Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CV Final > Atherosclerosis/Vascular Disease > Flashcards

Atherosclerosis/Vascular Disease Flashcards

1
Q

Triphasic wave form

A
  1. strong forward component of blood flow during systole
  2. short reversal of blood flow during early diastole
  3. low amplitude foward blood flow during remaining diastole (loses vacuum, going back)

INACTIVE - when exercise - both systolic and diastolic flow increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Bernoulli’s

A

as speed of a moving fluid increass, pressure within fluid decreases (and speed increases)

75% - flow begins to decreases and pressure downstream decreases to form a pressure gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

aneurysm vs diffuse ectasia

A

smaller increase generaly in diameter = de

aneurysm - widen, dilate (at least 50% increase over normal arterial diameter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

AAA

A

cystic medial degeneration - of elastic fibers

acuumulation of collagenous and mucoid material in the medial layer

mostly with aging and hypertension (marfan, ehlers danlos)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Type A Aortic Dissection

A

involves part of ascendinga aorta

surgical!

emergency and high mortality

lower BP in all

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Type B Aortic Dissection

A

does not involve ascending aorta

complicated - surgical

uncomplicated - medical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

AAA risk factors

A

increasing age

smoking

male

genetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

aortic wall tension

A

variation in wall tension in aneurysm

proportional to the product of pressure and radius

bigger radius = more tension = bigger chance of ruptiur

P is the same

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

AAA therapy

A

medican (smoking HTN)

endovascular/open therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

PAD mechanism

A

if stenosis - high resistance

turbulent flow - pressure drops across stenosis and impaired endothelial function

inapility to increase flow with execise

mismatched O2 supply and demand (IC)

inefficient oxidation

can’t dilate because endothelial dysfunction - angina and claudation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

claudication

A

cramping tightness aching fatigue

bluttock, hip, thigh, calf, foot

exercise induced

not with stating (relief)

less than 5 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

ABI

A

Under .90 is PAD!

measure P in both arms and legs

put highest angle P over highest arm P on eich side

add 2 numbers together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Toe Brachial Pressure

A

divide te pressure by higher of the two brachial ressures

when ABI not possible because calcified

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

PAD therapy

A

exercise

smoking cessation

STATINS

HTN

antiplatelets

symtomatic relief

revascularization (if gangrene, non healing ulcers, ischemic rest paid, bad claudication)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Raynauds Disease

A

rare disease that causes vasospasm of the arteries and reduces blood flow to fingers and toes

idiopathic or secondary (lupus, sjogrens)

vascular constriction - white/blue/numb extremities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment for Raynauds Disease

A

CCBs

Alpha block

ARBs (vasodilate)

surgery (rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

varicose veins

A

dilated tortuous veins

reflux bc valvular insufficiency

obesity, prenancy, familial

usually cosmetic - can be stasis dermatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Carotid artery disease therapy

A

can lead to stroke!

antiplatelet/anticoagulation

statins

risk factor modification (smoking, HTN, diabetes)

revascularization (stenting)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

arteriovenous malformation

A

embryonic/fetal development

direct connections between arteries and veins! more common in brain or SC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

risk factors for CAD

A

herediatry

lipids (high LDL)

smoking

diabetes

HTN

obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

CRP

A

inflammation marker

predictor of first MI/ischemic stroke (also high if another stressor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Atherosclerosis Pathway

A
  1. endothelial injury
  2. LDLs enter, smoooth muscle cells migrate
  3. macrophages roll and enter epithelial cell and eat LDL and turn into foam cell
  4. secrete cytokines to recruit more
  5. more macrophages enter - fatty streak
  6. TGF beta increases collagen

macrophages make MMP-9 which breaks down fatty cap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Thinning of fibrous cap

A

degraded by foam cells secreting MMP

rupture!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

synthesis of fibrous cap

A

smooth muscle cless promote collagen and elastin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

NO mechanism

A

ACH/sheer stress - cleave cNOS to NO

moves across wall and increases cGMP to stim smooth muscle cell relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

