Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Antihypertensives > Flashcards

Antihypertensives Flashcards

0
Q

ACE inhibitors mechanism

A

No reflex tachycardia, etc.
Decreased sodium and H2O retention
Increased renin
Increased bradykinin (potent vasodilator)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

ACE inhibitor drugs

A

Captopril
Enalapril
Lisinopril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ACE inhibitors Description

A

Decrease PVR therefore decrease BP

  • *Decrease diabetic nephropathy**
  • *Decrease albuminuria**
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ACE inhibitors indications

A

HTN-must effective in young white patients (black and elderly have low renin … add a diuretic)

CHF

DOC patients s/p MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ACE inhibitors Adverse

A

Hyperkalemia
Dry cough
Rash, fever, altered taste, hypotension
Angioedema (supervise first dose)*
Acute renal failure in patients with BILATERAL RENAL ARTERIAL STENOSIS
Decreased vasoconstriction on efferent therefore decreased GFR, elevated creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ACE inhibitor contraindications

A

Pregnancy–fetal hypotension leading to renal agenesis and anuria
Hyperkalemia
Bilateral renal a. stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Angiotensin receptor blockers (ARB) Drugs

A

Losartan

Valsartan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Angiotensin receptor blockers description

A

Alternative to ACE - I

Blocks the ATII receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Angiotensin receptor blockers mechanism

A

Very similar to ACE-I
Decreased PVR decreased BP
Decreased nephrotoxicity
No effect on bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Angiotensin receptor blockers Indication

A

HTN (white people)
CHF
s/p MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Angiotensin receptor blockers adverse effects

A

Similar to ACE-I

Angio edema risk is much lower (related to bradykinin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Angiotensin receptor blocker contraindications

A

Pregnancy - fetal hypotension, renal failure, anuria
Hyperkalemia
Bilateral renal a. stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Renin inhibitor drugs

A

Aliskiren

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Renin inhibitor mechanism

A

Inhibits production of both ATII and aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Aliskiren contraindications

A

Pregnancy
Bilateral renal a. stenosis
Hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Calcium channel blocker drugs

A

Verapamil
Diltiazem
Nifedipine
Amlodipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Verapamil Description

A

Calcium channel blocker
Non dihydropyridine
Least selective
Cardiac and vascular smooth muscle effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Verapamil mechanism

A

Bind to L type calcium channels in the heart and muscle of the peripheral vasculature ->decreased calcium entry -> relaxation of muscle -> -ve inotropism and/or vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Verapamil indication

A

Used in patients with angina, migraine or SVT
Used when first line agents are ineffective or contraindicated (patients with diabetes, asthma and PVD)
Effective in blacks and whites
Intrinsic natriuretic effect -> no need to add a diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Verapamil adverse

A

High dose of short acting -> increased risk for MI

  • *Reflex tachycardia**
  • Constipation*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Verapamil contraindication

A

**CHF due to -ve inotropic effects **

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Diltiazem description

A

Calcium channel blocker
Non dihydropyridine
A little more selective for vasculature than verapamil but still affects heart
Good side effect profile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Diltiazem mechanism

A

Bind to L type calcium channels in the heart and muscle of the peripheral vasculature -> decreased calcium entry -> relaxation of muscle -> -ve inotropic effects and/or vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Diltiazem indication

A

Pts with angina, migraine or SVT
Used when first line agents are ineffective or contraindicated (diabetes, asthma and PVD)
Effective in blacks and whites
Intrinsic natriuretic effect -> no need to add a diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Diltiazem Adverse

A

High dose short acting increases risk of MI

Reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Nifedipine and Amlodipine description

A

Dihydropyridines
Act only on smooth vascular muscle
Second gen amlodipine has little interaction with digoxin and warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Nifedipine and amlodipine mechanism

A

Calcium channel blockers
Greater affinity for vasculature so they don’t cause a decrease in CO
Very useful for HTN but not arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Nifedipine and amlodipine indication

A

Used when first line agents are ineffective or contraindicated (diabetes, asthma, PVD)
Effective in blacks and whites
Intrinsic natriuretic effect -> no need to add a diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Nifedipine and Amlodipine Adverse

