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78 Cards in this Set
- Front
- Back
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Quinidine CYP450
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inducer (some inhibition effect)
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Barbiturates CYP450
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inducer (primidone metabolite)
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St. John's wort CYP450
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inducer
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Phenytoin CYP450
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inducer
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Rifampin CYP450
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inducer
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Griseofulvin CYP450
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inducer
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Carbamazepine CYP450
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inducer
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Chronic alcohol use CYP450
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inducer
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HIV protease inhibitors CYP450
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inhibitor
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Ketoconazole CYP450
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inhibitor
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Erythromycin CYP450
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inhibitor
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Clarithromycin CYP450
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inhibitor
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Grapefruit juice CYP450
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inhibitor
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Acute alcohol use CYP450
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inhibitor
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Sulfonamides CYP450
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inhibitor
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Isoniazid CYP450
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inhibitor
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Cimetidine CYP450
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inhibitor
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Cotrimoxazole CYP450
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inhibitor
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Fluoxetine CYP450
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inhibitor
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Diltiazem CYP450
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inhibitor
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Amiodarone CYP450
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inhibitor
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Fluoroquinolones CYP450
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inhibitor
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Metronidazole CYP450
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inhibitor
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Ciprofloxacin CYP450
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inhibitor
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Digoxin and furosemide interaction
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Digoxin toxicity increases because furosemide reduced potassium
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Digoxin clinical use
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CHF (increases contractility)
a-fib (decreases AV node conduction, depresses SA node) |
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Digoxin mechanism (2)
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1. Positive inotropy (Na/K block)
2. Vagus stimulation |
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Digoxin cholinergic effects
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Nausea, vomiting, diarrhea, blurry yellow vision
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Digoxin EKG changes
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PR increased, QT decreased, ST segment scooping, T-wave inversion, other arrhythmias, hyperkalemia
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Digoxin and quinidine interaction
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Decreased digoxin clearance because quinidine displaces digoxin from tissue binding sites
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Digoxin clearance
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half-life is 40 hours
urinary excretion (bad in renal failure) |
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Digoxin toxicity antidote (5)
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1. Slowly normalize K
2. Lidocaine (or phenytoin) 3. Cardiac pacer 4. Anti-dig Fab fragments 5. Magnesium |
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Class I antiarrhythmics general
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1. Local anesthetics that block Na channels
2. Decrease slope of phase 0 in myocytes 3. Depress frequently depolarized cells |
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Class IA antiarrhythmic drugs
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Quinidine
Procainamide Disopyramide |
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Class IA effect on myocytes
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1. Increase AP duration
2. Increases effective refractory period 3. Increase QT interval 4. Increase phase 0 and 3 |
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Class IA arrhythmia treatments
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Mainly reentrant and ectopic supraventricular and ventricular tachycardia; procainamide for Wolf Parkinson White
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Quinidine toxicity
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cinchonism (headache, tinnitus), thrombocytopenia, torsades (QT increased)
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Procainamide toxicity
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reversible SLE
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Class IB antiarrhythmic drugs
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Lidocaine
Mexiletine Tocainide |
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Class IB effect on myocytes
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1. Decrease AP duration
2. Increase phase 0, decrease phase 3 |
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Class IB arrhythmia treatments
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Acute ventricular arrhythmias post-MI; digitalis-induced arrhythmias (lidocaine for v-tach)
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Class IB toxicity
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Local anesthetic
CNS stimulation/depression CV depression |
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Class IC antiarrhythmic drugs
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Flecainide
Encainide Propafenone |
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Class IC effect on myocytes
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1. No AP duration changes
2. Increased phase 0 only 3. Prolongs AV node refractory period (toxicity) |
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Class IC arrhythmia treatment
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V-tach that progress to VF
Intractable SVT (last resort) |
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Class IC toxicity
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Causes arrhythmias (don't use post MI)
AV node prolongation |
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Class II antiarrhythmic mechanism
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beta-blockers
decrease phase 4 slope in SA/AV node (increase PR interval); decreased cAMP and calcium currents |
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Class II antiarrhythmic drugs
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Propranolol
Esmolol Metoprolol Atenolol Timolol |
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Class II antiarrhythmic toxicity
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impotence
asthma exacerbation (not bad with metoprolol, atenolol) CV (bradycardia, AV block-atenolol, CHF) CNS (sedation) dyslipidemia (metoprolol) RX=glucagon |
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Class II antiarrhythmic clinical use
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V-tach, SVT, slow ventricular rate during a-fib and flutter, hypertrophic CM
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Class III antiarrhythmic general
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Increase AP duration, ERP, QT (last resort drugs); block potassium to increase phase 3
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Class III antiarrhythmic drugs
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Sotalol
Ibutilide Bretylium Dofetilide Amiodarone |
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Sotalol toxicity
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torsades
excessive beta block |
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ibutilide toxicity
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torsades
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bretylium toxicity
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new arrhythmias
hypotension |
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amiodarone toxicity
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pulmonary fibrosis
hepatotoxicity hypothyroidism/hyperthyroidism corneal deposits blue/gray skin deposits (photodermatitis) neurologic effects constipation CV (bradycardia, heart block, CHF) Class I, II, III, IV effects |
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Class IV antiarrhythmics general
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Decrease conduction velocity, increase ERP, increase PR; used to prevent nodal arrhythmias; decreases phase 0 slope in nodal cells, makes phase 3 less steep
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Class IV antiarrhythmic drugs
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Verapamil
Diltiazem |
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Adenosine
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Increases K out of cells making it harder to depolarize nodal tissue; treat SVT (not reentrant like WPW); toxicity of flushing and hypotension; short acting
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Theophylline
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Blocks adenosine by antagonizing receptor
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Potassium
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depresses ectopic pacemakers in hypokalemic patients
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Magnesium
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effective in torsades and dig toxicity
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Bruton's agammaglobulinemia
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XR; defective tyrosine kinase BTK
Blocked B cell maturation (reduced B cell count) Recurrent bacterial infections |
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Hyper-IgM syndrome
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Defect in CD40L (Th4 cells)
No class switch Severe pyogenic infections early IgM high; IgG very low (IgA, IgE low) |
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Selective Ig deficiency
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Isotype switching defect
Low IgA Sinus and lung infections, diarrhea |
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Common variable immunodeficiency
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Defective B cell maturation (normal number of B cells, decreased plasma cells)
Can occur in 20-30 age Risk of AI disease, lymphoma, sinopulmonary infections |
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Thymic aplasia (DiGeorge)
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22q11 deletion (failure of 3rd/4th pouches)
Thymus/parathyroid fail to develop (low T cells, low PTH, low calcium) Recurrent viral/fungal infections |
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IL-12 receptor deficiency
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Decreased Th1 response
Disseminated mycobacterial infections Decreased IFN-gamma |
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Hyper-IgE syndrome (Job's syndrome)
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Th cells fail to produce IFN-gamma so neutrophils don't respond to chemotactic stimuli
Increased IgE Coarse facies, staph abscesses (cold), eczema |
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Chronic mucocutaneous candidiasis
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T cell dysfunction
Get candida infections of skin and mucous membranes |
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Hereditary angioedema
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AR, deficiency C1 esterase inhibitor (normally deactivates classical complement pathway)
Get edema of mucosal surfaces |
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Myeloperoxidase deficiency
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Usually asymptomatic as long as NADPH oxidase still functional (makes HOCl normally)
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Severe combined immunodeficiency (SCID)
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Defective IL-2 receptor (XR), adenosine deaminase deficiency (AR), failure to synthesize MHCII antigens, or rag defects
Low B and T cells; increased adenine toxic to B and T cells (less dNTPs and DNA synthesis) Get infections of all types |
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Ataxia-telangiectasia
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Defective DNA repair
Ataxia, spider angioma, IgA deficiency Increased translocations and cancer risk |
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Wiskott-Aldrich syndrome
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XR, deletion of B and T cells (normal number, dysfunctional)
Thrombocytopenic purpura, Infections, Eczema High IgE, IgA; low IgM |
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Leukocyte adhesion deficiency (type I)
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AR defect in LFA-1 integrin (CD18) on phagocytes
Recurrent bacterial infections without pus; omphalitis Neutrophilia |
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Chédiak-Higashi syndrome
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AR defective MT function (decreased phagocytosis)
Recurrent pyogenic staph/strep infections; partial albinism; peripheral neuropathy/seizures |
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Chronic granulomatous disease
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Lack NADPH oxidase causing low ROS (superoxide)
Susceptible to catalase-positive organisms like staph, E. coli, Aspergillus, klebsiella, candida |
