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Pharmacology Exam 2 > Exam 2 Drugs > Flashcards

Exam 2 Drugs Flashcards

1
Q

Hydrochlorothiazide
chlorthalidone
metalozone
indapamide

A

thiazide diuretics

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2
Q

Furosemide
Torsemide
Bumetanide
Ethacrynic Acid

A

Loop Diuretics

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3
Q

Amiloride

Triamterene

A

Potassium-Sparing diuretics

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4
Q

Nifedipine

Amlodipine

A

Calcium Channel Blockers (Dihydropyridine)

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5
Q

Verapamil

Diltiazem

A

Calcium Channel Blockers (Non-dihydropiridine)

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6
Q 
Captopril
Enalapril
Fosinopril
Lisinopril
Perindopril
Quinapril
Ramipril
Trandolapril
A

ACE Inhibitors (“-opril”)

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7
Q 
Azilsartan
Candesartan
Eprosartan
Irbesartan
Losartan
Olmesartan
Temisartan
Vaslartan
A

ARBs (“-sartan”)

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8
Q

Doxazosin
Prazosin
Terazosin

A

Alpha-1 Antagonists (“-zosin”)

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9
Q

Clonidine
Methyldopa
Guanfacine
Guanabenz

A

Alpha-2 Agonists

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10
Q

Reserpine

A

Peripheral Sympathetic Inhibitor

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11
Q

Isosorbide dinitrate/hydralazine
Hydralazine
Minoxidil

A

Direct Vasodilators

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12
Q 
Atorvastatin
Fluvastatin
Lovastatin
Pravastatin
Rosuvastatin
Simvastatin
A

Statin

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13
Q

Alirocumab

Evolocumab

A

PCSK9 Inhibitor (cholesterol) - other treatments

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14
Q

Lovaza
Vascepa
Epanova
Omtryg

A

Omega 3 Fatty Acids (fish oil) - other cholesterol treatment

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15
Q

Digoxin - Method of Action

A

Use in Heart Failure (sometimes)

MOA: + inotropic effects (heart beats harder); decreases hospitalization, DOES NOT decrease or improve HF progression

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16
Q

ACE-I pharmacological use

A

blocks creation of angiotensin II

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17
Q

ARBs pharmacological use

A

blocks angiotensin II’s receptor

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18
Q

Fondaparinux

A

Xa Inhibitor (indirect)

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19
Q

Apixaban

Rivaroxaban

A

Xa inhibitor (direct)

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20
Q

Bivalirudin
Desirudin
Aragatroban
Dabigatrin

A

Direct Thrombin inhibitors

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21
Q

Amiodarone
Dofetilide
Ibutilide
Propafenone

A

Pharmacological Cardio Conversion

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22
Q

Dabigatran
Rivaroxaban
Warfarin
Apixaban

A

Anticoagulants

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23
Q

Aspirin

Dipyridamole

A

Antiplatelets

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24
Q

Clopidogrel
Prasugrel
Ticagrelor
Cangrelor (IV)

A

P2Y12 Inhibitor - reduces platelet activation/aggregation

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25
Q

Abciximab
Eptifibatide
Tirofiban

A

Glycoprotein lIb/IIIa Receptor Inhibitor

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26
Q

Alteplase
Reteplase
Tenecteplase

A

Fibrinolytics (fibrin-specific)

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27
Q

Streptokinase

Urokinase

A

Fibrinolytics (nonfibrin-specific)

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28
Q

Nitroglycerin

A

Short-acting nitrate (angina)

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29
Q

Nitroglycerin ER
Isosorbide dinitrate
isosorbide mononitrate

A

Long-acting nitrates

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30
Q

this diuretic used in Edema and Heart Failure, works on loop of henle, and can be used even in poor renal function (decreases renal vascular resistance, increased renal blood flow)

A

Loop Diuretics

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31
Q

this diuretic used commonly in Hypertension; decreases BP by increasing sodium and water excretion by the kidneys (decreases blood volume)

