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COMSAE Drugs study guide (latest update)

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Warfarin- Mechanism Interferes w/ vitamin K dependent clotting factors (II, VII, IX, X, C, S) Warfarin- Pathway, effect on PT/INR Extrinsic factor, increased PT Warfarin- Clinical Use Chronic anticoagulation Warfarin- Pregnancy CI in pregnant women--crosses placenta Warfarin- AE Bleeding, tissue necrosis Digoxin- MOA Direct inhibition of Na/K ATPase --> indirect inhibition of Na/Ca exchange Increased Calcium concentration --> positive ionotropy. Stimulates vagus nerve --> decrease HR Digoxin- Clinical use Heart failure (increase contractility) atrial fibrillation (decrease conduction at AV node and depression of SA node) Digoxin- AE Hyperkalemia, blurry yellow vision, arrhythmias, AV block Digoxin Toxicity- Treatment Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg+ Beta Blockers- Mechanism Decrease SA and AV nodal activity by decreasing cAMP/Ca2+ Decrease slope of phase 4 Beta Blockers- Use SVT, ventricular rate control for a-fib and a-flutter Beta Blockers- AE Exacerbation of COPD/asthma CV effects: bradycardia, AV block, HF Metronidazole- MOA Forms toxic free radical metabolites in bacteria. Bacteriocidal Metronidazole- Clinical Use GET GAP Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (C. diff), H. Pylori (penicillin injury) (Anaerobic infection below the diaphragm) Metronidazole- AE Disulfiram-like reaction (flushing, tachycardia, hypotension) with alcohol. Headache, metallic taste Typical antipsychotics (-azine)- MOA Block dopamine D2 receptor --> increase cAMP Typical antipsychotics - Clinical Use Schizophrenia, pyschosis, bipolar, Huntington, OCD Typical antipsychotics - AE EPS (ADAPT)- Acute dystonia, akathisia, parkinsonism, tardive dyskinesia Neuroleptic malignant syndrome (Malignant FEVER)- Myogllobinuria, fever, encephalopathy, vitals, increased enzymes, muscle rigidity Treatment: Dantrolene, D2 agonist (bromocriptine) Atypical antipsychotics (-apine, -peridone) - Clinical Use Schizophrenia, bipolar, OCD, anxiety, depression, mania, Tourettes Atypical Antipsychotics- AE All-- prolonged QT interval, fewer EPS/anticholinergic effects -pines: Metabolic syndrome Clozapine- agranulocytosis Respiridone- Hyperprolactinemia Lithium- Clinical Use Mood stabilizer Lithium- AE LiTHIUM: Low Thyroid, Heart (Ebstein anomaly), Insipidus (nephrogenic), Unwanted Movements (tremor) Cimetidine (-dines) - MOA H2 blockers Take H2 blockers before you dine; table for 2. Cimetidine- Use Peptic ulcer, gastritis, mild reflux Cimitidine- AE Inhibitor of cytochrome P450 Decrease renal excretion of creatinine Antiandrogenic, cross blood brain barrier Acetaminophen- MOA COX inhibitor (reversible) Acetaminophen- Use Antipyrogenic, analgesic NOT anti-inflammatory Use instead of aspirin to avoid Reye syndrome in children Acetaminophen- AE Hepatic necrosis; decrease glutathione (treatment: N-acetylcysteine) Furosemide, bumetanide, torsemide (-ides) Loop diuretics Loop diuretics- MOA Inhibit Na/K/2Cl in TAL Increase Ca excretion (Loops Lose Ca2+) Loop diuretics- Use Edema (HF, cirrhosis, nephrotic syndrome), HTN, hypercalcemia Loop diuretics- AE OHH DAANG Ototoxicity, Hypokalemia, Hypomagnesemia, Dehydration, Allergy (sulfa), Alkalosis, Nephritis, Gout Hydrochlorothiazide, chlorthalidone, metolazone Thiazide diuretics Thiazide diuretics- MOA Inhibit NaCl reabsorption in DCT--> decrease calcium excretion Thiazides- Clinical Use HTN, HF, nephrogenic diabetes insipidus, osteoporosis

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Uploaded on
August 3, 2024
Number of pages
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Written in
2024/2025
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COMSAE Drugs
study guide
(latest update)
Warfarin- Mechanism - answer Interferes w/
vitamin K dependent clotting factors (II, VII, IX, X,
C, S)


Warfarin- Pathway, effect on PT/INR - answer
Extrinsic factor, increased PT


Warfarin- Clinical Use - answer Chronic
anticoagulation


Warfarin- Pregnancy - answer CI in pregnant
women--crosses placenta


Warfarin- AE - answer Bleeding, tissue necrosis

, Digoxin- MOA - answer Direct inhibition of Na/K
ATPase --> indirect inhibition of Na/Ca exchange
Increased Calcium concentration --> positive
ionotropy.
Stimulates vagus nerve --> decrease HR


Digoxin- Clinical use - answer Heart failure
(increase contractility)
atrial fibrillation (decrease conduction at AV node
and depression of SA node)


Digoxin- AE - answer Hyperkalemia, blurry yellow
vision, arrhythmias, AV block


Digoxin Toxicity- Treatment - answer Slowly
normalize K+, cardiac pacer, anti-digoxin Fab
fragments, Mg+


Beta Blockers- Mechanism - answer Decrease SA
and AV nodal activity by decreasing cAMP/Ca2+
Decrease slope of phase 4

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