oxygen delivery cannot keep up with oxygen demand of this bigger muscle, decompensatory process may occur, such as heart failure. _____(HF)
b
usually adversely affects "full opening"
2) valve orifice is constricted & narrowed so blood cannot easily flow forward through it.
3) blood flowing through smaller opening generates more turbulence—there is a rumbling sound know as a murmur
A. incompetent (floppy)
B. stenosis
C. HF
D. CAD
a
this problem is also called valvular prolapse, insufficiency or
regurgitation
2) usually adversely affects "full closing"
3) results in regurgitation of blood back into the chamber it came from
4) backflow of regurgitation also can cause turbulence murmur.
A. incompetent (floppy)
B. stenosis
C. HF
D. CAD
c
occurs because of three possible pathologic precipitants:
a) PUMP PROBLEM: heart contractility has been weakened
and /or
b) INCREASED RESISTANCE: there is increased afterload to forward flow.
and /or
c) INCREASED PRELOAD: fluid volume overload (increased preload) has increased heart's workload.
A. incompetent (floppy)
B. stenosis
C. HF
D. CAD
hf, small, co, raas, harmful, work, harder
____(hf)
this results in two general sequelae:
a) diminished/_____(small) ____(CO), so that there is inadequate perfusion of tissues (the body not getting what it needs in terms of O2 & nutrients)
b) eventual problems related to "back-up" of fluid and general problems of fluid overload
3) as CO diminishes, the ________(RAAS) kicks in to try to compensate for what it perceives is a low blood volume problem
a) the RAAS is just trying to do its job, but IN THIS CASE it becomes __________(HARMFUL) to the body.
b) increased preload & afterload MAKE THE ALREADY STRUGGLING HEART HAVE TO _________(WORK) EVEN ________(HARDER) -- the initial problem is just exacerbated.
a
_________ must struggle against high afterload (AKA SVR --systemic vascular resistance) due to
1) HTN
and/or
2) pathologically increased, peripheral arterial, vasoconstriction
and/or
3) narrowed / blocked, systemic arteries.
A. LHF
B. RHF
C. DVT
D. None of the above
b
________ must struggle against high afterload (AKA PVR --pulmonary vascular resistance) due to
1) pathologically increased
pulmonary arterial
vasoconstriction
and/or
3) narrowed / blocked
pulmonary arteries.
and/or
4) lung problems such as
chronic bronchitis.
A. LHF
B. RHF
C. DVT
D. None of the above
hf, ventricle, ischemia, electrolyte, hr, preload
____(hf) _______(ventricle) is weak & has decreased contractility due to:
1) __________(ischemia) or MI,
and/or
2) ________(electrolyte) disturbances
and/or
3) ______(HR) & rhythm probs
is overwhelmed by fluid overload (increased __________((preload).
a
Vasoconstriction of peripheral arterial vessels occurs in an attempt to keep blood circulating in the central areas of the heart, brain, kidneys  further increase in afterload
A. LHF
B. RHF
C. DVT
D. None of the above
b
Increased aldosterone body "hangs on" to Na & therefore also hangs on to water  increase in preload --ie, worsening fluid overload occurs.
A. LHF
B. RHF
C. DVT
D. None of the above
a
general S&S of decreased CO; include:
fatigue, weakness, mental status change, deterioration of responsiveness, hypotension, dyspnea, prolonged capillary refill (>2 seconds), low urine output, S&S of fluid backup into lungs (lung congestion, ie, lung edema):pulmonary edema
A. LHF
B. RHF
C. DVT
D. None of the above
lhf, edema, crackles, hemoptysis, orthopnea, up, rr, low, so2
_____(lhf)
S&S of pulmonary _____(edema):
(1) ______(crackles) upon auscultation of lungs, cough, often with frothy blood-tinged sputum __________(hemoptysis), the froth is due to air mixed with fluid, the blood-tinged or pink color is due to back pressure pushing fluid and some RBCs into alveoli.
__________(orthopnea)--SOB upon lying down;
____(up) respiratory rate ______(RR)
_____(low) ____(SO2) (oxygen saturation)
b
S&S of decreased CO, S&S of fluid backup into periphery (i.e, peripheral edema):: jugular venous distention JVD
(2) liver congestion, so enlarged liver
(3) ascites --the state of extra fluid in the abdominal cavity due to fluid being pushed out of engorged abdominal
veins; think of this as a type of edema of the abdominal cavity
(4) edema of legs & feet.
A. LHF
B. RHF
C. DVT
D. None of the above
c
RHF due to a lung disease(Pulmonary Vascular Resistance)
A. Ischemia
B. pneumonia
C. Cor Pulmonela
D. Dyspnea
lung, congestion, caused, lhf
_______(Lung) __________(congestion) (pulmonary edema) is ________(caused) by _____(LHF) and its retrograde ("back-up") flow.
lung, congestion, causes, rhf
_______(Lung) _______(congestion) (such as in chronic bronchitis) _____(causes) ______(RHF) & retrograde venous flow.
treat, hf, positive, inotropic, vasodilator, diuretics
______(treat)ment of ___(HF):
1) to increase strength of "pump" & thus increase forward blood flow:
a) _____(positive) ______(inotropic) drugs such as digoxin
b) also, may need to decrease heart rate if too high so that workload of heart is lessened.
2) to help decrease resistance to forward flow (afterload —SVR & PVR) give ______(vasodilator) drugs such as NTG and ACE inhibitors
3) to help decrease preload give ______(diuretics) (remember, it is the characteristics of hanging on to fluid & back-up of fluid that give heart failure its often-used label of "congestive"—heart failure almost always has fluid overload as a main component, so diuresis is key part of treatment.)
b
an abnormally __________serum BNP level confirms that HF is occurring
A. small
B. elevated
C. normal
D. micro
c
A patient has intermittent claudication and a history of atherosclerosis. What other findings are most likely?
a. pitting edema of the ankles.
b. jugular vein distention.
c. cool feet with diminished pulses.
d. S&S of increased preload.
d
A patient is diagnosed with venous insufficiency. What treatment is most likely and why?
a. tissue plasminogen activator (tPA), because it is used to dissolve arterial clots.
b. drop the legs lower than the heart so that circulation can bypass DVTs.
c. complete bedrest, as venous stasis is the best way to prevent thrombosis.
d. elevation of feet as often as possible, because it enhances venous return.
b
A patient with a history of atherosclerosis and HTN is complaining of chest pain, SOB, and pain radiating to his left arm. He is diagnosed with an MI of his left ventricular wall.
3. What S&S would be expected and would indicate decreased CO /perfusion?
a. ankle edema and varicose veins.
b. oliguria and capillary refill of 4 seconds.
c. BP of 190/90 and capillary refill of 2 seconds.
d. bounding DP & PT pulses.
?
a
A patient with a history of atherosclerosis and HTN is complaining of chest pain, SOB, and pain radiating to his left arm. He is diagnosed with an MI of his left ventricular wall
Lab work done during the MI most likely shows high blood levels of certain substances, including:
a. troponin.
b. BNP.
c. histamine.
d. inotropes.
d
A patient with a history of atherosclerosis and HTN is complaining of chest pain, SOB, and pain radiating to his left arm. He is diagnosed with an MI of his left ventricular wall. He develops a blood pressure of 80/50. Which statement is most accurate?
a. The patient is in cardiogenic shock and should be given meds to increase SVR.
b. The patient should be given a negative inotrope, as this will cause vasodilation.
. c. The patient is hypotensive and should be given large volumes of fluid.
d. The patient is in cardiogenic shock and should be given a positive inotrope.
d
A patient with a history of atherosclerosis and HTN is complaining of chest pain, SOB, and pain radiating to his left arm. He is diagnosed with an MI of his left ventricular wall.
Several days later the patient manifests S&S of heart failure. Given the area of his heart involved in the MI, which are the most likely S&S?
a. increased preload & ankle edema.
b. decreased afterload & intermittent claudication.
c. tricuspid regurgitation & right atrial hypertrophy.
d. shortness of breath and lung crackles.
b
A patient with a history of atherosclerosis and HTN is complaining of chest pain, SOB, and pain radiating to his left arm. He is diagnosed with an MI of his left ventricular wall.
When the patient was suspected of developing the heart failure (HF), lab work was drawn that specifically corroborated the diagnosis of HF by showing that the ______was elevated.
a. CRP.
b. BNP.
c. CK.
d. RBC.
c
A 40-year-old man is undergoing a yearly physical. Everything is fine except that the nurse practitioner hears a murmur. All the following are likely etiologies EXCEPT:
a. pulmonic valve insufficiency.
b. a heart valve that is ischemic from a coronary artery blockage.
c. incompetent venous valves.
d. a stenotic mitral valve.
c
A patient with CAD reports that he gets angina only when he walks more than a mile. It always goes away when he rests or takes a NTG. Which statement best fits this patient?
a. He has unstable angina due to worsening of an atherosclerotic plaque.
b. He has ACS that is stable due to development of collateral circulation over time.
c. He has stable angina due to development of collateral circulation over time.
d. His pain is caused by increased preload from venous congestion.
d
A patient with CAD reports that he gets angina only when he walks more than a mile. It always goes away when he rests or takes a NTG.
The patient in the question above is on medications. All the following are likely EXCEPT that he takes
a. NTG to maximize coronary artery patency.
b. NTG to dilate coronaries.
c. aspirin to prevent inflammation that leads to increased plaque formation.
d. negative inotropic medications.
d
A patient in atrial fibrillation has an increased likelihood of
a. no cardiac output and dying immediately.
b. an arterial embolus to the lungs.
c. a venous embolus to the brain.
d. a thromboembolic event.
a
Lab work done on a heart patient shows a potassium of 5.5 (normal = 3.5 - 5.0). The patient is at risk for
a. ventricular fibrillation because his heart cells will be more irritable.
b. bradycardia because his heart cells will be more sluggish.
c. atrial fibrillation because he will be in heart failure.
d. increased afterload for the left ventricular because of systemic vasoconstriction.
b
A patient has a DVT of the right calf. Which of the following is the LEAST LIKELY to develop?
a. Pain at the DVT site.
b. Loss of pulse in right foot.
c. Erythema of the skin in the local DVT area.
d. Shortness of breath.
d
14. An otherwise healthy patient has had hypertension (HTN) for many years. Which of the following is most likely true?
a. He has secondary hypertension.
b. Etiologic factors of the HTN include epinephrine depletion.
c. The atrial natriuretic peptide system is in overdrive.
d. Etiologic factors of the HTN include pathologic overaction of the RAAS.
a
A patient with chronic bronchitis says: "Look how swollen my legs and feet and belly are. This has been increasing over the last couple of years. What's going on?" As his nurse, you would most likely suspect that the patient has all the following EXCEPT
a. edema from LHF.
b. cor pulmonale.
c. ascites from RHF backflow.
d. venous backflow from increased PVR.
b
A patient in the hospital is recovering from hip surgery.
She begins to complain of chest pain and dyspnea. Her RR is 30. A lung scan is performed and the V/Q ratio is reported to the nurse as "high." This patient has most likely suffered a(n)
a. MI.
b. pulmonary embolus.
c. atelectasis.
d. episode of pulmonary edema.
c
A patient in the hospital is recovering from hip surgery.
She begins to complain of chest pain and dyspnea. Her RR is 30.
Arterial blood gases (ABGs) are drawn. The results are: pH: 7.50; PaO2: 100; PaCO2: 29; HCO3: 26. This altered state is called
PCO2: 35-45, PO2: 80-100, HCO3: 22-26, SO2: 97-100
a. respiratory acidosis
b. metabolic acidosis
c. respiratory alkalosis.
d. metabolic alkalosis.
b
A patient in the hospital is recovering from hip surgery.
She begins to complain of chest pain and dyspnea. Her RR is 30. Arterial blood gases (ABGs) are drawn. The results are: pH: 7.50; PaO2: 100; PaCO2: 29; HCO3: 26.
PCO2: 35-45, PO2: 80-100, HCO3: 22-26
What mechanism is causing the disturbance noted?
a. Hypoventilation
b. Hyperventilation
c. Hemoptysis.
d. Orthopnea.
c
A child with laryngotracheobronchitis is likely to
a. have stridor from trying to exhale air from inflamed alveoli.
b. develop a walled-off area of viral infection in the laryngeal area.
c. have stridor from trying to inhale air through inflamed bronchi.
d. need a warm mist treatment.
d
A victim of a stab wound to the chest develops a pneumothorax. Which type of pneumothorax is most likely in his case?
a. Consolidative.
b. Tension
c. Bronchial
d. Open
a
A common denominator of a bed-ridden nursing home patient and an unconscious alcoholic is their high risk for
a. aspiration pneumonia.
b. bronchogenic carcinoma.
c. nosocomial pneumonia.
d. miliary tuberculosis.
c
The nurse taking care of a pulmonary patient notes that he is very thin and barrel-chested, has a respiratory rate of 28, and uses accessory muscles to breathe.
The nurse thinks it is most likely that the patient's S&S are due to
a. chronic bronchitis.
b. a VQ ratio.
c. emphysema.
d. Kussmaul respirations.
d
The nurse taking care of a pulmonary patient notes that he is very thin and barrel-chested, has a respiratory rate of 28, and uses accessory muscles to breathe.
An arterial blood gas report shows pH = 7.50, PCO2 = 32, PO2= 90, SO2= 92% HCO3 = 26.
PCO2: 35-45, PO2: 80-100, HCO3: 22-26
These numbers mean the patient
a. is in metabolic alkalosis.
b. has hypercapnia, which is his normal state of compensation.
c. is probably in respiratory failure.
d. is probably in his normal state of compensatory hyperventilation.
b
A patient complains of a one-week history of fever, cough, and purulent sputum. The nurse listening to the patient's lungs notes greatly diminished breath sounds in one area of the left lung and concludes that it is probably an area of consolidation. What statement reflects that the nurse has a good understanding of this situation?
a. The patient probably has TB, since he is coughing up blood.
b. The diagnosis is probably lobar pneumonia, which is consistent with having a consolidated area of lung tissue.
c. The nurse will prepare to help the physician insert a chest tube to reinflate the left lung, as the patient probably has a pneumothorax.
d. It is likely that the patient has chronic bronchitis and has developed cor pulmonale
?
c
A patient with a medical history of CHF presents to her health care provider complaining of PND, 2-pillow orthopnea, DOE, and hemoptysis. She most likely has
a. primary pulmonary hypertension. (error-- this wasn't in your notes)
b. noncardiogenic pulmonary edema.
c. cardiogenic pulmonary edema.
d. pleural effusion.
a
A patient has overdosed with heroin. He is unconscious and his RR is 8.
PCO2: 35-45, PO2: 80-100, HCO3: 22-26
Which of the following set of blood gases is most likely, given this information alone?
a. pH= 7.25; PaO2= 70; pCO2 = 50; HCO3= 24.
b. pH= 7.49; PaO2= 90; pCO2= 25; HCO3 = 25.
c. pH = 7.20; PaO2 = 80; pCO2 = 38; HCO3 = 18.
d. pH = 7.37; PO2 = 85; PCO2 = 36; HCO3 = 26.
a
A patient has overdosed with heroin. He is unconscious and his RR is 8.
PCO2: 35-45, PO2: 80-100, HCO3: 22-26
The correct answer above is called:
a. respiratory acidosis
b. metabolic acidosis
c. respiratory alkalosis.
d. metabolic alkalosis
so2, saturated, oximeter, 97, 100
____(SO2)
a) oxygen saturation—this indicates O2 that is carried by hemoglobin
b) cycle of oxygenation:
(1) in lungs, where the O2 concentration is high, Hgb will bind with O2 for transport to the tissues
(2) if all four O2-binding sites on the hemoglobin are "loaded up" with O2, the Hgb molecule is said to be _______(saturated),
(3) this is measured in the clinical setting as O2 saturation percent, or SO2 —ie, how great a percent of each Hgb molecule in the arterial circulation is saturated with O2?
c) measured by pulse __________(oximeter) on finger—light passes through blood vessels & "reads" the amount of O2 in each Hgb; sometimes considered the "5th VS"
d) normal SO2 = ___(97) to _____(100)% ; less than ~97% indicates some level of hypoxemia .
d
if the CO2 is out of norm, the acidosis or alkalosis has a ___________ origin.
A. neuro
B. pulmonary
C. metabolic
D. respiratory
c
if the HCO3 is out of norm, the acidosis or alkalosis has a ________ origin.
A. neuro
B. pulmonary
C. metabolic
D. respiratory
respiratory, acidosis, out, rr, low, co2, high
_______(Respiratory) _________(acidosis)
1) state of low pH caused by inhibition of normal breathing pattern, such as diminished effectiveness of breathing or decreased respiratory rate (hypoventilation).
2) this results in retention & accumulation of CO2 and therefore more acid gang in blood acid state (note: high PCO2 is called )
Patient unconscious____(out) & _____(RR) ______(low) from normal (16- 20) to 8 breaths a minute not breathing out enough CO2 retains_______( CO2) (hypercapnia) blood CO2 level is _____(high)
Kidneys increase hco3 and decrease its excretion, also rids co2
respiratory, alkalosis, hyperventilation, co2, low
__________(Respiratory) _________(alkalosis)
1) state of high pH caused by increase in normal breathing pattern, such as _____________(hyperventilation).
2) increased rate of breathing results in blowing off" more ______(CO2) less CO2 in the blood means not enough of the acid gang.
Classic state that causes hyperventilation: panic attack (Also can be seen in pts having acute asthma or emphysema exacerbations.) RR increases from normal (16- 20) to 28 breaths a minute breathing out too much CO2 blood CO2 level is ____(low)
Kidneys decrease hco3 and increase its excretion
metabolic, acidosis, hco3, low, dka
______(Metabolic) __________(acidosis)
1) state of low pH caused by accumulation of acid gang due to metabolic problems like renal failure & diabetic ketoacidosis
2) acid gang accumulation overwhelms the alkali guy, so _____(HCO3) will be ____(low).
Patient with ____(DKA) (diabetic ketoacidosis) has accumulated byproducts of sustained gluconeogenesis
Lungs then increase respiration to blow off co2
metabolic, alkalosis, hco3, high, vomiting
_________(Metabolic) _______(alkalosis)
1) state of high pH caused by metabolically- induced loss of acid gang and/or accumulation of alkali guy
2) _____(HCO3) will be _____(high).
Patient with extreme ___________(vomiting) loss of HCl
blood acid level becomes low making pH high
c
a pattern of rapid & deep breathing for the purpose of blowing off accumulated acid. metabolic acidosis
A. perfusion
B. ventilation
C. kussmaul
D. exhalation
b
_________ can be thought of as the portion of inhalation in which air passes into bronchi & alveoli (lung tissue) rest of the body.
A. perfusion
B. ventilation
C. kussmaul
D. exhalation
a
___________ can be thought of as the portion of inhalation in which the blood vessels of the lungs bring CO2 to the alveoli & take away O2 to pass on to the rest of the body.
A. perfusion
B. ventilation
C. kussmaul
D. exhalation
d
diaphragm & intercostal muscles "elastically" return to "resting state" and CO2 is expelled from the body.
A. perfusion
B. ventilation
C. kussmaul
D. exhalation
a
dyspnea upon lying down; usually related to LHF
A. orthopnea
B. dyspnea
C. hypoventilation, AKA bradypnea
D. hyperventilation, AKA tachypnea
c
defined as RR < 12 breaths per minute
A. orthopnea
B. dyspnea
C. hypoventilation, AKA bradypnea
D. hyperventilation, AKA tachypnea
d
defined as RR > 20 breaths per minute
A. orthopnea
B. dyspnea
C. hypoventilation, AKA bradypnea
D. hyperventilation, AKA tachypnea
a
shallow breathing.
A. hypopnea
B. hyperpnea
C. apnea
b
increased depth (tidal volume) of respirations
A. hypopnea
B. hyperpnea
C. apnea
c
no respirations at all
A. hypopnea
B. hyperpnea
C. apnea
a
disorders often seen in pulmonary diseases
A. nasal flaring in young children, hemoptysis, purulent sputum, inappropriate us of accessory muscles
B. nasal flaring in adults, hemoptysis, purulent sputum, inappropriate us of accessory muscles
C. nasal flaring in young children, oliguria, purulent sputum, inappropriate us of accessory muscles
D. none of the above
b
A patient presents who is complaining of dyspnea. He has a RR of 32 and an SO2 of 91%. He is using intercostal muscles during expiration. Altogether this describes one presentation of
A. Respiratory Failure
B. Respiratory Distress
C. Purulent Sputum
D. none of the above
a
patient can no longer breathe adequately on his own; usually the SO2 and PO2 are very low and the PCO2 is very high.
A. Respiratory Failure
B. Respiratory Distress
C. Purulent Sputum
D. none of the above
c
diseases refers to disease processes related to difficulty with inhalation.
b. since problems with inhalation usually means decreased O2 getting in, one sign often found with this category is hypoxemia
A. Constrictive
B. Obstructive
C. Restrictive
D. Destructive
c
measured numerically as low SO2 and/or low PO2, with pH & PCO2 only sometimes affected
A. Constrictive
B. Obstructive
C. Restrictive
D. Destructive
d
normal amount of air breathed in and out per minute is ~ 4 liters.
A. Perfusion
B. Inhalation
C. exhalation
D. Ventilation
a
normal amount of blood in the lungs available for gas exchange per minute is ~ 5 liters
A. Perfusion
B. Inhalation
C. exhalation
D. Ventilation
normal, v/q, 0.8
_____(normal) ____(V/Q) ratio: ____(0.8) (4 / 5)
vq, mismatch, can't, see, scan
"____(VQ) _________(mismatch)" means the V/Q ratio is out of the norm—either lower or higher than normal
a) ________(can't) actually "____(see)" a mismatch when assessing your patients, although it usually exists to some degree in most restrictive pulmonary diseases & contributes to S&S.
b) sometimes it can be actually measured in order to have a clear diagnosis -- measured by a nuclear imaging test called a V/Q _______(scan), but
even without quantification, we can guess what disturbance of ratio
our patients have by understanding the underlying cause.
b
is what happens if a person is having difficulty with ventilation—it is likely that he is not getting the usual number of liters of air from the atmosphere to the blood, in pneumonia, alveoli get filled up with secretions and portions collapse  less air can pass into the alveoli ie, low ventilation.
B. Low VQ disorder
C. High VQ disorder
c
is what happens if a person is having difficulty with perfusion—it is likely that during inhalation, he is not getting the usual number of liters of blood to alveoli for gas exchange a pulmonary embolus blocks one or more branches of the pulmonary arterial vasculature
B. Low VQ disorder
C. High VQ disorder
a
deformity-- kyphosis, obesity, neuromuscular weakness from diseases that affect the junction between neurons and muscle cells-- polio, myasthenia gravis.
A. Chest restriction
B. Airway restriction
C. Lung tissue Restriction
D. Pleural Restricion
b
foreign body, tumors of trachea & bronchi.
2) inflammation of upper airways—croup
a) most diseases that cause inflammation in larynx & bronchi are caused by virus inflammation airways narrowed stridor
is usually heard upon inspiration (a high pitched, raspy sound caused by turbulent flow in airways.
b) croup (laryngotracheobronchitis) - inflammation of larynx & bronchi
(1) usually occurs in infants & children younger than 1 year.
(2) S&S—fever, increased RR, barking cough, stridor
(3) tx—cool mist, sometimes steroids.
A. Chest restriction
B. Airway restriction
C. Lung tissue Restriction
D. Pleural Restricion
b
croup (laryngotracheobronchitis) - inflammation of larynx & bronchi
(1) usually occurs in infants & children younger than 1 year.
