• 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

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/71

Click to flip

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