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Carbonic Anhydrase Inhibitor Inhibits CA in the PCT → ↓ Na & HCO3- reabsorption Secreted into lumen via OA trx Inhibits 85% of PCT HCO3 reabs Inhibits 45% of total HCO3 reabs Metabolic acidosis, renal CaPO4 stones, hypokalemia, CNS, allergy Contraind: cirrhosis (encephalopathy) CHF edema, Glaucoma Urine alkalinization Mountain sickness |
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Loop Diuretic Inhibits Na+/K+/2Cl- trx in TAL → ↓Na & K & 2Cl reabsorption Secreted into lumen via OA trx Eliminated via kidney Hyponatremia/dehydration Hypocalcemia Hypokalemia Metabolic alkalosis Hypomagnesemia Hyperuricemia Ototoxicity Allergy Decrease luminal (+) potential (↓ K+ pushed out) → ↓Ca2+ & Mg2+ reabs Pulmonary edema Edema (CH, renal, cirrhosis) Hypercalcemia Hyperkalemia |
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Loop Diuretic Inhibits Na+/K+/2Cl- trx in TAL → ↓Na & K & 2Cl reabsorption Shorter acting 50% liver elimination (50% kidney elimination) Hyponatremia/dehydration Hypocalcemia Hypokalemia Metabolic alkalosis Hypomagnesemia Hyperuricemia Ototoxicity Allergy 40x more potent Pulmonary edema Edema (CH, renal, cirrhosis) Hypercalcemia Hyperkalemia |
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Loop Diuretic Inhibits Na+/K+/2Cl- trx in TAL → ↓Na & K & 2Cl reabsorption Longer acting Faster absorption 80% liver elimination Hyponatremia/dehydration Hypocalcemia Hypokalemia Metabolic alkalosis Hypomagnesemia Hyperuricemia Ototoxicity Allergy Pulmonary edema Edema (CH, renal, cirrhosis) Hypercalcemia Hyperkalemia |
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Loop Diuretic Loop - Inhibits Na+/K+/2Cl- trx in TAL → ↓Na & K & 2Cl reabsorption No sulfur group in its structure Only if allergic to other loops Worst ototoxicity |
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K+ Sparing Diuretic Competitive aldosterone receptor in DCT & CT → ↓ in Na+ channels & ↓ out K+ channels (Princ.) ↓ Na+ reabsorption & ↓ K+ secretion in Principal cells ↑ H+ secretion Intercalated cells Hyperkalemia, metabolic acidosis, gynecomastia, impotence, ↓ libido, GI, CNS effects Also inhibits DHT receptor → ↓ testosterone Only diuretic not acting in lumen Cirrhosis (ascites) Hyperaldosteronism Hypertension |
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K+ Sparing Diuretic Epoxy-spironolactone derivative Less anti-androgenic effects (less DHT & progesterone receptor binding) Heart failure |
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K+ Sparing Diuretic Blocks Na+ channels in Principal cells in DT & CT → ↓ Na+ reabs & ↓ K+ secretion Secreted unchanged into lumen via organic base transporter Eliminated unchanged via kidney Hyperkalemia (NSAIDs ↑ likelihood) Nausea, vomiting, diarrhea, leg cramps, headache, dizziness Edema; Hypertension |
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K+ Sparing Diuretic Blocks Na+ channels in Principal cells in DT & CT → ↓ Na+ reabs & ↓ K+ secretion Shorter acting Metabolized in liver → into kidney lumen → INSOLUABLE & PPTS OUT Photosensitivity 10x less potent than amiloride Edema Hypertension |
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Thiazide Diuretic Inhibits NaCl cotrx in DCT → ↓Na & Cl reabsorption Secreted into lumen via OA trx Absorbed orally Hyponatremia/dehydration Hypokalemia Metabolic alkalosis HYPERCALCEMIA Hyperglycemia Hyperuricemia Allergy Weakness Low Na in cell sucks Na through basolatera Na/Ca exchanger → ↑ Ca2+ reabsorption Hypertension CHF Idiopathic hypercalciuria (renal stones) Nephrogenic diabetes insipidus |
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Thiazide Diuretic Inhibits NaCl cotrx in DCT → ↓Na & Cl reabsorption Longer acting Hyponatremia/dehydration Hypokalemia Metabolic alkalosis HYPERCALCEMIA Hyperglycemia Hyperuricemia Allergy Weakness 10x more potent than HCT Different structure from thiazides Hypertension CHF Idiopathic hypercalciuria (renal stones) Nephrogenic diabetes insipidus |