CT scan

A

regular scan or use for coronary calcium studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

characteristics of angina

A

intermittent, recurrent

strangling, pain, pressure, tightness

location - retrosternal, shoulders - arms

dyspnea

30 s - 10 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

plaque and ischemic impact

A

stenotic - few, fibrotic, thick cap, less compensatory enlargement (ischemia - angina, postive stress test)

non-stenotic - many, lipid rich, thin cap, compensatory enlargement (infarction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

therapeutic targets

A

lower LDL (source of inflammation and building blocks of plaques) - stop progression and decrease chance of rupture

dampen inflammation and restore homeostasis

restore fibrous cap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

intima

A

where everything happens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

pathophysiology of atherosclerosis

A
  1. endothelial dysfunction (increased permeability, WBC adhesion)
  2. smooth muscleemigration from media to intima, macrophage activation
  3. liids from blood enter intima and phagocytosesd by macrophages in intima
  4. smooth muscle proliferation, collagen and other ecm deposition, extracellular lipid

1-2 don’t see anything, 3-4 do see

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

complications from atherosclerosis

A

thrombosis

embolism

aneurysm and rupture

dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

true aneurysm

A

dilation of segment of vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

false aneurysm

A

dissection

extravasation of blood

looks like true aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

fusiform aneurysm

A

true aneurysm

in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

saccular aneurysm

A

brain

true aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

etiologies of aneurysms

A

atherosclerotic**

infectious

inflammatiory

autoimmune

degenerative

traumatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Giant Cell Arteritis

A

large vessels - head

headches

visual problems

steroids!

usually older people, inflammation of arteries around forehead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Polyarteritis Nodosa

A

middle vessels

transmural inflammation

necrossis and thickening

fever, weight loss, abdominal pain

corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Wegener Granulomatosis

A

respirator involvement

acute necrotizing granulomas and vasculitis

fever, mucosal alterations

80% death if unreaed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

thromboangiitis obliterans (Buerger’s disease)

A

smokers,

segmntal thrombising infammation of distal limb arteries

ulcerations of toes, feet, fingers, gangrene

smoking cessation is only thing that helps!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

DVT etiology

A

OCP

dehydration

inactivity

surgery

trauma

MI

strok

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

DVT therapy

A

Heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

chylomicron

A

absorbed cholesterl from brush border into lymph to liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

primordial prevention

A

prevent the development of risk factors for CVD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

primary prevention

A

prevent the first CVD event

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

secondary prevention

A

prevent subsequent CVD events (decrease LDL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Bile Acids Mechanism

A

breakdown product of cholesterol - most is reabsorbed in the small bowel

act as a detergent - make cholesterol soluble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Bile Acid Resins

A

i.e. WelChol

No outcomes data!!

Used as add on for additional LDL lowering

inhibits cholesterol absorption

They disrupt the enterohepatic circulation of bile acids by combining with bile constituents and preventing their reabsorption from the gut

Liver makes more bile acids since it is not reabsorbled, which uses a lot of LDL cholesterol (liver compensates so not as effective)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Bile acid resin Side Effects

A

bloating

interfere with absorption of vitamins or meds

can raise TG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Ezetimibe

A

selective cholesterol absorption inhibitor

acts on brush border to inhibit reabsorption of cholesterol itself

Liver has to absorb more cholesterol from blood

** mainly add on to statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Ezitimide - decreases events?

A

yes!

with a statin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Niacin

A

decreases VLDL production, LDL formation, increases hepatic clearance of LDL precursors

raises HDL

NO decrease in events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Niacin side effects

A

gout!! elevated uric acid levls

hepatic toxicity

flushing and pruritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Fibrates Indications

A

lowers TG by a lot! no real effect on LDL, raises HDL a little

used for severe hypertriglyceridemia

hgih TH or low LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Fibrates Mechanism

A

activate PPAR alpha - activates lipoprotein lipase and increases lipoysis in the plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Fibrates side effects

A

avoid in patients wiht hepatic/renal function issues

increased risk with statins of rhabdomyolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

HMG-CoA Reductase Inhibitor Mechanism

A

Statin!!

if inhibit - increase HMG-CoA to make more cholesterol but also increase transcription of LDL R so take more out of blood and decrease LDL by a lot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Statin - decrease events?

A

yes!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Statin side effects

A

increase in transaminasess

muscle pain or weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Statin studies

A

primary prevention!

educe morbidity and mortality

cost effective

lifestyle also needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

PCSK9 mechanism

A

antibody to LDL -R that allows it to be destroyed - dysfunctional!

more LDL-R because it is recycled

decrease LDL by a olot - decrease events!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

PCSK9 Side Effects

A

injection site swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

how to lower TGs?

