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CSI Exam 4 > ACS, CAD, Thromboembolism > Flashcards

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
Q

Hibernation (chronic hypoxia) results in

A

O2 delivery adequate for myocyte survival, but NOT adequate myocyte function

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26
Q

Prolonged hypoxia

A

acute MI

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27
Q

Sx of underlying CAD

A

Angina that may radiate to neck, shoulder, jaw, back, or arm

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28
Q

Stable angina

A

angina on exertion that resolves w/ rest (may have angina w/ cold exposure or smoking) - 70% stenosis

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29
Q

Unstable angina

A

angina at rest, plaque rupture resulting in obstruction

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30
Q

Treatment for Stable angina

A

Aspirin, Nitro, anti-ischemic drugs

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31
Q

Treatment for Unstable angina

A

Aspirin, Nitro, anti-ischemic, heparin, G2b/3a inhibitors

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32
Q

Treatment for Prinzmetal

A

Nitrates

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33
Q

May see ST elevation w/

A

Unstable angina and/or Prinzmetal

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34
Q

3 non-invasive techniques for assessing possible ischemia

A

Stress Test, NM Profusion Study, ECHO

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35
Q

Exercise Stress Test

A

ischemic changes on EKG, decreased BP, poor exercise tolerance

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36
Q

NM Profusion Study

A

Thallium given followed by exercise, ischemic myocardium will show decreased uptake

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37
Q

Cardiac Catheterization

A

contrast dye injection to assess transient episodes of MI

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38
Q

NSTEMI

A

elevated biomarkers (troponin), no ST elevation, +/- angina

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39
Q

Unstable angina

A

No elevation in biomarkers, no ST elevation, + angina

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40
Q

MI is due to decreased

A

coronary blood flow, vasoconstriction, increased O2 demand

41
Q

Coronary blood flow slows due to

A

platelet aggregation and intra-coronary thrombus

42
Q

MI causes in the absence of CAD

A

Thyrotoxicosis, anemia, hypoxemia, uncontrolled HTN

43
Q

Sx of ACS

A

angina, radiating to arm, back, jaw, neck, etc; fatigue, SOB, weakness, dizziness, n/v, heartburn

44
Q

Unstable angina or NSTEMI risk determination - low risk

A

undergo exercise or pharmacologic stress testing

45
Q

Unstable angina or NSTEMI risk determination - high risk

A

antiplatelet therapy, heparin, angiography

46
Q

Most common cause of STEMI

A

occlusive thrombus

47
Q

Occlusive thrombus causes myocyte death after

A

15 minutes of occlusion

48
Q

TIMI Score for assessing risk of death and ischemic event sin pts w/ unstable angina or NSTEMI

A

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
Q

When patient presents w/ Sx of unstable angina or NSTEMI, you should

A

Order EKG w/in 10m, Cardiac enzymes, O2, Monitor, Meds

50
Q

What meds are given to a pt w/ Sx of unstable angina or NSTEMI

A

MONA (Morphine, O2, Nitro, Aspirin/Anti-coag)

51
Q

Why give morphine for unstable angina/NSTEMI?

A

opioid analgesic, sympathetic blockade, decreases O2 consumption

52
Q

Contraindications for Morphine

A

Hypotension, Bradycardia, Respiratory depression, Right ventricular infarction

53
Q

Why give Nitroglycerin for unstable angina/NSTEMI?

A

increases venous capacitance/venous pooling, decreases preload, dilates coronary arteries

54
Q

Contraindications for Nitroglycerin

A

Bradycardia, Hypotension, Inferior wall MI

55
Q

Why give Aspirin for unstable angina/NSTEMI?

A

Prevents COX and TBX A2 to prevent platelet aggregation

56
Q

Aspirin reduces mortality for unstable angina/NSTEMI by?

A

23%

57
Q

Why give Clopidogrel for unstable angina/NSTEMI?

A

irreversible platelet inhibitor

58
Q

Why give Heparin for unstable angina/NSTEMI?

A

inhibits clot propagation, no effect on bound thrombin in a thrombus (stabilizes it)

59
Q

Why give b-Blockers for unstable angina/NSTEMI?

A

decrease HR, decrease BP, prevents fatal arrhythmias, increased diastole and coronary perfusion

60
Q

Why give GP2a/3b blockers for unstable angina/NSTEMI?

A

block platelet activation

61
Q

Indications for GP2a/3b blockers

A

positive troponins, pts likely to receive PCI, medical stabilization UA/NSTEMI

62
Q

Why give Fibrinolytics for unstable angina/NSTEMI?

