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115 Cards in this Set

  • Front
  • Back
heart chambers
right and left atria
right and left ventricles
atrioventricular valves
tricuspid (right)
bicuspid (left)
semilunar valves
major heart vessels
vena cava(superior/inferior)
pulmonary trunk (right/left pulmonary arteries)
pulmonary veins (right/left; two pair)
Heart Failure
heart muscle cannot pump sufficient blood to meet body’s demand
left sided failure
decreased systemic perfusion (cannot push blood into aorta and into the system), low O2, left chambers
fail to empty and become dilated, left pressure rises, back up into
pulmonary veins and capillaries, forces fluid into alveoli (resulting in
not being able to move O2 and CO2)
a. most common causes: by MI, hypertension, valve diseases
b. results in: pulmonary edema
right sided failure
right chambers dilate, backs up into IVC/SVC,
reflected back as increased pressure in various organs (liver) and edema (lower extremeties)
a. caused by: chronic lung disease, chronic left sided failure
b. yields: venous congestion/peripheral edema
simultaneous R/L failure which comes from chronic severe left failure leading to increased back up pressure in lungs, this leads to back up in right heart
defined as increased blood pressure (diastolic > 90 mm Hg; systolic in men over 50 > 140, systolic in women > 160)
60 million cases in N. America alone (probably 1/3 of these are undiagnosed)
increases mortality by 50%
can be either systemic, pulmonary, or portal
two main types of HYPERTENSION
1. primary (essential)
2. secondary
primary (essential) hypertension
a. increases with age
b. accounts for 90% of cases
c. genetic predisposition
d. other risk factors include obesity, alcohol, decreased activity, smoking, stress, race (blacks are 2x as likely to be hypertensive as whites)
e. can be benign (long-term, slowly progressing) or malignant (acute, rapidly progressing)
f. unknown cause: possibly due to defects in the complex control mechanisms for blood pressure cardiac outputvolume overload-blood in chambers pressure overload-aorta peripheral resistance blood volume regulated at the arterioles aldsterone-NaCl
secondary hypertension
a. 10% of cases
b. usually due to pregnancy, renal disease, pheochromocytoma or diseases of the adrenal cortex: causes imbalances of water and sodium producing vasoconstriction
target organs involved with hypertension
1. heart: increased blood pressure leads to left ventricular hypertrophy, this leads to insufficient coronary blood flow, which leads to left ventricular failure, eventually right side also involved and congestive heart failure results
2. brain: cerebral hemorrhage
3. kidney: slowly progressive destruction of glomeruli leading to chronic renal failure
4. aorta: atheroma, aneurysms
can in turn cause arteriosclerosis, strokes and myocardial infarction
ISCHEMIA (Coronary Heart Disease)
A. most common heart disease: 30% of all males/23% of female deaths
B. caused by atheroma of coronary arteries
C. left ventricle more prone because it has a higher oxygen demand
D. angina: episodic chest pain with increased demand
myocardial infarction (MI)
death of heart muscle tissue due to ischemia (can measure increased enzymes for diagnosis; proportional to blood flow affected
MI short-term complications
a. dysrhythmias
b. left ventricular failure
c. L ventricular rupture as a result of an MI
(cardiac tamponade)
MI long-term complications
a. chronic left failure
b. ventricular aneurysm
c. recurrent MI
inflammation of the internal surface of the lining
-most often valves of the L side
Aggregates Aschoff bodies, aggregated lymphs and macrophages Aschoff bodies destroy myocardium
Causes dysrythmias
A. Acute inflammation of pericardial lining
Often with myocarditis-exudation
B. Infection leads to painful friction
C. Can result from MI, viral or bacterial (rheumatic fever) infection
Rheumatic Fever-cause unknown, suspect post strep, immune reaction is what is damaging-can lead to endocarditis
1. stenosis: narrowing or abnormal rigidity
2. incompetence: failure of closure (mitral valve prolapse)
