L32 HTN flashcards Flashcards by Scott Gunderson

DOC for HTN

Thiazides

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Sympathomimetic HTN drugs

Clonidine and methyldopa

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Mechanism of clonidine and methyldopa

a2 agonists, cause presynaptic inhibition of adrenergic and cholinergic signalling

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clonidine, methyldopa adverse

TCA’s inhibit clonidine

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Why are patches used for clonidine

Prevent peaks and troughs

reduce CNS side effects

Reduce peripheral (xerostomia)

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“big deal about methyldopa”

positive coombs test from damaged RBCs

Gynocomastia

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Other HTN drugs that alter symp function

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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Adrenergic neuron-blocking agents for HTN

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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a1 adrenergic antagonists (sin drugs)

block a1 without affecting a2 (prazosin)

Reduces a1 vasoconstriction
Vaso and arterialdilation

Reduces filling pressure and CO

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what is the first dose phenomenon?

Other a1 antag side effects?

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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B adrenergic antagonists for HTN

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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which B blocker doesnt have CNS effect?

Atenolol

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who should use B blockers for HTN

more effective in young white males:
HTN associated with stress

Less effective in African americans

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Which B blocker is a vasodilator?

nebivolol by increasing NO release

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B blocker side effects

heart and lung: bronchoconstriction

GI: diahrrea etc

CNS: sedative

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Adrenergics that increase decrease or have no effect on insulin release

no effect: ISA

B2 increase insulin release

A2 decrease insulin release

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B blocker effect for type II diabetics, type I?

Type II: decrease glucose tolerance

Type I: no effect because no insulin is released

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Who shouldn’t be given B blockers

asthmatics

Diabetics

Severe CHF

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

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preferred B blocker users

angina

Post MI

Migraine

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Hydralazine

precursor for NO like nitrates or nitrites

Dilates arterioles but not veins

Used only in sever hypertension

Big side effect of hydralazine

SLE in slow acetylators

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

HIP drugs

Hyrdalazine

Isoniazid

Procainimide

Sodium nitroprusside

VERY SHORT T1/2

IV only

Allows for quick pressure refulation

sodium nitroprusside toxicity

Cyanide accumulation

K+ channel openers

hyperpolarizes cell, stabilizes cell DILATES ARTERIOLES BUT NOT VEINS

Minoxidil

K channel opener, stimulates hair growth

Diazoxide

A thiazide without diuretic effect Opens ATP-sensitive K channels (vasodilation) ``` Decreases insulin release in B cells, Increases glucose (hyperglycemic) ``` Most effective for insuloma

adverse diazoxide effects

hyperglycemia Sodium and water retention Excessive hair growth

D1 agonist

Fenoldopam CAMP leads to vasodilation IV only, short t1/2

HTN Ca+ channel blocker mechanism

Block slow Ca channels in smooth muscle (heart and vessels) Reduced intracellualr Ca: Vasodilation and lower BP More effective in arteries

Strongest Ca channel blocker vasodilator:

dihydropyridines (nifedipine) Most effective in periphery Still contraindicated w/ CHF Little or no inhibition on SA or AV nodes

Strongest Ca channel blocker heart effects:

Verapamil

Most lipid soluble Ca channel blocker

nimodipine (crosses BBB)

Ca blockermin between verapamil and nifedipine

diltiazem

Ca channel blockers most effective in:

elderly, african americans

gingival hyperplasia

“dipines” Phenytoin Cyclosporin

Function of renin-angiotension system (RAS)

Guards GFR by increasing filtration pressure by constricting vessels

Three RAS inhibitor classes

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

What does angiotensin do?

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

Two “arms” of ACE

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

What is the normal function of ACE

To inactivate Bradykinin path, preventing vasodilation and protaglandin synth Activate angiotensin path to increase BP

Inhibiitng ACE will:

Block the angiotensin pathway, so it prevents an increase in BP Allow bradykinin path to lead to vasodilation and decreased BP

Positives of ACE inhibitors

Lower BP without compromising heart, brain or kidneys No lipid changes No reflex sympathetic (tachycardia) Effective orally

ACE inhibitor ('prils) uses

First choice HT drug for: Diabetics Chronic renal disease LV hypertrophy Use with thiazides!

Why should thiazides be used with ACE inhibitors?

Thiazeds lose K By blocking aldosterone, ACE inhibitors spare K Balance eachother out and both help wuth HT

ACE inhibitor Side effects

hypotension in hypovolemic patients Dry hacking cough Hyperkalemia CONTRAINDICATED IN PREGOS

ACE inhibitor drug interactions

potassium sparing diuretics (hyperkalemia) NSAIDS (prevents vasodilation by preventing prostaglandin synthesis)

ARBs (sartan's)

Same effect as ACE inhibitors EXCEPT it doesn't block bradykinin Also, doesnt produce dry cough

Renin antagonists

Aliskiren Not really used PREGNANCY RISK D