Path Flashcards
how are MPO/PR3 autoab bad?
ligate target to plasma mem of leuks & cross link w/ Fc receptors –> resp burst, release proteolytic granules, cytok –> alternative C’ –> rolling neu
ranges of nml vs elevated bp vs stage 1 HTN vs stage 2 HTN vs hypertensive crisis
<120/80 vs <130/80 vs <140 or 90 vs >/=140 or 90 vs >/=180/120
risk factors of HTN
black, age, obese/wt gain, alc, psychosocial stress, sedentary
does inc in cardiomyocyte size/hypertrophy inc vasc density?
no –> O2 & nutrients = less in hypertophied heart
forward vs backward failure
heart can’t pump blood forward to meet body’s metab demands vs inc pulm or systemic venous pressure -> fluid moves from capillaries to interstitium -> pulm and/or periph edema
HTN crisis: neuro vs cardiac vs renal vs ocular vs microangiopathic hemolytic anemia
HTN enceph vs LV fail, coronary syndrome, aortic dissection vs high BUN/Cr, hematuria vs HTN retinopathy, retinal hem, yellow exudates, papilledema vs fibrinoid necrotizing arteriolitis -> destroyed RBCs -> occlusion w/ schistocytes
L (cause; clin pres) vs R (cause) HTN/cor pulmonale heart dz
diastolic dysfxn, CHF, IHD; LV concentric w/ perivasc interstitial fibrosis, EKG showing lg V, afib showing lg A, eccentric, pulm edema vs RV overload, pulm HTN
causes and clin pres of AsD vs VsD
defect in interatrial septum -> L to R shunt -> R heart overload -> systemic edema. asx/murmur/sOB; CXR shows lg R heart vs defect in interventricular septum -> L heart overload. asx/murmur; pulm HTN, shunt reversal, Eisenmenger
coarct of aorta. clin pres for neonatal vs adult?
narrowing of abd aorta either proximal/preductal or distal/postductal to to L subclavian a & ductus arteriosus. CHF, shock vs UE HTN, dec LE pulse, aortic aneurysm, systolic murmur, CXR shows figure 3 config
PFO
failed postnatal fusion of septum primum & secundum -> no flap b/w RA & LA at fossa ovalis -> LAP > RAP to keep PFO closed but if RAP > LAP -> paradoxical embol (clot goes R to L to brain) -> cryptogenic stroke, migraines w/ aura
TOF. complications?
defect in conotruncal septum -> pulm valve/a stenosis, lg VSD, overriding aorta over VSD instead LV, RVH -> R to L shunt -> cyanosis, tet spells, squatting -> inc resistance -> more bloodflow to pulm circ. arterial thrombosis -> ischemic stroke
Eisenmenger syndrome. clin pres?
untxed L to R shunt inc pulm blood flow pulm vasc obstructive dz & vasc resistance pulm a HTN RV hypertrophy & failure. Fatigue, dyspnea, cyanosis, erythrocytosis; CXR shows enlarged RV & dilated pulm a
tricuspid atresia
no tricuspid valve & hypoplastic RV -> blood from RA to LA to LV (ASD) -> no blood to lungs -> cyanosis, CHF, digital club, fail to thrive
Ebstein anomaly
downward/apical displacement of tricuspid valve into RV -> incompetent tricuspid valve, shortened RV, enlarged RA -> R to L shunt
truncus arteriosus
arterial vessel from heart overrides vent septum -> supplies systemic & pulm circ from proximal ascending vessel -> cyanosis, polycythemia, finger clubbing, CHF, fail to thrive, recurrent resp infxns
TGA. D v L TGA
failed conotruncal septum to spiral & divide TA to pulm aa & aorta -> aorta = ant on RV, pulm a on LV. pulm & systemic circs in parallel not nml series -> incompatible w/ life w/o mixing circs vs nml circs but L/RV switched -> deO2 blood go to RA to LV to pulm aa, O2 blood go to pulm vv to LA to RV to aorta
general idea of L to R shunt vs R to L shunt
blood from L to R -> dec CO -> dec O2 to tissue -> Qp/Qs > 1.5:1-> R heart overload, inc pulm pressure/resistance, edema vs blood from R to L -> Qp/Qs < 1:1 -> L heart overload
Anomalous coronary a from pulm a
L>R coronary a -> LV perfused by desaturated blood under low pressure -> myocardial ischemia -> CP, syncope, sudden cardiac death, MI
xanthoma?
* Xanthelasma =
* Tuberous =
* Tendinous =
* Eruptive =
deposited lipid laden macs in skin or tendon. most common; soft & yellow vs extensors knees/elbows/butt d/t hyperchol & high LDL vs subq nodules on extensors hands/feet/Achilles vs pruritic red-yellow papules on extensors/butt/shoulders d/t hyperTG x/ IV; Can spont resolve in weeks
concentric vs eccentric hypertrophy
high overload -> new sarcomeres in parallel w/ long axes of cardiomyocytes vs vol-overload hypertrophy/aortic regurg -> vent dil -> new sarcomeres in series w/ existing sarcomeres
superficial vs DVT affects which vv? causes vs clin pres of DVT?
great/less saph vv vs iliac, fem, popliteal, tibial vv. immobile, cig smoke, obese, ocp, hormone replace, preg, surg/trauma, antiphospholipid ab, Factor V Leiden, prothrombin mutation vs pulm thromboembolism
cause vs clin pres vs complications of thrombophlebitis?
staph aureus, S. epidermidis, K. pneu, E. coli, Pseudomonas; IV cath, venipuncture for phlebotomy & IV injections vs fever/chills, limb swelling, tender vs sepsis, infective endocarditis
- Migratory thrombophlebitis/Trousseau
recurrent venous thrombosis preceding or concomitant w/ occult visceral malig from ca procoagulant or tissue factor
Cause of venous thrombosis?
Virchow’s triad: vessel wall injury; venous stasis from immobility; change in blood composition from factor V Leiden, lupus anticoag, protein C/S defic, antithrombin defic, malig
