Cardiovascular Flashcards

1
Q

What are the 3 types of ischemic heart disease?

A

1) . Arteriosclerosis
2) . Angina
3) . MI

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2
Q

3 major forms of angina

A

1) . exertional (stable)
2) . Variant (Prinzmetal’s)
3) . Unstable

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3
Q

Which type of of angina occurs prior to an MI?

A

Unstable, pain will increase with frequency, severity, and/or duration

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4
Q

Two common drug types used to treat angina pectoris?

A

Vasodilators and Cardiac Depressants

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5
Q

what are the subtypes of vasodilators?

A

Nitrates and Ca2+ blockers

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6
Q

what are the subtypes of cardiac depressants?

A

Beta-blockers and Ca2+ blockers

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7
Q

general goal of drugs treating angina pectoris?

A

relieve vasoconstriction and workload of the heart (reduce the O2 requirement)

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8
Q

where do nitrates work?

A

directly on vascular smooth muscle (not a receptor!)

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9
Q

general result of Nitrates

A

decrease preload/afterload –> reduce workload of heart -> reduce O2 demand

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10
Q

T/F: nitrates are DOC for acute angina attacks?

A

True, especially sublingual

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11
Q

Important patient education concerning Nitrates

A

proper storage and dosing

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12
Q

AE Nitrates

A

1) . reflex tachycardia
2) . dizziness
3) . OH
4) . weakness

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13
Q

what type of angina requires beta-blockers to treat?

A

stable angina along with short-acting nitrates

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14
Q

how do Ca2+ blockers work?

A

block Ca2+ channels resulting in decreased smooth muscle contractility

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15
Q

what are the zones injury MI?

A

1) . zone of ischemia
2) . zone of hypoxic injury
3) . zone of infarction

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16
Q

two types of MI based on ECG interpretation?

A

STEMI and NSTEMI

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17
Q

how is STEMI treated?

A

thrombolytic agent, aspirin, nitrates, beta-blockers

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18
Q

how is NSTEMI treated?

A

heparin

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19
Q

Peripheral vascular disease (PVD) can result in what?

A

development of venous thrombosis (VT)

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20
Q

a VT can result in what?

A

pulmonary embolism (PE)

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21
Q

what is a VT?

A

partial/complete occlusion of a vein by a thrombus

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22
Q

two types of VTs

A

superficial and deep

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23
Q

a DVT can result in what?

A

pulmonary embolism

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24
Q

Signs and symptoms of a pulmonary embolism?

A

1) . possible sudden death
2) . chest pain
3) . tachypnea
4) . hemoptysis
5) . anxiety, restlessness, apprehension
6) . dyspnesa
7) . persistent cough

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25
Q

Vascular injury results in what 2 immediate things?

A

1) . exposure of collagen and VWF

2) . Tissue factor exposure

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26
Q

exposure of collagen and VWF results in what?

A

platelets adhesion and release of ADP and thromboxane A2

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27
Q

once platelets adhere and release what happens?

A

more plates are recruited and activated

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28
Q

as more platelets are recruited and activated what results

A

platelet aggregation and ultimately platelet-fibrin thrombus formation

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29
Q

when tissue factors are exposed due to a tissue injury what is triggered?

A

coagulation pathways and thrombin generation

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30
Q

what does thrombin do?

A

recruit more platelets and convert fibrinogen to fibrin

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31
Q

how is fibrin important?

A

it binds platelets together to form a thrombus

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32
Q

primary hemostasis results in what?

A

platelet plug formation

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33
Q

secondary hemostasis results in what?

A

fibrin formation which is used to stabilize the platelet plug

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34
Q

What is artherosclerosis?

A

narrowing and hardening of the arteries

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35
Q

basic mechanism of artherosclerosis

A

injury occurs to arterial wall -> cholesterol begins to build up in the wall

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36
Q

what can atherosclerosis eventually cause?

A

thrombus formation -> MI, stroke, or other ischemic issues

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37
Q

what type of cholesterol is “good”?

A

High-density HDL

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38
Q

what are the 3 basic classes of drugs used to treat Artheroscerlosis?

A

1) . Statins
2) . PCSK9 inhibitors
3) . Cholesterol Absorption Inhibitor

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39
Q

true name of statins?

A

HMG-CoA reductase inhibitors

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40
Q

T/F: even with low LDL some populations must take a statin to reduce risk of stroke

A

TRUE

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41
Q

basic MOA statins

A

block cholesterol synthesis

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42
Q

statins common AE

A

myalgia

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43
Q

other Statins AE

A

dyspepsia, headache, increased liver enzymes, tendinopathy and tendon rupture?

44
Q

Rare AE of Statins

A

rhabdo and myopathy

45
Q

T/F: statins have a decreased risk of drug-drug interactions?

A

FALSE, increased risk (especially fibrates)

46
Q

how does grapefruit juice effect statins?

A

inhibits CYP enzymes - linked to statin rhabdo -> increased 6x hosptialization rate

47
Q

what are the 3 types of antithrombotic drugs classes?

A

1) . Antiplatelets
2) . anticoagulants
3) . fibrinolytics

48
Q

general concerns with antithrombotics as a whole?

A

bleeding or clotting

49
Q

what do antiplatelets do?

A

prevent thrombus

50
Q

basic MOA of antiplatelets

A

decrease platelet secretion and adhesion

51
Q

which antithrombotic class has boxed warnings?

A

antiplatelets, warning against CYP interaction, increase risk of bleeding

52
Q

suffix for antiplatelets

A

-gel/-grelor

53
Q

what do anticoagulants do?