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Thiazide Diuretic Inhibits NaCl cotrx in DCT → ↓Na & Cl reabsorption Longer acting Excellent oral absorption Eliminated via liver Hyponatremia/dehydration Hypokalemia Metabolic alkalosis HYPERCALCEMIA Hyperglycemia Hyperuricemia Allergy Weakness 20x more potent than HCT Different structure from thiazides Hypertension CHF Idiopathic hypercalciuria (renal stones) Nephrogenic diabetes insipidus |
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Thiazide Diuretic Inhibits NaCl cotrx in DCT → ↓Na & Cl reabsorption Longer acting Hyponatremia/dehydration Hypokalemia Metabolic alkalosis HYPERCALCEMIA Hyperglycemia Hyperuricemia Allergy Weakness Same potency as HCT Different structure from thiazides Hypertension CHF Idiopathic hypercalciuria (renal stones) Nephrogenic diabetes insipidus |
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Osmotic Diuretic Filtered & excreted exerting osmotic pull in PCT & loop of henle Must be given IV ↑ flow → ↑ urea excretion → ↓ ability to concentrate urine Headache, nausea, vomiting, hypernatremia/dehydration, pulmonary edema Initial rapid expansion of plamsa volume Intracranial pressure Renal ADH V2 receptor antagonistexcretion of toxins |
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ADH V2 Receptor Antagonist ADH V2 receptor antagonist → ↑ free H2O excretion & ↓ urea & Na+ reabsorption Heart failure |
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ADH V1a, V2 antagonist ADH V1a antagonist → ↓ vasocx & ↓ smooth muscle growth ADH V2 receptor antagonist → ↑ free H2O excretion & ↓ urea & Na+ reabsorption |
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Renin Inhibitor Binds to Renin preventing the conversion of Angiotensinogen to Angiotensin I |
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Class II Anti-arrhythmic Non-selective β blocker Na+ blocker at ↑ dose (membrane stabilization) ↓ AV conduction velocity, prolonged PR, ↓ automaticity in ectopic foci Myocardial depression, heart block, bronchospasm, ↑ insulin hypoglycemia, depression, rebound SNS if w/d Atrial flutter Atrial fibrilliation Ventricular arrhythmia (post-MI) Angina "golden child" |
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Class II Anti-arrhythmic Non-selective β blocker α blocker Antioxidant properties Atrial Flutter; Atrial fibrillation; Ventricular arrhythmia (post-MI); Angina |
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B1 B2 Blocker Treats Hypertension/Migraine/Chest Pain |
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B1 B2 Blocker with B1 ISA |
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a1 B1 B2 blocker with B2 ISA |
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B1 Blocker with B1 ISA Class II Anti-arrhythmic LUPUS-like syndrome Intrinsic SNS activity, but no membrane stabilizing effects Atrial flutter Atrial fibrilliation Ventricular arrhythmia (post-MI) Angina |
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Definition
B1 Blocker Class II Anti-arrhythmic Atrial Flutter; Atrial fibrillation; Ventricular arrhythmia (post-MI); Angina |
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β1 Blocker Class II Anti-arrhythmic Longer acting Less polar → less CNS effects Atrial flutter Atrial fibrilliation Ventricular arrhythmia (post-MI) Angina |
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β1 Blocker Class II Anti-arrhythmic Used IV when immediate block is needed Cleared quickly Atrial flutter Atrial fibrilliation Ventricular arrhythmia (post-MI) Angina |
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ACE Inhibitor Prevent A1 → A2 conversion Venous & arterial vasodilation → ↓ preload & afterload (+ ↑ bradykinin) Abrupt ↓ in BP w/first dose (vol dep) Rash, loss of taste, cough Heart failure |
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Definition
ACE Inhibitor Prevent A1 → A2 conversion Venous & arterial vasodilation → ↓ preload & afterload (+ ↑ bradykinin) Abrupt ↓ in BP w/first dose (vol dep) Rash, loss of taste, cough Heart failure |
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Definition
