final exam Flashcards
- Drug interactions w/ NSAIDs may block or reduce anti-HTN effect
- Not as good at preventing strokes as ACE-Is, ARBs, or CCBs
- Increase TGs and decrease HDL
- decreases renin and C.O.
beta blockers
- Clinical Use: HTN; anti-anginal
- MOA: selective beta-blocker
- AE: asthma, DM, cardiac depression
- Notes: give to a pt if they feel “worn out”
- *this term is used particularly with beta blockers that can show both agonism and antagonism at a given beta receptor
Acebutolol (ISA*), Atenolol, Metoprolol
- Clinical Use: HTN; anti-anginal
- MOA: non-selective beta-blocker
- AE: asthma, DM, cardiac depression
- Notes: mixed alpha AND beta blocker
Pindolol (ISA*), Labetalol, Propranolol
- Clinical Use: acute asthma
- MOA: selective beta-2-agonist
- AE: if given PO can cause tachycardia, nervousness, and tremors (“TNT”)
- Notes: use only if symptomatic; short-acting
Albuterol
- Clinical Use: acute asthma
- MOA: selective beta-2-agonist
- AE: tachycardia, nervousness, and tremors (“TNT”)
- Notes: use only if symptomatic; short-acting
Terbutaline
- Clinical Use: chronic asthma
- MOA: selective beta-2-agonist
- AE: unexplained deaths!!!; tachycardia, nervousness, tremors
Salmeterol, (Fomoterol)
• Properties
o Anti-inflammatory
• PGE2 and PGI2 cause erythema, incr blood flow
• Incr vascular permeability a/w other inflam mediators
o Analgesia
• PG’s cause hyperalgesia
o Antipyretic
• Pyrogens/cytokines incr endogenous hypothalamic formation of PGE2 which elevates body temp =incr in heat generation and DECR heat loss
• SE’s:
o gastric and intestinal ulceration–>mild dyspepsia and heartburn; may be accompanied by anemia from blood loss; local irritatin from drug PLS removal of PGE2 and PGI2
o inhibition of platelet fxn/CV risk–>NSAIDs inhibit platelet fxn which promote “stickiness” and clumping
o renal toxicity–>decr renal blood flow and GFR in pts with CHF; promote salt and H2O retention by PG-induced inhibition of both reabsorption of Cl- and action of ADH
o ASA intolerance–>pts may develop nasal polyps, asthma, chronic urticaria
o prolongation of gestation–>PG’s are uteotropic agents=their biosynthesis by the uterus incr dramatically in the hours before parturition; may provoke premature closure of ductus arteriosus
NSAIDs
- Clincal Use: Low doses=inhibit platelet function; moderate doses=provide analgesia and antipyresis; large doses=full anti-inflammatory and anti-rheumatoid effects
- MOA: irreversibly acetylates (blocks) COX-1 and COX-2=permanently inactivating
- AE: gastric irritation, ulceration, erosion, hemorrhage; incr bleeding time; decr renal fxn in pts at risk; hepatic injury (at large doses)
aspirin
- Clinical Use: adjunctive therapy for PD w/ L-DOPA
- MOA: D2 receptor agonist and D1 receptor ANTagonist
- AE: drug-induced tardive dyskinesia; NV; Orthostatic hypoTN and cardiac arrhythmias
- CI: females who are breast feeding or pregnant
- Notes: LOW GI absorption; only works in pts responsive to L-DOPA
Bromocriptine
- Clinical Use: PD; adjunctive therapy when L-DOPA effects decline
- MOA: inhibits DA catabolism (MAO-B irreversible inhibitor); enhances DA to brain
- AE: Hypertensive episodes
- CI: tricyclic antidepressants and SSRIs (i.e., Prozac)
- Notes: Good GI absorption; reaches CNS quickly; t1/2=1.5h; improves cognitive fxns a/w PD (early stages)
Selegiline
- Clinical Use: anti-epileptic (anticonvulsant)
- MOA: inactivation of Na+ channels=decr excitability
- AE: dizziness diplopia, nystagmus, blurred vision, ataxia, vertigo, N, confusion; H2O retention