1. congenital
25000 babies born annually
Minor and major classifications
Occur before 10 wks in utero
Cause unknown
Ventricular septal defect is most common
2. scarring: repair from infection (rheumatic fever)
3. age-related degeneration
Congenital Heart Diseases caused by viruses, alcohol or genetics
Septal Defects:
1. left to right shunts
2. can involve atria (patent foramen ovale)
3. can involve ventricle (VSD)
Patent Ductus Arteriosus: aorta to pulmonary trunk shunt
Tetralogy of Fallot:
1. ventricular septal defect
2. overriding aorta-movement from normal position (to the R) and
squeezes pulmonary trunk
3. pulmonary stenosis
4. right ventricular hypertrophy
1. extends from cricoid cartilage to stomach
2. lined by stratified squamous epithelium
a. high mitotic activity = high cancer rates
3. first 2/3 skeletal/lower 1/3 smooth muscle in wall
4. has a lower muscular sphincter
Esophageal reflux
1. reflux of stomach acid back up into esophagus
2. causes burning pain, “heartburn”
3. causes
a. fungal/viral infections
b. ingestion of caustic agents
c. increased abdominal pressure (pregnancy)
d. hiatal hernia
–organ is protruding into a space it doesn’t belong
-several types of hernia
e. smoking and/or alcohol (smoking-higher risk for esoph. cancer)
4. has potential to cause damage to epithelium
5. often causes metaplasia to columnar epithelium (adenocarcinoma)
-difficulty swallowing
1. most often due to obstruction
a. foreign body
b. tumors
c. achalasia: lower esophageal sphincter stenosis
2. sometimes psychosomatic
i.e. nerves, stress
ESOPHAGUS Tumors (Malignant) types
1. squamous: caused by alcohol, smoking; found in older men, spreads via lymph nodes, poor prognosis
2. adenocarcinoma: usually found in lower esophagus, often a metastasis from stomach, poor prognosis
1. three areas: cardia, body (fundus), pylorus (sphincter)
2. lined with columnar epithelium, special cell populations secrete HCl and intrinsic factor (body), gastrin (pylorus)
1. inflammation of gastric mucosa (mucosa is any lining open to the outside world)
a. Gastric mucosa starts in the oral and ends at the anal
b. mitotically active
2. acute
a. superficial damage
b. caused by alcohol, aspirin, alkalis, NSAIDs
c. can erode epithelium with vomiting
takes longer to heal with wear of the stomach lining vs. mucosa
3. chronic: all types can lead to metaplasia
a. Helicobacter pylori: affects pyloric epithelium, causes ulcers
b. autoimmune: pernicious anemia, found in elderly patients who have antibodies against parietal cells or intrinsic factor, causes failure to absorb vitamin B12, leads to impaired blood cell production
c. reactive: reflex from duodenum, caused by prolonged exposure to NSAIDs
1. damage to stomach lining by increased acid production, bacterial infection
2. can be acute or chronic
3. can cause hemorrhage, perforation, fibrous repair and loss of elasticity
-can cause anemia with continual on/off bleeding
1. Small intestine: duodenum, jejunum, ileum; all with columnar epithelium, smooth muscle, most digestion takes place in duodenum, ileum has Peyer’s patches (lymphocytes)
-most food products, enzymes all dumping into duodenum
-ileum has peyer’s patches, not much absorption, common for infections
2. large intestine: colon, rectum, anus; columnar epithelium with goblet cells, physiology is to add mucus, extract water
3. both collectively are called “gut”
intestinal infection causes
1. viruses

2. bacteria: E. coli, Salmonella, Shigella, Campylobacter (bacterial dysentery: blood/pus in stools)
3. protozoans: giardia-hide in C-curve of the duodenum
4. helminths
Small Intestine Malabsorption Syndromes
small intestine
a. celiac disease (sprue) british spelling-“coeliac”
1. atrophy of small intestinal villi
2. due to immune response to gluten (wheat flour)
Villi becomes flatten and ability to absorb and digest is hindered
Need to pay attention to labels
Large intestine Malabsorption Syndromes
. large intestine
a. Crohn’s disease(most common)
1. granulomatous inflammation of terminal ileum and bowel
2. affects women > men (autoimmune?)
