Cardiovascular Flashcards

Exam2

1
Q

ACE Inhibitor MOA?

A

ACE inhibition -> decreased angiotensin 2 -> dilated blood vessels -> decrease blood volume -> prevent/reverse pathological changes in heart d/t angiotensin 2 & aldosterone -> reduces cardiac afterload / increases cardia output

ACE inhibition -> increased bradykinin -> vasodilation -> promotes cough & angioedema

ACEi -> aldosterone inhibition -> dilation of renal blood vessels -> allows for sodium & water excretion -> decreases edema / decreases preload (venous return) -> prevents/reverses cardiac structure changes // slows/delays renal disease in diabetic nephropathy

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2
Q

ACE Inhibitor Indications?

A

Hypertension, heart failure, MI, diabetic (and non-) nephropathy, prevention of MI/Stroke/Death in pts at high cardiovascular risk

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3
Q

ACE Inhibitor Adverse Effects?

A

First dose hypotension <- widespread vasodilation <- lowered angiotensin 2 <- ACE inhibition

Cough: persistent, dry, nonproductive cough
ACE inhibition -> increased bradykinin -> cough & angioedema

Hyperkalemia:
ACE inhibition -> inhibition of aldosterone release -> increased potassium retention in kidneys

Acute kidney injury:
In those w bilateral renal artery stenosis (or stenosis in artery to a solitary kidney) bc their kidneys -> increased renin release -> increased levels of angiotensin 2 -> maintain glomerular filtration // inhibition of ACE interrupts the compensatory mechanism

Risk of hypoglycemia:
ACEi -> increased insulin uptake in muscles -> hypoglycemia

Renally adjusted

Increases lithium levels

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4
Q

What drugs are used for hypertension?

A

thiazide diuretic
ACEi
ARBs
Beta-blockers
Aplha1-blockers
CCB
Centrally acting alpha2-agonists
Vasodilators

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5
Q

What drug is a thiazide diuretic?

A

Hydrochlorothiazide

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6
Q

What drug is an ACEi?

A

Lisinopril

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7
Q

What drug is an ARB?

A

Losartan

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8
Q

What drugs are CCBs?

A

Dihydropyridine: Amlodipine

Non-dihydropyridine: Diltiazem

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9
Q

What drug is a beta-blocker?

A

Metoprolol

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10
Q

What drug is an Alpha1-blocker?

A

Prazosin

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11
Q

What drug is a centrally acting alpha2-agonist?

A

Methyldopa

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12
Q

What drug is a vasodilator?

A

Hydralazine

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13
Q

What drug is an aldosterone receptor antagonist?

A

Spironolactone

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14
Q

What drug is a loop diuretic?

A

Furosemide

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15
Q

What drug is a SGLT2i?

A

Dapagliflozin

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16
Q

Examples of causes of secondary hypertension?

A

Cushing’s syndrome
Pheochromocytoma
Medications
Lifestyle

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17
Q

What is the difference between primary and secondary hypertension?

A

Primary/essential hypertension: no identifiable cause

Secondary hypertension: secondary to identifiable cause

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18
Q

At what BP range are meds recommended versus lifestyle changes?

A

“elevated” 120-129 / less than 80: lifestyle change

HTN stage 1: 130-139 / 80-89: meds

HTN crisis: higher than 180 / 120: IV meds, emergent

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19
Q

Treatment of HTN goal?

A

BP maintenance at < 130 / < 80

Going lower can cause profound hypotension d/t being used to higher BP

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20
Q

Main part of diagnosing HTN?

A

Repeated BP readings above 130/80
(White coat syndrome)

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21
Q

Recommended sodium consumption?

A

<2300mg / day
<2.3g / day

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22
Q

What are lifestyle changes for managing HTN?

A

Reducing sodium intake
Diet: fruits/veggies, low fat/cholesterol
Lower alcohol
Increase exercise
Smoking cessation
Weight loss
Maintain potassium / calcium intake

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23
Q

First line agents for HTN?