(2) S&S—fever, increased RR, barking cough, stridor
(3) tx—cool mist, sometimes steroids.
A. Chest restriction
B. Airway restriction
C. Lung tissue Restriction
D. Pleural Restricion
c
extra fluid in pleural space
A. Closed Penumothorax
B. Open Pneumothorax
C. Pleural Effusion
D. pneumonia
d
normally, the space between the visceral and parietal pleura has very little fluid—just enough for lubrication
b) the amount increases when something causes irritation / inflammation to pleura: ex:
(1) cancer cells in the lung.
(2) heavy coughing from bronchitis, pneumonia, etc.
(1) can have chills and fever if related to infection
(2) pleuritic pain ("pleurisy") is typically described as pain upon deep breaths, cough, or movement in a local area of chest
(3) respirations often become more shallow—restricted by pain and fluid build-up.
A. Chest restriction
B. Airway restriction
C. Lung tissue Restriction
D. Pleural Restricion
c
cancer cells in the lung.
A. Closed Penumothorax
B. Open Pneumothorax
C. Pleural Effusion
D. pneumonia
a
presence of air in the pleural space caused by a rupture in the visceral pleura OR the parietal pleura & chest wall
a) results in disruption of normal negative pressure of lungs; ie, thorax pressure becomes the same as the atmosphere as air comes in pathologically.
b) affected lung begins to collapse as more & more air accumulates in the thorax around it
c) the two problems—lack of usual negative pressure to "guide" normal breathing process, plus the collapse of varying amount of lung tissue causes chest pain and SOB.
d) two types: open and closed
A. Pneumothorax
B. Airway restriction
C. Lung tissue Restriction
D. Pleural Effusion
b
when there is trauma from the outside.
(b) classic case—broken rib punctures pleura.
A. Closed Pneumothorax
B. Open Pneumothorax
a
when trauma is from the inside—often called a tension pneumothorax because air builds up in the thorax enough to put pressure on other lung too.
(b) can happen when a patient has an underlying disease, such as when a weakened, emphysemic alveoli ruptures (c) "spontaneous pneumothorax" can sometimes happen in healthy people of certain build—tall, thin, smokers.
A. Closed Pneumothorax
B. Open Pneumothorax
c
pneumonia—acute infection of the lower respiratory tract caused by bacteria, viruses, fungi, or parasites
a) overview
(1) 6th leading cause of death in the US; especially takes its toll on elderly
(2) risk factors: either end of age-spectrum; immunocompromised; underlying lung diseases (COPD, lupus, etc); alcoholism & other mechanisms of altered consciousness; smoking, endotracheal intubation; malnutrition; immobilization
b) types: community-acquired CAP hospital-acquired (nosocomial), & aspiration pneumonia; each usually involves different organisms & level of seriousness & need different treatment
A. Chest restriction
B. Airway restriction
C. Lung tissue Restriction
D. Pleural Restricion
d
Lung tissue Restriction, acute infection of the lower respiratory tract caused by bacteria, viruses, fungi, or parasites, 3 types
A. Closed Penumothorax
B. Open Pneumothorax
C. Pleural Effusion
D. pneumonia
a
Lung tissue Restriction organisms are most commonly gram positive and less virulent
(a) sometimes called "walking pneumonia"—don't have to be hospitalized)
(b) exception—immunocompromised & debilitated individuals in the community can get virulent CAP because they are
susceptible to opportunistic infections
A. CAP
B. Nosocomial Pneumonia
C. Aspiration Pneumonia
b
most commonly caused by virulent gram negative microbes like pseudomonas
(b) these patients need very strong antibiotics.
A. CAP
B. Nosocomial Pneumonia
C. Aspiration Pneumonia
c
aspiration usually means to inhale something that shouldn't be going into the lungs—nasal drip, food, liquid, foreign body —with resultant inflammation to lung tissue.
(b) this type of pneumonia can be a CAP or a nosocomial type
(c) usually happens in debilitated or other individuals whose gag, swallowing, and/or cough reflexes are depressed or absent
(i) elderly, weak patient can't swallow very well (dysphagia) food particles or fluid go into lungs instead of stomach creates breeding ground for microbes in lungs
(ii) alcoholic passes out: if he is supine, sometimes stomach contents will be regurgitated & go down trachea into lungs, because cough reflex has been suppressed by alcohol & deep unconsciousness  creates breeding ground for microbes in lungs.
(iii) other examples include brain injured; post-seizure; post-CPR
(e) NOTE: an alert, otherwise healthy person will not getit, as their cough, swallow, & gag reflexes are unimpaired.
A. CAP
B. Nosocomial Pneumonia
C. Aspiration Pneumonia
?
pnemonia, alveoli, debris, infilitrates collapse, lung, atelectasis, stiff
patho of ________(pneumonia):
(1) microorganisms settle into _______(alveoli) & are attacked by alveolar macrophages
(2) if this attack is ineffective or if body is overwhelmed by numbers of organisms, full-scale activation of body's defense mechanisms takes place
(3) inflammatory/infectious ____(debris) accumulate in alveoli and surrounding tissue -- these are called infiltrates
(4) ______(infiltrates) cause ______(collapse) of portions of _______(lung) tissue; this is called ______(atelectasis) & happens when groups of alveoli cave in due to blockage in the bronchioles (such as collections of mucus from inflammatory changes) air can't get into alveoli so they collapse.
(5) infiltrates + atelectasis = consolidation
(a) areas of lung that become ____(stiff )and have diminished function
(b) can be either a local area such as a single lobe (lobar pneumonia) OR may be more diffuse (bronchopneumonia)
pneumonia, crackles,small, breath, abnormal, xray
c) S&Ss of any kind of ______(pneumonia)
(1) fever, chills, malaise, pleural pain, cough, dyspnea
(2) upon auscultation:
(a) _______(crackles) (from inflammatory fluid in alveoli) or
(b) locally _______(small) ______(breath) sounds (consolidated tissue has no air going through it, so no sound)
(3) __________(abnormal) chest xray
d) dx—chest _____(xray), gram stain & cultures of sputum; treatment-- antibiotics, hydration, pulmonary toilet (cough, turn, deep breathe, suction)
pulmonary, edema, noncardiogenic, injury, increase, permeability, pink, sputum
________(pulmonary) _______(edema)—excess water in alveoli; see page 719
a) usually thought of as cardiogenic (already discussed in heart section) vs __________(noncardiogenic)
b) noncardiogenic etiology: ____(injury) to capillary endothelium (ex—smoke from a fire) _______(increase)d capillary ___________(permeability) and disruption of surfactant production by alveoli movement of fluid and plasma proteins from capillary to alveoli
c) S&Ss—cough, dyspnea, inspiratory crackles, ____(pink) frothy _____(sputum), hypoxemia (same S&S no matter what etiology of pulmonary edema).
a
arise from epithelium of respiratory tract (lung is also the site of metastasis for many other types of cancer)
a) most common cause (90%)—> cigarette smoking—one in 10 smokers will develop lung cancer
b) patho: carcinogens in tobacco smoke (has > 40) causes multiple genetic abnormalities in bronchial cells including deletions of chromosomes, activation of oncogenes, inactivation of tumor suppressor genes carcinoma in situ invasive carcinoma
c) types of bronchogenic cancer: to establish diagnosis, a bronchoscopy is done a sample of the suspicious area is taken and sent for biopsy
d) S&Ss—pleural effusion, cough, sputum, chest wall pain, SOB; anorexia, weight loss
A. Lung cancer
B. Open Pneumothorax
C. Pleural Effusion
D. pneumonia
high, vq, embolus, virchow
problems that result in ____(HIGH) ____(VQ) (can't get blood to the air—less perfusion than normal), ie, obstruction of vessel in lung
a. structural problems of vessels can cause this: strictures in pulmonary vessels, malformations, birth defects
b. most common perfusion problem is pulmonary ________(embolus)--occlusion of portion of pulmonary vessels by an embolus, which can be a blood clot, some type of tissue fragment, or an air bubble.
1) increased risk in patients with ______(Virchow)'s triad ( endothelial injury, hypercoagulability, venous stasis) venous thrombosis (DVT)dislodges & travels to lung
2) once embolus lodges in portion of pulmonary artery or its branches, it prohibits deoxygenated blood from getting to the air in the alveoli to be oxygenated, so the blood in the pulmonary veins that returns to the heart &beyond is less saturated with O2 & person will start to feel SOB & often chest pain; hemoptysis also occurs... see box below.
3) the seriousness depends on how large & how proximal the blockage is.
?
obstructive, accessory, pf
_________(obstructive) their S&S often are a result of this "forcing out:"
a) often patients must use ____________(accessory) muscles to do this; use of accessory muscles is often manifested as retractions—supraclavicular, substernal, & intercostal muscles "sucking in" upon expiration to help get air OUT of lungs.
b) some patients also have a prolonged expiratory phase as a compensatory mechanism (the length of time to exhale begins to get longer)
c) one test that is used to measure how well they can force out air is peak flow _____(PF) test
(1) measured by a PF meter—patient blows into it "like blowing out a candle"
(2) measures how many ml can be blown out in first second of exhalation
(3) the less the PF, the worse the obstructive pulmonary disease.
4) almost all patients in this category have patterns of maintenance (ie, normal state of daily disease) and exacerbation episodes (periods of worsening)
a
Obstructive Disorder:a chronic inflammatory disorder of the airways due to bronchial hyperresponsiveness to stimuli such as allergens in environment.
2) can begin at any age—about half of all cases develop in childhood and 1/3 in adulthood, usually under age 40.
b. patho: inhaled irritants inflammatory mediators (histamine, leukotriene,prostaglandins)
A. asthma
B. bronchitis
C. emphysema
D. cystic fibrosis
asthma, wheezing, alkalosis
Obstructive disorder _____(asthma( usually have ______(wheezing) upon exhalation, though in bad cases the wheezing can also be upon inhalation.
b) often have accessory muscle use—intercostal & supraclavicular retractions while exhaling—and prolonged expirations
c) SO2 can drop & patient will try to compensate for hypoxemia by hyperventilating (RR typically 24-28) during exacerbations, so ABGs during an asthma exacerbation usually show respiratory _____(alkalosis)
d) baseline PF lower than normal population, but will worsen even more during exacerbations.
b
Obstructive disorder a. collective term for emphysema and/or chronic bronchitis
1) patho is different, but some characteristics are the same in both.
a) in MOST cases, the cause of both types of is smoking
b) S&S in both include prolonged expirations, certain degree of accessory muscle use, and a chronically low PF; all these S&S are even worse than usual during exacerbation
c) treatment of both is similar (and much like treatment of asthma)— smoking cessation; giving O2 appropriately, bronchodilators, sometimes steroids
2) keep in mind that though they will be described separately, elements of emphysema and bronchitis are often BOTH seen in obstructive pulmonary disease and can complicate the "picture"
A. asthma
B. COPD
C. emphysema
D. cystic fibrosis
emphysema, elastase, breaks, protein, blebs
Obstructive disorder ________(emphysema) airway inflammation & abnormally increased activity of proteolytic enzymes like ___________(elastase) (an enzyme that _______(breaks) down the ______(protein) that make lungs so flexible & "elastic") due to this loss of elastic recoil, these areas act as air "traps"(large, over-inflated areas sometimes called "____(blebs)")
emphysema, tachypnea, pink, thin, ap, barrel, chest
Obstructive disorder_________(emphysema) a degree of ________(tachypnea) is almost always present—RR of 26 to 30/min
b) because of hyperventilation, patients with emphysema known as "pink puffers" --they can stay_____(pink) (ie, fairly well-oxygenated) as long as they keep "puffing."
b) this is hard work, so these patients usually are _____(thin) and have noappetite (no energy to eat)
c) they also have a typical feature of increased anteroposterior ____(AP) diameter of chest
(1) goes from normal AP-to-lateral diameter ratio of 1 to 2, to an equal diameter both ways (2:2), as a compensatory change to accommodate years of air trapping & lungs getting bigger
(2) the thorax is much "rounder" and is called a ______(barrel) _____(chest).
emphysema, help, tripod, pursed, alkalsosis
________(emphysema) often emphysemics will unconsciously use certain techniques to _____(help) to exhale and to get more air:
(1) "____(tripod)" position to maximize chest expansion
(2) "______(pursed) lip" breathing to increase pressure in chest to get air out & to prolong expiratory time
e) may have wheezing, but usually lung sounds are markedly diminished due to no air flow in many areas
f) ABGs: because an emphysemic patient is usually in a chronic state of compensatory hyperventilation, he or she therefore lives in a daily state of some degree of respiratory ________(alkalosis)
?
c
defined as hypersecretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years;
2) patho: inspired irritants (usually from smoking)
known as "blue bloaters"
also can have clubbing of the fingers
A. asthma
B. COPD
C. chronic bronchitis
D. cystic fibrosis
bronchitis, bloater, hyper, useless, acidosis
Obstructive Disorder chronic ________(bronchitis)
etiology of "______(bloater):"
(1) _____(hyper)ventilation won't do any good _____(useless)
(a) the body "knows" that, unlike the pink puffer, it will not help very much to increase the respiratory rate in an effort to "fight" for breath
(b) so they usually don't have weight loss like the thin, pink puffer; in fact they try to conserve energy by not moving much  often are a bit overweight ("bloated") (2)cor pulmonale— RHF due to a lung disease
(a) the patho of chronic bronchitis eventually makes it difficult for the right ventricle to get blood into the stiff, mucous-filled lungs.
(b) RV becomes strained & RHF results peripheral edema ("bloat")
(1) patients with chronic bronchitis more likely to chronically retain CO2 than emphysemics because of the inability to exchange gases --mucus, etc, prevents good diffusion of O2 in & CO2 out to alveoli.
(2) so, because of chronic hypercapnia, pt. lives in a baseline state of some degree of respiratory _______(acidosis)
a
Obstructive Disorder No barrel chest
Minimal changes in ventilatory patterns
Blue (chronically hypoxemiccyanotic, clubbed fingers)
No special position because it doesn't help; only "keeping still" helps a bit so they don't increase need for oxygen
Wt gain & edema from sedentary inclinations and from cor pulmonale ("bloater")
Usually have chronic hypercapnia & therefore chronic respiratory acidosis (hypoxic drive instead of normal CO2 drive)
bronchial component: cough, mucus, poor exchange of O2 & CO2
No tissue destruction
A. Chronic Bronchitis
B. Emphysema
C. Asthma
D. COPD
b
Obstructive Disorder Barrel chest (from air trapping lungs "huge")
Tripod position, hyperventilating as part of norm ("puffer").
Pink (adequate oxygenation unless having exacerbation)
Wt loss; very thin.
ABGs: chronic respiratory alkalosis (if becomes respiratory acidosis, patient is usually in trouble)Patho: no bronchial component
Equal destruction of alveoli & capillaries
A. Chronic Bronchitis
B. Emphysema
C. Asthma
D. COPD
b
Obstructive Disorder no bronchial component
Equal destruction of alveoli & capillaries
A. Chronic Bronchitis
B. Emphysema
C. Asthma
D. COPD
a
Obstructive Disorder Patho: bronchial component: cough, mucus, poor exchange of O2 & CO2
No tissue destruction
A. Chronic Bronchitis
B. Emphysema
C. Asthma
D. COPD
c
deficient HCO3
A. Respiratory Acidosis
B. Respiratory, Alkalosis
C. Metabolic Acidosis
D. Metabolic Alkalosis
d
Too much HCO3
A. Respiratory Acidosis
B. Respiratory, Alkalosis
C. Metabolic Acidosis
D. Metabolic Alkalosis
b
deficient HCO2
A. Respiratory Acidosis
B. Respiratory, Alkalosis
C. Metabolic Acidosis
D. Metabolic Alkalosis
a
Too much HCO2
A. Respiratory Acidosis
B. Respiratory, Alkalosis
C. Metabolic Acidosis
D. Metabolic Alkalosis
b
Gram Negative Pneumonia
A. CAP
B. Nosocomial
C. Aspiration
a
Gram Positive Pneumonia
A. CAP
B. Nosocomial
C. Aspiration
a
Venous injuries are
A. warm
B. cold
b
Arterial injuries
A. warm
B. cold
c
An 80-year old woman with a medical history of HTN and CAD goes to her NP for a check-up. She complains that her vision has been slightly blurry but otherwise has no changes in her usual S&S. Her VS (vital signs) are as follows: BP 168/100, HR 100, RR 20. Lab work is done which shows a high LDL and HDL of 38 (desired = > 40). Urinalysis is normal except for proteinuria and hematuria (normally there is no protein or blood in the urine).

16. The patient's blurred vision is likely caused by
a. accumulation of cholesterol on the sclera of both eyes.
b. coronary arterial blockage causing sudden myocardial infarction with resultant lack
of blood flow to the eyes.
c. chronic hypertensive damage to the retinal arterioles.
d. the low heart rate causing low cardiac output and thus ischemia to the optic nerve.
d
Which concept map best explains the proteinuria and/or hematuria?
a. Heart diseaseà high density lipoproteins accumulate and overcome renal
thresholdà spill into urineà proteinuriaà HDL now too low.
b. HTN + CAD à weakened walls of renal veinsàsubstances such as RBCs
pathologically spill into urineà hematuria.
c. Interaction between HDLs and LDLs cause damage to kidneysà spillage of
lipoproteins into urineà proteinuria.
d. Chronic HTNà high pressures inside renal arterial system cause damage and "leakiness"àspillage of substances into urine from renal capillariesà hematuria.
b
A patient with CAD presents to her NP with a change in her usual pattern of angina. Her usual pattern for the last several years is to have anginal pain (rated "3/10") after walking up a flight of stairs, but the pain usually quickly subsides after resting a few minutes. Now she says she has pain rated at "6/10" with minimal activity and it will only go away after taking 2 NTG pills. The NP hospitalizes the patient with a diagnosis of ACS.

18. To which category of CAD did this patient belong before the current change in anginal pattern?
a. Unstable angina.
b. Stable angina.
c. Stable aortic aneurysm.
d. CVI (chronic venous insufficiency).
a
A patient with CAD presents to her NP with a change in her usual pattern of angina. Her usual pattern for the last several years is to have anginal pain (rated "3/10") after walking up a flight of stairs, but the pain usually quickly subsides after resting a few minutes. Now she says she has pain rated at "6/10" with minimal activity and it will only go away after taking 2 NTG pills. The NP hospitalizes the patient with a diagnosis of ACS.
What concept map best explains the pathology behind the several years of unchanged anginal pattern?
a. Slow-developing plaque in coronary arteryàcompensatory collateral circulation
developsàdistal tissue receives enough O2 for all but most strenuous activities.
b. Small thrombi grow in coronary arteriesà emboli develop slowlyàblood flow not blocked off till emboli break off and fill lumen.
c. Slow-developing plaque in coronary arteryàcompensatory higher venous pressures in distal tissueà perfusion stays steady for many years.
d. Ischemic pain from CAD actually worsens but patient ignores the anginaà only seeks help when higher activity levels cause shortness of breath (SOB) and nausea.
?
d
In the hospital, the patient begins complaining of worsening pain ("8/10"). The RN suspects she is having a myocardial infarction, and the MI is located in her right ventricle. All of the following fit with the RN's thinking EXCEPT
a. the patient's EKG monitor shows bradycardia, which is often associated with sino-atrial (SA) node ischemia from a right coronary artery blockage.
b. it is likely that a previously stable right coronary plaque has ruptured and completely
blocked off flow to distal tissue.
c. the high level of pain indicates there are areas of myocardial tissue that are
undergoing necrosis because of lack of O2.
d. the patient has a heart rate (HR) of 90 beats/minute and a BP of 118/80, indicating probable high preload and afterload.
b
pathology underlying why diuretics (meds that increase urination) are given in a person with heart failure ______?
A. decreased cardiac outputàkidneys sense this and increase renin as a compensatory responseà RAAS kicks in but its results exacerbate the problem.
B. increased preload is almost always part of the heart failure picture
C. one of the S&S associated with RHF
D. right ventricular MIàmyocardial tissue damageàRV can't pump forward as wellà back pressure accumulatesàfluid eventually forced from veins of legs and feet into tissue (peripheral edema)
E classic picture of cor pulmonale
F. increases during heart failure because body is "frantically" trying to rid of fluid
?
g
mini-concept map that explains S&S of LHF
A. decreased cardiac outputàkidneys sense this and increase renin as a compensatory responseà RAAS kicks in but its results exacerbate the problem.
J. classic pulmonary edema S&S of SOB, orthopnea, hemoptysis
C. one of the S&S associated with RHF
G. left ventricular MIàmyocardial tissue damageàLV can't pump forward as wellà back pressure accumulatesàfluid eventually forced from capillaries of lungs into the alveoli (pulmonary edema)
E classic picture of cor pulmonale
F. increases during heart failure because body is "frantically" trying to rid of fluid
e
person has chronic lung disease-lungs very stiff-pulmonary vascular resistance increases-RV struggles to push blood into the high pressure pulmonary system -RV fails-back pressure eventually results in peripheral edema
A. decreased cardiac outputàkidneys sense this and increase renin as a compensatory responseà RAAS kicks in but its results exacerbate the problem.
J. classic pulmonary edema S&S of SOB, orthopnea, hemoptysis
C. one of the S&S associated with RHF
G. left ventricular MIàmyocardial tissue damageàLV can't pump forward as wellà back pressure accumulatesàfluid eventually forced from capillaries of lungs into the alveoli (pulmonary edema)
E classic picture of cor pulmonale
F. increases during heart failure because body is "frantically" trying to rid of fluid
j
clinical presentation of LHF
A. decreased cardiac outputàkidneys sense this and increase renin as a compensatory responseà RAAS kicks in but its results exacerbate the problem.
J. classic pulmonary edema S&S of SOB, orthopnea, hemoptysis
C. one of the S&S associated with RHF
G. left ventricular MIàmyocardial tissue damageàLV can't pump forward as wellà back pressure accumulatesàfluid eventually forced from capillaries of lungs into the alveoli (pulmonary edema)
E classic picture of cor pulmonale
F. increases during heart failure because body is "frantically" trying to rid of fluid
i
a treatment for a person with heart failure
A. decreased cardiac outputàkidneys sense this and increase renin as a compensatory responseà RAAS kicks in but its results exacerbate the problem.
I. decrease systemic vascular resistance (SVR), a type of afterload, by giving vasodilating drugs
C. one of the S&S associated with RHF
G. left ventricular MIàmyocardial tissue damageàLV can't pump forward as wellà back pressure accumulatesàfluid eventually forced from capillaries of lungs into the alveoli (pulmonary edema)
D. right ventricular MIàmyocardial tissue damageàRV can't pump forward as wellà back pressure accumulatesàfluid eventually forced from veins of legs and feet into tissue (peripheral edema)
F. increases during heart failure because body is "frantically" trying to rid of fluid
c
jugular venous distention
A. decreased cardiac outputàkidneys sense this and increase renin as a compensatory responseà RAAS kicks in but its results exacerbate the problem.
I. decrease systemic vascular resistance (SVR), a type of afterload, by giving vasodilating drugs
C. one of the S&S associated with RHF
G. left ventricular MIàmyocardial tissue damageàLV can't pump forward as wellà back pressure accumulatesàfluid eventually forced from capillaries of lungs into the alveoli (pulmonary edema)
D. right ventricular MIàmyocardial tissue damageàRV can't pump forward as wellà back pressure accumulatesàfluid eventually forced from veins of legs and feet into tissue (peripheral edema)
F. increases during heart failure because body is "frantically" trying to rid of fluid
a
main etiology of fluid overload in any kind of heart failure
A. decreased cardiac output-kidneys sense this and increase renin as a compensatory responseà RAAS kicks in but its results exacerbate the problem.
