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Pharmacology > Anti Hypertensive Drugs > Flashcards

Anti Hypertensive Drugs Flashcards

1
Q

Primary Risk Factors for HTN

A 
Family history
African ethnicity
Male gender
Post-menopausal women
>20 lbs excess body weight
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2
Q

Associated Risk Factors for HTN

A

Diabetes
Excess Alcohol
Oral contraceptives
Inactivity

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3
Q

What are pre hypertensive BPs?

A

120-139/80-89

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4
Q

What are stage 1 hypertensive BPs?

A

140-159/90-99

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5
Q

What are stage 2 hypertensive BPs?

A

160/100 and up

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6
Q

In patients less than 60 years old, what is the lowest blood pressure when you would prescribe anti-hypertensive meds?
What would you recommend before then to lower their BP?

A

When they get above 140/90, you need to prescribe meds.

Before that, use lifestyle modifications to treat HTN

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7
Q

In patients older than 60, at what BP do you start prescribing meds for HTN?

A

150/90

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8
Q

What are the 4 classes of first-line DOC anti-hypertensives?

A

Diuretics
Ca2+ channel blockers
ACE Inhibitors
Angiotensin receptor blockers

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9
Q

Thiazide Diuretics

MOA

A

Block the Na+/Cl- channels in the distal convoluted tubule, increasing Na+ loss and urinary volume.
K+ wasting
Cause some vasodilation via prostaglandin release

Cause increased aldosterone production and insertion of ENaC channels into luminal membrane of principal cells, driving K+ out of the lumen

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10
Q

Thiazide Diuretics

Adverse Effects

A 
Hyponatremia
Hyperglycemia
Hypokalemia
Increased LDL/HDL
Metabolic alkalosis
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11
Q

Thiazide Diuretics

What drugs would be OK to coadminister with thiazides to prevent K+ wasting?

A

Prevent aldosterone from reabsorbing more Na+ in collecting ducts, thus prevent K+ wasting

  • Beta Blockers
  • ACE inhibitors
  • Angiotensin receptor antagonists
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12
Q

Thiazide Diuretics

What drugs should you not coadminister thiazides with?

A

NSAIDs

May block the vasodilatory effects of the prostaglandins released by the thiazides

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13
Q

Thiazide Diuretics

Contraindications

A

Hypokalemia

Pregnancy

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14
Q

Thiazide Diuretics

What is their interaction with beta blockers?

A

May cause hyperglycemia together, though beta blockers may be coadministered to help prevent hypokalemia

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15
Q

List the thiazide diuretics

A

Hydrochlorothiazide

Chlorthalidone

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16
Q

Loop Diuretics

MOA

A

Block the Na+/K+/Cl- channel in the thick ascending limb of the loop of Henle
K+ wasting
Venous dilation via Prostaglandin release
Also cause excretion of Mg2+ and Ca2+

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17
Q

Loop Diuretics

List them

A

Furosemide
Ethacrynic acid (last resort)
Bumetanide
Torsemide

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18
Q

Loop Diuretics

Side Effects

A 
Hypokalemia
Metabolic alkalosis
Dehydration
Hyponatremia
Hypomagnesemia
Impaired diabetes control
Increased LDL/HDL
Ototoxicity
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19
Q

Loop Diuretics

Drugs Interactions

A

Aminoglycosides - exacerbates ototoxicity

NSAIDs- block vasodilatory effects of prostaglandins

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20
Q

List the K+ Sparing Diuretics

A

Spironolactone
Eplerenone
Amiloride
Triamterene

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21
Q

Spironolactone

MOA

A

Blocks the aldosterone receptor, thus preventing insertion of ENaC channels into the luminal membrane of the principal cells.
Increase Na+ excretion and spare K+

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22
Q

Spironolactone

Adverse Effects

A

Hyperkalemia

Anti-androgenic effects - gynecomastia, amenorrhea, impotence

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23
Q

Eplerenone

MOA

A

Blocks the aldosterone receptor, thus preventing insertion of ENaC channels into the luminal membrane of the principal cells.
Increase Na+ excretion and spare K+