A

Thiazide Diuretics

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32
Q

This diuretic is good for RESISTANT hypertension; they increase NaCl excretion, decrease K+ secretion), diminishing cardiac remodeling in heart failure

A

Aldosterone antagonists
spironolactone
eplerenone

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33
Q

Adverse effects of potassium sparing diuretics

A

HyperK; decrease or D/C K+ supplements and avoid high potassium foods

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34
Q

Spironolactone

Eplerenone

A

Aldosterone antagonists (diuretic)

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35
Q

Types of Diuretics?

A

Thiazide, Loop, Potassium Sparing, Aldosterone Antagonists

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36
Q

Aspirin MOA?

A

inhibits COX (cyclooxygenase)

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37
Q

Types of antiplatelets

A

aspirin, dipyridamole, P2Y12 inhibitors, Glycoprotein IIa/IIIb inhibitors

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38
Q

when to use fibrinolytics?

A

Acute Coronary syndrome if PCI is too far away, in ischemic stroke, in VTE

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39
Q

treatment for acute stroke; give within 3 hours after onset to reverse symptoms

A

Alteplase (fibrinolytics)

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40
Q

how do potassium sparing diuretics work?

A

inhibit sodium transport at late distal and collecting ducts

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41
Q

dihydropiridines vs. nondihydropyridines (CCB)

A

dihydropyridines have greater affinity for peripheral vasculature calcium channels (legs), while nondihydropyridines have affinity for both peripheral and cardiac calcium channels (not just legs)

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42
Q

DO’s and DONT’s of using nondihydropyridines (CCBs)

A

DONT use if EF is low; use for angina, Afib, HTN (blocks cardiac conduction through AV node, has vasodilating properties)

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43
Q

Which dihydropyridine (CCB) is safe for reduced EF?

A

Amlodipine

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44
Q

Verapamil

Diltliazem

A

Non-dihydropyridine (CCB)

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45
Q

Nifedipine

Amlodipine

A

dihydropyridine (CCB)

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46
Q

method of action ARBs?

A

block angiotensin II from binding to angiotensin receptor (RAAS)

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47
Q

Aliskren

A

Direct Renin Inhibitor (antihypertensive) - less common. MOA: directly inhibits renin

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48
Q

Doxazosin
Prazosin
Terazosin

A

Alpha-1 Antagonists (antihypertensive) - less common. MOA: add-on treatment, NOT monotherapy due to a risk for increase in cardiovascular events

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49
Q

Clonidine
Methyldopa
Guanfacine
Guanabenz

A

Alpha-2 agonists (antihypertensives) - less common. MOA: reduces sympathetic outflow, enhances parasympathetic activity

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50
Q

1st line medication for hypertension in PREGNANCY?

A

methyldopa - alpha 2 agonist. Labetalol ok too

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51
Q

Reserpine

A

peripheral sympathetic inhibitors. MOA: reduces sympathetic tone and peripheral resistance, depletes NE from nerve endings. (anti-hypertensive) - not tolerated well

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52
Q

isosorbide dinitrate/hydralazine
hydralazine
minoxidil

A

Direct Vasodilators (antihypertensive) - MOA: relaxes smooth muscle in arterioles, activates baroreceptors.

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53
Q

best time to prescribe direct vasodilators? (antihypertensive)

A

Resistant hypertension, but also ADD diuretics and BB (causes reflex tachycardia)

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54
Q

Blood pressure definition?

A

BP = CO x PVR
(CO: cardiac output)
PVR: peripheral vascular resistance

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55
Q

role of angiotensin II in Heart failure?

A

increases systemic vascular resistance, increasing BP. ALSO, potentiates release of NE, inducing vascular hypertrophy = cardiac remodeling

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56
Q

ACE-Inhibitor function?

A

blocks conversion of angiotensin I –> angiotensin II

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57
Q

ARB function?