I. decrease systemic vascular resistance (SVR), a type of afterload, by giving vasodilating drugs
C. one of the S&S associated with RHF
G. left ventricular MIàmyocardial tissue damage-LV can't pump forward as wellà back pressure accumulates-fluid eventually forced from capillaries of lungs into the alveoli (pulmonary edema)
D. right ventricular MIàmyocardial tissue damage-RV can't pump forward as well- back pressure accumulates-fluid eventually forced from veins of legs and feet into tissue (peripheral edema)
F. increases during heart failure because body is "frantically" trying to rid of fluid
d
mini-concept map that explains S&S of RHF
A. decreased cardiac output-kidneys sense this and increase renin as a compensatory responseà RAAS kicks in but its results exacerbate the problem.
I. decrease systemic vascular resistance (SVR), a type of afterload, by giving vasodilating drugs
C. one of the S&S associated with RHF
G. left ventricular MIàmyocardial tissue damage-LV can't pump forward as wellà back pressure accumulates-fluid eventually forced from capillaries of lungs into the alveoli (pulmonary edema)
D. right ventricular MIàmyocardial tissue damage-RV can't pump forward as well- back pressure accumulates-fluid eventually forced from veins of legs and feet into tissue (peripheral edema)
F. increases during heart failure because body is "frantically" trying to rid of fluid
f
BNP (B-type natriuretic peptide)
A. decreased cardiac output-kidneys sense this and increase renin as a compensatory responseà RAAS kicks in but its results exacerbate the problem.
I. decrease systemic vascular resistance (SVR), a type of afterload, by giving vasodilating drugs
C. one of the S&S associated with RHF
H. sound of air going through fluid in alveoli when there is pulmonary edema
D. right ventricular MIàmyocardial tissue damage-RV can't pump forward as well- back pressure accumulates-fluid eventually forced from veins of legs and feet into tissue (peripheral edema)
F. increases during heart failure because body is "frantically" trying to rid of fluid
h
explains crackles heard in lungs upon auscultation with a stethoscope
A. decreased cardiac output-kidneys sense this and increase renin as a compensatory responseà RAAS kicks in but its results exacerbate the problem.
I. decrease systemic vascular resistance (SVR), a type of afterload, by giving vasodilating drugs
C. one of the S&S associated with RHF
H. sound of air going through fluid in alveoli when there is pulmonary edema
D. right ventricular MIàmyocardial tissue damage-RV can't pump forward as well- back pressure accumulates-fluid eventually forced from veins of legs and feet into tissue (peripheral edema)
F. increases during heart failure because body is "frantically" trying to rid of fluid
stroke, volume, contractility, preload, afterload
stroke, volume, contractility, preload, afterload
b
central nervous system (CNS) reaction to pain- N&V, large amount of sweating ______
A. perfusion
B. diaphoresis
C. kussmaul
D. kinase
a
High RR low SO2
A. respiratory distress
B. respiratory failure
C. respiratory furious
D. none of the above
b
Low SO2, O2, and PH with high PCO2
A. respiratory distress
B. respiratory failure
C. respiratory furious
D. none of the above
b
If the lungs are sick the _____compensate
A. Lungs
B. Kidneys
C. metabolic
D. none of the above
a
If the metabolic side is sick the _____compensate
A. Lungs
B. Kidneys
C. metabolic
D. none of the above
Innate, born
________(Innate) (AKA "natural") resistance-- the defense mechanisms we are ____(born) with; this includes
1st, physical, immediate, non-specific
___(1st) line of resistance (first defense against invasion)--body's _________(physical) barriers, which are ________(immediate) (response occurs at the time of contact with a stressor) and ________(non-specific) (the response process is the same, regardless of the type of stressor).
2nd, inflammation, immediate
__(2nd) line of resistance (secondary defense against invasion)-- ___________(inflammation), which is also _________(immediate) and non-specific
acquired, 3rd, immunocyte, delayed, specific
______(Acquired) (AKA "adaptive") immunity-- ___(3rd) line of defense
1. being able to resist certain diseases or conditions due to _________(immunocyte) involvement
2. this type of response is _______(delayed) and __________(specific) immunocytes are lymphocytes
(B-cells & T-cells)
skin, sweat, acidic
various glands in __(skin) secrete _____(sweat), which has antibacterial & antifungal properties:
1) attack cell walls of certain bacteria.
2) contribute to making the skin actually _____(acidic) (ph 3 to 5), making it inhospitable to most bacteria.
sjogren, autoimmune, dries, body
______________(sjogren) syndrome—_________(autoimmune) disease that
_____(dries) up all lubricating fluids in the _____(body)
changes, bowel, flora, antibiotics
bowels:
1) in the normal bowel are many "good flora" - microbes which do not harm us but do keep out malicious microbes by competing for food.
2) defecation: gets rid of injurious agents such as harmful bacteria.
e. stressors that can breach these defenses:
1) Sjogren's—dries up saliva, so less protection in mouth
2) anything that _____(changes) the _______(bowel) _____(flora) can leave us open to invading microbes; ex of something that might change the bowel flora: ______________________(antibiotics)
b
shedding of skin cells = bacteria shed too
A. sjogren
B. desquamation
C. flora
D. inflammation
stressors, breach, stones, douching
flow of urine washes away microbes
b. vaginal secretions slightly acidic—kills bacteria.
c. ______(stressors) that can ______(breach) these defenses
1) decreased urine flow, as in kidney ______(stones) or kidney failure
2) anything that changes vaginal acidity, such as _______(douching)
d
expected manifestations such as a certain ("normal") degree of swelling, heat, redness (erythema), & pain.
A. sjogren
B. desquamation
C. flora
D. inflammation
c
defend the body by direct attack against invading microbes.
A. B-lymphocytes
B. desquamation
C. T-lymphocytes
D. inflammation
a
plasma cells then create antibodies to the microbe that has attacked the body.
A. B-lymphocytes
B. desquamation
C. T-lymphocytes
D. inflammation
b, remember, take, time
____(B)-lymphocytes a particular set of antibodies now will always "______(remember)" and "lay in waiting" for that specific microbe.
b. being delayed and specific
1) meaning of "specific" - immunocytes only respond fully to microbes that they recognize (have developed memory of).
2) meaning of "delayed"— it _____(take) _____(time) to develop the ability to recognize and destroy microbes.
cilia, bronchi, sweep, foreign
________(cilia) of cells in ________(bronchi) can "_____(sweep)" away ______(foreign) bodies
active, immunity, own, developed, antibodies
the key criterion for categorizing someone as having _______(ACTIVE) acquired ______(immunity) is that their ______(own) immunocyte system __________(developed) the _________(antibodies) that established immunity.
b) this can happen two ways: naturally or artificially
a
since the lymphocytes cannot mount a full-on defense this first time around, this person will actually "get" meningitis—that is, have the S&S (& probably will be pretty sick!).
2) but even though the lymphocytes can't help much NOW, they have begun to create & establish "memory," AKA "recognition" of the meningitis microbe...the plasma cells are busy making antibodies, so that in the FUTURE, this person will be protected & won't have S&S again....
this is when a person's plasma cells build up antibodies in response to a microbially-induced illness, as in the meningitis example above
A. NATURAL active acquired immunity
B. ARTIFICIAL active acquired immunity
C. NATURAL passive acquired immunity
D. ARTIFICIAL passive acquired immunity
?
b
: this is when a person's plasma cells build up antibodies in response to receiving inoculations of a much-weakened or inactive microbe; example of this process:
(a) a child gets inoculated (AKA vaccinated) with the MMR (measles, mumps, rubella) vaccine
(b) this means a weak mixture of the actual live viruses is given to the child; the mixture is TOO WEAK to actually cause S&S but does mobilize the child's own immunocyte system to create antibodies specific to those viruses.
A. NATURAL active acquired immunity
B. ARTIFICIAL active acquired immunity
C. NATURAL passive acquired immunity
D. ARTIFICIAL passive acquired immunity
passive, immunity, do, not, develop, antibodies
_______________(passive) acquired __________(immunity)
a) the key criterion for categorizing someone as having PASSIVE acquired immunity is that they have been given someone else's antibodies; they __(do) ___(not) _____(develop) the ______(antibodies) on their own.
c
this occurs when there is transfer of antibodies from mom to baby via:
(a) the placenta
i. antibodies that the mom has in her body
(MatAb) crosses the placental membrane
from her blood to fetus's
ii. MatAb disintegrate by the time baby is 2-3 months old
(b) breast milk—some MatAbs can transfer during breast feeding
i. soon after breast feeding stops, the MatAbs
disintegrate.
ii. by then, baby has own antibodies or has been vaccinated.
A. NATURAL active acquired immunity
B. ARTIFICIAL active acquired immunity
C. NATURAL passive acquired immunity
D. ARTIFICIAL passive acquired immunity
d
this occurs when antibodies are injected during treatment, usually in
emergencies or as a stop-gap measure until active immunity can develop
(a) usually given as intramuscular injection of antibodies to a disease that you have a high risk of contracting (i.e., the microbe may have entered your body via a recent laceration, being coughed upon, sharing body fluids, etc ) because you have never previously had the disease and therefore have no antibodies to it.
A. NATURAL active acquired immunity
B. ARTIFICIAL active acquired immunity
C. NATURAL passive acquired immunity
D. ARTIFICIAL passive acquired immunity
normal, inflammation, acute, short
a ___________(normal) ___________(inflammation) process is usually ____(acute) and _____(short)-lived
inflammatory, shifting, substances, into, injured
purposes of ________(inflammatory) response--to facilitate __________(shifting) of _______(substances) from blood ________(into) ________(injured) / irritated tissue to:
a. "clean up" the area, begin the clotting process, and ultimately promote healing.
b. stimulate and enhance immunocyte response (i.e, the 3rd line of defense) as needed
injury, stimulates, leakiness
step 1: irritation /_____(injury) of tissue triggers same response anywhere in your body  ________(stimulates) "_____________(LEAKINESS)" in three ways:
mast, degranulation, leukotrienes, histamine, prostaglandins
also, ____(mast) cell __________(degranulation)(=leaking) occurs:
a) here & there throughout any tissue area in the body are a specialized type of cell called MAST CELLS
b) when they are stimulated by an irritant or injury, they will degranulate—that is, "leak" chemical "granules"
c) these are local inflammatory mediators called _________(leukotrienes), _________(histamine), and ___________(prostaglandins).
leukotrienes, histamine, prostaglandins, capillaries, relax
a) here & there throughout any tissue area in the body are a specialized type of cell called MAST CELLS
b) when they are stimulated by an irritant or injury, they will degranulate—that is, "leak" chemical "granules"
c) these are local inflammatory mediators called _________(leukotrienes), _________(histamine), and ___________(prostaglandins).
they cause __________(capillaries) in the area to swell up but at the same time sort of "____(relax)" (this is called vasodilation) & become more permeable, so they "leak" plasma from blood into tissue
a) the "leaked" plasma contains neutrophils, clotting factors & fibrin.
b) if more inflammation is needed, the SYSTEMIC inflammatory mediators come to the area via the bloodstream to pour "FUEL ON THE FIRE;" these are called acute phase reactants -- examples are CRP , circulating prostaglandins (& many others).
?
capillaries, relax, leak, neutrophils, clotting, fibrin
they cause __________(capillaries) in the area to swell up but at the same time sort of "____(relax)" (this is called vasodilation) & become more permeable, so they "leak" plasma from blood into tissue
a) the "____(leak)ed" plasma contains ___________(neutrophils), _________(clotting) factors & _______(fibrin).
b) if more inflammation is needed, the SYSTEMIC inflammatory mediators come to the area via the bloodstream to pour "FUEL ON THE FIRE;" these are called acute phase reactants -- examples are CRP , circulating prostaglandins (& many others).
more, inflammation, systemic, acute, crp, prostaglandins
if _______(more) ________(inflammation) is needed, the __________(SYSTEMIC) inflammatory mediators come to the area via the bloodstream to pour "FUEL ON THE FIRE;" these are called ______(acute) phase reactants -- examples are ____(CRP) (measurable), circulating ______________(prostaglandins) (& many others).
they increase inflammation
compliment, acute, weaken, bacteria
________(compliment) is ______(acute) phase reactants
__________(weaken) ________(bacteria)
vasodilation, leakiness, inflammation, permeability
vasodilation, leakiness, inflammation, permeability
neutrophils, blood, macrophages, phagocytize, debris
the________(neutrophils) (phagocytic WBCs from the ________(blood)) and _________(macrophages)(phagocytic cells in the (tissue)) _______(phagocytize) ("eat" & destroy) any dirt, _____(debris), dying tissue, and/or microbes they might find in the tissue area.
combination, plasma, phagocytes, dead, exudate
the ______(combination) of ________(plasma), __________(phagocytes), ____(dead) tissue cells, bacteria, fibrin, etc, results in a thick fluid called _______(exudate)
2) when there is little microbe involvement this exudate is a
clear gold color (the color of the plasma that is leaking out in the area) and is called serous exudate; if there is also some blood, it is called serosanguinous.
3) if there is more microbe & WBC involvement—ie, infection—the
exudate becomes especially thick & whitish or yellowish; this is known as purulent exudate or pus.
little, microbe, exudate, gold, serous, blood, serosanguinous
the combination of plasma, phagocytes, dead tissue cells, bacteria, fibrin, etc, results in a thick fluid called exudate
2) when there is ________(little) ________(microbe) involvement this _______(exudate) is a
clear _________(gold) color (the color of the plasma that is leaking out in the area) and is called ______(serous) exudate; if there is also some_____( blood), it is called _____________(serosanguinous).
3) if there is more microbe & WBC involvement—ie, infection—the
exudate becomes especially thick & whitish or yellowish; this is known as purulent exudate or pus.
more, microbe, wbc, exudate, thick, whitish, purulent, pus
the combination of plasma, phagocytes, dead tissue cells, bacteria, fibrin, etc, results in a thick fluid called exudate
2) when there is little microbe involvement this exudate is a
clear gold color (the color of the plasma that is leaking out in the area) and is called serous exudate; if there is also some blood, it is called serosanguinous.
3) if there is ______(more) _________(microbe) & _________(WBC) involvement—ie, infection—the
_________(exudate) becomes especially ______(thick) & __________(whitish) or yellowish; this is known as ___________(purulent) exudate or ________(pus).
c
: if bacteria, viruses, or other microbes are a part of the "mix" above, macrophages will have phagocytized & processed them and now need help from the 3rd line of defense—
A. granulating
B. desquamation
C. lymphocytes
D. inflammation
macrophages, secrete, immunocytes, display, remnants, microbes
the lymphocytes—which will help to kill the microbes, but will also create memory (immunity) of the microbe; to involve the lymphocytes, the _______(macrophages) will:
1) ________(secrete) chemotactic substances to "call" ____________(immunocytes) (AKA,
T or B lymphocytes) to come to the area via the bloodstream
2) __________(display) ________(remnants) of the ________(microbes) on their cell membranes as a guide to the lymphocytes: "this is our enemy... now create some more defenses."
a
clotting factors, platelets, and fibrin come together in various ways in the area to create healing, _____________________ tissue.
A. granulating
B. desquamation
C. lymphocytes
D. phospholipases
inflammatory, local, systemic
_________(inflammatory) response can be __________(local) (either local externally or local internally) or ___________(systemic) (see #6)
a. local external example—laceration or abrasion to skin.
b. local internal examples:
1) appendix gets irritated by a piece of food or microbe normal inflammation responds to the irritation appendicitis (appendicitis becomes a disease process, because it is ultimately harmful to the body, but the initial inflammation was a normal defense of the body.)
2) pleuritis—inflammation of pleura when irritated by, for example, a lung cancer cell.
3) thyroiditis—thyroid is inflamed because of autoimmune attack.
inflammatory, local, laceration, appendix, irritated , pleuritis, cancer, thyroiditis
_________(inflammatory) response can be __________(local) (either local externally or local internally or systemic (see #6)
a. local external example—_________(laceration) or abrasion to skin.
b. local internal examples:
1) __________(appendix) gets ______________(irritated) by a piece of food or microbe normal inflammation responds to the irritation appendicitis (appendicitis becomes a disease process, because it is ultimately harmful to the body, but the initial inflammation was a normal defense of the body.)
2) _________(pleuritis)—inflammation of pleura when irritated by, for example, a lung ________(cancer) cell.
3) __________(thyroiditis)—thyroid is inflamed because of autoimmune attack.
systemic, inflammatory, leukocytes, acute
NORMAL __________(systemic) ______________________(inflammatory) response
a. overview
1) the steps in a systemic response are basically the same as a local one, but without a specific focus; systemic inflammatory response happens when the body needs the extra help of the systemic "cavalry" like more ____________(leukocytes) (leukocytosis) and more ___________(acute) phase reactants (often causing fever)
2) basic steps can be seen below in discussion of sepsis, but can also apply to any disease process which involves normal body's response to a systemic invasion/disorder (ex—the flu, chicken pox, measles... etc).
c
normal systemic response
1) when a microbe or its toxins enter the blood and are carried throughout the body, a system-wide inflammation is triggered called
A. granulating
B. desquamation
C. septicemia/sepsis
D. phospholipases
sepsis, inflammatory, systemic, immunocyte
when a microbe or its toxins enter the blood and are carried throughout the body, a system-wide inflammation is triggered called septicemia or ________(sepsis)
2) often (but not always), it starts with a localized infection microbe may invade the blood directly or may proliferate locally and release their toxins into the blood stream
3) activates ___________(inflammatory) process __________(systemic)ally (cast of characters in the inflammatory mix: histamine, prostaglandin, leukotrienes, acute phase reactants such as CRP, large numbers of WBCs.)
4) at this point the patient may slowly get better as the inflammatory response activates the _________(immunocyte) response (3rd line of defense) to help and/or, or situation may deteriorate into an extreme, abnormal situation called septic shock (more about this later).
systemic, inflammation, malaise, fever, increased, prostaglandins, acute
S&S of _____________(systemic) _____________(inflammation) may include
1) ________(malaise), aches & pains
2) ______(fever) (from response to _________(increased) _________(prostaglandins) & ______(acute) phase reactants)
a) purpose of fever: has beneficial effect of directly killing some microorganisms
b) but also can have deleterious effects
fever, hypotension, increases, metabolic
(1) _______(fever) can dilate blood vessels too much vasodilation = ________(hypotension)
(2) also, fever ________(increases) ___________(metabolic) rate may cause decompensation in very ill, debilitated, and/ or elderly patients
heat dilates cool constricts
inflammation, leukocytosis, leukocytes, increase, neutrophils, crp
__________(inflammation) CBC will show increased WBCs-- ____________(leukocytosis)
(1) ___________(leukocytes) (WBCs) __________(increase) in number as they are "summoned" to the areas of inflammation.
(2) the WBC subtype that is usually most increased is ____________(neutrophils) neutrophilia; ex of lab report showing leukocytosis and neutrophilia:
(a) total WBCs count = 15,000 K/ul (norm~5- 10,000) (b) percentage of neutrophils = 88% (norm~50-75%)
and ____(crp)
low, inflammation, quantitative, leukopenia, neutropenia
Abnormalities of inflammation: "not enough"______(low) ________(inflammation)
1. defect in phagocytic functions
a. _______(quantitative) defect (example-- from chemotherapy)
1) ___________(leukopenia) --deficiency in WBCs
2) specific deficiency in neutrophils-- ___________(neutropenia)
\
low, inflammation, qualitative, chemotactic, defects, won't, respond
Abnormalities of inflammation: "not enough"______(low) ________(inflammation)
__________(qualitative) defects
1) _________(chemotactic) ________(defects)—________(won't) __________(respond) appropriately when "summoned."
2) impaired function; ex—phagocytes damaged by diabetes mellitus have decreased ability to fight microbes.
low, inflammation, qualitative, phagocytes, damaged, diabetes
Abnormalities of inflammation: "not enough"______(low) ________(inflammation)
__________(qualitative) defects
2) impaired function; ex—__________(phagocytes) ________(damaged) by _______(diabetes) mellitus have decreased ability to fight microbes.
complement, deficiencies, genetic
__________(complement) __________(deficiencies)
a. these are a group of disorders that stem from a ______(genetic) defect in synthesis of complement proteins
b. patients who have defects in these have problems that are very similar to those seen in patients with antibody deficiencies— they will be extra susceptible to infections.
inflammation, overdrive, septic, shock, chronic
abnormal ___________(inflammation) is one in which inflammation goes into "________(overdrive)" and/or becomes chronic; examples include ______________(septic) ________(shock) & _____(chronic) inflammation disorders.
high, inflammatory, vasodilation, floppy, hypotension
______(high) levels of __________(inflammatory) mediators trigger widespread, extreme _________(vasodilation)= no arterial vessel "tone" as
arteries become too relaxed, "________(floppy)" blood pools in periphery instead of being part of circulationeventually low blood volume reduces amount of O2 being brought to tissues as well as decreasing BP ________________(hypotension)
septic, shock, elevated, crp, esr, ischemia,brain, kidneys
S&S of _____(septic) _________(shock):
1) same as in "normal" systemic inflammatory response, only worse: malaise, etc; fever, leukocytosis, __________(elevated) ___(CRP) & ____(ESR)
2) low BP results in ___________(ischemia) to organs such as _______(brain), _______(kidneys),
etc, so patient can have altered mental function, renal failure, heart failure, death.
?
antiinflammatories, suppress, prostaglandins, steroids, nsaids
to minimize the pain and swelling of inflammation (whether it's "normal" inflammation or "too much inflammation"), certain medications can be given, called "_____________(antiinflammatories)."
2) the mechanism of action of most antiinflammatories is to ___________(suppress) the effects of __________(prostaglandins), which works well in suppressing inflammation but can result in side effects.