3. 20-60 yrs old
4. shows cobblestone pattern of mucosal lining
5. stenosis and adhesions leading to obstruction
6. remitting/relapsing disorder

7. often presents with referred lower back pain
b. ulcerative colitis
1. chronic inflammation of rectal mucosa
2. shallow ulcers develop in mucosa
3. patients are predisposed to colon cancer
4. thought to be assoc’d with emotional problems (esp with children)
Malabsorption Syndromes
1. impairment of production/secretion of pancreatic/liver/intestinal enzymes or defects in epithelial surface for absorption
2. symptoms are weight loss, diarrhea, distended abdomen
3. pancreatic insufficiency found in cystic fibrosis, tumors, parasites
intestinal tumors
1. most common in large intestine as precancerous polyps
2. derived from epithelium: adenocarcinoma
3. incidence increase with age, related to diet and genetic predisposition
4. third most fatal malignancy
5. males>females
Older the more risk, >50 every 10 years
6. presents with abdominal pain, vomiting, blood loss in stool
7. 80% of tumors found in lower colon
8. prognosis related to staging
-early detection is the key
a. usually due to blockage
b. presents with diffuse abdominal pain
c. increased severity of infection localizes pain to right lower quadrant of abdomen
d. can lead to perforation, peritonitis
2 layer sac around all the abdominal organs, it compartmentalizes the abdomen
1. usually an extension of abdominal infection
2. causes decreased gut motility
3. can precipitate fluid accumulation (ascites
1. oval-shaped bodies found along the course of the lymphatic vascular system
a. collection of lymphocytes
2. function to filter lymph (plasma filtrate), produce antibodies (plasma cells) and serve as a site for macrophage phagocytosis
a. collection of all the extracellular fluids/one way flow
b. 3 ways to go in but only one way to go out
enlargement of nodes due to immune response (influenza,
mononucleosis, AIDS)
1. swelling due to bacterial or viral infections
a. flow increased because lymph is carrying more stuff
b. lymphs are increasing and dividing
Hodgkins Disease
Lymphoma-cancer involving lymphocytes
–too many lymphs in one little area
1. proliferation of Reed-Sternberg cells (atypical lymphocytes)
a. lymph nodes are a tumor site of lymphocytes uncontrollably dividing
b. normal lymph have a nucleus and an atypical lymph with lymphoma is multilobed or bilobed (owled eyed lymphs)
2. presents as enlarged nodes, spreads to other nodal groups and organs (typically spleen, liver, bone marrow)
a. patients typically present with night sweats-unknown
3. diagnosed by biopsy, staged with CT/MRI
a. must be owled eyed in order to diagnose
4. prognosis related to type/stage, overall five year survival 50-75%
a. diagnosis with early detection is key
b. requires chemotherapy
Non-Hodgkins Lymphoma
too may lymphs that are not in a lymphnode, but form a tumor somewhere in the body
1. proliferation of B/T lymphocytes
-mostly well differentiated, but can be aplastic
2. grades
a. high: increased mitotic index, rapid expansion, poor prognosis without treatment
b. low grade: slow growing-high grade: fast growing
faster growing will show signs sooner, more curable because its identified sooner
c. intermediate
Prognosis: high grade often more curable because diagnosis is early and
treated with aggressive chemotherapy; low grade disease is often
disseminated, can be treated but often relapses
*radiation is more commonly used due to degree of spreading
Non-Hodgkins Lymphoma Types
a. B cell: majority of cases, can be diffuse or follicular (grow in
germinal center formations)
b. T cell: <10%
A. Pluripotent stem cell produces all blood cells
B. Four major cell lines
1. Lymphoid linelymphocytes
2. Erythroid lineerythrocytes (RBC)-no nucleus, cannot divide or make
proteins, 120 day lifespan, shape will change as they age
a. no nucleus provides room for hgb
b. concave shape allows for flexibility
3. Myeloid line (all the rest of WBC)