A

blocks receptors of angiotensin II

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58
Q

CONTRAINDICATIONS for ACE-I/ARB?

A

pregnancy, renal artery stenosis (ACE can cause decline in renal function)

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59
Q

function of nitrates in HF?

A

venous dilation = reduced preload

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60
Q

function of hydralazine in HF?

A

direct arterial smooth muscle relaxation = reduce AFTERLOAD

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61
Q

Purpose of Beta Blockers in HF?

A

block influence of SNS (NE) at beta adrenergic receptors, improving EF and reducing hospitalizations

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62
Q

Do you give BB with volume overload?

A

NO! wait until euvolemic and initiate a low-dose

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63
Q

Aldosterone impact on HF? Why are aldosterone antagonists important for treating HF?

A

Aldosterone is responsible for sodium and water retention, electrolyte abnormalities. ALDOSTERONE ANTAGONISTS are important because ACE-I do not suppress production/release of aldosterone

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64
Q

Importance of antiplatelets (aspirin and warfarin) in Heart Failure?

A

Bad valves can cause stasis blood, endothelial dysfunction, hypercoagulability increasing risk of thromboembolic events

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65
Q

importance of Aspirin in HF?

A

reduces risk of stroke (embolism)

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66
Q

importance of anticoagulant in HF?

A

prevents blood clots, especially in LV dysfunction and prosthetic valves

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67
Q

Role of Digoxin in HF?

A

Positive inotropic effects = heart beats harder (increases intracellular Na by binding to Na and K pumps)
Restoration baroreceptor sensitivity
if AFib too, use to slow HR
DOES NOT decrease progression of HF, but has a role in decreasing hospitalizations due to HF

68
Q

Risks of Digoxin

A

high risk of toxicity; monitor electrolytes

69
Q

Heart failure with PRESERVED LVEF also known as?

A

diastolic HF - impaired ventricular relaxation and filling; EF not affected

70
Q

How to manage ACUTE heart failure episode?

A

FIRST: manage congestion and hypoperfusion:

congestion: IV diuretic (furosemide) & IV vasodilators (nitro)
hypoperfusion: positive inotropes to make heart beat faster (dobutamine)

71
Q

What are the 4 groups that need a statin?

A
  1. Established ASCVD
  2. LDL > 190
  3. Diabetic, age 40-70, LDL 70-189
  4. Nondiabetic, age 40-75, LDL 70-189, 10 year risk >7.5%
72
Q

What do statins do?

A

inhibit MHG-CoA reductase, responsible for cholesterol synthesis

73
Q

Atorvastatin
Fluvastatin
Lovastatin
Pravastatin

A

Statins

74
Q

Low intensity statins?

A

Lovastatin
Pravastatin
(10-20 mg)

75
Q

Moderate intensity statins

A

all of them…(40 mg)

reduces LDL by 30-50%

76
Q

high intensity statins

A

Atorvastatin
Rosuvastatin
(40-80 mg)
reduces LDL by 50%

77
Q

Adverse effects of statins

A

constipation, abdominal pain

Severe: myopathy, rhabdo, elevated liver function tests

78
Q

Treatment for hypercholesterolemia?

A

1st: LIFESTYLE TREATMENT

then statins

79
Q

If NOT using statin for high cholesterol, other options?

A 
Ezetimibe
PCSK9 inhibitor
Nicotinic Acid
Fibric acid derivatives
Omega 3 fatty acids
80
Q

MOA ezetimibe?

A

inhibit cholesterol absorption in small intestine and prevents delivery to liver. used post CV event.

81
Q

Alirocumab

Evolocumab

A

PCSK9 inhibitor : used in combo with statin. Binds to LDL receptor and prevents its degradation–> longer breakdown and excretion of LDL. NEW, so don’t be the first!

82
Q

Type of antihypertensive to use for resistant HTN?

