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Pharmacology > Module 3.1: ANTI-HYPERTENSIVE (ANTI-HPN) > Flashcards

Module 3.1: ANTI-HYPERTENSIVE (ANTI-HPN) Flashcards

1
Q

Normal bp

A
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2
Q

Prehypertension

A

120–135/80–89

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3
Q

Hypertension

A

≥ 140/90

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4
Q

Stage 1

A

140–159/90–99

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5
Q

Stage 2

A

≥ 160/100

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6
Q
  • No specific cause can be determined
  • investigation of autonomic nervous system function, baroreceptor reflexes, the RAAS, and the kidney has failed to identify a single abnormality as the cause of increased peripheral vascular resistance
A

ESSENTIAL/ PRIMARY HTN

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7
Q
  • Specific cause identified
  • Possible causes: renal artery constriction, coarctation of the aorta, pheochromocytoma, Cushing’s disease, and primary aldosteronism.
A

SECONDARY HTN

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8
Q

BP is maintained by three anatomic sites:

A

o Arterioles
o postcapillary venules (capacitance vessels)
o heart

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9
Q

…contributes to maintenance of blood pressure by regulating the volume of intravascular fluid (triggering the juxtaglomerular aparatus)

A

kidneys

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10
Q

…mediated by autonomic nerves, act in combination with humoral mechanisms, including RAAS, to coordinate those anatomical sites’ functions and to maintain normal blood pressure

A

Baroreflexes

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11
Q
  • responsible for rapid, moment-to-moment adjustments in blood pressure: transition from a reclining to an upright posture
  • Central sympathetic neurons arising from the vasomotor area of the medulla are tonically active
A

Postural Baroreflex

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12
Q

stretch of the vessel walls brought about by the internal pressure (arterial blood pressure).

A

Carotid baroreceptors:

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13
Q

…causes (1) direct constriction of resistance vessels and (2) stimulation of aldosterone synthesis in the adrenal cortex ->increases renal sodium absorption and intra- vascular blood volume

A

Angiotensin II

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14
Q

…regulate water reabsorption by the kidney

A

Vasopressin (posterior pituitary gland)

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15
Q

Prehypertension

A

120–135/80–89

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16
Q

Hypertension

A

≥ 140/90

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17
Q

Stage 1

A

140–159/90–99

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18
Q

Stage 2

A

≥ 160/100

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19
Q
  • No specific cause can be determined
  • investigation of autonomic nervous system function, baroreceptor reflexes, the RAAS, and the kidney has failed to identify a single abnormality as the cause of increased peripheral vascular resistance
A

ESSENTIAL/ PRIMARY HTN

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20
Q
  • Specific cause identified
  • Possible causes: renal artery constriction, coarctation of the aorta, pheochromocytoma, Cushing’s disease, and primary aldosteronism.
A

SECONDARY HTN

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21
Q

BP is maintained by three anatomic sites:

A

o Arterioles
o postcapillary venules (capacitance vessels)
o heart

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22
Q

…contributes to maintenance of blood pressure by regulating the volume of intravascular fluid (triggering the juxtaglomerular aparatus)

A

kidneys

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23
Q

…mediated by autonomic nerves, act in combination with humoral mechanisms, including RAAS, to coordinate those anatomical sites’ functions and to maintain normal blood pressure

A

Baroreflexes

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24
Q
  • responsible for rapid, moment-to-moment adjustments in blood pressure: transition from a reclining to an upright posture
  • Central sympathetic neurons arising from the vasomotor area of the medulla are tonically active
A

Postural Baroreflex

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25
Q

MECHANISM OF ACTION:
 Reduction of HR and CO
 CNS effect
 Inhibition of renin release
 Reduction in venous return and plasma volume
 Reduction in peripheral vascular resistance
 Reduction in vasomotor tone
 Improvement in vascular compliance
 Resetting of baroreceptor levels
 Effects on prejunctional B receptors, reduction in NE release
 Attenuation of pressor response to catecholamines with exercise and stress (newer generation decrease in ADRS due to B1 selectivity; B1 is the adrenergic receptor in the heart)