ACE Inhibitor Pro-drug, longer duration Prevent A1 → A2 conversion Venous & arterial vasodilation → ↓ preload & afterload (+ ↑ bradykinin) Abrupt ↓ in BP w/first dose (vol dep) Rash, loss of taste, cough Heart failure |
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Definition
ACE Inhibitor Pro-drug, longer duration Prevent A1 → A2 conversion Venous & arterial vasodilation → ↓ preload & afterload (+ ↑ bradykinin) Abrupt ↓ in BP w/first dose (vol dep) Rash, loss of taste, cough, Hyperkalemia Heart failure |
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Definition
ARB Vasculature A2 receptor blocker, sim. to ACE inhib. but no cough |
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Definition
ARB Vasculature A2 receptor blocker, like ACE inhib. but no cough, less effective in Africans |
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Definition
Vasodilator Class IV Anti-arrhythmic (dihydropyridines primarely work on VASCULATURE) Blocks L-type Ca2+ channel → ARTERIAL vasodiltn & ↓HR & ↓CX (less deg.) Highly protein bound (~90%) Liver metabolized Worsening angina, worsening HF, heart block (in AV dz), bradycardia, hypotension, edema, resp, GI Not helpful for systolic dysfx Helpful for diastolic dysfx (cardiac filling) Heart failure / HTN Reentry arrhythmia Angina (vasospastic/exer) |
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Definition
Vasodilator Class IV Anti-arrhythmic Blocks L-type Ca2+ channels ↓ HR, ↓ CX, ↓ conduction velocity (AV), prolongs AV refractory period Hypotension → reflex tachy, VERY NEGATIVELY INOTROPIC (don't use w/ b block), heart block (AV conduction dz), bradycardia (SA conduction dz), GI Given orally but IV is better More active L-isomer first pass met. SVT (acute or chronic) |
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Definition
Vasodilator Class IV Anti-arrhythmic Blocks L-type Ca2+ channels ↓ HR, ↓ CX, ↓ conduction velocity (AV), prolongs AV refractory period Hypotension → reflex tachy, neg. inotropy, heart block (AV conduction dz), bradycardia (SA conduction dz), GI Less negative inotropic effects (less ↓ CX) SVT (acute or chronic) |
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Definition
Vascular Smooth Muscle Dilator ↑ NO + ↑ K+ perm. ARTERIAL vasodilation → ↓afterload, ↑CX, renal dilation → ↑renal blood flow SE: LUPUS-LIKE SYNDROME |
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Definition
Vascular Smooth Muscle Dilator Metabolized to NO→AC→ ↑cGMP → vasodiltn VENOUS & ARTERIAL vasodilation → ↓preload & afterload |
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Definition
Vasodilator Metabolized to NO → VENOUS & ARTERIAL vasodiltn → ↓ preload & afterload Flushing, headache, hypotension, reflex tachycardia, Fast first pass metabolism Tolerance develops rapidly CHF (acute & chronic) Vasospastic Angina (w/Ca2+ blockers) |
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Definition
Vasodilator Metabolized to NO → VENOUS & ARTERIAL vasodilation → ↓preload & afterload CHF, Vasospastic Angina (w/Ca2+ blockers) |
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Definition
Class 1A Na+ Blocker (Intermediate r) Blocks V-G Na+ channels & K+ channels Blocks α-adren & vagus ↓ automaticity, ↑ AP = prolonged QT, widened QRS, ↑ SA & AV node conduction velocity; "1A has Added AP" GI, hepatic granulomas, torsades, cinchonism, LUPUS-LIKE syndrome (rarely), inhibits P450; will prolong P450 drugs Can cause PARADOXICAL ↑ IN HEART RATE in ATRIAL FLUTTER Chronic SVT (2nd line) |
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Definition
Class 1A Na+ Blocker (Intermediate r) Blocks V-G Na+ channels & K+ channels (no ANS effects) ↓ automaticity ↑ refractory period ↓ conduction velocity; ↑ AP = prolonged QT "1A has Added AP" GI, hypotension, torsades, heart block, AGRANULOCYTOSIS, LUPUS-LIKE SYNDROME (20-50%longterm) Converted to active metabolite NAPA → no Na+ channel activity but blocks K+ channels Ventricular tachycardia; SVT (2nd line if DC cardioversion doesn't work; WPW syndrome |
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Definition
