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Cardio quiz 2b

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eem8u's version from 2016-12-17 16:39

Disease of Aorta and Blood Vessels (Lec 19)

Question Answer
calculate flowQ = d-pressure / resistance
as radius decreases, resistance_______INCREASES R ~ L / r^4
calculate flow, fx of velocityQ = Area x velocity
in smaller vessel flow is laminar/turbulentturbulent
***elevation pallor /dependent rumor seen withcritical limb ischemia
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High or low resistance system?
Question Answer
muscular arterieshigh
mesenteric (pre-prandial)high
ICAlow
vertebrallow
renallow
mesenteric (post-prandial)low
venouslow
respiratory variation in venous systeminspiration > forward flow (b/c of negative intrathoracic P)
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Disease of aorta
Question Answer
hollenhurst plaque - definedindicates Atheromatous Embolization of the eyes
sx of Atheromatous Embolization in extremities (2)livido reticular and digital ulcers/gangrene
***aneurysm form from min. diameter of≥ 3 cm
80% of aneurysms occur@ renal arteries/aortic bifurcation
thoracic vs aortic aneurysm - etiologygenetic vs traditional CV risk factors
***Aortic dissection - type Ain ascending aorta, before L subclavian branch point
Aortic dissection - type Bafter L subclavian branch point
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Peripheral Artery Dx
Question Answer
Includes which vesselsaorta, iliac, lower extremities
% of adults w/ PAD in western world16%
highest risk factorssmoking, diabetes
***clinical manifestation (2)(continuum) intermittent claudication (occurs with *exertion*) > critical limb ischemia (pain at rest)
frequency of involvement - 3 major areasfemoral popliteal > > tibial / peroneal >> aorta/iliac
****Leriche Triadbilateral butt/thigh claudication + impotence + global atrophy
****Ankle brachial index- calculationhighest ankle SBP / highest brachial SBP
***Ankle brachial index - calcificationCalcified > 1.4
****ankle brachial index - normal0.91 – 1.4
*****ankle brachial index - severe obstruction< 0.4
****ulceration is rare in primary/secondary raynaudPrimary
****how do arterial pulse volume waveforms change in PADsee 20.42 ---- flattened peak (loss of sharp upstroke & dicrotic notch)
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Acute Limb Ischemia
Question Answer
Class Ino pain at rest, ankle pressure > 50 mm Hg
class IIIschemic rest pain, ankle pressure < 50 mm Hg (Salvageable)
class IIIanesthesia/ paralysis (AMPUTATION necessary)
****Buerger’s Dx / thromboangiitis obliterates - triad of sxthrombophlebitis (clot in superficial vein) / raynaud’s / distal arterial occlusion
****Buerger’s Dx / thromboangiitis obliterates - definedsegmental inflammation of MEDIUM sized vessels >> thrombosis and vasospasm
*****Buerger’s Dx / thromboangiitis obliterates - 3 risk factorsmen/ under 40 / SMOKER
****Buerger’s Dx / thromboangiitis obliterates- diagnosis required (2)at least TWO extremities involved / rule out PAD
raynaud’s Disese vs phenomenonbilateral/ no clear cuase/ ULCERATION RARE vs secondary to other condition/can develop gangrene
***tx for Acute LipodermatosclerosisCOMPRESSION
***Lipedema vs Lymphedemaankle cutoff/ALWAYS bilateral vs whole lower limb
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PATHOLOGY of Aortic Atherosclerosis, Aneurysmal Disease and Acute Aortic Syndrome, Aortic Atherosclerosis (Lec 20)

