Week 4 Flashcards
(199 cards)
1
Q
lipoprotein
A
cholesterol transport. composed of hydrophobic core (cholesterol and TG) and hydrophilic shell (phospholipids and apo)
2
Q
relationship between size and density of lipoproteins
A
larger=less dense=more fat
3
Q
apoB lipoproteins
A
atherogenic. nonHDL lipoproteins (VLDL, chylomicrons, LDL, etc)
4
Q
exogenous pathway of lipoprotein metabolism
A
dietary lipids are exported into the lymph as chylomicrons, LPL then hydrolyzes the TG into FFA, which tissues take in for energy and storage. the chylomicron remnant is then taken in by the liver via LDLR
5
Q
apoB48
A
associated with chylomicrons
6
Q
apoC
A
cofactor for LPL
7
Q
apoE
A
associated with chlyomicron remnants-interacts with LDLR
8
Q
endogenous pathway of lipoprotein metabolism
A
in fasting states, the adipose tissue releases FFAs, which get repackaged in the liver and excreted as VLDLs. remnants after tissue uptake are LDLs
9
Q
apoB100
A
associated with LDL
10
Q
secondary causes of hypercholesterolemia
A
diet, alcohol, hypothyroidism, medications
-most importantly T2D or insulin resistance
11
Q
T2D relationship to hypercholesterolemia
A
increased insulin=overproduction of VLDL=increased LDL
12
Q
lipoprotein (a)
A
Lp(a)=independent risk factor for CHD
13
Q
HDL
A
tiny, dense lipoprotein with inverse relationship to CHD. associated with apoA
14
Q
reverse cholesterol transport
A
nascent HDL stimulates release of LDL from macrophages. LDL is esterified and added to HDL =mature HDL, which transports the LDL to the liver
15
Q
causes of hypoalphalipoproteinemia (decreased HDL)
A
ApoA mutation (nonfunctional nascent HDL=rapid catabolism), Tangiers Disease (ABCA1 mutation=LDL can’t be removed from macrophase=HDL catabolism), LCAT deficiency (mature HDL can’t be formed)
16
Q
which HDL mutation causes swollen tonsils and lymph nodes?
A
Tangiers disease
17
Q
which HDL mutation causes cloudy corneas?
A
LCAT deficiency
18
Q
primary target in lowering cholesterol?
A
reduction in LDL (<50 for women)
19
Q
secondary targets in lowering cholesterol?
A
reduction in TG, increase in HDL
20
Q
why don’t patients with FH respond to statins, CAIs, or BASs?
A
these patients don’t have working LDLR so up regulating these receptors does nothing for them in terms of decreasing plasma LDL
21
Q
treatments for FH?
A
LDL apheresis, drugs that target apoB/MTP to decrease liver production of VLDL
22
Q
treatments for patients who don’t tolerate statins due to muscle pain or who are already on highest dose possible?
A
LDL apheresis, drugs that target apoB/MTP to decrease liver production of VLDL, antibody drugs that eliminate Psck9 (decreased LDLR degradation)
23
Q
fibrates
A
activate PARPalpha in liver to increase the activity of LPL to
24
Q
jugular venous pressure (JVP)
A
way to assess for RAP. position patient at 30 degrees and look at how high you can see the pulsatile jugular vein above the angle of louis.
25
venous vs arterial pulsation
venous is a double pulsation if there is atrial contraction (a and v waves)
26
when would you not see a double venous pulse?
in atrial fibrillation-no atrial contraction
27
S1 heart sound
AV closure, start of systole, just after a wave. louder at apex since direction of flow is inferior
28
S2 heart sound
semilunar closure, start of diastole, corresponds to v wave. louder superiorly
29
splitting
upon inspiration, S2 might split due to a delay in closing the pulmonic valve bc the R side of the heart is getting more volume with increased SVC/ICV pressure
30
S3 heart sound
early diastolic filling. indicates increased LAP. heard best at apex
31
S4 heart sound
late diastolic filling due to atrial kick. indicates blood bouncing off a stiff ventricle. heard best at apex
32
heart sounds and MR
laterally displaced apical impulse (from eccentric LVH) and holosystolic murmur
33
aortic stenosis and heart sounds
sustained apical impulse from concentric LVH, diminished carotid pulse, crescendo decrescendo systolic murmur
34
differences between regurgitation and stenosis
in regurgitation: can better increase SV/CO, can be acute or chronic, two chambers are affected
35
type of LVH that accompanies regurgitation?
