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Pharma Recall - Pharmacology > Ch 20 - Antihypertensive drugs - DONE > Flashcards

Ch 20 - Antihypertensive drugs - DONE Flashcards

1
Q

Define hypertention:

A

persistent diastolic pressure greater than 90 mm Hg and systolic pressure greater than 140 mm Hg

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2
Q

What is the most common presenting sign of hypertention?

A

There is none! When patients are first diagnosed they are usually asymptomatic

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3
Q

What are some of the potential complications of hypertention?

A
  • Coronary artery diesease
  • cardiac and renal failure
  • stroke
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4
Q

What is the hydraulic equation for blood pressure?

A

BP = Cardiac output (CO) x total peripheral vascular resistance (PVR)

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5
Q

What conclusion can be drawn from the hydraulic equation for blood pressure?

A

drugs that reduce either CO or total PVR will produce a reduction in BP

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6
Q

What are the major classes of drugs that are used to treat hypertention?

A
  • Sympatholytic agents
  • Diuretics
  • Vaodilators
  • Angiotensin-converting enzyme (ACE) inhibitor
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7
Q

Give examples of sympatholytic agents:

A
  • methyldopa
  • clonidine
  • guanfacine
  • α- and β-blockers
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8
Q

Give examples of vasodilators:

A
  • hydralazine
  • minoxidil
  • sodium nitroprusside
  • diazoxide
  • calcium channel blockers
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9
Q

Give examples of angiotensin-converting enzyme (ACE) inhibitors, and angiotensin II receptor antagonis:

A
  • captopril
  • enalapril
  • lisinopril
  • losartan
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10
Q

What does the sympatholytic agents do?

A

all of them reduce PVR or CO

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11
Q

What does the vasodilators do?

A

reduce PVR

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12
Q

What does the angiotensin-converting enzyme (ACE) do?

A
  • PVR

- reduce blood volume by reducing the secretion of aldosterone

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13
Q

Which antihypertensive drugs have their site of action at the vasomotor center?

A
  • Methyldopa

- Clonidine

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14
Q

Which antihypertensive drugs have their site of action at the sympathetic nerve terminals?

A
  • Guanethidine

- Reserpine

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15
Q

Which antihypertensive drugs have their site of action at the β-receptors of the heart?

A
  • Propanolol and other β-blockers
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16
Q

Which antihypertensive drugs have their site of action at the sympathetic ganglia?

A
  • Trimethapan
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17
Q

Which antihypertensive drugs have their site of action at angiotensin receptors of vessels?

A

Losartan

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18
Q

Which antihypertensive drugs have their site of action at α-receptors of vessels?

A
  • Prazosin and other α1- blockers
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19
Q

Which antihypertensive drugs have their site of action at vascular smooth muscle?

A
  • Hydralazine
  • Minoxidil
  • Nitroprusside
  • Diazoxide
  • Verapamil and other calcium channel blockers
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20
Q

Which antihypertensive drugs have their site of action at the kidney tubules?

A
  • Thiazide etc.
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21
Q

Which antihypertensive drugs have their site of action at β-receptors of Juxtaglomerular cells that release Renin?

A
  • Propanolol and other β-blockers
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22
Q

Which antihypertensive drugs have their site of action on the Angiotensin-converting enzyme (ACE)?

A
  • Captopril and other ACE inhibitors
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23
Q

What are sympatholytic agents?

A

centrally acting hypertensives

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24
Q

Methyldopa mechanism of action:

A

stimulates central presynaptic α2- adrenergic receptors and inhibits the release of norepinephrine

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25
Q

What is the primary effect of Methyldopa?

A
  • the decreased sympathetic outflow results in decreased PVR

- it also creates some reduction in CO

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26
Q

What is the route of administration of Methyldopa?

A
  • oral

- IV

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27
Q

What is the clinical indication for Methyldopa?

A
  • moderate hypertention
  • often given to patients with renal insufficiency since it does not decrease blood flow to the kidney
  • can be used safely in pregnancy
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28
Q

What are the potential toxicities of Methyldopa?

A
  • A drug induced positive Coombs test that is sometimes associated with hemolytic anemia
  • Lactation associated with increased prolactin release
  • Edema
  • Sedation
  • Impotence
  • Dry mouth
  • Hepatitis
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29
Q

Clonidine mechanism of action:

A
  • Like Methyldopa, Clonidine stimulates central presynaptic α2- adrenergic receptors wich results in diminished central adrenergic outflow.
  • Decrease PVR
  • Decreases also heart rate and CO
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30
Q

When is Clonidine used clinically?

A
  • for mild-to-moderate hypertention

- usually a second line agent

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31
Q

What is the route for administration of Clonidine?

