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128 Cards in this Set
- Front
- Back
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GI
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digestive tract-
alimentary canal- gut- |
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GI
Accessory organs |
Salivary glands
Liver Pancreas Gallbladder |
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GI - Anorexia
What? |
a loss of appetite.
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GI - Anorexia
Why? |
Protective
signal the presence of disease remove noxious agents |
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GI - Anorexia
How? |
Brain: Hypothalamus &
Cranial nerve I Emotions: fear, depression, frustration, and anxiety- Diseases: renal d/t increased urea- Cancer: Tumor break down from tx or advanced metastasis releases substances that influence the satiety center of the brain. Medications |
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GI - Nausea
What? |
an ill-defined and unpleasant subjective sensation that often precedes or accompanies vomiting
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GI - Nausea
Why? |
controlled by medulla in brain
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GI - Vomting or Emesis
What? |
the sudden and forceful expulsion of stomach and intestinal (chime) contents
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GI - Vomting or Emesis
Why? |
controlled by medulla-
it is a basic physio protective mechanism limiting damage from ingested noxious agents by emptying the contents of the stomach and portions of the small intestines |
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GI - Vomiting or Emesis
How? |
Inflammation of any of the intra-abdominal organs such-
Rationale: Stimulate visceral afferent pathways that talk to vomiting center. Distention or irritation of the GI tract- Rationale: Stimulate visceral afferent neurons. Hypoxia- exerts direct effect on vomiting center. Meds- such as Zoloft. |
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GI - Vomiting or Emesis
Physiologic responses to vomiting: |
Respirations cease
Decreased BP Bradycardia-Valsalva maneuver, or sympathetic nervous system response & Tachycardia Dizziness, Light-headedness |
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GI - Constipation
What? |
It is the infrequent passage of stools. The difficulty with this definition arises from the many individual variation of what is normal
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GI - Constipation
Why? |
Neurogenic disorders
Low residue diet, Sedentary life style, Lack of toilet Diseases-hypothyroidism causes decrease bowel motility Medications-calcium containing antacids, and codeine Advanced age due to change in neuromuscular functions |
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GI - Constipation & Pain
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Pain is diffuse and vague- RATIONALE: This is because nerve endings in abdominal organs are sparse-
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GI - Diarrhea
What? |
excessive or frequent passage of liquid stools
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GI - Diarrhea
Why? |
Lactose deficiencies
Infections-clostridium difficle (occurs from antibiotic therapy) Diseases-colitis, Crohn’s |
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GI - Abdominal Pain
What? |
abdm organs are sensitive to stretching and distention putting pressure on the nerve endings, the sensation is pain
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GI - Abdominal Pain
Why? |
inflammatory response mediators such as histamine, bradykinin, and serotonin, stimulate nerve endings producing pain, associated edema and vascular congestion contributes to the pain, the distention leads to obstruction & lack of blood flow & pain associated with ischemia
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GI - Abdominal Pain
Type - Parietal What? |
pertaining to a cavity-
pain arising from the parietal peritoneum- |
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GI - Abdominal Pain
Type - Parietal How it presents? |
Intense, localized pain that lateralizes (goes to one side). The parietal peritoneum is innervated from only 1 side of nervous system
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GI - Abdominal Pain
Type - Visceral What? |
pain arising from the visceral peritoneum-
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GI - Abdominal Pain
Type - Visceral How it presents? |
it is pain that is poorly localized-
the pain radiates- |
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GI - Abdominal Pain
Type - Referred What? |
visceral pain felt at some distance from a diseased organ-
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GI - Abdominal Pain
Type - Referred How it presents? |
this pain is well localized-
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GI - Upper GI Bleed
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Severity of bleeding depends on the origin:
Venous, capillary or arterial |
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GI - Upper GI Bleed
Arterial Source |
bleeding is profuse-
massive blood loss of more than 1500 mL or 25% intravascular blood volume- Color- bright red, OR 'coffee ground' vomitus if contact with stomach acid |
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GI - Upper GI Bleed
Melena What? |
is black, sticky, tarry foul-smelling stool
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GI - Upper GI Bleed
Melena Why? |
indicates slow bleed from an upper GI source. The longer the passage of blood through the intestines, the darker the color of stool
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GI - Upper GI Bleed
How it presents? |
*ESOPHAGEAL VARICES*
Increased BUN: d/t blood protein digestion during bleed S/S of Shock: Decreased BP & Increased HR- Hgb and HCT: is decreased but may not show until after fluid is replaced 4-6h |
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GI - Dysphagia
What? |
difficulty in swallowing
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GI - Dysphagia
How? |
swallowing is coordinated by the tongue and pharynx. These structures are innervated by the following cranial nerves (CN): V, IX, X and XII
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GI - Dysphagia
Why? |
Altered cranial nerve(s) fx as with CVA-
Disorders that produce narrowing of the esophagus such as tumor or strictures |
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GI - Achalasia
What? |
condition where the lower esophageal sphincter fails to relax; food that has been swallowed has difficulty passing into the stomach
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GI - Achalasia
Complication? |
this is possible especially if the person lies down immediately after eating.
