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CV Final Material > Hypertension Drugs 1 > Flashcards

Hypertension Drugs 1 Flashcards

1
Q

How is blood pressure related to risk of stroke and CV disease?

A

Risk rises exponentially with increasing blood pressure

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2
Q

What is the distribution of hypertension within the general population?

A

hypertension exhibits normal distribution

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3
Q

Who gets hypertension the most?

A

older women

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4
Q

What percentage of US adults has hypertension?

A

30.4% about 67 million people

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5
Q

What percentage of US adults with hypertension are under good control?

A

46.5% about 31 million people which means that 53.5% are uncontrolled

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6
Q

What percentage of US adults with uncontrolled hypertension are unaware they have it?

A

about 40%

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7
Q

What adverse CV events can be associated with hypertension?

A 
heart failure
myocardial ischemia & infarction
stroke
aortic aneurysm & dissection
retinopathy
nephrosclerosis
renal failure
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8
Q

According to JNC8, what is the target BP for people >60 years?

A

<90

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9
Q

According to JNC8, what is the target BP for people 18 years with CKD, and >18 years with diabetes?

A

<90

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10
Q

What are the 4 major classes of anti-hypertensive drugs?

A
  • vasodilators
  • adrenergic affecting agents
  • RAS affecting agents
  • diuretics
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11
Q

How do vasodilators in general decrease BP?

A
  • decrease vascular tone which decreases peripheral resistance
  • causes degrees of increased SNS output usually increasing heart rate
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12
Q

What are some direct arterial vasodilators?

A
  • Hydralazine
  • Minoxidil
  • Diazoxide
  • Nitroprusside
  • Fenoldopam
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13
Q

Arterial vasodilators cause direct smooth muscle relaxation reducing perfusion pressure which activates what reflexes?

A

– baroreceptor activation: compensatory increase in sympathetic outflow; tachyphylaxis can cause loss of antihypertensive effect
– Reflex release of renin (which can be blocked by beta-blockers)

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14
Q

What is hypertensive crisis?

A

BP> 180/120

needs to be brought down gradually

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15
Q

What is hypertensive urgency?

A

elevated BP with no acute or progressing target-organ injury

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16
Q

What is hypertensive emergency?

A

high BP with acute or progressing target-organ damage

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17
Q

Hypertensive emergency can result in what?

A

encephalopathy, intracranial hemorrhage, acute left ventricular failure with pulmonary edema, dissecting aortic aneurysm, unstable angina, eclampsia

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18
Q

What is the MOA of nitric oxide donors?

A

NO binds receptor and causes increase in cGMP/protein kinase G

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19
Q

Do nitric oxide donors only work on arteries?

A

No, some venous component

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20
Q

Which nitric oxide donor can cause cyanide toxicity?

A

nitroprusside

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21
Q

General adverse effects of direct arterial vasodilators?

A

– sodium / water retention

– tachycardia / angina

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22
Q

Adverse effect of hydralazine?

A

Hydralazine can cause lupus-like syndrome

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23
Q

Adverse effect of minoxidil?

A

Minoxidil can cause hair growth

24
Q

How could you counteract the fluid retention and reflex tachycardia?

A

Use with diuretic (preferably thiazide) & β-blocker

25
Q

In general, how do Ca channel blockers affect hypertension?

A
  • decrease vascular tone which decrease peripheral resistance
  • there is a small increase in heart rate due to SNS
26
Q

What are some Ca channel blockers?

A
  • Nifedipine
  • Diltiazem
  • Verapamil
  • Amlolodipine
27
Q

What are some non-dihyrdopyridines?

A

diltiazem & verapamil

28
Q

What are some dihyrdopyridines?

A

amlodipine, felodipine & nifedipine

29
Q

Adverse effects of all Ca channel blockers?

A

flushing & headaches

30
Q

Ca channel blockers that cause negative inotropic effect?

A

verapamil > diltiazem > nifedipine

31
Q

Ca channel blockers that cause constipation?

A

verapamil > diltiazem or nifedipine

32
Q

Ca channel blockers that cause decreased AV conduction?