Class 1B Na+ Blocker (Rapid r) Blocks Na+ channels, ↑ gK in fast fibers during phase 3 & 4 IV use only (↑ first pass metab) B/c of rapid r only works on ischemic or heavily-driven tissue ↓automaticity, ↓ action potential "1B has Brief AP", ↓ conduction velocity, Widened QRS but shorter QT SEIZURES Nystagmus, tremor, dysarthria, altered sernsorium Ventricular tachycardia; Ventricular fibrillation (after amiodarone) |
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Definition
Class 1B Na+ Blocker (Rapid r) Blocks Na+ channels, ↑ gK in fast fibers during phase 3 & 4 orally available B/c of rapid r only works on ischemic or heavily-driven tissue; ↓automaticity, ↓ action potential, ↓ conduction velocity; Widened QRS with shortened QT Nausea, tremor, CNS effects Orally active Neuropathic Pain (DM pts); Ventricular Tachycardia; ventricular fibrillation (but only after amiodarone) |
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Definition
Class 1C Na+ Blocker (very long r) Blocks Na+ channels Blocks K+ channels Blocks Ca2+ channels ↓ conduction velocity, widened QRS, ↑ action potential "1C continuous AP", prolonged QT, prolonged PR Proarrhythmic (after MI) Exacerbate CHF by ↓ LV fxn (low Ca) Heart block (in AV node dz) Atrial arrhythmia (in NO other heart disease ie Young PPL) |
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Definition
Class 1C Na+ Blocker (very long r) Blocks Na+ channels Blocks K+ channels Blocks β-adrenergic ↓ conduction velocity, widened QRS, ↑ action potential "1C continuous AP", prolonged QT, prolonged PR Proarrhythmic (after MI) Exacerbate CHF by ↓ LV fxn Heart block (in AV node dz), torsades Bradycardia & bronchospasm (β block) Metab by P450 Atrial arrhythmia "causes more arrhythmias than it's worth" |
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Definition
Class III K+ Channel Blocker Blocks K+ channels Blocks Na+ & Ca2+ channels Non-competitive SNS blocker Prolonged QT, ↓ automaticity, ↓ conduction velocity, widened QRS, prolonged PR Corneal deposits (100%), LIVER DZ, HYPO & HYPERTHYROIDISM, PULM FIBROSIS, vasodilation, photosensitivity/skin color Highly lipophilic, extensive tissue distrib + LONG hl First line agent in ACLS code Active metabolite: desethyl-amio Atrial tachycardia; Ventricular tachycardia; Long term stab. with ICD |
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Definition
Class III - K+ Channel Blocker Blocks K+ channels Non-selective β blocker ↑ action potential, ↓ automaticity, ↓ conduction velocity (AV only), prolongs AV refractory period Torsades (especially in hypokalemia) β blocker SE's Renal excretion of unchanged drug β blocker w/Class III effects Atrial arrhythmias (chronic) |
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Definition
Class III - K+ Channel Blocker Blocks K+ channels Non-selective β blocker IV use only, Delays repolarization, ↑ action potential, QRS stays same Torsades Contraindicated in hypokalemia IV use only Atrial Arrhythmias (Acute) |
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Definition
Class III - K+ Channel Blocker Blocks K+ channels (rapid delayed rectifier K+ current)↑ action potential, QRS stays same Greater effect on atrial than ventricles Torsades Rx Interax: ↑ [Dofetilide] Interfere w/cation trx in kidney, prolong QT interval, use liver metab. Atrial Arrhythmias (chronic) |
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Definition
Anti-arrhythmic Binds adenosine receptors → opens ACh-sens. K+ channel (in SA/AV/atria), anti-sympathetic tone (↓Na, ↓Ca) Shortens atrial AP, ↓ automaticity, ↑ AV refractory period, ↓ AV conduction velocity Transient: asystole, dyspnea, bronchoCX Atrial fibrillation Flushing IV use only Rx Interax: theophylline & caffeine block adenosine receptors Atrial tachycardia; Atial fibrillation; Produce controlled hypotension |
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Definition
Anti-arrhythmic (AV Nodal Depressant) MOA: Direct: Blocks Na+/K+ ATPase Indirect: vagal stimulation ↑ CX (↑ Ca2+) Vagal: ↓ atrial AP, ↓ SA automaticity & ↓ AV conduction velocity Rx Interax: ↑ [Digoxin] quinidine & verapamil SVT (Acute or Chronic); CHF (↑CO) |
