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Pharmacology Exam 2 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Where are beta 1 receptors located?

A

In the heart (responsible for pulse)

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2
Q

Where are beta 2 receptors located?

A

In the bronchioles and blood vessels (responsible for vasodilation)

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3
Q

What is the minimum MAP needed to perfuse the brain?

A

> 65

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4
Q

Equation CO

A

CO = SV x HR

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5
Q

What is stroke volume (SV)?

A

amount ejected with each ventricular beat

influences pulse pressure

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6
Q

What is ejection fraction (EF)?

A

Fraction of end diastolic volume (EDV) ejected with a ventricular beat
(related to contractility)

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7
Q

What are changes in the HR by an increase or decrease in firing of SA node?

A

chronotrophy

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8
Q

What are changes in conduction velocity at the AV node and influences the PR interval on EKG?

A

dromotrophy (how fast)

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9
Q

What happens if there is a sudden decrease in preload?

A

baroreceptor reflex activation resulting in reflex tachycardia and angina

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10
Q

What is known as the force of the contraction?

A

inotropy

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11
Q

What mineral concentration effects inotropy?

A

calcium

increased calcium increases force of contraction

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12
Q

What is responsible for minute to minute BP regulation?

A

baroreceptors

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13
Q

The goal of HTN management is to protect which four organs?

A

eyes
brain
heart
kidneys

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14
Q

Which Rx meds can worsen control of BP?

A

stimulants for ADHD
tricyclic antidepressants (TCA)
venlafaxine (Effexor)
Desvenlafaxine (Pristiq)

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15
Q

Hypertensive urgency vs emergency

A

both have bp >180/110
Urgency DOES NOT target organ damage and hospital admission can be considered
Emergency DOES target organ damage and admitted for management

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16
Q

*Chlorthalidone, chlorothiazide, hydrochlorothiazide, indapamide and metolazone - Class?

A

Thiazide Diuretic

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17
Q

*Thiazide Diuretic - MOA

A

inhibits reabsorption of Na and water by blocking Na/Cl co-transporter on the luminal side of the tubule = decreased plasma volume –> decreased preload

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18
Q

*Can Thiazide Diuretics be used as mono therapy?

A

yes, in early HTN

1st line

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19
Q

Thiazide diuretics - side effects

A

hypokalemia
hyperuricemia –> gout
hyponatremia
metabolic acidosis

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20
Q

*Amiloride (Midamore) and Triamterene (Dyrenium) - class?

A

potassium sparing diuretics

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21
Q

*Potassium sparing diuretics - MOA

A

decrease in membrane permeability to Na by inhibiting epithelial sodium transport at the late distal tubule = bloks the Na and keeps the K

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22
Q

Are potassium sparing diuretics used as mono therapy?

A

usually not

used with thiazide diuretic to off set hypokalemia potential

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23
Q

*Eplerenone (Inspra) and spironolactone (aldactone) - class?

A

Aldosterone antagonists

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24
Q

*Aldosterone antagonists - MOA

A

competitively binds to mineralcorticoid receptor in the distal tubule to prevent the intracellular gene transcription necessary to up regulate the critical components for Na and water reabsorption.

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25
Q

Teaching - why avoid salt subs for many anti-hypertensives?

A

high in K

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26
Q

Good drug choice if Chem 7 shows high Na and low K…

A

Spironolactone

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27
Q

Aldosterone antagonists - side effects

A

hyperkalemia
gynecomastia (spironolactone - 10%)
metabolic acidosis

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28
Q

Eplerenone (Inspra) - DDI

A

CYP450 substrate - caution with inhibitors (if a DDI increases eplerenone, hyper k can worsen)

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29
Q

Aldosterone Antagonists - contraindications

A

K >5.5
CrCl <50 for HTN
concurrent CYP450 inhibitors

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30
Q

*ACE inhibitors - MOA

A

inhibits ACE –>reduces formation of ATII

after load and preload are reduced and acts mainly as a functional vasodilator

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31
Q

*Captopril (Capoten), Enalapril (Vasotec), Lisinopril (Zestril)…-Class?

A

ACE inhibitors

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32
Q

*ACEI or ARB in pregnancy?

A

No - D

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33
Q

Why are Thiazide diuretics not effective with low CrCl?

A

the drug has to get to the renal tubule to work and if CrCl<30 it will not

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34
Q

*ACEI and ARB - DDI

A

NSAIDS with decrease effectiveness of ACEI because prostaglandin blocking will constrict tubules and Jg cells will compensate by increase renin, increase aldosterone and decrease effectiveness.

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35
Q

*ACE inhibitors vs ARB - side effects

A

hypotension, angioedema (emergency b/c airway could close), hyperkalemia
only ACE has dry, non-productive cough (b/c accumulation of bradykinin is irritating)

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36
Q

*Angiotensin Receptor Blockers (ARB) - MOA

A

inhibits the ability of ATII to bind to the AT subtype 1 receptor
–> vasoconstriction, vascular remodeling (important in HF)

Very specific (AT1 subtype)

Same MOA as ACE inhibitors except does not inhibit bradykinin

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37
Q

*Candesartan, Eprosartan, Irbesartan…-class?

A

ARB

“-artan”

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38
Q

Why do new cardiac drugs have a T:P>50?

A

QD dosing

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39
Q

Can ACEI and ARB be used as mono therapy?

A

Yes because do not cause “pseudo” tolerance as with other vasodilators

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40
Q

*Tekturna (Aliskiren) - class?

A

The only renin inhibitor

no clinically relevant benefits over other classes so not 1st line

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41
Q

*Renin inhibitor in Pregnancy?

A

No - D

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42
Q

*Acebutolol, Atenolol, Bisoprolol, Esmolol, Metoprolol, Nebivolol - class?

A

beta blocker - B1 selective

“A-M”

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43
Q

*Nadolol, Pindolol, Propranolol - class?

A

beta blocker non selective B1 and B2

44
Q

*Beta blockers - MOA (brain)

A

decrease sympathetic NS outflow - protects sudden cardiac death

45
Q

*Beta blockers - MOA (heart)

A

effect phase 4 depolarization
decrease O2 demand so improves ischemia
decreases force of contraction

46
Q

*Beta blockers - MOA (vessels)

A

inhibits B2 receptors - vasoconstriction
inhibits alpha1 and alpha2 - vasodilation
*better at HR control than BP

47
Q

*Beta blockers - MOA (kidneys)

A

inhibits B1 receptors –> reduces renin –> reduces Na

48
Q

*Beta blockers - side effects

A 
bradycardia
AV heart block (prolonged PR interval)
bronchospasm in hyperactive airway disease
fatigue
depression
decreased sexual function
Mask hypoglycemia b/c won't get tachy
49
Q

*Beta blockers in pregnancy?

A

YES :)

50
Q

*Diltiazem and Verapamil - class?

A

Non-DHP CCB

act on heart and periphery

51
Q

*Amlodipine, Nicardipine, Nifedipine, Nimodipine…-class?

A

Dihydropyridine (DHP) CCB

act on periphery

52
Q

*CCB - MOA

A

inhibits Ca entry by blocking channels in the SA and AV nodes
–>decreased HR
–>decreased force of contraction
decreases O2 demand

53
Q

*CCB for HF?

A

No! does not protect against sudden death because no remodeling
*Contraindicated

54
Q

*CCB - 2 drugs with DDI because sub/inhib CYP3A4

A

Diltiazem and Verapamil

55
Q

*CCB - side effects

A 
bradycardia
reflex tachy
AV heart block
constipation
*lower extremity edema*
56
Q

CCB in WPW?

A

caution! can worsen condition because has accessory pathways around AV node and can cause increased pulse because bypasses

57
Q

*Which 2 Mixed Beta Blockers require tedious titration?

A

Esmolol and Carvedilol

58
Q

*Clonidine and Methyldopa - class?

A

Alpha 2 receptor agonist

59
Q

*Preferred HTN treatment in pregnancy

A

Methyldopa

60
Q

*Alpha 2 receptor agonist - MOA?

A

work in CNS to decrease sympathetic outflow onto the heart, blood vessels and kidneys

Reduce preload and after load

61
Q

*Alpha 2 receptor agonist - side effects

A

sedation
erectile dysfunction
*rebound HTN and tachy if abruptly stopped

62
Q

What is the most commonly prescribed Thiazide diuretic?

A

hydrochlorathiazide (HCTZ)

63
Q

HCTZ - Pregnancy?

A

Yes - B

64
Q

Why might Chlorthalidone be more effective than HCTZ?

A

longer T1/2
more potent
greater lowering of BP
maybe less cardiac events

65
Q

Digoxin - what needs to be monitored?

A

Levels b/c narrow TI

66
Q

What 2 classes are known substrates of CYP2D6?

A

Beta Blockers (anti-hypertensive) and antiarrhythmics

67
Q

Which 2 populations are at greatest risk for being a poor metabolizer of CYP2D6?