A

Thiazide diuretics
ACEi
ARBs
CCBs

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24
Q

Drugs that aid in HTN & heartfailure

A

ACEi
Aldosterone antagonist
ARB
Beta blocker
CCB- DHP
Diuretic

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25
Q

Drugs that aid in HTN and recurrent stroke prevention

A

ACEi
Diuretic

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26
Q

Drugs that aid in HTN and risk of CAD

A

ACEi
Beta blocker
CCB
Diuretic

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27
Q

Drugs that aid in HTN & post-MI

A

ACEi
Aldosterone antagonist
Beta blocker

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28
Q

Drugs that aid in HTN & diabetes

A

ACEi
ARBs
Beta blocker
CCB
Diuretic

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29
Q

Drugs that aid in HTN & CKD

A

ACEi
ARBs

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30
Q

Drugs that are safe to aid HTN in pregnancy

A

Labetalol
Nifedipine
Methyldopa

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31
Q

Drugs for HTN that are contraindicated in pregnancy

A

ACEi
ARBs
Direct renin inhibitors

All teratogenic

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32
Q

Thiazide diuretics- MOA

A

Prevents re-absorption of sodium in distal renal tubules

Promotes urinary excretion of sodium, water, potassium, hydrogen

Calcium, glucose, uric acid sparing

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33
Q

Thiazide diuretics- adverse effects

A

Photosensitivity - wear sunscreen

Electrolyte disturbances- hypokalemia, hypomagnesemia, hyponatremia, hypercalcemia

Orthostatic hypertension

Gout

Contains sulfa moiety (cross-reactivity w sulfa antibiotics is low)

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34
Q

ARBs Indications?

A

HTN
Heart failure
diabetic nephropathy
MI

Prevention of:
MI
Stroke
Death for high risk of cardiovascular events

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35
Q

ACEi and ARBs: main difference?

A

ARBs have lower risk of coughing or hyperkalemia

ACE are first choice, ARBs if not tolerated

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36
Q

ARBs MOA?

A

Prevents angiotensin 2 from binding to receptor -> decreased vasoconstriction -> vasodilation -> increased blood flow -> decreased BP //

decreased aldosterone -> decreased re-absorption of sodium and water -> decreased blood volume -> decreased BP

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37
Q

ACEi: Contraindications?

A

Idiopathic/hereditary angioedema

Coadministration within 36hours with a neprilysin inhibitor (ex. sacubitril)

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38
Q

ARBs: side effects?

A

Acute kidney injury
Hyperkalemia
First-dose hypotension
Fetal injury
Angioedema (less than ACEi)

Monitor:
Serum potassium (palpitations, irregular heart beat)
Renal function (BUN/Cr/urine output

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39
Q

CCBs: MOA?

A

CCB block calcium from entering heart muscle -> vasodilation -> decreased contractility -> reduced HR

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40
Q

Effects calcium has on the heart?

A

Increased calcium influx into the heart -> increased vasoconstriction / contraction

More calcium = constriction & contraction

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41
Q

What is a dihydropyridine (DHP) CCB?

A

Acts mostly on blood vessels

Amlodipine

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42
Q

DHP CCB: side effects?

A

Flushing
Peripheral edema
First-dose hypotension
Gingival hyperplasia - advise to floss regularly
Hyperglycemia
Headache

(Amlodipine)

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43
Q

What drug is a nondihydropyridine?

A

Acts on heart and blood vessels

(Diltiazem- CCB)

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44
Q

NDHP CCBs: Indications?

A

Arrythmias
Angina
HTN

(Diltiazem)

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45
Q

Main difference between NDHP and DHP?

A

Non-dihydropyridine: affects heart AND blood vessels (Diltiazem)

Dihydropyridine: affects only blood vessels (Amlodipine)

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46
Q

NDHP CCBs: MOA

A

Blocks calcium channels in vessels -> vasodilation -> decreased BP

Blocks calcium channels in heart -> increases relaxation -> increases vasodilation -> increases coronary perfusion

Blocks calcium channels at SA node -> decreases HR

and heart -> decreases AV node conduction -> decreases dysrhythmias

(Diltiazem)

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47
Q

NDHP CCB: side effect?

A

Constipation d/t CCB in GI
Peripheral edema/flushing d/t vasodilation
Bradycardia d/t CCB at SA node

Hyperglycemia
Heart failure
Gingival hyperplasia- floss regularly

Avoid grapefruit juice & st. John’s Wort d/t inhibition of drug metabolism -> increased drug levels

Contraindicated with heart failure or EF<40%

(Diltiazem- less potent than verapamil)

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48
Q

DHP CCB: Indications?

A

Angina- vasospastic
HTN

(Amlodipine)

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49
Q

What drug is a beta blocker?

A

Metoprolol

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50
Q

Beta blocker- MOA?

