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Patophysio 2017 final review

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alapaj's version from 2017-03-23 23:47

pulmonary quick review

Question Answer
asthmadenudation of airway epithelium, collagen deposition beneath the basement membrane, edema, mast cell activation, inflammation, bronchospasm
acute bronchitisinflammation of trachea and bronchi. lots of mucus and loss of ciliary function
chronic bronchitistype B COPD 'blue bloater', scarring, fibrosis hypertrophy and hyperplasia of glands, increased bronchial wall thickness
emphysematype A COPD "pink puffer' barrel chest, alveoli destruction, abnormal enlargement of distal air sacs
bronchiectasis(rozstrzenie oskrzeli)recurrent inflammation of bronchial walls, dilation of bronchioles, purulent foul-smelling sputum
bronchiolitisbronchiolar inflammation, mucosal swelling, increased mucus, bronchial muscle constriction
CF (mucoviscidosis)autosomal recessive disorder of exocrine glands and mucus cells. Thick secretion ause airway obstruction, atelectasis and air trapping
ARDS characteristic abormalities1-injury to the alveoli, 2-changes in alveoli diameter, 3-injury to the pulmonary circulation, 4-disruption in oxygen transport and utilization
ARDS typical findingssevere hypoxemia due to shunting, decreased lung compliance, decrease in FRC, Diffuse, fluffy alveolar infiltrates on chest radiograph, non-cardiogenic pulmonary edema
PE RFVirchow's triad ; venous stasis, hypercoagulability, intimal injury
pulmonary infarction definitiondeath, necrosis of lung parenchyma
Alfa 1 antytripsin functioninhibits proteolytic breakdown of alveolar tissue
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hemostasis

Question Answer
primary hemostasisvasoconstriction, platelet plug formation
secondary hemostasisformation of fibrin clot, activation of clotting factors, conversion of fibrynogen to fibrin
thrombocytopenia causesbone marrow supression, DIC, heparin, splenomegaly, hyperthermia, massive transfusion
factor 12 is activated byHMWK, Kallikrein
Bernard Soulier syndromegiant platelet syndrome, gp1b defficiency
Glanzman thromboblasteniaGP2b3a defficiency - abn. aggregation
teleangiectasiadilated & weakend vessel wall, hallmark often epistaxis
hemophilia Afactor 8 defficiency, interfere with intrinsic pathway, ↑aPTT
hemophilia B(Christmas disease), factor 9 defficiency
vitamin K dependent factors2,7,9,10, PC, PS
von Willebrand diseaseabnormal protein 8 carrier, F8 defficiency in circulation, decreased platelet adhesion
DICCF and PT are consumed, blood clots are formed in small vessels
hemostasis disturbancies during pregnancy↑activation of clotting system (intrinsic pathway)
qualitative platelet disorder lab values↑BT, PTC normal
BTassess primary hemostasis, screening for PT disorder
PTassess extrinsic pathway
aPTTassess intrinsic pathway
TT the time required for plasma fibrinogen to form thrombin
F1fibrynogen
F2Prothrombin
F3tissue (factor) thromboplastin
F4calcium ions
F9Christmas factor
F12Hageman factor
F13HMWK
d-dimer testmeasures a substance that is released when a blood clot breaks up (fibrynolysis)
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endocrine fast review

Question Answer
mineralocorticoids are regulated byRAAS
glucocorticoids are regulated byACTH, CRH
Addison's diseaseprimary adrenocortical insufficiency (adrenal gland hypofunction)
Cushing's syndromehypercortisolism
Pheochromocytomaexcessive catecholamines production
Increased androgens males symptomsearly puberty
Increased androgens females symptomsmasculinization
Function of aldosteronsalt and water retention by the kidney
level of ADH in central diabetes insipiduslow
level of ADH in nephrogenic diabetes insipidusnormal
hyperparathyroidism symptomspainful bones, renal stones, abdominal groans, mental moans
microvascular complications of DMnefropathy and retinopathy
macrovascular changes of DMdamaged large vessels - heart, brain, extremities
GH effects on the liverrelease glucose during hypoglycemia, ↑lean body mass, ↓fat tisue
Conn syndromeprimary hyperaldosteronism
causes of hyperprolactinemiaprimary hypothyroid, CRF, liver cirrhosis
↑GH adults results inacromegaly
↑GH children results ingigantism
Addison's disease symptomshypotension, hypoglycemia, hyperpigmentation, weight loss, hyperkalemia, hyponatremia
Cushing syndrome sympromsHTN, truncal obesity, moon face, hypokalemia, glucose intolerance
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GI