A

Blacks and Asians

68
Q

How does amiodarone increase risk for hyperthyroidism?

A

contains a large amount of iodine. Get baseline TSH and repeated levels q 6-12 mos.

69
Q

Licorice contains glycyrizzhic acid and can cause…

A 
hypertension
hypokalemia
hypervolemia
Na retention
edema
70
Q

Garlic for HTN - dosing

A

Kwai (garlic powder) 600-900 mg/day

71
Q

Beta blockers - inhibit sympathetic or parasympathetic NS?

A

sympathetic

72
Q

BP goal for non-DM or chronic kidney disease (CKD)

A

<140/90

73
Q

BP goal if DM or CKD

A

<130/80

74
Q

Garlic for HTN - MOA

A

inhibits ACE
increases NO
(some pts reduce BP by >20%)

75
Q

Why can diabetics still sweat on beta blockers?

A

postganglionic sympathetic nerve fibers secrete Ach (most sympathetic responses are related to norepinephrine)

76
Q

Which beta blocker do patients tend to feel worse before better?

A

Carvedilol (Coreg)

10-14 days

77
Q

Garlic - effect on blood vessels

A

dilates (lowers BP)

78
Q

Which aldosterone antagonist has more DDI (CYP450)?

A

Eplerenone

78
Q

Treatment secondary hypertension r/t hyperaldosteronism and what labs would you see?

A

Aldosterone antagonist

Lab: high na, low k

78
Q

Why do thiazides diuretics potentially cause more hyponatremia?

A

Work on the last place for reabsorption - distal tubule

78
Q

What does aldosterone do?

A

Changes the cell membrane so more Na can be reabsorbed.

78
Q

What does angiotensin do?

A

Vasoconstricts and remodels

78
Q

What enzyme facilitates conversion of angiotensin I to II?

A

ACE

78
Q

Why are thiazide diuretics useful in osteoporosis?

A

Improves Ca reabsorption

79
Q

Which diet is recommended for hypertension?

A

DASH

80
Q

ACEI or ARB as mono therapy?

A

Yes, very good

81
Q

Why are ACEI or ARB less effective as mono therapy in AAs?

A

Make less renin (combo therapy is not an issue)

82
Q

How do ACEI and ARB confer “renal protective effects” in diabetics?

A

Decrease glomerular filtration pressures –> Block angio 2 vasoconstriction and decreases pressure.

83
Q

Why does ARB not have cough as ADE if MOA is same as ACEi?

A

Same but does not inhibit bradykinin –> buildup causes cough in ACEI.

84
Q

Are renin inhibitor used as first line?

A

No advantage over ACEI and ARB. Only one drug (aliskiren)

Same ADE, preg,etc.

85
Q

Why is it beneficial to reduce remodeling of the myocardium?

A

Leads to angina

Disorganized myocardial fibers make contraction less effective

86
Q

Which classes of anti hypertensives reduce remodeling?

A

ACEI
ARB
BB

Not DHP CCB (dilt and verapamil)

87
Q

Preferred class for HF?

A

Beta blockers

88
Q

Are BB effective as BP lowering?

A

No, better at rate control b/c don’t have the beta 2 vasodilation effect.

89
Q

What happens when renin is released?

A

Release aldosterone –> Na/water reabsorption and increase plasma volume.

90
Q

What are the only 3 BB FDA approved for HF?

A

Bisoprolol
Metoprolol succinctness
Carvedilol

91
Q

Which non selective BB is hydrophilic (renal), long T 1/2 (qd dosing)?

A

Nadolol

Be careful in renal pts

92
Q

Which non selective BB is lipophilic (liver), has more DDI, short t1/2?

A

Propranolol

Careful in cirrhosis and decreased hepatic function.

93
Q

Can you crush metoprolol succinctness (toprol XL)?

A

No, but can break on scored line.

94
Q

CCB - phase if action

A

Dromotropy

95
Q

BB phase of action

A

Inotrophy

96
Q

Which DHP CCB can be used as a tocolytic?

A

Nifedipine.

97
Q

Clonus one, guanfacine, methyldopa - class?

A

Alpha 2 receptor agonist

98
Q

Non stimulant options for ADHD (alpha 2 Receptor agonist)

A

Clonidine

Guanfacine

99
Q

Which alpha 2 receptor agonist can be used for opiate/benzo/ethos withdrawal?

A

Clonidine

100
Q

Which alpha 2 agonist can cause hemolytic anemia?

A

Methyldopa

Pharmacology Exam 2 (9 decks)

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