Rapid Review: Lab/Diagnostic Findings and Clinical Presentations; and MISC! Flashcards
Question: Lab/Diagnostic Finding or Clinical Presentation Answer: Diagnosis/Disease associated with finding/presentation
Anticentromere antibodies
Scleroderma (have excessive fibrosis and collagen deposition throughout the body; 2 types. the type associated with anti-centromere antibodies is the Crest type: CREST syndrome = Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly, Telangiectasia)
Antidesmoglein (epithelial) antibodies
Pemphigus vulgaris (blistering)
List the 4 most important pharmacokinetics equations: (Vd, Cl, LD, MD)
1) Vd = (amount of drug given)/([drug] in plasma)2) Cl = (Vd X 0.7)/t1/23) LD = Css X Vd4) MD = Css X Cl
List the 4 most important pharmacokinetics equations: (Vd, Cl, LD, MD)
1) Vd = (amount of drug given)/([drug] in plasma)2) Cl = (Vd X 0.7)/t1/23) LD = Css X Vd4) MD = Css X Cl
Anti-glomerular basement membrane antibodies
Goodpasture’s syndrome (glomerulonephritis and hemoptysis)
competitive vs noncompetitive inhibitors:1) Resemble substrate?2) Overcome by increased [S]?3) Bind active site?4) Effect on Vmax?5) Effect on Km?6) Pharmacodynamics: effect on potency? efficacy?
Competitive inhibitors:1) Yes2) Yes3) Yes4) Vmax does not change5) Km increases6) decreased potency (increased Km, decreased potency); no effect on efficacyNoncompetitive inhibitors:1) No2) No3) No4) Vmax decreases5) Km does not change6) decreased efficacy (decreased Vmax, decreased efficacy); no effect on potentcy
competitive vs noncompetitive inhibitors:1) Resemble substrate?2) Overcome by increased [S]?3) Bind active site?4) Effect on Vmax?5) Effect on Km?6) Pharmacodynamics: effect on potency? efficacy?
Competitive inhibitors:1) Yes2) Yes3) Yes4) Vmax does not change5) Km increases6) decreased potency (increased Km, decreased potency); no effect on efficacyNoncompetitive inhibitors:1) No2) No3) No4) Vmax decreases5) Km does not change6) decreased efficacy (decreased Vmax, decreased efficacy); no effect on potentcy
antihistone antibodies
drug-induced SLE. drugs:
1) hydralazine - treats severe HTN (1st line for HTN in pregnancy, with methyldopa), CHF
2) isoniazid (INH) - treatment and prophylaxis for Mycobacterium tuberculosis
3) phenytoin - anti-epileptic
4) procainamide - anti-arrhythmic
Zero-order elimination
rate of elimination of drug is constant, regardless of the plasma concentration; Cp decreases linearly with time.Examples = PEA: Phenytoin, Ethanol, Aspirin
Zero-order elimination
rate of elimination of drug is constant, regardless of the plasma concentration; Cp decreases linearly with time.Examples = PEA: Phenytoin, Ethanol, Aspirin
Anti-IgG antibodies
Rheumatoid arthritis (systemic inflammation, joint pannus, boutonniere deformity)
First-order elimination
Rate of elimination is proportional to drug concentration (a constant fraction of the drug is eliminated per unit time); the plasma concentration decreases exponentially with time.
First-order elimination
Rate of elimination is proportional to drug concentration (a constant fraction of the drug is eliminated per unit time); the plasma concentration decreases exponentially with time.
antimitochondrial antibodies (AMAs)
Primary biliary cirrhosis (female>male; autoimmune disease of liver - get slow progressive destruction of bile canaliculi, so bile builds up in liver = cholestasis, and damages tissue over time, leading to scarring, fibrosis, cirrhosis; portal hypertension)
Phase I vs Phase 2 metabolism:Which phase do geriatric patients lose first?
Phase I: -reduction, oxydation, hydrolysis-usually yields slightly polar, water-soluble metabolites (often still active)-cytochrome P-450Phase II:-GAS: Glucuronidation, Acetylation, Sulfation-usually yields very polar, inactive metabolites (renally excreted)*Geriatric patients lose phase 1 first
Phase I vs Phase 2 metabolism:Which phase do geriatric patients lose first?
Phase I: -reduction, oxydation, hydrolysis-usually yields slightly polar, water-soluble metabolites (often still active)-cytochrome P-450Phase II:-GAS: Glucuronidation, Acetylation, Sulfation-usually yields very polar, inactive metabolites (renally excreted)*Geriatric patients lose phase 1 first
antineutrophil cytoplasmic antibodies (ANCAs)
vasculitis
1) c-ANCA: Wegener’s granulomatosis (a rapidly progressive (crescentic) glomerulonephritis (RPGN))
2) p-ANCA: microscopic polyangiitis (pauci-immune glomerulonerphritis, RPGN), and Churg-Strauss syndrome (pauci-immune, asthma, sinusitis, palpable purpura, peripheral neuropathy))
* “pauci-immune” = form of vasculitis associated with minimal evidence of hypersensitivity upon immunofluorescence.
Efficacy vs Potency
Efficacy: -proportional to Vmax (increase Vmax, increase efficacy)-maximal effect a drug can produce-high efficacy drugs: analgesics, antibiotics, antihistamines, decongestantsPotency:-inversely proportional to Km (increase Km, decrease potency)-amount of drug needed for a given effect-increased potency, increased affinity for receptor-highly potent drugs: chemo drugs, anti-hypertensive drugs, antilipid drugs
Efficacy vs Potency
Efficacy: -proportional to Vmax (increase Vmax, increase efficacy)-maximal effect a drug can produce-high efficacy drugs: analgesics, antibiotics, antihistamines, decongestantsPotency:-inversely proportional to Km (increase Km, decrease potency)-amount of drug needed for a given effect-increased potency, increased affinity for receptor-highly potent drugs: chemo drugs, anti-hypertensive drugs, antilipid drugs
antinuclear antibodies (ANAs: anti-Smith and anti-dsDNA)
SLE (type III hypersensitivity)
Pharmacodynamics: Effects of adding competitive antagonists, noncompetitive antagonists, and partial agonists to an agonist on pharmacodynamic curves:
1) Competitive antagonist + agonist –> shift curve to the right = decreased potency (increased Km); no change on efficacy2) Noncompetitive antagonist plus agonist: shift curve down = decreased efficacy (decreased Vmax); no effect on potency3) Partial agonist: acts at the same site as a full agonist, but with reduced maximal effect. Get decreased efficacy (decreased Vmax); potency is variable, can be either increased or decreased.
Pharmacodynamics: Effects of adding competitive antagonists, noncompetitive antagonists, and partial agonists to an agonist on pharmacodynamic curves:
1) Competitive antagonist + agonist –> shift curve to the right = decreased potency (increased Km); no change on efficacy2) Noncompetitive antagonist plus agonist: shift curve down = decreased efficacy (decreased Vmax); no effect on potency3) Partial agonist: acts at the same site as a full agonist, but with reduced maximal effect. Get decreased efficacy (decreased Vmax); potency is variable, can be either increased or decreased.
antiplatelet antibodies
ITP (idiopathic thrombocytopenic purpura)
Therapeutic Index: What is it? What’s the equation? Is it safer to have a higher or lower TI?*Examples of drugs with low TI?
TI = measurement of drug safetyTI = LD50/ED50 = median lethal dose/median effective dose(“TILE”)Safer drugs have higher TI valuesExamples of drugs with low TI (must monitor these patients!):-Phenobarbital-Lithium-Digoxin-Coumadin/Warfarin