A

fibrates

niacin

fish oil

(not as important as LDL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

how to lower LDL?

A

statins

ezetimibe

pcsk9 abs

bile acid resins

niacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what happens from vessel injury?

A

vasoconstriction (reduced blood flow)

platelet adhesion/activation/aggregation

blood coagulation cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

local control of vasoconstriction

A

thromboxane and other local controls released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

systemic control of vasoconstriction

A

epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

extrinsic pathway

A

damage to tissue outside the vessel activates factor X

first pathway to start but turns off when a little factor Xa is made

vessel injury

triggered by tissue factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

intrinsic pathway

A

after extrinsic pathway makes a little Xa and is turned off

most fibrin is made from intrinsic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

initation of the clotting cascade

A

interaction of plasma bound TF exposed by vascular injury

interacts with factor 7 (extrinsic)

activates factor 10

10a acivates a small amount of thrombin and TFPI which rapidly inactivates the pathway!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Extrinsic Xase

A

TF + VIIa

activates factor XI and facor X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

thrombin generation

A

primed by extrinsic pathway but becomes reliant on intrinsic pathway to make Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Intrinsic Xase

A

IXa + VIIIa

greatly amplifies Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Prothrombinase Complex

A

Xa + Va

explosive generation of thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Factor v Leiden

A

mutated form of factor V cannot be inactivated by protein C

tons of V –> clots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What does thrombin activate?

A

XI, V, 13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

formation and stabilization of fibrin

A

thrombin hydrolyzes fibrinogen to fibrin

calcium - acts like glue to hold fibrin monomers together (loose insoluble fibrin polymer - clot)

factor XII also activated by thrombin and stabilizes the fibrin polymers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what does thrombin do?

A
  1. activate protein C (anti inflammatory - helps dissolve clot)
  2. activate platelests
  3. form fibrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Vitamin K dependent factors

A

thrombin, Vii, IX, X

protein C and S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

TFPI

A

synthesized in endothelial cells

present in plasma and platelets

inhibits Xa, VIIa and TF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Antithrombin

A

circulating plasma protease inhibotr

neutralizes many enzymes in the clotting cascade (esp thrombin and factor Xa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Protein C/Protein S

A

inhibit coagulation cofactors V and VIII (inactivate prothrombinase and Intrinsic Xase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

fibrinolysis

A

normal hemostatic response to vascular injury (body doesn’t need clot anymore

plasminogen –> plasmin (intrinsic and extrinsic factors

release of tPA from endothelial cells!

plasmin digest many of the proteins cleave peptide bonds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

intrinsic activation of plamsin

A

XIIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

extrinsic activation of plasmin

A

tPA and urokinase

activate plasmin

activate fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

d dimer

A

major fibrin degredation factors

sign that high clot burden

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

tissue factor

A

initates coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

prostacyclin

A

vasodilation/inhibition of platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

NO

A

vasodilation/inhibition of platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

vWF

A

platelet collagen adhesion - complex with factor VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

AT

A

inhibition of blood coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

tPA

A

fibrinolysis

94
Q

factors of plaque vulnerability

A

size of atheromatous core

thickness of fibrous cap

inflammation and repair of fibrous cap

95
Q

subendocardial vs transmural MI

A
96
Q

Diagnostic criteria of abnormal Q waves

A

width > .04 s

depth > 25% of R wave

97
Q

EKG of AMI - acutely

A

ST elevation

98
Q

EKG hours after AMI

A

ST elevation

decreased R wave

Q wave begins

99
Q

ekg after ami 1-2 days later

A

t wave inversion

deep q wave

100
Q

ekg days after acute mi

A

st normalizes

t wave inverted

101
Q

ekg weeks after ami

A

st and t are normal

q wave persists

102
Q

cardiac markers

A

CK (start late peak early)

troponin (start early peak late)

103
Q

left ventricle dysfynction - complications

A

heart failure (rales)

pulmonary edema

cardiogenic shock

104
Q

myocardial healing complications

A

VSD

ventricular free wall rupture

aneurysm formation

105
Q

process of thrombolysis

A

plasminogen –> plasmin

plasmin breaks down fibrin (in thrombus and circulating)