A

plasminogen activators (binds fibrin to break up clot)

63
Q

Indications for fibrinolytics

A

STEMI if Tx is < 6-12hrs from onset, ST elevation >1mm

64
Q

ST elevation definition

A

.2mV in Males or .15mV in Females ST elevation

65
Q

ST elevation indicates

A

infarction

66
Q

Reprofusion/Angioplasty is used as Tx for

A

STEMI

67
Q

Tx for STEMI

A

antiplatlets, Antithrombin, b-blockers/ACE-I, Nitrate, AND angioplasty

68
Q

Virchow’s Triad for Venous Thrombosis

A

Venous stasis, Endothelial injury, Hypercoaguable state

69
Q

Venous stasis causes

A

tumor, immobility, venous insufficiency, Afib

70
Q

Endothelial injury causes

A

Valve disease, atherosclerosis, indwelling catheter, trauma/surgery

71
Q

Hypercoaguable state causes

A

malignancy, sepsis, pregnancy, oral BC, trauma/surgery

72
Q

DVT Sx

A

erythema, calf tenderness, warmth, edema

73
Q

+ Homan’s Sign

A

flex calf and pain, indicating DVT

74
Q

Differential for DVT

A

cellulitis, venous insufficiency, edema d/t CHF, popliteal cyst

75
Q

D-dimer

A

fibrin degradation product present in blood after a blood clot is degraded

76
Q

Negative D-dimer and suspicion is low

A

rules out DVT

77
Q

Positive D-dimer

A

suspicious for thrombus formed in the past 72 hrs

78
Q

False D-dimer positive causes

A

advanced age, pregnancy, AAA, malignancy, infection, acute MI, underlying AID

79
Q

Lower extremity DVT, typically in 3 veins of origin

A

femoral, popliteal, ileofemoral

80
Q

Upper extremity DVT, typically in 2 veins of origin

A

axillary and subclavian

81
Q

Primary Thrombosis in UE

A

Idiopathic, Paget-Schroetter Syndrome

82
Q

Paget-Schroetter Syndrome

A

thrombosis of the subclavian v. after exercise

83
Q

Secondary Thrombosis in UE

A

CVC/PICC line placement, Malignancy, pacemaker

84
Q

Wells Criteria for DVT

A

Cancer, Calf swelling, entire leg swelling, tenderness to deep palpation, immobility, previous DVT, clinical signs of DVT

85
Q

Work-up for Suspected DVT

A

CBC, CMP, PT/PTT/INR, D-dimer, Protein C/S, Doppler

86
Q

PE S/S

A

some level of hypoxia/decreased O2, chest pain, dyspnea, tachypnea, hemoptysis, syncope, hypotension, tachycardia, weakness

87
Q

PE Diagnosis

A

pulmonary angiography (gold standard), spiral CT

88
Q

Wells Criteria for PE

A

DVT Sx, tachycardia, 3d immobilization or w/in 30d of surgery, thromboembolism in past, cough/hemoptysis, cancer

89
Q

PERC (rule out PE) criteria

A

< 50y/o, HR < 100, O2 > 94%, no Hx of DVT/PE, no recent trauma, no hemoptysis, no oral BC, no signs of DVT

90
Q

Acquired risks for PE

A

Cancer, calf swelling, entire leg swelling, tenderness, paralysis, immobility, previous DVT, signs of DVT

91
Q

Inherited risks for PE

A

Antithrombin III deficiency, Protein C/S deficiency, Factor V Leiden, Disfribrinogenemia, Non-O blood type

92
Q

Work-up for PE

A

CBC, CMP, PT/PTT/INR, CXR/EKG, D-dimer, Biomarkers, CT w/ contrast, Pulmonary agiogram

93
Q

Manage PE w/

A

Enoxaparin/Lovenox or Heparin

94
Q

pathognomonic EKG for PE

A

S-wave on Lead 1, negative deflection of Q wave on Lead 3, inverted T wave on Lead 3 (S1Q3T3)

95
Q

Additional EKG findings for PE

A

R heart strain, T-wave inversion in V1-V4, R axis deviation, RBBB

96
Q

Most common EKG presentation seen w/ acute PE

A

sinus tachycardia

97
Q

Differential for PE

A

asthma, abdominal pathology, MI, pericarditis, HF, pneumonia

98
Q

If PE patient is hemodynamically unstable, Sx include:

A

hypotensive, cardiac arrest, decreased LV SV

99
Q

Management for PE pt w/ hemodynamic instability

A

streptokinase, urokinase, tPA, intervention

CSI Exam 4 (11 decks)

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