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Pharmacology Test 2 > Cardiovascular > Flashcards

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
Vascular injury results in what 2 immediate things?
1) . exposure of collagen and VWF | 2) . Tissue factor exposure
26
exposure of collagen and VWF results in what?
platelets adhesion and release of ADP and thromboxane A2
27
once platelets adhere and release what happens?
more plates are recruited and activated
28
as more platelets are recruited and activated what results
platelet aggregation and ultimately platelet-fibrin thrombus formation
29
when tissue factors are exposed due to a tissue injury what is triggered?
coagulation pathways and thrombin generation
30
what does thrombin do?
recruit more platelets and convert fibrinogen to fibrin
31
how is fibrin important?
it binds platelets together to form a thrombus
32
primary hemostasis results in what?
platelet plug formation
33
secondary hemostasis results in what?
fibrin formation which is used to stabilize the platelet plug
34
What is artherosclerosis?
narrowing and hardening of the arteries
35
basic mechanism of artherosclerosis
injury occurs to arterial wall -> cholesterol begins to build up in the wall
36
what can atherosclerosis eventually cause?
thrombus formation -> MI, stroke, or other ischemic issues
37
what type of cholesterol is "good"?
High-density HDL
38
what are the 3 basic classes of drugs used to treat Artheroscerlosis?
1) . Statins 2) . PCSK9 inhibitors 3) . Cholesterol Absorption Inhibitor
39
true name of statins?
HMG-CoA reductase inhibitors
40
T/F: even with low LDL some populations must take a statin to reduce risk of stroke
TRUE
41
basic MOA statins
block cholesterol synthesis
42
statins common AE
myalgia
43
other Statins AE
dyspepsia, headache, increased liver enzymes, tendinopathy and tendon rupture?
44
Rare AE of Statins
rhabdo and myopathy
45
T/F: statins have a decreased risk of drug-drug interactions?
FALSE, increased risk (especially fibrates)
46
how does grapefruit juice effect statins?
inhibits CYP enzymes - linked to statin rhabdo -> increased 6x hosptialization rate
47
what are the 3 types of antithrombotic drugs classes?
1) . Antiplatelets 2) . anticoagulants 3) . fibrinolytics
48
general concerns with antithrombotics as a whole?
bleeding or clotting
49
what do antiplatelets do?
prevent thrombus
50
basic MOA of antiplatelets
decrease platelet secretion and adhesion
51
which antithrombotic class has boxed warnings?
antiplatelets, warning against CYP interaction, increase risk of bleeding
52
suffix for antiplatelets
-gel/-grelor
53
what do anticoagulants do?
prevents thrombus & thrombus growth
54
LMWH and Heparin basic MOA
increase antithrombin to decrease thrombin
55
Heparin and Direct thrombin inhibitor basic MOA
prevents conversion of fibrinogen -> fibrin
56
Arixtra basic MOA
selectively inhibits factor Xa
57
Anticoagulants that are administered via IV
LMWH, Heparin, Direct thrombin inhibitor, Arixtra
58
Anticoagulants that are administered via PO
Direct thrombin inhibitor, Factor Xa inhibitor, and Warfarin (VKa)
59
Direct thrombin inhibitor and Factor Xa are further classified as what?
DOAC
60
DOAC has less of a risk of what?
intercranial bleeding
61
Warfarin basic MOA
inhibits vitamin K - inhibits coagulation cascade indirectly (reduces factor formation)
62
Atrixtra is what type of anticoagulant?
factor Xa inhibitor
63
AE of Warfarin
intercranial bleeding , rare: skin necrosis, DDI with leafy green
64
Fibrinolytics generally do what?
lyse active thrombus
65
Fibrinolytics basic MOA
breaks fibrin links in active thrombus
66
when are Fibrinolytics prescribed?
immediately following stroke, MI, and PE
67
Fibrinolytics suffix
-kinase/-plase
68
what is the continuum from least to most risk of HIT(heparin induced thrombocytopenia) (for anticoagulants)
Atrixtra - direct thrombin inhibitor - LMWH - Heparin
69
Cholesterol Absorption Inhibitor MOA
inhibits absorption of cholesterol in small intestine
70
When might a cholesterol absorption inhibitor be used?
if a pt. is experiencing a lot of myalgia from statins
71
Cholesterol absorption inhibitors DDI
not metabolized by CYP enzymes, less DDI
72
basic MOA for PCSK9 Inhibitors
increase LDL uptake for degradation
73
PCSK9 common AE
injection site reactions
74
what is CHF?
heart is unable to pump sufficient blood to supply the needs of the body
75
How is CHF progressive?
structural changes over time lead to reduced cardiac contractility
76
Conditions that can lead to CHF
ischemic and hypertensive heart disease, cardiomyopathy, valve disease
77
What is compensated CHF?
pt is med stable. Combined efforts of 3 compensatory phases achieve a normal CO
78
what is decompensated CHF?
unable to maintain adequate circulation. Life-threatening: fluid overload and total heart failure
79
clinical manifestation of L ven CHF
1) . dyspnea 2) . fatigue and muscular weakness 3) . renal changes 4) . nocturia
80
in general R ven CHF deals with what?
fluid build up in the periphery
81
in general L ven CHF deals with what?
fluid build up in the lungs
82
which ventricular failure can result in pulmonary edema?
Left ventricle heart failure
83
HF with preserved ejection fraction results from what?
diastolic heart failure, cardiac hypertrophy -> reduced volume capacity in L ven
84
HF with reduced ejection fraction is caused by what?
systolic heart failure, heart unable to adequately contract
85
which HF is more often related to aging and cardiac hypertrophy?
HFpEF (preserved heart failure)
86
goals of HFpEF
1) . treat underlying comorbidities 2) . give diuretics 3) . may add aldosterone antagonist
87
general goal of HFpEF?
get rid of fluid, can't fix just treat symptoms
88
Goals of HFrEF
improve QOL and prolong survival
89
corresponding meds for HFrEF
diruretics, + inotropic drugs (digoxin), vasodilators
90
Entresto is what?
a type of ARB (higher risk of angioedema than other ARBS)
91
T/F: Digoxin reduces mortality?
FALSE
92
T/F: Digoxin is an NTI
TRUE
93
rEF Baseline Trx
ACEi or ARB, + beta-blocker, + diuretic (prn)
94
when is digoxin prescribed?
as a last resort if sympotoms not controlled on other therapy
95
what is an arrhythmia?
disturbance of HR due to SA node irregularities (origin, pattern, speed/rate)
96
Overall symptoms of arrhythmias
increase/decrease in HR palpitations
97
general symptoms of arrhythmias
fatigue, dyspnea, syncope, dizziness, angina, diaphoreseis (profuse sweating)
98
Anti-arrhythmic drug therapeutic concerns
also causes arrhythmia, take HR for 60s, decreases exercise tolerance, 30-60% efficacy
99
Amiodarone MOA
prolong duration of AP by blocking ion channels (K+, Na+, Ca2+)
100
Amiodrone indication
ventricular arrhytmia
101
Amiodarone AEs
LFTs, TFT, PFTs, bluish discoloration
102
considerations for Amiodrone
50 day half life
103
Digoxin MOA
increase contractility (Na+/K+ ATPase)
104
Digoxin indication
arrhythmia & CHF (last resort)
105
Digoxin AE
GI (Beer's list) CNS - blurred vision, confusion, lethargy Arrhythmia
106
Digoxin considerations
avoid pt who has kidney dysfunction (metabolized by kidneys) *medical emergency if given to them

Pharmacology Test 2 (9 decks)

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