106
Q

streptokinase

A

binds with plasminogen

sk-plasminogen complex cleaves plasminogen to plasmin

plasmin breaks down fibrin

107
Q

tPA

A

binds with fibrin

cleaves plasminogen to plasmin

breaks down fibrinogen to fibrin

108
Q

kringle dowmains

A

on tpa

allow tpa to recognize and bind to fibrin

create higher affinity

109
Q

TNKase

A

tPA mutant form to increase half life and specificity

also retaplase

110
Q

indications for thrombolysis or stent

A
  1. chest pain consistent with AMI
  2. EKG changes (ST segment elevation, new BBB)
  3. time from onset less than 12h
111
Q

determinants of survival (MI)

A
  1. rapidity of reperfusion
  2. magnitude of restortation of flow
  3. persistence of flow
  4. major complications (bleeding, reinfarction)
112
Q

drugs with SURVIVAL BENEFIT post-mi

A

BB

ACEI

aspirin

statins

113
Q

stable angina

A

no change in frequency, severity, duration, or precipitating factors in the previous 60 days

generally occurs with xexertion and relieved by rest

good prognosis

114
Q

pathophysiology of stable angina

A

one or more severe narrowings in large epicardial coronary artery

generlly atherosclerosis (no superimposed thrombus)

115
Q

treatment goals of stable angina

A

relieve discomfort (supply ad demand)

revascularization of medical therapy fails

prevent progression

116
Q

medications for stable angina

A

BB

CCBs

nitrates

asirin

statins

(ranolazine if resistant)

117
Q

vasospastic angina

A

at rest or exertion

may be associated w atherosclerosis

118
Q

treatment of vasospastic angina

A

nitrates

CCBs

statins + aspirin

119
Q

unstable angina

A

angina increasing in frequency, intesnity, or duration

at rest!

transient ECG changes

high risk of MI and death

120
Q

pathophysiology of unstblae angina

A

ruptured atherosclerotic plaque

partially occluding thrombus in lumen of large coronary artery

high mechanical stress points

cap may thin due to monocyte production of proteases - chemically digest plaque cap

121
Q

coronary thrombosis

A

underlying tissue is exposed, clotting mechanisms are activated

thrombus forms

thrombus may be non occlusive and eventually incorporated into atherosclerotic plaque (subclinical)

partially occlusive –> unstable angina, STEMI

122
Q

AMI

A

thrombus is totally occlusive and leds to AMI

severe chest pain

st segment elevation

123
Q

treatment goals for unstable angina

A

relieve discomfort (supply demand)

prevent MI

aggressive revascularization

124
Q

medications for unstable angina

A

BB

CCBs

nitrates

aspirin

heparin (unfractionated and LMW)

newer anti platelets (GB2b/3a)

statins

125
Q

First line antianginal

A

nitrates

CCBs

BBs

126
Q

second line antianginal

A

ranolazine

127
Q

nitrates mechanism

A

venodilation!

reduce preload - decrease size of heart

decrease BP - decrease afterload

stop vasospasm!

128
Q

nitrate effect in angina

A

decreased myocardial oxygen requirement (decrease wall stress)

129
Q

cellular affect of nitrates

A

enzymatic degredation to NO –> activate guanylyl cyclase in smooth muscle

inactivate A-M and vasodilate

only affects smooth muscle

viagra is the same!! can’t mix

130
Q

nitrates - adverse effects

A

hypotension, reflex tachy, headache due to hypotension

tolerance!

rebound due to withdrawl (don’t give 24/7) = decrease blood flow to kidneys so retain water and salt

131
Q

CCB mechanism

A

arterial vasodilation

lowers BP

coronary vasodilation (choice for coro vasospasm!)
negative inotropy

negative chronotropy

132
Q

CCB cellular mechanism

A

block voltage dep L type ca channels

decrease transmembrane calcium flux

skeletal muscle not depressed (uses intracellular pools)

133
Q

CCB effects in angina

A

increase oxygen (relieves vasospasm)

decrease demand (neg inotrope, vasodilation decreases wall pressure, some slow HR)

134
Q

Verapamil

A

CCB

useful as antiarrhythmic for SVT

135
Q

Diltiazem

A

CCB

136
Q

Amlodipine

A

safest CCB for CHF

well tolerated

137
Q

CCB side effects

A

lower extremity edema

sinus brady/av block

138
Q

BB mechanism

A

neg chrono, neg ino

lower BP

increase duration of diastole

anti arrhythmic (suppress)

survival benefit - post MI and comp CHF

139
Q

BB adverse effects

A

bronchospasm

exacerbation of CHF

impotensce/depression

excessive sinus brady and AV block

140
Q

Ranolazine

A

indicated for patients with angina on meds or can’t tolerate

block late I(na) channels (some are open during plateau phase so Na enters during systole - if block, less cytosolic Ca)

low HR, low BP, CHF, DM

prevents intracellular calcium overload!