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Definition
Digitalis Glycoside MOA: Inhibit Na+/K+ ATPase binding extracellularly on α subunit Prefers E1-P form → stabilize to E2-P form Na & Mg favor binding K favors release MET: 25% plasma protein bound Renal elimination, 2 day half-life SE: Fatigue, malaise, dizziness, confusion, delirium, anorexia, N/V, abdominal pain color vision, halos, bradycardia, AV block, ectopic beats, SA arrest, ventricular arrhythmias, EKG changes OTH: Aglycone portion = for cardiac activity; Monosaccharide chain = metab.; Eubacterium lentum in gut inactivates USE: Heart Failure |
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Definition
Digitalis Glycoside MOA: Inhibit Na+/K+ ATPase binding extracellularly on α subunit Prefers E1-P form → stabilize to E2-P form Na & Mg favor binding K favors release MET: >90% plasma protein bound Hepatic elimination, 7 day half-life SE: Fatigue, malaise, dizziness, confusion, delirium, anorexia, N/V, abdominal pain color vision, halos, bradycardia, AV block, ectopic beats, SA arrest, ventricular arrhythmias, EKG changes OTH: Aglycone portion = for cardiac activity; Monosaccharide chain = metab.; Eubacterium lentum in gut inactivates USE: Heart Failure |
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Definition
Misc. Inotropes Stimulate β1 receptors → ↑ CX SE: Dopamine: tachycardia, arrhymthia Dobutamine: tolerance, vasodilation (via β2 receptors) OTH: Dopamine vasodilates renal vasculature via D1 receptors USE: Heart Failure (serious) |
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Phosphodiesterase Inhibitor MOA: Inhibits phosphodiesterase-III → vasodilation & ↑ CX MET: PDE-III selectively found in cardiac & smooth muscle SE: Nausea, vomiting Thrombocytopenia, liver damage Arrhythmia OTH: Does more harm than good when used long term USE: Heart Failure (serious) |
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Alcoholism Trx MOA: Interacts with NMDA & GABA-A receptors MET: Taurine derivative OTH: Reduces hyperexcitability during withdrawal USE: Alcoholism |
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Alcoholism Trx MOA: Irreversibly inhibit ALDH → ↑acetaldehyde MET: Converted to active metabolites (which inhibit ALDH) TOX: Acetaldehyde syndrome → alcohol flush reaction USE: Alcoholism |
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Alcoholism Trx MOA: Opiate µOR antagonist Blocks alcohol reinforcement OTH: Reduces craving Reduces relapse rates by 50% USE: Alcoholism |
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Definition
Alcoholism Trx Methanol −ADH→ formaldehyde −ALDH→ formic acid TOX: Headache, vertigo, vomiting, abd/back pain, dyspnea, met. Acidosis, coma, resp. failure OTH: Can cause blindness (15mL) USE: Toxic |
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Alcoholism Trx MOA: Ethgly −ADH→ glycoaldehyde −ALDH→ glycolic acid → glyoxylic & oxalic acid TOX: Metabolic acidosis Renal failure (oxalate deposits) OTH: Treat with EtOH Treat w/fomepizole: ADH inhibitor USE: Antifreeze |
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Ethylene Glycol Trx MOA: Alcohol Dehydrogenase Inhibitor |
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Drug of Abuse ↑ excess DA release and reverses the transport of DA, thus is more potent and longer acting than cocaine SEL: Presynaptic DA terminal MET: <12h; hih lasts 8-24hr SHORT TERM USE: Euphoria rush; rapidly ↑ HR, BP; ↑ attention and decreased fatigue; ↑ activity (violent behaviors); ↓ appetite; ↑ respiration; hyperthermia LONG TERM USE: Depletes DA in NAc (DA neve terminal damage); Dependence & psychotic symptoms; Paranoia; Hallucination; Mood disturbances; Repetitive motor activity |
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Definition
Drug of Abuse MOA: Binds to DA transporters to prevent reuptake of DA allowing an ↑ in DA-R1 effect (reward); Also ↓ VMAT2 SEL: DA transporters USE: Local anesthetic; ↑ HR and BP; ↑ arousal and alertness; rush and euphoria; ↑ involuntary motor behaviors; stereotyped behaviors; paranoia; psychological dependence; Heart SE: cardiac arrhythmias (v fib), myocardial ischemia, cerebral vasoconstriction, seizures |
