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Pharmacology > Anti-Hypertensive > Flashcards

Anti-Hypertensive Flashcards

1
Q

Cardiovascular mortality risk doubles with each what BP increment?

A

20/10mmHG

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2
Q

What is hypertension?

A

> 130/>80

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3
Q

CO=

A

SV X HR

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4
Q

SV=

A

EDV-ESV

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5
Q

BP=

A

CO X SVR

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6
Q

Rationale for reducing CO?

A

Reduce blood volume
Reduce HR
Reduce SV

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7
Q

Rationale for reducing SVR?

A

Dilate systemic vasculature

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8
Q

5 anatomical site of BP control:

A
  1. Resistance arterioles
  2. Capacitance venules
  3. Pump output heart
  4. Volume kidneys
  5. CNS- sympathetic nerves
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9
Q

4 Renin angiotensin aldosterone system (RAAS) antagonists

A
  1. Angiotensin-converting enzyme (ACE) inhibitors
  2. Angiotensin II receptor blocker (ARBs)
  3. Neprilysin inhibitor plus ARBs
  4. Aldosterone antagonists (Potassium sparing diuretics)
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10
Q

Pathway for renin angiotensin aldosterone system (RAAS)

A 
Angiotensinogen (liver)
Angiotensin I from renin (kidney)
Angiotensin II from ACE (lungs)
Arteriole vasoconstriction and adrenal cortex 
Aldosterone 
Sodium retention
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11
Q

What does ACE inhibit

A

Angiotensin I and bradykinin

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12
Q

5 common clinical uses for ACE inhibitors

A
  1. Heart failure
  2. CAD
  3. HTN
  4. Chronic renal disease with proteinuria
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13
Q

5 adverse effects from ACE inhibitors

A
  1. Increase serum potassium
  2. Acute renal failure
  3. Pregnancy
  4. Dry cough and angioedema (rare)
  5. Hypotension in patients with volume and/or salt depletion
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14
Q

What does ACE inhibitors drug name end with?

A

“pril”

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15
Q

What does ARBs inhibit?

A

Angiotensin II attaching to the receptors to allow for vasoconstriction and aldosterone secretion

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16
Q

4 common clinical uses for ARBs

A
  1. Heart failure
  2. CAD
  3. HTN
  4. Chronic kidney disease with proteinuria
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17
Q

When is ARBs most common used?

A

As an alternative to ACE inhibitors when patients develop dry cough

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18
Q

4 adverse effects for ARBs

A
  1. Increase serum potassium
  2. Acute renal failure
  3. Pregnancy
  4. Hypotension in patients with volume and/or salt depletion
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19
Q

What does ARBs dug name end in?

A

“sartan”

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20
Q

What does neprilysin inhibitor plus ARBs inhibit?

A

Block break down of peptides (valsartan and LBQ675)

Block angiotensin II connecting to it’s receptors

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21
Q

Common clinical uses for neprilysin inhibitor plus ARB

A

Heart failure

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22
Q

5 Adverse effects of neprilysin inhibitor plus ARB

A 
Hyperkalemia 
Cough 
Angioedema 
Renal function deterioration 
Hypotension
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23
Q

3 Contraindications for neprilysin inhibitor plus ARB

A

36 hours of ACE inhibitors (angioedema)
Pregnancy
Bilateral renal artery stenosis

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24
Q

What does direct renin inhibitor (DRI) inhibit?

A

Renin

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25
Q

Clinical uses for DRI

A

HTN

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26
Q

What is DRI available to be in combo with?

A

Amlodipine + HCTZ

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27
Q

What is the is the drug name for DRI?

A

Aliskiren (tekturna)

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28
Q

5 Adverse effects for DRI

A 
Hyperkalemia 
Angioedema 
Renal function deterioration 
Diarrhea 
Hypotension in patients with volume and/or salt depletion
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29
Q

2 Contraindications for DRI

A

Aliskiren with ARBs or ACEIs in patients with DM

Pregnancy

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30
Q

Risk of hyperkalemia and renal impairment elevates when DRI is used with what in DM patients?

A

ARBs and ACEIs

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31
Q

Aldosterone antagonists inhibit what?

A

Sodium and water retention

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32
Q

What 2 drugs are aldosterone antagonists

A

Spironolactone

Eplerenone

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33
Q

How does aldosterone antagonists increase BP?

A

Induce sodium and water retention

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34
Q

4 clinical uses for aldosterone antagonists

A

Hyperaldosteronism
Resistant HTN
Heart failure
MI with LV dysfunction

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35
Q

3 Adverse effects for aldosterone antagonists

A

Renal dysfunction
Hyperkalemia
Endocrine abnormalities

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36
Q

What can aldosterone antagonists cause?