A

Alpha-2 agonists

83
Q

How to D/C clonidine? (Alpha-2 agonist)

A

Avoid severe rebound HTN. Taper B.B. first, wait several days, and then taper clonidine

84
Q

What to do if INR >10?

A

Vitamin K! Takes 24 hours to see effects

85
Q

INR >4 , under 10 - what do you do?

A

Hold warfarin until therapeutic

86
Q

How long does warfarin take to be eliminated?

A

5-7 days

87
Q

fondaparinoux (indirect Xa inhibitor) MOA?

A

Accelerates antithrombin (binds to AT)

88
Q

Warfarin MOA? When to use?

A

Vitamin K antagonist

Treatment of VTE and stroke prevention in Afib

89
Q

How to dose warfarin

A

Start it in combo w/ heparin, because it’s effects take 5-7 days. D/C warfarin 5 days before surgery and restart 12-24 hours post-op

90
Q

Fondaparinoux MOA

A

SubQ; indirectly inhibits Xa in coagulation cascade - no effect against thrombin
Binds to Antithrombin

91
Q

Contraindications and cautions of Fondaparinoux

A

CrCl<30 (rental impairment)
Hypersensitivity, thrombocytopenia

CAUTION in elderly (bleeding)

92
Q

Apixaban and rivaroxaban MOA?

A

Inhibit Xa directly; bind reversible to Xa and prevent thrombus formation

93
Q

Things to know about direct Xa inhibitors

A

Shorter 1/2 life than warfarin, missed doses more serious, no labs to measure effectiveness, no antidotes

94
Q

Which anticoagulant to use with patient who has Heparin induced thrombocytopenia(HIT)?

A

Direct thrombin inhibitors

Bivalirudin, aragatroban

95
Q

Drug of choice for RAPID anticoagulation?

A

Infractioned heparin

96
Q

True or false: UFH dissolves a formed clot.

A

False! Prevents propagation and growth

97
Q

UFH is eliminated enzymatically in low doses and renally in high doses (true or false)

A

True

98
Q

What is HIT?

A

Heparin-induced thrombocytopenia- when platelets drop by >50%; discontinue UFH / LMWH immediately!!! Switch to direct thrombin inhibitors or fondaparinoux

99
Q

Dalteparin

Enoxaparin

A

LMWH

100
Q

LMWH MOA?

A

Prevent growth of formed thrombus, inhibits thrombin (factor IIa and factor Xa)

101
Q

Is LMWF safe in treating pregnancy?
Dalteparin
Enoxaparin

A

Yes- does not cross placenta

102
Q

Are nitrates done first at ER?

A

No- they relieve angina but they do not change outcomes

103
Q

Adverse effects of P2Y12 Inhibitors?

A

bleeding, TTP (thrombotic thrombocytopenic purpura) (clopidogrel), dyspnea, bradyarrhythmias

104
Q

How to dose P2Y12 inhibitors post-procedure

A

start immediately, continue for 2 weeks to 12 months

105
Q

What Antiplatelet do you Rx for patient with poor CYP2C19 metabolizers?

A

Prasugrel or Ticagrelor; Clopidogrel is converted to active form by CYP2C19, so won’t be as effective in these patients

106
Q

What do you do with antiplatelet meds for person who is having surgery?

A

WITHHOLD for 7 days to decrease chances of uncontrolled bleeding

107
Q

When to use GP lib/llla?

A

for antiplatelet therapy; specifically when P2Y12 inhibitor are not adequate OR in large thrombus burden - not recommended if patient is on fibrinolytics or bivalrudin (bleed risk)

108
Q

Role of thrombolytics?

A

break up life-threatening thrombus

109
Q

Types of Antiplatelets

A

Aspirin
Dipyridamole
P2Y12 Inhibitors
GP lib/llla receptor inhibitors

110
Q

Which drug is considered 1st line therapy in ACS?