141
Q

treatment of stable angina

A
  1. BB (first line) + aspirin + statin
  2. give bottle of sublingual nitroglycerin
  3. CCBs if BB are not tolerated (added if angina persists or to treat HTN)

4 ranolazine for persistant angina

  1. risk stratification
142
Q

strategies for treatment of unstable angina

A
  1. hospitalization
  2. treatment with nitrates and BB
  3. treatment of ruptured plaque with throbus (aspirin, plavix, statin, antithrombin like heparin)
  4. cardiac cath to determine risk
143
Q

significant coronary stenosis

A

greater than 75% (with exercise)

greater than 90 - symptoms at rest, no compensatory dilation

144
Q

AMI path - 1 day

A

wavy fibers

interstital edema

after sarcolemma has been disrupted but before inflammation

145
Q

AMI Path - 3-4 days

A

coagulative necrosis of myocytes

loss of nuclei and cross striations

dense interstital neutrophilic infiltrates

pm breaks - exposes

increase neutrophils to clean up dead myocytes

146
Q

AMI path: 7-10days

A

nearly complete phagocytosis of necrotic myocytes by macrophages

keep BP down! don’t want to pressure wall

147
Q

AMI path 10-14 days

A

granualtion tissue with new vessels and collagen

148
Q

AMI path after 2 months

A

necrotic myocardium is replaced by dense collagenous scar

149
Q

stunned myocardium

A

reperfusion injury!

biochemically altered myocytes after reperfusion

prolonged cardiac failure induced by short term ischemia that recovers after a fw days

short period of cardiac failure you wouldn’t predict

150
Q

coronary artery spasm

A

with or without atherosclerosis

smokers, alcohol withdrawl

stimulants - cocaine, meth

presents with angina - key is removing stimulating factors

151
Q

coronary artery dissection

A

presenting symptom - angina

pre meno women

hypertension

surgery

stents

thrombolytics

152
Q

ADP

A

recruit circulating platlnts

after platelets are activated they release ADP to create a plug

153
Q

initation of platelet activation

A

collagen! via vWF

shape change (to increase SA) and degranulation (platelet is circulating drug delivery system)

154
Q

glycoprotein IIB/IIIa

A

receptor on platelets

when stimmulated - platelets cloumb together

final common pathway in platelet aggregation

155
Q

anti-platelet drugs

A

salicylates (aspirin)

ADP receptor antagonists

cAMP agonists

thrombin receptor (PAR-1)

g IIb/IIIa antagonists

156
Q

salicylates indications

A

aspirin

weak platelet antagonists - impairs plately function

MI, secondary prevention of MI, stroke prevention with low CHADS score

157
Q

salicylates mechanism

A

irreversible acetylation and inactivation of COX

blocks TxA2 production

158
Q

salicylates side effects

A

GI bleeding

159
Q

ADP antagonists mechanism

A

anti-platelet

block P2Y12 receptor, prevent recruitment of circulating platelets

clinical effects irreversible for days

(clopidogrel)

more potent than ASA!

160
Q

ADP receptor indications

A

strok prevention (secondary)

1 year after ACS

2/4 weeks after bare metal stent

prolonged course after drug eluding stents

161
Q

ADP recptor agonist side effects

A

irreversible for days

drug drug (CYP450)

162
Q

cAMP antagonist mechanism

A

inhibits uptake of adenosine by platelets, endothelial cells, RBCs

increases local adenosine levels

inhibit platelets and vasodilate

antiplatelet!

163
Q

indications for cAMP antagonists

A

stroke prevention (if NSR)

vasodilater in vascular disease

164
Q

PPAR-1 antagonist

A

aka Thrombin receptor antagonist

another receptor to antagonize on PLATELETS

165
Q

indication for PPAR-1 antagonist

A

secondary prevention post MI

166
Q

Side effects of PPAR1 antagonists

A

increased risk of ICH in patients with prior stroke

167
Q

glycoprotein IIb/IIIa mechanism

A

antiplatelet

most potent platelet antagonizer

IV ONLY!!!

abs

only anti=platelet that is IV!!!!