a. granulocytes (eosinophils, basophils, neutrophils)
b. agranulocytes (monocytes)
4. Megakaryocyte line: pieces break off platelets
C. bone marrow d/o can be a problem with one or all the blood lines
normal lab values hematocrit
(volume of packed RBCs/spun)
1. 40-50% male
2. 35-45% female
normal lab values RBC concentration
1. 5 million/uL male
2. 4.5-5 million/uL women
reduced RBCs in circulation, shown by low hemoglobin, low RBC count, low hematocrit
1. body compensates by increasing cardiac output and RBC production
-increase in RETIC
Anemia Causes
a. iron deficiency: impaired uptake, increased blood loss, increased
b. chronic blood loss: peptic ulcers, stomach and colon cancers
c. B12/folic acid deficiencies: pernicious anemia (lack of intrinsic
factor) which causes megaloblastic anemia –immature cells in
bone marrow not making enough
d. RBC production failure: (aplastic anemia) productive marrow is
replaced by fat, affects production of all blood cell types
-decrease in WBC also, immune response problems
e. chronic underlying diseases: eg. autoimmune disorders
f. RBC destruction: (hemolytic anemia)
hemolytic anemia
1. hereditary spherocytosis: RBC membrane cytoskeletal
defect which makes cells fragile, cells are convex
2. G6P dehydrogenase deficiency: x-linked, renders RBCs
suseptible to destruction by certain drugs/infectious
3. thalassemia: defective hemoglobin synthesis, hereditary,
common in Mediterranean and Middle/Far East
4. sickle cell disease: point mutation miscoding for
hemoglobin synthesis, affects African population, RBCs
sickle-shaped, fragile, occlude vessels, multiple
complications pair is incorrect
5. mechanical/immune-mediated destruction
-can be caused by H157 E coli (HUS-jaundice, flu-like sx., cola-colored urine)
increased red cell mass, increased hematocrit, induced by
hypoxia, if hematocrit rises above 50% causes hyperviscosity (very thick)
-olympians train in Colorado due to higher altitude, produce more RBC
and when they leave to compete, they have high O2 levels
a. granulocytes (life span of days-weeks)
1. neutrophils: 60-70% of circulating WBCs, segmented nuclei, light blue granules, non-specific phagocytes
2. eosinophils: 1-4%, segmented nuclei, pink granules, phagocytose parasites
3. basophils: 1%, segmented nuclei, dark blue granules, release heparin and histamine
b. agranulocytes (life span of months-years)
1. monocytes: 3-8%, horseshoe-shaped nuclei, non-specific phagocytes
2. lymphocytes: 20-25%, spherical nucleus, immune response, antibody production
Changes in WBCs
1. Reduction: neutropenia (cancer patients…leukemia)
-lymphoma collects lymphs that forms a mass
-leukemia is too many blood cells in circulation
2. Increase: leukocytosis, response to infection
most common WBC neoplasm, shows as increased number of
circulating neoplastic cells with decreased production of other normal cells (anemia, infection, bleeding)
-high WBC, decreased RBC and platelets
1. Normal hematopoesis
2. Myeloid leukemias (acute or chronic)
-more common than lymphoid
3. Lymphoid leukemias (acute or chronic
*pediatric leukemias are usually acute and elderly are usually chronic
-both are treatable, chemotherapy
1. cell derived from lymphocytes, found in peripheral tissue, “clockface” nucleus
2. lymph cell is out in circulation
3. involved in immune response
Multiple Myeloma
affects patients >50, neoplastic proliferation of a clone of plasma cells, causes plasma cells to grow in bone marrow (bone destruction with pain)
-very commonly found in spine and usually found too late
fragments of megakaryocytes from bone marrow, involved in blood clotting
Thrombocytopenia: decreased platelet production
C. Hemophilia: hereditary defects in making coagulation factors
D. Disseminated Intravascular Coagulation (DIC)
1. excessive activation of coagulation in small blood vessels
2. causes hemolysis because vessels are occluded with thrombi
3. increased fibrin production in small vessels
4. decreased platelet count resulting from excessive clotting in small