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GI - Diverticulosis/Diverticulitis
What? |
saccular dilation or outpouch through the circular smooth mucle of the intestinal wall
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GI - Diverticulosis/Diverticulitis
Cause? |
No known cause
Deficiency in dietary fiber prevalent where diets are high in refined carbs- virtually unknown in areas such as rural Africa, w/ high-fiber diets 80% of those older than 85 % |
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GI - Diverticulosis/Diverticulitis
Patho- |
Slow transit time of colon
^ water absorb from stool Decrease stool bulk & narrowed sigmoid lumen- ^ intraluminal pressure- diverticula forms- Retain stool/bacteria in diverticulum=inflammation spreads, edema # 1 Abscess formation, Perf, Obstruction, |
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GI - Diverticulosis
How it presents? |
majority have no symptoms-
crampy abdm pain located in the LLQ usually relieved by passage of flatus or BM Alternate constipation and diarrhea- |
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GI - Diverticulitis
How it presents? |
Abdm pain localized over involved area of the colon.
Tender, LLQ mass may be palpated. fever, chills, nausea and anorexia Leukocytosis elderly patients frequently afebrile, normal WBC, and little, if any, abdm tenderness. hematochezia passage of bright red stool |
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GI - GERD
What? |
not a disease, a syndrome produced by reflux of gastric secretions into the esophagus
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GI - GERD
Why? |
d/t weak or incompetent lower esophageal sphincter or delayed gastric emptying-
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GI - GERD
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Gastric acid has pH < than 4. This is very caustic and erosive to the esophageal mucosa
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GI - GERD
Result of reflux? |
inflammatory response. histamine causes hyperemia(congestion of blood) that leads to increased capillary permeability, edema, tissue fragility and erosion of the esophagus. The erosion leads to formation of scarring and strictures d/t the thick scar tissue
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GI - GERD
Barrett’s Esophagus? ^ risks of cancer- |
Reparative process where squamous mucosa that normally lines the esophagus is replaced by columnar epithelium like stomach-
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GI - GERD
How it presents? |
dyspepsia/heartburn- most common after 30-60 min of meals. worse by bending at waist or lying flat- belching, CP
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GI - GERD
Respiratory- |
Wheezing, Chronic cough
Hoarseness Asthma-Link of GERD with asthma. Rationale: Asthma caused by aspiration, laryngeal injury and vagal-mediated bronchiospasms. |
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GI - Peptic Ulcer
What? 2 types: gastric duodenal |
erosion of the GI mucosa results from digestive action of HCL acid and pepsin.