3) in general two types of antiinflammatories exist—__________(STEROIDS), and ___________(NSAIDs)—"non-steroidal antiinflammatory drugs."
prostaglandins, created, arachidonic , pro-inflammatory,
____________(prostaglandins) (PGs) are a group of mediators that have a huge variety of functions
1) PGs are _______(created) in the cell membrane of most cells in body, in a series of steps called the _________(arachidonic) pathway (see next page, also Prep)
2) PGs are generally categorized as either being protective or proinflammatory.
a) certain types of PGs stimulate further inflammation by increasing vascular permeability and also induce fever &
pain
these PGs are "________(pro-inflammatory)" PGs
b) others types have protective characteristics that are important in many ways throughout the body; they are what I call "protective" PGs.
d
_____________work here; they are enzymes that catalyze the creation of arachidonic acid from the phospholipids of the cell membrane
A. granulating
B. desquamation
C. septicemia/sepsis
D. phospholipases
natural, steroids, cortisol, suppress, proinflammatory, prostaglandins
in the body there are _________(natural) occurring _________(steroids), the most common of which is ________(cortisol)
b. synthetic examples are drugs based on the structure of cortisol such as prednisone & solumedrol.
c. steroids are non-specific in their inhibition of prostaglandins, ie, steroids ______(suppress) both ___________(proinflammatory) AND protective types of ___________(prostaglandins)
d. they do this by suppressing phospholipase, the enzyme high up in the arachidonic pathway which catalyzes the creation of arachidonic acid from the phospholipids in cell membranes.
e. steroids are the strongest and best antiinflammatories because they work so high up in the arachidonic pathway, thus blocking both prostaglandins and leukotrienes
steroids, side, ulcers, bleeding, diminish, kidney, combat, htn
it makes _______(steroids) the worst of all anti-inflammatories in
creating ___(side)-effects related to suppression of the protective roles of prostaglandins
2) some of these potential side effects are stomach________(ulcers), easier _______(bleeding), __________(diminish)ed _______(kidney) function, diminished capacity to ________(combat) infection, increased skin fragility, ___(HTN)
nsaids, work, lower, not, powerful, side
non-steroidal antiinflammatories - _______(NSAIDs)
a. these suppress inflammation also, but do so at a lower place in the arachidonic pathway.
b. since NSAIDs ____(work) _______(lower) in the arachidonic pathway they are ___(not) as ______(powerful) as steroids, nor do they have as bad of ___(side) effects, so they are used more for problems such as headaches, general aches and pains, etc, rather than to suppress more serious inflammatory conditions.
c. examples of NSAIDs—aspirin, ibuprofen (Motrin), naproxen
NSAIDs, for, headaches, aspirin, naproxen
non-steroidal antiinflammatories - ______(NSAIDs)
a. these suppress inflammation also, but do so at a lower place in the arachidonic pathway.
b. since NSAIDs work lower in the arachidonic pathway they are not as powerful as steroids, nor do they have as bad of side effects, so they are used more ____(for) problems such as _________(headaches), general aches and pains, etc, rather than to suppress more serious inflammatory conditions.
c. examples of NSAIDs—______(aspirin), ibuprofen (Motrin), __________(naproxen)
t, cd4, intro, cd8, direct
Subtypes of ___(T)-lymphocytes include:
(1) ____(CD4) cells (AKA helper-T)— act as "_____(intro)ductory" cells.
(2) ____(CD8) cells (AKA cytotoxic T-cells)—act as ______(direct) killers
(3) Memory T cells
t, cell, b, humoral
if the ___(T) cell is "in charge" of developing immunity, you can say the person developed "____(cell)-mediated" immunity.
2) if the ___(B) cell is "in charge" of developing immunity, you can say the person developed "________(humoral)" immunity.
antibodies, defeat, neutralization, binding, toxins
___________(antibodies) _______(defeat) microbes in several ways, including:
1) ________(neutralization) (inactivation):
a) neutralize bacterial toxins by ________(binding) to the toxins of bacteria, thus rendering the _____(toxins) unable to bind to host tissues
opsonization, coats, phagocytosis, optimized
_______________(opsonization): "___(coats)" bacteria—this promotes ___________(phagocytosis) by _____________(optimized) recognition and "digestibility" of antigen for phagocytes
abnormal, immunocyte, Hypersensitivities, much
___________(Abnormal)ities in __________(immunocyte) response: ___________(Hypersensitivities)—" too ______(much)" immunocyte response
allergic, response, hypersensitivity, environment
_____________(allergic) _______(response) ("allergic reaction"): ___________(hypersensitivity) to a target antigen from the __________(environment), called an allergen.
alloimmune, hypersensitivity, another's, antigens
_____________(alloimmune) response: _____________(hypersensitivity) to ________(another's) person's ________(antigens) (the target antigen), such as when an organ is transplanted
autoimmune, hypersensitivity, self-antigens
____________(autoimmune) response: _________(hypersensitivity) to _________(self-antigens) (the target antigen) - a reaction of our body to our own antigens.
allergic, ige, degranulation, histamine, binds, h1
_________(allergic) response but if you are an individual who is genetically programmed, ie, "predisposed" to an allergic response, there is a pathologic response to that substance that in particular involves the ______(IgE) antibody.
3) after initial exposure to that substance (which we will now call an "allergen" because you are predisposed to be allergic to it), IgE pathologically binds to mast cells instead "standing down" —this "sensitizes" the mast cell
4) on repeated exposure to that allergen, the allergen's receptors bind to the IgE on the sensitized mast cell and quickly initiates _______(degranulation) of mast cell ________(histamine) release histamine __________(binds) to ________(H1) receptors of surrounding tissue & causes systemic and/or local reactions.
allergic, rash, anaphylaxis, hives, urticaria, angioedema, vasodilation
___________(allergic) reaction once a person is sensitized, the S&S appear immediately upon 2nd or more exposure
2) localized reaction: (such as with dermatitis--skin reaction): local ___(rash), itching, swelling, from histamine, leukotriene, prostaglandin effects.
3) systemic reaction-- _________(anaphylaxis)
a) occurs when someone is more severely allergic to the antigen (determined by previous exposures and person's genetic makeup)
b) histamine, leukotrienes, PGs, and acute phase reactants such as complement system are overactivated throughout body—all the S&S noted for localized reactions become systemic.
(1) itching all over; ____(hives) (____________)(urticaria)
(2) ______________(angioedema)----abnormal _________(vasodilation)
and edema of small blood vessels; usually occurs in lips & hands
3717
allergic, wheezing, leukotriene, hypotension
___________(allergic) reaction once a person is sensitized, the S&S appear immediately upon 2nd or more exposure
_______(wheezing) (from bronchial edema, but also from ___________(leukotriene)-induced bronchoconstriction), dyspnea; possibly laryngeal edema
(4) ______(hypotension) & shock if bad enough—what causes the hypotension in this context?
allergic, treatment, antihistamines, steroids, leukotriene, blockers
__________(allergic) reaction
_______(treatment)—meds that work against
a) histamine—_______(antihistamines)
b) inflammatory properties of PGs: _____________(steroids)
c) against bronchoconstrictive properties of leukotrienes: _______(leukotriene) ________(blockers) (FYI--Singulair).
autoimmune, genetic, hla, hlab27, psoriasis, females
__________(autoimmune) reaction
also, ______(genetic) factors important in autoimmune dzs —presence of certain ___(HLA) antigens in people with certain autoimmune diseases is statistically significant
ex. ______(hlab27) causes _______(psoriasis)
c) gender effect is a consideration—10 :1 ratio ___________(females) to males
?
tissue, autoimmune, sclerosis, t, destroy, myelin, weakness
________(tissue)-specific _______(autoimmune) diseases
1) multiple ________(sclerosis)--
a) ___(T)-lymphocytes ________(destroy) random patches of the ________(myelin) sheath that insulates the fibers of neurons in the brain
b) results in asymmetric _______(weakness) and/or malfunction of various areas of the body.
tissue, autoimmune, graves, hyperthyroidism, goodpasture, pulmonary, glomerular
________(tissue)-specific _______(autoimmune) diseases
______(Graves) disease
a) disease that causes most cases of _________(hyperthyroidism)
b) autoantibody stimulates thyroid gland cells to oversecrete thyroid hormone (TH), causing S&Ss of hyperthyroidism
3) _______(Goodpasture)'s syndrome
a) autoantibody attacks connective tissue in _______(pulmonary) &__________(glomerular basement membrane.
b) results in pulmonary hemorrhage & glomerulonephritis
4) myasthenia gravis
a) autoantibody attacks acetylcholine receptors on cells of muscles
b) this means that acetylcholine would not have enough effective post-synaptic gap receptor; what kinds of S&S?_______________
?
tissue, autoimmune, myasthenia, acetylcholine, type-1, celiac, intolerance, gluten
________(tissue)-specific _______(autoimmune) diseases
4) ________(myasthenia) gravis
a) autoantibody attacks ________(acetylcholine) receptors on cells of muscles
b) this means that acetylcholine would not have enough effective post-synaptic gap receptor;
5) _____(type-1) diabetes
a) T-cells destroy insulin-producing cells.
b) without insulin, glucose accumulates in blood + no energy source for cells
6) ________(celiac) disease (AKA "sprue"):
a) caused by individual's _______(intolerance) of a protein called _______(gluten) found in wheat and other foods
b) gluten triggers an attack by T-cells on own intestinal lining & causes diarrhea
autoimmune hemolytic anemia
a) a trigger such as a drug causes autoantibodies to attack RBCs
b) the result is abnormally high hemolysis (destruction of RBCs) &
resultant low numbers of them (anemia)
systemic, autoimmune, immune-complex, vessels, inflammation, vasculitis
_______(systemic) _________(autoimmune) diseases
1) overview
a) these are autoimmune reactions in which antibody & self-antigen pair up into a molecule called an _____________
____________________(immune-complex)
the immune complex irritates the blood ______(vessels) & causes _________(inflammation) of them (_____)(vasculitis)
systemic, lupus, women, autoantibodies, nucleic
________(systemic) ____(lupus) erythematosus (SLE), sometimes just called "lupus"
a) genetic predisposition & mostly seen in _____(women)
b) pathogenesis / S&S /dx:
(1) in everyone, there are normally always bits of degraded
cells & nucleic acids like DNA in the blood on their way to being disposed of in the spleen, liver, etc.
(2) due to a not well-understood mechanism, some antibodies that happen to be circulating in the blood
become __________(autoantibodies) when they encounter some of these bits of the person's own _____(nucleic) acids.
(3) they attach themselves to the DNA_ & together they become immune complexes
lupus, malar, arthritis, serositis,
_____(lupus) often there are skin rashes such as classic butterfly" ____(malar) rash (across cheeks)—in a crude way, this rash creates a wolf-like facial
appearance —hence the Latin "lupus)"—"wolf"
(c) joints: nonerosive _______(arthritis) of at least 2 peripheral joints
(d) _______(serositis) - inflammation of serous compartments (sacs in body such as pleura and pericardial sac)—causes pleurisy, pericarditis.
(e) kidneys—proteinuria
(f) neurons of brain—seizures
(g) fatigue (almost always found in autoimmune diseases of all types)
sle, elevated, crp, ana
(7) ____(SLE) diagnosis
(a) by clinical findings above
(b) lab tests:
o ______(elevated) ___(CRP)—non-specific inflammatory test
o more specific for lupus—____(ANA)--stands for antinuclear antibody—ie, this tests looks for the presence of the immune complexes made up of antibody + nucleic acid (DNA)
20
systemic, autoimmune, rheumatoid, autoantibody, collagen, joint, iritis
________(systemic) ___________(autoimmune) __________(rheumatoid) arthritis (RA):
a) etiology—similar to SLE, but instead of the autoantibody / nucleic acid immune complex, the RA immune complex consists of an -___________(autoantibody) attached to _________(collagen)
b) inflammation develops anywhere there is collagen but most
commonly in synovial membranes (synovial refers to lining of joints) of small joints such as hands
c) S&S
(1) fatigue
(2) ____(joint) pain, swelling & deformation
(3) also can have inflammatory S&S of eyes, heart, lungs, almost any tissue.___(iritis)
rheumatoid, autoimmune, ra, any, age, morning
__________(rheumatoid) arthritis (RA): _______(autoimmune)
a) etiology—similar to SLE, but instead of the autoantibody / nucleic acid immune complex, the RA immune complex consists of an autoantibody attached to collagen
elevated CRP
(b) more specific for ___(RA)—rheumatoid factor ( )-- this tests looks for the presence of the immune complexes made up of antibody + collagen
begins at ____(any) _____(age) & is due to inflammation that damages joints
(b) other areas of body often become inflamed and painful as well.
(c) pain tends to be worse in ____________(morning) & lessens as day goes on
alloimmune, histocompatibility, hla
4. ________(alloimmune) hypersensitivity
a. overview
1) the target antigen in this category is someone else's cells.
2) this type of hypersensitivity is in some respects not a "true" hypersensitivity
to be able to distinguish "self" from foreign, almost all body's cell membranes have "self-antigens" composed of protein; these are called ___________(histocompatibility) antigens (histo = "tissue") and are commonly known as "____(HLA)s"--human leukocyte antigens (because they were first discovered on leukocytes)
abo, ab, any
____(ABO) compatibility issues ___(ab) ____(any)
without, rh, given, ok, first, second, reaction
so, a person ___________(without) the ____(RH) factor who is ______(given) RH+ blood will be ___(ok) the ______(first) time he gets the blood, since he hasn't developed antibodies yet
3) if he receives Rh + blood a _________(second) time, may have a transfusion __________(reaction) (like described above).
never, problem, mom, rh, +, or, baby, negative
never, problem, mom, rh, +, or, baby, negative
mom, rh, negative, baby, positive, cure, rhogam
mom, rh, negative, baby, positive, cure, rhogam
no, rhogam, baby, get, erythroblastosis
no, rhogam, baby, get, erythroblastosis
immunodeficiencies, only, opportunistic
_____________(immunodeficiencies) -- "not enough" immunocyte response greatly increase the chance of the immunocompromised person ____(only) getting __________(opportunistic) diseases
a) these are diseases caused by an increased susceptibility to diseases that immunocompetent people DON'T get, ie, to microbes that are normally harmless.
combined, b, t, deficiency, congenital, scids, genetic
______(combined) __(B)-cell & __(T)-cell immuno__________(deficiency) - essentially the diminishment or absence of BOTH humoral and cell-mediated immunity.
1) _______(congenital): ________(SCIDS)—severe combined immunodeficiency syndrome— caused by diverse _________(genetic) mutations that lead to complete absence of all immune function ("bubble boy")
2) acquired
a) irradiation & cytotoxic drugs for cancer wipe out bone marrow, so don't have enough T AND B lymphocytes.
b) immunosuppressant drugs post-transplant
c) aging
combined, b, t, deficiency, irradiation, aging
______(combined) __(B)-cell & __(T)-cell immuno__________(deficiency) - essentially the diminishment or absence of BOTH humoral and cell-mediated immunity.
2) acquired
a) ________(irradiation) & cytotoxic drugs for cancer wipe out bone marrow, so don't have enough T AND B lymphocytes.
b) immunosuppressant drugs post-transplant
c) ______(aging)
humoral, b, deficiency, congenital, igg, missing
______(humoral) (___(B)-cell) immuno__________(deficiency)—most commonly a ________(congenital) problem—example is X-linked hypogammaglobulinemia
1) ___(IgG) ___________(missing) or lessened in amount
2) what would be sequela
congenital, DiGeorge, 22, failure, thymus
_____(congenital)-- ______(DiGeorge)s syndrome-- genetic defect on chromosome ___(22) that causes _______(failure) of development of _________(thymus);
aids, kills, cd4
acquired-- ___(AIDS)—Acquired Immunodeficiency Syndrome
a) caused by human immunodeficiency virus (HIV)
b) virus invades ____(kills) ___(CD4) cells & begins killing them— decreases ability to mount immune responses because the CD4 cell is so important as an "introductory" component to development of various immunities
hiv, rna, retrovirus
___(HIV) is an ____(RNA) ________(retrovirus)
a) a regular RNA virus inserts its RNA into cytoplasm of host cell & takes over ribosomal protein-building for its own propagation
b) a retrovirus inserts its RNA into a host cell cytoplasm, converts its own RNA into DNA, then back into RNA.
less CD4 cells = increased susceptibility to infections in general and opportunistic infections in particular.
diagnosis, hiv, elisa, confirm, western
_____(diagnosis) of _____(HIV):
1) lab test called an ________(elisa) (enzyme-linked immunosorbent assay)-is used first.
a) this tests for presence of antibodies to HIV (as soon as the virus entered the body, the immune response is triggered & antibodies are usually detectable by 1-2 weeks or so.)
b) 96% of all infected individuals will test positive within 2 to 12 weeks of the initial infection
c) if the ELISA is negative, recommendations for further testing depends on several factors, such as patient risk status and timing of the testing.
if ELISA is positive, a second test, or ________(confirm)atory test is done called __________(western) blot—more expensive, but more specific &
very few false positives
c
man presents to an ER with a large laceration sustained at a construction site 3 days before. The area around the laceration is erythematous, painful, and swollen.
1. The erythema and swelling can be explained at a cellular level by all the following EXCEPT
a. mast cell degranulation and release of histamine.
b. pro-inflammatory prostaglandins are released.
c. immunoglobulins are reacting to HLA antigens.
d. local reaction to acute phase reactants.
?
d
man presents to an ER with a large laceration sustained at a construction site 3 days before. The area around the laceration is erythematous, painful, and swollen.
The patient is given a TIG (tetanus immunoglobulin) injection because the wound is high risk for tetanus exposure and he doesn't remember ever having a tetanus vaccination. The purpose of the TIG is to
a. prevent any tetanus bacteria from activating the inflammatory system.
b. introduce tetanus bacteria so that the immune system can create antibodies to tetanus.
c. prevent an autoimmune reaction to any tetanus bacteria that might be present.
d. provide tetanus antibodies to fight any tetanus bacteria that might be present.
a
man presents to an ER with a large laceration sustained at a construction site 3 days before. The area around the laceration is erythematous, painful, and swollen.
3. The patient ______(should or should not) also get a tetanus vaccination, because_____.
a. should: he needs protection against future tetanus exposure.
b. should: the vaccination will provide additional passive immunity.
c. should not: the TIG is enough, as it will provide long term active acquired immunity
d. should not: the vaccine will do nothing for the current exposure.
d
A microbe invades the body for the first time. Which statement is most likely about the processes that follow?
a. Plasma cells will immediately secrete T-cells specific to that microbe.
b. CD4 cells will introduce remnants of the microbe to the B-cells, which directly phagocytize the remnants.
c. Antigens will be created from the memory cells of immunocytes.
d. Immunocytes will begin the process of developing memory to that microbe.
c
A patient has a systemic inflammation. All the following are likely associated with his condition EXCEPT
a. increased acute phase reactants.
b. lab results showing a high C-reactive protein (CRP).
c. lab results showing leukopenia.
d. increased pro-inflammatory prostaglandins.
b
A baby who has received immunoglobulins against the "XYZ" virus via its mother's milk
now has
a. natural active acquired immunity.
b. natural passive acquired immunity.
c. passive innate immunity.
d. active innate immunity.
b
A baby who has received immunoglobulins against the "XYZ" virus via its mother's milk
now has
The baby in question 6 will ________.
a. have lifelong immunity to the XYZ virus because of receiving the immunoglobulins that are specific to that particular microbe.
b. develop temporary immunity to the XYZ virus due to receiving Mom's antibodies that are specific to that particular microbe.
c. now have complete 2nd line of defense protection, having received it in the breast milk.
d. develop an immunodeficiency : receiving defective immunocytes in the breast milk.
d
A patient presents with generalized itching, urticaria, and wheezing. She says it started after she was stung by a bee.
8. The patient is most likely experiencing
a. the effects of complement system opsonization of an invading microbe.
b. localized effects of mast cell degranulation.
c. a cell-mediated response.
d. anaphylaxis.
?
a
The wheezing is at least partly caused by
a. bronchoconstriction due to leukotriene over-release from mast cells throughout the body.
b. over-active response to immune complex deposition in the lung tissue.
c. bronchoconstriction from humoral immunodeficiency.
d. vasoconstriction from the effect of autoimmune over-degranulation
b
A patient presents with generalized itching, urticaria, and wheezing. She says it started after she was stung by a bee.
The most appropriate treatment for this patient is to __________, because _______.
a. give an NSAID: it suppresses phospholipase enzymes.
b. give a steroid: it will suppress prostaglandin activity.
c. do a CRP test: it will determine the degree of hypersensitivity.
d. give an antihistamine: it will suppress IgE
d
A patient has just had a liver transplant and is beginning to display signs S&S consistent with rejection. The following is most likely a true statement about the situation:
a. The patient is undergoing an autoimmune hypersensitivity.
b. The patient is undergoing an IgE-mediated hypersensitivity reaction.
c. The donor's immunoglobulins are attacking the HLA's on the patient's RBCs.
d. The recipient's immunoglobulins are attacking the HLA's on the donor liver.
d
A woman has just been diagnosed with SLE.
12. In educating the patient about her disease, the nurse shows complete understanding of the pathophysiology of SLE when he tells the patient:
a. "Unfortunately, you will need to be on a gluten-free diet."
b. "You should expect to have swelling in the area of your thyroid."
c. "Fortunately SLE only affects one area, usually the joints in your hands."
d. "You may have a variety of symptoms that come and go."
?
c
A woman has just been diagnosed with SLE.
13. Lab tests are done. Which of the following is most likely?
a. Test results that indicate hemolytic anemia.
b. A low CRP.
c. A positive ANA.
d. Test results that indicate a low ANA.
b
A woman has just been diagnosed with SLE.
The pathophysiology related to the above test is best described by which of the following?
a. Vasculitis caused breakdown of RBCs, resulting in anemia that this lab test detects.
b. SLE is a hypersensitivity disorder in which autoantibodies attack nucleic acids and form detectable complexes that circulate in the blood; the blood is tested for the circulatory presence of these complexes.
c. SLE is a hypersensitivity disorder in which autoantibodies attack DNA and form detectable complexes that migrate to one type of tissue; that tissue is tested for presence of these complexes.
d. Immune complexes invade CD4 cells, a phenomenon which is detected by lab tests as a low ANA.
c
. A patient tells her nurse practitioner (NP) that he had rheumatic fever as a child. Knowing the pathophysiology behind this disease, the NP will need to assess the patient for
a. angioedema.
b. S&S of immunodeficiency.
c. heart valve problems.
d. urticaria.
a
A patient who receives blood with an incompatible blood type may develop
a. an alloimmune reaction.
b. an opportunistic infection.
c. a humoral autoimmune reaction.
d. a chemotactic autoimmune reaction.
b
Which of the following compatibility situations is most likely? A patient who is
a. B positive and receives B negative blood will have a transfusion reaction.
b. AB positive and receives B negative blood will do fine.
c. A negative and receives A positive blood will do fine.
d. A negative and receives O negative blood will have a transfusion reaction.
d
A patient presents to the ED with fever, chills, myalgia, and a dry cough. He says he has recently traveled to China. He says he got a flu shot a year ago.
1. Which is most likely in this case?
a. This disease is pertussis, probably contracted from an unvaccinated contact when he visited China.
b. The disease is probably not influenza, since he had a flu shot during last year's flu season.
c. The diagnosis is influenza, probably contracted via fecal/oral route while in China.
d. The diagnosis is influenza, possibly contracted because patient did not have this year's flu shot.
?
c
A patient presents to the ED with fever, chills, myalgia, and a dry cough. He says he has recently traveled to China. He says he got a flu shot a year ago.
2. The disease mentioned above has the following characteristic:
a. The causative microbe can also cause a membrane across the pharynx.
b. This disease is difficult to treat because of the antigenic drift of its exotoxin.
c. New mutations of proteins on its cell membrane cause a variety of types.
d. A later outbreak may include skin lesions in a dermatome pattern.
b
A commonality of genital herpes, chicken pox, and shingles is that
a. each is caused by a bacterial organism that penetrates the nervous system.
b. the causative microbe can remain dormant in the nervous system.
c. the causative microbe causes bloody diarrhea.
d. each is transmitted via vector.
a
Otherwise healthy persons whose water supply comes from a well are more at risk for________.
a. a protozoa that causes diarrhea.
b. helminthic infection.
c. c diff infection.
d. the malaria protozoa.
a
4 year old patient presents with bloody diarrhea. Possible causes include ___ because____.
a. shigella: the microbe has caused inflammation in the lining of the intestines.
b. pseudomembranous colitis: C. diff has eradicated normal flora.
c. giardia: this protozoa invades the intestinal wall and causes necrosis.
d. diphtheria: this bacteria causes parotid enlargement.
a
A 4 year old patient presents with bloody diarrhea.
The child above becomes very sick, with S&S that include low BP and altered mental status. The cause of his S&S is likely
a. wide-spread inflammatory mediators causing vasodilation.
b. re-awakening of a dormant microorganism.
c. post-infection autoimmune syndrome.
d. neuraminidase invasion of the CNS.