5. patients become ischemic and have hemolytic anemia
6. caused by septicemia, systemic shock, delivery complications
nephron Anatomy
have about a million
glomerulus -is only one capillary
2. Bowman’s capsule-around glomerulus
3. tubule system-give a lot of surface and time to filtrate and move ions around, what you need goes back into the blood stream and what you don’t need, goes into urine
a. proximal tubule
b. loop of Henle
c. distal tubule
d. collecting duct
kidney function
1. selective filtration of blood plasma (glomerulus)
2. selective reabsorption of glucose, amino acids, water, Na, K, Ca,
PO4,H+(tubule system)
3. production of erythroprotein for hematopoesis
4. production of renin which activates angiotensin which stimulates the
secretion of aldosterone (hormone responsible for increased sodium
5. all functions together maintain homeostatic ionic balance, plasma
volume, blood pressure
A. Caused by diseases which alter the structure of the glomerulus
B. Disruption in the glomerulus affects all structures/functions downstream
C. Renal Failure
Renal Failure types
1. partial kidney failure
A. nephritic syndrome: disturbance of glomerular structure that
involves reactive cellular proliferation (endothelium, mesangial
cells (phagocytes)), low renal blood flow
a. oliguria: reduced glomerular blood flow leading to reduced urine output
b. hematuria: leakage of RBCs into urine
c. uremia: retention of waste products in the body
d. activation of renin:angiotensin system leading to fluid retention and hypertension
e. acute glomerulonephritis
B. nephrotic syndrome: abnormality of basement membrane
(thickening), glomerulus unable to selectively retain proteins
a. proteinuria: loss of protein into urine
b. hypoalbuminemia: lack of protein in blood, leads to
c. decreased immunity due to loss of IgG and complement
d. increased thromboses due to fibrinogen in blood
e. hyperlipedemia
f. membranous nephropathy
2. total kidney failure
A. acute: where majority of glomeruli simultaneously stop working
a. dramatic oliguria to anuria
b. caused by immune-mediated damage to glomeruli or tubular disruption due to hypoxia, toxins, infections or vascular problems (hypovolemic shock)
c. can be reversed if harmful stimulus is removed; no opportunity for metabolic compensation (causes electrolyte imbalance)
B. chronic: slow, progressive, irreversible destruction of glomeruli;
opportunity for metabolic compensation
a. progressive uremia (retention of wastes); causes destruction of renal cells and loss of erythropoetin production
b. polyuria: excretion of large amounts of dilute urine
c. caused by vascular diseases (hypertension), glomerulonephritis (immune-mediated)
VASCULAR DISEASES-big vessels, not glomerulus, but renal artery
A. hypertension: causes ischemia
1. can be caused by blood not getting to kidney
B. occlusion: causes infarction
C. renal artery stenosis: may cause (correctable) hypertension
D. benign hypertension: causes chronic ischemia with slow destruction of glomeruli
E. malignant hypertension: necrosis of afferent arterioles and glomeruli
F. renal infarction: renal artery emboli
G. DIC (disseminated intravascular coagulation): fibrin thrombi, hemolysis
A. Anatomy
1. ureter
2. bladder
3. urethra
B. Physiology: transport and storage of urine
A. tubular inflammation
B. caused by ascending bacterial infection or septicemia, urine reflux, obstruction
C. symptoms include fever, rigors, back pain
D. diagnose with urine culture
E. gross/microscopic: small abcesses with proliferation of neutrophils
F. may spread systemically and cause renal necrosis, chronic condition causes scar
A. necrosis of renal tubular epithelial cells usually due to trauma
B. due to ischemia (hypotension, hemorrhage, burns, shock) or toxic causes
C. regeneration possible if stimulus removed
A. increased mode of treatment for end-stage renal failure
B. disease can recur or can have vascular thromboses
C. rejection
1. hyperacute: immediate reaction, widespread intravascular thromboses,
