Exam 3 Review SHeet Flashcards
Thiazide Diuretics
hydrocholorthiazide
P: Hydodiuril
other drugs end in “zide”
Used most for hypertension tx d/t low cost and short acting (half life: 1-2 hrs)
act on distal convoluted tubule in nephron
Indication for use of hydrocholothiazide
Used in CHF, HTN & edema patients
MOA for hydrocholothiazide
Inhibits Na/Cl pump = decrease Na/Cl absorption and increase excretion of Na/Cl and eventually H2O
Modest diuresis
Some K and Mg excreted also
Check electrolyte levels and BP before admin
Cautions for hydrocholothiazide
Gout (Inhibits uric acid secretion)
Women have a greater decrease in K than men
Hypercalcemia
Do not give to severe renal impairement, diabetics (Increase blood sugar), hyperlipidemia, lupus & sulfa patients
Adverse effects of hydrocholorthiazide
Orthostatic hypotension, dizziness Drowsiness N/GI upset - take with food if discomfort Electrolyte imbalance Increase blood glucose Headache Rash Hyperuricemia (Blocks uric acid secretion Hyperlipidemia
Nursing implications for hydrocholothiazide
Take in the AM
Monitor I&O
Avoid high Na foods and increase K foods
Monitor electrolytes and blood sugars
Caution with position changes = orthostatic hypotension
Men can have possible ED
Be aware of hyponatremia s/s – craving salt, cramps, wt loss
Drug Interactions with hydrocholorothiazide
Many
High Na foods decrease effectiveness
Potassium sparing diuretics
Na channel blockers: triamterene (P) Dyrenium
Aldostersone antagosnists: spironolactone (P) Aldactone
triamterene (Dryenium) and spironolactone (Aldactone) characteristics
Weaker diuresis and antihypertensive effects when used alone
Usually used with other K wasting diuretics to maintain K levels
Indications for use of triamterene (Dryenium) and spironolactone (Aldactone)
HTN, edema, and cirrhosis
MOA of spironolactone (Aldactone)
Works in the distal tuble
Increase Na and H2O loss while keeping K
Aldosterone antagonist
MOA of triamterene (Dyrenium)
Works in distal tubule
Increase sodium, Cl, H20, Ca, and bicarb loss but keeps K and Mg (Watch for arrhythmia’s)
Inhibits uric acid secretion = increase uric acid levels
Independent of aldosterone
Cautions with triamterene (Dyrenium) and sprironolactone (Alactone)
Renal insufficiency, pre existing hyperkalemia
Liver disease
Diabetes (Increase BS)
Pts on ACE inhibitors (Increase K), NSAIDS or K supplements (Increase K)
No Mrs. Dash (Increase K)
Adverse effects of triamterene and spironolactone
Hyperkalemia (Muscle cramping, arrhythmias, tingling/numbness, confusion Electrolyte imbalance Hypotension N/V/D Weakness, fatigue Headache Gynecomastia Nephrotoxic – triamterene (rare)
Nursing implications/education of triamterene and spironolactone
Take in the AM or early PM (if bid) to prevent nocturia
I&O
Monitor electrolytes and BS
Caution with position changes = orthostatic hypotension
Men can have possible ED
Be aware of hyponatremia s/s= craving salt, cramps, wt loss
Loop diuretics
furosemide (Lasix)
other drugs end in “zide”
Cause a greater natriuresis than thiazides
PO and IV form - PUSH IV SLOW (tinnitus or CV collapse)
Short onset: 15-30 min, lasts 6-8 hours
Furosimide less bioavailablility than other d/t increase protein bound
Torsemide less renal cleared so easier on kidneys/renal patients
MOA of furosemide (Lasix)
Act in loop of henle
Inhibit Na/K/Cl channel = prevents reabsorption of Na/Cl and eventually H2O
Increase K/Ca/Mg excretion
Cautions with furosemide (Lasix)
Gout
Impaired glucose intolerance
Renal disease
Elderly and PG pts
Adverse effects of furosemide (Lasix)
Hypokalemia Orthostatic Hypotension Dehydration Hypomagnesium Ototoxicity Hyperuricemia
Drug interactions with furosemide (Lasix)
Other ototoxic drugs - amnioglycosides (abx), aspirin
Beta Blockers - increase level
Many others - see book
Nursing implications/Education on furosemide (Lasix)
Take in the AM or early PM (if bid) to prevent nocturia
I&O
Increase K foods
Monitor electrolytes and blood sugars
Caution with position changes = orthostatic hypotension
Men can have possible ED
Be aware of hyponoctremia s/s = craving salt, cramps, and wt loss
Beta Blockers
propranolol (Inderal)
Other drugs end in “olol”
Good absorption, onset 30 min, duration 6-12 hrs
Some large first pass effect: propranolol, labetalol
Some highly protein bound: propranolol, penbutolol, carvedilol
Takes 2-3 weeks for full effect of beta blockers to be achieved
Cardioprotective: BB occupy catecholemine receptors so they cant bind = Decrease sympathetic nervous system (HR/BP)
Indications for use of propranolol (Inderal)
HTN, angina, MI, irregular cardiac rhythyms
Stable CHF
Migraines, anxiety, substance withdrawl
Tremors (Mask s/s of hypoglycemia)
MOA of propranolol (Inderal)
Part of ANS - blocks beta 1 (Heart) and beta 2 (lungs) receptors
- Some are selective and others are non-selelctive
Vasodilation = decrease BP/HR
Decreased force of contractions (NOT good for Unstable CHF pts.)