A

Hypotension -> dizziness, HA, fatigue, peripheral edema
Bradycardia
Heart block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Thiazides drugs

A

Chlorthalidone
Hydrochlorothiazide
Metolazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Thiazide indications

A

DOC for black and elderly (with normal renal and cardiac function)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Thiazide Mechanism

A

Increased sodium and H2O excretion therefore decreased ECF -> decreased CO and renal blood flow (in the long term, there is normal plasma volume but decreased PVR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Thiazide adverse

A 
**Hypokalemia**
Hyperuricemia
Hyperglycemia
Hypomagnesium
Hyperlipidemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Thiazide contraindications

A

Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Loop Diuretics

A

Ethacrynic acid
Furosemide
Torsemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Loop diuretics description

A

Prompt action in pts with poor renal function or heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Loop diuretic mechanism

A

decreased renal vascular resistance

increased renal blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Loop diuretics indication

A

DOC for pts with poor renal function or unresponsive to other diuretics ex. thiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Amiloride and Triamterene

A

ENaC

Decrease the potassium lost in urine caused by thiazide or loop diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Disopyramide description

Antiarrhythmic

A 
Class 1A
Stronger -ve inotrope than quinidine and procainamide
Strong antimuscarinic properties
Causes peripheral vasoconstriction
Blocks K channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Disopyramide indication

Antiarrhythmic

A

Supraventricular and ventricular arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Disopyramide adverse

Antiarrhythmic

A

Pronounced -ve inotropic effects
Cardiac failure without preexisting myocardial dysfunction
Severe antitmuscarinic effects (dry mouth, urine retention, blurred vision, constipation, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Class 1 A general

Antiarrhythmic

A

Sodium channel blockers
Never drug of choice
Ventricular and Supraventricular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Class 1A effect

Antiarrhythmic

A

Slow phase 0 depolarization (sodium channels)
Also prolongs phase 3 (potassium channels)

Slowing of conduction, prolonging AP & increase ventricular effective refractory period

Intermediate speed of association with activated and inactivated Na channels -> affects normal healthy tissue too

Procainamide, Disopyramide, and Quinidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Class 1 B general

Antiarrhythmic

A

Sodium channel blocker

Ventricular only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Class 1 B effect

Antiarrhythmic

A

Slows phase 0 and decreases slope of phase 4
Minimally shortens phase 3 repolarization (no clinical effect)
Little effect of depolarization in normal cells
Rapid association/dissociation with sodium channels

Used primarily in ventricular arrhythmia (atria is too fast)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Tocainide adverse

Antiarrhythmic

A

Severe hematological and pulmonary toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Mexiletine adverse

Antiarrhythmic

A

Mainly CNS and GI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Lidocaine is drug of choice when?

Antiarrhythmic

A

DOC for V tach and V fib after cardioversion in acute ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Lidocaine toxic dose produces

Antiarrhythmic

A

Convulsions and coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Class 1 C general

Antiarrhythmic

A

Sodium channel blocker

Ventricular and supraventricular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Class 1C effect

Antiarrhythmic

A

Markedly depress phase 0 of AP, no change in repolarization (K)
Slowing of conduction of AP, but little effect on duration or ventricular effective refractory period

Associate and re-associates slowly with sodium channels -> prominent effects even in normal cells
***Most likely of class 1s to cause arrhythmia***
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Propafenone description

Antiarrhythmic

A

Class 1C
Decreases slope of phase 0 without affecting duration of AP

Prolongs conduction and refractoriness in all areas of the myocardium

Reduces spontaneous automaticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Propafenone indication

Antiarrhythmic

A

Life threatening ventricular arrhythmia and maintenance of normal sinus rhythm in patients with symptomatic a fib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Class II mechanism

Antiarrhythmic

A

Beta blockers

Supraventricular only

56
Q

Class II effect

Antiarrhythmic

A

Reduce HR and myocardial contractility (beta 1)