Does NOT have the anti-androgenic effects of spironolactone

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24
Q

Spironolactone and Eplerenone

Drug Interactions

A

NSAIDs

ACE inhibitors and Angiotensin Receptor Blockers - can exacerbate hyperkalemia by inhibiting aldosterone’s production

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25
Q

Amiloride and Triamterene

MOA

A

Block the ENaC channel in the principal cells

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26
Q

Amiloride and Triamterene

Drug Interactions

A

NSAIDs

ACE Inhibitors and Angiotensin Receptor Blockers - may exacerbate hyperkalemia

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27
Q

Would you ever use a K+ sparing diuretic as a monotherapy?

A

No. Not very strong on their own, but they are good in combination with loop or thiazide diuretics (the K+ wasting drugs)

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28
Q

Ca2+ Channel Blockers

Dihydropyridines are selective for? What is the dihydropyridine drug and its MOA?

A

Selective for vascular smooth muscle.

Nefedipine is used only in HTN by blocking vascular Ca2+ channels

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29
Q

Ca2+ Channel Blockers

What are the non-dihydropyridine drugs? What are they selective for?

A

Verapamil and Diltiazem

They act on both vascular and cardiac smooth muscle (though verapamil has a much more potent effect on cardiac smooth muscle)

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30
Q

Nefedipine

Adverse Effects

A

Acute tachycardia

Peripheral edema

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31
Q

Diltiazem

Adverse Effects

A

Bradycardia

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32
Q

Verapamil

Adverse Effects

A

Constipation

Bradycardia

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33
Q

Verapamil and Diltiazem are contraindicated in…?

A

Patients with conduction disturbances (heart block, etc)

34
Q

Clonidine

MOA

A

Alpha-2 receptor agonist

Activates a G-alpha-i cascade, inhibiting adenylyl cyclase to decrease sympathetic outflow from the CNS

35
Q

Clonidine

Adverse Effects

A

Sudden withdrawal may lead to a hypertensive crisis

Sedation
Dry mouth
Dermatitis

36
Q

Why might guanfacine be used in place of clonidine?

A

Guanfacine has a longer half life, so it is less likely to cause rebound HTN when a patient misses a dose

37
Q

Methyldopa

MOA

A

Alpha-2 receptor agonist

Also competes with LDOPA for dopamine decarboxylase, inhibiting dopamine production

38
Q

Methyldopa

Indications

A

Used for hypertensive control in pregnant women

39
Q

Methyldopa

Adverse Effects

A

Sedation
Hyperprolactinemia
Anemia

40
Q

Reserpine

MOA

A

Blocks VMAT vesicular transporter, preventing storage of NE in vesicles. MAO will digest NT in the cytosol.

41
Q

Reserpine

Indications

A

Hypertensive patients who are resistant to other drugs

42
Q

Reserpine

Adverse Effects

A

Depression

Nasal Congestion

43
Q

Reserpine

Drug Interactions

A

Do not give reserpine with a MAO inhibitor, which could reverse reserpine’s effects and cause a hypertensive crisis

44
Q

Phenoxybenzamine

MOA

A

Non selective alpha adrenergic antagonist

45
Q

Phenoxybenzamine

Indications

A

Pheochromocytoma

46
Q

Phenoxybenzamine

Adverse Effects

A

Tachycardia (due to NE binding beta receptors instead of alpha)

47
Q

Prazosin

MOA

A

Selective alpha-1-antagonist

48
Q

Prazosin

Indications

A

Primary HTN

Benign Prostatic Hyperplasia

49
Q

Prazosin

Adverse Effects

A

Orthostatic Hypotension

Dizziness

50
Q

Beta Blockers

General MOA

A

Lower contractility of the heart
Lower HR
Prevent renin release, thus decreasing angiotensin II production

51
Q

What is the prototypical beta blocker?