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Drug of Abuse MOA: Agonst at Gi ↓ cAMP and PKA, thus ↓ Ca; K current ↑; Inhibitory response ↓ NT release; ↑ DA release in mesocorticallimbic system; Chronic use ↑ cAMP and PKA, thus activation CREB, which is inolvd in tolerance and dependance SEL: MOR WITHDRAWAL TRX: Methadone; Clonidine; Naltrexone; Buprenorphine USE: euphoria, rapid tolerance to euphoria; RESP. DEPRESSION; sedation; analgesia; emetic effects; Miosis (Edinger-Westphal Stim) "Pinpoint Pupils"; Physical Dependence |
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Lysergic Acid Diethylamide |
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Definition
Drugs of Abuse MOA: thought to activate several types of 5HT receptors MET: rapidly absorbed from oral; onset 40-60 min. peak 2-4 hrs lasting ~8hr USE: perceptual distortions; profound hallucinations; mood changes; intense arousal; portentiousness |
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Drugs of Abuse MOA: THC binds to CBR1 receptors on GABA neurons in the NAc, inhibiting GABA release and disinhibiting DA release to ↑ DA R1 mediated signaling SEL: CBR1's in NAc USE: ↑ euphoria to minimize migraine; ↓ intraocular pressure (glaucoma); calm muscle spasms; restore appetite; anti-emetic SX: lower flow to limbs; irritates lungs/airways; may lower sperm # or quality |
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Drugs of Abuse MOA: Stimulates the nAchR, on the mesoaccumbens DA system in the VTA SEL: nAchR TRX WITHDRAWAL: sprays, gums, patches; Buproprion (Wellbutrin); Mecamylamine nAchR antagonist |
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Drugs of Abuse MOA: Dissociative Anesthetic; binds Sigma receptors and NMDA-type of glutamate receptor (antagonist) TRX WITHDRAWAL: haloperidol for psychosis USE: emotional withdrawal; bizarre unpredictable aggressive behavior; psychosis |
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Strong Opoid Potent MOR agonist 30% absorbed in gut 90% first pass metabolism Analgesia, sedation, euphoria, dysphoria, miosis, N/V, OH, resp. & cough suppression Pinpoint pupils = opioid OD Constipation Mod-severe pain Myocardial infarction Dyspnea, anxiety |
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Strong Opoid Potent MOR agonist Same potency as morphine bioavailability than morphine Long acting No euphoria Prevents W/D signs Mod-severe pain Opioid addiction |
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Definition
Strong Opoid Potent MOR Agonist 1/5 morphine potency 1/4 morphine duration No cough suppression Less constipation No labor prolongation OB/Surg analgesia Mod-severe pain |
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Strong Opoid Potent MOR Agonist 80x morphine potency Less nausea Sufentanyl = ↑ fentanyl Alfentanyl = ↓ fentanyl Post-op pain Anesthetic (w/droperidol) |
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Moderate Opoid Agonists Weaker MOR agonist Metabolized in part to morphine Excellent bioavailability Few SE Mild-moderate pain Cough |
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Definition
Moderate Opoid Agonist Weaker MOR agonist Given w/aspirin or acetaminophen Abuse |
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Moderate Opoid Agonist Weaker MOR agonist 1/2 codeine potency Given w/acetaminophen Interax: alcohol/sedatives (fatal) Mild-moderate pain |
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Mixed Opoid Agon/Antag KOR agonist MOR antagonist Same potency as morphine 5x pentazocine potency Sedation (KOR) Sweating, dizziness Psychotomimetic effects Anxiety, nausea, vomiting Less psychotomimetic effects Less MOR antagonist activity Moderate-Severe Pain |
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Mixed Opoid Agon/Antag KOR agonist MOR antagonist 25-50x morphine potency (pain) Sedation (KOR) Sweating, dizziness Psychotomimetic effects Anxiety, nausea, vomiting Worse sedation & resp. depression than morphine Binds MOR w/high affinity Mod-severe pain; Reduce Craving for Morphine |
