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Pharmacology > Anti-Hypertensive Agents > Flashcards

Anti-Hypertensive Agents Flashcards

1
Q

What is the pre-hypertensive state?

A

Systolic 120-139

Diastolic 80-89

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2
Q

What is Stage I HTN?

A

140-159/90-99

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3
Q

What is Stage II HTN?

A

≥ 160 systolic OR ≥ 100 diastolic

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4
Q

What are the 4 sites of action for HTN drugs?

A
  1. Arterial resistance
  2. Venule capacitance
  3. Kidney volume
  4. Cardiac output
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5
Q

What drugs alter arteriole resistance?

A 
Diuretics
Calcium Channel Blockers (CCBs)
Alpha Adrenergic Blockers 
Beta Adrenergic Blockers (BBs) 
Vasodilators
Angiotensin Receptor Blockers (ARBs)
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6
Q

What drugs alter venous capacitance?

A

Vasodilators

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7
Q

What drugs alter cardiac output?

A

Beta-blockers

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8
Q

What drugs alter the volume excreted by the kidneys?

A

Diuretics
ACE Inhibitors
Beta-blockers (inhibit renin)

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9
Q

What are the drugs of choice for uncomplicated HTN?

A

Diuretics

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10
Q

Thiazide MOA

A

Inhibits Na+/Cl co-transporter

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11
Q

Thiazide SE

A

Hyponatremia
Hyperglycemia
Increased LDL/HDL
Hypokalemia

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12
Q

How do thiazides stimulate hypokalemia?

A

Low Na stimulate aldosterone which causes increased delivery of Na+ to collecting duct cells increases Na+ diffusion.

K+ loss from principal cells and H+ loss from intercalated cells due to resulting neg. charge on lumen side following Na reuptake.

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13
Q

What are the 4 first line drugs for HTN?

A
  • Diuretics
  • Calcium Channel Blockers (CCBs)
  • Angiotensin Converting Enzyme inhibitors (ACEIs) *Angiotensin Receptor Blockers (ARBs)
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14
Q

What are the interactions of thiazides with NSAIDs and beta blockers?

A

NSAIDs – inhibits prostaglandin production, reduces efficacy

ß-blockers – enhances hyperlipidemia and hyperglycemia

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15
Q

Thiazide Contraindications

A

Hypokalemia

Pregnancy (starting after pregnant)

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16
Q

Loop Diuretic MOA

A

Blocks Na+/K+/Cl co-transporter, causes venous dilation via prostaglandins

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17
Q

Loop Diuretic SE

A 
Dehydration/hyponatremia 
Hypokalemia
Increased LDL/HDL
Impaired diabetes control
Ototoxicity
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18
Q

What are the drug interactions of the loop diuretics?

A

NSAIDS - inhibit prostaglandins which are required for efficacy

Aminoglycosides – enhance ototoxicity and nephrotoxicity

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19
Q

K+ Sparing Diuretics MOA

A

Aldosterone receptor blocker – combine with diuretics, not used for monotherapy of HT

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20
Q

K+ Sparing Diuretics SE

A

Hyperkalemia

Gynecomastia (spironolactone)

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21
Q

K+ Sparing Diuretics Contraindications

A

Renin System Inhibitors (they will inhibit aldosterone which will further contribute to hyperkalemia)

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22
Q

Ca Channel Blockers MOA

A

All reduce vascular resistance by reducing calcium influx in VSM Non-dihydropyridines also reduce pacemaker potentials, AV node conduction, and contractility

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23
Q

CCB - Nifedipine Action and SE

A

Nifedipine – dihydropyridine, limited effect on pacemaker or conduction
SE: acute tachycardia, peripheral edema (arteriolar dilation > venodilation)

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24
Q

CCB - Diltiazem Action and SE

A

Diltiazem – non-dihydropyridine, reduces pacemaker and conduction currents
SE: bradycardia

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25
Q

CCB - Verapamil Action and SE

A

Verapamil – non-dihydropyridine, more pronounced reduction of currents
SE: constipation, bradycardia

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26
Q

CCB - non-dihydropyridine Contraindications

A

Non-dihydropyridines are contraindicated in pts with conduction disturbances.

  • Use with care in patients on beta blockers
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27
Q

Clonidine MOA

A

Alpha-2 agonist that causes peripheral vasoconstriction but decreases sympathetic outflow from CNS resulting in vasodilation

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28
Q

Clonidine SE

A

Sedation
Dry Mouth
Dermatitis
Rebound HTN with withdrawal of the drug

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29
Q

What is the analog of clonidine that has less chance of rebound?

