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316 Pharmacology > Exam 2: Hypertension > Flashcards

Exam 2: Hypertension Flashcards

1
Q

How many Americans have hypertension

A

76 million Americans

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2
Q

If uncontrolled, HTN can lead to serious heart problems like

A
  • Damage to heart and vessel
  • Kidney damage
  • Stroke
  • erectile dysfunction
  • Vision loss
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3
Q

Examples of damage to heart and vessel from HTN

A

Angina

Peripheral artery disease

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4
Q

What is the number one cause of stroke

A

Hypertension

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5
Q

Essential hypertension

A

Chronic elevation in BP with no clearly identifiable etiology (except genetics/environmental)

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6
Q

Essential hypertension accounts for ____% of hypertension

A

90-95%

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7
Q

Onset age for essential hypertension

A

40’s to 50’s

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8
Q

Blood pressure =

A

(Peripheral vascular resistance)(Cardiac output)

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9
Q

Cardiac output =

A

(Heart rate) (stroke volume)

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10
Q

Stroke volume =

A

End diastolic volume - end systolic volume

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11
Q

Genetic predisposition/ _____ of patients have family history of essential hypertension

A

70-80

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12
Q

Goal of treatment for essential hypertension

A

BP < 140/90 and minimizing morbidity and mortality

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13
Q

Secondary hypertension has a

A

Identifiable etiology

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14
Q

For secondary hypertension. many factors influencing CO, SVR, and BP can be disrupted by disease processes that impact:

A

Volume status
Adrenergic tone
Peripheral Vascular resistance

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15
Q

goal of treatment for secondary hypertension

A

Treat underlying cause and minimizing morbidly and morality

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16
Q

Symptoms, when present, are caused

A

By long term effects of HTN on susceptible organs

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17
Q

Essential hypertension complications/target organ damage

A 
RENAL disease 
Heart 
Brain 
Peripheral vasculature 
Eyes
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18
Q

examples of heart complications due to essential hypertension

A

Left ventricular hypertrophy
Angina
Myocardial infarction
Heart failure

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19
Q

examples of brain complications due to essential hypertension

A

Stroke or transient ischemic attack

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20
Q

examples of peripheral vasculature complications due to essential hypertension

A

Peripheral arterial disease

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21
Q

examples of eyes complications due to essential hypertension

A

retinopathy

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22
Q

Classifications of antihypertensives

A 
Ace inhibitors 
ARBs 
Aldosterone inhibitors 
Renin inhibitors 
Vasodilators 
Diuretics 
CCBs 
Sympatholytics
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23
Q

Acronym to remember antihypertensive classifications

A 
Always 
Accept 
A 
Red 
Valentine's 
Day
Card 
Surprise
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24
Q

Ace inhibitors end in

A

-Prils

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25
Q

All Ace inhibitors are administered

A

PO

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26
Q

Which ace inhibitor is not administered PO

A

Enalaprilat

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27
Q

All ace inhibitors are prodrugs besides

A

Captopril and lisinopril

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28
Q

Indications for ace inhibitor/ captopril

A

hypertension
heart failure
Diabetic nephropathy
Left ventricular dysfunction following MI

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29
Q

MoA of ACE inhibitors/ CaptoPRIL

A

Blocks ACE from converting angiotensin I to angiotensin II, leading to decreased

  • vasoconstriction
  • Peripheral vascular resistance
  • Aldosteron production
  • Fluid volume
  • – Overall decreased BP
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30
Q

Adverse effects of captopril (& other ACE inhibitors)

A

Hypotension: Especially in 1st dose due to abrupt lowering of angiotensin II
Dry, persistent cough (ACE COUGH; secondary to increase bradykinin)
Hyperkalemia: secondary to inhibition of aldosterone; rare, but increase risk if also taking potassium-sparing diuretic, potassium supplements
Swelling of tissues (angioedema)

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31
Q

Hyperkalemia

A

High potassium levels

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32
Q

Most common reason for discontinuing ACE inhibitor therapy

A

Dry, persistent cough: ACE cough

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33
Q

Advise individuals to not take ____ during ACE inhibitors

A

Do not take K+ supplements or salt substitutes

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34
Q

Ace inhibitors are good antihypertensives for diabetics because

A

they limit damage to renal blood vessels often seen in diabetic patients and other patients with renal disorders

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35
Q

Black box warning for ACE inhibitors

A

Drugs that act on RAAS can cause injury/death to developing fetus

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36
Q

Should ACE inhibitors be given to pregnant women

A

No!

