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AFN Pharm I > Antihypertensives Part I > Flashcards

Antihypertensives Part I Flashcards

1
Q

What is normal blood pressure range

A

< 120/80

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2
Q

What is the range for elevated blood pressure, but not yet stage 1 HTN?

A

120-129 / <80

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3
Q

Stage 1 HTN parameters

A

130-139 systolic

OR

80-89 diastolic

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4
Q

Stage II HTN parameters

A

> =140 systolic

OR

> =90 diastolic

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5
Q

HTN crisis parameters

A

> =180 systolic

OR

> =120 diastolic

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6
Q

(t/f) Mild HTN (130/80) will not cause end-organ damage

A

False,

*Starting at 115/75 CV disease risk doubles every increment of 20/10 increase

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7
Q

Starting at ___/___ CV disease risk doubles every increment of ___/___ increase

A

115/75

20/10

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8
Q

(t/f) Isolated systolic HTN alone is associated with end-organ damage

A

True

*Both systolic and diastolic HTN are associated with end-organ damage

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9
Q

The risk of end-organ damage d/t HTN is increased in what population?

A

African Americans

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10
Q

The risk of end-organ damage d/t HTN is decreased in what population?

A

Premenopausal women

*(when compared to men)

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11
Q

(t/f) HTN is usually asymptomatic until end-organ damage has already occured

A

True

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12
Q

(t/f) You have HTN

A

If you don’t know this you should probably check

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13
Q

Pts who no specific cause can be found for their HTN have what type of HTN?

A

Essential or Primary HTN

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14
Q

Pts who a specific cause can be indentified for their HTN have what type of HTN?

A

Secondary HTN

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15
Q

(t/f) In most cases of HTN, CO is decreased

A

False

*CO remains normal despite increases in SVR (systemic vascular resistance, AKA arterial resistance, AKA afterload)

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16
Q

What is more common, secondary or essential HTN?

A

Essential HTN

*Secondary HTN only accounts for 10-15% of cases

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17
Q

Although we can’t pinpoint what causes essential/primary HTN via studies, what are 3 factors that we think cause it?

A

-Genetics

-Stress

-Diet (increased Na & decreased K or Ca)

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18
Q

What 2 hemodynamic factors make up blood pressure?

A

CO & PVR

*the hydraulic equation of BP is BP = CO x PVR

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19
Q

(t/f) SVR (systemic vascular resistance) is the same as PVR (peripheral vascular resistance)

*not to be confused w/ PVR (pulmonary vascular resistance)

A

True

*whoever labeled it as peripheral vascular resistance should be imprisoned

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20
Q

What is sensing site of BP regulation (MAP specifically) via autonomic/CNS control?

A

Baroreceptors found in the aortic arch & carotid sinus

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21
Q

Increase baroreceptor firing d/t HTN causes what baroreflex response?

A

Inhibition of sympathetic action on BP

*Can also cause parasympathetic stimulation that can only decrease HR to combat the increase in MAP/vessel wall stretch

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22
Q

Decreased baroreceptor firing d/t HoTN causes what baroreflex response?

A

Sympathetic stimulation (increase in PVR, venous tone, and contractility of heart) to increase BP

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23
Q

The endogenous, local release of _____________ from the vascular endothelium causes vasoconstriction

A

Endothelin-1

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24
Q

The endogenous, local release of _____________ from the vascular endothelium causes vasodilation

A

NO (nitric oxide)

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25
Q

With baroreflexive and renal autoregulation of BP, why do pts remain hypertensive chronically?

A

Their baroreceptors and the renal blood volume-pressure control systems are “set” at a higher level of BP

*this is straight from the book in Chpt 11 pg. 3 directly beneath the diagram

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26
Q

What mechanism of BP autoregulation controls BP during postural changes?

A

Baroreflexes

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27
Q

What mechanism of BP autoregulation controls BP over the long term?

A

Renal system

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28
Q

What two actions does the kidney do when it senses an decrease in renal perfusion pressure?

A

-increased reabsorption of Na & H2O

-increased production of renin

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29
Q

How does the kidney increase production of renin without sensing a decrease in renal perfusion pressure?

A

Stimulation of B1 receptors in the JGA

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30
Q

What things does angiotensin II do?

A

-Systemic vasoconstriction (increase SVR, efferent arteriole of kidney)

-stimulation of aldosterone production in the adrenal cortex (reabsorption of Na)

-SNS stimulation

-increases the breakdown bradykinin

-Na+ reabsorption in the PCT

-Increased ADH/Aldosterone

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31
Q

____________ released from the posterior pituitary gland also plays a role in maintainance of blood pressure through its ability to regulate water reabsorption by the kidney.

A

Vasopressin (ADH)

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32
Q

What are the 4 categories of antihypertensive agents?

(think about the different mechanisms of autoregulation and what drugs need to do to lower blood pressure)

A

-Diuretics

-Blocking production or action of angiotensin

-Direct vasodilators

-Sympathoplegic agents (AKA sympatholytics, AKA antisympathetics)

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33
Q

You give hydralazine to a pt (think long term therapy) and their BP is not responding like it should. What other 2 drugs could you give in conjunction with hydralazine?

A

Beta-blocker & Diuretic

*hydralazine dilates arteries, reducing SVR. Compensatory mechanisms, via the baroreceptors & kidneys evoke tachycardia & Na/H2O retention. The BB drops the HR and diuretic prevents Na/H2O reabsorption

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34
Q

If ACEIs only lower BP less than 10mmHg, why do we give them even in severe HTN?

A

-They prevent/reduce renal disease in DM pts

-They reduce chance of HF

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35
Q

Say you have a pt on ACEI, BB, & Diuretic and you need to add another drug. What drug is particularly useful?

A

Spironolactone

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36
Q

What type of drug is spironolactone?

A

Mineralocorticoid antagonist

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37
Q

What are the 3 main actions of glucocorticoids?

A

-converting sugar, fat, and protein stores to useable energy

-inhibiting swelling and inflammation

-suppressing immune responses.

(think stress hormones/steroids. Glucocorticoids increase muscle and fat metabolism to increase serum glucose to fuel the fight or flight response)

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38
Q

What do mineralcorticoids do?

A

-Na absorption

-K+ excretion

*Aldosterone is the only endogenous mineralocorticoid

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39
Q

What is aldosterone?

A

A mineralocorticoid

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40
Q

What does spironolactone block?

A

Aldosterone

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41
Q

Diuretics lower blood pressure primarily by depleting body _______ stores

A

Na

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42
Q

How does increased serum Na cause vessel stiffness?

(this is a minor/newly found effect)

A

Altered Na/Ca exchange leading to increase intracellular Ca. This can lead to vessel stiffness and increased neural reactivity.

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43
Q

Whats another name for aldosterone receptor antagonists?

A

Potassium-sparing diuretics

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44
Q

_________ diuretics are appropriate for most patients w/ mild or moderate HTN & normal renal & cardiac function

A

Thiazide diuretics

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45
Q

_______ diuretics are indicated in severe HTN. Also when multiple drugs that retain ____ are used, in _______ insufficiency (GFR < __-__) and in _______ failure or _________ when there is increase Na retention

A

-Loop diuretics

-retain Na

-renal insufficiency

-GFR < 30-40

-cardiac failure or cirrhosis

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46
Q

Is the antihypertensive effects of thiazide diuretics dose dependent?

A

No

*lower doses of thiazide diuretics exert as much anti-HTN effects as larger doses even though the larger doses are more natriuretic (depletes Na). These diuretics work on the DCT so they can only achieve a certain level of anti-HTN as compared to their stronger colleagues, loop-diuretics.

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47
Q

Are the anti-HTN effects of loop diuretics dose dependent?

A

Yes

*high doses produce more anti-HTN effects

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48
Q

Renin release is stimulated by what 3 things?

A

-low renal artery BP

-sympathetic stimulation (B1 receptors)

-low Na delivery or high Na concentration @ DCT

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49
Q

What converts angiotensin I to angiotensin II?

A

ACE (angiotensin converting enzyme)

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50
Q

Angiotensin II & III stimulate ___________ release

A

Aldosterone

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51
Q

ACEIs help prevent cardiac __________

A

remodeling

*cardiac remodeling happens through a angiotensin cascade in the heart

52
Q

What 4 classes of drugs act on RAAS

A

-ACEI

-ARBs

-Renin blockers (aliskiren)

-Aldosterone antagonists

53
Q

What class of drug is aliskiren?

A

Renin blocker

54
Q

(t/f) BBs can reduce renin secretion

A

True

*we went over this already bro

55
Q

Bradykinin is a potent vaso________ and stimulates the release of _______ & _________

A

-vasodilator

-NO (nitric oxide)

-Prostacyclins

56
Q

Baroreceptor is __________ as the RAAS system is __________

A

Short-term/immediate

Long-term

57
Q

Why are ARBs more effective in blocking RAAS?

A

They block the ACE independent pathway to get from angiotensin I to II, unlike ACEIs

58
Q

Aldosterone cause _______ re-absorption where as ADH (vasopressin) causes ______ reabsorption

A

-Na

-H2O

59
Q

NO (nitric oxide) causes smooth muscle _________ by binding to ________ _________ to convert GTP to ________

A

-diation

-guanylyl cyclase

-cGMP

60
Q

cGMP does what to smooth muscle?

A

Relaxes

61
Q

Which one is a direct vasodilator?

Sodium nitroprusside

or

Nitroglycerin

A

Sodium nitroprusside

*Na nitroprusside converts straight to NO while nitroglycerin has to undergo a few metabolic processes to become NO

62
Q

What is the primary humoral mechanism responsible for BP control?

A

RAAS

63
Q

What vascular substances are involved in the regulation SVR?

A

-Endothelin-1

-NO

64
Q

2 main comphensatory mechanisms after giving vasodilator (hydralazine)

A

-tachycardia

-Na/H2O retention

65
Q

Diuretics can increase your ________ ______ _______ & impair ________ tolerance

A

-serum lipid profile

-glucose tolerance

66
Q

B2 stimulation cause smooth muscle _________ in vasculature and airway

A

Dilation

67
Q

Renin & _____________ combine to make angiotensin I

A

-angiotensinogen

68
Q

What 2 organs can convert angiotensin II to III?

A

Brain

adrenal gland

69
Q

ACEIs will ________ renin levels

A

Increase

70
Q

Aliskiren (renin blocker) reduces plasma renin activity but increases plasma renin levels by up to ___x

A

10x

71
Q

Ending of ACEIs drug names

A

“pril”

72
Q

Endings of ARBs drug names

A

“sartan”

73
Q

Endings of Anti-lipid drug names

A

“statin”

74
Q

Do ACEIs cause reflex SNS activation?

A

No

*they are long-term and act on the long term system (RAAS). The baroreceptors are a reflex and for short-term control and won’t counteract the RAAS inhibition

75
Q

All ACEIs are prodrugs except __________

A

Lisinopril

76
Q

Lisinopril __________ muscle relaxant effects of depolarizing NMBs (succs)

A

increases

77
Q

In what 2 ways do ACEIs lower BP?

A

-blocking angiotensin II formation

-blocking bradykinin metabolism

*bradykinin is a vasodilator so if you stop its metabolism then you have more of it, duh

78
Q

ACEIs have no reflex sypathetic activation so they are safe in pts with _________ _________ disease

*type of cardiac disease

A

Ischemic heart disease

79
Q

3 main adverse effects of ACEIs

A

-dry cough

-angioedema

-hyperkalemia

80
Q

__________ block bradykinin-mediated vasodilation, therefore impair the effect of ACEIs

A

NSAIDs

81
Q

ACEIs/ARBs are contraindicated in _____________ and pts with bilateral ________ artery stenosis

A

-pregnancy

-bilateral renal artery stenosis

82
Q

Why are ACEIs/ARBs contraindicated in bilateral renal artery stenosis?

A

Angiotensin II constricts the efferent arteriole more than the afferent. The efferent (exit) arteriole being constricted helps maintain pressure in the glomerulus to increase GFR. By inhibiting efferent constriction in the case of renal artery stenosis, which will result in decreased afferent blood flow, you will have an extremely reduced GFR. Bilateral knocks out GFR in both kidneys so not good bro.

83
Q

Big take-away differences that ARBs have from ACEIs?

A

-don’t interfere with bradykinin metabolism (no dry cough)

-block RAAS more effecitively cause they also block the ACE independent pathway

84
Q

(t/f) you can give ACEI/ARB in unilateral renal artery stenosis

A

Yep

*you got another kidney

85
Q

Hydralazine dilates _______ more than ________

A

Arteries more than veins

86
Q

Hydralazine doesn’t dilate ________ arteries

A

epicardial arteries

87
Q

Calcium combines with _________ to activate myosin light chain kinase, which induces smooth muscle contraction in the vasculature

A

Calmodulin

88
Q

What does IP3 do mainly?

A

Releases Ca++ from the sarcoplasmic reticulum of smooth muscle (then Ca++ combines with calmodulin to activate myosin light chain kinase to cause contraction)

89
Q

What are the 3 mechanisms of action for hydralazine?