Prolongs repolarization at AV node and decreased slope of phase 4 (blocking adrenergic release) -> slows conduction of impulses through the myocardial conduction

Reduce rate of spontaneous depolarization in cells with pacemaker activity
Little effect on AP in most myocardial cells

57
Q

Class III mechanism

Antiarrhythmic

A

K channel blockers

Ventricular and supraventricular

58
Q

Class III effect

Antiarrhythmic

A 
Blocks repolarizing K channels
Prolongs AP (and QT interval) without altering phase 0 or resting membrane potential 
Prolongs effective refractory period

ALL have potential to induce arrhythmia

59
Q

Amiodarone adverse main

Antiarrhythmic

A

Interstitial pulmonary fibrosis

Blue / gray skin discoloration due to iodine accumulation

60
Q

Amiodarone contraindications

Antiarrhythmic

A

Patients taking digoxin, theophylline, warfarin, quinidine or have bradycardia, SA or AV block, severe hypotension, or respiratory failure

61
Q

Dofetilide

Antiarrhythmic

A

Potent and pure K channel blocker

Class III

62
Q

Dofetilide indication

Antiarrhythmic

A

Maintaining or conversion to norma sinus rhythm in chronic a fib / flutter

63
Q

Dofetilide Adverse

Antiarrhythmic

A

HA, chest pain, dizziness, v tach, Torsades (prolongs QT interval)

64
Q

Class IV mechanism

Antiarrhythmic

A

Calcium channel blockers

Supraventricular only

65
Q

Class IV effect

Antiarrhythmic

A

Blocks L type calcium channels
Decrease inward calcium current -> decrease rate of phase 4 spontaneous depolarization
Slows conduction in SA and AV nodes
Major effects on vascular smooth muscles and heart

Use primarily for supraventricular arrhythmia

66
Q

Digoxin description

Antiarrhythmic

A

Shorten refractory period in atrial and ventricular myocardial cells

Prolongs effective refractory period and diminishes conduction velocity in AV node

67
Q

Digoxin Indication

Antiarrhythmic

A

Control ventricular response rate in A fib and flutter with impaired left ventricular function or heart failure

Mechanism of action
Heart failure- +ve inotrope -> increases intracellular calcium
Arrhythmia - Direct AV node blocking effects (inhibits calcium currents) and vagomimetic properties (activates ACh mediated K currents in the atrium)

Major indirect actions
Hyperpolarization, shorten atrial APs, increase AV node refractoriness -> decrease fraction of impulses that are conducted through the node

68
Q

Digoxin adverse

Antiarrhythmic

A

Toxic dose -> ectopic ventricular beats (v tach and V fib)

69
Q

Adenosine description

Antiarrhythmic

A

Naturally occurring nucleoside (P1r agonist)

High dose: Decrease conduction velocity and prolongs refractory period as well as decreases automaticity in AV node

70
Q

Adenosine indication

Antiarrhythmic

A

DOC for abolishing acute SVT (emergency situations)
Lidocaine is used in acute V tach emergencies

Mechanism of action
Enhanced K conductance; decrease cAMP mediated Calcium influx -> hyperpolarization, especially in the AV node

71
Q

Adenosine PK

Antiarrhythmic

A

half life 15 sec

72
Q

Adenosine adverse

Antiarrhythmic

A

Low toxicity - Flushing, burning, chest pain (similar to MI, hypotension)

Bronchoconstriction in asthmatics (may last up to 30 mins)

73
Q

Magnesium description

Antiarrhythmic

A

Functional calcium antagonist

74
Q

Magnesium indication

Antiarrhythmic

A

Torsades de pointes (prolonged QT interval)
Digitalis induced arrhythmia (lidocaine also used)
Prophylaxis of arrhythmia in acute MI

75
Q

Atropine indication

Antiarrhythmic

A

Used in bradyarrhythmia to decrease vagal tone -> increased HR

76
Q

Rhythm control

Antiarrhythmic

A 
Restore and maintain sinus rhythm -> generally involves drugs acting on the AV node to slow conduction
Class IC (flecainide and propfenone) and Class III (amiodarone and dofetilide)
77
Q

Rate Control

Antiarrhythmic

A

Control ventricular rate while allowing atrial fibrillation to continue
-ve dromotropic agents to slow conduction in the AV node

Calcium channel blockers, Beta blockers, digoxin

78
Q 
In the treatment of hypertension, a reduction in cardiac output is most likely to result in the development of which of the following?
Chronic cough
Periorbital edema
Peripheral edema
Peripheral neuropathy
Type 2 Diabetes
A

Peripheral edema

79
Q

A reduction in body fluid volume is most likely to result in the development of what?