due to antigen-antibody reaction, now rare due to improved screening
2. acute: occurs within one week of surgery, T-cell reaction with
infiltration of new kidney with lymphocytes, neutrophil proliferation,
cellular necrosis, can respond to treatment
3. accelerated acute: occurs in patient with previous unsuccessful
transplant experience
4. chronic: takes months, slow breakdown of immune tolerance,
permanent loss of nephrons
Nephroblastoma (Wilms’ tumor)
1. embryological origin
2. peak incidence in children ages 1-4 yrs of age
3. diagnosis due to abdominal mass with hematuria
4. prognosis related to spread/differentiation
5. high cure rate with radiation/chemotherapy
Transitional cell carcinoma
1. found in lower urinary tract, usually bladder
-cells that line the bladder are called transitional cells because it can change shapes, cells flatten out as the bladder expands
2. related to environmental factors (organics/chemicals, smoking)
3. more common in men
4. good prognosis: 80% are low grade, non-invasive tumors, respond to
surgical removal
typically can be spot treated and don’t need chemo or radiation
Renal cell carcinoma
–usually occurs only on 1 side
1. most common tumor involving the kidney
2. more common in men, some link to smoking
3. often discovered accidentally when investigating non-renal symptoms
4. poor prognosis
-if found early, can remove kidney and still have another
A. transfer of GI bacteria to lower urinary tract
B. more common in women because of short urethra
C. localized to urethra/bladder; may progress to cause pyelonephritis
A. blockage of ureters causing hydronephrosis, bilateral obstruction causes renal failure
B. calculi: stones (Ca, PO4) caused by stasis of urine or infection
Polycystic disease
–often bilateral
1. autosomal dominant inheritance
2. detected in childhood
3. manifested in adult
4. causes chronic renal failure and hypertension
5. predisposition to berry aneurysms (arterial/venous malformation in a vessel to the brain which if it ruptures, will cause hemorrhagie stroke)
A. digestive organ made up of hepatocytes arranged in lobules, centered around a central vein
B. lobules bordered by portal triads (portal vein, hepatic artery, bile duct)
LIVER functions
1. carbohydrate, lipid and protein metabolism
2. production of bile-compound that emulsifies/breaks down fat
-bile is stored in gallbladder
3. storage of glucose (glycogen) and fat-soluble vitamins (A,D,E & K)
-fat soluable vitamins can build up to a toxic level
-water soluable are excreted when not needed
4. albumin synthesis
5. detoxification of many drugs and hormones
6. makes cholesterol
Main Causes Of Liver Disease
1. toxins: alcohol (accumulation of acetaldehyde leading to irreversible fatty
liver), drugs (medications, illegal/recreational)
2. infectious agents
3. vascular (hypertension, arthersclerosis)
4. tumors (lots of primary cancers will spread in liver)
Manifestations Of Liver Disease
1. jaundice: yellow discoloration of skin/sclera resulting from increased plasma bilirubin (hemoglobin breakdown product
2. hepatitis: inflammation of liver
3. cholestasis: bile duct damage causing backup of bile into liver
4. cirrhosis: extensive scarring causing disruption of normal liver structure, impaired blood flow (portal hypertension), ascites, irreversibly reduced
hepatocyte function, causes hepatic jaundice
hemolytic anemia and blood production disorders (prehepatic)
Gilbert’s syndrome
autosomal dominant disease affecting 5-10% of population, failure of liver to clear bilirubin (prehepatic)
-some yellowing to skin and puritis
neonatal jaundice cause
incomplete enzyme function usually due to prematurity, can lead to kernicterus (permanent brain/motor damage)
-very common
-treat with bili lights
symptoms of jaundice caused by obstruction
pale stools, dark urine, impaired fat absorption, itching
inflammation of liver
acute: cell death with inflammation, 80% fatal, causes hepatic jaundice