eccentric LVH
36
functional classification of regurgitation
1. Normal leaflet movement
2. increased leaflet movement
3. decreased leaflet movement
37
anatomic examples of normal leaflet movement regurgitation
perforation of a normal leaflet due to endocarditis
38
anatomic examples of increased leaflet movement regurgitation
myxomatous degeneration caused chordae rupture (mitral valve prolapse or flail leaflet)
39
anatomic examples of decreased leaflet movement regurgitation
rheumatic disease HFrEF (dilation due to remodeling), or dilation due to ischemia
40
acute mitral regurgitation
regurgitant volume into LA=increased LAP (v wave)=pulmonary edema; FSV decreased bc split between two outlets (decreased CO); increased LVEF due to increased preload (extra LA volume) and decreased afterload (LAP is lower than aortic & decrease ESV)
41
compensatory mechanisms of acute MR
LV dilation=increased preload to increase SV
| adrenergic stimulation=increased HR (increase CO) and contractility (to decrease ESV)
42
chronic MR
eccentric LVH allows continued LVEDV increase with decreased LVEDP (increases compliance, normalizes afterload, increases FSV)
increases RV so RF remains the same
LVEF reduced towards normal
43
chronic decompensated MR
loss of contractile function=decreased LVEF to normal, decreased FSV, increased RF
44
aortic regurgitation
higher preload and afterload so that the LV must eject at a higher pressure=massive eccentric LVH
45
why does tachycardia/exercise help with AR?
tachycardia decreases the diastolic time, thereby reducing the time for reverse flow to occur
46
AR on pressure waveform
sharp drop in aortic diastolic pressure due to reverse flow
47
MR on pressure waveform
large v wave due to increased atrial inflow
48
why is AR susceptible to ischemia?
coronary perfusion is driven by the pressure gradient between aortic diastolic pressure and LVEDP. because of rebound backwards flow, the ADP is decreased and additionally, the LVEDP is increased (less drive)
49
fatigue
represents a chronic mild impairment of CO in combination with a chronic moderate elevation of pulmonary capillary pressure
50
dyspnea on exertion
inappropriate increase in pulmonary cap pressure during physical exertion
51
chest discomfort on exertion
development of myocardial ischemia during exertion. supply-demand imbalance
52
lightheadedness on exertion
falling systemic arterial pressure during exercise due tot he inability to increase the CO commensurately to the systemic vasodilation that accompanies exercise
53
valve diseases that can cause ischemia (angina, pain)
AS, AR
54
valve diseases that cause LVH
AS, AR, MR
55
define atherosclerosis
arterial intimal disease of large/med arteries characterized by lipid accumulation and inflammation in the neointimal space
56
medial response associated with atherosclerosis
VSMC migration, fibrous cap formation
57
adventitia response associated with atherosclerosis
neovascularization once lesion reaches certain size
58
main points to remember about atherosclerosis initiation
1. risk factors promote endothelial damage
2. activated endothelium expressed receptor that attract monocytes
3. LDL enters intima, becomes oxidized and engulfed by macrophages=foam cell accumulation
4. TH1 cells propagate inflammation
59
risk factors that promote endothelial damage
HTN (shear stress), smoking (oxidative stress), diet, inactive lifestyle, etc
60
in atherosclerosis, where does the initiating endothelial damage usually occur?
arterial branch points and bifurcations
61
what endothelial receptors mediate monocyte attraction?
- selectins promote rolling
- VCAM/ICAM promote adhesion
- CCR promotes diadapesis
62
main points to remember about evolution of lipid accumulation to intermediate lesions
VSMCs switch to secretion function and form fibrous cap and neointimal calcification. compensatory vasodilation maintains luminal diameter (asymptomatic), neovascularization occurs when plaque passes supply/demand threshold
63
what type of fibrous cap is most stable/less likely to rupture
thick caps
64
what drives plaque rupture?
inflammatory T cells increase inflammatory mediators and VSMC apoptosis.
MMPs eat away at fibrous cap
65
is stability of plaque related to its degree of stenosis?
