Pharm Exam 2 Flashcards
Narcan
MOA: Structural analog of morphine that is a competing antagonist at the opioid receptors.
Indications: Opioid overdose, reversal of post-op opioid actions, reversal of neonatal respiratory depression.
Hypertension: Categories
Pre-hypertension: 120-139 / 80-89
Stage 1 Hype: 140-159 / 90-99
Stage 2 Hype: 160 / >100
Beta Adrenergic Blockers
eg Metoprolol
MOA: impede action of catecholamines (epi, norepi, dopamine) at heart receptors
- reduces HR
- reduces cardiac contractility
- reduces cardiac impulses through AV node
- Reduces renin production in kidney
Non selective - block Beta1 & Beta2 - Propranolol - can cause bronchospasm, impaired glucose metab, treat for hyperthyroidism, tremors, migraines
Selective - more effective on Beta1 - Metoprolol - less bronchospasm
Hypertension: Nonpharmoc. Interventions
Stress mngmt Restrict Salt Excercise Reduce weight DC smoking/tobacco Limit Alcohol Lower fats/triglycerides Breath as stress reducer
Alpha1 Adrenergic Agonists
Decongestants
MOA: activate Alpha1 Adren. Receptors in nasal blood vessels
Shrink nasal membranes that are inflamed
Angiotensin II Receptor Blockers (ARBS): MOA
Angio II constricts systemic and renal blood vessels
Receptor blockers prevent constriction, lowering BP
Action: Blocks Angio II after it is formed. Receptors in smooth muscle and adrenal gland, drop BP by affecting renin-angio cycle. Block vasoconstriction and secretion of aldosterone. Similar to ACE inhibitors, minus cough.
ARBs more effective after MI, do not treat BP as effectively in CHF
Diltiazem (Cardizem) - Calcium Channel Blockers
Less vasodilation Used in atrial arrythmias. - Blocks calcium influx into cells - Reduces cardiac contractility - Smooth muscle cells in vasculature effected by vasodilation - Decrease HR
SE: Hypotension, arrythmias, chest pain, peripheral edema, GI sx
Antihypertensives for Severe Hypertension
First-line: Thiazide-type diuretics, calcium channel blockers, ACEIs, ARBs
Second/Third-line: Higher doses and combinations
Clonidine (Catapress)
Centrally-acting Alpha2 Agonists
MOA: Act centrally on brain
- Reduces vasoconstriction
- Reduces renin (precursor of Angio1->Angio2->potent VC
Potassium & Diuretics
Thiazide causes loss of K+, as do loop diuretics such as furosemide (Lasix).
K+ sparing= Spironolactone (Aldactone). Block aldosterone, which allows Na+ to be released. Sod/Pot pumps inhibited, causing Na+ secretion and K+ retention
Tetracycline: SE/AE
GI issues, discoloration of teeth, suprainfection, hepatoxicity, renal toxicity. High doses can correlate to liver damage
Melatonin Agonists
Ambien, Ramelteon (Rozerem)
Newer hypnotic used for chronic insomnia.
MOA: melatonin receptor activation. Short onset and short duration. Induces sleep well but does not maintain
Agonist/Antagonist Opioids
4 groups: Pentazocine, nalbuphine, butorphanol, buprenorphine
Low potential for abuse, less powerful analgesic. Produces less respiratory depression than more powerful opioids.
MRSA medication
Vancomycin
Most widely used ABX in hospitals
MOA: bacterial cell wall lysis. Only gram +
SE/AE: renal failure, admin. low doses
Muscle Spasm Meds
Two groups: Analgesic Anti-inflamms (e.g. Aspirin) and muscle relaxers–>
Baclofen (Lioresal), Carisoprodol (Soma), Diazepam (Valium), Cyclobenzaprine (Flexeril)
Baclofen & Diazepam relieve spasticity by acting on CNS
Dantrolene acts directly on skeletal muscle