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37
Q

Angiotensin II receptor blockers (ARBs) end with

A

-sartans

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38
Q

All angiotensin II receptor blockers (ARBs) are given how?

A

All PO

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39
Q

Indications for Angiotensin II receptor blockers (ARBs) / Iosartan

A

Hypertension
Congestive Heart Failure
Myocardial infarction
Stroke Prevention

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40
Q

MoA ARBs

A 
Blocks actions of angiotensin II which causes vasodilation and decreased 
- peripheral vascular resistance 
- aldosterone production 
- fluid volume 
and overall decreased BP
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41
Q

All anihypertensives can cause what adverse effect

A

hypotension

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42
Q

Adverse effects for angiotensin II receptor blockers (ARBs)

A

Hypotension

Hyperkalemia

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43
Q

Rare adverse effects for ARBs

A

Thrombocytopenia
Rhabdomyolysis
Angioedema

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44
Q

Black boxed warnings for ARBs

A

drugs that act on RAAS can cause injury/death to developing fetus

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45
Q

Should ARBs be given to pregnant women

A

No!

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46
Q

Aldosteron inhibitors in this unit end in

A

-one

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47
Q

Indications for aldosterone inhibitors (spironolactone)

A

Hypertension
Heart failure
and following Myocardial infarction

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48
Q

MoA for aldosterone inhibitors

A

Blocks the release of aldosterone, leading to the urinary excretion of Na and H2O, also causes retention of K+

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49
Q

Retention of K+ or hyperkalemia can be due to

A

no exchange of Na, this can be done from urinary excretion of Na or reuptake of Na as oppose to Na/K exchange

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50
Q

Side effects of aldosterone inhibitors

A

Hypotension and Hyperkalemia

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51
Q

The only Direct Renin Inhibitor (DRI) currently on the market

A

Aliskiren

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52
Q

Aliskiren drug class

A

Renin inhibitors

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53
Q

Aliskiren is given

A

PO only

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54
Q

Aliskiren MoA

A

Binds to renin to inhibit conversion of angiotensinogen to angiotensin I, thereby suppressing the RAAS

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55
Q

When aliskiren is administered with high fat meals, it

A

decrease absorption

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56
Q

Adverse effects of aliskiren

A

Hypotension and hyperkalemia

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57
Q

are long term benefits and safety of aliskiren known?

A

No, they are not known yet

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58
Q

As a drug that affects RAAS, should aliskiren be given to pregnant women

A

No!

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59
Q

Vasodilator examples

A

Fenoldopam
Hydralazine
Minoxidil
Nitroprusside

60
Q

Indications for vasodilators

A

Hypertension
Heart failure
Pulmonary Hypertension

61
Q

MoA vasodilators

A

Vasodilation leads to decreased arterial pressure and decreased peripheral vascular resistance, as a result, we also see an increase heart rate and increase contractility of the heart

62
Q

Adverse effects of vasodilators

A

Hypotension
Palpitations
Tachycardia
W/ high doses—> fluid retention edema, systemic lupus erythematous like S/S

63
Q

systemic lupus erythematous like symptoms and signs

A

Facial rash, joint pain, fever, nephritis, and pericarditis

64
Q

Nitroprusside (nitropress) drug class

A

Vasodilator, antihypertensive

65
Q

MoA for nitroprusside

A

produces peripheral dilation by direct action on both arteriolar and venous smooth muscle, which caused decreased peripheral vascular resistance

66
Q

Black box warning for nitroprusside

A

Never inject directly!! dilute first!