Question Answer
abdominal visceral paindiffuse, poorly localized f.e. distended organ
somatic painsharp, well localized f.e. ruptured organ
hiatal herniaprzepuklina rozworu przełykowego
Mallory Weiss syndromebleeding caused by tears in lower esophagus or upper stomach. Factors alcohol, salicyates, VOMITING
Diagnostic feature of Crohnspresence of granulomas
enterocollitiszapalenie jelita cienkiego i okrężnicy
Ulcerative Collitis affectslarge intestine only, destroys mucosa and submucosa only
UC which parts of GI affectedrectum & colon - crypts of Liberkuhn
UC characteristic featureno malabsorption
Crohn's may results fromblockage and inflammation of lymphatic vessels
CD affect which part of GIproximal colon
Diverticula causeslow fiber food, high intraluminal pressure
IBSdiarrhea and constipation
volvulustwisting bowel by itself
Intussusceptiontelescoping of the bowel into adjacent distal portion
Hirschprung diseaseabsence of autonomic nerve ganglia in smooth muscle, no peristalsis
Celiac diseasegluten intolerance (wheat) ; protein called gliadin
tropical sprueatrophy of small intestine mucosa, B12 & folate malabsorption
Dysphagia type 1 causelack of neuromuscular coordination, initiation of swallowing, worse with liquids than solids
Dysphagia type 2 causeperistalsis altered; diverticula, achalasia, tumors
Dysphagia type 3 causeLES function impaired
CRC causeshigh fat low fiber diet, UC, CD
Lecitin functionenhance solubility of cholesterol
acute pancreatitisCCK & secretin regulation impaired resulting in ↑pancreatic enzymes release
acute pancreatitis causesbiliary tract disease, hypertrigliceridemia, ethanol consumption
acute pancreatitis most prominent factorobstruction of pancreatic duct→release of enzymes→activation→autodigestion
acute pancreatitis lab findingsserum lipase↑ and amylase↑, leukocytosis, hyperlipidemia, hypocalcemia
chronic pancreatitis featurecalcifications
chronic pancreatitis is associated withalcohol consumption
pancreatic cancer RFobesity, cigarettes
cholelithiasischolesterol stone in gallbladder
cholelithiasis 3 phasessupersaturation, nucleation, hypomotility
cholelithiasis RFhypomotility stasis of bile in gallbladder, oral contraceptive, pregnancy, obesity, DM
cholecystitisgallbladder wall inflammation
cholecystitis symptomsRUQ pain radiating to the back, fat intolerance, sweating
GE varices causecirrhosis due to alcoholism or viral hepatitis
hepatic encephalopathy definitioncomplex neuropsychiatric syndrome chracterized by symptoms from mild confusion to sturpor and coma
hepatic encephalopathy is worsened by↑ammonia
hepatic encephalopathy classical findingasterixis - spastic jerking of muscles held in forceful extension
hepatic encephalopathy clinical manifesthypokalemia, hyponatremia, alkalosis, hypoxia, hypercarbia
hepatic encephalopathy grades1- confusion, no flap, 2- bahavioral changes, flap, 3- marked confusion, slurred speach, flap, 4-coma, no flap
cerebral edema often present in patients wth grade 3 and 4 hepatic encephalopathy
cerebral edema symptomsdeeping coma, systolic HTN, extensor rigidity, respiratory arrest
Ascites RFhypoalbuminemia, portal HTN
SBP↓ opsonic activity of ascitic fluid, ↓ reticuloendothelial function, migration of bacteria from the gut
SBP worsens following conditionshepatic encephalopathy, renal failure
hepatorenal syndrome due toimbalance between vasodilators and vasoconstrictors agents caused by liver disease
Hepatocellular failure manifestjaundice, ↓CF, hypoalbuminemia, ↓vit D,K, feminization
portal HTN resultGI congestion, esophageal varices, hemorrhoids, ascites, splenomegaly
what prevents gastrocarcinomaaspirin
causes of prehepatic jaundicehemolysis and ineffective erythropoesis
causes of hepatic jaundiceviral hepatitis, alcoholic liver disease, autoimmune hepatitis
causes of posthepatic jaundicecholestasis, Dubin-Johnson syndrome, Rotor syndrome
osmotic diarrheaosmotic active solutes in the lumen causing influx of H2O and sodium
secretory diarrheabacteria triggering chloride ions and H2O secretion
exudative diarrheamucous/blood/protein inflammation in the lumen, increased osmotic load (UC,CD)
hormones increasing glucose levelglucagon, catecholamines, cortisol, GH
↑ALP indicateintra/extrahepatic cholestasis
↑AST indicatecirrhosis, inflammation, hepatitis
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kidneys