A

verapamil = diltiazem > nifedipine

33
Q

Ca channel blockers that cause edema?

A

nifedipine > verapamil or diltiazem

34
Q

Which adrenergic receptors on the heart increase contractility and HR?

A

beta-1

35
Q

Which adrenergic receptors on arterioles causes vasoconstriciton?

A

alpha-1

36
Q

Which adrenergic receptors on arterioles cause vasodilation?

A

beta-2

37
Q

Which adrenergic receptors on the lungs cause bronchodilation?

A

beta-2

38
Q

Which adrenergic receptors on the kidneys cause increased renin?

A

alpha-1 and beta-1

39
Q

In general, how to mixed alpha blockers lower blood pressure?

A
  • block alpha-1 decreasing vascular tone which decreases peripheral resistance
  • block alpha-2 decreasing venous tone decreases venous return which decrease CO
  • large increase in HR due to SNS
40
Q

What are alpha-1/alpha-2 blocker drugs?

A

Phenoxybenzamine & Phentolamine

41
Q

MOA of alpha-1/alpha-2 blocker drugs?

A

inhibit smooth muscle catecholamine uptake in peripheral vasculature: vasodilation & BP lowering

42
Q

In general, how to alpha-1 specific blockers lower blood pressure?

A
  • block alpha-1 decreasing vascular tone which decreases peripheral resistance
  • smaller increase in HR due to SNS
43
Q

What are some alpha-1 specific blockers?

A
  • Prazozin
  • Terazosin
  • Doxazosin
44
Q

Benefits of being alpha-1 specific?

A
  • Smaller increase in heart rate
  • Do not stimulate renin release
  • Does not block α2 – thus NE can inhibit its own release
45
Q

Alpha-1 blockers have a first dose effect, what’s that?

A

– orthostatic hypotension
– transient dizziness, faintness, palpitations, syncope within 1 to 3 hours of 1st dose
– reflex tachycardia
– first dose at bedtime to minimize effect

46
Q

A mixed α1 /β Blocker can help minimize first dose effect, what’s up with that?

A

– α1 competitive inhibitor
– β1& β2 competitive inhibitor
– Mild orthostatic hypotension & headaches

47
Q

In general, how do beta-blockers lower blood pressure?

A
  • inhibit beta-1 on kidneys decreases renin decreasing ATII decreases vascular tone decreasing peripheral resistance
  • inhibit beta-1 on heart decreasing rate which decreases CO
48
Q

Stimulating beta-1 receptors does what?

A

– heart, kidney

– stimulation increases HR, contractility, renin release

49
Q

Stimulating beta-2 receptors dose what?

A

– lungs, liver, pancreas, arteriolar smooth muscle
– stimulation causes bronchodilation & vasodilation
– mediate insulin secretion & glycogenolysis

50
Q

What are some beta-blocker drugs?

A
  • Propranolol - β1 / β2
  • Metropolol – β1
  • Atenolol – β1
  • Labetalol – β1 / β2 / α1
51
Q

Beta-blockers work best in young adults and work well in older adults in combo with what?

A

diuretics

52
Q

Which beta-blockers are cardio selective?

A

Metropolol & Atenolol have greater affinity for β1 than β2 receptors
– inhibit β1 receptors at low to moderate dose
– higher doses block β2 receptors

53
Q

Cardio selective beta-blockers are safer for who?

A

Safer in patients with bronchospastic disease, peripheral arterial disease, diabetes – may exacerbate bronchospastic disease when selectivity lost at high doses

54
Q

Generally preferred β-blockers for hypertension?

A

Metropolol & Atenolol

55
Q

Potential adverse effects of beta blockers?

A

– Glucose intolerance, masked hypoglycemia
– Bradycardia, dizziness
– Bronchospasm
– Increased triglycerides and decreased HDL
– CNS: Depression, fatigue, sleep disturbances
– Reduced C.O., exacerbation of heart failure
– Impotence
– Exercise intolerance

CV Final Material (16 decks)

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