- Notes: CYP3A4 induction
carbamazepine
- Clinical Use: anti-epileptic (anticonvulsant)
- MOA: inactivation of Na+ channels=decr excitability
- AE: dizziness, blurred vision, HA, ataxia; 10% of pts may get a rash that can evolve into Steven-Johnson Syndrome
lamotrigine
- Clinical Use: anti-epileptic (anticonvulsant)
- MOA: increases GABA effects
- AE: sedation, GI upset, diarrhea, tremor, ataxia, platelet dysfxn; hepatotoxicity, weight gain; hair loss; spina bifida (teratogenicity)
- Notes: drug of choice for MOST seizures
valproate
- Clinical Use: anti-epileptic (anticonvulsant); EtOH dependence; migraines
- MOA: blocks Na+ channels; augments GABA activity; antagonizes glutamate receptors; inhibits carbonic anhydrase
- AE: CNS effects, weight loss, kidney stones, metabolic acidosis
topiramate
- Clinical Use: as stated above
- MOA: binds BZD receptor, enhancing GABA effects
- AE: sedation, dizziness, ataxia, fatigue, confusion, diplopia
- Notes: intermediate t1/2; overdose is reversed by Flumazenil
clonazepam
- Clinical Use: anti-epileptic (status epilepticus)
- MOA: binds BZD receptor, enhancing GABA effects
- AE: sedation, dizziness, ataxia, fatigue, confusion, diplopia
- Notes: intermediate t1/2; overdose is reversed by Flumazenil
diazepam
- Clinical Use: anti-epileptic (status epilepticus=PERFERRED DRUG)
- MOA: binds BZD receptor, enhancing GABA effects
- AE: sedation, dizziness, ataxia, fatigue, confusion, diplopia
- Notes: LONG t1/2; overdose is reversed by Flumazenil
lorazepam
- Clinical Use: IV/IM pre-anesthetic and intra-operative medication
- MOA: binds BZD receptor, enhancing GABA effects
- Notes: short-acting IV for intubations
midazolam
- Clinical Use: HTN; drug and nicotine withdrawal
- MOA: centrally-acting alpha-2 receptor agonist
- AE: dry mouth, sedation, decreased libido, orthostatic hypoTN, rebound HTN (w/ abrupt withdrawal)
- Notes: reduces LVH and lowers total cholesterol w/o reducing HDL=good for ppl w/ hypercholesterolemia; no CNS effects; imidazoline receptor agonist
clonidine
• Long-acting; used topically; more anti-inflammatory; ZERO salt retention and LESS potent than cortisol
dexamethasone
- Short-acting; LESS salt retention; more anti-inflammatory; ZERO salt retention and LESS potent than cortisol
- Used as an adjunctive medication in cancer treatment (MOPP, CVPP)
prednisone
- Clinical Use: shock (adjunct tx); CHF; bradycardia; cardiac output maintenance–>stimulates contractility
- MOA: stimulates DA receptors and beta-1 adrenergic receptors (at high doses)
- AE: tachycardia; proarrhythmogenic
- Notes: (+) inotrope; at low doses=produces renal/splanchnic vasodilatory effects; at HIGH doses=produces pressor effects
dopamine
=inotrope
- Clinical Use: HTN, BPH
- MOA: Competitive, selective alpha-1-receptor blockers–>decr peripheral resistance and MAP; incr HR and CO; improve urine flow
- AE: postural hypoTN, tachycardia, nasal stiffness, weight gain, psychomotor slowing
- Notes: reversed by epinephrine
Doxazosin, Prazosin
-alpha blocker
• Clinical Use: anaphylaxis, vasoconstrictor in local anesthetics, topical hemostatic, cardiac rescue
o peripheral excitatory - α1: vasoconstriction, pupil dilation
o Cardiac excitatory - β1: increase HR and contraction force
o Peripheral inhibitory - β2: vasodilator, bronchodilation, gut relaxation
o Metabolic Actions - α1, β2, β3: increase blood Glc, lactate, free fatty acids.
o CNS Stim - α and β: respiratory stim, wakefulness, reduced appetite.