67
Q

Indications for nitroprusside

A

Lower blood rapidly in hypertensive emergencies

Controlled hypotension during surgical procedures

68
Q

Continuous BP monitoring of nitroprusside should be done by

A

experienced personnel

69
Q

Extensive hypotension from nitroprusside can result in

A

hypo perfusion of vital organs may occur

70
Q

Adverse effects of nitroprusside

A

Hypotension: if administration is too rapid, it can cause a precipitous fall in BP
Sodium and water retention
Cyanide toxicity

71
Q

How to combat sodium and water retention from nitroprusside

A

Furosemide

72
Q

Cyanide toxicity and nitroprusside

A

nitroprusside contains 5 cyanide groups which are split free in the 1st step of nitroprusside metabolism

73
Q

Nitroprusside gives rise to large cyanide quantities except when

A

used briefly or at low infusion rates

74
Q

Hydralazine drug class

A

Hypertension, pre-eclampsia/eclampsia, heart failure

75
Q

MoA hydralazine

A

Direct vasodilation of arterioles (little effects on veins) which cause decreased systemic resistance

76
Q

Nursing considerations/adverse effects of hydralazine

A

Hypotension: orthostatic precautions should be observed

Peripheral neuritis

77
Q

Peripheral neuritis (from hydralazine) symptoms

A

Numbness, paresthesia, tingling

Secondary to antipyridoxine effect

78
Q

Types of diuretics

A

Thiazide diuretics
Loop diuretics
Potassium Sparing diuretics

79
Q

Thiazide diuretics include

A

Chlorthiazide, hydrochlorothiazide

80
Q

Thiazide diuretics indications

A

Hypertension
Heart failure
Liver Cirrhosis
Renal failure

81
Q

MoA of thiazide diuretics

A

In the DISTAL CONVOLUTED TUBULE of the nephron, block NA and Cl reabsorption, leading to increase excretion of Na, Cl, H2O, K+

82
Q

Adverse/side effects of thiazide diuretics

A 
F/E imbalances such as 
-Hyponatremia 
-Hypochloremia 
-Hypokalemia 
-Dehydration
-Hyperglycemia 
and increased uric acid
83
Q

F/E imbalances refer to

A

loss of both water and solutes in the same proportion from the extracellular fluid space

84
Q

Loop diuretics include

A

Bumethanide
Furosemide
Ethacrynic acid
Torsemide

85
Q

Loop diuretics indications

A

Hypertension
Heart failure
Edema

86
Q

Loop diuretics MoA

A

in the ASCENDING LOOP OF HENLE, blocks Na, Cl, K+ and water reabsorption, leading to increase excretion of Na, Cl, H2O and K+

87
Q

Loop diuretics’ effect is much more

A

potent than other diuretics

88
Q

Adverse and side effect of loop diuretics

A

F/E imbalances such as hyponatremia, hypochloremia, hypokalemia, dehydration, orthostatic hypotension, hyperglycemia, AND
-Increase uric acid
ALSO- ototoxicity

89
Q

Examples of potassium sparing diuretics

A

Amiloride
Spironolactone
Triamterene

90
Q

Potassium sparing diuretics indications

A 
Hypertension 
Heart Failure 
Edema 
Cirrhosis 
Nephrotic syndrome 
HYPOkalemia
91
Q

MoA Potassium Sparing Diuretics

A 
in the DISTAL PORTION OF NEPHRON, blocks Na, Cl, and water reabsorption, 
which leads to 
- increased excretion of NA
- Smaller loss of H2O
- Decreased excretion of K+
92
Q

Adverse/side effects of Potassium Sparing Diuretics

A

Hyperkalemia

Gynecomastia in males

93
Q

Gynecomastia

A

overdevelopment or enlargement of breast tissue in mens/boys

94
Q

Calcium channel blockers prevent the

A

movement of calcium ions into cardiac and vascular smooth muscle cells

95
Q

Calcium channel blockers have major

A

therapeutic effects on heart and arteries

96
Q

Calcium channel blockers indication

A

Hypertension
Angina pectoris
Cardiac dysrhythmias

97
Q

Calcium channels are

A

Gated pored in the plasma membrane that regulate the entry of calcium ions into cells

98
Q

Calcium plays an important role in

A

function of vascular smooth muscle and heart

99
Q

At therapeutic doses, calcium channel blockers act

A

SELECTIVELY on the peripheral arterioles and/or cardiac arteries/arterioles

100
Q

When an action potential travels down surface of smooth muscle cells, what happens to calcium channels?