?
b
After coming home from an overseas assignment a young army officer begins complaining of extreme fatigue and arthralgia. He has a very high fever and is anemic. The most likely etiology of his S&S is
a. infection with rabies virus.
b. protozoal invasion of his RBCs
c. Staph aureus-related cellulitis.
d. Guinea worm infestation.
?
b
A young woman presents to her nurse practitioner complaining of SOB and fatigue. She states that her periods have been very heavy. (norm RBC = 4-6million; norm MCV = 80-95).
1. What is her most likely diagnosis and CBC results?
a. macrocytic anemia; RBCs = 3 mill & MCV = 102.
b. microcytic anemia; RBCs = 3 mill & MCV = 70.
c. normocytic anemia; RBCs = 3 mill & MCV = 90.
d. polycythemia vera; RBCs = 20 mill & MCV = 90.
?
c
A young woman presents to her nurse practitioner complaining of SOB and fatigue. She states that her periods have been very heavy. (norm RBC = 4-6million; norm MCV = 80-95).
Based on the diagnosis, the patient's S&S can be explained by the following:
a. a malfunction in DNA during erythropoiesis causes inadequate ATP formation.
b. an underlying chronic disease causes a steady loss in RBCs.
c. a steady loss of iron results in insufficient hemoglobin production.
d. a malformed hemoglobin molecule that decreases oxygen-carrying capacity of each RBC.
a
A young woman presents to her nurse practitioner complaining of SOB and fatigue. She states that her periods have been very heavy. (norm RBC = 4-6million; norm MCV = 80-95).
The patient probably has a certain degree of hypoxemia because
a. her low levels of iron have decreased the O2-carrying capacity of her Hgb.
b. a secondary polycythemia has resulted from an underlying lung disease.
c. she is not breathing in enough oxygen, resulting in unsaturated Hgb molecules.
d. her heavy periods have led to a loss of Von Willebrand factor.
a
A young woman presents to her nurse practitioner complaining of SOB and fatigue. She states that her periods have been very heavy. (norm RBC = 4-6million; norm MCV = 80-95).
Which of the following will most likely be part of the treatment rationales for this patient?
a. iron (Fe) supplements will help the SOB by increasing the capacity of Hgb to carry O2.
b. a well-rounded diet will provide nutrients to increase production of intrinsic factor.
c. treating the underlying disease process will restore normal eythropoiesis.
d. injections of vitamin B12 will increase the size of the RBCs.
d
A patient recently diagnosed with a vertebral fracture says, "I can't understand how I broke it. I sat down a little too hard, but not hard enough to break anything." His diagnosis is possibly _____because _____.
a. leukemia : excessive, non-functional white blood cells increase risk of infection.
b. idiopathic thrombocytopenia purpura (ITP): the low platelet count causes increased risk of bleeding.
c. aplastic anemia: suppression of bone marrow stem cell proliferation causes pancytopenia.
d. multiple myeloma: increased osteoclastic activity causes osteoporosis.
c
A patient recently diagnosed with a vertebral fracture says, "I can't understand how I broke it. I sat down a little too hard, but not hard enough to break anything."
The correct answer for the patient above most likely causes additional S&S, including
a. multiple petechiae due to coagulopathy.
b. leukocytosis due to the infection and inflammation.
c. lethargy from the hypercalcemia.
d. decreased production of clotting factors.
b
A person notices ecchymosis under her skin in several areas of her body but denies any substantial trauma to those areas. These ecchymoses could be related to the presence of all the following EXCEPT:
a. liver disease resulting in decreased clotting factors.
b. compensatory erythrocytosis from living in higher elevation.
c. hypersplenism.
d. thrombocytopenia.
a
. local chronic inflammatory tissue reaction
A. granuloma
B. erythema
C. leukopenia
D. chemotactic defect
E. decrease in phagocytic functions
b
reddened, inflamed appearance of skin
A. granuloma
B. erythema
C. leukopenia
D. chemotactic defect
E. decrease in phagocytic functions
e
results in decreased inflammatory response and less healing ability
A. granuloma
B. erythema
C. leukopenia
D. chemotactic defect
E. decrease in phagocytic functions
d
example of qualitative defect of "not enough" inflammatory function
A. granuloma
B. erythema
C. leukopenia
D. chemotactic defect
E. decrease in phagocytic functions
e
breach of first line of defense
A. vasodilation
B. mast cells of tissue
C. leukopenia
D. serosanguinous exudate
E. Sjogren's syndrome
d
wound fluid leakage contains serous fluid and blood
A. vasodilation
B. mast cells of tissue
C. leukopenia
D. serosanguinous exudate
E. Sjogren's syndrome
c
example of quantitative defect of "not enough" inflammatory function
A. vasodilation
B. mast cells of tissue
C. leukopenia
D. serosanguinous exudate
E. Sjogren's syndrome
b
degranulation releases histamine, prostaglandins, leukotrienes
A. vasodilation
B. mast cells of tissue
C. leukopenia
D. serosanguinous exudate
E. Sjogren's syndrome
a
part of inflammation in which vasomotor tone of capillaries "relaxes"
A. vasodilation
B. mast cells of tissue
C. leukopenia
D. serosanguinous exudate
E. Sjogren's syndrome
a
a way of conferring artificial passive immunity
A. booster shot
B. steroid
C. stomach ulcers
D. antibiotics
E. endemic
c
steroidal suppression of protective prostaglandins
A. booster shot
B. steroid
C. stomach ulcers
D. antibiotics
E. endemic
b
. suppresses pro-inflammatory aspects of prostaglandins
A. booster shot
B. steroid
C. stomach ulcers
D. antibiotics
E. endemic
d
negative effect on normal bowel flora resulting in breach of body's defenses
A. booster shot
B. steroid
C. stomach ulcers
D. antibiotics
E. endemic
e
used to describe a disease that exists all the time in certain communities; ex— "malaria is _______ to parts of Africa."
A. booster shot
B. steroid
C. stomach ulcers
D. antibiotics
E. endemic
a
an outbreak of a disease that spreads within a certain time frame to people of one or several communities; ex—"There is often a yearly flu __________ in some U.S. communities."
A. epidemic
B. pandemic
C. infection
D. antibiotics
E. endemic
b
the disease outbreak spreads from being epidemic (a few communities) to being worldwide; ex—"The Spanish flu of 1918 began as an
epidemic amongst soldiers at U.S. army bases, then became __________when they went to Europe during WWI."
A. epidemic
B. pandemic
C. infection
D. antibiotics
E. endemic
c
invading organism is pathogen—an organism that causes harm
c. types of pathogens—bacteria, viruses, rickettsia & chlamydia, fungi, parasites
A. epidemic
B. pandemic
C. infection
D. antibiotics
E. endemic
breach, airborne, fecal, blood
______(breach) of integrity of skin and/or mucous membranes—scrapes, lacerations, bites, sexual activity (sexual transmission), etc
2) _____(airborne)— sent out via coughing, sneezing, etc, and inhaled.
3) oral / ____(fecal) route --entry via GI tract --means organism is
ingested, sometimes by directly drinking/ eating it, or by taking in
microscopic fecal material on hands (good handwashing helps prevent!)
4) _______(blood) borne—blood-to-blood or blood-to-open skin
a) almost any disease can become blood-borne under right circumstances—example: hepatitis C & HIV are most often sexually-transmitted but can be received into the blood via IV-drug abuse needles or blood transfusions
b) but as a general rule, blood-borne diseases mean that they are less infectious—harder to "catch" than the other portals of entry.
course, disease, incubation, replication, prodromal, s&s, acute, maximum
_______(course) of a ______(disease)— stages that are pathogen-specific & affected by all above factors
a. ________(incubation) period—phase during which the pathogen begins active _______(replication) but doesn't produce S&Ss; varies in length: salmonella—6 to 8 hrs, hep B—50 to 180 days
b. ________(prodromal) stage - initial appearance of ____(S&S)s—may be mild
c. ________(acute) stage—______(maximum) impact, with very pronounced & specific S&Ss
d. convalescent period—containment of infection & resolution of S&Ss
e. resolution - total elimination of pathogen without remaining S&Ss
beta, lactamase, destroy, penicillin, mrsa, strept
beta lactam resistance
1) overview
a) penicillin and its derivatives are called beta-lactam antibiotics because they all have a molecular structure called a beta-lactam ring; ex of penicillins—methicillin, amoxicillin, etc.
b) beta lactams used to be effective against a wide spectrum of microbe
c) then certain microbes mutated and developed an enzyme called
___________(beta) ________(lactamase), which can _____(destroy) beta-lactam ________(penicillin)antibiotics by dismantling the beta lactam ring..
d) specific beta-lactamase microbes: ____(MRSA) & resistant _______(Strept)ococcus pneumoniae
mrsa, methicillin, long, nosocomial, fomites
________(MRSA) developed in 1960's in hospitalized patients that had been on ________(methicillin) so ________(long) that one strain of the staph bacteria mutated and became resistant.
c) now rampant in some hospital settings, nursing homes, etc, and is still generally known as a ________(nosocomial) disease—spread by (1) direct patient-to-hands-to-patient contact
(2) colonization of nares of healthcare workers
(3) occasionally __________(fomites) such as stethoscopes.
the drug vancomycin is now one of the few drugs that will destroy MRSA
strept, otitis
resistant ____(Strept)ococcus pneumoniae
a) most common microbe causing _____(otitis) media (inner ear infection)
b) used to be easily treated with penicillin until ear infections became overtreated or treated inappropriately (antibiotics don't cure viral ear infections)
c) new strain of strep developed that makes beta lactamase & now many ear infections are much harder
a
_________--infection of the dermis and subcutaneous tissue
a. pathogenesis:
1) most commonly, an organism such as Staphylococcus aureas that normally dwells on TOP of the skin (ie, on epidermis layer), gains deeper entry after a laceration, puncture, etc (sometimes the breach is microscopic)
2) or sometimes _______follows a milder staph infection of the skin such as impetigo, an eruption of blisters usually around nose & mouth that are itchy, crusty, and contagious.
b. infected area is erythematous, swollen, painful
c. tx (treatment) for ______—abx (antibiotics)
A. cellulitis
B. botulism
C. tetanus
D. rabies
E. malaria
b
caused by the toxin of Clostridium botulinum, a bacillus that can invade the body via food or soil (dirt-to-wound).
b. toxin heads for neuromuscular nerve synapses & blocks acetyl choline muscle receptor cells.
c. typical S&S is a descending, symmetric paralysis, including respiratory
d. ex—"floppy baby syndrome"—seen in children that eat honey contaminated
with C. botulinum.
e. considered one of top candidates for bioterrorism use.
f. tx—temporary mechanical ventilation, other supportive tx
A. cellulitis
B. botulism
C. tetanus
D. rabies
E. malaria
c
vaccination as part of DPT (diphtheria, pertussis, tetanus) but immunity weakens so must get boosters every 10 years.
b. pathogenesis of ______ disease:
1) caused by Clostridium tetanii, a bacillus which can live in soil as a spore  when deposited in a wound, will then germinate
2) as it becomes active, will release exotoxin blocks
inhibitory neurotransmitters & causes uninterrupted nerve impulses to muscle cells can cause jaw muscle tightening called trismus (lockjaw), or more severe-- condition characterized by muscle twitching, cramps, convulsions,
c. tx—antibx & TIG.
A. cellulitis
B. botulism
C. tetanus
D. rabies
E. malaria
d
a. a virus transmitted in saliva of infected host, usually by bite to the skin (most common vector is a bat)
b. virus travels via peripheral nervous system (PNS) to the brain & spinal cord (central nervous system -- CNS) and causes brain inflammation leads to S&S of anxiety, agitation, confusion, convulsions
c. other S&S include production of large amount saliva, plus dysphagia = "foaming at the mouth" & "hydrophobia" (not really a fear of water, just can't swallow).
d. tx:
1) treatment needs to begin within first 14 days with post-exposure prophylaxis (PEP) -- one dose of _____ immunoglobulin and five doses of ______ vaccine over first 30days.
2) if not treated within this time, the _____virus will continue it "trip" all the way up to the CNS—once CNS infected, there is no cure.
3) without tx, almost always fatal.
A. cellulitis
B. botulism
C. tetanus
D. rabies
E. malaria
e
responsible for 2 million deaths in the world yearly.
b. caused by protozoa that is transmitted via mosquito vector.
c. protozoa reproduces in liver cells (hepatocytes) and then is released into
blood, where it infects RBCs & causes them to rupture (hemolysis) as the RBCs rupture, they trigger a flooding of acute phase reactants into blood causes S&S
d. S&S - high fever, chills, arthralgia, anemia, splenomegaly, cerebral ischemia, heart failure
e. tx—prophylaxis with quinine-based drugs; antibiotics
A. cellulitis
B. botulism
C. tetanus
D. rabies
E. malaria
a
invades via coughing, sneezing
b. S&S - red, sore throat, often white patches on tonsils
c. with certain strains of it, can get scarlet fever (AKA "scarlatina") along with above S&S—a fever and rash that can cover whole body.
d. VERY important for infected person to get antibx early on: getting an early and thorough treatment of antibx will lessen chance of autoimmune disease like rheumatic fever.
A. strep throat
B. diphtheria
C. pertussis
D. mumps
E. malaria
b
very contagious upper respiratory infection (URI) caused by bacterium transmitted by cough, sneeze, etc
b. S&S - sore throat, fever, pseudomembrane across tonsils & throat
A. strep throat
B. diphtheria
C. pertussis
D. mumps
E. malaria
c
a highly contagious disease that is one of the leading causes of vaccine-preventable deaths in underdeveloped countries
b. also known as whooping cough, since one of S&S are horrible violent coughing fits that can be so bad that the person cannot eat & becomes malnourished (vaccine for diphtheria & pertussis given with tetanus as DPT)
A. strep throat
B. diphtheria
C. pertussis
D. mumps
E. malaria
d
virus that invades parotid glands—swelling, fever
b. main complication is infertility in males.
c. rarely seen in developed countries because of vaccine (MMR)
A. strep throat
B. diphtheria
C. pertussis
D. mumps
E. malaria
?
e
________
a. ________(nickname-- "two-week ______" or just "the ______")
1) virus passed by coughing, sneezing, etc
2) S&S -- dense red maculopapular rash starting on head & going down to body; also fever, cough, runny nose, conjunctivitis.
3) can have serious complications such as encephalitis (literally =inflammation of brain but usually refers to inflammation from microorganism)
4) rarely seen in developed countries except in immunocompromised or those not vaccinated with MMR, but still endemic in certain underdeveloped areas.
A. measles rubella
B. varicella
C. pertussis
D. mumps
E. measles rubeola
a
_______(nickname—"three-day ______" or "German ______")
1) milder virus & mild S&S—fever, rash, swollen glands.
2) main concern is if a woman contracts the disease in early pregnancy:
a) can cause baby to be born with problems like mental retardation, eye problems, hearing problems, and others
b) child-bearing age women should always have a _________ _______ done, and if low, need to be vaccinated.
3) vaccine (MMR) has eradicated it in US & certain other countries.
A. measles rubella
B. varicella
C. variola
D. zoster
E. measles rubeola
b
"pox" diseases (herpetic diseases)
a. overview of herpetic diseases
1) all are caused by some version of the herpes virus
2) a herpes virus, once in the body, never leaves the body—instead, "hides out in the nerves;" fortunately, most of the time it never "comes back out;" exceptions—genital & oral herpes; shingles.
b. ________ (nickname "chicken pox")
1) very contagious—spread via direct inhalation of virus from an infected person exhaling, sneezing, etc
2) manifests as vesicles (fluid-filled blisters) that begin on trunk and move outward & have different stages of development-- they appear, break, & crust in clusters at different times
3) person is contagious till the last lesion crusts
4) mortality very low, except in the immunocompromised person
5) chicken pox vaccine now part of normal immunization schedule
A. measles rubella
B. varicella
C. variola
D. zoster
E. influenza
c
_______(nickname "small pox")
1) also very contagious, inhaled virus, and also manifests as vesicles, but
different look & pattern than chicken pox—small pox lesions are dense
clusters that are all the same stage, start in the face & extremities and move toward the trunk.
2) besides lesions, and depending on the type of small pox virus, a patient may get high fever, severe flu-like S&S, painful pustules in mouth & esophagus; sometimes hemorrhage from the virulence of the virus toxin.
3) eradicated in the world (except for certain labs—feared as possible bioterrorist use)
A. measles rubella
B. varicella
C. variola
D. zoster
E. influenza
d
________(AKA herpes zoster; nickname—"shingles")
1) after having chicken pox, the varicella virus remains in one's system for life, becoming dormant in nervous system like herpes simplex
2) in most people it never travels to the skin again, but in some, especially with age and/or immunocompromised status, will "pop out" as painful lesions of the skin along a dermatome.
3) most people have a single episode
4) tx—antiviral meds, creams.
A. measles rubella
B. varicella
C. variola
D. zoster
E. influenza
e
_______("flu")
a. an acute viral illness of the upper and lower respiratory system with S&S of fever, chills, myalgia, malaise, dry cough, headaches.
b. self-limiting and usually not serious except in certain people of high risk: very young, elderly, chronically ill and debilitated, immunocompromised persons.
c. epidemiology
1) transmitted airborne respiratory droplets & occurs primarily in winter months
2) Type A circulates yearly, with epidemics every 3-5 years & with major pandemics every 25-35 years due to major mutations
3) yearly flu outbreaks almost always begin in Asian countries that have a high number of people that live close to animals, since animals such as pigs & birds such as chickens are the natural reservoir for the flu
d. pathogenesis of type A flu:
1) single stranded RNA virus with proteins on the viral cell envelope called neuraminidase and hemagglutinin.
2) these proteins catalyze the process of viral invasion of our respiratory cells, replication, and the release of the new viral progeny.
3) each time new progeny are released, host cells die necrosis of superficial respiratory cells and inflammation, causing S&S (see above) & also leaving host susceptible to bacterial pneumonia
A. measles rubella
B. varicella
C. variola
D. zoster
E. influenza
nomenclature, mutate, a, antigenic, hn
e. _______(nomenclature)
1) it is the neuraminidase and hemagglutinin viral proteins that ________(mutate) and cause yearly changes in Type _____(A) influenza viral makeup—this is called __________________(antigenic) drift or shift, depending on how
major the change is.
2) usually an ___(HN) designation is given according to the type of mutation' the avian flu, for example, was H5N1.
a
general etiologies & types of infectious _______
a. _____
1) mild S&S-- usually cause vomiting and watery diarrhea
2) sometimes called "stomach flu" but is not a true influenza
A. diarrhea viral
B. varicella
C. dysentery
D. zoster
E. influenza
b
_________ (causing non-bloody diarrhea)
1) spectrum of severity from mild to very severe & life-threatening watery diarrhea.
2) examples of organisms causing _________ enteritis:
a) E. coli-- certain strains can be ingested in undercooked meat & other foods (certain forms of E. coli normally found in our intestines do not cause diarrhea)
b) salmonella
(1) cows and chickens are reservoir and carry it in theguts-- it is spread in their stool.
(2) transmitted through feces-contaminated beef or chicken that is not cooked properly (milk and eggs can be affected).
A. diarrhea viral
B. bacterial diarrhea
C. dysentery
D. zoster
E. influenza
c
this is what infectious diarrhea is called when it is bloody & severe.
1) types of _____:
a) bacillary —etiology is a bacillus; most common is shigella
b) amoebic —etiology is protozoa found in water
2) patho / S&S of dysentery
a) unlike "regular," non-bloody diarrhea-causing microbes, the above microbes causes damage to the mucosal surface of the gut, so the diarrhea is characterized by blood & mucous as well as pain with bowel movements—all this is due to infection & inflammation of intestinal lining
b) other S&S include fever and dehydration
A. diarrhea viral
B. bacterial diarrhea
C. dysentery
D. zoster
E. influenza
long, antibiotic, diarrhea, clostridum, nosocomial
_____(long) ________(antibiotic) -associated ________(diarrhea)
1) this type of infectious diarrhea also called pseudomembranous colitis.
("colitis"—inflammation of colon; "pseudomembranous"—as part of infection, causes internal lining of intestines to develop yellowish membrane-like debris)
2) caused by being on long-term antibiotics wipes out normal gutflora a bacteria called ________(Clostridium) difficile (AKA "C-diff") moves in & causes an inflammatory state of the intestines ("colitis")
3) most common cause of iatrogenic / ____________(nosocomial) diarrhea
4) tx: stop antibiotics, IV fluids, put on other c-diff specific antibx
5) infection can reoccur, no prevention
a
___________characteristics
a. type of cancer of the hematopoietic system in which there is uncontrolled proliferation of leukocytes, causing over-crowding of bone marrow & decreased production of normal hematopoietic cells
b. S&S
1) leukocytosis; ex. of a WBC count you might see on a blood test-- 50,000 (norm count = 6 to 10,000)
2) thrombocytopenia easy bleeding & bruising
3) anemia fatigue, SOB.
4) ease of infection because the WBC immunocyte function is impaired.
2. classified according to predominant cell (myeloid vs lymphoid) and the onset (either acute or chronic)
A. Leukemia
B. Multiple myeloma
C. dysentery
D. zoster
E. influenza
b
____________
overview
a. a type of cancer that is mostly idiopathic etiologically, but also may have genetic component
b. predominant cell involved in becoming cancerous is B-lymphocytes, specifically the plasma cells.
S&S / tx
a. osteoporosis, which leads to pathological fractures (bone breakage that occurs with minimal stimulus).
b. hypercalcemia with its S&S of confusion, lethargy, weakness, kidney stones & kidney failure
e. tx -- chemotherapy, radiation, bone marrow transplantation
A. Leukemia
B. Multiple myeloma
C. dysentery
D. zoster
E. influenza
?
multiple, myeloma, plasma, malignant, increase, osteoclastic, hypercalcemia
_______(Multiple) _________(myeloma)
1. overview
a. a type of cancer that is mostly idiopathic etiologically, but also may have genetic component
b. predominant cell involved in becoming cancerous is B-lymphocytes, specifically the plasma cells.
2. pathogenesis
a. normally,______( plasma) cells (the cells that develop from B-cells and secrete immunoglobulins) selectively produce immunoglobulins on as-needed basis.
b. with multiple myeloma, some of the plasma cells become __________(malignant) and begin overproducing immunoglobulins.
c. these immunoglobulins infiltrate bones (and certain organs as well, but mainly bones), causing multiple malignant tumors that ________(increase) ___________(osteoclastic) activity
1) remember that osteoclasts are hematopoietic cells that normally migrate along bone capillary walls and "chew up" bone cells when calcium is needed in the body (pg 5 Prep 3, altered tissue)
2) in multiple myeloma, osteoclasts go into overdrive and chew up more bone cells than normal
3) thus the bones get weaker & there is a pathologically high amount of calcium in the blood _________(hypercalcemia)
decreased, rbc, anemia
Disorders due to pathologically _________(decreased) number of ________(RBC)s; these are called
______________(anemia)
anemia, decrease, quality, hgb, result, disease,
________(anemia) = less than normal number of total circulating
erythrocytes and /or a _________(decrease) in the ________(quality) or quantity of ______(Hgb).
2) anemia is the _________(RESULT) of a _________(disease) processes; it is a "state" or
"condition," and/ or can be considered a SIGN of a disease, but
only in certain cases is it considered a disease process in itself
increased, rbc, polycythemias, Erythrocytosis
Disorders due to pathologically
_________(increased) number of ______(RBC)s --
_____________(polycythemias)/______________ (Erythrocytosis)
primary, polycythemia, vera, slow, hyperproliferation
_______(primary) _________(polycythemia)
1) also known as polycythemia ______(vera)—a rare condition in which there is ________(slow) development of ___________________(hyperproliferation) of bone marrow stem cells.