A

fibrin-specific (Alteplase, Reteplase, Tenecteplase); opens greater percentage of infarcted arteries

111
Q

Contraindications for Fibrinolytics

A

for use in NSTE-ACS and if too much time has passed since the cardiac event

112
Q

Fibrinolytics in VTE?

A

Streptokinase, Urokinase, Alteplase - use for treatment in VTE ONLY IF shock, hypotension, massive DVT w/ limb gangrene

113
Q

If PCI is too far away, what do you do?

A

use fibrinolytics - FIRST LINE (fibrin-specific)

114
Q

HTN treatment >140/90 blacks?

A

Thiazide diuretic OR CCB

115
Q

HTN treatment >140/90 white/nonblack?

A

ACE-I/ARB (or thiazide/CCB)

116
Q

HTN treatment for >140/90 in patients with CKD

A

Add ACE-I/ARB, even in African Americans.

117
Q

Guidelines for starting TWO Hypertensive drugs?

A

systolic >20mmHg or diastolic >10mmHg

118
Q

What are the types of direct cardioversion? DCC

A

unstable (emergency- shock) and stable (medication)

sedate before electrical cardioversion

119
Q

When thinking Rate vs Rhythm control, which do we try and achieve first?

A

RATE! - be careful with amiodarone, works like K blocker, CCB, BB - last ditch effort

120
Q

When can you consider DCC?

A

w/ Afib lasting <48 hours

121
Q

When is Delayed cardioversion considered?

A

in patients with Afib >48 hours; MUST anticoagulate for 3 weeks PRIOR to conversion and continue for 4 weeks AFTER as well.

122
Q

Treatment for PCI (including time)

A

preferred treatment, within 90 min!

Dual antiplatelet therapy: ASA + P2Y12, anticoagulate w/ UFH

123
Q

Treatment for Fibrinolysis

A

within 30 min! do if PCI not available. Dual antiplatelet therapy (ASA + clopidogrel P2Y12), and Anticoagulate with IV UFH

124
Q

Two factors to address in acute heart failure episode

A

congestion and hypoperfusion, use

IV diuretics, IV vasodilators, Dobutamine (positive inotropes)

125
Q

Purpose of amiodarone

A

treat Afib and ventricular arrhythmias

126
Q

Factors that describe stage B HF

A

Previous MI, LV remodeling, low EF, valvular disease (but no symptoms)

Treat w/ ACEI + BB

127
Q

Factors describing stage A HF

A

risk factors: HTN, smoking, lipids, DM, lack of exercise

Treat w/ ACEI

128
Q

Stage C HF

A

Symptoms! DOE, edema, SOB, fatigue

Treat w/ ACEI, BB, Diuretic

129
Q

ACE-I and renal function

A

ACE-I can cause renal insufficiency, and is CONTRAINDICATED in bilateral renal stenosis, however it can be beneficial chronically

130
Q

Nitrates reduce _______ and hydralazine reduces ___________

A

preload, afterload

131
Q

when do you initiate beta blockers in HF?

A

wait until patient is euvolemically stable (volume overload + BB = worsening effects)

132
Q

When to use nondihydropyridines vs dihydropyridines

A

nondihydros - angina and AFib

dihydros - peripheral vasodilation

133
Q

in acute HF exacerbation, we give IV diuretics, IV vasodilators, and IV positive inotropes (dobutamine)…why?

A

IV dobutamine - increases cardiac contractility, makes heart pump harder
IV vasodilators - rapidly decreases arterial tone
IV diuretics - decrease blood volume/fluid

134
Q

CCB Method of Action?

A

Relaxes arterioles by blocking calcium from entering cell

135
Q

True or False: Rechallenging statins in those who experience rhabdomyolysis is okay, but wait 2-4 weeks

A

FALSE! If patient has rhabdo from a statin, DO NOT rechallenge that same one! In other cases, where patient simply does not tolerate, re-challenging is ok, but wait 2-4 weeks.

136
Q

Safest CCB to use in reduced EF?