NO
66
why is plaque rupture bad?
rupture exposes the lumen to tissue factor and other prothrombotic molecules that promote platelet driven thrombosis==complete stenosis or embolization
67
why is aspirin good to take if you have atherosclerosis?
it deactivates platelets via COX inhibition. ruptured clots are then less likely to form a thrombus
68
most important risk factor for atherosclerosis
T2D--as much risk as past MI
69
metabolic syndrome
- 3+ symptoms that increase risk for CVD, T2D, stroke
| - increased abdominal girth, high TG, low HDL, high bp, high fasting glucose
70
important inflammatory markers for atherosclerosis
CRP and LpPLA2
71
atherosclerosis imaging
ultrasonography of carotids, electron beam imaging of coronaries (looking for calcification), MRI of aorta/carotids/coronaries
72
ADAMTS7-atherosclerosis
encodes MMP that modulates inflammation and accelerates VSMC migration and intimal thickening
73
ABO blood group and atherosclerosis
predictive of plaque rupture
| increased risk with A and B blood groups
74
who has a greater absolute risk for MI? (W/M)
men
75
BMI qualifying someone as overweight or obese?
25-30=overweight
| 30+=obese
76
healthy diet
- decreases bp/inflammatory markers/insulin resistance/metabolic symptoms
- improves lipid profile
77
low fat diet
- reduces the energy density profile of diet (fewer cals per meal since people tend to eat the same amount of food consistently)
- reduces total cholesterol, LDL, HDL (regression of atherosclerosis)
78
low carb diet
- theory that if we don't ingest glc, body will think it's fasting (glucagon) and break down fats
- best for initial weight loss (diuretic effect)
- atherogenic since eating more fats. also bad for kidneys/liver in long run
79
mediterranean diet
- most balanced. best
- no trans fat. only good cis unsaturated fats
- reduces risk of T2D, CVD, weight loss similar to atkins
- easy to adhere to
80
the low down on exercise
- a low amount of moderate intensity exercise is sufficient to increase aerobic fitness and decrease CV risk (and decrease weight).
- increasing the intensity and amount of exercise compounds these effects
81
what should you say to patients who are worried about exacerbating or initiating a cardiac event during exercise?
heat stroke is more dangerous and more likely
82
leading cause of death in US
CVD
83
stages of atherosclerotic lesion progression
1. initial lesion- monocyte adhesion/migration
2. fatty streak-lipid laden foam cells
3. intermediate lesion-foam cells secrete lipids
4. atheroma-lipid core develops
5. fibroatheroma-fibrous cap develops
6. complicated lesion-rupture leads to hemorrhage, thrombosis, aneurysm, ischemia
84
PCI (percutaneous coronary intervention)
cather balloon and stenting. used to treat patients with unstable angina and acute MI. improves LV function
85
restenosis
stent damages internal lamina so that VSMC migrate into lumen, proliferate, secrete ECM-->entirely iatrogenic
86
growth factors involved in restenosis
- PDGF-VSMC migration
- FGF & Ang2- VSMC proliferation
- TGFb-ECM secretion
87
solution to restenosis?
- drug eluting stents: rapamycin (inhibits VSCM proliferation) and paclitaxel (inhibits replication and migration of VSCM)
- target cell cycles
88
challenges of drug eluting stents?
thrombosis-because you also inhibit endothelial proliferation
89
types of familial cardiomyopathies
hypertrophic, dilated, restrictive
90
mutations in hypertrophic cardiomyopathy
involve myofibril disarray and interstitial fibrosis
91
mutations in dilated cardiomyopathy
mutated cytoskeletal proteins
92
theory behind cardiomyopathies
mutant muscle is more sensitive to Ca and consumes more ATP (higher energy cost=eventual failure)
93
long QT syndrome
defects in repolarization (channelopathies) that predispose to polymorphic VTs (torsades de pointes)
94
ischemia
imbalance of supply and demand due to inadequate perfusion--hypoxia and accumulation of waste products
95
determinants of myocardial oxygen demand
HR, systolic wall tension, myocardial contractility
96
O2 demand-HR
theory behind treating ischemia with beta blockers is that they are negatively chronotropic
97
O2 demand-wall tension
higher tension=elevated EDVs=higher P=higher o2 necessary
| -diuretics and nitrates reduce pressure and volume (preload)
98
O2 demand-contractility
beta blockers are negative inotropes and can therefore be used to reset the supply demand balance by reducing demand
99
determinants of myocardial oxygen supply
oxygen content & coronary blood flow
100
o2 supply: blood o2 content
determined by O2 sat & Hgb--need to maintain adequate oxygenation and hematocrit in ischemia to increase supply
101
o2 supply: coronary blood flow
dependent on driving pressure and coronary vascular resistance
102
driving pressure of coronary blood flow
greatest during diastolic phase, when wall tension is the lowest bc of relaxation and decreased pressure
103
why are tachycardias so bad in terms of o2 supply?