• MOA : α1 α2 β1 β2, β3 stimulator (sympathomimetic)
• AE:
• Drug interactions:
• Notes: decreases TPR, increases HR, mean BP unchanged (systolic increases, diastolic decreases). Tyrosine monooxygenase is rate limiting step in Epi synthesis
epinephrine
• Clinical Use: acute/chronic pain; premedication prior to surgery
• MOA: Strong μ** agonist
• AE: somnolence, NV, dizziness, confusion, nervousness
• Notes: highly lipophilic=distributes to brain RAPIDLY; 100X more potent than morphine
• **Other strong μ agonists are:
o Morphine- Gold Standard; DOC dor Dyspnea-Associated Pulmonary Edema; LARGE first-pass effect; crosses BBB slowly
o Meperidine- active metabolite is a proconvulsant=contraindicated in pts at risk for seizures
o Methadone- long-acting; used to tx pts w/ opioid addiction
o Levorphanol- long t1/2=12-16h
fentanyl
- Clinical Use: acute/chronic pain
* Notes: 1000X more potent than morphine (10X more potent than fentanyl)
sulfentanil
- Clinical Use: prostate CA
- MOA: inhibits androgen uptake and binding to androgen receptors
- AE: gynecomastia, ALT/AST elevated, NVD, nervousness
flutamide
- Clinical Use: COPD; bronchial asthma
- MOA: antagonizes Ach receptors @ M3 receptor producing bronchodilation
- AE: dry mouth, sedation
- Notes: used in combo w/ beta-2-agonists and steroids
Muscarinic Antagonists
Ipratropium, Tiotropium
- Clinical Use: antifungal
- MOA: inhibits P450 impairing ergosterol synthesis==>impairs fungal membrane formation
- AE: MANY (NV, photophobia, hepatic toxicity and necrosis)
- DI: inhibits CYP3A4=lots of drug interactions; absorption is reduced by drugs that decrease gastric activity
- Notes: Imidazole (along w/ Clotrimazole and Miconazole); can be used as steroid antagonist; selective activity due to difference in membrane steroids
ketoconazole
- Clinical Use: decrease immune effects of asthma
- MOA: selectively binds cysteinyl LT receptors
- AE: none
- Notes: in children, used in combo w/ steroid plus beta-2-agonist
montelukast
- Clinical Use: decrease immune effects of asthma
- MOA: antagonizes LTC4 and LTD4 receptors
- AE: since taken PO, virtually no adverse effects
- Notes: in children, used in combo w/ steroid plus beta-2-agonist
zafirlukast
- Clinical Use: edema; HTN; primary hyperaldosteronism; hypokalemia; CHF; hirsutism
- MOA: antagonizes aldosterone-specific mineralcorticoid (and androgen receptors=inhibits 17-alpha-hydroxylase) receptors, primarily in the DCT, decreasing Na+ and H2O reabsorption and increasing K+ retention
- AE: hyperkalemia, metabolic acidosis, gynecomastia, impotence, decr libido, GI upset (ulcers), HA, fatigue, ataxia, confusion
Potassium-Sparing Diuretics
Spironolactone
- Clinical Use: sedation prior to anesthesia
- MOA: Low doses=potentiate GABA actions; High doses=directly impair Na+ and K+ channel operation–>direct depression of neuronal activity
- AE: OD possible w/ no effective antagonist; dose-dependent decrease in BP and respiration
- Notes: avoid extravasation or inadvertent intra-arterial injection
Barbituates Thiopental (ultra short-acting), Phenobarbital (long-acting)
- Penicillins
- Beta-lactamase inhibitors
- Cephalosporins
- Carbapenems
- Monobactams
- Vancomycin (d-Ala-d-Ala)
- Bacitracin
Cell wall synthesis inhibitors
- Streptogramins
- Oxazolidinones
- Macrolides (“MACE”=Macrolides: Azithromycin, Clarithromycin, Erythromycin)
- Ketolides
- Lincosamides (Clindamycin)
- Aminoglycosides (“A SGT”=Aminoglycosides: Streptomycin, Gentamicin, Tobramycin)
- Glycycylines (Tigecycline)
Protein Synthesis Inhibitors
- Sulfonamides (Sulfamethoxazole, Sulfasalazine, Sulfadiazene)
- Trimethoprim
folate metabolism inhibitors
• Fluoroquinilones (Ciprofloxacin, Levofloxacin)
dna replication and transcription
- Metronidzaole
- Nitrofurantoin
- Methenamine
- Mupirocin
- Polymyxins
UTI antiseptics
- Clinical Use: acute promyelocytic leukemia (APL); surface acne
- MOA: stimulates transcription of genes that have retinoic acid receptors=induces differentiation
- AE: Retinoic Acid Syndrome; VitA toxicity
Tretinoin (Differentiating Agent)
- Clinical Use: antineoplastic; genital warts; HBV & HCV; Kaposi’s sarcoma (HHV-8); multiple melanomas; MS; RA
- MOA: activate JAK-STAT pathway–>upregulation of specific proteins–>inhibit cellular protein synthesis==>immunomodulatory, antiproliferative, antiviral
- AE: fever, chills, myelosuppression, neurotoxicity
interfeon-alpha
- Clinical Use: transplant rejection; atopic dermatitis; psoriasis
- MOA: calcineurin inhibitor; inhibits production of interleukins, interferons, and other antigen-stimulated products in T-cells; inhibits the release of pre-formed mediators from skin mast cells and basophils
- AE: dose-limiting reversible nephrotoxicity, vasoconstriction, neurotoxicity, hyperlipidemia
- DI: metabolized by CYP3A4=MANY drug interactions
- Notes: 10-100X more potent that cyclosporine
tacrolimus