168
Q

indication for 2b3a

A

treatment of ACS

only anti=platelet that is IV!!!!

169
Q

side effect of 2b/3a

A

excessive bleeding

170
Q

anticoagulants

A

warfarin

unfractionatedheparin

low MW heparin

Xa inhibitor

direct thrombin inhibitors

171
Q

warfarin mechanism

A

inhibits synthesis of vitamin K dependent clotting factors

II, VIII IX, X

inhibits protein c and s

oral - chronic use

172
Q

indications for warfarin

A

mechanical heart valve

a fib

PE/DVT

recent anterior wall MI

173
Q

warfarin side effects

A

bleeding!

hemorrhagic skin necrossis

teratogenic

(slow onset, requires INR, interacts with everything)

174
Q

warfarin reversal

A

vitamin K

IV = temporary low dose

PO = prolonged

intravenous fresh froxen plasma - replace clotting factors

175
Q

NOAC mechanism

A

direct thrombin inhibitor

(now reversal agent for one of them)

176
Q

NOAC indications

A

stroke prevention (a fib)

DVT

no monitoring, no interactions, safer

177
Q

NOAC side effects

A

no reversal agents (until now)

$$

bleeding

178
Q

unfractionated heparin mechanism

A

from pig and cow

binds to and activates ATIII - inhibits thrombin, Xa, enhances TFPI

reversable (protamin)

length of heparin sugars indicate if it binds to thrombin or XA

179
Q

heparin indications

A

anti coagulation bridge to warfarin

ACS

cardiac cath/surg

SQ = prophylaxis of venous thrombo embolic disease

180
Q

side effects of heparin

A

bleeding

hypercoagulble period

heparin induced thrombocytopenia (abs bind to platelets - clotting but platelet count decreases!!

non specific - need testing

181
Q

low molecular weight heparin indications

A

same mechanism of action as heparin - binds ATIII

less potein binding (more reliable)

SQ administration

fewer side effects

182
Q

Xa inhibitors mechanism

A

ATIII mediated inhibition of Xa

SQ

183
Q

Xa inhibitor indications

A

prevention of DVT

ACS

stroke (a fib)

184
Q

direct thrombin inhibitors indication

A

i.e. bivalrudin

ACS

185
Q

IV anticoagulants

A

direct thrombin inhibitors, unfractionated heparin

186
Q

SC anti-coagulants

A

heparin (unfractionated, low MW)

Xa inhibitors

187
Q

PO anticoagulants

A

Warfarin, NOACs

188
Q

Anti-coag for Afib

A

Warfarin

NOACs

Unfractionated heparin (inpatinet - IV)

189
Q

anti-coag for ACS

A

heparin (Both)

Xa inhibitors

thrombin inhibotrs

190
Q

fibrinolytics mechanism

A

convert plasminogen to plasmin - beaks down fibrin clot

191
Q

indications for fibronolytic (thrombolytic) therapy

A

acute MI only (not effective in unstable angina

chestpain under 6 hours in duration

ecg changes (ST elevation in 2 limb leads or big elevation in 2 precordal leads or LBBB)

192
Q

absolute contraindications to thrombolytic therapy

A

A: aortic dissection
P: pregnancy
E: expected bleeding
S: surgery (2 weeks)
H: hypertension (chronic > 200/100)
I: internal bleeding (known)
T: trauma (recent 2 weeks, hemorrhagic, head)

193
Q

streptokinase

A

thrombolytic

can use once!

194
Q

obstructive CAD

A

more than 70% cross sectional arrowing in a major coronary artery

195
Q

small vessel CAD

A

abnormal flow in coronary arteries not typically visualized by angiogram

often due to endothelial disfunction

196
Q

stable angina

A

stable (un-ruptured) plaque with ischemic symptoms that do not occur at rest and are predictably provoked

innapropriate vasoconstriction

197
Q

unstable angina

A

ruptured plaque that causes ischemic symptoms to occur at rest or with progressively less exertion

no myocardial injury!! no biomarkers!

thrombus formation

198
Q

MI

A

myocardial injury from ruptured coronary plaue or severe supply demand mismatch

199
Q

Carotid IMT

A

no radiation

no contrast

visual of carotid thickening in I-M layer before palaque

surrogate - if it’s there it’s likely to be anywhere

TEST: to asses presence of atherosclerosis (not ischemia)

200
Q

Coronary calcium scan

A

minimal radiation

no contrast

Ca on coro arteries - likely older because have to have hard plaque

201
Q

tests to assess presence of atherosclerosis (not ischemia)

A

Carotid IMT

Coronary Ca Scan

202
Q

people with atypical angin

A

women

elderly

diabetes

203
Q

features of unstable angina

A

rest symptoms

increasing frequency

increasing duration

lower threshold for symptoms

biomarker negative!

NO stress test if unstable angina, stemi, nstemi

204
Q

supply and demand balance

A

if you give a man a FiSH he will eat What He Can

Flow

saturation

hgb

wall stress

HR

contractility

205
Q

myocardial energy supply

A

usually fatty acids (if have a lot of oxygen available –> more ATP)

in ischemia - switches to glucose

206
Q

coronary effect of vasoconstriction

A

hypoxic vasoconstriction

icchemic regions - dilate inhpoxic regions (opp of lungs)

(opp of lungs)

207
Q

vasodilation in ischemia - mechanism

A

during ischemia, can’t make ATP - ADP,AMP are converted to adenosine

adenosine is a vasodilator and prime mediator of vascular tone (decreased Ca into the cells –> relaxation/vasodilation)

NO - vasodilation via cGMP

increased sheer stress - Ach, thrombin, plateless = NO released to compensate lead to vasodilation

208
Q

Ach and coronary arteries

A

Ach - vasoconstrction of smooth muscles (without endothelial lining)

vasodilation (with endothelial lining)

Ach –> No in endothelial cells –> vasodilation

209
Q

Endothelial dependent vasodialtors

A

Ach, thrombin, serotonin, sheer stress

210
Q

endolthelial independent factors

A

nitroglycerine (makes NO in the smooth muscle cell)

211
Q

healthy endothelium vs endothelial dysfunction

A

dysfunction - don’t make NO, no relaxation signals to smooth muscle, contraction WINS

212
Q

decrease in coronary pressure affects what part of the heart

A

higher flow at epicardial level (where bv come from) then endocardial level

213
Q

threholds of stenossi

A

less than 70% - little change in blood flow at rest, artery can dilate in exercise

70-90 - autodilation of the resistance vessels at rest and normal flow, exercise - can’t dilate further and ischemia

90 - max dilation at rest, may be suboptimal

214
Q

stunning myocardium

A

acute ischemia!!

related to time of ischemia

perfusion is normal following ischemia

function returns to normal in 1 week

oart of heart is stunnd, doesn’t just start moving normally

215
Q

hibernating mycoardium

A

frequent or prolonged ischemia

perfusion is usually reduced!

downregulation of ATP uptake and oxygen consumption

216
Q

preconditioning

A

upregulation of factors (NO synthase) to condition - less infarction

217
Q

ischemic cascade

A
  1. metabolic alteration
  2. perfusion abnormalities
  3. diastolic dysfunction
  4. regional wall motion changes
  5. ECG changes
  6. Angina
218
Q

C/I stress test

A

AMI

unstable angina

decompensated HF

arrhytmias

AV block

myocardiits

aortic stenosis

HOCM

uncontroleld HTN

acute systemic illness

219
Q

mechanisms of stress (Stress Test)

A

treadmill/bike

adenosine

domutamine (beta agonist)

220
Q

PET - when?

A

earliest (metabolism changes)

221
Q

Cardiac MRI - when?

A

Early (perfusion changes)

222
Q

Nuclear imaging - when?

A

early (perfusion changes)

223
Q

ECG - when?

A

late - systolic dysfunction

224
Q

ECG - when?

A

latest

225
Q

Max stress test

A

85% of predicted HR

Max Predicted HR = 220-age

226
Q

Nuclear Evidence of ischemia

A

after exercise - less uptake of isotope - not normal

227
Q

PET and ischemia

A

abnormal metabolism - if using glucose it is abnormal

228
Q

adenosine stress test

A

if stenosis - max dilated

give adenosine - more update and more flow

onl arterioles distal to normal epicardial artery can dilate!!

at rest - normal flow to both

in stress - relatively increased to one area (others are already max dilated)

229
Q

sensitivity

A

unlikely to miss a Negative

good screening test!

SNOut

Sensitive test when negative rules out

230
Q

specificity

A

Unlikely to wrongly label a Positive (good conformation test )

SpIN specific test when Positive rules IN

CV Final (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions