Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
71 Cards in this Set
- Front
- Back
Diuretic MOA
|
Acutely cause diuresis, chronic use associated w/ decreased peripheral vascular resistance
|
|
Thiazide and thiazide-like diuretics pros
|
*decreased morbidity and mortaility, effective, low-cost
*may be of benefit in salt-sensitive patients, including African-Americans |
|
Thiazide and thiazide-like adverse effects
|
*frequent urination
*increase in uric acid levels *increase calcium levels *glucose intolerance/lipid changes *photosensitivity/rash |
|
Indication for thiazide diuretics
|
Diuretic of choice for HTN w/ normal renal function
|
|
How long may it take for thiazides to reduce blood pressure?
|
3-4 weeks
|
|
Hydrochlorothiazide dose
|
12.5-50mg QD (Esidrix, Microzide)
|
|
Metolazone dose
|
2.5mg QD (Zaroxolyn)
|
|
Loop diuretics pros
|
*useful in patients w/ CrCl<30 ml/min
*decreased morbidity and mortality, low-cost *may be of benefit in salt-sensitive patients, including Arican-Americans |
|
Loop diuretics adverse effects
|
*frequent urination
*increase uric acid levels *decrease calcium levels *metabolic effects (less common than w/ thiazides) *photosensitivity/rash *tinnitus/loss of hearing |
|
What loop diuretic does not have a sulfa group?
|
Ethacrynic acid (phenoxyacetic acid derivative)
|
|
Potassium-sparing diuretics pros
|
effective in combination to prevent hypokalemia
|
|
Potassium-sparing diuretics adverse effects
|
*increase K+
*increase uric acid levels *gynecomastia *irregular menses |
|
Diuretic drug interactions
|
NSAIDs and steroids
|
|
Diuretic monitoring parameters
|
BP, SCr, electrolytes, uric acid, weight
|
|
Diuretic patient education
|
*thirst and dry mouth -> try sugarless hard candy or sugarless gum
*sodium restriction important *notify of s/sx of gout and electrolyte abnormalities (leg cramps, muscle weakness) |
|
Furosemide dose
|
10-40mg BID
|
|
Beta-blockers MOA
|
*decrease in CO due to decrease in HR and contractility (decrease SV)
*reduction in plasma renin activity; inhibition of NE release via presynaptic beta-blockade |
|
Beta-blocker pros
|
*decreased morbidity and mortality
*Good choice post-MI; also effective for angina *Beneficial for patients w/ migraine, essential tremor, anxiety |
|
BB adverse effects
|
*bradycardia
*exercise intolerance *bronchospasm *glucose intolerance *masks symptoms of hypoglycemia |
|
Caution/relative contraindications for BB
|
asthma, COPD, diabetes, peripheral vascular disease, sleep apnea
|
|
Cardioselective BB's to be used in aforementioned patients
|
low-dose:
*Bisoprolol *metoprolol *atenolol *acebutolol |
|
CNS adverse effects (depression) seen with what lipid soluble BB's?
|
Propanolol
|
|
ISA/partial Beta-receptor agonist agents
|
*pindolol
*penbutolol *carteolol *acebutolol |
|
Combined alpha/beta-blocker
|
labetalol
|
|
What beta-blocker undergo extensive first-pass metabolism?
What beta-blockers are excreted renally? |
propanolol and metoprolol
atenolol and nadolol |
|
Beta-blocker drug interactions
|
*concomitant non-dihydropyridine calcium channel blockers may lead to heart block
*Unopposed alpha vasoconstriction with sympathomimetics (cocaine, amphetamines) |
|
Beta-blocker monitoring parameters
|
BP, HR
|
|
Beta-blocker patient education
|
*do not discontinue abruptly (may cause tachycardia, aggravation of angina, or death)
*educate patients w/ diabetes of effect on masking hypoglycemia (except sweating) |
|
ACE-Inhibitors pros
|
*documented to slow progression of diabetic nephropathy
*decreased morbidity and mortality in heart failure and acute-MI |
|
ACE-Inhibitors adverse effects
|
*non-productive, dry cough
*Hyperkalemia *Angioedema |
|
Contraindications of ACE-Inhibitors
|
*Bilateral renal artery stenosis (cause renal failure)
*pregnancy |
|
ACE-Inhibitors comments
|
*hyperkalemia in patients w/ renal disease or diabetes or in patients w/ concomitant NSAIDs, potassium supplements or potassium sparing diuretics
*Rash and taste disturbances may occur especially w/ captopril due to sulfhydryl group |
|
ACE-Inhibitors drug interactions
|
*NSAIDs decrease efficacy of ACE-I
*May increase serum lithium levels *caution with concomitant use of potassium supplements |
|
ACE-Inhibitors monitoring parameters
|
BP, K, SCr, Cough, Angioedema
|
|
ACE-Inhibitors patient education
|
*seek medical attention if facial swelling occurs