A

Propranalol

52
Q

Nadolol

A

Nonselective Beta blocker

Longer half life

53
Q

Pindolol

A

Partial agonist of Beta receptors
Nonselective
Causes less bradycardia than other beta blockers

54
Q

Metoprolol

A

B1-selective beta blocker

Lipophilic

55
Q

Atenolol

A

B1-selective

Hydrophilic

56
Q

Labetolol

A

Beta blocker with some alpha-blocking activity

Lipophilic

57
Q

Carvedilol

A

Nonselective beta blocker that also has alpha-receptor antagonist activity
Vasodilation
Lipophilic

58
Q

What are the lipophilic beta blockers?

A

Metoprolol
Labetolol
Carvedilol

59
Q

Beta Blockers

Side Effects of all BBs

A 
Bradycardia
Increased triglycerides
Decreased HDLs
Hyperglycemia
Impaired exercise tolerance
60
Q

Beta Blockers

Side effects of Nonselective BBs

A

Bronchiole constriction (increased airway resistance)

61
Q

Beta Blockers

Side Effects of Lipophilic BBs

A

Insomnia
Chronic fatigue
Depression

62
Q

Contraindications for Beta Blockers

A

Sinus bradycardia
Cardiogenic shock
Heart block
Asthma

63
Q

Beta Blockers

Drug Interactions

A

Calcium Channel Blockers - causes reduced contractility and conduction

64
Q

Vasodilators

General MOA

A

Vasodilation of small vessels, primarily the arterioles

65
Q

Hydralazine

MOA and Indications

A

Vasodilator used in drug resistant HTN and emergencies

66
Q

Hydralazine

Side Effects

A

Tachycardia
Angina aggravation
Fluid Retention

NSAIDs can reduce effectiveness

67
Q

Minoxidil

MOA and Indications

A

Vasodilator used for drug resistant HTN

68
Q

Minoxidil

Adverse Effects

A

Hypertrichosis
Tachycardia
Angina Aggravation
Fluid retention

69
Q

Nitroprusside

MOA and Indications

A

Vasodilator used in emergencies

70
Q

Nitroprusside

Adverse Effects

A

Cyanide poisoning (gets converted to a cyanide-like metabolite in the liver)

71
Q

ACE Inhibitors

General MOA

A 
Block production of angiotensin II
Prevent vasoconstriction
Prevent aldosterone activation
Prevent bradykinin degradation
Prevent some NE release, growth, and inflammation
72
Q

List the ACE Inhibitors

A

Captopril
Enalapril
Lisinopril

73
Q

Why is Lisinopril the most commonly used ACE inhibitor today?

A

Captopril had a very short half life.
Enalapril had a longer half life but needed to be metabolically converted, making half life and drug effects more unpredictable

Lisinopril has a rapid onset of action and a more predictable half life

74
Q

ACE Inhibitors

Adverse Effects

A

Hyperkalemia
Dry cough
Angioedema (rare)

75
Q

ACE Inhibitors

Contraindications

A

Should not be given with K+ sparing drugs

Pregnancy
Bilateral renal stenosis

76
Q

How do ACE inhibitors help patients who have HF or LV dysfunction?

A

Prolongs survival by preventing cardiac remodeling

77
Q

Angiotensin II Receptor Blockers

Which one do we use most?

A

Losartan

- selective AT1 receptor antagonist

78
Q

Angiotensin II Receptor Blockers

Adverse Effects

A

Hyperkalemia

79
Q

Angiotensin II Receptor Blockers

Contraindications

A

Pregnancy

Should not be used with K+ sparing drugs

80
Q

How should you best treat HTN in African Americans?

A

Monotherapy with diuretics or Calcium channel blockers

81
Q

What anti-hypertensive meds should you avoid in pregnancy?

A

ACE inhibitors
Angiotensin receptor blockers
Beta Blockers

82
Q

What anti-hypertensive meds should you use in pregnancy?

A

Methyldopa

Pharmacology (67 decks)

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