Decreased renin secretion
Hard to increase HR with exercise/stress test
Bronchospastic disease (Never give COPD/asthma/resp pts)
Mask s/s of hypoglycemia
Adverse effects of propranolol (Inderal)
Hypotension Arrythmias Bronchospams Hypoglycemia Bradycardia, depression, ED, elevated liver enzymes, dizziness, fatigue, lethargy, hyperlipidemia
Nursing implications/Education for propranolol (Inderal)
Do not stop abruptly - can cause rebound HTN and MI
Check VS (esp HR) before administering
Change positions slowly (orthostatic hypotension)
Alert diabetics about hypoglycemia
Eat high fiber diet to avoid constipation
Lifestyle changes: Wacth Na intake, diet and exercise
Can cause sexual dysfunction (esp. in men)
Cautions and Contraindications Mnemonic for propranolol (Inderal)
A: Asthma B: block (Heart block) C: COPD D: Diabetes mellitus E: Electrolyte (Hyperkalemia)
Ace inhibitors
captopril (Capoten)
other drugs end in “pril” (A-pril)
Most are prodrugs = need good liver function to metab into active form
Takes up to 4 weeks to get full effect
Indications for use of captopril (Capoten)
HTN, CHF, DM neuropathy, L ventricular dysfunction, Acute MI
Unlabeled uses: RA, dementia (Decrease inflammation in the brain)
MOA of captopril (Capoten)
Inhibit conversion of angiotensin I to angiotensin II = decrease aldosterone secretion
- leads to decrease Na and H2O rentention
Prevents breakdown of bradykinin (vasodilator) = Increase badykinin levels = Increase vasodilation
Decrease in K excretion (Know K levels before giving)
Effects of captopril (Capoten)
Decrease systemic vascular resistance
No change in HR
Increase renal perfusion/Decrease renal vascular resistance
- renal protective, give to DM pts to prevent nephropathy
Prevent ventricular remodeling
Cautions of captopril (Capoten)
Do not give to PG pts - Category D
Cautions of captopril (Capoten)
Do not give to PG pts - Category D
Renal insufficiency
Photosensitivity (Wear sunscreen to prevent burning)
Captopril and moexipril need to be taken on an empty stomach (Watch for proteinuria w/in first 2-4 wks)
Adverse effects of captopril (Capoten)
Cough
Orthostatic Hypotension
Hyperkalemia (Cramping, arrythmias)
Angioedema
ACE w/diuretic = 1st dose phenomenon (Decrease BP)
- Hold diuretic for a few days to get used to ACE then add diuretic again
Rach (rare), N/D/Constipation, leukopenia, myalgia, headache
Drug interactions of captopril (Capoten)
Increase levels of digoxin, lithium, and potassium
Decrease levels of ACE by antacids and indomethacin use
Potassium sparing diuretics
Potassium Supplements
Angiotensin II Receptor Blockers (ARBs)
losartan (Cozaar)
other drugs end in “sartan”, they “sartanly” resemble ACE
High 1st pass effect, highly protein bound, renal/hepatic elimination
MOA of losartan (Cozaar)
Much like ACE, block binding of angiotensin II to receptors
AT1 receptors prevent vasoconstriction and aldosteron relsease
AT2 may have vasodilary effects
No effect on bradykinin pathway
Cautions of ARBs/losartan/Cozaar
Do not give pregnant women - Category D
Adverse effects of ARBs/losartan/Cozaar
Hypotension Angioedema (rare) Thrombocytopenia Rhabdomyolysis Diarrhea, Dizziness, fatigue
Drug interactions with ARBs/losartan/Cozaar
Termisartan with other hepatically cleared drugs - increase digoxen and warfarin levels Potassium sparing diuretics Potassium supplements Grapefruit (metab by CYP also)
Selective Aldosterone blockers
eplerenone (Inspra)
Less side effects than spironolactone because they are selective
Natuetic = Decrease Na and H2O retention
Indications for use of Selective Aldosterone Blockers/eplerenone/Inspra
HTN and Heart Failure after an MI
MOA for Selective Aldosterone Blockers/eplerenone/Inspra
Bind to mineralcorticoid receptors so aldosterone can’t bind = Decrease Na and H20 retention
K not excreted - watch K levels
Contraindications of selective aldosterone blockers/eplerenone/Inspras
Hyperkalemia, Diabetics with microalbuminuria, renal pts.