A

prevents thrombus & thrombus growth

54
Q

LMWH and Heparin basic MOA

A

increase antithrombin to decrease thrombin

55
Q

Heparin and Direct thrombin inhibitor basic MOA

A

prevents conversion of fibrinogen -> fibrin

56
Q

Arixtra basic MOA

A

selectively inhibits factor Xa

57
Q

Anticoagulants that are administered via IV

A

LMWH, Heparin, Direct thrombin inhibitor, Arixtra

58
Q

Anticoagulants that are administered via PO

A

Direct thrombin inhibitor, Factor Xa inhibitor, and Warfarin (VKa)

59
Q

Direct thrombin inhibitor and Factor Xa are further classified as what?

A

DOAC

60
Q

DOAC has less of a risk of what?

A

intercranial bleeding

61
Q

Warfarin basic MOA

A

inhibits vitamin K - inhibits coagulation cascade indirectly (reduces factor formation)

62
Q

Atrixtra is what type of anticoagulant?

A

factor Xa inhibitor

63
Q

AE of Warfarin

A

intercranial bleeding , rare: skin necrosis, DDI with leafy green

64
Q

Fibrinolytics generally do what?

A

lyse active thrombus

65
Q

Fibrinolytics basic MOA

A

breaks fibrin links in active thrombus

66
Q

when are Fibrinolytics prescribed?

A

immediately following stroke, MI, and PE

67
Q

Fibrinolytics suffix

A

-kinase/-plase

68
Q

what is the continuum from least to most risk of HIT(heparin induced thrombocytopenia) (for anticoagulants)

A

Atrixtra - direct thrombin inhibitor - LMWH - Heparin

69
Q

Cholesterol Absorption Inhibitor MOA

A

inhibits absorption of cholesterol in small intestine

70
Q

When might a cholesterol absorption inhibitor be used?

A

if a pt. is experiencing a lot of myalgia from statins

71
Q

Cholesterol absorption inhibitors DDI

A

not metabolized by CYP enzymes, less DDI

72
Q

basic MOA for PCSK9 Inhibitors

A

increase LDL uptake for degradation

73
Q

PCSK9 common AE

A

injection site reactions

74
Q

what is CHF?

A

heart is unable to pump sufficient blood to supply the needs of the body

75
Q

How is CHF progressive?

A

structural changes over time lead to reduced cardiac contractility

76
Q

Conditions that can lead to CHF

A

ischemic and hypertensive heart disease, cardiomyopathy, valve disease

77
Q

What is compensated CHF?

A

pt is med stable. Combined efforts of 3 compensatory phases achieve a normal CO

78
Q

what is decompensated CHF?

A

unable to maintain adequate circulation. Life-threatening: fluid overload and total heart failure

79
Q

clinical manifestation of L ven CHF

A

1) . dyspnea
2) . fatigue and muscular weakness
3) . renal changes
4) . nocturia

80
Q

in general R ven CHF deals with what?

A

fluid build up in the periphery

81
Q

in general L ven CHF deals with what?

A

fluid build up in the lungs

82
Q

which ventricular failure can result in pulmonary edema?

A

Left ventricle heart failure

83
Q

HF with preserved ejection fraction results from what?

A

diastolic heart failure, cardiac hypertrophy -> reduced volume capacity in L ven

84
Q

HF with reduced ejection fraction is caused by what?

A

systolic heart failure, heart unable to adequately contract

85
Q

which HF is more often related to aging and cardiac hypertrophy?

A

HFpEF (preserved heart failure)

86
Q

goals of HFpEF

A

1) . treat underlying comorbidities
2) . give diuretics
3) . may add aldosterone antagonist

87
Q

general goal of HFpEF?

A

get rid of fluid, can’t fix just treat symptoms

88
Q

Goals of HFrEF

A

improve QOL and prolong survival

89
Q

corresponding meds for HFrEF

A

diruretics, + inotropic drugs (digoxin), vasodilators

90
Q

Entresto is what?

A

a type of ARB (higher risk of angioedema than other ARBS)

91
Q

T/F: Digoxin reduces mortality?

A

FALSE

92
Q

T/F: Digoxin is an NTI

A

TRUE

93
Q

rEF Baseline Trx

A

ACEi or ARB, + beta-blocker, + diuretic (prn)

94
Q

when is digoxin prescribed?

A

as a last resort if sympotoms not controlled on other therapy

95
Q

what is an arrhythmia?

A

disturbance of HR due to SA node irregularities (origin, pattern, speed/rate)

96
Q

Overall symptoms of arrhythmias

A

increase/decrease in HR palpitations

97
Q

general symptoms of arrhythmias

A

fatigue, dyspnea, syncope, dizziness, angina, diaphoreseis (profuse sweating)

98
Q

Anti-arrhythmic drug therapeutic concerns

A

also causes arrhythmia, take HR for 60s, decreases exercise tolerance, 30-60% efficacy

99
Q

Amiodarone MOA

A

prolong duration of AP by blocking ion channels (K+, Na+, Ca2+)

100
Q

Amiodrone indication

A

ventricular arrhytmia

101
Q

Amiodarone AEs

A

LFTs, TFT, PFTs, bluish discoloration

102
Q

considerations for Amiodrone

A

50 day half life

103
Q

Digoxin MOA

A

increase contractility (Na+/K+ ATPase)

104
Q

Digoxin indication

A

arrhythmia & CHF (last resort)

105
Q

Digoxin AE

A

GI (Beer’s list)
CNS - blurred vision, confusion, lethargy
Arrhythmia

106
Q

Digoxin considerations

A

avoid pt who has kidney dysfunction (metabolized by kidneys) *medical emergency if given to them