A

Amlodipine

137
Q

Why do we take a baseline CK when prescribing statins?

A

Need to have a baseline INCASE patients complain of myopathy, muscle pain, weakness, brown urine (signs of rhabdo)

138
Q

True or False: Rechallenging statins in those who experience rhabdomyolysis is okay, but wait 3-4 weeks

A

FALSE! If patient has rhabdo from a statin, DO NOT rechallenge that same one! In other cases, where patient simply does not tolerate, re-challenging is ok.

139
Q

Statins metabolized by which enzyme?

A

CYP450s

140
Q

Quinidine
Procainamide
Disopyramide

A

Class 1A Na channel blockers (antiarrhythmic class)

-intermediate potency

141
Q

Lidocaine

Mexilitine

A

Class 1B Na channel blockers (antiarrhythmics)

-lowest potency

142
Q

Flecainide

Propafenone

A

Class 1C Na channel blockers (antiarrhythmics

-greatest potency

143
Q

Class 2 antiarrhythmics?

A

Beta Blockers

144
Q

Class 3 antiarrhythmics?

A

Potassium channel blockers

Amiodarone
Dofetilide
Dronedarone
Ibutilide
Sotolol
145
Q

which anticoagulants bind the Von Willebrand factor in the coagulation cascade?

A

heparin

146
Q

Adenosine MOA

A

Direct AV node inhibition; drug of choice for PSVT

147
Q

Uses for anticoagulation

A

Prevention of stroke, VTE, thrombus formation (Afib, procedures), thromboembolism (PE)

148
Q

Types of Anticoagulants

A 
Warfarin
Xa Inhibitors
Direct Thrombin inhibitors
Heparin
LMWH
149
Q

What is the importance of aPPT in UFH dosing?

A

adjust dose based on the aPPT; should be 1.5-2.5x control aPPT value

150
Q

What do you do if there is HIT or thrombosis while patient is on UFH?

A

D/C immediately and switch to direct thrombin inhibitors OR Fondaparinoux

151
Q

Dalteparin

Enoxaparin

A

LMWH

152
Q

Which anticoagulants have antidotes, and what are they?

A

Protamine –> LMWH
Vit K –> warfarin
Praxbind –> direct thrombin inhibitors

153
Q

which antiarrhythmics are IV form?

A

Class 1A and 1B Na channel blockers

154
Q

Which antiarrhythmics are PO?

A

Class 1C Na channel blockers

155
Q

Where in conduction system do BB affect rhythm?

A

Blocks conduction at AV node

156
Q

does Amiodarone have a long or short 1/2 life?

A

EXTREMELY long (antiarrhythmic)

157
Q

common side effects and severe side effects of Amiodarone

A

hypotension, sinus bradycardia (acts like all classes of antiarrhythmics)

pulm toxicity, hepatotoxicity, hypo/hyperthyroidism, exacerbated arrhythmias

158
Q

Which antiarrhythmics slow conduction at AV node?

A

BB and CCB (class 2 and 4)

159
Q

Why are we cautious with verapamil + digoxin?

A

verapamil (CCB) can mess with concentration of digoxin (digoxin has low therapeutic index, so small changes can cause large effects)

160
Q

Which antiarrhythmic causes DIRECT AV nodal inhibition?

A

Adenosine

161
Q

Which antiarrhythmic drug is 1st line choice in treating PSVT?

A

Adenosine

162
Q

How can you tell if your patient has digoxin toxicity?

A

CNS effects(psychosis confusion), GI effects (nausea, vomiting), Visual disturbances (green halos around objects), new cardiac arrhythmias

163
Q

How to monitor for digoxin toxicity

A

Look for HypoK, HypoMg

164
Q

which drugs provide 24 hour protection for angina?

A

BB and CCB

165
Q

door-to-needle time for Alteplase in stroke?

A

60 minutes

Pharmacology Exam 2 (1 decks)

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