2) tx—removal of 300 to 500 ml of blood 3 to 4 times per month
secondary, polycythemia, hypoxic, smoking, copd
_________(secondary) _________(polycythemia):
1) compensatory increase in RBCs in response to _________(hypoxic) conditions s such as living at higher altitudes (>10,000 feet); ________(smoking) (due to increased level of CO2); chronic low-O2 conditions such as _______(COPD)
2) mechanism of compensation: low O2 body increases erythropoietin secretionmore RBCs made
anemia, classification, test, cbc
diagnosis of an _______(anemia) AND its ___________(classification) by a blood ______(test) called a _______(CBC)
(complete blood count)
anemia, rbc, less, 4
first look at RBC count--normal is 4 to 6 million/L (males); patient has _______(anemia) when the ______(RBC) count is _____(less) than <__(4) million.
name, anemia, mcv, microcytic, less, 80
to _____(NAME) the type of _______(anemia), next look at the _______(MCV) (mean corpuscular volume), which is the size of each RBC;
normal range = 80 to 95
a) pt. has _______(microcytic) anemia when the MCV is ____(less) <__(80)
macrocytic, anemia, mcv, greater, 95
pt. has_________(macrocytic) _________(anemia) when the _______(MCV) is _________(greater)>___(95)
anemia, low, hgb, hct
other numbers you might see in an _______(anemia) person's CBC:
1) ____(low) hemoglobin _____(Hgb); normal Hgb = 14-18 gm / L, so
< 14 may be seen in anemia.
2) low hematocrit _____(Hct) - the percentage of RBCs in the
blood; normal = 42 to 52%, so < 42% may be anemia.
polycythemia, rbc, hematocrit, greater, 6, 52
on CBC, _________(polycythemia) is
characterized by:
a. ______(RBC)s and ________(hematocrit) ____(greater) than ___(6) million and ___(52)%
?
polycythemia, thickness, sludge, ischemia, heart, lung, failure
linking S&S of _______(polycythemia) with patho
a. problems related to
overproliferation of RBCs most
often are due to the
"________(thickness)" of the blood: extra
RBCs = "______(sludge)-like" blood.
b. sequelae of above is high risk
for distal tissue ______(ischemia), since
blood that is "thick" and slow-
moving (stasis) can increase
chance of clots forming &
blocking blood vessels.
c. also, "thickened" blood can cause
extra workload on heart & lungs
= higher risk for failure in these
organs.
d. so, because of above, S&S of
polycythemia can include
1) ischemic pain
2) ___(heart) & ____(lung) ____(failure)-related issues.
microcytic, heavy, menses, occult, gi, bleeding, iron, deficiency
_______(microcytic) anemia:
1) an anemia in which the size (MCV) is smaller than normal, so CBC would show RBCs of less 4 million and MCV of less than 80
a) something causes the body to slowly, chronically, lose RBCs and thus it begins to "run low" on material to make enough full-sized replacement RBCs
(1) so over period of time, the bone marrow tries to "catch up" by churning out RBCs that are smaller (less mature).
(2) this compensatory response is not enough to bring the RBC numbers up all the way to normal, but it is better than nothing. b) examples of chronic, steady loss of RBCs:
(1) women with _______(heavy) ______(menses)
(2) _____(occult) (hidden) __(GI) ________(bleeding)
c) sometimes microcytic anemia is called "_____(iron) __________(deficiency) anemia" because iron (Fe) is an essential part of the Hgb molecules which are lost with the RBCs.
3) S&S of microcytic anemia
a) in common with MOST anemias are: RBC <4million, fatigue, weakness, sometimes SOB & dull mentation.
4) treatment—stop blood loss if possible and give iron supplements
normocytic, rapid, chronic, erythropoietin
1) ______(normocytic) an anemia in which the size of the RBC is normal, so CBC would show RBCs of less 4 million and MCV that is normal
a) something causes ____(RAPID) blood loss, so that there is no time for compensatory response of smaller RBCs; ex—traumatic hemorrhage. OR
b) a ______(chronic) disease cause a slow-down in production of RBCs—they get produced in their normal size, but just more slowly & in less numbers; ex-- AIDS, lupus, chronic renal failure
3) S&S of normocytic anemia
a) in common with MOST anemias are: RBC <4million, fatigue, weakness, sometimes SOB & dull mentation.
b) particular to its classification you would see normal MCV.
4) treatment
a) for acute blood loss-- stop blood loss if possible and give units of blood as needed to replace.
b) for chronic disease-- give a type of growth hormone called ____________(erythropoietin) to stimulate bone marrow to make more RBCs.
anemia, fatigue, weakness, sob, mentation
) in common with MOST ______(anemia)s are: RBC <4million, __________(fatigue), ________(weakness), sometimes _____(SOB) & dull _________(mentation)
macrocytic, pernicious, elderly, diminished, intrinsic
_______(macrocytic) anemia:
1) an anemia in which the size (MCV) is larger than normal so CBC would show RBCs of less 4 million and MCV of greater 95
a) certain disease processes cause faulty DNA coding of RBC size so that the RBCs are larger than normal (but don't function right!)
b) most common example of a macrocytic anemia is _______(pernicious) anemia.
(1) mostly seen in the __________(elderly), in patients with GI absorption disorders, and in people with inadequate nutrition (eg, alcoholics)
(2) often begins with _________(diminished) production of intrinsic factor a hormone made by parietal cells in stomach.
(3) without ________(intrinsic) factor, vitamin B12 cannot be adequately absorbed from digested food
a) in common with MOST anemias are: RBC less 4 million fatigue, weakness, sometimes SOB & dull mentation.
(1) MCV less than 95
(2) glossitis ("inflammation of tongue") swollen, beefy red, smooth, painful tongue
(3) neuropathies, most often of the legs, such as paresthesia
(a) often described as "pins and needles" or burning
(b) caused from lack of B12 as an important nerve modulator
4) treatment—usually B12 as an injection.
macrocytic, glossitis, paresthesia, treat, b12
_______(macrocytic) anemia:
1) an anemia in which the size (MCV) is larger than normal so CBC would show RBCs of less 4 million and MCV of greater 95
(4) without vitamin B12, DNA malfunctions & makes coding error in RBC creation too made AND they are larger than normal (but don't function right!).
3) S&S of macrocytic anemia
RBC less 4 million fatigue, weakness, sometimes SOB & dull mentation.
(1) MCV less than 95
(2) ___________(glossitis) ("inflammation of tongue") swollen, beefy red, smooth, painful tongue
(3) neuropathies, most often of the legs, such as _________(paresthesia)
(a) often described as "pins and needles" or burning
(b) caused from lack of B12 as an important nerve modulator
4) _____(treat)ment—usually ___(B12) as an injection.
frank, bleeding, petechiae, spots, purpura, ecchymosis, collection
_____(frank) __________(bleeding) ("frank" in this case means " pretty obvious"); examples:
1) under the skin:
a) ________(petechiae) - pinpoint red _____(spots) that don't blanche
b) __________(purpura) - larger areas that look purplish
c) _________(ecchymosis)—general term for ________(collection) of blood under skin greater than~1cm
c
________________ - "hidden" bleeding; ex-- in GI tract if the bleeding is slow & not in areas where blood can be digested, stools may appear normal but actually have blood in them
A. von Willebrand disease
B. thrombocytopenia
C. GI bleeding
D. Frank bleeding
E. hemophilia
b
_____________ causes
a) congenital problems (rare)
b) nutritional
c) certain drugs & chronic diseases
d) autoimmune:
(1) IgG attacks platelets, diminishing their effectiveness
(2) called -ITP
2) S&S
a) usually platelet count on CBC is less than 100,000 (normal is around 250,000)
b) bleeding as noted above.
A. von Willebrand disease
B. thrombocytopenia
C. GI bleeding
D. Frank bleeding
E. hemophilia
e
___________refers to several possible different hereditary deficiencies of coagulation factors, usually X-linked recessive problem
a) S&Ss— spontaneous bleeding or bleeding that is out of proportion to amount of trauma
b) txs:
(1) transfuse plasma—plasma has clotting factors
(2) transfuse concentrates of whichever clotting factor is deficient.
A. von Willebrand disease
B. thrombocytopenia
C. GI bleeding
D. Frank bleeding
E. hemophilia
a
von Willebrand Factor is found in the blood and in the tissue in various forms.
(1) one example—a type of vWF is released by injured tissue
(2) it "calls" platelets and binds to them and to fibrinogen to promote clotting—a "platelet plug."
b) , like hemophilia, is an inherited disorder & it is the most common clotting disease - every 1 in 100 person has a variation of it.
c) S&S—various types of cause varied severity of S&S
(1) mostly very mild clotting deficiency with mild incidences of "easy bleeding."
(2) ex—some women manifest very heavy periods due to a type of .
d) tx—usually none needed, or symptomatic; certain more severe forms receive transfusions of vWF.
A. von Willebrand disease
B. thrombocytopenia
C. GI bleeding
D. Frank bleeding
E. thrombocytosis
e
_________— platelet greater than 400,000
a. can be from a genetic myeloproliferative disorder or from secondary cause such as RA, cancer, or after splenectomy
b. causes hypercoagulation which can manifest as thrombotic disorder-- proliferation of blood clot formation
A. thrombus
B. embolus
C. GI bleeding
D. Frank bleeding
E. thrombocytosis
a
an arterial or venous clot attached to vessel wall
A. thrombus
B. embolus
C. GI bleeding
D. Frank bleeding
E. thrombocytosis
b
an arterial or venous thrombus that has broken loose and travels in the circulatory system.
A. thrombus
B. embolus
C. GI bleeding
D. Frank bleeding
E. thrombocytosis
Splenomegaly, hematologic, infection, abo, incompatibility, hypersplenism
__________(Splenomegaly)—enlargement of spleen
1. causes can be categorized as _________(hematologic), _________(infection), malignancies, or physiologic:
a. hematologic: any time there is increased hemolysis of RBC's, the spleen can enlarge because it has more RBC "debris" to process; examples:
1) Rh blood type incompatibility (erythroblastosis fetalis)
2) ____(abo) blood type __________(incompatibility)
3) hemolytic problems from:
a) drug reactions and autoimmune diseases in which there is a triggering of antibody attack on RBCs
b) infections in which RBCs are attacked, such as malaria
b. infection/inflammation
a) viral -hepatitis, mononucleosis (Epstein-Barr virus), CMV
b) bacterial-- TB
c. malignancies, especially leukemia; huge numbers of WBCs come through spleen & it swells.
d. physiologic splenomegaly—usually an individualistic quirk; idiopathic etiology & no S&S.
2. S&S of splenomegaly:
a. palpably large spleen (normally you can't palpate it)
b. may have pain
c. may have __________(hypersplenism)
Hypersplenism, splenomegaly, pancytopenia, easy
___________(Hypersplenism)
a. a condition that results from __________(splenomegaly): due to the enlarged spleen, RBCs, WBCs, and thrombocytes (platelets) become trapped there—ie, sequestered.
b. all the cells begin to be "chewed up," destroyed en masse; two sequelae:
1) spleen becomes even more engorged & enlarged.
2) ___________(pancytopenia) —low numbers of all cells in blood.
c. S&S: anemia, increased risk of infection, "________(easy) bleeding."
a
disease that causes most cases of hyperthyroidism
b) autoantibody stimulates thyroid gland cells to oversecrete thyroid hormone (TH), causing S&Ss of hyperthyroidism
A. Graves disease
B. Goodpasture's syndrome
C. myasthenia gravis
D. celiac disease
E. autoimmune hemolytic anemia
b
autoantibody attacks connective tissue in pulmonary & glomerular basement membrane.
b) results in pulmonary hemorrhage & glomerulonephritis
A. Graves disease
B. Goodpasture's syndrome
C. myasthenia gravis
D. celiac disease
E. autoimmune hemolytic anemia
c
autoantibody attacks acetylcholine receptors on cells of muscles
b) this means that acetylcholine would not have enough effective post-synaptic gap receptor
A. Graves disease
B. Goodpasture's syndrome
C. myasthenia gravis
D. celiac disease
E. autoimmune hemolytic anemia
d
caused by individual's intolerance of a protein called gluten found in wheat and other foods
b) gluten triggers an attack by T-cells on own intestinal lining & causes diarrhea
b) this means that acetylcholine would not have enough effective post-synaptic gap receptor
A. Graves disease
B. Goodpasture's syndrome
C. myasthenia gravis
D. celiac disease
E. autoimmune hemolytic anemia
e
a trigger such as a drug causes autoantibodies to attack RBCs
b) the result is abnormally high hemolysis (destruction of RBCs) &
resultant low numbers of them (anemia)
A. Graves disease
B. Goodpasture's syndrome
C. myasthenia gravis
D. celiac disease
E. autoimmune hemolytic anemia
?
b
Study of functions and processes that occur in the body, mostly normal processes.
A. pathophysiology
B. physiology
C. well being
a
the study of the underlying changes in body physiology that result from disease or injury
A. pathophysiology
B. physiology
C. homeostasis
c
maintenance of constant conditions in the body's internal environment
A. pathophysiology
B. physiology
C. homeostasis
genetic, inherited, spontaneously
_________(genetic) disorders can be ___________(inherited) (like sickle cell & many others) or arise ___________(spontaneously) in response to an influence in the womb such as alcohol or an irritant such as smoking that might stimulate the development of a cancer gene (oncogene)
a
majority of DNA is found in nucleus of cells but small bits of DNA are also found in mitochondria
A. mitochondrial DNA
B. multifactorial,
C. chromosomal
D. single-gene
b
combination of environmental triggers and variations / mutations of genes, plus sometimes inherited tendencies; examples:
a. various cancers such as lung cancer: begins by smoke & toxins irritating bronchial tissue one or more genes in cells of that tissue begin to be deranged—oncogenes created code for wild, uncontrolled growth of cells.
b. many common diseases such as hypertension (HTN), coronary artery disease (CAD) & diabetes mellitus (DM) are now known to be caused or highly influenced by a mix of environmental and inherited components
A. mitochondrial DNA
B. multifactorial,
C. chromosomal
D. single-gene
c
problems can be aberrations of NUMBER, such as Down's syndrome, AKA trisomy 21—this is known as a polysomy, because there is an extra chromosome (at the 21st site.)
problems can be aberrations of STRUCTURE, such as translocation; an instance of this is seen in the development of the Philadelphia chromosome, which leads to CML (more info in cancer section at end)
A. mitochondrial DNA
B. multifactorial,
C. chromosomal
D. single-gene
d
Be able to use Punnett square for figuring out percent chance of child getting the disease, being homozygous for a disease, being heterozygous, etc, based on different combinations of parents;
A. mitochondrial DNA
B. multifactorial,
C. chromosomal
D. single-gene
d
breakdown of glycogen, which is a form of stored glucose.
A. pathophysiology
B. physiology
C. homeostasis
D. glycogenolysis
lost, blood, water, rate, increase
Example of compensatory response to pathologic stressors: if
you've ___(lost) a lot of____(blood) (massive bleeding) or ____(water) (dehydration), the body uses certain compensatory techniques to keep remaining fluid volume circulating as effectively as possible (temporary measures until the cause of the problem gets fixed) :
a) heart ____(rate) would ___________________(increase).
b) also, arteries in your periphery (arms and legs) would
constrict, shunting whatever blood volume is left to the central areas, that is, to your most important organs—brain, heart, lungs, kidneys.
a
an _________ disorder occurs when a mutated ("diseased"), recessive ("weak") gene partners up with an allele that is also recessive & diseased; those alleles are notated with two lower-case letters.
2) the protein that they code for will then malfunction & an abnormality/disease/ disorder will occur that relates to that "bad" protein
b. example of disorder--sickle cell anemia
A. autosomal recessive
B. autosomal dominant
C. homeostasis
D. glycogenolysis
a
____________________________— the failure to compensate, adapt, heal, etc.
A. decomposition
B. multifactorial,
C. chromosomal
D. single-gene
stressors
Disease vs disorder vs syndrome are ________(stressors)
b
factors that or contribute to and/or increase probability that a dz will occur ..."setting the stage"
ex-- heredity, age, ethnicity, lifestyle (smoking, eating habits, etc), environment
A. decomposition
B. risk factors
C. precipitating factor
D. single-gene
c
a condition or event that triggers a pathologic event or disorder ....
the "kick-off"
b. ex—"an asthma attack can be precipitated by exertion"
A. decomposition
B. risk factors
C. precipitating factor
D. single-gene
autosomal, abnormal, dominant
• _________(autosomal) dominant:
--key feature is that at a given site on a pair of chromosomes, the normal allele is recessive & the _______(abnormal) allele is ______(dominant)
-- greater chance for someone to get this dz, because unlike recessive disorders, in which only a homozygous recessive genotype gets the dz, there are two dominant genotypes that can result in phenotype—homozygous dominant & heterozygous
-- ex—PKD -- mutated ("bad") gene codes for malfunction in development of kidneys cysts throughout kidney tissue S&S of hematuria, pain, kidney failure.
d
the cause of a disease; includes all factors that contribute to development of dz; examples:
a. etiology of AIDS: HIV (human immunodeficiency virus)
b. etiology of rheumatic heart disease: autoimmune reaction
c. TB (tuberculosis): mycobacterium
A. idiopathic
B. risk factors
C. precipitating factor
D. etiology
a
dz (disease) with unidentifiable cause
A. idiopathic
B. iatrogenic
C. nosocomial
D. etiology
b
_________ occurs as result of medical tx
• ex—if kidney failure is due to improper use of antibiotics prescribed by a healthcare provider you could say "the etiology of the kidney failure was ______."
A. idiopathic
B. iatrogenic
C. nosocomial
D. etiology
c
____________________problems—result as consequence of being in hospital environment
• ex— urinary tract infection is called a nosocomial infection if it developed while patient was in the hospital.
A. idiopathic
B. iatrogenic
C. nosocomial
D. Clinical manifestations
d
the demonstration of the presence of a
sign and/or symptom of a disease
a. signs-- manifestations that can be objectively identified by a trained
observer
b. symptoms -- subjective manifestations that can only be reported by
the person experiencing them-- pain, nausea, fatigue
A. idiopathic
B. iatrogenic
C. nosocomial
D. Clinical manifestations (signs and symptoms)
much, glucose, conversion
if too ____(much) ____(glucose), glycogen ________(conversion) called glycogenesis
systemic, hives, malaise
others are ____(systemic), such as fever, urticaria ____(hives), _____malaise ("I feel dragged out" or "awful all over"), systemic lymphadenopathy
acute, rapid, short
_____(acute) S&S:
a) fairly ______(rapid) appearance of S&S of dz (over a day to several days); usually last only a ____(short) time
chronic, slowly, insidious, longer
______(chronic) S&S —develop more _______(slowly); S&S are often ______(insidious) and
last ____(longer) and/or wax and wane over months or years.
a
periods when S&S disappear or diminish
significantly (wane)
A. remission
B. exacerbations
C. nosocomial
D. Clinical manifestations (signs and symptoms)
b
periods when S&S become worse or more severe (wax); exacerbate—to provoke, to make worse.
• ex: "The patient had an _____________ of his chronic asthma and had to go to the hospital."
A. remission
B. exacerbations
C. nosocomial
D. Clinical manifestations (signs and symptoms)
c
usually refers to problem, situation, etc, that is occurring towards the center, or "core," of the body
b) often used when referring to essential organ systems
like brain, heart, lungs, kidneys;
A. remission
B. exacerbations
C. central
D. proximal
d
the more central an area or problem is, the more
A. remission
B. exacerbations
C. central
D. proximal
a
refers to problem, situation, etc, that is occurring
towards the outer parts of the body, away from core
ex—if we lose a lot of blood, the blood vessels of
the periphery often constrict so that not a lot of blood can circulate into those areas (mainly arms & legs)
A. peripheral
B. exacerbations
C. shock
D. proximal
b
Basic definition of _______
low BP plus S&S of not getting enough blood to different parts of the body (ex—confusion from not getting blood to brain).
A. peripheral
B. shock
C. prognosis
D. proximal
c
the predicted outcome of a dz based on certain factors:
a. the usual course of that particular dz
A. comorbidities
B. shock
C. prognosis
D. proximal
a
two or more coexisting medical conditions; this increases chance of poor prognosis
• ex—"The patient's __________ of heart disease and lung disease contributed to his poor prognosis in recovering from pneumonia."
A. comorbidities
B. sequela
C. prognosis
D. proximal
b
aftermath of a disease
1. a ______ is any abnormal condition that follows and is the result of disease, injury, or treatment; synonym = complications
2. occasionally the term is used as simply "outcome," mostly used in negative context
A. comorbidities
B. sequela
C. prognosis
D. proximal
c
A 55-year-old man with emphysema (a type of lung disease) who has smoked 2 packs of cigarettes per day for 40 years is hospitalized for acute onset of cough productive of bloody sputum. After a few days of testing and treatment, the patient's nurse reads a physician's note on the chart: "I have told the patient that the etiologies of his presenting problem are: 1) exacerbation of his chronic emphysema and 2) the new diagnosis of lung cancer. The onset of both were contributed to by his longstanding smoking."
1. The patient asks the nurse for more information. Which of the following explanations to the patient best indicates a full understanding of the patient's situation?
a. "You have a new disease process that was directly caused by all the coughing you've been doing from cigarette smoking."
b. "You have a sudden onset of a chronic lung disease that was brought on by lung cancer."
c. "The coughing up of blood is caused by a worsening of a disease you've had for a long time plus a new problem-- lung cancer."
d. "These diseases have been creeping up on you for probably 20 years; it just goes to
show that you should never have taken up smoking."
?
d
: A 55-year-old man with emphysema (a type of lung disease) who has smoked 2 packs of cigarettes per day for 40 years is hospitalized for acute onset of cough productive of bloody sputum. After a few days of testing and treatment, the patient's nurse reads a physician's note on the chart: "I have told the patient that the etiologies of his presenting problem are: 1) exacerbation of his chronic emphysema and 2) the new diagnosis of lung cancer. The onset of both were contributed to by his longstanding smoking."
2. Based on the scenario, which statement is most likely correct?
a. The patient has a poor prognosis because of the comorbidities of lung cancer and
cigarette smoking.
b. The patient's age is a risk factor for lung cancer.
c. A precipitating factor for the acute hospitalization was the history of emphysema.
d. Heavy cigarette smoking was a risk factor in the patient's developing emphysema
and lung cancer.
b
An 80-year-old patient is in shock from loss of blood following an accident. His vital signs are: BP 80/50 (normal ~ 120/80), HR 120 (norm = 60-100), RR 20 (norm = 12 to 20), T 98.6 (norm ~ 98.6).
3. In assessing this patient, the nurse understands that the abnormal HR is
a. probably the etiology for the patient's low BP.
b. due to the patient's heart compensating for low blood volume by pumping faster.
c. the normal compensatory response of shunting blood volume to the periphery.
d. due to multiple risk factors.
c
An 80-year-old patient is in shock from loss of blood following an accident. His vital signs are: BP 80/50 (normal ~ 120/80), HR 120 (norm = 60-100), RR 20 (norm = 12 to 20), T 98.6 (norm ~ 98.6).
