ACS, CAD, Thromboembolism Flashcards

1
Q

Atherosclerosis build-up is due to

A

lipoprotein build-up, endothelial damage, inflammation

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2
Q

When do you begin to see signs of atherosclerotic disease?

A

early! 1:6 adults had endothelial changes as teens

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3
Q

Mechanism of Atherosclerosis

A

lipoproteins penetrate injured endothelium

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4
Q

Atherosclerosis is a build up of lipoproteins in the ______ layer

A

intimal layer

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5
Q

Factors that accelerate atherosclerosis

A

smoking, HTN, sheer forces, cholesterol

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6
Q

Inflammation and damage to the endothelial wall causes

A

adhesion molecule expression, binding of monocytes

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7
Q

Monocytes migrate to the endothelial damage site and

A

ingest lipoproteins

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8
Q

Foam cells

A

monocytes w/ ingested lipoprotein -> fatty streaks

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9
Q

Endothelial signs of pre-atherosclerosis

A

fatty streaks

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10
Q

Inflammation enhances

A

thrombotic state

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11
Q

Fibrous cap

A

foam cells generate an unstable fibrous cap

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12
Q

3 non-modifiable risk factors

for plaque formation

A

age, Male, FHx (post-menopausal women catch up to men)

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13
Q

8 modifiable risk factors

for plaque formation

A

Cigarette smoking, hypertension, diabetes, cholesterol, obesity, alcohol, sedentary lifestyle, metabolic syndrome

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14
Q

Sx begin at ____% stenosis

A

70% stenosis, exertional Sx (stable angina)

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15
Q

Sx at rest occur at ____% stenosis

A

90% stenosis, resting Sx (unstable angina)

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16
Q

Metabolic Syndrome

A

Central Obesity + any 2: TGs>150, HDL130/>85 or previous HTN, fasting glue >100

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17
Q

HDL role

A

carries cholesterol from the body to the liver - protective effects

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18
Q

LDL

A

Delivers cholesterol to body

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19
Q

HDL > ___ is cardioprotective and negates another risk factor

A

60

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20
Q

Non-Atherosclerotic CAD

A

Trauma, tumor, aortic dissection, Kawasaki’s, Takayasu’s, Infectious endocarditis, Lupus

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21
Q

What 3 things determine coronary a. perfusion?

A

functioning endothelium, autonomic tone, endothelial structure

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22
Q

Coronary artery atherosclerosis causes

A

stenosis of the vessels and results in ischemia

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23
Q

Why would you see intracellular acidosis and disordered Ca2+ homeostasis w/ ischemia?