*Use salt-substitutes sparingly *If c/o cough: use sugar-free gum/candy to help reduce cough |
|
Angiotensin-II Receptor Blockers (ARBs) Pros
|
*evidence of slowing of progression of diabeteic nephropathy
*Heart failure |
|
Calcium Channel Blockers (CCBs) Non-dihydropyridine Pros
|
*useful in patients w/ tachyarrhythmias and/or atrial fibrillation
*delay onset of diabetic nephropathy *no change in lipid profiles |
|
CCCs Non-dihydropyridine adverse effects
|
*bradycardia
*1st-degree heart block *negative inotropic effects *constipation (V > D) |
|
CCBs Non-dihydropyridine monitoring parameters
|
BP, HR, constipation
|
|
CCBs Non-dihydropyridine patient education
|
*constipation management
*do not crush or chew sustained-released product |
|
CCBs Dihydropyridine pros
|
efficacious and no changes in lipid profiles
|
|
CCBs Dihydropyridine adverse effects
|
*HA
*Peripheral edema *Reflex tachycardia (especially nifedipine) |
|
CCBs Dihydropyridine comments
|
*long-acting preferred over short-acting products
*short-acting dihydropyridines, such as sublingual nifedipine, may increase morbidity/mortality *Avoid in systolic heart failure (except amlodipine or felodipine) |
|
CCBs Dihydropyridine monitoring parameters
|
BP, HR, peripheral edema, reflex tachycardia
|
|
CCBs Dihydropyridine patient education
|
*educate about possibility of peripheral edema
*do not crush or chew SR products |
|
Diltiazem SR dose
|
90-180mg BID
|
|
Verapamil SR dose
|
QD or BID - dose range =180-480mg/day
|
|
Amlodipine dose
|
2.5-10mg QD (Norvasc)
|
|
Nifedipine long-acting dose
|
30-90mg QD (Adalat CC, Procardia XL)
|
|
Felodipine dose
|
5-20mg QD (Plendil)
|
|
Losartan dose
|
50-100mg QD or divide BID
|
|
Valsartan dose
|
80-320mg QD (Diovan)
|
|
Alpha blockers Pros
|
*improved lipid profile
*beneficial effects in patients w/ BPH |
|
Alpha blockers adverse effects
|
*first-dose syncope (use 1mg hs)
*tachycardia *edema |
|
Alpha-blocker place in therapy
|
*Do not use as initial first-line therapy or as monotherapy
*Reasonable to consider in patients w/ HTN and BPH, if added to diuretic, beta-blocker, or ACE *Use other agents for BPH before trying this *If used, must use in combo w/ diuretic to limit fluid retention |
|
Alpha-blocker monitoring parameters
|
BP, orthostatics
|
|
Alpha-blocker patient education
|
*take HS
*Rise slowly from seated/supine position |
|
Central alpha2-agonists pros
|
*no effects on lipids
*Clonidine in patch form may improve compliance *methyldopa is DOC in pregnancy |
|
Central alpha2-agonists adverse effects
|
*anticholinergic
*bradycardia *sexual dysfunction *skin rash *depression RARE: *hemolytic anemia and hepatic dysfunction (methyldopa) |
|
Central alpha2-agonists comments
|
*significant rebound HTN upon withdrawal
*best in combination w/ diuretic therapy to minimize fluid retention |
|
Central alpha2-agonists monitoring parameters
|
BP, adverse effects
|
|
Central alpha2-agonists patient education
|
Change patch every week
|
|
Direct vasodilators pros
|
effective for refractory HTN
|
|
Direct vasodilators adverse effects
|
Both: tachycardia, fluid retention, worsening angina,
Minoxidil: tachycardia, fluid retention, worsening angina, hypertrichosis Hydralazine: HA, drug-induced lupus, peripheral neuropathy |
|
Direct vasodilators comments
|
*need diuretic and beta-blocker used in combination to counteract reflex increase in sympathetic outflow to compensate for profound vasodilation
*Last-line therapy |
|
Direct vasodilators monitoring parameters
|
BP, HR, edema, adverse effects
|
|
How does ACEI and ARBs affect kidneys? |
Reduce GF pressure via vasodilation of efferent arteriole |
|
How do diureticz affect kidneys? |
Reduce blood flow to glomerulus via intravascular volume depletion |
|
How do NSAIDS affect kidneys? |
Reduce blood flow to glomerulus by inhibiting production of vadodilating prostaglandins |
|
Compensatory mechanism of kidney when renal perfusion is impaired |
Renin production and angiotensin II pfoduction is triggered - > vasoconstricts efferent arteriole to maintain intraglomerular pressure which improves renal blood flow Prostaglandins dilate afferent arteriole to increase blood flow to glomerulus. |
|
Good alternative to diuretics in patients on ACEI and NSAIDS |
Dihydropyridine calcium channel blocker They dilate afferent arteriole, the opposite of what NSAIDs do |