4. The patient would also most likely have all of the following EXCEPT
a. S&S of cool feet and hands from the body's compensatory response to shock.
b. S&S of feeling faint and weak from blood loss.
c. a risk factor of shock.
d. a more guarded (ie, "poorer") prognosis because of his age.
b
A young, otherwise healthy patient is admitted to the hospital with a diagnosis of heart failure of unknown cause. The etiology of the heart failure would be termed
a. iatrogenic.
b. idiopathic.
c. nosocomial.
d. acute.
b
To do well on tests in this course, a student should
a. closely memorize verbatim all of the notes.
b. be able to explain concepts and apply them to different situations.
c. wait till a week before the tests to seek help from the instructor.
d. avoid extensive studying till the week before the test.
a
a segment of a DNA molecule that is composed of an ordered sequence of nucleotide bases (adenine, guanine, cytosine, thymine)
a. gene.
b. idiopathic.
c. nosocomial.
d. acute.
genes, coding, proteins
Main functions of ____(genes): ____(coding) for synthesis of _____(proteins) that form our traits and functional characteristics.
1) Examples of these include "permanent" proteins such as eye pigment, hair color, and blood type in a developing fetus, as well as more subtle inherited traits like outgoing personality or susceptibility to certain diseases.
b
When there is a ________ of a gene, the protein it is responsible for often malfunctions.
a. gene.
b. mutation.
c. chromosome.
d. acute.
c
Packaging of genes: __________
a. The DNA helix containing genes goes through many shapes during the cell life but at one point takes the shape that we are most familiar with- the rod-shaped body in the nucleus of cells called a
a. gene.
b. mutation.
c. chromosome.
d. acute.
23, each, 46
A person receives __(23) chromosomes from ___(each) parent, so you end up with 23 pairs, or a total of ___(46).
Last pair determine sex 23rd pair.
d
are ________- ie, NOT sex chromosomes
a. gene.
b. mutation.
c. chromosome.
d. autosomal.
a
Partner genes have the same location ("locus") on each respective chromosome, code for the same trait, and are called "a pair of ______
a. alleles.
b. mutation.
c. chromosome.
d. autosomal.
b
The combinations are called _______ & represent what was inherited from mom & dad.
a. alleles.
b. genotypes .
c. chromosome.
d. autosomal.
a
a disease caused by abnormalities in an individual's genetic material, when gene is mutated
a. genetic disorders.
b. genotypes .
c. chromosome.
d. autosomal.
b
_________ disorders:
1) a teratogen is any influence — eg, drugs, radiation, viruses-- that can cause congenital defects
2) congenital defects are abnormalities that are either detectable at birth and/or can be attributed to fetal development "glitches." Ex. fetal alcohol syndrome
a. genetic disorders.
b. teratogenic.
c. chromosome.
d. autosomal.
c
_________ disorder: a type of genetic disorder that results from alterations to the development or structure of a chromosome, which in turn alters the "local" genes (genes in the immediate area)--the genes' functionality is disrupted and they don't code proteins correctly, giving rise to the phenotype (S&S) of the disorder.
b. one well-known example of _______ disorders: Down's syndrome caused by disorder of structure or too many numbers.
a. genetic disorders.
b. teratogenic.
c. chromosomal
d. autosomal.
d
____________ disorders are usually due to an inherited mutated gene
b. since genes code for proteins, when a gene mutates so that its protein product can no longer carry out its normal function, a disorder can result.
c. ______ disorders are inherited in recognizable patterns: autosomal recessive, autosomal dominant, and sex-linked.
a. genetic disorders.
b. teratogenic.
c. chromosomal
d. single-gene .
a
less-than-normal numbers of RBCs
a. anemia.
b. teratogenic.
c. chromosomal
d. single-gene .
b
___________pain, from sickle cell, especially in the joints; patho of this type of pain:
(1) the deformed RBCs "clog" up the capillaries that usually carry O2-rich blood to the tissues
(2) this results in distal tissues that are starved to O2 & "cry out" in pain.
a. anemia.
b. ischemia.
c. chromosomal
d. single-gene .
trait, mild
Someone with sickle cell ___(trait) has the genotype Ss but has ___(mild) S&S of sickle cell disease.)
a
_______ disorders
a. overview
1) occurs when a person inherits a mutated, diseased gene that is dominant
2) ie, the gene that codes for a certain disease characteristic is dominant, and the gene that codes for the normal characteristic is recessive (exactly opposite of autosomal recessive) polycystic kidney disease (PKD)
a. autosomal dominant .
b. autosomal recessive.
c. recombinant DNA
d. single-gene .
c
________ form of genetic engineering
1. many alterations in DNA came about as a natural part of evolution, but now we can deliberately alter DNA in the interests of medicine and science.
2. ________ is a "new" DNA that results from purposefully combining two or more different sources of DNA; ex-- altering ("engineering") DNA codons in bacteria to make proteins the bacteria would not ordinarily produce
a. autosomal dominant .
b. autosomal recessive.
c. recombinant DNA
d. single-gene .
c
A child is born to a couple, one of whom is heterozygous for an autosomal dominant disease. The other parent is homozygous normal. What would be the child's chances of having the disease? (Use a Punnett square to figure this out—see weekly prep for help).
a. 0%
b. 25%
c. 50%
d. 75%
a
A child is born to a couple, one of whom is heterozygous for an autosomal recessive disease. The other parent is homozygous normal. What would be the child's chances of having the disease? (Use a Punnett square to figure this out—see weekly prep).
a. 0%
b. 25%
c. 50%
d. 75%
c
A child is born to a couple, one of whom is heterozygous for an autosomal recessive disease. The other parent is homozygous normal. In the question above, what are the chances that the child will be a carrier?
a. 0%
b. 25%
c. 50%
d. 75%
d
Which of the following is the result of defective protein synthesis caused by a nuclear single-gene malfunction?
a. fetal alcohol syndrome.
b. Down's syndrome.
c. mitochondrial DNA disorder.
d. cysts in the kidneys.
a
A nurse explaining to a new mother the patho of her baby's teratogenic defect shows complete understanding of the situation when he says,
a. "Certain chromosomes in your baby may have been injured before you finally kicked your cocaine addiction in your 6th month of pregnancy."
b. "Your baby inherited a gene from you or his father that caused a defect in important protein-based structures."
c. "Your baby inherited a gene that caused a defect called trisomy 21."
d. "Since your little guy was born with the Philadelphia chromosome, he will be a life-long Phillies fan."
d
A child with sickle cell anemia presents with pain all over, especially the joints. Which of the following best links the patho with S&S?
a. Cyst formation in the kidneys leads to blood spillage from the circulation into the
urine, thus causing anemia.
b. A single-gene mutation causes malfunction of tissue protein, leading to stiffening of
and ischemic pain of the joints.
c. Chromosomal aberrancy causes malformation of RBCs in the blood supply to the joints and subsequent pain due to lack of oxygen.
d. A single-gene mutation causes malfunction in RBC O2-carrying capacity, leading to ischemic pain in the joint tissues.
?
c
decrease in amount of oxygen to cell or ability to use oxygen appropriately
A. dypoxia
B. Aerobic
C. hypoxia
D. Anaerobic
b
O2 is present
(this is the ideal, "normal" situation).
A. dypoxia
B. Aerobic
C. hypoxia
D. Anaerobic
d
low or absent O2.
A. dypoxia
B. Aerobic
C. hypoxia
D. Anaerobic
positive, anaerobic, 2, atp, temporary
______(positive) side to ______(anaerobic) glycolysis:
a. it can give _(2) molecules of ___(ATP) per molecule of glucose to give energy to the cell.
b. thus, it is a _______(temporary) stop-gap measure that keeps your body going until the cells can get more O2 so that aerobic metabolism can be re- established
hypoxia, deficiency, atp, altered, acidosis
sequela result from _____(hypoxia):
a. _______(deficiency) of +____(ATP) for cellular functions; ex—without ATP, the Na / K pump of each cell cannot maintain normal electrical cell membrane status and propagation of electrical impulses will be disrupted.
?
b. ______(altered) acid/ base balance, especially _______(acidosis); significance: acidosis from something like hypoxia or reliance on gluconeogenesis (more on this in next section) can dangerously tip body pH out of its narrow, desirable range fairly quickly
?
eaten, glucose, up, hyperglycemia, insulin
if you have just _____(eaten), _______(glucose) in the blood normally goes ____(up), a state of temporary _________(hyperglycemia); this triggers the pancreas to secrete ___________(insulin)
to circulate to cells and assist in getting glucose molecules from the blood
into the cells to use as the main source of cellular energy.
food, greater, glycogen, glycogenesis
if intake of _____(food) / glucose is _____(greater) than immediate cellular energy needs,
insulin directs the excess glucose to be stored as ______________________(glycogen) in the liver. This is called _____________________________________(glycogenesis) .
hypoglycemia, counterregulatory, epinephrine, cortisol, gh, glucagon
___________(hypoglycemia)certain hormones called the ______(counterregulatory) hormones are triggered by low blood glucose:
1) _______(epinephrine) from the adrenal medulla
2) _________(cortisol) from the adrenal cortex
3) growth hormone ______(GH) from the pituitary
4) _________________(glucagon) from the pancreas
causes, glycogenolysis
first, back-up, glycogenolysis, higher, sugar
if you don't eat, the body takes the ______(first) step in its "________(back-up) plan:" the counterregulatory hormones stimulate the conversion of glycogen to glucose.
this process is called ___________(glycogenolysis) &
results in a ________(higher) blood ________(sugar), correcting the hypoglycemia &
making glucose available to the cells for energy use.
b) many times a day if our body needs some glucose & we cannot immediately take it orally, glycogenolysis takes place as a "stop gap measure" till we can take in glucose
b
the use of any other substance besides carbohydrates for cellular energy; this means breaking down fats and proteins for energy. get ketones
A. dypoxia
B. gluconeogenesis
C. hypoxia
D. Anaerobic
hyperketonemia, low, ph, ketoacidosis, ketonuria
__________(hyperketonemia) is manifested by:
1) blood test showing high serum ketones.
2) AND usually the following as well:
a) blood test showing ______(low) blood ___(pH)—this would be called _______(ketoacidosis)—a form of acidosis; and/or
b) urine test which shows________(ketonuria) (ketones spill into urine); and/or
c) S&S such as acetone breath (excretion via lungs).
negative, glycolysis, 2, not, enough, acidosis
______(negative) side to anaerobic _________(glycolysis):
a. __(2) molecule of ATP is ___(not) ____(enough) to keep going for a long time.
b. also, every time the metabolic process must "recycle" through glycolysis, multiple molecules of pyruvate (pyruvic acid) accumulate, resulting in ___________.(acidosis)
rmp, normally, negative
____(rmp) is _______(normally) the way of ____________(negative)
gluconeogenesis, ketones, some, energy, acids, can't, brain
____________(gluconeogenesis) "good" characteristic of _____(ketones): they can offer the body _____(some) ______(energy)—usually enough to be a "stop gap" till glucose is available.
b) two "bad" characteristics of ketones:
(1) they are ______(acids)-- over time there is a danger of acidosis
(2) they ______(can't) be used by _______(brain) cells—brain cells MUST have glucose for energy.
McCardle, can't, glycogenolysis, intolerance
______(McCardle)'s _____(can't) use _______________(glycogenolysis) as back-up plan so has exercise ____________(intolerance).
1, diabetes, not, insulin, sustained, gluconeogensis, hyperketonemia
Type __(1) __________(diabetes): gluconeogenesis taken to extreme: (gluconeogenesis is normal body back-up process, but if disease process alters it or causes sustained usage, then has potentially detrimental consequences)
a. people with Type I diabetes mellitus do ____(not) make ______(insulin) without insulin, glucose unable to get into cells, glycogen is eventually used up, (so BACK-UP PLAN #1 is used up), and body turns to ________(sustained) _________(gluconeogenesis) (BACK-UP PLAN #2) as its main energy pathway.
b. this is ok for awhile, but eventually sustained gluconeogenesis causes ketone over-accumulation, resulting in _________(hyperketonemia) (high levels of ketones in the blood)
urine test which shows ketonuria (ketones spill into urine); and/or breath
alcoholic, iron, deficiency, anemia, lethargy
often an _________(alcoholic) has very poor diet—obtains minimal ______(iron) and B vitamins such as thiamine (as well as countless other deficiencies)
2) as a sequela of iron __________(deficiency), may develop iron-deficiency ______(anemia)(not enough rbc); seeing iron's role in the metabolic pathway, what kinds of S&S do you think might this patient have? _________(lethargy), shortness of breath
beriberi, lack, thiamine, wernicke, ataxia, staggering
 _______(beriberi) (____(lack )of ______(thiamine))— probs w/ memory, paresthesia; one type is ______(Wernicke) Korsakoff associated w/ alcoholism. _____(ataxia) ______(staggering), uncoordinated gait
(2) parathesia--numbness & tingling or other unusual sensations, usually in legs (this is seen in B12 deficiency too).
higher, k, hyperkalemia
potassium (K+); _____(higher)-than-normal numbers of ___(K) in blood is called
______________________(hyperkalemia)
HYPOPOLARIZED, more, positive, shortening, sensitive, tics, chvostek
______________(HYPOPOLARIZED) states: situations in which membranes of cells have been reset to a ______(MORE) _________(positive) number than normal, _________(shortening) the polar gap status & making them more ________(sensitive)
&S of hypopolarization:
1) pathologic hypopolarization of cells manifests clinically as muscles that
are too sensitive - ie, hyperactive, "irritable"
2) they contract with smaller-than-normal stimulation, often resulting in muscle ___(tics) or spasms (example—positive __________(chvostek) sign)
3) if the spasms are severe and/or unrelenting, this is called tetany
hypopolarized, hyperkalemia, hypernatremia, hypocalcemia
examples of states in which cells become ______________(hypopolarized): __________________(hyperkalemia), _______________(hypernatremia), ____________(hypocalcemia )
hyperkalemia, hypernatremia, cations, cells
___________(hyperkalemia) & ____________(hypernatremia) are easy to understand: more cations in the blood mean that eventually more cations will diffuse from blood into cells
a) within the cell, this creates a more "positive" state, ie, increased positivity since more _______(cations) have moved in
b) so instead of the usual RMP of -90mV, the ____(cells) membrane is RESET to more positive RMP
hypocalcemia, increases, na, cell
2) __________(hypocalcemia) is a little harder to understand:
a) the very presence of low calcium levels in the blood as the blood circulates in tissue beds triggers an _________(INCREASEs) in permeability of cell membranes to Na+ so that MORE ___(Na)+ is allowed INTO the ___(cell) than normal
increased, positivity, hypopolarization, hypersensitivity, hyperactive
_____________(increased) _________(positivity)= ______________(hypopolarization) (shortened polar gap) = cell ___________(hypersensitivity) = "__________(hyperactive)" S&S
HYPERPOLARIZED, lengthening
___________(HYPERPOLARIZED) states: situations in which membranes of cells have been reset to a LESS positive number than normal, ___________(lengthening) the polar gap status & making them less sensitive
hyperpolarized, hypokalemia, hyponatremia, hypercalcemia
examples of states in which cells become ___________(hyperpolarized): ___________(hypokalemia), ____________(hyponatremia), _____________(hypercalcemia)
hypercalcemia, less, na, hyperpolarization
___________(hypercalcemia) is a little harder to understand:
a) the very presence of high calcium levels in the blood as the blood circulates in tissue beds triggers an DECREASE in permeability of cell membranes to Na+ so that ___(LESS) __(Na)+ is allowed INTO the cell than normal
b) so now the situation is exactly like any other in which there are more cations LEAVING the cell  decreased cations in cell = decreased positivity = ______________(hyperpolarization).
hyperpolarization, fatigue, bradycardia
__________(hyperpolarization):
1) pathologic hypopolarization of cells manifests clinically as muscles that
are less sensitive than usual- ie, hypoactive.
2) they contract more slowly, often resulting in patients complaining of _______(fatigue), lethargy, mental slowness, even can cause low heart rate, called __________(bradycardia).
co2, h, acid
o For our purposes in this class, think of ___(CO2) & __(H)+ as the main members of the "___(ACID) GANG
HCO3, alkali
________(HCO3) as the "_____(ALKALI) GUY."
metabolic, acidosis, kidneys, low, hco3
__________(metabolic) __________(acidosis) (think of the word metabolic in the ABGs context as meaning that the acid/ base imbalance is related to a problem in the _______(kidneys) and/or any other disorder/body system EXCEPT the lungs (respiratory system). 27.35
Also caused by ___(low) ___(hco3)
metabolic, acidosis, kidney, failure, diabetes, poison
other examples of processes that may result in __________(metabolic) ________(acidosis):
a) ______(kidney) _________(failure): because sick kidneys can't excrete H+ or make HCO3 acid accumulation acidosis.
b) _____(diabetes) ketoacidosis: ketones accumulate
c) ____(poison), drug overdose, alcohol: breakdown products are acidotic
metabolic, acidosis, lungs, decrease, acid
compensation for _____(metabolic) __________(acidosis) (the body's attempt to return to
normal acid/base balance):
a) the primary means of compensating for metabolic acidosis is via the _______(lungs).
b) the lungs try to _________(decrease) the ______(acid) gang in the body by increasing the amount of CO2 that is exhaled
c) they do this by increasing the rate & / or depth of respirations.
d) end result is that the pH is increased back to normal.
respiratory, acidosis, lungs, retention, co2
________(respiratory) __________(acidosis)
1) state of low pH caused by a ventilation problem such as diminished effectiveness of breathing or decreased respiratory rate (more on this in pulmonary lecture).
2) this results is that the _____(lungs) ________(retention) of _____(CO2) (accumulation of an acid)acidosis
3) compensation is by the kidneys: HCO3 will be increased to buffer the situation, ie, to counteract the acid (CO2) that has accumulated from poor ventilation.
metabolic, alkalosis, excess, hco3, vomiting
_______(metabolic) ________(alkalosis)
1) etiology-- a metabolic problem that results in one or more of the following:
a) _____(excess) accumulation of HCO3 in the body
b) not enough excretion of _____(HCO3) in the urine.
c) too much acid (H+ and others) being excreted in the urine or lost in other metabolic ways.
d) not enough acid being made
some causes of metabolic alkalosis:
a) large amount of ______(vomiting). Why does vomiting sometimes cause alkalosis
b) over-ingestion of bicarbonate (HCO3).
4) compensation is via lungs, by rate & depth of respirations.
over ingesting of antacids
respiratory, alkalosis, hyperventilation, anxiety
________(respiratory) ________(alkalosis)
1) state of high pH caused by __________(hyperventilation)—increased rate of breathing results in "blowing off" more CO2— less CO2 in the blood = LESS ACID GANG = higher pH. (more on this in pulmonary lecture).
2) example of a cause of respiratory alkalosis: _________(anxiety)
metabolic, acidosis, fix, lungs, increasing
______(metabolic) ______(acidosis) the ____(fix) is the _____(lungs) start ______(increasing) respirations
water, move, more, concentrated
rule of osmosis: ____(water) will always want to ______(move) from a more dilute compartment to a _______(more) ________(concentrated) compartment—ie, from a compartment of less % of solutes to one with greater % of solutes (the body wants to return to having the compartments equally concentrated.)
concentration calls!
high, osmolality, high, concentration
When we have ______(high) _______(osmolality) we have _____(high) _______(concentration) so water will follow
tonicity, salinity
______(tonicity)— interchangeable with the term "________(salinity)" (the "saltiness" of a
fluid, how much of it is made of salt, ie NaCl)
26:30
oncotic, pressure, protein
_______(oncotic) __________(pressure) (AKA colloidal osmotic pressure)—exactly the same principle as osmotic pressure, but refers specifically to _______(protein) molecules.
water, lost, body, causes, tissue, to, blood
________(water) is pathologically _______(LOST) by the ______(body), so that there is increased concentration (osmolality) of the plasma space (blood); ultimately this ______(causes) a ________(tissue)-____(to)-__________(blood) (T to B) fluid shift.
t, to, b, dehydration, turgor, oliguria, cns
S&S caused by __(T)-___(to)-____(B) fluid shift such as examples above
a. think "_______(dehydration);" in nursespeak, we would think of this state as a "fluid volume deficit."
dry mucus membranes
2) poor skin ___(turgor) -- skin loose, "tents" when pinched, won't "snap back."
3) sunken eyes
4) sunken fontanels in babies
5) diminished urinary output ______(oliguria) & also urine concentration increases.
6) sometimes low BP; why? lower volume fluid= less pressure
7) acute _____(CNS) (central nervous system) changes related to dehydrated brain cells-- restlessness, confusion, unconsciousness, convulsions.
Hyperosmolar
raas, renin, osmolality, high, 2, aldosterone, hold, na, water
____(RAAS)—Renin-Angiotensin-Aldosterone System
1) increased _______(renin) is secreted by the kidneys in the following situations: a) when blood ________(osmolality) is ____(high) (usually because of water loss)
and/or
b) when fluid volume in the circulation is low due to blood loss
and /or
c) BP is low
2) renin stimulates secretion of angiotensin I  becomes angiotensin ___(2) with the "help" of ACE (angiotensin converting enzyme)
secretion of aldosterone from the adrenal gland
________(aldosterone) causes kidney tubules to "___(hold) on" to ___(Na)+ water follows Na+ back into circulation instead of going out with urine urine output decreases____(water) in blood and general circulatory volume increases
excess, water, b, to, t
2. _____(excess) _____(water)
a. general mechanisms & sequelae
1) pathologic increase of water in the circulation can occur from several etiologies (see following sections), with the result being a dilution of the blood and a lower serum osmolality than its next-door neighbor, the tissue (as per the "rule," the vascular compartment is the first to change its composition)
2) since the blood has changed to a lower osmolality than the nextdoor tissue compartment, which way will water will be PULLED ("called")?
INTO the tissue or INTO the blood? (ie, T to B or ___(B) __(to) __(T)?)
excess, fluid, tissue, edema
as ____(excess) _____(fluid) is pulled into the ______(tissue), the resultant pathologic accumulation is called _______(edema), which can impair body processes such as healing and oxygen exchange because of increased distance for nutrients and waste products to move between capillaries and cells
excess, water, siadh, increased, adh
_____(excess) _____(water): hormonal problems such as ____(SIADH)-syndrome of inappropriate antidiuretic hormone (think of the "I" in SIADH as "_______(increased)" ____(ADH)).
a) possible etiologies of SIADH
(1) ectopically-produced (ectopic = "outside usual") ADH such as from small-cell bronchogenic cancer
(2) various drugs, especially general anesthetics (SIADH sometimes seen in post-op recovery period).
(3) trauma to brain such as brain tumors, head injury, etc. (swelling of brain puts pressure on pituitary gland)
excess, water, oliguria, hypoproteinemia
____(excess) ____(water) S&S include decreased urine output _________(oliguria) because your body is holding onto water inappropriately and other
fluid volume excess S&S (see next page)
some causes of __________(hypoproteinemia)
b, to, t, pulmonary, edema, swelling, brain
S&S caused by __(B)-___(to)-_(T) fluid shifts
a. in "nurseland", we generally think of a person with B-to-T fluid shifts as being in a state of "fluid volume overload or excess."
b. as tissues "pull in" water from the diluted vascular system, they eventually show their water overload as edema that can occur anywhere in body; examples:
1) under skin: skin appears tight & puffy; assessed by pushing into skin & seeing indentation ("pitting edema")-- rated on scale from 1+ to 4+
2) in lung tissue—________(pulmonary) _______(edema) ("wet lungs"): manifested as cough and/or SOB &/or crackles while listening with stethoscope.