A

Myocardial, renal, and vascular fibrosis

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37
Q

Contraindication for aldosterone antagonists

A
  1. SCr >2.5 (men) >2 (women)

2. Potassium >5

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38
Q

2 mechanism of actions for diuretics (decrease BP)

A
  1. Depleting body of sodium and H2O

2. Reducing blood volume (decrease SV)

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39
Q

6 types of diuretics

A
  1. Loop diuretics
  2. Thiazide diuretics
  3. Potassium sparing diuretics
  4. Osmotic diuretics
  5. Carbonic anhydrase inhibitors
  6. Vasopressin (ADH) antagonists
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40
Q

3 uses for loop diuretics

A
  1. Edematous
  2. Hyperkalemia
  3. HTN (2nd line)
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41
Q

7 Adverse effects for loop diuretics

A
  1. Na/volume depletion
  2. Hypokalemia
  3. Hypocalcemia
  4. Hypomagnesemia
  5. Metabolic alkalosis
  6. Hyperuricemia
  7. Ototoxicity
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42
Q

4 thiazides

A

Hydrochlorothiazide
Chlorthalidone
Indapamide
Metolazone

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43
Q

Is thiazide 1st or 2nd line to treat HTN?

A

First line

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44
Q

Is thiazide more or less potent than loops?

A

Less potent

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45
Q

8 adverse effects of thiazide

A
  1. Hypovolemia
  2. Hypokalemia
  3. Hypoatremia
  4. Hypochloremia
  5. Hypomagnesemia
  6. Hyperkalemia
  7. Hyperuricemia
  8. Metabolic alkalosis
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46
Q

2 different potassium sparing diuretics

A

Sodium channel blockers

Aldosterone receptor antagonists

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47
Q

Are potassium sparing diuretics weak or strong diuretics

A

Weak

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48
Q

What is the adverse effect for potassium sparing diuretics?

A

Hyperkalemia

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49
Q

What do central anti-adrenergics target?

A

Adrenergic neurons in CNS

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50
Q

What does central anti-adrenergics prevent?

A

Releasing of catecholamines

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51
Q

How is central anti-adrenergics controlled?

A

Negative feedback inhibition (alpha 2= inhibit NE release)

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52
Q

Where on the brain is the inhibitory effect on NE located at?

A

Prefrontal cortex

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53
Q

What drug is a central anti-adrenergic (alpha2 agonists)

A

Clonidine

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54
Q

What 4 things specifically lower BP in central anti-adrenergics?

A
  1. Lower venous return
  2. Lower TPR
  3. Lower HR
  4. Lower SV
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55
Q

What does methyldopa get converted into?

A

Methylnorepinephrine

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56
Q

What does methylnorepinephrine do when released?

A

NOT activate adrenergic receptors

CAN act on the alpha2 receptors (further inhibit NE release)

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57
Q

What is a big adverse effect of central anti-adrenergic?

A

Rebound HTN with withdrawal

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58
Q

4 clinical uses of central anti-adrenergic

A
  1. HTN (NOT 1st line and resistant HTN)
  2. ADHD
  3. HTN in pregnancy
  4. Treatment of withdrawal
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59
Q

2 non-selective alpha antagonists

A

Phenoxybenzamine

Phentolamine

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60
Q

What is phenoxybenzamine?

A

Irreversible, non-competitive antagonist

61
Q

What is phentolamine?

A

Reversible, competitive antagonist

62
Q

How are phenoxybenzamine and phentolamine treated?

A

Pheochromocytoma

63
Q

When is phentolamine used?

A

HTN crisis

64
Q

4 adverse effects of nonselective alpha antagonists

A
  1. Reflex tachycardia
  2. Postural hypotension
  3. Cardiac arrhythmias
  4. Ischemic cardiac events
65
Q

Adverse effect of phentolamine?

A

Stimulates GI SM and enhance gastric acid secretion

66
Q

Adverse effects of phenoxybenzamine?

A

Mutagenic

67
Q

What does alpha1 antagonists do?

A

Inhibit binding of NE to Postsynaptic alpha1 receptors

68
Q

What does alpha1 antagonists cause?

A

Relax SM

Decrease PVR and venous return

69
Q

Clinical use of selective alpha1 antagonists

A

HTN (not 1st line)

70
Q

5 adverse effects of selective alpha1 antagonists

A
  1. Postural hypotension
  2. Syncope
  3. Fluid retention
  4. Nasal congestion
  5. Drowsiness
71
Q

What is 1st does phenomenon

A

Faintness and/or syncope within 30min-6hrs after initial dose
Use low initial dose at bedtime
Titrate slowly

72
Q

What 3 locations at beta1 receptors?

A

Heart
SA and AV node
Kidneys

73
Q

What 3 locations are beta2 receptor

A

Lungs
Vascular SM
Liver/pancreas

74
Q

Beta1 blockade cause?