A

BETA BLOCKERS {-OLOL}

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26
Q

…causes (1) direct constriction of resistance vessels and (2) stimulation of aldosterone synthesis in the adrenal cortex ->increases renal sodium absorption and intra- vascular blood volume

A

Angiotensin II

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27
Q

…regulate water reabsorption by the kidney

A

Vasopressin (posterior pituitary gland)

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28
Q

Normal bp

A
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29
Q

Goal of Anti-HTN:

1. REGULATE CO

A

Tachycardia -> Dec filling time -> Dec stroke volume -> Dec cardiac output

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30
Q

Goal of Anti-HTN:

2. PERIPHERAL RESISTANCE

A

muscle relaxation -> arteries dilatation, fall in Peripheral Resistance [PR], then BP goes down

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31
Q

right part of the heart; blood returning to the heart; aka degree of distention particularly your right atrium

A

Preload

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32
Q

anything that decrease venous return

A

preload unloaders

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33
Q

decrease vasoconstriction in arterioles and arteries

A

Afterload unloaders

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34
Q

lower blood pressure by depleting the body of sodium and reducing blood volume

A

Diuretics

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35
Q

ower blood pressure by reducing peripheral vascular resistance, inhibiting cardiac function, and increasing venous pooling in capacitance vessels.

A

Sympathoplegic agents

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36
Q

reduce pressure by relaxing vascular smooth muscle, thus dilating resistance vessels and—to varying degrees—increasing capacitance as well

A

Direct vasodilators

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37
Q

 Appropriate for the treatment of arterial HTN, esp in patients who have concomitant ischemic heart disease, HF or arrhythmias

A

BETA BLOCKERS {-OLOL}

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38
Q

 They are highly heterogenous with respect to various properties
 They reduce mortality, nonfatal re-infarction rates and improve clinical outcomes in patients with stable ventricular dysfunction who are receiving conventional HF treatment

A

BETA BLOCKERS {-OLOL}

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39
Q

MECHANISM OF ACTION:
 Reduction of HR and CO
 CNS effect
 Inhibition of renin release
 Reduction in venous return and plasma volume
 Reduction in peripheral vascular resistance
 Reduction in vasomotor tone
 Improvement in vascular compliance
 Resetting of baroreceptor levels
 Effects on prejunctional B receptors, reduction in NE release
 Attenuation of pressor response to catecholamines with exercise and stress (newer generation decrease in ADRS due to B1 selectivity; B1 is the adrenergic receptor in the heart)

A

BETA BLOCKERS {-OLOL}

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40
Q

INDICATION:
- Treatment for arterial hypertension; especially in concomitant ischemic heart failure and arrhythmia
 would not only control pressure, also decrease ischemia by decreasing O2 demand;
 arrhythmia: block electric conduction>reduction in heart rate

A

BETA BLOCKERS {-OLOL}

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41
Q

improve survival after MI

A

METOPROLOL, CARVEDILOL

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42
Q

 MOA: reduce arterial pressure by dilating both resistance and capacitance vessels
 DOC for Pt with HTN due to BPH

A

ALPHA BLOCKERS

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43
Q

…lower BP by blocking postsynaptic vasoconstrictor effects of Norepinephrine

A

Selective Alpha1 adrenergic antagonists

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44
Q

…cause balanced arterial and venous dilation, with no increase in CO

A

Hemodynamically, selec a1 receptor inihibitors

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45
Q

[ALPHA BLOCKERS] ADVERSE DRUG REACTION:

Tend to cause greater BP lowering in the upright compared to supine position

A

ORTHOSTATIC HYPOTENSION]

46
Q

Non-selective alpha blockers given for patients diagnosed with pheochromocytoma

A

PRAZOCIN, TAMSULOSIN]

47
Q

…reduce BP by decreasing SNS outflow, systemic vascular resistance and HR

A

Central alpha 2 sympathetic agonists

48
Q

…is an agonist for both central a2 and II-imidazoline receptors

49
Q

…deplete nerve terminal with NE, decrease reflex peripheral arterial and venous constriction, and predispose to orthostatic hypotension