3) acute CNS (central nervous system) changes related to
_______(swelling) of _______(brain) cells -- restlessness, confusion, unconsciousness, convulsions.
c. if we did lab work, we would see a low serum osmolality (we would consider this patient's blood to be hypoosmolar, hypotonic, have low oncotic pressure, and low osmotic pressure—all similar terms-- compared to normal blood)
correct, fluid, overload, nps, anp, bnp, increase, urination
compensatory mechanisms to ____(correct) ______(fluid) _______(overload): natriuretic peptide system _____(NPS)
a. when fluid volume is high, the right atrium and left ventricle detect that too much fluid is reaching them.
b. they secrete ___(ANP) (atrial natriuretic peptide) & ___(BNP) (b-type natriuretic peptide these peptides reach the kidneys via the circulation & stimulate them to _______(increase) _______(urination) (diuresis) fluid volume goes down.
c. when fluid volume is low, this system is suppressed.
cells, differentiation, erythropoietin, growth, rbc
birth & growth of ___(cells): most cells have very well-defined growth and development of structure & function
a. as programmed by their genetic makeup, cells have different degrees of ________(differentiation)(synonyms: "organization"
and/or "specialization").
b. there is a spectrum from fairly rudimentary all the way to highly differentiated cells, such as nerve cells and cardiac cells.
c. this development is helped along by many hormones such as _____________(erythropoietin) and other _______(growth) mediators.
erythropoietin: made by the kidneys, it is important in stimulating growth and development of _____(RBC)s.
cell, normal, death, apoptosis, 10
death of cells
a. ____(cell) death can be the culmination of ____(normal) cycle of cell and/ or aging process, or can be as a result of a pathologic event.
b. "normal ____(death)"-- ______(apoptosis)
1) apoptosis is a form of "programmed death," or cell "suicide"
2) our bodies create & kill ___(10) billion new cells a day-- if cells didn't die, we would have gigantic and/or distorted bodies.
3) also, body has to get rid of cells that have been worn out, developed improperly, or have genetic damage
abnormal, cell, death, necrosis
_______(abnormal)" _____(cell) _____(death) -_______(necrosis) occurs when a cell is injured and reaches the irreversible point on this spectrum:
inflammation, first, step, healing
no matter what part of the continuum, the commonality of all injury to cells/tissue is ___________(inflammation), which is one of the _____(first) _____(step)s to ________(healing).
injury, irritation, swelling
______(injury)/inflammation of various tissue is part of almost every disease process in some way
a) so if I mention injury and/or _________(irritation) as part of a disease process, always think of "_______(swelling) & leakage" as part of the picture
ischemia, hypoxia, arterial
_______(Ischemia)
1. overview
a. definition: ischemia is oxygen deprivation to cells _______(hypoxia) due to decrease in _______(arterial) circulation to the area
b. there are many etiologies for hypoxia of tissue, but ischemia is the most common.
c. underlying mechanism of ischemia is narrowed and/or blocked arteries
d. this narrowing or blockage can be acute or chronic
acute, ischemia, embolus, sickle
________(acute) ________(ischemia)-- hypoxia to tissues from sudden lack of blood supply; examples:
a. arterial _______(embolus): clot that travels in the arteries till it suddenly gets lodged in a smaller blood vessel (arteriole or capillary) distal tissues quickly become hypoxic.
b. _____(sickle) cell crisis: abnormally shaped RBCs get stuck in capillaries &
decreases blood supply to joints, etcischemia ischemic pain.
chronic, ischemia, tolerated, atherosclerosis
________(chronic) __________(ischemia): better _________(tolerated) because tissues can adapt to some degree over time; examples of causes of this gradual ischemia:
a. gradual narrowing of arteries from _____________(atherosclerosis).
b. slow-developing clot (thrombus) in leg artery or coronary artery.
infarction, any, ischemic, arterial
______(infarction)
a. if ___(ANY) __________(ischemic) situation, acute or chronic, is not treated, can lead to infarction-- cell death (necrosis) that is specifically caused by lack of _________(arterial) blood supply to an area
sore, decubitus
unrelieved pressure on skin, such as lying immobile prevents skin capillaries from receiving oxygenated blood (ischemia)  tissue injury & breakdown in this situation is called a pressure ulcer, stasis ulcer, "bed ____(sore)," or ______(decubitus)
co, damage, nervous
mechanism of action, S&S, treatment:
a. ____(CO) has a high affinity for hemoglobin (Hgb)-- about 3000 times more so than oxygen → binds to Hgb, forming carboxyhemoglobin (HgCO)
b. HgCO prevents O2 from binding to Hgb, so tissues become hypoxiccell _____(damage)S&S .
c. S&S mostly relate to ___(nervous) system & depend on % of HgCO in body
--headache, giddiness, confusion, seizures, coma.
d. treatment—100% O2 by oxygen mask and/or hyperbaric chamber until HgCO levels come down to normal.
abnormal, cellular, lipids, liver, urates, gout
_________(Abnormal) _______(cellular) accumulations
1. when substances accumulate in the cells pathologically they can interfere with normal cellular functions & ultimately cause cell injury; examples follow..
2. ______(lipids); ex-- fatty ____(liver) from dz processes such as alcoholism
3. _______(urates) (AKA uric acid) accumulation; ex—____(gout):
free, radicals, aging, pollutants
______(free) _______(radicals) can be thought of as a separate molecular "species,"
because they don't behave like "normal" atoms & molecules.
b. they act differently because they are a "spin-off" of abnormal, accelerated, and/or uncontrolled reactions, especially certain oxidation/ reduction ("redox") reactions
c. typical generators of these free-radical-producing reactions are:
1) simple _____(aging)
2) environmental ________(pollutants)
3) certain drugs, & alcohol abuse
4) various types of radiation damage, including too much sun
5) certain foods such as those high in preservatives and charred meat.
cell, proliferation, multiplication,
________(cell) ________(proliferation)-- the ___________(multiplication) or reproduction of cells, resulting in the rapid expansion of a cell population.
2. this is part of normal growth and development of cells
a. ex—our hematopoietic system (birthplace of blood cells) is chiefly located in the bone marrow
b. basic stem cell differentiates into several types of blood cells, which then mature, proliferate (multiply), & are released into the blood
malignant, poor, differentiation
___________(malignant) tumor or "malignancy;" interchangeable with "cancer"
1) key characteristics—very rapid growth rate of cells that are ______(poor) _________(differentiation)
2) location
a) can occur in a specific site; ex-- local malignant tumor such as cancerous skin lesion
b) and/or metastasis can occur (verb: metastasize)
(1) refers to propensity of malignant cells to invade sites distant to immediate area
(2) metastasis is major cause of illness and death resulting from most human malignant dz
c) some cancers by nature are wide-spread, such as leukemia
genetic, mutation, cancer, oncogene
the ______(genetic) _________(mutation) that sets ___________(cancer) into motion is often called an _____(oncogene)
clonal, proliferation, overreact, little, differentiation, anaplasia
the oncogene promotes ______(clonal) _____(proliferation)—a rapid increase in growth & development—by:
1) stimulating cells to "______(overreact)" to growth factor signals—causes wild, rapid duplication but very ______(little) ________(differentiation).
a) instead of differentiating into a specific tissue type with a specific function, as normal cells do, cancer cells do not differentiate; they stay in a younger stage of development and continue to replicate.
b) this loss of differentiation is called ________(anaplasia)
angiogenesis, cancer, divert, nourishment
—________(angiogenesis) development
of new blood vessels); this is partly why ______(cancer) kills—cancer cells ________(divert) ________(nourishment) from our other cells
markers, predict, cml, exchange, short, philadelphia
genetic _____(markers)— genetic abnormalities that are found in some people that _____(predict) odds of having certain types of cancers; example:
1) chronic myeloid (AKA myelocytic or myelogenous) leukemia _______(CML) develops because of a translocation ________(exchange) of pieces of chromosome; in this case, one chromosome gets shortened (sort of "squashed") in this process—this ______(short) chromosome is called the _______(Philadelphia) chromosome
t0, no, cancer, n0, no, lymph
T= size of tumor.
a) ___(T0) = ___(no) ______(cancer) cells
b) T1- T3 = cancerous tumor size; increasing severity & poorer prognosis with higher #.
2) N = extent of lymph nodes involvement.
a) ____(N0) = ____(no) _____(lymph) node involvement.
b) N1- N3 = nodes involved (usually the ones closest to the
cancer site; increasing severity & poorer prognosis with higher #.
3) M = metastasis ("mets") —spread to other tissues beyond local lymph nodes (ex: colon cancer spreading to liver)
a) M0 = no metastasis
b) M1- M3 = mets present; increasing severity & poorer prognosis with higher #.
m, other, tissues, no
T= size of tumor.
a) T0 = no cancer cells
b) T1- T3 = cancerous tumor size; increasing severity & poorer prognosis with higher #.
2) N = extent of lymph nodes involvement.
a) N0 = no lymph node involvement.
b) N1- N3 = nodes involved (usually the ones closest to the
cancer site; increasing severity & poorer prognosis with higher #.
3) ____(M) = metastasis ("mets") —spread to _______(other) ______(tissues) beyond local lymph nodes (ex: colon cancer spreading to liver)
a) M0 = ___(no) metastasis
b) M1- M3 = mets present; increasing severity & poorer prognosis with higher #.
b
A 28-year-old man presents with a low blood pressure due to blood loss from a gunshot wound.
The regulatory action that will best compensate for this patient's fluid volume deficit is:
a. increased action of the natriuretic peptide system
b. increased action of the RAAS.
c. inhibition of renin secretion.
d. conversion of aldosterone into angiotensin II.
?
c
A 28-year-old man presents with a low blood pressure due to blood loss from a gunshot wound.
The regulatory action that will best compensate for this patient's fluid volume As a result of the action in , all the following will occur EXCEPT:
a. the patient's body will "hang on" to fluids.
yes, this will happen-- see above explanation.
b. Na+ will be retained by the kidneys. - yes, see above
c. Na+ excretion in the urine will increase. - if more Na is excreted in the urine, H2O will follow, and the blood volume will diminish, not increase as needed. This action correlates more with the system that is opposite of the RAAS—the natriuretic system.
d. blood pressure will increase. - yes, because blood volume increases as a result of the RAAS action.
b
(Normal labs: Na+ = 135 to 145; K+ = 3.5 - 5.0; osmo = 180- 195; HCO3 = 22-28).
Questions 3 & 4 refer to the following: A patient is hospitalized in renal failure. Because of her kidneys' inability to excrete water, she has generalized edema & a serum sodium of 129. Because the kidneys have also lost the ability to appropriately regulate potassium, she has a serum potassium of 5.9.
?
3. These lab results show:
a. hypernatremia & hypokalemia.
b. hyperkalemia & hyponatremia.
c. hyperosmolality & hypernatremia.
d. hypoosmolality & hypocalcemia.
?
a
(Normal labs: Na+ = 135 to 145; K+ = 3.5 - 5.0; osmo = 180- 195; HCO3 = 22-28).
A patient is hospitalized in renal failure. Because of her kidneys' inability to excrete water, she has generalized edema & a serum sodium of 129. Because the kidneys have also lost the ability to appropriately regulate potassium, she has a serum potassium of 5.9.
The edema is most likely due to fluid shifting from the intravascular space into interstitial spaces secondary to all the following except:
a. hypertonicity of the plasma space
b. hypotonicity of the plasma space.
c. hypoosmolality of the blood.
d. diminished osmotic pressure of the blood.
a
: A patient is in a coma from advanced liver disease. Blood tests reveal that his serum albumin level is very low, also that his blood pH is 7.30 & HCO3 is 18 (normal HCO3 = 22-28).
5. What fluid shifts would the nurse expect and why?
a. Water would shift from blood (B) to tissue (T) because of decreased plasma oncotic pressure.
b. There would be an increased intravascular volume due to increased plasma oncotic pressure.
c. There would be dehydrated brain cells due to fluid shifting from T to B.
d. Water would shift from T to B because of increased osmolality of the vascular space.
?
c
A patient is in a coma from advanced liver disease. Blood tests reveal that his serum albumin level is very low, also that his blood pH is 7.30 & HCO3 is 18 (normal HCO3 = 22-28). The patient's acid/base imbalance is called metabolic ____.
a. alkalosis, as manifested by the low pH & HCO3.
b. alkalosis, most likely due to accumulation of "alkali guy" substances such as HCO3.
c. acidosis, most likely due to accumulation of "acid gang" substances such as H+.
d. acidosis, as manifested by the high pH & low HCO3.
b
A patient is in a coma from advanced liver disease. Blood tests reveal that his serum albumin level is very low, also that his blood pH is 7.30 & HCO3 is 18 (normal HCO3 = 22-28). A patient who just came out of general anesthesia has lab work done. The serum osmo is 165. The patient also has pitting edema. The nurse taking care of this patient suspects that the _________ is due to ____________.
a. hyperosmolality: dehydration.
b. hypoosmolality: syndrome of inappropriate ADH (SIADH).
c. hypertonicity: SIADH.
d. high oncotic pressure: a state of hyperpolarization inside the cells.
b
A patient is in a coma from advanced liver disease. Blood tests reveal that his serum albumin level is very low, also that his blood pH is 7.30 & HCO3 is 18 (normal HCO3 = 22-28). A patient who just came out of general anesthesia has lab work done. The serum osmo is 165. The patient also has pitting edema.The nurse in the previous question would expect all the following S&S EXCEPT:
a. signs of cerebral edema such as irritability.
b. signs of cerebral cell dehydration such as headache.
c. pitting edema
d. crackles in the lungs upon auscultation
b
A patient is in a coma from advanced liver disease. Blood tests reveal that his serum albumin level is very low, also that his blood pH is 7.30 & HCO3 is 18 (normal HCO3 = 22-28). A patient who just came out of general anesthesia has lab work done. The serum osmo is 165. The patient also has pitting edema.The nurse in the previous question would expect all the following S&S EXCEPT:Re: the patient in the previous two questions: As an intervention to return the patient to normal serum osmolality, the nurse is likely to be ordered to hang an IV bag of _______ because once the fluid is distributed in the blood it will __________ and help return fluid compartment status to homeostasis. (see page 15)
a. 0.45 NaCl: cause water to shift from tissue (T) to blood (B).
b. 3% NaCl : cause water to shift from T to B.
c. 0.25 NaCl : shift water from B to T.
d. NS : shift water from B to T.
d
A child accidentally ingests an insecticide with the ingredient cyanide. Knowing that cyanide suppresses the actions of cytochrome oxidase in the electron transport chain, what signs might an RN expect and why?
a. ketonuria due to increased glycogenesis.
b. hypertonicity due to acetyl Co-A suppression.
c. enhanced metabolic state due to increased production of ATP.
d. shortness of breath due to decreased ATP to use for the work of breathing.
?
c
A patient who is having hyposecretion of ADH (antidiuretic hormone) would MOST LIKELY have the following sign:
a. serum osmolality of 270 mOsm/kg.
b. oliguria. ERROR—should say: hypoosmolar concentration status of the blood
c. serum osmolality of 300 mOsm/kg
d. edema.
?
b
A patient with a serum calcium of 6.0 (norm = 8.5- 10.5) is most likely to ______ because_______.
a. be lethargic: the cells are hypopolarized.
b. have muscle spasms: more Na+ has entered the cells.
c. be weak: Na+ has left the cells.
d. have hyperirritable muscles: the cells are hyperpolarized.
c
A diabetic patient has pathological changes to his arteries that result in narrowing and blockage. He is diagnosed with gangrene of the toes (gangrene is when LOTS of tissue dies). Lab work is drawn and shows an elevated CK. Which pathological process accurately explains this type of occurrence?
a. necrosisgangreneischemia creatine kinase spillage into blood.
b. infarct cellular differentiation release of urea.
c. ischemia cell swellingspillage of cellular enzymes into blood.
d. metastasis superoxide dismutase release of free radicals.
c
A patient that has been recently diagnosed with a neuroma on the sole of his foot is very anxious. Of the following, which information shows that the nurse understands the nomenclature of neoplasms when explaining the situation to the patient?
a. "You should have the neuroma removed, as this is a cancer that will spread to other parts of the body."
b. "This is most likely a malignancy that will metastasize to your lymph nodes."
c. "Neuromas are benign growths that usually will not spread."
d. "You will soon have the irresistible urge to put on tap shoes and dance in a Broadway musical."
b
A family nurse practitioner (FNP) tells a patient that her biopsy shows leiomyosarcoma staged at T2N2M0.
3. This patient has a
a. benign tumor of the endometrium.
b. smooth muscle tumor that has spread to the lymph nodes.
c. a malignancy of the uterus that has spread to distant sites.
d. muscle cell tumor that is a carcinoma.
c
patient who smokes expresses concern to his nurse about the metaplastic changes of the bronchi that were seen during his bronchoscopy. The nurse bases her response on the knowledge that this metaplasia is
a. an irreversible cellular adaptation pattern.
b. considered a precancerous cellular change.
c. a reversible cellular adaptation pattern.
d. due to a physiologic hyperplasia.
d
Which sets of information are correctly linked?
a. a patient with kidney disease: erythropoietin injections are needed to counteract overproliferation of red blood cells.
b. chronic myelocytic leukemia: counteracted by a medication that stimulates the Philadelphia chromosome.
c. gout: caused by diet high in urea.
d. carbon monoxide: binds to Hgb in oxygen's place.
a
A patient has a post-stroke sequela of right-sided hemiparesis. The muscles on his left side grow larger than normal to compensate for the weakness on the right. This muscle adaptation is called
a. hypertrophy.
b. atrophy.
c. clonal proliferation.
d. calcification.
a
Link the genetic etiology with the S&S of CML:
a. Genes on a defective chromosome malfunction and cause extreme leukocytosis.
b. A sex-linked monosomy results in a gene on the X chromosome that causes leukocytosis.
c. An autosomal dominant disorder that manifests later in life cause a single gene to code for wild leukocyte growth.
d. Genes on an extra chromosome malfunction and cause defects in leukocyte development, resulting in leukopenia
metaplasia, reversible, replacement, mature, chronic
______(metaplasia)—_______(reversible) ___________(replacement) of one ______(mature) cell by another type of mature cell; happens when cells are being subjected to ______(chronic) injury or irritation
a. ex--when normal columnar ciliated epithelial cells of bronchial linings in lungs of smokers are replaced by stratified squamous epithelial cells
b. begins to reverse & normalize as soon as the irritant (such as smoking) is removed
hyperplasia, increased, cells, from, division
_______(hyperplasia)—__________(increased) in number of ________(cells) resulting ______(from) increased rate of cell _________(division)
a. physiologic example-- certain organs can regenerate using hyperplasia; ex—removal of part of liver leads to hyperplasia of liver cells (hepatocytes); even with removal of 70% of liver, regeneration is complete in 2 weeks.
b. pathologic hyperplasia— benign prostatic hyperplasia (BPH); as a man gets older, prostate enlarges from increase numbers of cells;
considered a pathology, yet is a very, very common problem in men
over 50-ish.
dysplasia, abnormal, changes, cells, pre-cancer
________(dysplasia) --
a. ________(abnormal) ________(changes) in size, shape, & organization of mature ______(cells) due to persistent, severe cell injury or irritation
b. in some resources dysplasia is not considered a true "adaptive" process-- consider it one step beyond "adaptation," but not quite "cancer."
1) sometimes called "_______(pre-cancer)" because the cells are much less differentiated than normal, but not quite as undifferentiated & disorganized as cancer cells.
2) remember, the less the differentiation = the lower the
function = the less specialized = the more likely to divide &
proliferate = more potential to be disorganized & cancer-like.
c. ex—PAP smears can reveal dysplastic cells of cervix that often must undergo laser-type treatment or close watching to make sure they do not deteriorate into a cervical cancer.
atrophy, decrease, size
________(atrophy)—_______(decrease) or shrinkage in cellular ______(size)
a. physiologic—occurs in early development; ex—thymus gland
b. pathologic
1) often occurs as result of decreases in "work load"—an area or an organ is no longer stimulated very much to do its "work," so the cells shrink
2) ex—disuse atrophy
a) patient in bed for a long time or immobilized in some way b) having a cast, for example—those cells shrink up while
cast is on, then grow slowly back to normal when cast is off & the cells are "stimulate to "work" again.
benign, neuroma
______(benign) nerve cell tumor would be: _____(neuroma)
c
A 59 year old man is diagnosed with CML—chronic myelocytic leukemia. All of the following help to explain the genetic etiology of the CML EXCEPT
a. a chromosomal structural defect called translocation occurs.
b. pieces of two chromosomes are exchanged.
c. a chromosomal aneuploidy defect called translocation occurs.
d. a short, defective chromosome called the Philadelphia chromosome develops.
rhabdomyosarcoma, skeletal, muscle
_____________(rhabdomyosarcoma)
striated ("rhabdo"), AKA ______(skeletal) _________(muscle)--
metabolic acidosis
ABGs for normal HCO3= 22 to 28
ph 7.28 HCO3 19
this person has?
metabolic alkalosis
ABGs for normal HCO3= 22 to 28
ph 7.50 HCO3: 30
this person has?
a
The patient says she has read that free radicals might be partly responsible for the development of her disease process. She wants to know more information and if there is anything that can counteract free radicals. The nurse's explanation will be based on understanding that all of the following statements are true EXCEPT
a. an example of a free radical is cytochrome oxide.
b. free radical molecules initiate harmful reactions such as lipid peroxidation, which damages the lipids of cell membranes.
c. the body's way to counteract free radicals include enzymes such as superoxide dismutase.
d. free radicals are molecules that are in a highly reactive state and can be calmed by taking certain vitamins..
low, gfr, edema
low, gfr, edema
24hr, stroke, tia
24hr, stroke, tia
ige, hypersensitivity, degranulation mast, cell
ige, hypersensitivity, degranulation mast, cell
urticaria, itching, histamine
urticaria, itching, histamine
a+, not, receive, b-
a+, not, receive, b-
steroid, inhibit, prostaglandin
steroid, inhibit, prostaglandin
rhogam, needed, ab-, ab+
rhogam, needed, ab-, ab+
steroids, cause, kidney, failure
steroids, cause, kidney, failure
low, protein, bruising
low, protein, bruising
normal, aging, dry, mouth, eyes
normal, aging, dry, mouth, eyes
joint, pain, rash, sle
joint, pain, rash, sle
giardiasis, frothy, greasy, diarrhea
giardiasis, frothy, greasy, diarrhea
antigenic, drift, flu
antigenic, drift, flu
strept, rheumatoid
strept, rheumatoid
malnourished, parathesia
malnourished, parathesia
vaccine, artificial, active
vaccine, artificial, active
chills, anemia
chills, anemia
gout, uric, acid
gout, uric, acid
poor, skin, renin, raas
poor, skin, renin, raas
rheumatoid, autoimmune
rheumatoid, autoimmune
laceration, erythemia, swelling, clear, normal
laceration, erythemia, swelling, clear, normal
mcv, high, macro
mcv, high, macro
fatigue, glossitis, intrinsic, lack, b12
fatigue, glossitis, intrinsic, lack, b12
celiac, gluten, intestinal
celiac, gluten, intestinal
pcp, humoral
pcp, humoral
oi, cmv, retinitis, aids
oi, cmv, retinitis, aids
mrsa, found, in, nose, hospital, not, gene
mrsa, found, in, nose, hospital, not, gene
increased, hemolysis, prehepatic
increased, hemolysis, prehepatic
cirrhosis, hf, edema
cirrhosis, hf, edema
increased, urea, kidney, problem
increased, urea, kidney, problem
increased, ammonia, liver
increased, ammonia, liver