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Mixed Opoid Agon/Antag KOR agonist MOR antagonist 30x pentazocine antagonism 20x pentazocine analgesia Sedation (KOR) Sweating, dizziness Psychotomimetic effects Anxiety, nausea, vomiting Mod-severe pain (acute) |
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Definition
Mixed Opoid Agon/Antag KOR agonist MOR antagonist Given w/naloxone IV to avoid analgesic & euphoric effects Sedation (KOR) Sweating, dizziness Psychotomimetic effects Anxiety, nausea, vomiting Combined w/tripelennamine ("T's & blues") → heroin-like Moderate pain |
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Opoid Antagonists Competitive opioid antagonist (MOR) Fast onset T-REX is bigger than an OX, and a T-REX is more orally active! Precipitates opioid W/D Opioid overdose |
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Definition
Opoid Antagonist Competitive opioid antagonist (MOR)3-5x naloxone potency Long acting Orally active (moreso) Opioid addiction (highly motivated) |
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Definition
Misc. Opoids Weak MOR agonist Inhibits NE & 5-HT reuptake in CNS (MAR-I) stops pain trns spinal cord 1/10 codeine MOR affinity 6000x less morphine MOR affinity Less potential for abuse & respiratory depression Dual mechanism of action Dental pain Acute Musculoskeletal pain Cancer pain |
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Local Anesthetic (Ester) Block V-G Na+ channels in high frequency pain fibers (spend lots of time "open") ~ Weak bases (pKa=8-9) 1) uncharged into axoplasm 2) ionized & trapped inside 3) binds open Na+ channel ~ Quickly metabolized by PChE SHORT ACTING (metabolized by plasma ChE) Given w/EPI Aunt Ester had allergies …but she was a peach! (PChE) Infiltration Nerve block Spinal anesthesia |
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Definition
Local Anesthetic (Ester) Block V-G Na+ channels in high frequency pain fibers (spend lots of time "open") ~ Weak bases (pKa=8-9) 1) uncharged into axoplasm 2) ionized & trapped inside 3) binds open Na+ channel ~ Quickly metabolized by PChE SHORT ACTING (metabolized by plasma ChE) Given w/EPI Aunt Ester had allergies …but she was a peach! (PChE) Infiltration Nerve block Spinal anesthesia |
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Local Anesthetic (Ester) More lipophilic than Pro/Coke: Rapider onset, potenter LONG ACTING MOST COMMONLY USED DRUG FOR SPINAL ANESTHESIA Topical LA |
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Definition
Local Anesthetic (Ester) Block V-G Na+ channels in high frequency pain fibers (spend lots of time "open") ~ Weak bases (pKa=8-9) 1) uncharged into axoplasm 2) ionized & trapped inside 3) binds open Na+ channel ~ Quickly metabolized by PChE Poorly water soluble So poorly water soluble that systemic toxicity potential is zero. DUSTING POWDER/OINTMENT (burns/ulcerations) |
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Definition
Local Anesthetic (Amide) Block V-G Na+ channels in high frequency pain fibers (spend lots of time "open") ~ Weak bases (pKa=8-9) 1) uncharged into axoplasm 2) ionized & trapped inside 3) binds open Na+ channel Metab in Liver P450; Pts w/ Liver dx will see tox More lipophilic than Pro/Coke: Rapider onset, potenter INTERMEDIATE ACTING Drowsiness Used in ester-allergic individuals LA Cardiac arrhythmias |
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Definition
Local Anesthetic (Amide) Block V-G Na+ channels in high frequency pain fibers (spend lots of time "open") ~ Weak bases (pKa=8-9) 1) uncharged into axoplasm 2) ionized & trapped inside 3) binds open Na+ channel Metab in Liver P450; Pts w/ Liver dx will see tox More lipophilic than Pro/Coke: Rapider onset, potenter INTERMEDIATE ACTING Drowsiness Used in ester-allergic individuals LA Cardiac arrhythmias |
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Definition
