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Exam 2 - Anti-hypertensives Flashcards

1
Q

What are the four major groups of antihypertensive agents?

A
  • Diuretics
  • Sympathoplegic agents
  • Direct vasodilators
  • Angiotension inhibitors
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2
Q

How is efficacy increased and toxicity decreased in antihypertensive drugs?

A

Combination of drugs from different groups

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3
Q

What are some common side effects of diuretics and how can these be avoided?

A
  • ED
  • Increased renin secretion
  • K+ depletion leading to hypokalemia
  • Reduced glucose tolerance and increased plasma lipid concentration (not good for diabetics)

Most can be avoided by using lower doses. Anti-hypertensive doses are much lower than those for diuresis.

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4
Q

What are the initial recommended drugs in hypertension?

A
  • Thiazides
  • ACE-I
  • ARB
  • CCB
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5
Q

Thiazide diuretics are more effective in what race?

A

More effective in African Americans than in Caucasians

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6
Q

When would you consider a Thiazide diuretic for HTN?

A

Mild to moderate HTN

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7
Q

When would you consider a Loop diuretic for HTN?

A

Severe cases (renal insufficiency, HF)

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8
Q

When would you consider a Potassium diuretic for HTN?

A

In combination with a thiazide or loop diuretic to decrease the loss of potassium

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9
Q

What is the general MOA of Sympatholytics in HTN?

A
  • Decrease BP by reducing sympathetic vasomotor tone

- Activate baroreflexes

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10
Q

Other than a decrease in BP, what do Sympatholytics generally cause? How can you prevent this?

A

Generally cause Na+ and H2O retention.

Best when combined with a diuretic to prevent water retention.

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11
Q

What type of anti-HTN are Clonidine and Methyldopa?

A

Centrally Acting Sympatholytics (alpha agonist)

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12
Q

What is the MOA for Clonidine and Methyldopa?

A
  • Stimulate medullary a2 adrenergic receptors leading to decreased peripheral sympathetic nerve activity in blood vessels, kidney, and heart
  • Decreased SNS outflow and decreased renin secretion leads to decreased BP
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13
Q

When is Methyldopa preferred for treatment over clonidine?

A

HTN in pregnancy

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14
Q

What are differences in the effects/administration of clonidine compared to methyldopa?

A

Clonidine reduces HR and CO more than methyldopa

While both are oral, clonidine can also be used as a patch

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15
Q

What are some adverse effects of Centrally Acting Sympatholytics (clonidine, methyldopa)?

What are some effects specific to Methyldopa?

A
  • Sedation and other CNS
  • Xerostomia (common)

Methyldopa:

  • Hemolytic anemia with a positive Coombs test
  • Hepatotoxic
  • Gynecomastia/lactation due to increased prolactin
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16
Q

What are some contraindications/precautions of Centrally Acting Sympatholytics (clonidine, methyldopa)?

A
  • No monotherapy
  • Sudden withdrawal of clonodine can lead to HTN crisis
  • TCA can inhibit clonidine’s therapeutic action
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17
Q

What is the MOA for Prazosin?

A

Block a1-adrenergic receptors

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18
Q

What are indications/therapeutic effects of Prazosin?

A
  • Reduces norepinephrine vasoconstriction –> dilate arteries and veins
  • Decreased BP due to decreased peripheral resistance
  • BPH
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19
Q

What is the DOC for a patient suffering from both HTN and BPH?

A

Prazosin

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20
Q

What are some adverse effects of Prazosin?

A
  • Postural hypotension may be pronounced with first dose (“first dose phenomenon”)
  • Na+ and water retention due to increased renin
  • Reflex tachycardia
  • Dizziness, palpitations, headache
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21
Q

In what population would B-blockers produce the best effects?

A

Young white males

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22
Q

Why are B-blockers combined with other drugs?

A

Counteract reflex tachycardia and increased renin

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23
Q

While B-blockers are no longer recommended for monotherapy, what are some compelling indications to do so?

A

Patient with

  • Angina
  • MI
  • Migraine
  • HF
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24
Q

What can Nebivolol be helpful in?

A

ED

Increases NO –> direct vasodilation –> decreased ED

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25
What are some contraindications to using B-blockers?
- Diabetes - Severe (end-stage) HF - Severe bradycardia - Heart block - Asthma (as causes bronchoconstriction)
26
What is the DOC for HTN in pregnancy?
Methyldopa
27
What anti-HTN drugs can be used in pregnancy?
- Methyldopa - Labetalol - Hydralazine - Nifedipine
28
What are indications/therapeutic effects of Combined a1/B-blockers (Labetalol, Carvedilol)?
- Vasodilation without reflex tachycardia Labetalol: - Decrease BP in HTN emergencies - Pregnancy Carvedilol: - HTN and HF, especially after MI
29
What are adverse effects of Combined a1/B-blockers (Labetalol, Carvedilol)?
- Orthostatic hypotension - Bronchoconstriction Labetalol: - Hepatotoxic --> emergency use only!
30
What are contraindications of Combined a1/B-blockers (Labetalol, Carvedilol)?
Asthma
31
Hypotension from any vasodilator may be accomapnied by what?
- Reflex tachycardia and increased myocardial contraction - Increased renin secretion - Fluid retention - HA, flushing (vasodilation in brain and skin) - Palpitations, dizziness (from orthostatic hypotension)
32
What is the MOA for Hydralazine?
Dilates arterioles but not veins via direct action of NO
33
What are the uses of Hydralazine?
Used in chronic therapy of severe HTN **Last choice though and only used in combination when other drugs have failed Also used for severe HTN or HTN emergency in pregnancy (compelling indication)
34
What are some adverse effects of Hydralazine?
- SLE in slow acetylators (HIP drug) - HA, nausea, palpitations, sweating, flushing - Angina
35
What is the MOA for Sodium nitroprusside (Nitropress)?
Rapidly lowers BP (in minutes) via direct action of NO, and effect disappears in minutes after discontinuation
36
What are the uses of Sodium nitroprusside (Nitropress)?
Used for emergency HTN situations (IV and disappears quickly, so not for chronic use)
37
What are the pharmacokinetics of Sodium nitropresside (Nitropress)?
- Metabolized by liver rapidly to thiocyanate and excreted by the kidney - IV ONLY
38
What are adverse effects of Sodium nitropresside?
- Cyanide accumulation which can be caused by too high of infusion, severe kidney disease, anuria - Metabolic acidosis , arrhythmias, hypotension, death in patients with deficiency in cyanide metabolism or severe liver disease
39
What is the MOA for Fenoldopam?
D1 receptor agonist - relaxes arteriolar smooth muscle
40
What are the uses of Fenoldopam?
Used for emergency HTN situations
41
Nifedipine, Amlodipine, Diltiazem, and Verapamil belong to what drug class?
Calcium Channel Blockers
42
What is the MOA of CCB?
Bind to L-type calcium channels in the: - Myocardium to decrease contractility, impulse generation, and conduction - Vascular smooth muscle to relax it and produce vasodilation
43
What specific CCB is vascular smooth muscle the most sensitive to?
Nifedipine
44
What specific CCB is cardiac muscle most sensitive to?
Verapamil
45
Even though Nifedipine and Verapamil are both CCBs, how do they differ in their effect on the heart?
- Nefedipine: Increases HR (as main effect is vasodilation in smooth muscle which will initiate baroreflex and cause reflex tachycardia) - Verapamil: Decreases HR
46
Which CCBs are classified as Dihydropyridines?
Nifedipine and Amlodipine
47
What are adverse effects of Dihydropyridine CCBs (Nifedipine and Amlodipine)?
- Vascular-like effects such as reflex tachycardia, HA, flushing, dizziness, peripheral edema - Gingival hyperplasia
48
What is the most common side effect of verpamil (CCB)?
Constipation
49
What are some contraindications/precautions of Verapamil and Diltiazem (CCBs)?
- SA or AV node abnormalities or use with B-blockers (can lead to excessive bradycardia or heart block) - HF (these drugs decrease inotropic ability which a patient with HF is already struggling with)
50
What are some contraindications/precautions of Dihydropyridines (CCBs)?
Use caution in HTN patients with HF
51
What two classes of drugs are considered Inhibitors of the Renin-Angiotensin System?
- ACE-I ("prils") | - ARBs ("sartans")
52
What is the MOA for ACE-I?
Inhibiting ACE --> Decrease in angiotensin II --> Decreased BP (reduced direct vasoconstriction by angiotensin II and reduced release of aldosterone)
53
What are advantages of using an ACE-I?
- Lower BP without compromising heart, brain, or kidneys | - Do not cause reflex sympathetic activation/tachycardia due to baroreceptor resetting
54
ACE-I are definitive DOC for HTN in patients with what other complications?
- Diabetes - CKD - HFrEF
55
What do ACE-I do in regards to diuretics?
- Enhance the anti-HTN efficacy of diuretic drugs | - Balance the adverse effects of diuretics (increased K+ will oppose the diuretic-induced hypokalemia)
56
What is DOC for CKD even w/o HTN?
ACE-I
57
What is DOC for patient with HTN + DM?
ACE-I
58
What is DOC for patient with HTN + CKD?
ACE-I
59
What is DOC for patient with HTN + HFrEF?
ACE-I
60
What are some adverse effects of ACE-I?
- Orthostatic hypotension and dizziness (severe in hypovolemic patients/diuretic users) - Cough (due to increased bradykinin) - Angioneurotic edema (due to increased bradykinin) - Hyperkalemia due to inhibited aldosterone secretion - Acute renal failure in patients with bilateral renal artery stenosis
61
In what population can ACE-I cause severe orthostatic hypotension and dizziness?
Hypovolemic/diuretic users
62
What are some contraindications/precautions of ACE-I?
- 2nd/3rd trimester of pregnancy due to being teratogenic - Use with K+ sparing diuretics --> hyperkalemia - Combination with NSAIDs will cause decreased vasodilation
63
What is the MOA of ARBs?
Block AT1 receptors selectively without affecting AT2 receptors
64
What is the difference in side effects between ACE-I and ARBs?
ARBs do not cause cough or angioedema as they do not increase bradykinin
65
In what population are ACE-I least effective?
Elderly African-Americans

Pharm II (10 decks)

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