Question Answer
PKD symptoms↓GFR, ↓ability to concentrate urine, late HTN, pain, 20% kidney stones, UTI
ADPKDliver and other organs affected
RCC RFcigarettes obesity, DM, HTN, asbestos, long term renal dialysis, kidney transplant
Wilms tumornephroblastoma, common childchood kidney cancer
Hematogenous UTI agentsStaphylococcus, E. Coli
Ascending UTI agentsE. Coli, proteus, enterobacter
Upper UTI synonympyelonephritis
UTI RFvesicourethral reflux, female gender, pregnancy, catheter, urinary obstruction, AIDS, DM
acute pyelonephritis symptomsfever, pain at costovertebral angle, nausea, vomiting, anorexia,
upper UTI characteristic featureWBC casts
chronic pyelonephritis findingsfibrosis, scarring, loss o nephron function
Nephrolithiasis RFhyperparathyroidism, gout, HTN, UTI, IBS, ↑dietary sodium, obesity DM2, dehydratation, prolonged immobility
gromerulopathyalterations in structure and function of gromerular capilaries
Nephrotic syndromeloss of protein > 3.5g/24h, proteinuria, hyperlipidemia, hypoalbuminemia
nephrotic syndrome most common primary causesDM, MN, FSGS, MCD
Membranous Neuropathythickening of glomerular basement membrane
Focal Segmental Glomelurosclerosisscarring of podocytes, epithelial and endothelial damage→proteinuria
Minimal Change Diseasepodocytes altered →↓GF →proteinuria
Nephritic syndromehematuria, RBC casts, proteinuria, HTN, edema
acute glomeruonephritis symptomshematuria, ptoteinuria, oliguria, azotemia, edema, HTN
Acute GN characteristic featureantibodies complex deposition IgG
RPGNcreshend shape depositions – epithelial cells, macrophages and fibrin in Bowman's space
chronic GN↓renal function, fibrosis, sclerosis, small kidneys → ESRD
AKI↓kidney function, electrolytes and acid imbalance, ↑creatinine, ↓GFR
AKI RFCDV disease, DM, HTN, HF, BPH, maligancies
prerenal KI causes (↓GFR)hemorrhage, burns, dehydratation, shock, ↓CO, HF, MI, renal artery stenosis
postrenal KI causesBPH, obstructed catheter, calculi, tumors
intrarenal KI causesATN, ischemia, glomerulonephritis, pyelonephritis, nephrotoxins
ATN causesnephrotoxins, ischemia, vasculitis, emboli,
ATN prodromal phaseinjury, normal UO, ↑BUN and ↑creatine
ATN oliguric phaseoliguria/anuria, hyperkalemia, azotemia, metabolic acidosis, HTN
ATN postoliguric phasefluid volume deficit. lab values begin to normalize
CKDireversible loss of nephrons > 75% > 3months
CKD RFDM, HTN, ATN, DI, hyperparathyroidism, gout, amyloidosis,
ESRD>90% of all nephron lost
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heart

Question Answer
pulsus paradoxusabnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration
prinzmetal angina etiologyvasospasm unrelated to increased activity, stress or HR
ECG changes in MIdeep wide ! wave, inverted T wave, ST segment elevation
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