chronic: long term inflammation lasting > 6 months, presence of abnormal liver function tests, fibrosis
hepatitis types
1. A/E
a. from fecal contamination
b. four week incubation period
c. complete recovery with immunity
2. B
a. from infected blood, semen, saliva
b. can be mild/acute with recovery and immunity
c. can be mild/chronic (> 6 months duration) with
recovery and immunity
d. chronic can be a carrier and have increased rates of

3. C
a. non A/non B (blood-borne)
b. two month incubation with acute onset
c. symptoms similar to B, but less severe
4. D
a. concurrent only with B
b. two month incubation
c. 50% are chronic
Storage Diseases
1. Wilson’s disease
2. hemochromatosis/hemosiderosis
3. glycogen storage diseases
Wilson’s disease
autosomal recessive, increased levels of copper
-bronze/coppery look to skin
autosomal recessive/alcoholism, increased levels of iron
glycogen storage diseases
genetically transmitted, usually diagnosed young
and usually fatal
a. Gaucher’s
b. Niemann-Pick
Vascular Disease (Liver)
1. normal portal circulation
no direct venous drainage from GI system to the inferior vena cava, it all dumps into the portal vein and is very “dirty” blood
2. portal hypertension: increased blood pressure in portal vein causes abdominal
ascites, splenomegaly; caput medusa, has multiple causes
-blood is shunted to other vessels and not into the portal vein, increases blood pressure, can reopen umbilical pathways (medusa)
Liver Carcinoma
1. highly malignant
-spreads fast and easily
2. more common in men than women (5:1)
3. often associated with cirrhosis, HBV, HCV
4. benign growths often associated with oral contraceptives
If large enough, can take over and impair function of the liver, but is not malignant
5. liver is a common site for metastasis
1. oral cavity
2. pharynx/larynx
3. trachea/bronchii
4. lungs/alveoli
cells in lungs/alveoli
a. Type I cells –allow for passage of air
b. Type II cells-secrete/release surfactant
respitory system functions
1. Gas exchange: oxygen in/carbon dioxide out
2. PAO2 = 80 - 100 mm Hg
3. PACO2 = 35 - 45 mm Hg
4. ability for lungs to expand/contract
5. need positive pressure
Type I: low PAO2 (<60 mm Hg, < 30 mm Hg unconscious), normal PACO2
Type II: low PAO2, elevated PACO2 (>50 mm Hg, hypercapnia = coma)
disease, airway obstruction, mechanical impairment, CNS involvement
a. pulmonary hypertension
b. polycythemia
1. excess RBC production
2. increased blood viscosity
3. thrombus formation
4. decreased blood flow
incomplete expansion of the lungs/collapse of lung
causes of Atelectasis
a. airway obstruction
b. compression: pleural fluid
c. scarring
d. loss of surfactant
e. mucous plugging
Pulmonary edema
increased fluid in alveoli from left ventricular failure
inflammation and consolidation of lung
1. fifth most common cause of death in US
2. common in infants and the elderly (decreased mobility)
3. primary infection can be in the bronchioles or in the lobes
4. may be alveolar or interstitial
5. caused by various bacteria/viruses
Virus is Atypical and causes milder symptoms
6. airways fill with neutrophils and exudates/fluid
Hypostatic pneumonia
from chronic lung infection
Mycoplasma pneumoniae
causes interstitial pneumonia
Primarily in kids
Affects all the lung and you hear Rales
chronic bronchitis
chronic obstructive pulmonary disease (COPD)
small airway obstruction with bronchospasm, mucus production
1. common disorder among both children and adults
Children can grow out of it
2. increasing incidence due to environmental factors
3. chronic inflammatory response with periods of acute exacerbation and
excess mucus production
4. triggered by cold, allergens, exercise, stress, infection
Intrinsic-exercise, infection, aspirin, stress
-non-immune mediators
Extrinsic-allergens (allergic triad)
5. Treatment:
Medications: albueterol-stops spasms
corticosteroids to decrease inflammation
leukotrienes help with the mast cells
Chronic asthma sufferers have permanent smooth muscle hyperplasia and