A

Calcium channels open and calcium ions flow inward, initiating contraction

101
Q

Blockage of the calcium prevents

A

Contraction, resulting in vasodilation

102
Q

Calcium entry into myocardium has a

A

Positive inotropic effect

103
Q

Positive inotropic effects mean

A

strengthen the heart’s contractions, so it can pump more blood with fewer heartbeats

104
Q

Cardiac effects of calcium on the SA node

A

Open calcium channels in SA node cause an increase spontaneous discharge of SA node

105
Q

Cardiac effects of calcium on the AV node

A

Open calcium channels in AV node cause AV node to fire more readily

106
Q

Calcium Channel Blockers can be categorized as

A

Dihydropyridines

Non-Dihydropyridines

107
Q

Dihydropyridines

A

Work primarily on the smooth muscles of there arteries; vasodilation

108
Q

Examples of Dihydropyridines calcium channel blockers

A

Amlodipine
Felodipine
Nicardipine
Nifedipine

109
Q

Non-Dihydropyridines

A

Negative inotropic effect on the heart;
Slow conduction through AV node
Decrease rate of SA node firing

110
Q

Examples of non-Dihydropyridines calcium channel blockers

A

Diltiazem

Verapamil

111
Q

non-dihydropyridines calcium channel blockers MoA

A

inhibits the movement of calcium ions across the membranes of cardiac & arterial muscle cells:

  • coronary vasodilation
  • peripheral vasodilation
  • negative chronotrope
  • negative inotrope
  • negative fromotrope
  • increased CO
  • Decrease BP
  • Decrease myocardial O2 consumption and increase blood supply to heart
112
Q

Adverse effects of non-dihydropyridines calcium channel blockers

A

Hypotension
Bradycardia
Peripheral edema
Heart block (increased risk with concurrent digoxin)
Constipation
Headache
Cardriosuppressant effects of beta blockers intensified with concurrent CCB

113
Q

When taking non-Dihydropyridines calcium channel blockers, patients should avoid

A

Grapefruit juice as it can delay CCB metabolism and produce toxic levels

114
Q

examples of sympatholytics

A

Alpha-1 adrenergic blockers
Beta adrenergic blockers
Alpha and Beta adrenergic blockers
Centrally acting alpha-2 agonists

115
Q

Examples of alpha 1 adrenergic blocking agents

A

Doxazosin
Prazosin
Terazosin

116
Q

Alpha 1 adrenergic blocking agents end in

A

-zosin

117
Q

Alpha 1 adrenergic blocking agent indication

A

Hypertension
Benign prostatic hyperplasia
-not listed treatment of PHEOCHROMOCYTOMA, extravasation

118
Q

MoA of alpha 1 adrenergic blocking agents, antagonist

A

Blocks alpha 1 receptors along the walls of peripheral blood vessels,
Leading to VASODILATION

119
Q

Side effects of alpha 1 adrenergic blocking agents

A

Orthostatic hypotension
Reflex tachycardia
Headache

120
Q

Most therapeutic effects are due to

A

Blockage of alpha 1 receptors on the vasculature

121
Q

Indications for alpha 1 adrenergic blocking agents

A
  • Hypertension: blocks alpha 1 on arterioles and veins, leading decrease in peripheral vascular resistance, which causes a decrease in blood pressure
  • reversal of sympathomimetic drug effects! (epinephrine) in cases of OD/toxicity
  • Prevention of tissue necrosis following extravasation of drugs that produce vasoconstriction (phentolamine approved for use)
  • Benign prostatic hyperplasia: selective blockage of alpha-1 receptors on bladder beck, prostatic capsule)
  • Pheochromocytoma (catecholamine-secreting tumor)
122
Q

Terazosin drug class

A

Alpha 1 adrenergic blockers

123
Q

Terazosin administration

A

PO only

124
Q

Terazosin MoA

A

Competitive antagonist that produces SELECTIVE blockage of alpha-1 adrenergic receptors