A

Decrease HR
Decrease contractility
Decrease renin release

75
Q

Beta2 blockade cause?

A

Bronchoconstriction
Decrease insulin secretion
Vasoconstriction

76
Q

Theorized effect on beta-blockers

A

Inhibit release of NT and decrease sympathetic activity

77
Q

Beta1 selectivity for heart

A

Bradycardia
Negative inotropy
Decrease BP

78
Q

Beta1 selective on lungs

A

Less bronchospasm

79
Q

Beta1 selectivity with peripheral effects

A

Metabolic effects

Circulatory

80
Q

2 effects on non-selective beta1 and beta2

A
  1. Similar cardiac and antiHTN effects

2. More pulmonary and peripheral effects

81
Q

What does beta blocker drugs name end in?

A

“olol”

82
Q

5 beta blocking effects

A
  1. Negative chronotropic
  2. Negative dromotropic
  3. Anti-arrhythmic
  4. Negative inotropic
  5. Anti-ischemic
83
Q

3 non-vasodilation BB hemodynamics:

A
  1. Acute decrease in CO ~20% with compensatory reflex rise in SVR
  2. SVR returns to baseline
  3. BP lowers chronically from decreased HR and CO
84
Q

Are BB first line antiHTN?

A

NO

85
Q

Why aren’t BB 1st line antiHTN? (3)

A
  1. Other drugs have better CV protection
  2. Lowers brachial BP but not central BP
  3. Mortality may be higher with atenolol
86
Q

What does vasodilation BB BP reduction come from?

A

Decreased HR and SVR

87
Q

4 BB contraindications

A
  1. Bradycardia
  2. Severe asthma or bronchospasm
  3. Severe depression
  4. Cardiogenic shock or hypotension
88
Q

6 BB adverse effects

A
  1. Smooth muscle spasm
  2. Exaggeration of the cardiac therapeutic actions
  3. CNS penetration
  4. Worsened quality of life
  5. Adverse metabolic side effects
  6. Withdrawal phenomenon
89
Q

3 main clinical uses for BB

A
  1. Ischemic heart disease (chronic stable angina and acute coronary syndrome)
  2. Heart failure with reduced EF (metoprolol succinct, carvedilol, bisoprolol)
  3. Tachyarrhythmias
90
Q

2 different types of Ca++ channels:

A
  1. T(transient) type

2. L type

91
Q

What is t-type Ca channel?

A
  • opens at more negative potentials

- dominant in SA node

92
Q

What is L-type Ca channel?

A
  • located on vascular SM, cardiac myocytes, cardiac nodal tissue
  • dominant in AV node
  • required for initiation of contraction via Ca++
93
Q

2 types of Ca channel blockers?

A
  1. Non-dihydropyridines (NON-DHPs)

2. Dihydropyridines (DHPs)

94
Q

What do NON-DHPs effect?

A

SA
AV
Contractility

95
Q

What do DHP effect?

A

Contractility

Vasodilation

96
Q

NON-DHPs effect on:

SA, AV, inotropic, myocardial blood flow, peripheral arterioles

A 
Normal/decrease 
Decrease 
Decrease
Increase 
Increase
97
Q

DHPs effect on:

SA, AV, inotropic, myocardial blood flow, peripheral arterioles

A 
Normal
Normal
Normal
Increase 
Increase
98
Q

BB effects on:

SA, AV, inotropic, myocardial blood flow, peripheral arterioles

A

Decrease all

99
Q

2 NON-DHPs medications

A

Verapamil

Diltiazem

100
Q

Verapamil

A

More cardio selective
More potent HR lowering effect
Stronger suppression of contractility

101
Q

Diltiazem

A

More effective vasodilator
Better antiHTN
Moderate suppression of contractility

102
Q

Clinical uses for NON-DHPs (4)

A

HTN
Supreventricular tachyarrhythmias
Chronic stable angina
Coronary spasm

103
Q

3 contraindications of NON-DHPs

A

Severe hypotension or cardiogenic shock
LV dysfunction (<40%)
Bradycardia

104
Q

Is nifedipine DHPs long or short acting?

A

Short

105
Q

How does DHPs work?

A

Rapid vasodilation
Rapid drop BP
Rapid reflex adrenergic activation with tachycardia
Increase demand

106
Q

Unusual side effects of DHPs (4)

A

Muscle cramps
Myalgia
Hypokalemia
Gingival swelling

107
Q

How long or short acting DHPs preferred?

A

Long

108
Q

Is DHPs first or second line HTN?

A

First

109
Q

4 clinical uses for DHPs

A

HTN
Chronic stable angina
Coronary spasm
Raynaud’s phenomenon

110
Q

Chief side effect of DHPs?

A

Ankle edema

111
Q

2 HTN emergency meds

A

Nicardipine IV

Clevidipine IV

112
Q

Tunica intima

A

Endothelial cells

113
Q

Tunica medica

A

SM cells

Sheets of elastin

114
Q

Tunica externa

A

Loosely woven fibers of collagen

115
Q

How do nitroglycerin (glyceryl trinitratel, NTG) work?

A

NTG produce NO
NO goes to SM cells
Stimulate guanylyl cyclase
Increase cGMP (vasodilates veins and arteries)

116
Q

What do organic nitrates do to preload and afterload?

A

Decrease because of the vasodilation

117
Q

What does organic nitrates do to myocardial oxygen consumption and oxygen delivery to heart tissue?

A

Decrease myocardial oxygen consumption

Increase oxygen delivery to heart tissue

118
Q

3 most common ways to receive NTG?

A

Sublingual/spray
IV
Transdermal patch

119
Q

2 nitrate preparations:

A 
Isosorbid dinitrate (ISDN)
Isosorbid mononitrate (ISMN)
120
Q

What is isosorbid dinitrate?

A

Low bioavailability, high first pass metabolism

Converted to active mononitrate metabolite (via liver)

121
Q

What is isosorbide mononitrate?

A

High bioavailability, no first pass metabolism

122
Q

How does nitrate preparations produce vasodilation?

A

ISDN -> ISMN -> NO -> cGMP -> vasodilation

123
Q

5 clinical uses of organic nitrates

A
  1. Chronic stable angina
  2. Unstable angina and ACS
  3. Acute HR and pulmonary edema
  4. Chronic heart failure
  5. HTN
124
Q

Contraindication of nitrate?

A

Right ventricular infarction

125
Q

4 Adverse effects of nitrate?

A

Headache
Hypotension, dizzy, syncope
Reflex tachycardia
Halitosis (bad breath)

126
Q

Serious nitrate interaction

A

Decrease BP
Syncope
Erection

127
Q

Nitrate tolerance (tachyphylaxis) (3)

A
  • loss of nitrate-induced vasodilation
  • reduced nitrate-induced BP lowering effect
  • attenuation of nitrate-induced anti-ischemic effect
128
Q

What is Monday disease at explosive factory?

A

Nitrate tolerance

129
Q

How long does nitrate tolerance occur?

A

2-3days

130
Q

What are 2 parenteral vasodilators?

A

Sodium nitroprusside

Fenoldopam

131
Q

What 3 things are nitroprusside?

A

Complex of iron
Cyanide groups
Nitro so moiety

132
Q

Does sodium nitroprusside cause tolerance?

A

No

133
Q

How does sodium nitroprusside cause vasodilation?

A

Rapid uptake by RBCs
NO and cyanide
NO activates GC -> cGMP and causes vasodilation

134
Q

What does sodium nitroprusside cause in preload and afterload?

A

Decreases in both

135
Q

What does normal LV function do with sodium nitroprusside?

A

Decrease BP

136
Q

What does severely impaired LV function do with sodium nitroprusside?

A

Decrease afterload leads to rise in SV and CO

137
Q

What is sodium nitroprusside toxicity?

A

Cyanide toxicity

138
Q

What is treatment for cyanide toxicity with sodium nitroprusside?

A

Hydroxocobalamin, sodium thiosulfate

139
Q

3 additional toxicity problems with sodium nitroprusside?

A

Hypotension
Coronary steal
Increase ICP

140
Q

3 Sodium nitroprusside clinical uses?

A

HTN emergencies
Acute decompensated HF
Perioperative HTN in cardiac surgery

141
Q

In HF, a reduced afterload can do what to SV and CO?

A

Enhance them

142
Q

2 therapeutic uses for hydralazine (oral direct vasodilator)?

A

HTN

HF with reduced EF

143
Q

Therapeutic uses of minoxidil (oral direct vasodilator)?

A

Severe HTN poorly responsive to other HTN drugs

LAST RESORT

144
Q

3 adverse effects of oral direct vasodilators

A

Headaches, flushing
Baroreceptor (mediated reflex tachycardia)
Salt and water retention (edema)

145
Q

What is fenoldopam?

A

Selective agonist of D1-like dopamine receptor

146
Q

Is fenoldopam rapid or slow acting?

A

Rapid acting arteriolar vasodilator

147
Q

When is fenoldopam used?

A

HTN emergencies and postop HTN

148
Q

What are the 2 major toxicities with fenoldopam?

A

Reflex tachycardia

Hypokalemia

149
Q

What should be done when BB are used with fenoldopam?

A

With caution: substantial hypotension because BB inhibit sympathetic reflex

Pharmacology (14 decks)

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