A

Guanfacine

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30
Q

Methyldopa MOA

A

It is converted to methylnorepinephrine and is a α2-adrenergic receptor agonist

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31
Q

Methyldopa SE

A

Sedation

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32
Q

Methyldopa Drug Interactions

A

L-DOPA - inhibits DOPA decarboxylase

33
Q

Methyldopa Contraindications

A

Liver Disease

34
Q

What is the major indication of methyldopa?

A

Most extensively used anti-hypertensive in pregnancy

35
Q

Reserpine MOA

A

Blocks VMAT vesicular transporter, prevents storage of NE centrally and peripherally

36
Q

How is reserpine used?

A

Combined with diuretics

Used for mild and moderate hypertension.

37
Q

Reserpine SE

A

Depression

Nasal Congestion

38
Q

Phenoxybenzamine MOA

A

Non-selective α-receptor antagonist

39
Q

Phenoxybenzamine SE

A

Tachycardia

40
Q

Phenoxybenzamine Indications

A

Pheochromocytoma

41
Q

Prazosin MOA

A

Selective α1-adrenergic antagonist - less tachycardia than direct vasodilators

42
Q

Prazosin SE

A

Hypotension with the 1st dose

43
Q

Beta Blocker MOA

A

Decreased cardiac contractility and CO, decreased renin secretion

44
Q

Propranolol

A

Non-selective, used for mild to moderate hypertension, used as adjunct to prevent tachycardia with vasodilators and is lipophilic

45
Q

Nadolol

A

Non-selective with longer half life than propranolol

46
Q

Pindolol

A

Non-selective partial agonist that causes less bradycardia than propranolol

47
Q

Metoprolol

A

ß1-selective and somewhat lipophilic

48
Q

Atenolol

A

ß1-selective and hydrophilic

49
Q

Labetolol

A

Mixed beta/alpha receptor antagonist; lipophilic

50
Q

Carvedilol

A

Non-selective blocker with additional alpha receptor antagonist properties, vasodilatory

51
Q

What is the difference between atenolol and metoprolol?

A

Metoprolol crosses the BBB while atenolol does not

52
Q

What are the side effects of the beta blockers?

A 
Bradycardia
Impotence
Increased triglycerides 
Decreased HDLs 
Hyperglycemia
Impaired exercise tolerance
53
Q

What are the drug interactions of the beta blockers?

A

CCBs (reduced contractility and conduction)

54
Q

Beta Blocker Contraindications

A

Cardiogenic Shock
Sinus bradycardia
Asthma
Severe heart failure

55
Q

Vasodilator MOA

A

Vasodilation of small vessels, primarily arterioles

56
Q

Hydralazine Indications

A

Orally effective, used in drug resistant hypertension and in emergencies, long term efficacy is poor.

57
Q

Hydralazine SE

A

Tachycardia, angina aggravation, fluid retention

NSAIDS can reduce effectiveness

58
Q

Minoxidil Indications

A

Drug resistant hypertension - similar to hydralazine

59
Q

What is another use for minoxidil?

A

Hair growth

60
Q

Nitroprusside MOA

A

Vasodilator

61
Q

Nitroprusside Indications

A

Emergencies

62
Q

Nitroprusside SE

A

Cyanide poisoning

63
Q

ACE Inhibitor MOA

A

Blocks production of Angiotensin II and Ang II-mediated-

vasoconstriction

64
Q

Captopril

A

Short half life ACE-I

65
Q

Enalapril

A

Converted to active metabolite enalaprilat, longer onset of action, longer half-life ACE-I than captopril

66
Q

Lisinopril

A

Water soluble, excreted unchanged by kidney, longer half-life, allows 1x daily dosing

67
Q

ACE-I SE

A

Hyperkalemia, dry cough, angioedema

68
Q

ACE-I Contraindications

A

Pregnancy and bilateral renal stenosis

69
Q

ACE-I Indications

A

Prolongs survival in pts with HF or LV dysfunction after MI Preserves renal function in diabetic patients

70
Q

ANG-II Receptor Blocker MOA

A

ANG-II receptor antagonist

71
Q

Losartan MOA

A

Selective AT1 receptor antagonist

72
Q

Losartan SE

A

Hyperkalemia

73
Q

Losartan Contraindications

A

Pregnancy

K+ Sparing Diuretics

74
Q

What are good combinations of drugs for HTN?

A
  • Thiazide or Loop diuretic with K+ sparing diuretic
  • Thiazide diuretic with BB’s
  • CCBs with ACEI
75
Q

What is the main HTN drug for diabetics?

76
Q

What is the main HTN for HF?

A

ACE-I combined with diuretics

77
Q

What are the main HTN drugs for MI?

A

ACE-I and beta blockers

78
Q

What drugs are less effective in African Americans?

A

Monotherapy with BBs and ACEIs not as effective

Pharmacology (74 decks)

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