they increase the heart rate (increased demand) and they decrease the time in diastole, therefore decreasing the time for coronary flow (decreased supply)
104
reactive hyperemia of the coronaries
mediators (NO, adenosine, ACh) reduce the resistance of the coronary vascular bed in order to augment blood flow in conditions of higher O2 demand
105
coronary flow reserve
the difference between resting coronary blood flow and maximal flow as a result of reactive hyperemia
106
metabolic effects of ischemia
- reduced production of ATP=Na accumulation=swelling and membrane damage
- glycolysis predominates=generation of lactate that is inadequately perfused away=acidosis
- acyl coA accumulation=inhibits esterification of FFAs=impaired fatty acid oxidation pool
107
electrophysiological effects of ischemia
- disruption of sarcolemma=NaK ATPase failure=increased extracellular K=acidosis
- and leads to reductions in Vm, AP upstroke, amplitude, velocity
108
systolic impairment associated with ischemia
- contractile dysfunction due to interference with Ca binding to troponin=decreased SV
- dyskinesis (outward bulging) in central zone of ischemia, akinesia in adjacent regions, compensatory hyperkinesia in unaffected regions
109
diastolic impairment associated with ischemia
- because relaxation also requires energy, it is impaired=stiffness and decreased compliance=increased LVEDP
- one of the earliest signs of ischemia
110
VC version of what is happening to the LV during ischemia
incomplete emptying & resistance to filling==predisposes to HF and cardiogenic shock
111
what part of the heart is most susceptible to ischemia?
subendocardium--subject to more compressive forces and gets blood at the end of the line
112
stunning
acute ischemia followed by re-perfusion so that cells don't die. leads to a prolonged period of contractile dysfunction (fully recoverable)
113
what causes stunning?
accumulation of toxins leading to an altered Ca uptake
114
hibernation
chronic hypo perfusion that causes contractile dysfunction but no cell death. usually encountered in setting of severe CAD. akinesia results--looks like MI on echo. reversible
115
angina
sensation of chest discomfort-substernal pain that radiates to the L arm/neck/jaw
116
what causes angina?
anaerobic byproducts stimulate cervicothoracic nociceptors
117
stable angina
provoked by oxygen supply demand mismatch in the setting of fixed coronary artery stenosis. resolves after stressor
118
unstable angina
results from progressive narrowing at the site of flow limiting stenosis
119
variant angina
printzmetal angina--vasospasm causes an abrupt reduction in blood flow. typically occurs in the morning and at rest
120
silent angina/ischemia
occurs in patients who have autonomic neuropathy (diabetes, deinnervated transplanted hearts)
121
ECG diagnosis of ischemia
ST segment depression away from area of ischemia. ***but the ecg must be taken at time of ischemia for it to show up***
122
goal of treatment of ischemia
restore O2 supply-demand imbalance
123
first line treatment for ischemia
beta blockers--reduce HR, bp, contractility (decrease demand) and reduction in HR also increases supply by increasing diastolic time
124
second line therapy for ischemia
ca channel antagonists-reduce preload and afterload, negativly inotropic and chronotropic
125
aspirin and ischemia
all patients without contraindications should receive it--limits platelet aggregation by inhibiting COX
126
heparin and ischemia
should be given to patients with unstable angina--disrupts coagulation cascade
127
mechanical interventions for ischemia
PTCA, stent, CABG
128
clinical causes of infarction
coronary thrombosis, coronary embolism, severe vasospasm, trauma, extreme increases in myocardial O2 demand
129
define infarction
prolonged ischemia that leads to irreversible myocardial damage (death)
130
molecular cause of infarction
lipid rich foam cells release MMPs (macrophage derived metalloproteinases) that degrade the matrix of the fibrous cap
131
symptoms of infarction
usually preceded by severe and persistent unstable angina.