Adverse effects selective aldosterone blockers/eplerenone/Inspras
Hyperkalemia, Hyponatremia, Increase Triglicerides, dizziness, angina, MI
Drug interactions with selective aldosterone blockers/eplerenone/Inspra
Potassium supplements/potassim sparing diuretics = Increase K levels/ret
ACE/ARB’s = Increase K levels/ret
Grapefruit may increase effects of Inspra
Alpha 1 blockers
praxosin (Minipress) - given via patch, 1st dose effect
terazosin (Hytrin)
doxazosin (Cardura)
Indicated for HTN
Central ALpha 2 agonist
Not first line tx for HTN, usually added with other HTN meds
clonidine (Catapress)
methyldopa (Aldomet) - ok for pregnant patients, can darken urine
Alpha Beta blockers
Usually used in ICU via drip, lying flat
labetolol
Direct acting vasodilators
hydralazine
side effects: palpatations, tachy, angina
Usually also on BB to stop tachy
Direct acting vasodilators
hydralazine
side effects: palpatations, tachy, angina
Usually also on BB to stop tachy
Cardiac Glycosides
digoxin helps with a-fib/flutter/HR 60-80% oral absorp, 36 hour half life Not recommended by dialysis Give loading dose to speed up therapeutic effect
MOA for cardiac glycosides/digoxin
Inhibit Na-K-ATPase pump = Na & Ca can’t leave cell = Increase in Ca = Increase force of contraction
Effects of cardiac glycosides/digoxin
Increase force of contraction - positive inotrope
Depress SA node = Decrease HR (negative chronotrope)
Prolongs refractory period of AV node (negative dromotrope)
Cautions for cardiac glycosides/digoxin
Renal insuff
Can cause electrolyte imbalance - hypokalemia, hypercalcemia, hypomagnesemia
Contraindicated for v-fib, v-tach, heart block patients
Thyroid patients - need to know thyroid levels before admin and adjust dose
High bran fiber diets reduce absorption
Monitoring for cardiac glycosides/digoxin
Dig levels: therapeutic 1-2 ng/mL
Electrolyte levels (K/Ca/Mg)
Heart rate
Signs of digoxin toxicity
N/V (extreme) Arrythmias Visual disturbances (Halos/yellow) Fatigue, weakness, diarrhea ANTIDOTE: digoxin immune fab (Digibind) - IVP slow (15-30 min) - does not change dig levels, can only tell if working by decrease s/s
Adverse effects of digoxin
Anorexia, N/V, abd discomfort
Headache, weakness, visual disurbances
Arrythmias, confusion, aggitation
Very similar to toxicity - get levels to determin dig tox
Drug interactions with digoxin
MANY, may increase digoxin levels
Patient education on digoxin
Take pulse before taking medication, Call MD if below 60 bpm
Do not d/c w/o approval from MD
NO OTC antacids, cough/cold, dietary supplements w/o approval from MD
Do not take with food - absorbes better on an empty stomach
Eat K rich foods, do not eat high fiber
Keep away from kids (Deadly)
Keep lab appointments
If missed dose, do not double up.
Natriuretic Peptides
nesiritides (Natrecor)
MOA of Natriuretic Peptides/nesiritides (Natrecor)
Promotes smooth muscle relaxation and dilation of vein and arteries
Decrease vascular resistance
Decrease fatigue and dyspnea
Decrease aldosterone levels = Decreased Na and H2O
Given by IV bolus and infusion