A

Beta blocker -> blocks beta 1(heart/kidneys) -> decreases HR, contractility, cardiac output, inhibits renin release

Beta blocker -> blocks beta 2 (lungs, pancreas, arteriolar muscle) -> peripheral vasoconstriction (decrease blood flow to extremities) / bronchoconstriction (caution w/ asthma)

Decreases HF risks, decreases BP, decreases risk of sudden cardiac death

(Metoprolol)
(Metoprolol succinate for HF- beta 1 selective)

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51
Q

Beta blockers- side effects?

A

Bradyarrhythmia
Fatigue, insomnia
SOB/Bronchospasm- avoid starting if pt already experiencing
Rebound hypertension- if stopped abruptly

Avoid if pt is decompensated- more for Tx not for acute

Counsel on abrupt withdrawal d/t increased mortality and avoid rapid titrations d/t side effects

Hyperglycemia (masked Sx- tremors, palpitations, hunger, irritability)

Hyperkalemia
Increase cholesterol

Intensify adverse effects of diltiazem (NDHP CCB)

(Metoprolol)

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52
Q

Beta blocker- contraindications?

A

Bradycardia (HR < 45)
AV block without functioning pacemaker
Cardiogenic shock
Acute heart failure exacerbation

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53
Q

What drug is an Alpha1-Blocker?

A

Prazosin

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54
Q

What drug class is prazosin?

A

Alpha1-Blocker

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55
Q

Alpha1-blocker- MOA?

A

Blocks alpha1 receptors -> prevents norepinephrine binding -> vascular vasodilation -> dilation of arterioles/veins & relaxation of smooth muscle -> decreases BP

(Prazosin)

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56
Q

Alpha1-blocker- indications?

A

HTN- not first choice d/t hypotension

BPH- off-label
PTSD-related nightmares- off-label

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57
Q

Alpha1-blocker- side effects?

A

Orthostatic hypotension
Angina

Reflex tachycardia
Nasal congestion
Dizziness/drowsiness

Not first-choice for HTN

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58
Q

What drug is a Centrally Acting Alpha2-Agonist?

A

Methyldopa

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59
Q

What drug class is Methyldopa?

A

Centrally acting alpha2-agonists

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60
Q

Alpha2-agonist- MOA?

A

Stimulates alpha2 receptor (in brain) -> decrease sympathetic outflow (norepinephrine release) -> -> decrease SNS activity -> decreases peripheral resistance
renal vascular resistance
heart rate
blood pressure

(Methyldopa)

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61
Q

Alpha2-agonist- indication?

A

Hypertension
HTN in pregnancy

(methyldopa)

62
Q

Alpha2-agonist- side effects?

A

Neurologic effects- depression at higher doses- can worsen depression or increase risk of suicidal ideation- counsel

Hemolytic anemia
Transient sedation w initiation or dose increase

Contraindicated w/ use of MAO inhibitors- counsel

63
Q

What drug is a vasodilator?

A

Hydralazine

64
Q

What drug class is hydralazine?

A

Vasodilator

65
Q

Vasodilator- MOA?

A

Selective vasodilation of arterioles

(Hydralazine)

66
Q

Vasodilator- side effects?

A

Reflex tachycardia
Increases intracranial pressure

Headache, dizziness, weakness/fatigue, increased blood volume

Not first-choice for HTN/HF
(Hydralazine)

67
Q

What are some common causes for arrythmias?

A

MI
Electrolyte imbalances: decreased potassium or decreased magnesium

68
Q

What are the classes of antiarrhythmics?

A

Class 2: beta blockers (Metoprolol)
Class 3: Potassium channel blockers (Amiodarone)
Class 4: NDHP if no HF (Diltiazem)

69
Q

What drug is a potassium channel blocker?

A

Amiodarone

70
Q

What drug class is Amiodarone?

A

Potassium channel blocker

71
Q

Potassium channel blocker- side effects?

A

Hyper/hypothyroidism
Hepatotoxic
Optic neuropathy
Pulmonary toxicity
Bradycardia
Hypotension

Avoid grapefruit juice/ st.John’s Wort
Take with food (avoids GI upset)
Limit sun exposure

Long half-life (58days)
Correct hypokalemia, hypomagnesemia, hypocalcemia prior to starting

Contraindications:
Iodine sensitivity

(Amiodarone)

72
Q

Amiodarone- indications?

A

Arrhythmias - not first-choice d/t toxicities

73
Q

Potassium channel blocker- MOA?

A

Blocks potassium channels -> blocks repolarization of heart muscle -> prolongs AP

(Amiodarone)

74
Q

Which cholesterol increases risk for ASCVD?