  • Decrease in arterial tone, leading to decrease peripheral vascular resistance, which leads to DECREASE IN BP
  • Relaxation of bladder neck & prostatic capsule (used for benign prostatic hyperplasia)
125
Q

Adverse/side effects of terazosin

A 
Orthostatic hypotension 
Tachycardia 
Syncope following 1st dose 
Impotence, decreasing libido 
Retention of sodium and water (often combined with diuretic to counteract this effect) 
Nasal congestion 
Dizziness
126
Q

Beta adrenergic antagonists

A

Beta blockers
Nonselective - blocks beta 1 and beta 2
Selective - blocks only beta 1

127
Q

Major therapeutic effects of beta adrenergic antagonists

A

Blockage of beta 1 receptors in the heart

128
Q

**. Indications of beta adrenergic antagonists

A

Angina pectoris: decrease cardiac workload and decrease O2 consumption
Cardiac dysrhythmias: Decrease rate of sinus nodal discharge & suppress conduction of atrial impulses through AV node which prevents ventricles from being driven by excessive rate
Myocardial infarction: decrease infarct size, decrease risk on reinfarction, and decrease in mortality
Hypertension
Migraine prophylaxis
also used in pain management

129
Q

Beta adrenergic blockers end in

A
  • olol
130
Q

Metoprolol drug class

A

Caridioselective Beta 1 adrenergic antagonist, beta blocker

131
Q

Advantages of metoprolol

A

@ normal, therapeutic dosages, blocks Beta 1 receptor sites only (Although selectivity is not absolute)
- may be used in proteins with bronchospastic disease with caution

132
Q

Metoprolol MoA

A

Selective inhibitor of B-1 adrenergic receptors leads to multiple therapeutic effects:

  • Decrease in conduction through AV node (decrease heart rate)
  • Decrease in force of cardiac contraction
  • Decrease in renin secretion
133
Q

Adverse effects and side effects of metoprolol

A 
Hypotension 
Bradycardia 
Dizziness 
Heart block 
Heart failure 
-Drowsiness 
-Vertigo 
- Contraindicated in patients with history of severe allergy 
--- CAUTION IN DIABETICS
134
Q

Black box warning for metoprolol

A

Not be withdrawn abruptly! gradually taper (over 1-2 weeks) to avoid acute tachycardia, hypertension, and/or ischemia

135
Q

Alpha and beta adrenergic antagonists examples

A

Carvedilol

Labetolol

136
Q

Alpha and Beta Adrenergic antagonist MoA

A

Blocks both Alpha-1 and Beta adrenergic receptors

  • Vasodilation
  • Decrease Heart rate
  • Decrease force of contraction
  • Decrease release of renin from kidneys
137
Q

Adverse and side effects of alpha and beta adrenergic antagonists

A

Dizziness
Hypotension
Bradycardia

138
Q

Examples of centrally acting alpha-2 adrenergic agonists

A

Clonidine
Guanfacine
Methyldopa

139
Q

MoA centrally acting alpha-2 adrenergic agonists

A

-inhibits innervation of sympathetic neurons in the CNS, leading to a
- Decreased outflow of NE,
- Decrease heart rate
- Decrease contractility
Vasodilation

140
Q

Adverse/side effects of centrally acting alpha-2 adrenergic agonists

A

Drowsiness
Dizziness
Rebound hypertension if abruptly discontinued

141
Q

Clonidine drug class

A

Alpha- 2 adrenergic agonist

142
Q

MoA clonidine

A
  • stimulates alpha-2 adrenoceptors in brain stem (in areas associated with autonomic regulating of CV system) LEADS TO
  • activation on inhibitory neurons
  • Decrease in sympathetic outflow from CNS to CV system
  • Decrease in peripheral vascular resistance
  • Decrease in cardiac output
  • Decrease in blood pressure
143
Q

Clonidine administration

A

PO or transdermal patch

144
Q

Adverse effects of clonidine

A

Bradycardia, hypotension, CNS depression (causing drowsiness); discontinue by tapering slowly to avoid rebound hypertension

145
Q

Clonidine can also be used to prevent

A
  • Cancer pains ( can be used as a pain medication because it prevents pain signal transmission)
  • indicated for ADHD

316 Pharmacology (19 decks)

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