Question Answer
atheroma precipitatesinflammation / neovascularization / intraplaque hemorrhage
complications - coronary vs aortic plaquecoronary - plaque erosin /// aortic - penetrating ulcer (b/c of high degree of vascularization)
structure - aortic vs coronary plaqueaortic plaques more variegated and vascularized (via vasovasorum)
key microscopic fea. of aortic plaquenecrotic lipid core (as in all plaques)
3 sequelae of Aortic Atherosclerosis1- thromboemolus OR atheroma >> ischemia/stroke/gangren 2- aneurysm 3- Acute Aortic Syndrome (includes dissection, penetrating ulcer, hematoma)
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Aortic Aneurysm
Question Answer
definedabnormal DILATION of aorta due to weekend wall
cause of true aneurysm (3)atherosclerosis, congenital (Marfan), ***syphillis
cause of false aneurysm (1)trauma
true vs false aneurysmin false, communication with EXTRAVASCULAR space (w/ hematoma) // in true, wall intact b/ tHINNED
***cause- nutritional deficiencybit C —> altered collagen cross-linking
cause - infectionsyphillis
HOW does atherosclerosis weaken wallthick intimate >> medial ISCHEMIA >> fibrosis >> loss of elastic fibers
***WHERE does atherosclerosis weaken wall(lower abdominal aorta >> below renals /above bifurc of iliac
WHERE does hypertension weaken wallascending aorta (closer heart)
HOW does hypertension weaken wall shear stress
primary genetic causemarfans
***Loeys-Dietz syndrome - mechanismTGbeta mutation —> abnormal elastin/collagen 1/ collagen 3
****ehler’s danlos syndrome - mechanismcollagen III defective synthesis >>> EEEE for collagen THREE
WHERE do genetic syndromes usually cause aneurysmASCENDING AORTA
****rupture risk is > 50% with _____ cm diameter8 cm !!
rupture risk is ~0% with _____ cm diameter<4cm !!
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Marfan Syndrome & Aneurysm
Question Answer
genefibrillin - 1
mechanismfibrillin secreted by fibroblasts >> ECM to form elastic fibers (absence causes severe weakness)
type of genetic disorderAD
****most common site of aneurysmascending aorta
path characteristic of tunic media “cystic medial degenerationsee 19.22
****also assc w/aortic dissection!!
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Acute Aortic Syndromes (AAS)
Question Answer
2 risk factors of AASatherosclerosis / HTN
general mechanism of AAS1- weakening tunica media / 2- rupture of vasa vasorum
***aortic dissection - mechanismmedial degeneration >> TEAR in tunica intimate and media >> false and true lumen >> propagation in either direction >> obstruction of branch vessels
***aortic dissection - risk populationmen, 40-60 w/ HTN (in younger patients, Marfan)
***aortic dissection - most commonly locatedASCENDING aorta
Penetrating Atherosclerotic Ulcer - mechanismatheroma ulceration (intimal disruption) >> erosion of media and **inner elastic layer
****Penetrating Atherosclerotic Ulcer - most commonly locatedDESCENDING thoracic aorta
Intramural Hematoma - mechanism (2)1- focal penetrating ath. ulcer 2- hemorrhage of vas vasorum >>> hematoma (and can lead to DISSECTION)
Intramural Hematoma - mortality increases at ___ locationat valve and ascending aorta
Intramural Hematoma - locationboth ascending and descending
NO intimal tear seen w/Intramural Hematoma
aortic dissection - radiation to neckascending aorta
****aortic dissection - radiation to back -- location?DESCENDING aorta
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Pathology of Atherosclerotic Coronary Artery Dx (Lec 22)

Pathogenesis of Atherosclerosis
Question Answer
worldwide, CAD accounts for ____ of all deaths30%
3 most common sites of atherosclerosis1- lower aorta/iliacs / 2-proximal coronaries / 3- femorals/popliteals/thoracic
fibrous cap - compositionfoam cells, t-lymph, **smooth muscle, ECM (collagen/proteoglycan)
necrotic lipid core - compositioncholesterol crystals, esters, foam cells, calcium
earliest grossly recognizable form of atherosclerosisfatty streak (22.11)
3 key pathogenic features of plaque progressioninflammation / neovascularization / intraplaque hemorrhage
****describe process of plaque inflammationmonocytes adhere to *dysfx endothelium* > inflammatory c migrate to subendo space > infiltrate deep intimate > disrupt internal elastic lamina
describe process of plaque NEOvascularizationthickened diffusion barrier > vasa vasorum proliferate from inside / outside artery and from VEIN > vessels are THIN and fragile > easy rupture
****thickness of normal diffusion barrier in blood vessels< 0.5 mm
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Classification of Ahterosclerosis (AHA)
Question Answer
type Ieccentric intimal thickened / isolated macrophage foam cells / **NO lipid deposition (22.19)
type IIfoam cells in layers / **INTRACELLULAR lipid deposition / NO lipid core (22.20)
type III(preatheroma) scattered foam cell / lipid both INTRA and EXRAcellular / NO lipid core (22.21)
****type IV**FIBROUS cap formation w/ NECROTIC lipid core (22.22)
type V-aFibro/collagenous CAP w/ expanded lipid core & smooth muscle cells(22.23)
type V-bsmaller lipid core w/ **Calcification** (22.23)
type V-cSTABLE plaque >> fibro-collagenous w/ Lipid core absent (22.23)
type VIDISRUPTED cap > thrombus & hemorrhage (22.24)
positive remodeling (plaque progression) = unstable, lipid rich, decreased lumen
negative remodeling(plaque regression) = fibrotic plaque, lumen shape preserved
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Complicated Plaque Morphology
Question Answer
rupture-thrombosis—describe microscopy**communication b/t thrombus and lipid-rich core w/ hemorrhage (22.31)
****rupture-thrombosis—size of cap< 65 um (22.30)
plaque erosion - microscopy**NO communication w/ necrotic core / area of thrombus *denudation* = surface epithelium absent (see 22.33)
calcified nodule - microscopyplaque CALCIFIED nodule protruding into lumen (through disrupted cap) (see 22.34)
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Neoatherosclerosis
Question Answer
stent restenosis - incidence rate17-47% after procedure
stent restenosis - pathopyhsVESSEL WALL injury >> myofibroblast proliferation >> ECM deposition >> NEOintimal
describe microscopy of atherosclerosis in vein graft (22.42)no lipid core/ no Fibrous great, less inflation
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