A

-hyperpolarizes smooth muscle by opening K+ channels

-Inhibits IP3 (decreasing Ca++ release)

-Stimulates formation of NO

90
Q

Given hydralazine’s stimulation of the sympathetic nervous system (baroreceptor mediated reflex), it consequently leas to ____________ and _____________

A

-Tachyphylaxis

-Tachycardia

91
Q

A major side effect of hydralazine is a reversible ______-like syndrome at higher doses

A

-lupus-like syndrome

*don’t ask me why

92
Q

Hydralazine onset is ___-___ minutes and peak effect is __-__ mins and duration is __-__ hrs so it may be difficult to titrate

A

-Onset = 10-20mins

-peak = 10-80mins

-duration = 1-4hrs

93
Q

Nitroglycerin dilate _______ more than ________ at low doses

A

Veins more than arteries

94
Q

Minoxidil is similar to ________

A

hydralazine

95
Q

Minoxidil dilates _________

A

arteries

96
Q

Mechanism of action of minoxidil

A

-hyperpolarization by opening K+ channels

97
Q

Is minoxidil stronger than hydralazine?

A

Yes

98
Q

Minoxidil must be given with a ________ and ________ because it is such a strong arterial vasodilator

A

-Beta-blocker

-Diuretic

99
Q

Fenoldopam is a ______ agonsist

A

D1 agonist

100
Q

What 2 things does fenoldopam do?

A

-arterial dilator

-natriuresis/diuresis

101
Q

Beware of fenoldopam in ___________ because it __________ IOP

A

-glaucoma

-increases IOP

102
Q

cGMP _________ platlet aggregation

A

decreases

103
Q

What 4 things does NO do?

A

-vascular smooth muscle dilation

-inhibits plt aggregation

-inhibits leukocyte-endothelial interactions (WBC inflammatory response)

-prevents reabsorption of Na+ & H2O

104
Q

(t/f) SNP (sodium nitroprusside) and nitrate dilate arteries and veins

A

True

105
Q

NTG (administered sublingually) can be administered orally via the drugs _________ __________ & ___________

A

-Isosorbide dinitrate & mononitrate

106
Q

Do you get relfex tachycardia w/ nitrates?

A

Yep

107
Q

__________ is a metabolite of nitroprusside

*nitroprusside get broken down into NO and this compound

A

Cyanide

108
Q

Nitroprusside leads to ________ toxicity

A

Cyanide toxicity

109
Q

To tx cyanide toxicity, you will give ________ __________

A

Sodium thiosulfate

110
Q

What 3 steps to treat cyanide toxicity?

A

1 - stop NTP

2 - 100% O2

3 - sodium thiosulfate

111
Q

Cyanide toxicity leads to ______________ which impairs oxygenation

A

Methemoglobinemia

112
Q

CCBs only work on __-type Ca++ channels

A

L-type

113
Q

Which type of CCBs don’t affect the heart that much?

*aka don’t cause decrease in HR, contractility, conduction velocity, etc.

A

Dihydropyridines

114
Q

Nifedipine, amlodipine, & nicardipine & clevidipine are what kind of CCB?

A

Dihydropyridines

115
Q

Verapamil is what type of CCB?

A

Phenylalkylamine

116
Q

What 2 types of CCBs affect the heart?

*aka decrease HR, contractility, conduction velocity, etc.

A

Phenylalkylamines & Benzothiazepines

117
Q

Diltiazem is what kind of CCB?

A

Benzothiazepines

118
Q

What 2 common CCB drugs affect the heart?

A

-verapamil

-diltiazem

119
Q

What type of CCB affects the heart and vasculature?

A

Benzothiazepines
(diltiazem)

120
Q

What type of CCB only acts mainly on the heart?

A

Phenylaklylamines (verapamil)

121
Q

Dihydropyridine CCBs dilate ________ more than _______

A

arteries more than veins

122
Q

With CCBs, avoid concominant use with ________

A

BBs

123
Q

CCBs are most effective prophylactic tx of _______ angina

A

-variant (prinzmetals) angina

*aka coronary vasospasms

124
Q

Verapamil should be cautioned in pts taking ________

A

Digoxin

125
Q

Which CCB can lead to digoxin toxicity

A

Verapamil

126
Q

(t/f) CCBs are more for rate control because they affect the cardia nodal cells moreso than the myocardial cells

A

True fact bro

127
Q

What CCB has a greater affinity for the cerebral vascular bed?

A

Nicardipine

AFN Pharm I (7 decks)

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