A
  • Oral
  • IV
  • Transdermal (for extended use)
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32
Q

Clonidine AE:

A
  • Sedation
  • Dizziness
  • Dry mouth
  • Rebound hypertention after sudden withdrawal from high doses
  • Bradycardia especially in patients with AV nodal disease
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33
Q

What do you use to treat Rebound hypertention after sudden withdrawal from high doses of Clonidine?

A
  • Labetalol

- Nitroprusside

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34
Q

What drug interactions should the physician be concerned about before giving Clonidine?

A

Clonidine should not be given with tricyclic dugs. This combination may inhibit the actions of Clonidine.

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35
Q

What is Guanfacine?

A

a centrally acting antihypertensive with a mechanism of action and side-effect profile very similar to those of Clonidine.

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36
Q

Give some examples of α1-adrenergic blockers:

A
  • Prazosin
  • Terazosin
  • Doxazosin
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37
Q

How does the α-blockers work?

A

They block the α1-adrenergic receptors

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38
Q

What are the antihypertensive effect of α-blockers?

A
  • decrease PVR

- exert minimal effects on CO

39
Q

Describe the clinical use of α-adrenergic blockers:

A
  • moderate hypertention

- benign prostatic hypertrophy (relaxes the smooth muscles in the bladder neck)

40
Q

AE of Prazosin and its synthetic analogues:

A
  • Dizziness
  • Orthostatic hypotention - especially after the first dose (first-dose effect)
  • Headache
41
Q

Give some examples of β-blockers:

A
  • Propanolol
  • Metoprolol
  • Atenolol
  • Labetalol (both α-blocker and β-blocker)
  • Carvedilol
42
Q

Name a drug that is both a α-blocker and β-blocker:

A

Labetalol

43
Q

β-blockers mechanism of action:

A

Blockade of β1- and β2- adrenergic receptors

44
Q

What is the clinical use of β-blockers?

A
  • Often one of the first-line agents chosen to treat patients with mild-to-moderate hypertention and a concominant disease such as angina and chronic heart failure.
  • These drugs may be of particular use in high renin states because they reduce renin release
45
Q

When should the β-blockers be avoided?

A
  • peripheral vascular disease
  • asthma
  • acute heart failure
46
Q

β-blockers SE:

A
  • Sedation
  • Fatigue
  • Bronchoconstriction
  • Impotence
  • May decrease HDL and increase plasma triacyglycerol
47
Q

Give two examples of ganglionic blockers:

A
  • trimethaphan

- hexamethonium

48
Q

What is the clinical use of ganglionic blockers?

A
  • no longer in use because of severe SE
49
Q

Ganglionic blockers AE:

A
  • parasympathetic blockade (urinary retention, blurred vision, and so forth)
  • sympathetic blockade (sexual dysfunction and orthostatic hypotention)
50
Q

Give two examples of Postganglionic adrenergic neuronal blockers:

A
  • Reserpine

- Guanethidine

51
Q

What is the mechanism of action of Postganglionic adrenergic neuronal blockers?

A

block the release of stored norepinephrine

52
Q

What is the clinical use of Postganglionic adrenergic neuronal blockers?

A
  • rarely used to treat hypertention because of low efficacy and significant AE
53
Q

Name the most effective Diuretics:

A
  • loop diuretics

- Thiazide diuretics

54
Q

How are the Diuretics used therapeutically?

A
  • first-line agent

- mild-to-moderate hypertention

55
Q

Diuretics SE:

A
  • Potassium depletion (most common effect)
  • Possible impairment of glucose tolerance
  • Possible increase in plasma lipid concentration
56
Q

Hydralazine mechanism of action:

A
  • vasodilator of ARTERIOLAR smooth muscle => decreased PVR
    • this reduction in resistance is usually followed by a reflex tachycardia and fluid retention
  • β-blockers are often coadministered to minimize the sympathetic effect
57
Q

How is Hydralazine clinically used?

A

For moderate hypertention and CHF (chronic heart failure)

58
Q

Hydralazine AE:

A
  • Lupus-like syndrome
  • Cadriovascular effects:
    • hypotention
    • reflex tachycardia
    • palpitations
    • angina
  • Headache
  • Nausea
  • Diarrhea
59
Q

Minoxidil mechanism of action:

A

ARTERIAL vasodilator that works by opening potassium channels, which results in hyperpolarization and relaxation of smooth muscle cells

60
Q

How is Minoxidil clinically used?

A
  • For severe hypertention refractory to other drugs
  • For hair replacement (Rogaine)
  • Often administered with β-blockers and diuretics
61
Q

Minoxidil AE:

A
  • Edema due to sodium and water retention
  • Reflex tachycardia
  • Flushing
  • Headache
  • Hypertrichosis (increased hair growth)
62
Q

Sodium Nitroprusside mechanism of action:

A

Sodium Nitroprusside release Nitric oxide (NO), which stimulates the enzyme guanylyl cyclase and increases the intracellular production of cGMP concenctrations.
-> This results in decrease of intracellular calcium ions and consequent relaxation of vascular smooth muscle (BOTH ARTERIAL AND VENOUS)

63
Q

How is Sodium Nitroprusside clinically used?