A

Reflex tachycardia

80
Q 
One of the potential consequences of reducing blood pressure is increasing renin activity.  Which of the following agents affects the renin-angiotensin process in the body?
Atenolol
Captopril
Minoxidil
Nifedipine
Verapamil
81
Q

Spironolactone

Eplerenone

A

Aldosterone antagonist -> inhibition of Na+ and H2O retention -> inhibition of vasoconstriction
Decreased cardiac remodeling
1st line in patients with HTN and severe LV dysfunction
-reduced K+ excretion-> risk of hyperkalemia

82
Q

Atenolol & Metoprolol mechanism

A

Beta 1 selective
Decreased CO, contractility and HR
Decreased CNS sympathetic output (especially with exercise)
Decreased NE and renin (Beta1) -> decreased ATII and aldosterone

83
Q

Atenolol & Metoprolol, Propanolol, Pindolol indication

A

More effective in young/white patient

DOC only for patients with CAD or left ventricular dysfunction and HTN

84
Q

Atenolol & Metoprolol, Propranolol, Pindolol PK

A

May take weeks to develop full effects

85
Q

Atenolol, Metoprolol, Propranolol, Pindolol Adverse

A

Bradycardia, CNS effects, hypotension, impotence, lipid disturbance (decreased HDL, increased TAG), hypoglycemia
Abrupt withdrawal -> angina and MI in patients with heart disease

86
Q

Propranolol contraindication

A

Asthma and COPD, sinus bradycardia

87
Q

Pindolol, Propranolol, Atenolol, Metoprolol Contraindication

A

Sinus bradycardia, mask symptoms of hypoglycemia (diabetics)

88
Q

Pindolol indication

A

B partial agonist

Preferred beta blocker in pregnancy

89
Q

Doxazosin, Prazosin, Terazosin Class

A

alpha blockers

90
Q

Alpha blocker drugs for HTN

A

Doxazosin, Prazosin, Terazosin

91
Q

Doxazosin, Prazosin, Terazosin Mechanism

A

Alpha blockers
Decreased PVR and MAP by relaxation of arterial and venous smooth muscle

Minimal change in CO, renal blood flow and GFR -> no long term tachycardia

92
Q

Doxazosin, Prazosin, Terazosin Description

A

Competitive inhibition of alpha one receptors

Sodium and Water retention-> usually give with a diuretic

93
Q

Doxazosin, Prazosin, Terazosin Indication

A

Alpha blocker
Mild to moderate HTN in combination with propranolol or a diuretic (less common now due to adverse effects)

BPH

94
Q

Doxazosin, Prazosin, Terazosin Adverse

A

**Reflex tachycardia and orthostatic hypotension may be seen with first dose, but not long term (alpha 2 blocks response by inhibiting NE) -> ameliorate with beta blocker

Dizziness, drowsiness, HA, fatigue, nausea, palpitations

95
Q

Doxazosin contraindications

A

Has been shown to increase rate of CHF

96
Q

Labetalol class

A

mixed alpha beta blocker

97
Q

Labetalol description

A

NO reflex tachycardia or increased CO (beta 1 effect is greater)
Safe in PREGNANCY

98
Q

Labetalol indication

A

long term treatment of HTN

HTN emergencies: IV admin-> rapid drop in BP

99
Q

Labetalol Adverse effects

A

Orthostatic hypotension

100
Q

Labetalol contraindication

A

Pheochromocytoma

101
Q

Clonidine & methyldopa class

A

central acting alpha 2 agonist

102
Q

Central acting alpha 2 agonist description

Clonidine & Methyldopa

A

Does not decrease renal blood flow or GFR

103
Q

Clonidine mechanism

A

Decreases sympathetic outflow (NE) by acting on presynaptic auto receptors -> decreases PVR and CO -> decreases BP