A

anaerobic glycolysis -> lactate production

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24
Q

Transient hypoxia results in

A

myocardial stunning and reversible effects

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25
Hibernation (chronic hypoxia) results in
O2 delivery adequate for myocyte survival, but NOT adequate myocyte function
26
Prolonged hypoxia
acute MI
27
Sx of underlying CAD
Angina that may radiate to neck, shoulder, jaw, back, or arm
28
Stable angina
angina on exertion that resolves w/ rest (may have angina w/ cold exposure or smoking) - 70% stenosis
29
Unstable angina
angina at rest, plaque rupture resulting in obstruction
30
Treatment for Stable angina
Aspirin, Nitro, anti-ischemic drugs
31
Treatment for Unstable angina
Aspirin, Nitro, anti-ischemic, heparin, G2b/3a inhibitors
32
Treatment for Prinzmetal
Nitrates
33
May see ST elevation w/
Unstable angina and/or Prinzmetal
34
3 non-invasive techniques for assessing possible ischemia
Stress Test, NM Profusion Study, ECHO
35
Exercise Stress Test
ischemic changes on EKG, decreased BP, poor exercise tolerance
36
NM Profusion Study
Thallium given followed by exercise, ischemic myocardium will show decreased uptake
37
Cardiac Catheterization
contrast dye injection to assess transient episodes of MI
38
NSTEMI
elevated biomarkers (troponin), no ST elevation, +/- angina
39
Unstable angina
No elevation in biomarkers, no ST elevation, + angina
40
MI is due to decreased
coronary blood flow, vasoconstriction, increased O2 demand
41
Coronary blood flow slows due to
platelet aggregation and intra-coronary thrombus
42
MI causes in the absence of CAD
Thyrotoxicosis, anemia, hypoxemia, uncontrolled HTN
43
Sx of ACS
angina, radiating to arm, back, jaw, neck, etc; fatigue, SOB, weakness, dizziness, n/v, heartburn
44
Unstable angina or NSTEMI risk determination - low risk
undergo exercise or pharmacologic stress testing
45
Unstable angina or NSTEMI risk determination - high risk
antiplatelet therapy, heparin, angiography
46
Most common cause of STEMI
occlusive thrombus
47
Occlusive thrombus causes myocyte death after
15 minutes of occlusion
48
TIMI Score for assessing risk of death and ischemic event sin pts w/ unstable angina or NSTEMI
1 pt/factor ->all 7 = 40% risk of ischemia >65 y/o, elevates biomarkers, EKG changes (ST depression), 3+ CAD risk factors, ischemia, CAD > 50% stenosis, aspirin use
49
When patient presents w/ Sx of unstable angina or NSTEMI, you should
Order EKG w/in 10m, Cardiac enzymes, O2, Monitor, Meds
50
What meds are given to a pt w/ Sx of unstable angina or NSTEMI
MONA (Morphine, O2, Nitro, Aspirin/Anti-coag)
51
Why give morphine for unstable angina/NSTEMI?
opioid analgesic, sympathetic blockade, decreases O2 consumption
52
Contraindications for Morphine
Hypotension, Bradycardia, Respiratory depression, Right ventricular infarction
53
Why give Nitroglycerin for unstable angina/NSTEMI?
increases venous capacitance/venous pooling, decreases preload, dilates coronary arteries
54
Contraindications for Nitroglycerin
Bradycardia, Hypotension, Inferior wall MI
55
Why give Aspirin for unstable angina/NSTEMI?
Prevents COX and TBX A2 to prevent platelet aggregation
56
Aspirin reduces mortality for unstable angina/NSTEMI by?
23%
57
Why give Clopidogrel for unstable angina/NSTEMI?
irreversible platelet inhibitor
58
Why give Heparin for unstable angina/NSTEMI?
inhibits clot propagation, no effect on bound thrombin in a thrombus (stabilizes it)
59
Why give b-Blockers for unstable angina/NSTEMI?
decrease HR, decrease BP, prevents fatal arrhythmias, increased diastole and coronary perfusion
60
Why give GP2a/3b blockers for unstable angina/NSTEMI?
block platelet activation
61
Indications for GP2a/3b blockers
positive troponins, pts likely to receive PCI, medical stabilization UA/NSTEMI
62
Why give Fibrinolytics for unstable angina/NSTEMI?
plasminogen activators (binds fibrin to break up clot)
63
Indications for fibrinolytics
STEMI if Tx is < 6-12hrs from onset, ST elevation >1mm
64
ST elevation definition
.2mV in Males or .15mV in Females ST elevation
65
ST elevation indicates
infarction
66
Reprofusion/Angioplasty is used as Tx for
STEMI
67
Tx for STEMI
antiplatlets, Antithrombin, b-blockers/ACE-I, Nitrate, AND angioplasty
68
Virchow's Triad for Venous Thrombosis
Venous stasis, Endothelial injury, Hypercoaguable state
69
Venous stasis causes
tumor, immobility, venous insufficiency, Afib
70
Endothelial injury causes
Valve disease, atherosclerosis, indwelling catheter, trauma/surgery
71
Hypercoaguable state causes
malignancy, sepsis, pregnancy, oral BC, trauma/surgery
72
DVT Sx
erythema, calf tenderness, warmth, edema
73
+ Homan's Sign
flex calf and pain, indicating DVT
74
Differential for DVT
cellulitis, venous insufficiency, edema d/t CHF, popliteal cyst
75
D-dimer
fibrin degradation product present in blood after a blood clot is degraded
76
Negative D-dimer and suspicion is low
rules out DVT
77
Positive D-dimer
suspicious for thrombus formed in the past 72 hrs
78
False D-dimer positive causes
advanced age, pregnancy, AAA, malignancy, infection, acute MI, underlying AID
79
Lower extremity DVT, typically in 3 veins of origin
femoral, popliteal, ileofemoral
80
Upper extremity DVT, typically in 2 veins of origin
axillary and subclavian
81
Primary Thrombosis in UE
Idiopathic, Paget-Schroetter Syndrome
82
Paget-Schroetter Syndrome
thrombosis of the subclavian v. after exercise
83
Secondary Thrombosis in UE
CVC/PICC line placement, Malignancy, pacemaker
84
Wells Criteria for DVT
Cancer, Calf swelling, entire leg swelling, tenderness to deep palpation, immobility, previous DVT, clinical signs of DVT
85
Work-up for Suspected DVT
CBC, CMP, PT/PTT/INR, D-dimer, Protein C/S, Doppler
86
PE S/S
some level of hypoxia/decreased O2, chest pain, dyspnea, tachypnea, hemoptysis, syncope, hypotension, tachycardia, weakness
87
PE Diagnosis
pulmonary angiography (gold standard), spiral CT
88
Wells Criteria for PE
DVT Sx, tachycardia, 3d immobilization or w/in 30d of surgery, thromboembolism in past, cough/hemoptysis, cancer
89
PERC (rule out PE) criteria
< 50y/o, HR < 100, O2 > 94%, no Hx of DVT/PE, no recent trauma, no hemoptysis, no oral BC, no signs of DVT
90
Acquired risks for PE
Cancer, calf swelling, entire leg swelling, tenderness, paralysis, immobility, previous DVT, signs of DVT
91
Inherited risks for PE
Antithrombin III deficiency, Protein C/S deficiency, Factor V Leiden, Disfribrinogenemia, Non-O blood type
92
Work-up for PE
CBC, CMP, PT/PTT/INR, CXR/EKG, D-dimer, Biomarkers, CT w/ contrast, Pulmonary agiogram
93
Manage PE w/
Enoxaparin/Lovenox or Heparin
94
pathognomonic EKG for PE
S-wave on Lead 1, negative deflection of Q wave on Lead 3, inverted T wave on Lead 3 (S1Q3T3)
95
Additional EKG findings for PE
R heart strain, T-wave inversion in V1-V4, R axis deviation, RBBB
96
Most common EKG presentation seen w/ acute PE
sinus tachycardia
97
Differential for PE
asthma, abdominal pathology, MI, pericarditis, HF, pneumonia
98
If PE patient is hemodynamically unstable, Sx include:
hypotensive, cardiac arrest, decreased LV SV
99
Management for PE pt w/ hemodynamic instability
streptokinase, urokinase, tPA, intervention