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GI - Peptic Ulcer
Pepsin? |
Pepsin is an enzyme that converts protein into usable substances with the body
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GI - Peptic Ulcer
Stomach protection? |
protected rom autodigestion-
regenerates q 3 days can repair itself unless cell breakdown exceeds the repair ability- also mucus, and bicarbonate |
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GI - Peptic Ulcer
Why? |
H. pylori (common cause)
NSAIDs, Aspirin, ^ emptying more parietal cells mucosa, smoking, alcohol, caffeine, ingestion, decrease in mucosal bicarb secretion- Intense emotional response- CNS Lesions Corticosteroids-decrease mucous cell renewal- hypoxic/hypotensive episode cause shunting of blood from GI, blood bypasses gastric mucosa, an imbalance b/t HCL, pepsin & protective factors ensues, superficial erosions result |
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GI - Peptic Ulcer
Patho of H. Pylori? |
H. pylori forms amonia in the stomach- causes inflammation
histamine from mast cells and prostaglandins act as vasodilators increases cap blood flow & edema, edema causes disruption of capillary walls * loss of plasma & blood into gastric lumen. The break in musus barrier allows back-diffusion of acid leading to tissue injury |
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GI - Peptic Ulcer
Gastric How it presents? |
Pain: No pain to pain (burning, gaseous) No pain d/t gastric mucosa not rich in pain fibers. high in epigastric area, 1-2h p.c.
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GI - Peptic Ulcer
Duodenal How it presents? |
Pain: No pain to pain (burning, cramp like)
Midepigastrium region beneath xiphoid process. If ulcer on posterior aspect of the duodenum pain will be in back. 2-3h p.c. |
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GI - Peptic Ulcer
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some do not exp. pain until presence of ulcer is shown through complications such as hemorrhage or perf. This is seen in those who take aspirin, NSAID, or anticoag.
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GI - Peptic Ulcer
Duodenal |
Duodenal Ulcer pain is relieved with food or antacids. because pain of duodenal ulcer is brought on by the HCL on empty stomach.
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GI - Peptic Ulcer
Treatment? |
eradication of H. pylori-triple antibiotic therapy
avoid gastric irritation-aspirin, NSAIDs Conventional pharmaco tx |
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Inflammatory Bowel Disease (IBD) Ulcerative Colitis
What? |
inflammation and ulceration of the colon and rectum. begins in rectum and spreads proximally affecting mostly mucosal layer
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Inflammatory Bowel Disease (IBD) Ulcerative Colitis
Patho? |
inflammatory process runs together- mucosa is hyperemic (dark red & velvety) has edema.
begins in crypts of Lieberkuhn (which is intestinal glands) and coalesces into ulcers which lead to abscess & necrosis- inflammation causes tongue-like projections that resemble polyps called pseudopolyps. Granulation tissue thickens the muscle, shortens the colon. |
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Inflammatory Bowel Disease (IBD) Ulcerative Colitis
How it presents? |
most common bloody diarrhea and abdm pain-
from destruction of mucosal epithelium, pain range from cramp to severe. diarrhea frequency is 30 to 40 q d in severe cases. Dehydration Electrolyte imbalance Fever- from inflammation |
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Inflammatory Bowel Disease (IBD) Ulcerative Colitis
Characterized by? |
acute fulminating (spread)crisis or chronic disorder
Remissions or exacerbations 20 to 40 years of age with second peak 50 to 80 equal in men and women. common in Jewish and white urban pop. ^ risk of colon cancer |
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Inflammatory Bowel Disease (IBD) Ulcerative Colitis
Treatment? |
rest bowel, control flammation.
infection control, nutrition alleviate stress, symptomatic relief using drug therapy. Antimicrobial, Corticosteroids Anticholinergic: decrease GI motility and relief of smooth muscle spasms. Sedatives, Antidiarrheal Immunosuprresives- Iron and Vitamins- |
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Inflammatory Bowel Disease (IBD) Crohn's Disease
What? |
recurrent, granulomatous inflammatory response that affects any area of the GI tract from mouth to anus
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Inflammatory Bowel Disease (IBD) Crohn's Disease
Patho? |
interspersed lesions 'skip lesions' on all layers of bowel w/ submucosal layer most involved- surface has cobblestone appearance” from fissures & crevices surrounded by areas of submucosal edema- bowel thickens, 'hose like', strictures form, abscess/fistula tracts develop communicating w/ other loops of bowel, skin, bladder, rectum or vagina
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Inflammatory Bowel Disease (IBD) Crohn's Disease
Charateized by? |
slow progressive, relentless often disabling disease.
onset is insidious, begins at 10-30 years old. common among person of European hx, higher among Jews remissions & exacerbations |
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Inflammatory Bowel Disease (IBD) Crohn's Disease
How it presents? |
less bloody diarrhea than with ulcerative colitis b/c Crohn’s affects the sub layer more than other layers
onset is insidious so there are nonspecific complaints such as fatigue, abdm pain, wt loss, fever |
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Inflammatory Bowel Disease (IBD) Crohn's Disease
Treatment? |
*same as for ulcerative colitis*
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Liver - Cirrhosis
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9th leading COD in U.S.
4th leading COD in persons 35-54; 2x common in men as women; single most cause or is excessive alcohol Chronic progressive disease Represents end stage of chronic liver disease |
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Liver - Cirrhosis
Causes? |
4 Causes of Cirrhosis
excess alcohol: accumulates fat in liver- postnecrotic: by virus, toxin, autoimmnue- biliary obstruction and infection- right side heart failure- mineral deposits: hemochromatosis - iron and Wilson's - copper |
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Liver - Cirrhosis
Patho? |
Cell necrosis
Disorganized regen process Scar tissue formation Compression of hepatic veins and bile ducts Portal hypertension, extra hepatic portosystemic shunts and no flow of bile |
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Liver
Functions- |
carb, protein, fat metabolism, body detox, steroid metabolism, form/excrete bile, convert bilirubin, store glycogen, fat vitamins ADEK, fatty acids, iron, copper, albumin, phagocyte RBC, WBC, bacteria
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Liver - Cirrhosis
How it presents? |
Onset insidious-
variable ranging from asymptomatic hepatomegaly to hepatic failure- often none until advaned- |
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Liver - Cirrhosis
Complication - Portal Hypertension |
abnormally high BP in the portal venous system-
compression and destruction of the portal, hepatic veins and capillaries Obstruction to blood flow through portal system Development of collateral circulation |
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Liver - Cirrhosis
Complication - Esophageal Varices is most common/life threatening- |
esophageal varices are extremely dilated sub-mucosal veins in the lower esophagus, very fragile, cant tolerate high pressures-
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Liver - Cirrhosis
Complication - Esophageal Varices factors of irritation- |
alcohol, swallow poorly chewed food, ingest coarse food, acid reflux-
^ abdm pressure from: Nausea, Vomiting Straining, Coughing Sneezing Lift heavy objects |
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Liver - Cirrhosis
Complication - Esophageal Varices. How it presents? |
Melena or hematemesis
Massive hemorrhage-MEDICAL EMERGENCY |
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Liver - Cirrhosis
Complication - Esophageal Varices. Treatment? |
IV vasopressin- vasoconstriction of splanchnic arterial bed, decreases portal blood flow and portal hypertension
IV nitroglycerin-reduces detrimental effects of vasopressin, enhances beneficial effects |
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Liver - Cirrhosis
Complication - Esophageal Varices. Treatment? |
Minnesota or Sengstaken-Blakemore Tube
Minnesota has 1 GI balloon & 1 port for GI aspiration Sengstaken-Blakemore Tube has 2 balloons one for GI, one for esophageal compression. and third port for GI irrigation. Blood admin; Vita K admin Histamine (H2) Blocker or Proton Pump Inhibitor |
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Liver - Cirrhosis
Complication - Splenomegaly |
increased spleen size-
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Liver - Cirrhosis
Complication - Splenomegaly |
Portal Hypertension cause
increased pressure in the splenic vein- Enlargement of spleen - increases filtering/sequestering capacity Reduces number of circulating blood cells |
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Liver - Cirrhosis
Complication - Splenomegaly |
Leads to anemia, thrombocytopenia, leukopenia
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Liver - Cirrhosis
Complication - Peripheral edema |
Usually precedes ascites, sometimes development coincides with or occurs after ascites. From decreased liver synthesis of albumin.
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Liver - Cirrhosis
Complication - Ascites What? |
accumulation of serous fluid in the peritoneal or abdominal cavity
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Liver - Cirrhosis
Complication - Ascites 3 causes? |
Portal Hypertension- ^ BP in forces albumin out large pores of capillaries into lymph space, lymph unable to carry them off so they leak back into peritoneal cavity and increase osmotic pressure-
Hypoalbuminemia- liver unable to synthesize albumin, decreases colloidal pressure Hyperaldosteronism- hepatocytes can't metabolize aldosterone, aldosterone levels ^ = ^ sodium reabsorption, and water retention. |
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Liver - Cirrhosis Complication
Ascites (Complication) |
Renal Failure
such edema formation decreases intravascular volume and subsequently decreases renal blood flow & filtration |
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Liver - Cirrhosis
Complication - Ascites How it presents? |
wt gain, abdm distention, everted umbilicus, striae, dyspnea, S/S of dehydration, decrease UOP, decreased potassium
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Liver - Cirrhosis
Complication - Ascites Treatment? |
restrict sodium, diuretics, paracentesis, daily weights,
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Liver - Cirrhosis
Complication - Hepatic Encephalopathy What? |
potentially-reversible neuropsychiatric abnormality in the setting of liver failure
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Liver - Cirrhosis
Complication - Hepatic Encephalopathy Why? |
Disorder of protein metabolism and excretion
Main agents are nitrogenous ammonia and amino acids- toxic substances normally removed by the liver accumulate in blood and impair brain function- |
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Liver - Cirrhosis
Complication - Hepatic Encephalopathy How it presents? |
Euphoria, Depression, Confusion, Yawning;
Change in orientation Asterixis- tremors Fetor hepaticus-musty, sweet odor of patient’s breath |
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Liver - Cirrhosis
Complication - Hepatic Encephalopathy Treatment? |
reduce amonia-restrict protein, Neomycin Sulfate (PO or enema) to sterile intestines-
Lactulose (Cephulac) lower pH; laxative effect to excrete ammonia. Preferred drug to decrease ammonia over Neomycin, it is < toxic |
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Liver - Cirrhosis
Complication - Hepatorenal Syndrome What? |
Functional RF no structural abnorm of kidneys;
RF from the redistribution of blood flow from the kidneys to peripheral and splanchnic circulations, or hypovolemia secondary to ascites- |
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Liver - Cirrhosis
Complication - Hepatorenal Syndrome Treatment? |
IV admin of salt poor albumin.
Salt and water restrictions Diuretic therapy |
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Liver - Cirrhosis
How it presents? |
Gonadal:
Women- amenorrhea and loss of libido. Men- testes atrophy, loss of libido, impotence, and gynecomastia. |
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Liver - Cirrhosis
How it presents? |
Adrenal:
Decrease aldosterone metabolism, sodium & water retention, low serum K+, skin manifestations (estrogen), jaundice: inability to conjugate and excrete bilirubin |
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Hepatitis
What? |
inflammation of the liver
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Hepatitis
Why? |
acute viral- most common
Noninfectious-drugs and other chemicals Bacteria Autoimmune |
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Liver - Hepatitis
Patho? |
Inflammation of liver tissue
Hepatic cell degen. & necrosis Obstruction of canaliculi Cholestasis- no bile flow Jaundice- cant conjugate bilirubin or excrete in bile |
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Liver - Hepatitis
How it presents? |
No symptoms
Wide range of symptoms |
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Liver - Hepatitis
3 Phases. Number 1? |
Prodromal Phase:
Begins 2 wks after exposure, ends with appearance of jaundice. Last up to 21 days. Fatigue, anorexia, N/V, HA, cough and low grade fever |
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Liver - Hepatitis
3 Phases. Number 2? |
Icteric Phase:
Last up to 6 weeks. Jaundice, clay colored stools, liver enlarged and tender |
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Liver - Hepatitis
3 Phases. Number 3? |
Posticteric/Recovery Phase:
jaundice is disappearing and lasts for up to 4 months. Malaise and easy fatigability |
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Liver - Hepatitis
3 Phases. Treatment? |
Rest and nutrition
High in carbs, low in fat and protein. No specific tx for viral hep. |
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Liver - Hepatitis A
Mode of transmission? |
Fecal - Oral
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Liver - Hepatitis A
Source of infection? |
crowded conditions-
poor hygiene- sexual contact- contam. shellfish- |
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Liver - Hepatitis B
Mode of transmission? |
Parenteral, permucosal-semen, vaginal secretions, saliva, perinantal
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Liver - Hepatitis B
Source of infection? |
contam. needles-
sexual contact- tattoo/piercings- blood products- |
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Liver - Hepatitis C
Mode of transmission? |
same as B
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Liver - Hepatitis C
Source of infection? |
same as B
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Liver - Hepatitis D
Mode of transmission? |
same as B, if you have D then you have B
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Liver - Hepatitis D
Source of infection? |
same as B, if you have D then you have B
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Liver - Hepatitis E
Mode of transmission? |
Fecal - Oral
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Liver - Hepatitis E
Source of infection? |
crowded conditions-
poor hygiene- contam. water- third world- |
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Liver - Hepatitis G
coexist with other virus- Mode of transmission? |
IV & sexual contact-
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Liver - Hepatitis G
Source of infection? |
blood transfusions-
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Pancreatitis
What? |
inflammatory process of the pancreas, results in edema to severe hemorrhagic necrosis-
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Pancreatitis
Why? |
biliary tract disease
alcoholism, trauma/surgery viruses, drugs- metabolic disorders-hyperthyroidism, renal failure idiopathic |
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Pancreatitis
Normal fx? |
Contributes to digestion
Produce hormones (glucagon, insulin) that facilitate the formation and cellular uptake of glucose |
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Pancreatitis
How it presents? |
Pain in LUQ, or mid-epigastri, may radiate to back.
Severe, deep, piercing, and continuous or steady Flushing, cyanosis and SOB Cyanotic or greenish to yellow-brown color of the abdom wall. Ecchymoses of the flanks area ^ serum and urine amylase ^ serum lipase- |
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Pancreatitis
Treatment? |
Meperidine (Demerol)
IV Albumin, NPO w/ NG suctn Somatostatin, ^ carb diet, Ca+ gluconate to treat hypocalcemia & L/R |
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Cholelithiasis
What? |
stones in the gallbladder
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Cholelithiasis
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common of bile system
8% to 10% US adults Higher in women Fair, Fat, Forty ^ in Caucasians High in the Native-American Sedentary, Obesity |
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Cholelithiasis
Cause? |
actual cause unknown-
dvps when holesterol, bile salts, and Ca+ solution is altered so that precipitation occurs |
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Cholecystitis
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occurs if the bile can't escape, however, w/ some blockage bile can continue to flow
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GB function?
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Store and concentrate bile bile has bile salts, cholesterol, bilirubin, lecithin, fatty acids, water and electrolytes
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Bile function?
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aids in fat digestion. emulsifies the fat
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Cholecystitis
How it presents? |
jaundice- no bile
dark, amber urine- bili in pee clay-colored stool- no urobili pruritis- deposit bile salt in skin; cant eat fatty foods; bleeding disorder- no Vita K |
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Cholecystitis
How it presents? |
Steatorrhea- no bile in duodenum, preventing fat emulsion
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Cholecystitis
How it presents? Biliary Colic? attempts to move stones- |
mod/severe pain accomm by N/V, restlessness, Tachy & diaphoresis; occurs 3 to 6 hours after heavy meal or in recumbent position; pain in RUQ or referred to R shoulder
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