A

Peripheral sympatholytics

50
Q

ADR: orthostatic hypotension; rebound hypertension especially when you suddenly stopped using the drug
IND: acute hypertension

51
Q

ADR: x’ss tachycardia causing increase in myocardial o2 demand

A

Nifedipine

52
Q

IND: pregnancy induced hypertension

A

Alpha methyldopa [aldomet]

53
Q

[ACE-Inhibitors]

ADVERSE DRUG RESPONSE

A
  • in pt with hypovolemia leads to severe hypotension;
  • acute renal failure (particularly in patients with bilateral renal artery stenosis or stenosis of the renal artery of a solitary kidney),
  • dry cough sometimes accompanied by wheezing, and
  • angioedema
54
Q

ADR: orthostatic hyptension, sedation, increase prolactin production (M and F)

A

METHYLDOPA

55
Q

 Effective work primarily by selective blockade of AT-I receptors; leading to the same effect as ACE-I
 Effective as monotherapy but when combined with other antihypertensive agents, are effective in virtually all populations

A

ANGIOTENSIN (AT) RECEPTOR BLOCKERS [ARB] {-SARTAN}

56
Q

Contraindication: depressive pt; TCA may block antiHTN effect of…

57
Q

inhibits the release of norepinephrine from sympathetic nerve endings

A

ADRENERGIC NEURON-BLOCKING AGENT

58
Q

ADR: HYPOTENSION, delayed or retrograde ejaculation (returns back into the bladder), diarrhea, HTN crisis among pt with pherochromocytoma

A

ADRENERGIC NEURON-BLOCKING AGENT

59
Q

CI:TCA, may lead to severe HTN crisis

A

ADRENERGIC NEURON-BLOCKING AGENT

60
Q

for treatment of patients with HF and Chronic kidney diseases

A

RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM [RAAS] BLOCKERS

61
Q
  • increases BK [bradykinin] concentration – leading to cough [remember patho: bradykinin is one of the chemicals release by neutrophils during asthmatic attacks; this causes irritation to the bronchial airways causing cough as ADR]
  • Long term use may lead to angiotensin escape
A

ACE INHIBITORS [ACE-I] {- PRIL}

62
Q

With the exception of_____ & _____, ACE-I are prodrugs, which improves their absorption before hydrolysis to active diacids in the liver or intestines
[EX. ENALAPRIL  ENALAPRILAT the active metabolite]

A

LISINOPRIL and CAPTOPRIL

63
Q

ACE-I drug whose action could be cancelled by ICATIBANT

64
Q

ACE-I drug which is also a lysine derivative of enalaprilat

A

LISINOPRIL

65
Q

ACE-Inhibitors are distinguished by…

A

sulfhydryl (captopril), phosphinyl (fosinopril), or carboxyl side groups

66
Q

chronic kidney disease patients taking ACE-Inhibitors would lead to…

A

HYPERkalemia

67
Q

[ACE-Inhibitors]

ADVERSE DRUG EFFECT

A
  • in pt with hypovolemia leads to severe hypotension;
  • acute renal failure (particularly in patients with bilateral renal artery stenosis or stenosis of the renal artery of a solitary kidney),
  • dry cough sometimes accompanied by wheezing, and
  • angioedema
68
Q

[ACE-Inhibitors]

CONTRAINDICATION

69
Q

 Effective work primarily by selective blockade of AT-I receptors; leading to the same effect as ACE-I
 Effective as monotherapy but when combined with other antihypertensive agents, are effective in virtually all populations

A

ANGIOTENSIN (AT) RECEPTOR BLOCKERS [ARB] {-SARTAN}

70
Q

…act by binding selectively to the AT-I receptor

A

ANGIOTENSIN (AT) RECEPTOR BLOCKERS [ARB]

- competitive (IRBESARTAN, VALSARTAN) or - insurmountable (CANDESARTAN or LOSARTAN)

71
Q

[ARB]

ADVERSE DRUG RESPONSE

A

ERECTILE DYSFUNCTION

72
Q

Renin converts angiotensinogen to angiotensin I. Block by _____ blocks the sequence at its start.