A

Increased LDL (bad cholesterol) or decreased HDL (good cholesterol)

75
Q

What are some ASCVD events?

A

MI
Ischemic stroke
Transient ischemic attack
Coronary artery disease

76
Q

What is the 10-year ASCVD score?

A

Concerned when score is >7.5%

77
Q

What enzyme synthesizes cholesterol?

A

HMG-CoA Reductase- the main target for statins

78
Q

What is the main target for statins?

A

HMG-CoA Reductase- the enzyme that synthesizes cholesterol

79
Q

What range is ideal for total cholesterol?

A

<200mg/dL

200-239mg/dL borderline
>240mg/dL high

80
Q

What is primary prevention of ASCVD?

A

No history of ASCVD event, at risk

Increased LDL > 190

Age 40-75 > 7.5% 10-year CV risk

81
Q

What is secondary prevention of ASCVD?

A

History of ASCVD event -> more likely for another

Age > 75: moderate intensity statin
Age < 75: high intensity statin

82
Q

What drug is a statin?

A

Atrovastatin

83
Q

What drug class is atrovastatin?

84
Q

Statin- MOA?

A

Competitively inhibits HMG-CoA reductase -> decreased cholesterol synthesis ->
decreased LDL production

increased LDL receptor expression -> LDLs get pulled from blood by liver -> increased LDL excretion -> decreased overall cholesterol

mild increase in HDL

(Atorvastatin)

85
Q

Statins- Indications?

A

Hyperlipidemia
Lowers risk of heart failure, MI & sudden death- primary and secondary prevention

(Atorvastatin)

86
Q

Statins- side effects?

A

Myalgia (muscle pain)
Myopathy (muscle weakness/pain)- higher risk with higher log p (lipophilicity)
Rhabdomyolysis (muscles breaking down -> release creatinine kinase increasing level // monitor creatinine kinase to check this)

Headache
Rash
GI discomfort
Memory issues

Monitor LFTs and discontinue if severely low

CYP substrate- Avoid grapefruit juice to prevent accumulation effect

Try to take at night- when cholesterol synthesis is highest

(Atorvastatin)

87
Q

What drug is a bile acid seqeusterant?

A

Cholestyramine

88
Q

What drug class is cholestyramine?

A

Bile acid sequestrant

89
Q

Bile acid sequestrant- indications?

A

Hyperlipidemia
Hypercholesteremia (high LDL)

Used commonly with statins or if statin-tolerant

(cholestyramine)

90
Q

Bile acid sequestrant- MOA?

A

Non-digestible positive charge -> displaces chloride & binds to bile acids in GI -> form insoluble complex -> bile-acid bound LDL -> excreted in feces -> decreases LDL

(Cholestyramine)

91
Q

Bile acid sequestrant- side effects?

A

Constipation/GI upset
Elevated triglycerides- don’t take if TG> 500
Teeth discoloration/erosion/decay of tooth enamel- counsel on dental hygiene

Don’t take if bowel obstruction

Other meds taken 1 hour before or 4-6hours after

Oral contraceptives/fat-soluble vitamins (A, D, E, K) 4 hours prior or 6-12 hours after
Can cause hemorrhage from lack of vit K

Swallowing dry can cause esophageal irritation- counsel to mix powder with fluid

(Cholestyramine)

92
Q

Tiers of ASCVD therapy, what drug is high-, medium-, and low-intensity?

A

High: Atorvastatin 40-80mg, >50% lower

Med.: Atorvastatin 10mg, 30-50%

Low: Cholestyramine, 20% alone (40-60% combo w/ statin)

93
Q

What drug is a fibric acid (fibrate) derivative?

A

Fenofibrate

94
Q

What drug class is fenofibrate?

A

Fibrates derivative

95
Q

Fibrates- indications?

A

High TG, ASCVD, high cholesterol

Third-line drug d/t interactions, side effects, etc.

(Fenofibrate)

96
Q

Fibrates- MOA?

A

Activates PPAR-a in liver -> increased fat burned by liver -> increased breakdown of TG -> decreased TG

Activates PPAR-a in liver -> decreased bad fats produced by liver -> decreased TG

Increases HDL

Reduces cholesterol buildup in blood

Little to no effect on LDL

(Fenofibrate)

97
Q

Fibrates- side effects?

A

GI discomfort- take with food to avoid (high fat meal for absorption)
Gallstones- contraindicated for preexisting gallbladder disease
Myopathy
Liver toxicity
AKI

Avoid grapefruit juice- accumulation effect

Can be cautiously combined with statin (except gemfibrozil)

(Fenofibrate)

98
Q

What drug is a lipid lowering agent?