basement membrane thickening
–completely irreversible
1. permanent dilation of alveoli, destruction of tissue with scarring
2. loss of elasticity and surface area for gas exchange, tachypnea
3. decreased oxygen delivery
4. compensatory rapid respiratory rate and barrel chest (pink puffer)
5. related to smoking (biggest cause)
chronic bronchitis
1. defined as productive cough for > 3 months over a 2 yr period
2. abnormally high mucus production, surface epithelium preserved
3. coughing may be so severe as to cause dyspnea and hypoxia (blue
a. green sputum (more neutrophils)
4. related to smoking
chronic obstructive pulmonary disease (COPD)
combination of asthma, emphysema, chronic bronchitis
adult respiratory distress syndrome (ARDS)
tuberculosis (TB)
adult respiratory distress syndrome (ARDS)
1. caused by systemic sepsis (bacterial infection) and/or trauma
2. high mortality (70%)
3. treat with continuous airway pressure and cardiac/renal support
4. damage to alveolar lining, air spaces dilate
1. coal dust
Accumulation of CO2
Most retained in nasal passages
Located in centrolobulr zone
Fibrosis can occur
2. silicosis (miner’s disease)
Stone cutting/mining
Develop after 10-20 yrs exposure
3. asbestosis
Pulm fibrosis
Pleural fibrosis and plaques
a. molecules engulfed by macrophages
b. release of cytokines
tuberculosis (TB)
1. caused by Mycobacterium tuberculosis
2. chronic inflammation with granuloma formation
a. No acute purulent infection elicit granulomas
3. formation of tubercles
4. can wax and wane, appear to heal, and recur
5. can spread
6. of concern in developing countries, AIDS
7. new strains emerging resistant to current antibiotics

Normal PPD result within 48 hours and wheal <10 mm
AIDS should have < 5 mm due to immunocompromised
A. Most common neoplasias in developed countries
-lifestyle, pollution,
B. Incidence peaks between 40-70 years of age
-very slow growing, insidious
-cannot be picked up on chest X-ray, but can be by CT
-by the time its found, its usually too late
-70% who smoke will develop lung cancer
C. Male = Female
D. Related to smoking, environmental exposure
-secondhand smoke is said to be worse because of the carcinogens that people are blowing out and the smoke people are from inhaling from the cigarette itself
Highly metastatic to brain, bone, liver, adrenal glands (Fig. 8-27 (p 200))
G. No early signs/symptoms; cough, chest pain, dyspnea, hemoptysis, cachexia
H. Staging/typing (TNM)
I. Poor five year survival; some types very sensitive to radiation/chemotherapy
-6 mths to 2 years with no intervention depending on health of patient
-Up to 5 years with interventions
(70% bronchial/30% alveolar)
1. squamous cell (50%): keratin (protein on skin surface, squamous cells
no longer alive but serving a function on the skin) producing
-Squamous metaplasia from chronic irritation, can still repair itself if they quit smoking
-Squamouc cell carcinoma is from persistent exposure and cannot be repaired
2. small cell anaplastic (oat cell) (20%): most malignant, endocrine
-Starts making excess hormones
3. adenocarcinoma (20%): peripheral location in lung, slow growing
4. large cell anaplastic (10%): poorly differentiated, poor prognosis
air in pleural space, causes atelectasis, results from chest
wounds, disease, iatrogenic causes (hospital/physician induced)
-trauma such as gunshot wounds can introduce air in the space
-chest tubes, central line, etc…
inflammation of the pleura; viral/bacterial
Pediatric respitory diseases
neonatal respiratory distress syndrome (NRDS)
cystic fibrosis
neonatal respiratory distress syndrome (NRDS)
surfactant (soapy film that lines the alveoli to keep it from
-7 mths gestation, fetus begins to make surfactant
-very common in premature infants
cystic fibrosis
a. genetic disease
b. autosomal recessive
c. most common genetic disease in Caucasian population
d. results in increased mucus production
e. caused by defective chloride transport across cell membranes
f. survival of about 30 years