A

for hypertensive emergenises and CHF

64
Q

What is the route of administration of Sodium Nitroprusside?

A

IV

65
Q

Sodium Nitroprusside AE:

A
  • Hypotention
  • Metabolic acidosis
  • Cyanide toxicities (cyanide is produced during the metabolim of Sodium Nitroprusside)
  • Thiocyanate toxicitiy
66
Q

Diazoxide mechanism of action:

A

prevents arterial smooth muscle contraction by opening potassium channels and stabilizing membrane potentials

67
Q

What other action does Diazoxide have?

A

it prevents insulin release from the pancreas

68
Q

The rout of administration of Diazoxide

A

IV

69
Q

How is Diazoxide clinically used?

A

for hypertensive emergensies

70
Q

Diazoxide AE:

A
  • hypotention
  • reflex tachycardia
  • hyperglycemia
71
Q

Give three examples of Calcium channel blockers:

A
  • nifedipine
  • verapamil
  • diltiazem
72
Q

Calcium channel blockers mechanism of action:

A

Inhibition of calcium influx into smooth muscle cells.

Nifedipine is the most selective for the peripheral vasculature

73
Q

Calcium channel blockers AE:

A
  • constipation
  • headache
  • dizziness
74
Q

What are ACE inhibitors?

A

ACE inhibitors are angiotensin-converting enzyme inhibitors

75
Q

Against which physiological system are ACE inhibitors effective?

A

the renin-angiotensin-aldosterone system

76
Q

EXPLAIN THIS SYSTEM

A

PAGE 167… LONG

77
Q

Give examples of ACE inhibitors:

A
  • captopril
  • lisinopril
  • enalapril
  • benazepril
78
Q

ACE inhibitors mechanism of action:

A
  • block the conversion of angiotensin I to angiotensin II and also increase levels of bradykinin, which is a potent vasodilator.
  • these drugs do not have much of an effect on CO and heart rate
79
Q

For what condition does a physician prescribe ACE inhibitors?

A
  • mild-to-moderate hypertention
  • CHF (vasodilatory effect)
  • Diabetic nephropathy.
80
Q

Describe the absorption of captopril:

A

it is well absorbed orally, but does not enter the CNS

81
Q

How is captorpil eliminated?

A

elimination occurs primarily through the urine

82
Q

ACE inhibitors AE:

A
  • dizziness
  • cough
  • angioedema
  • hyperkalemia
  • sudden drop in blood pressure after an initial dose
  • renal failure in patients who have bilateral renal artery stenosis
  • proteinuria
  • neutropenia
83
Q

Should ACE inhibitors be administered in pregnant women?

A

No! in the second and third trimester there is a risk of fetal hypotention, anuria, and malformation.

84
Q

What drug interactions should physician monitor while administrating ACE inhibitors?

A

Nonsteroidal anti-inflammatory drugs (NSAIDs) may reduce the vasodilatory effects of ACE inhibitors, because NSAIDs block the actions of bradykinin.

85
Q

Name four Angiotensin II receptor antagonists:

A
  • losartan
  • valsartan
  • candesartan
  • irbesartan
86
Q

Angiotensin II receptor antagonists mechanism of action:

A
  • They block angiotensin II at its receptor site, thus inhibiting both the vasoconstriction and aldosterone-secreting effects of angiotensin II.
  • They DO NOT affect the bradykinin system
87
Q

What is the route of administration of Angiotensin II receptor antagonists?

A

oral

88
Q

How are the Angiotensin II receptor antagonists used clinically?

A

for mild-to-moderate hypertention

89
Q

Angiotensin II receptor antagonists AE:

A
  • headache
  • hyperkalemia: especially in patients taking potassium-sparing diuretics
  • hypotention
    • they DO NOT cause the cough seen in ACE inhibitors
90
Q

Angiotensin II receptor antagonists CI:

A

Like ACE inhibitors, losartan and valsartan are CI in pregnancy becase they may cause fetal malformations, anuria, and hypotention.

91
Q

What is malignant hypertention?

A

hypertention associated with target-organ vascular damage (i.e., hypertensive encephalopathy, retinal hemorrhage, angina)

92
Q

How is malignant hypertention treated?

A

in the initial stages antihypertensive drugs such as diazoxide, labetalol and sodium nitroprusside are used. The goal is not normalization of blood pressure but rather a 25% reduction, because sudden hypoperfusion may result in brain injury. Excess fluid may be removed with loop diuretics or, if necessary, dialysis

93
Q

Dialysis def (google):

A

the separation of particles in a liquid on the basis of differences in their ability to pass through a membrane.

Pharma Recall - Pharmacology (14 decks)

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