99
Q

What drug type is Ezetimibe?

A

Lipid lowering agent

100
Q

Ezetimibe- indications?

A

high cholesterol

Adjunct to max statin
Monotherapy if statin intolerant

101
Q

Ezetimibe- MOA?

A

Binds to NPC1L1 protein in small intestine -> inhibits cholesterol absorption -> decreases absorbed cholesterol -> decreases effects of dietary cholesterol

102
Q

Ezetimibe- side effects?

A

Myopathy/rhabdomyolysis
Gallstones- when used w/ fibrates
Hepatotoxicity- when used w/ statins

Adjunct to max statin when high LDL
Monotherapy if statin intolerant

103
Q

What is angina pectoris?

A

Sudden pain beneath sternum, common to radiate to left shoulder, left arm and jaw

Occurs when the heart isn’t receiving enough oxygen to meet the body’s demands

Secondary to atherosclerosis of coronary arteries

Can lead to MI, myocardial ischemia, anginal pain, death

104
Q

What is chronic stable angina?

A

Triggered by physical activity, emotional excitement, large meals, cold exposure

Underlying cause: CAD

Treatment: decreasing cardiac oxygen demand <- vasodilation (only symptomatic relief)

105
Q

What is an antianginal drug?

A

Nitroglycerin

106
Q

What drug class is Nitroglycerine?

A

Antianginal agent

107
Q

Nitroglycerin- indications?

A

Stable angina

108
Q

Nitroglycerin- MOA?

A

Increases vasodilation -> decreases venous return -> decreases preload -> decreases oxygen demand

109
Q

Nitroglycerine- side effects?

A

Headache- improves over time

Washout period from last doses of sildenafil & tadalafil: 24- and 48-hours (all vasodilatory)

Drug holiday to prevent tolerance

Don’t d/c abruptly- withdrawal effects/vasospasms

110
Q

Nitroglycerine- doses allowed?

A

Repeat every 5 minutes, 3 doses max, call 911 if not alleviated

Open bottle mist be replaced 6months d/t patch deterioration

111
Q

Beta blocker- indications?

A

Angina -first line for angina w/ effort (decreases cardiac oxygen demands)

Arrythmias (decreases HR / contractility)
HTN (decreases HR)

HF (metoprolol succinate)

(Metoprolol)

112
Q

What drug is an injectable anticoagulant?

A

Enoxaparin

113
Q

What drug class is enoxaparin?

A

Injectable anticoagulant

114
Q

Enoxaparin- MOA?

A

Inactivation of clotting factors: thrombin and factor Xa -> -> decreases fibrin production -> clotting suppressed -> prevents thrombosis

115
Q

Enoxaparin- side effects?

A

Hemorrhage
Spinal/epidural hematoma
Heparin-Induced thrombocytopenia (HIT)

Contraindicated for hx of HIT or uncontrolled active bleeding

Monitor PTT/Xa levels on heparin drip

Pork based

Short half-life: 1.5hours
From porcine products

117
Q

What drug is a vitamin K antagonist?

118
Q

What drug class is Warfarin?

A

Vitamin K antagonist

119
Q

Warfarin- MOA?

A

Inhibits VKORC1 (enzyme that converts inactive vitamin K to active form) -> inactive vitamin K -> decreased production of vitamin K dependent clotting factors (SNTT) -> delayed anticoagulant effect

INR goal: 2-3
INR goal for mitral valve replace.: 2.5-3.5

120
Q

Warfarin- side effects?

A

Hemorrhage/bleeding
Fetal harm

Overdoes- tx w/ vitamin K (takes some time, only works w/ functioning liver)

Narrow therapeutic index- monitor INR
Goal: 2-3

121
Q

Warfarin- indications?

A

Anticoagulation
Preventing blood clots
VTE

122
Q

What drug is a direct thrombin inhibitor?

A

Dabigatran

123
Q

What drug class is dabigatran?

A

Direct thrombin inhibitor

124
Q

Dabigatran- indications?

A

DVT/PE Tx- 5 days of parenteral anticoagulation & dabigatran

Stroke prevention w/ nonvalvular AFib
VTE prevention after knee/hip replacement surgery

Doesn’t need anticoagulation monitoring
few drug/food interactions

(Direct thrombin inhibitor)

125
Q

Dabigatran vs. Warfarin?

A

Dabigatran has higher efficacy and lower incidence of bleeding

126
Q

Dabigatran- MOA?