104
Q

Clonidine PK

A

Oral; well absorbed. Administer with diuretic (sodium and water retention)

105
Q

Clonidine adverse

A

Sedation, dry mouth, dizziness, HA, sexual dysfunction are common
Rebound HTN after abrupt withdrawal

106
Q

Methyldopa mechanism

A

Decreased sympathetic outflow -> decreased PVR and BP

CO not affected

107
Q

Methyldopa indication

A

DOC Pregnancy induced HTN

Renal insufficiency

108
Q

Methyldopa PK

A

Oral; well absorbed

Administer with diuretic

109
Q

Methyldopa adverse

A

Sedation, dry mouth, dizziness, HA, sexual dysfunction are common
Rebound HTN after abrupt withdrawal

110
Q

Methyldopa contraindication

A

Can cause positive Coombs test, hemolytic anemia, hepatitis

111
Q

Hydralazine class

A

Direct vasodilator

112
Q

Hydralazine description

A

Never 1st line treatment
Direct acting smooth muscle relaxant
Reflex tachycardia, increased plasma renin ->Sodium and water retention
(coadmin with a diuretic and betablocker)

113
Q

Hydralazine Mechanism

A

Opening of Potassium channels in smooth muscle -> arteriolar dilation (NOT venous)

114
Q

Hydralazine Indication

A

DOC pregnancy induced hypertensive emergencies related to eclampsia

115
Q

Hydralazine PK

A

Oral or IV

116
Q

Hydralazine Adverse

A

HA, tachycardia, nausea, sweating, flushing
Lupus like syndrome
Reflex tachycardia and fluid retention
Volume overload -> edema and CHF

117
Q

Minoxidil (Rogaine) class

A

direct vasodilator

118
Q

Minoxidil (Rogaine) description

A

Never 1st line treatment
Direct acting smooth muscle relaxant
Reflex tachycardia, increased plasma renin ->Sodium and water retention
(coadmin with a diuretic and betablocker)

119
Q

Minoxidil (Rogaine) mechanism

A

Opening of Potassium channels in smooth muscle -> arteriolar dilation (NOT venous)

120
Q

Minoxidil (Rogaine) Indication

A

Severe malignant HTN

Male pattern baldness (hypertrichosis)

121
Q

Minoxidil (Rogaine) Adverse

A

HA, tachycardia, nausea, sweating, flushing
Reflex tachycardia and fluid retention
Volume overload -> edema and CHF

122
Q

Bosentan class

A

Non selective endothelin receptor blocker

123
Q

Bosentan description

A

Blocks the endothelin mediated (ETa and ETb) vasoconstriction

124
Q

Bosentan contraindications

A

PREGNANCY CATEGORY X

125
Q

Epoprostenol description

A

synthetic PGI2

126
Q

Epoprostenol mechanism

A

Lowers peripheral, pulmonary and coronary resistance

127
Q

Bosentan indication

A

Pulmonary HTN

128
Q

Epoprostenol indication

A

Pulmonary HTN

129
Q

Epoprostenol PK

A

continuous IV infusion

130
Q

Epoprostenol Adverse

A

Flushing, HA, JAW PAIN, diarrhea, arthralgia

131
Q

Typical 1st line treatment

A

ACE-I’s ARB’s

132
Q

1st line in patients with acute or chronic CAD

A

ACE-I’s, or ARB’s and add Beta blocker

133
Q

Patients with LV dysfunction first line treatment

A

Thiazide or loop diuretic and beta blocker along with ACE-I or ARB (plus hydralazine and isosorbide dinitrate if black)

134
Q

HTN treatment for MI patients

A

Begin on beta blocker before adding ACE-I or ARB

135
Q

HTN treatment for patients who have a history of ischemic stroke

A

Get an ACE-I or ARB and a thiazide diuretic

Pharmacology (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions