Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/14

Click to flip

14 Cards in this Set

  • Front
  • Back
Adrenergic Neuron Fxn blockers: Guanadrel
antiHTN

exogenous false NT replaces NE in storage vesiclebut is inactive at adrenergic receptors.

Initially, IV dose cause NE release and BP elevation so CONTRAINDICATED in pheochromocytoma.

During blockade, effector cells become super sensitive to NE, similar to postGN sympathetic denervation.
Adrenergic Neuron Fxn blockers: Reserpine
AntiHTN

binds tightly to adrenergic storage vesicles in CNS and PNS, inhibiting vesicular catecholamine transporter that facilitate vesicular storage. Thus nerve ending lose capacity to concentrate and store NE and DA.

Recovery requires synthesis of storage vesicles
Centrally acting sympatholytics: Clonidine, guanabenz, guanfacine
stimulate alph2a-adr-r causing reduction in symp activity.

higher doses can cause activation of alpha2-b-r, causing vasocontriction and loss of therapeutic effect.
Direct vasodilator drugs: Hydralazine
arteriolar vasodilator (unknown mech), lowers TPR and hence afterload and BP, with reflexive increase in HR and cardiac contractility, renin and fluid retention.

prevents dev'p of nitrate tolerance.

Rapid dev'p of tachyphylaxis.

Beneficial in combo HTN and cardiac failure.

Useful in HTN emergencies assoc. w/ PREGNANCY

contraindicated in pts with both HTN and coronary heart dz, due to reflex relatedHR increase and cardiac contractility.
Direct vasodilator drugs: Minoxidil
K ch opener, causing hyperpolarization in ARTERIOLAR s.m. w/ little effect on venous.

Tx for HTN refractory to other drugs.

similar adverse effects as hydralazine i.e. increase in HR, cardiac ischemia etc... so usually co-admin. w/ beta blockers.

HAIR GROWTH seen in pts. Topical minoxidil (rogaine) now used for baldness.
Direct vasodilator drugs: sodium nitroprusside
nitrate compound with nitrous group, 5 cyanide groups and iron. NO is released spontaneously nonenzymatically, hence causing dilation of BOTH arteries and veins.

Cause decrease in TPR and venous return (so both afterload and preload decreased). This results in reflex increase in cardiac stimulation but less than with other vasodilators.
sodium nitroprusside indications?
IV for potent hemodynamic control in hypertensive emergencies and severe cardiac failure due to rapid action, short duration and high efficacy.

MUST monitor blood pressure.

Rx toxicity: The cyanide is converted to thiocyanate in liver which is then excreted by kidneys.... so pts with renal issue: excessive thiocyanate accum. resulting in disorientation, psychosis, muscle spasm and convulsions.

Pts with liver issues: cynide accumulation leading to acid-base distrubrances, cardiac arrhythmias and even death.
Ca Channel blockers
act on both vasculature sm and myocardium. It is different from organic nitrates in that it is predominantly arteriolar dilator, while nitrates are mainly venodilatory.
Nifedipine (dihyropyridine), Verapamil (non-dihydropyridine)
Nifedipine and Verapamil, inhibit the alpha subunit of L-type ca channel, hence inhibiting Ca entry through L-type channel... resulting in SM relaxation.

In myocytes, reduce Ca influx causes decreased cardiac contractility., SA and AV node conduction vel.

SKELETAL MUSC. NOT affected because it depends mainly on intracellular pools of Ca, and not as much transmembrane Ca influx through L type channel.
CV effects: Nifedipine and other DIHYDROPYRIDINE
Increase: coronary and peripheral vasodilation >> results in reflex increase in HR, contractility. No changes in AV conduction or rate of recovery of Ca channels.
CV affect: Verapamil and other non-dihydropyridines
coronary and periph vasodilation. NO REFLEX HR increase or contractility. Instead, HR, contractility, AV conduction and Ca channel recovery are ALL DECREASED.
Ca channel blocker applications?
Esp. effective in LOW renin pts, blacks, and elderly.

Hypertension, HTN emergencies, angina, heart failure, cerebral artery spasm (dihydropyridines).

In pts with arrhythmias, stick to Verapamil.
Ca channel blocker: side effects
AV node block (verapamil), excessive vasodilation, CO depression and CHF (verapamil)
PDE inhibitors
prevent cAMP or cGMP breakdown via hydrolysis, causing vasodilation. Increase cAMP has pos. ionotropic effect on myocardium as well (hence aka ino-dilator).

ex: sildenafil (PDE type 5) used in ED.