A

Inhibits thrombin (in blood and bound to clots) -> prevents conversion of fibrinogen into fibrin (req. thrombin) -> decreases coagulation -> decreases VTE/PE/aFib
(Direct thrombin inhibitor)

127
Q

What does thrombin do?

A

Converts fibrinogen into fibrin- essential for coagulation

128
Q

Dabigatran- side effects?

A

Bleeding
GI discomfort

Can’t be crushed

Premature d/c can increase thrombotic events

129
Q

What drug is a direct oral anticoagulant
Factor Xa inhibitor?

A

Rivaroxaban

130
Q

What drug class is Rivaroxiban in?

A

Direct Oral anticoagulant (DOAC)
Factor Xa Inhibitor

131
Q

Rivaroxaban- MOA?

A

Inhibition of factor Xa -> inhibits production of thrombin -> decreases coagulation

132
Q

Rivaroxaban- indications?

A

DVT/PE Tx
DVT/PE prevention after hip/knee replace. surgery
Stroke prevention for those w/ aFib

133
Q

Rivaroxaban vs. Warfarin?

A

Rivaroxaban is:
faster onset
fixed dose-consistent dosing
lower bleed risk
few drug/food interactions
No INR monitoring

134
Q

Roxaroxaban- side effects?

A

Bleeding (less risk than Warfarin)
Doses >10mg taken w high fat food for increased absorption

Not safe in pregnancy

Avoid grapefruit juice

135
Q

What drug class is sacubitril/valsartan?

A

Angiotensin receptor neprilysin inhibitor (ARNI)

136
Q

Sacubitril/valsartan- MOA?

A

inhibits breakdown of BNP and blocks angiotensin -> increased vasodilation -> decreased cardiac workload

BNP- hormone that helps with loss of sodium/water and vasodilation
(ARNI)

137
Q

Sacubitril/valsartan- indications?

A

Heart failure

(ARNI)

138
Q

Sacubitril/valsartan- side effects?

A

Dizziness- reduce diuresis is management, chronic diuretic dose might be reduced 50%

Hyperkalemia

RAASi first choice- transition ACEi/ARBs to ARNI

ANGIOEDEMA- contraindication

If taking ACEi- need 36hr washout period prior to taking ARNI

(ARNI)

139
Q

Sacubitril/valsartan compared to ACEi/ARBs

A

Both are anti-RAAS

ACEi/ARBs still used for HF and HFrEF

Cost difference
Sacubitril/valsartan- more hypotensive

140
Q

What drug is a sodium glucose co-transporter 2 inhibitor (SGL2i)?

A

Dapagliflozin

141
Q

What drug class is dapagliflozin in?

A

Sodium glucose co-transporter 2 inhibitor (SGL2i)

142
Q

Dapagliflozin- indications?

143
Q

Dapagliflozin- MOA?

A

Inhibits SGLT-2 in kidneys -> decreases SNS response -> decreases glucose & sodium reabsorption (kidneys) -> decreases plasma volume -> decreases cardiac workload

increases mild ketosis -> ‘sick’ myocardium prefers ketone metabolism -> cardiac muscle has more ‘food’ available

Can improve tolerance to MRAs & ARNI/ACEi/ARBs by decreasing hyperkalemia caused by them

(SGL2i)

144
Q

Dapagliflozin- side effects?

A

Glucosuria- increased risk of UTI

Risk of yeast infection- proper urinary hygiene

Volume losses- decrease diuretics 50% & correct volume depletion prior to starting SGL2i

Increased urination/thirst

Euglycemic ketoacidosis

Necrotizing fasciitis risk

Contraindicated for dialysis

Control high blood sugar prior to starting
Euglycemic ketoacidosis d/t NPO

145
Q

What drug is a mineralocorticoid receptor agonist (MRA)?

A

Spironolactone

146
Q

What drug class is spironolactone in?

A

Mineralocorticoid receptor agonist (MRA)

147
Q

Spironolactone- indications?

A

HF (HFrEF)
HTN

148
Q

Spironolactone- MOA?

A

Antagonist of aldosterone receptors (in kidneys) -> decreases sodium & water retention & increase potassium retention // -> stops progression of myocardial scaring -> reverses remodeling

(MRA)

149
Q

Spironolactone- side effects?

A

Risk of hyperkalemia- caution w/ CKD: stop K+ supp. / oral K+ binder- check levels

Gynecomastia

Abnormal uterine bleeding- post-menopausal

Check renal function

(MRA)