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final exam Flashcards

1
Q
  • 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.
A

beta blockers

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2
Q
  • 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
A

Acebutolol (ISA*), Atenolol, Metoprolol

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3
Q
  • Clinical Use: HTN; anti-anginal
  • MOA: non-selective beta-blocker
  • AE: asthma, DM, cardiac depression
  • Notes: mixed alpha AND beta blocker
A

Pindolol (ISA*), Labetalol, Propranolol

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4
Q
  • 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
A

Albuterol

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5
Q
  • Clinical Use: acute asthma
  • MOA: selective beta-2-agonist
  • AE: tachycardia, nervousness, and tremors (“TNT”)
  • Notes: use only if symptomatic; short-acting
A

Terbutaline

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6
Q
  • Clinical Use: chronic asthma
  • MOA: selective beta-2-agonist
  • AE: unexplained deaths!!!; tachycardia, nervousness, tremors
A

Salmeterol, (Fomoterol)

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7
Q

• 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

A

NSAIDs

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8
Q
  • 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)
A

aspirin

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9
Q
  • 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
A

Bromocriptine

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10
Q
  • 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)
A

Selegiline

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11
Q
  • 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
A

carbamazepine

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12
Q
  • 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
A

lamotrigine

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13
Q
  • 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
A

valproate

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14
Q
  • 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
A

topiramate

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15
Q
  • 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
A

clonazepam

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16
Q
  • 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
A

diazepam

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17
Q
  • 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
A

lorazepam

18
Q
  • Clinical Use: IV/IM pre-anesthetic and intra-operative medication
  • MOA: binds BZD receptor, enhancing GABA effects
  • Notes: short-acting IV for intubations
A

midazolam

19
Q
  • 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
A

clonidine

20
Q

• Long-acting; used topically; more anti-inflammatory; ZERO salt retention and LESS potent than cortisol

A

dexamethasone

21
Q
  • 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)
A

prednisone

22
Q
  • 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
A

dopamine

=inotrope

23
Q
  • 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
A

Doxazosin, Prazosin

-alpha blocker

24
Q

• 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

A

epinephrine

25
Q

• 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

A

fentanyl

26
Q
  • Clinical Use: acute/chronic pain

* Notes: 1000X more potent than morphine (10X more potent than fentanyl)

A

sulfentanil

27
Q
  • Clinical Use: prostate CA
  • MOA: inhibits androgen uptake and binding to androgen receptors
  • AE: gynecomastia, ALT/AST elevated, NVD, nervousness
A

flutamide

28
Q
  • 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
A

Muscarinic Antagonists

Ipratropium, Tiotropium

29
Q
  • 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
A

ketoconazole

30
Q
  • 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
A

montelukast

31
Q
  • 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
A

zafirlukast

32
Q
  • 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
A

Potassium-Sparing Diuretics

Spironolactone

33
Q
  • 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
A 
Barbituates
Thiopental (ultra short-acting), Phenobarbital (long-acting)
34
Q
  • Penicillins
  • Beta-lactamase inhibitors
  • Cephalosporins
  • Carbapenems
  • Monobactams
  • Vancomycin (d-Ala-d-Ala)
  • Bacitracin
A

Cell wall synthesis inhibitors

35
Q
  • Streptogramins
  • Oxazolidinones
  • Macrolides (“MACE”=Macrolides: Azithromycin, Clarithromycin, Erythromycin)
  • Ketolides
  • Lincosamides (Clindamycin)
  • Aminoglycosides (“A SGT”=Aminoglycosides: Streptomycin, Gentamicin, Tobramycin)
  • Glycycylines (Tigecycline)
A

Protein Synthesis Inhibitors

36
Q
  • Sulfonamides (Sulfamethoxazole, Sulfasalazine, Sulfadiazene)
  • Trimethoprim
A

folate metabolism inhibitors

37
Q

• Fluoroquinilones (Ciprofloxacin, Levofloxacin)

A

dna replication and transcription

38
Q
  • Metronidzaole
  • Nitrofurantoin
  • Methenamine
  • Mupirocin
  • Polymyxins
A

UTI antiseptics

39
Q
  • 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
A

Tretinoin (Differentiating Agent)

40
Q
  • 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
A

interfeon-alpha

41
Q
  • 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
A

tacrolimus

Pharm (19 decks)

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