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Pharm Exam 3 > L32 HTN flashcards > Flashcards

L32 HTN flashcards

1
Q

DOC for HTN

A

Thiazides

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2
Q

Sympathomimetic HTN drugs

A

Clonidine and methyldopa

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3
Q

Mechanism of clonidine and methyldopa

A

a2 agonists, cause presynaptic inhibition of adrenergic and cholinergic signalling

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4
Q

clonidine, methyldopa adverse

A

TCA’s inhibit clonidine

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5
Q

Why are patches used for clonidine

A

Prevent peaks and troughs

reduce CNS side effects

Reduce peripheral (xerostomia)

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6
Q

“big deal about methyldopa”

A

positive coombs test from damaged RBCs

Gynocomastia

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7
Q

Other HTN drugs that alter symp function

A

Ganglion blockers

MAOI’s: allows tyramine to be to octopamine
10x less potent than norepi
So sympathetic tone is decreased
Alpha don’t constrict vessels

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8
Q

Adrenergic neuron-blocking agents for HTN

A

reserpine: prevents amaine uptake
Prevents sympathetic tone

Guanethidine: replace NE in vesicles
Blocks release of NE
Coke etc inhibit its effect

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9
Q

a1 adrenergic antagonists (sin drugs)

A

block a1 without affecting a2 (prazosin)

Reduces a1 vasoconstriction
Vaso and arterialdilation

Reduces filling pressure and CO

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10
Q

what is the first dose phenomenon?

Other a1 antag side effects?

A

postural hypotenion

Other side effects:
Palpitations from reflex tachycardia

Decreases GFR = increased renin released
= increased salt & water retention

Note: Do not effect plasma lipids

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11
Q

B adrenergic antagonists for HTN

A

Lower BP by blocking B receptors in:

Heart: lower CO
Kidneys: reduce renin secretion
CNS: reduce sympathetic vasomotor tone

If a vasodilator is used, B blockers can prevent reflex tachycardia

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12
Q

which B blocker doesnt have CNS effect?

A

Atenolol

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13
Q

who should use B blockers for HTN

A

more effective in young white males:
HTN associated with stress

Less effective in African americans

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14
Q

Which B blocker is a vasodilator?

A

nebivolol by increasing NO release

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15
Q

B blocker side effects

A

heart and lung: bronchoconstriction

GI: diahrrea etc

CNS: sedative

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16
Q

Adrenergics that increase decrease or have no effect on insulin release

A

no effect: ISA

B2 increase insulin release

A2 decrease insulin release

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17
Q

B blocker effect for type II diabetics, type I?

A

Type II: decrease glucose tolerance

Type I: no effect because no insulin is released

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18
Q

Who shouldn’t be given B blockers

A

asthmatics

Diabetics

Severe CHF

Heart block: exacerbated in combo with
Ca channel blockers and digoxin

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19
Q

preferred B blocker users

A

angina

Post MI

Migraine

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20
Q

Hydralazine

A

precursor for NO like nitrates or nitrites

Dilates arterioles but not veins

Used only in sever hypertension

21
Q

Big side effect of hydralazine

A

SLE in slow acetylators

Drop in diastolic pressure can cause palpitations,
Angina, arrhythmias, especially with narrow coronary arteries

22
Q

HIP drugs

A

Hyrdalazine

Isoniazid

Procainimide

23
Q

Sodium nitroprusside

A

VERY SHORT T1/2

IV only

Allows for quick pressure refulation

24
Q

sodium nitroprusside toxicity

A

Cyanide accumulation

25
Q

K+ channel openers

A

hyperpolarizes cell, stabilizes cell

DILATES ARTERIOLES BUT NOT VEINS

26
Q

Minoxidil

A

K channel opener, stimulates hair growth

27
Q

Diazoxide

A

A thiazide without diuretic effect

Opens ATP-sensitive K channels (vasodilation)

Decreases insulin release in B cells, 
Increases glucose (hyperglycemic)

Most effective for insuloma

28
Q

adverse diazoxide effects

A

hyperglycemia

Sodium and water retention

Excessive hair growth

29
Q

D1 agonist

A

Fenoldopam

CAMP leads to vasodilation

IV only, short t1/2

30
Q

HTN Ca+ channel blocker mechanism

A

Block slow Ca channels in smooth muscle
(heart and vessels)

Reduced intracellualr Ca:
Vasodilation and lower BP

More effective in arteries

31
Q

Strongest Ca channel blocker vasodilator:

A

dihydropyridines (nifedipine)

Most effective in periphery
Still contraindicated w/ CHF

Little or no inhibition on SA or AV nodes

32
Q

Strongest Ca channel blocker heart effects:

A

Verapamil

33
Q

Most lipid soluble Ca channel blocker

A

nimodipine (crosses BBB)

34
Q

Ca blockermin between verapamil and nifedipine

A

diltiazem

35
Q

Ca channel blockers most effective in:

A

elderly, african americans

36
Q

gingival hyperplasia

A

“dipines”
Phenytoin
Cyclosporin

37
Q

Function of renin-angiotension system (RAS)

A

Guards GFR by increasing filtration pressure by constricting vessels

38
Q

Three RAS inhibitor classes

A

Inhibit:

  1. Angiotensin converting enzyme (ACE)
  2. Angiotensin II receptors (AT1 receptor)
    (ARBs)
  3. Inhibit Renin
39
Q

What does angiotensin do?

A
  1. direct/indirect vasoconstriction
  2. increased aldosterone secretion
    Promotes water and salt retention
  3. promotes cardiac remodeling
40
Q

Two “arms” of ACE

A

Angiotension II: Vasoconstriction
Converts angio I to angioII
(Na and H2O retention can be reversed with K+ sparing diuretics: spironolactone, eplerenon)

Bradykinin Arm: Vasodilation
From increased prostaglandin synthesis

41
Q

What is the normal function of ACE

A

To inactivate Bradykinin path, preventing vasodilation and protaglandin synth

Activate angiotensin path to increase BP

42
Q

Inhibiitng ACE will:

A

Block the angiotensin pathway, so it prevents an increase in BP

Allow bradykinin path to lead to vasodilation and decreased BP

43
Q

Positives of ACE inhibitors

A

Lower BP without compromising heart, brain or kidneys

No lipid changes

No reflex sympathetic (tachycardia)

Effective orally

44
Q

ACE inhibitor (‘prils) uses

A

First choice HT drug for:
Diabetics
Chronic renal disease
LV hypertrophy

Use with thiazides!

45
Q

Why should thiazides be used with ACE inhibitors?

A

Thiazeds lose K

By blocking aldosterone, ACE inhibitors spare K

Balance eachother out and both help wuth HT

46
Q

ACE inhibitor Side effects

A

hypotension in hypovolemic patients

Dry hacking cough

Hyperkalemia

CONTRAINDICATED IN PREGOS

47
Q

ACE inhibitor drug interactions

A

potassium sparing diuretics (hyperkalemia)

NSAIDS (prevents vasodilation by preventing prostaglandin synthesis)

48
Q

ARBs (sartan’s)

A

Same effect as ACE inhibitors EXCEPT it doesn’t block bradykinin

Also, doesnt produce dry cough

49
Q

Renin antagonists

A

Aliskiren

Not really used

PREGNANCY RISK D

Pharm Exam 3 (3 decks)

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