73
Q

ACE is responsible for activating angiotensin I to angiotensin II and for inactivating bradykinin, a vasodilator normally present in very low concentrations. ______ block this enzyme thus decreases the concentration of a vasoconstrictor and increases the concentration of a vasodilator.

74
Q

The ___________ lack the effect on bradykinin levels, which may explain the lower incidence of cough observed with these agents.

A

AT1 receptor antagonists

75
Q

MOA:
Block Na/K/2Cl transporter in renal loop of Henle

EFFECT:
Reduce blood volume and poorly understood vascular effects + greater efficacy

INDICATION:
Severe hypertension, heart
failure

A

Loop diuretics:

Furosemide

76
Q

These CCBs are more CARDIOSELECTIVE

A

VERAPAMIL AND DILTIAZEM

77
Q

These CCBs are more VASOSELECTIVE

A

DIHYDROPYRIDINE

78
Q
  • opening of potassium channels in smooth muscle membranes by minoxidil sulfate, the active metabolite
  • arteriolar dilation
  • PO drug/orally active
  • ADR: Headache, sweating, hypertrichosis
79
Q
  • arterial dilation; given with nitrates for HF and HTN patients
  • in Pt with IHD, may lead to reflex tachycardia and sympathetic stimulation may provoke angina or ischemic arrhythmias
  • PO drug/orally active
  • ADR: nausea, anorexia, palpitations, sweating, and flushing
A

HYDRALAZINE

80
Q
  • treating hypertensive emergencies as well as severe heart failure
  • BOTH arteries and vein dilatation
  • activation of guanylyl cyclase, either via release of nitric oxide or by direct stimulation of the enzyme resulting to an increase in cGMP leading to smooth muscle relaxation
A

NITROPRUSSIDE

81
Q
  • rapid fall in systemic vascular resistance and mean arterial blood pressure
  • MOA: opening potassium channels and stabilizing the membrane potential at the resting level
  • arteriolar dilatation
82
Q

ADR: excessive hypotension, resulting from the recommendation to use a fixed dose of 300 mg in all patients

83
Q

ADR: accumulation of cyanide; metabolic acidosis, arrhythmias, excessive hypotension, and death

A

NITROPRUSSIDE

84
Q
  • peripheral arteriolar dilator used for hypertensive

- emergencies and postoperative hypertension

A

FENOLDOPAM

85
Q
  • ADR: reflex tachycardia, headache, and flushing

- CI: glaucoma Pt – increases IOP more

A

FENOLDOPAM

86
Q

Direct Renin Inhibitors

87
Q

Dopamine agonists

A

FENOLDOPAM

88
Q

MOA:
Block Na/Cl transporter in
renal distal convoluted tubule

EFFECT:
Reduce blood volume and poorly understood vascular effects

INDICATION:
Hypertension, mild heart
failure

A

Thiazides:

Hydrochlorothiazide

89
Q

MOA:
Block Na/K/2Cl transporter in renal loop of Henle

EFFECT:
Reduce blood volume and poorly understood vascular effects + greater efficacy

INDICATION:
Severe hypertension, heart
failure

A

Loop diuretics:

Furosemide

90
Q

MOA: Releases nitric oxide

EFFECT: Powerful vasodilation

INDICATION: Hypertensive emergencies

ROA: Parenteral • short duration

TOXICITY: Excessive
hypotension, shock

A

Nitroprusside

91
Q

SYMPATHOPLEGICS, CENTRALLY ACTING Toxicity:

hemolytic anemia

A

methyldopa

92
Q

also used in withdrawal

from abused drugs

93
Q

MOA:
Blocks vesicular amine
transporter in noradrenergic
nerves and depletes transmitter stores

EFFECTS:
Reduce all sympathetic effects, especially cardiovascular, and reduce blood pressure

