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
risk factors vs clin pres of varicose vv of LE
fhx, age, female, multipara; obese, occupation vs Chronic insufficiency of LE, Pitting edema; Venous stasis, ulcer; Superficial thrombophlebitis
primary vs secondary lymphedema
in children; Milroy dz: auto dom VEGFR3 -> dec lymp vessel -> can’t absorb lymph fluid -> painless chronic LE lymphedema vs in adults; Brca, rads therapy, extensive skin resect, extreme obese
varicose vv of LE. primary vs secondary?
subq dil vessels in LE esp great/less saph vv -> inc venous pressure, dec venous return. downreg P2X1 receptors -> lose ctxile cells -> can’t vasoconstrict, just dil -> secondary valve dz vs inflam & destruction of vessel wall -> inc venous pressure -> more inflam & venous destruction
examples of complicated plaques
calcification in lipid core; superficial v deep rupture; chol crystal in small/med aa esp abd aorta -> livedo reticularis, blue toe syndrome, LE pain; plaque hem from rupture of newly formed capillaries
non vs modifiable factors of atherosclerosis
fhx, age, gender vs HLD, DM, HTN; homocysteine, metab d/o; cig smoke; inflam/infxn
tunica intima vs media vs adventitia
simple sq endothel cells vs symph circular sm mm cells, have lumen that shrinks when cells constrict vs merges w/ surrounding tissue
elastic aa. vasa vasorum?
largest aa containing cirumferential & fenestrated sheets of elastic fibers in tunic media, in/external lamina –> stretches heart in systole. blood vessels in tunica media
muscular/distributing aa
branches off elastic aa to supply organs & extremities. constrict/dil to ctrl blood flow to specific organs. respond to neural, hormonal, & local metab stimuli
arterioles -> metarterioles -> capillaries
smooth cell mm layer = still continuous, ctrls blood flow/pressure vs scatter sm mm cells, ctrls blood flow thru capillaries vs not continuous, 1 cell thick for diffusion, contains pericytes
cont vs fenest vs sinusoid capillaries
most common, no defects vs pores -> more permeable; GI, endocrine glands, kid, choroid plexus vs bigger pores -> WBC pass thru, highly fenestrated basal lamina; liver, spleen, bone marrow, some endocrine glands
post capillary vs collecting vs muscular venules
receive blood from capillaries, have pericytes, WBC migration vs mult layers of pericytes, tunica media vs smooth mm fibers instead of pericytes, tunica media
lymph vessels
run parallel to capillary & vv; move lymph via muscle compression; have valves to prevent backflow; low pressure vs endothel cells not tightly joined -> edges loosely overlap & have minivalves to prevent backflow; fibers anchor endothel cells -> expose slits & keep vessels from collapsing
what do cardiac cells vs Purkinje look like histo?
central nuclei, striations, lots of capillaries, intercalated discs (desmosomes/adherent jxns/gap jxns); no regen -> fibrosis/scar vs must fine tune microscope -> bigger cells w/ frothy central cyto w/ few peripheral striations
endo vs myo vs epicardium
simple sq vs thickest; atria has lowest pressure -> thinnest myocardium, LV has highest pressure -> thickest myocardium vs simple sq w/ adipose
papillary mm vs chordae tendinae vs heart valves
collagen fibers providing tension for chordae tendinae vs collagen & elastic thata prevent prolapse of AV valves vs prevent backflow; lamina fibrosa = central cartil plate, covered by endocardium
sA & AV nodes vs Purkinje
irreg twirl of small fibers lacking intercalated discs embedded in collagen connective tissue vs binucleated bigger myocytes w/ less myofibrils = terminal branches of condxn in ventricles, lg glycogen stores -> clear halo around nucleus
