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

1/45

Click to flip

45 Cards in this Set

  • Front
  • Back
Thiazide diuretics: What drugs?
Chlorothazide
Hydrochlorothiazide
Thiazide diuretics: effects?
decrease plasma volume (PV)

decrease venous return, which causes a decrease in cardiac output (CO)

cardiopulmonary reflexes respond to decreased BP due to decreased PV

reflexes causes:
increased peripheral resistance
increased heart rate
increased plasma renin levels

decrease systemic vascular resistance w/ chronic use which balances the CV reflex reaction
Thiazide diuretics: mechanism of action?
increase sodium and water excretion by inhibiting reabsorption of sodium and chloride ions in the distal nephron

relaxation of vascular smooth muscle w/ chronic use
Thiazide diurectics: therapeutic uses?
used alone to control BP in Stage 1 & Stage 2 HT

Combined w/ other anti-HT drugs to control fluid
retention and edema caused by the other drug
Thiazide diuretics: adverse effects?
muscle weakness

fatigue

Potassium loss: leads to muscle crams and cardiac arrythmias

hyperglycemia (problem only in diabetics)

increased total cholesterol due to increased VLDL

impotence

also, metabolic acidosis, hyponatremia, volume depletion, and hyperuricemia
Potassium sparing diuretics: what drugs?
spironolactone

triamterene

amiloride
Potassium sparing diuretics: effects?
decrease potassium loss
Potassium sparing diuretics: therapeutic use?
used in combination w/ thiazide and loop diuretics to decrease potassium
Loop diuretics: effects?
decrease fluid retention

decrease peripheral vascular resistance
Loop diuretics: therapeutic use?
used in combination w/ anti-HT drugs which cause pronounced fluid retention
B-adrenergic receptor blockers: what drugs?
propranolol(non-selective, B1 & B2)

nadolol(non-selective, B1 & B2)

metoprolol(cardioselective, B1 only)

atenolol(cardioselective, B1 only)

pindolol(non-cardioselective)

labetalol(non-cardioselective)
B-blocker: effects?
B-1 receptor block
decrease in HR
decrease in contractility

B-2 receptor block
decrease norepinephrine release

Non-selective B block
in addition to previous affects:
increase total cholesterol
increase LDL
decrease HDL
B-blocker: mechanism of action?
B-2 receptor block: blocks presynaptic B-2 receptors that mediate a feedback facilitation of norepinephrine release, leaving A-2 receptor mediated inhibition of norepinephrine release unopposed
Labetalol (B-blocker): effects?
decreases peripheral vascular resistance

HR is not decreased
Labetalol: mechanism of action?
blocks B-receptors and A-receptors
Calcium channel blockers: what drugs?
nifedipine (dihydropyridine)

verapamil (non-dihydropyridine)

diltiazem (non-dihydropyridine)
Calcium channel blockers: effect?
decrease cardiac automaticity

decrease AV conduction

decrease cardiac contractility

dihydropyridines have a greater effect on blood vessels

non-dyhydropyridines have a greater effect on the heart

vasodilation
Calcium channel blockers: mechanism of action?
blocks L-type calcium channels: channels responsible for the generation of action potentials in vascular smooth muscle
Calcium channel blockers: therapeutic use?
used alone in therapy of Stage 1, 2, & 3 HT

used in combination w/ a thiazide diuretic or an ACE-inhibitor in therapy of stages of HT
Calcium channel blockers: adverse effects?
Dihydropyridines
headache

tachycardia

digital dysesthesia

ankle edema

Non-dihydropyridines
bradycardia

constipation

Contraindicated in pts. with ejection fraction less than 30%, sinus bradycardia, atrial ventricular conduction disturbances
Angiotensin Converting Enzyme (ACE) Inhibitors: what drugs?
Captopril

Enalapril

Lisinopril
ACE Inhibitors: effects?
decrease angiotensin II

decrease aldosterone

decrease BP

decrease cardiac preload and cardiac afterload
ACE Inhibitors: mechanism of action?
prevents the conversion of angiotensin I to angiotensin to by inhibiting angiotensin converting enzyme

prevent the enzymatic inactivation of bradykinin
ACE Inhibitors: therapeutic use?
used alone in the treatment of Stage 1, 2, & 3 HT

used in combination w/ thiazide diuretics, calcium channel blockers, or b-blockers in the therapy of Stage 4 HT
ACE Inhibitors: adverse effects?
severe hypotension w/ 1st dose

dry cough

hyperkalemia

dysgeusia (loss of taste sensation)

maculopapular rasch

angioedema

Can cause fetal mortality in 2nd and 3rd trimesters
Angiotensin receptor blocking agent: what drugs?
Losartan
Losartan: effects?
decreases preload

decreases afterload
Losartan: mechanism of action?
competitive inhibitor of angiotensin II on the angiotensin 1 (AT-1) receptor
Losartan: therapeutic use?
used alone for Stage 1, 2, & 3

used in combo w/ thiazide diuretics, calcium channel blockers, & B-blockers in therapy for Stage 4 HT
Losartan: adverse effects?
dizziness
Alpha adrenergic blockers: what drugs?
Prazosin

Terazosin
A-blockers: effect?
decreases preload (venous dilation)

decreases afterload (arterial dilation)
A-blockers: mechanism of action?
blocks A-1 receptor
A-blockers: therapeutic use?
used alone for Stage 1 HT

used w/ a diuretic for Stage 2 HT
A-blockers: adverse effects
prazosin
postural hypotension w/ first dose (first doese effect) due to venous vasodilation

dizziness

headache

tachycardia

delayed ejaculation

incontinence

orthostatic hypotension

nasal stuffiness
Centrally acting drugs: what drugs?
Clonidine

Methyldopa

Guanabenz

Guanfacine
Centrally acting drugs: effect?
Clonidine
decrease sympathetic activity

increase parasympathetic activity

decrease norepinephrine release

decrease peripheral vascular resistance

decrease cardiac output
Centrally acting drugs: mechanism of action?
Clonidine
stimulate central A-2 receptors

stimulate peripheral presynaptic A-2 receptors

Methyldopa
converted by enzymes DOPA decarboxylase and dopamine-B-hydroxylase to a-methylnorepinephrine which is stored in synaptic vesicle s and released in response to nerve activity

stimulates central and peripheral A-2 receptors
Centrally acting drugs: therapeutic use?
used in combo w/ diuretics for all Stages of HT
Centrally acting drugs: adverse effects?
sedation

dry mouth

bradycardia

constipation

Rebound hypertension upon abrupt withdrawal(dramatic rise in HR and BP, profuse sweating)

methyl dopa specific effects
decreased liver function

positive Coomb's test

mental lassitude

impaired concentration
Peripheral adrenergic blockers: what drugs?
Reserpine

Guanethidine
Peripheral adrenergic blockers: effect?
decreased cardiac preload

decreased cardiac afterload
Peripheral adrenergic blockers: mechanism of action?
Reserpine

interferes w/ the transport of norepinephrine and dopamine from the cytosol into synaptic vesicles
Peripheral adrenergic blockers: therapeutic use?
Reserpine
use w/ a diuretic for all Stages of HT

Guanethidine
severe HT
Peripheral adrenergic blockers: adverse effects?
Reserpine
Psychic depression

sedation

inability to concentrate

bradycardia

orthostatic hypotension

nausea

diarrhea

nasal congestion

delayed ejaculation

attenuation of sexual orgasm