INIDICATION: Hypertension but rarely used

TOXICITY: psychiatric depression, gastrointestinal
disturbances

94
Q

MOA:
Interferes with amine release
and replaces norepinephrine
in vesicles

EFFECTS:
Reduce all sympathetic effects, especially cardiovascular, and
reduce blood pressure

INIDICATION: Hypertension but rarely used

TOXICITY: Severe orthostatic hypotension; sexual dysfunction

A

Guanethidine

95
Q

MOA:
Selectively block α1
adrenoceptors

EFFECTS:
Prevent sympathetic
vasoconstriction • reduce
prostatic smooth muscle tone

INDICATION:
Hypertension • benign prostatic hyperplasia

TOXICITY:
Orthostatic hypotension

A

ALPHA BLOCKERS
• Prazosin
• Terazosin
• Doxazosin

96
Q

Nonselective prototype BETA blocker

A

Propranolol

97
Q

Very widely used b1-selective blocker

98
Q

MOA: Block β1 receptors

EFFECTS: Prevent sympathetic cardiac
stimulation • reduce renin secretion

INDICATION:
Hypertension • heart
failure

A

BETA BLOCKERS
• Metoprolol, others
• Carvedilol

99
Q

also blocks α receptors

A

carvedilol

100
Q

MOA: Nonselective block of L-type calcium channels

EFFECTS:
Reduce cardiac rate and output • reduce vascular resistance

INDICATION:
Hypertension, angina,
arrhythmias

A
  • Verapamil

* Diltiazem

101
Q

MOA:
Block vascular calcium
channels > cardiac calcium
channels

EFFECTS:
Reduce vascular resistance

INDICATION:
Hypertension, angina

A

Nifedipine,
amlodipine, other
dihydropyridines

102
Q

MOA: Causes nitric oxide release

EFFECTS:
Vasodilation • reduce vascular resistance • arterioles more sensitive than veins • reflex tachycardia

INDICATION: Hypertension

TOXICITY: Angina,
tachycardia • Lupus-like syndrome

A

Hydralazine

103
Q

MOA:
Metabolite opens K channels
in vascular smooth muscle

INDICATION: Hypertension •
also used to treat hair loss

TOXICITY: Angina,
tachycardia • Hypertrichosis

104
Q

MOA: Releases nitric oxide

EFFECT: Powerful vasodilation

INDICAtion

A

Nitroprusside

105
Q

MOA: Activates D1 receptors

EFFECT: Powerful vasodilation

INDICATION: Hypertensive emergencies

ROA: Parenteral • short duration

TOXICITY: Excessive
hypotension, shock

A

Fenoldopam

106
Q

MOA: Opens K channels

EFFECT: Powerful vasodilation

INDICATION: Hypertensive emergencies

ROA: Parenteral • short duration

TOXICITY: Excessive
hypotension, shock

107
Q

MOA: α, β blocker

EFFECT: Powerful vasodilation

INDICATION: Hypertensive emergencies

ROA: Parenteral • short duration

TOXICITY: Excessive
hypotension, shock

108
Q

MOA: Inhibit angiotensin converting enzyme

EFFECTS:
Reduce angiotensin II levels •
reduce vasoconstriction and
aldosterone secretion • increase bradykinin

INDICATION:
Hypertension • heart failure, diabetes

ROA: Oral

TOXICITY: Cough, angioedema • hyperkalemia
• renal impairment
• teratogenic

A

(ACE-I) Captopril

109
Q

MOA: Block AT1 angiotensin
receptors

EFFECTS:
Reduce angiotensin II levels •
reduce vasoconstriction and
aldosterone secretion

INDICATION:
Hypertension • heart failure

ROA: Oral

TOXICITY: less Cough, angioedema • hyperkalemia
• renal impairment
• teratogenic

A

(ARBs) Losartan

110
Q

MOA: Inhibits enzyme activity of renin

EFFECT: Reduces angiotensin I and II and
aldosterone

INDICATION: Hypertension

ROA: Oral

TOXICITY: Hyperkalemia,
renal impairment • potential
teratogen

A

RENIN INHIBITOR

• Aliskiren

Pharmacology (4 decks)

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