132
ECG diagnosis of infarction
ST segment elevation at site of infarction, q waves signify dead territory
133
why is there ST elevation in infarction?
excess voltage is flowing out of the necrosed area
134
why is there ST depression in ischemia?
conduction flows towards areas of ischemia, so areas not affected experience a drop in voltage
135
protein diagnosis of MI
elevated levels of creatine kinase (CK), myobglobin, troponin I and troponin T--indicative of release of dying cell contents
136
common rhythmic sequelae of infarction
dysarrhythmias and conduction block
137
LV dysfunction complications of MI
- decreased LV compliance=increased P=pulmonary edema
- systolic dysfunction=systemic hypoperfusion (high risk for cardiogenic shock)
- pericarditis
- wall/septum/pap muscle rupture
- wall aneurysm
- remodeling
138
how can one diagnose pericarditis?
friction rubs and distant heart sounds
139
what treatment can be used to prevent ventricular remodeling following MI?
ACEi
140
thrombolytic agents approved for use in MI
streptokinase, tPA
141
what type of necrosis occurs in ischemia?
coagulative
142
most common cause of ischemia
atherosclerosis
143
which tissue is most susceptible to ischemia?
subendocardium
144
myocardial changes that occur in ischemia
switch to anaerobic glycolysis, stop contracting=myofibril relaxation=myocytes stretch=cell membrane damage=coagulative necrosis=phagocytotic clearance=granulation=fibrotic scar
145
when do myocardial stretching/changes become irreversible?
20-40 minutes after onset of ischemia. TREAT QUICKLY
146
acute coronary syndrome
- unstable angina, acute MI, sudden death
| - associated with abrupt plaque changes (rupture of vulnerable plaques)
147
how long does an MI take to reach its full extent (i.e. become transmural)
4-6 hours. leaves some time to act and TREAT QUICKLY
148
minutes after MI
micro: thin/wavy myocytes stretched by adjacent tissue
gross: only detected via TTC stains
149
6-24 hours after MI
micro: coagulative necrosis (loss of nuclei/striations), hypereosinophilia
gross: dark mottling due to trapped deoxygenated blood
150
1-3 days after MI
micro: PMN infiltration
gross: tan/yellow pallor
151
7-10 days after MI
micro: macrophage infiltration to clear debris
gross: hyperemic border with yellow/pale center
152
what causes hyperemic border week after MI?
normal tissue vasodilates to allow ingress of macros to clear debris
153
2-4 weeks after MI
micro: ingrowth of granulation tissue
gross: grey/red periphery
154
8-10 weeks after MI
micro: collagenous scar
| - gross: grey/white
155
three results of reperfusion
1. rescue non lethally injured myocytes (stunning or hibernation)
2. alter the pattern of necrosis (contraction band necrosis from influx of Ca and hyper contraction of those not yet dead)
3. reperfusion injury (oxygen free radicals kill healthy, noninvolved myocytes=hemorrhage)
156
complications of MI associated only with transmural MI
pericarditis, ventricular rupture, anuerysm
157
when is an MI area most susceptible to rupture?
3-5 days post-- when PMN infiltrate is maximal
158
LV psuedoanuerysm
LV rupture that is contained- won't lead to tamponade
159
leading cause of mortality in women?
CVD
160
who has a higher rate of CVD occurrence? higher mortality?
men, women
161
why do we think estrogen might be cardioprotective?
women tend not to be affected until post menopause
-also, estrogen decreases LDL, increases HDL, facilitates NO mediated vasodilation, and inhibits atherosclerosis by inhibiting vessel response to injury
162
since we think estrogen is cardioprotective, what do we think about hormone replacement therapy (HRT)?
not currently recommended: there seems to be an early protective promise, but no sig diff in the long run and even increased risk of breast cancer. badness.
163
thoughts on why HRT doesn't seem to be doing it?
it might be beneficial in healthy vessels (increases vasodilation and decreases inflammation) but seems to be detrimental in atherosclerotic vessels (increases MMP)
-ladies in the trials that concluded it was not recommended were all fairly old and might have fallen into this later category
164
effects of testosterone on CVD?
- causes vasodilation, reduces angina threshold, shortens the QT
- low levels could be associated with CV risk
165
hemodynamic changes associated with pregnancy
- decreased PVR, bp, peripheral resistance
| - increased uterine flow, blood volume, HR/SV (CO), venous pressure
166
hemodynamic changes associated with labor/delivery
- each contraction releases 500ml of blood into the circulation (increased CO, bp)
- lose 400mL with vaginal delivery vs 800 for C section
- increase in venous return afterwards since baby is no longer squishing your IVC
167
high risk states for pregnancy
pulmonary HTN, stenosis, regurgitation, cyanotic heart disease, prosthetic valves
168
condition associated with the worst mortality during pregnancy?
pulmonary HTN
169
what usually causes pulm. HTN?
VSD/PDA/ASD shunts
170
why is pulm. HTN bad during pregnancy?
the volume load of pregnancy compromises poorly functioning RV=HF (also eventually reaches the point where LV is not preloaded)
-pregnancy is actually not advised or termination is advised
171
stenosis in pregnancy
pressure overload state reduces the body's ability to increase CO needed in pregnancy.
-LAP further increased by increased blood flow of pregnancy, increased HR of pregnancy reduces CO and can cause a fib.
172
how to manage stenosis in pregnancy
beta blockers and diuretics. balloon valvotomy if severe enough
173
regurgitation in pregnancy
better tolerated than stenosis because you can still augment SV and accommodate increased flow
174
cyanotic heart disease
congenital R to L shunt. augmented by decreasing peripheral resistance in pregnancy. increased risk of paradoxical embolism. hypoxia impedes fetal growth
175
which prosthetic valves in pregnancy are best?
- tissue valves are less thrombogenic so they don't require heparin but also will def need to be replaced at some point
- mechanical valves are thrombogenic and def need anticoagulation therapy but last forever(ish)
176
problem with anticoagulation therapy during pregnancy?
- higher risk of thromboembolization in mother (increased clotting factors and platelet adhesiveness in pregnancy)
- higher risk of placental hemorrhage
- embryopathy with warfarin in first trimester
177
how to deal with necessary anticoagulation therapy during pregnancy?
since heparin doesn't cross the placenta, give that until week 14 and then switch to warfarin. switch back to heparin towards ends since it has a shorter longevity and you can wean quickly for delivery
178
peropartum cardiomyopathy
occurs during last month of pregnancy or within five months of delivery. usually within one month though
179
three causes of ACS
1. plaque rupture
2. intravascular thrombosis
3. vasoconstriction/spasm
180
high risk unstable angina vs NSTEMI
similar clinically and on ECG (ST depression)--difference is that NSTEMI has myocardial damage and will therefore be positive for biomarkers
181
difference between STEMI and NSTEMI
- in a STEMI the entire vessel is occluded and the ischemia is transmural.
- STEMI is more unstable=higher biomarker levels, lower LV function, higher risk of CHF
182
STEMI vs NSTEMI in regards to mortality
NSTEMI has higher rates of mortality-- more prone to recurrent ischemia and STEMI symptoms are more in your face, so they are recognized and treated more quickly
-although the potential for damage is much greater in STEMI
183
acute care of ACS
1. anti-ischemic therapy (nitroglycerin, beta blockers, CCBs)
2. antithrombotics: antiplatelets (aspirin, thienopyridines, glycoprotein inhibitors) and anticoagulants (heparin, thrombin inhibitors)
3. reperfusion: PCI, CABG
184
explain "TIME IS MUSCLE"
myocardial necrosis starts around 6 hours after ischemic event. If you catch and treat infarction within 60 minutes, you can save almost all of the tissue!!
185
which tissue has the least amount of blood flow at rest?
skeletal
186
at what percent of stenosis does flow begin to decrease?
75%
187
claudication
pain caused by too little blood flow during exercise
188
ankle brachial index (ABI)
systolic pressure taken at ankle (dorsal is pedis/posterior tibial) divided by brachial systolic pressure
-ratio of less than 0.9 indicates PAD
189
change in blood flow pattern after stenosis
the blood flow distal to the stenosis becomes broad and mono phasic (on doppler) as opposed to the normal systolic/diastolic differentiation
190
effect of exercise on ABI
- normal response: equal arm and leg pressure with exercise
| - PAD: abnormla decrease in pressure at the ankle
191
critical limb ischemia
blood flow to legs doesn't meet demands. usually occurs when ABI<0.35
192
causes of stroke
mostly embolic, then large vessel/small vessel occlusion, then hemorrhage
193
only branch of the ICA?
opthalmic artery
194
hollenhorst plaque
retinal cholesterol embolus from ICA (into opthalmic artery)
195
subclavian steal syndrome
stenosis to subclavian--> vertebral artery fills retrograde to supply it=dizziness, vertigo since blood is being "stolen" from the brain as a result
196
consequence of renal ischemia
HTN due to increased renin release
197
which artery increases its flow in response to a meal?
SMA
198
clinical syndrome of mesenteric ischemia
postprandial abdominal pain, weight loss (food fear, malabsorption), nausea, vomiting, diarrhea, constipation
199
DVT
normal phasic flow becomes continuous