Local Anesthetic (Amide) Block V-G Na+ channels in high frequency pain fibers (spend lots of time "open") ~ Weak bases (pKa=8-9) 1) uncharged into axoplasm 2) ionized & trapped inside 3) binds open Na+ channel Met. in Liver P450; Pts w/ Liver dx will see tox More lipophilic than Pro/Coke Rapider onset, potenter INTERMEDIATE ACTING LAXITY IN NEONATES; OB LA |
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Definition
Local Anesthetic (Amide) Block V-G Na+ channels in high frequency pain fibers (spend lots of time "open") ~ Weak bases (pKa=8-9) 1) uncharged into axoplasm 2) ionized & trapped inside 3) binds open Na+ channel Met. in Liver P450; Pts w/ Liver dx will see tox More lipophilic than Mep/Lido: LONG ACTING Highly plasma protein bound CARDIOTOXIC Particularly long acting (some nerve blocks last 24+ hrs!) Analgesia + abdominal muscle control Epidural anesthesia ;(OB) Nerve blocks |
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Local Anesthetic (Amide) Block V-G Na+ channels in high frequency pain fibers (spend lots of time "open") ~ Weak bases (pKa=8-9) 1) uncharged into axoplasm 2) ionized & trapped inside 3) binds open Na+ channel Met. in Liver P450; Pts w/ Liver dx will see tox More lipophilic than Mep/Lido: LONG ACTING Highly plasma protein bound Cardiotoxic Particularly long acting (some nerve blocks last 24+ hrs!) Analgesia + abdominal muscle control Epidural anesthesia (OB) Nerve blocks |
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a1 a2 B1 B2 Agonist Vasoconstrictor All LA except Cocaine produce vasodilation → systemic absorption. LA formulated w/ Epi to ↓ system absorp. Localizes LA at desired site and lowers tox by allowing time for body to metabolize. |
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General Inhaled Anesthetic Nonspecific interactions w/ lipid bilayer Block K+ channels → hyperpolarization Activate or facilitate GABA Slow induction (↑ blood:gas) Most potent (↓MAC) HEPATOTOXICITY (free radicals) SENSITIZES MYOCARDIUM to NE/EPI ↑cerebral blood flow Halo = Heart |
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General Inhaled Anesthetic Nonspecific interactions w/ lipid bilayer Block K+ channels → hyperpolarization Activate or facilitate GABA Fluranes fluoride floppy muscles Intermediate induction Intermediate potency Fluranes (fluoride) can be nephrotoxic ↓minute volume Muscle relaxation |
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General Inhaled Anesthetic Nonspecific interactions w/ lipid bilayer Block K+ channels → hyperpolarization Activate or facilitate GABA Fluranes fluoride floppy muscles Intermediate induction Intermediate potency Fluranes (fluoride) can be nephrotoxic ↓minute volume Muscle relaxation |
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General Inhaled Anesthetic Nonspecific interactions w/ lipid bilayer Block K+ channels → hyperpolarization Activate or facilitate GABA Fast Induction (↓ blood:gas) Low Potentcy (↑MAC) Fluranes fluoride floppy muscles Fluranes (fluoride) can be nephrotoxic (sevo less) ↓minute volume Muscle relaxation |
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General Inhaled Anesthetic Nonspecific interactions w/ lipid bilayer Block K+ channels → hyperpolarization Activate or facilitate GABA Fast Induction (↓ blood:gas) Low Potentcy (↑MAC) Fluranes fluoride floppy muscles Fluranes (fluoride) can be nephrotoxic (sevo less) ↓minute volume Muscle relaxation |
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General Inhaled Anesthetic Nonspecific interactions w/ lipid bilayer Block K+ channels → hyperpolarization Activate or facilitate GABA Fast induction (↓ blood:gas) Least potent (↑MAC) NO potency |
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General IV Anesthetics Barbiturate Ultra short acting Rapid onset, short anesthesia Diffuses out of brain May produce "hangover" Myocardial/Respiratory depression ↓cerebral/renal blood flow, ↓GFR NOT Analgesic Thio huxtable is ultra short |
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General IV Anesthetic Benzodiazepines Slower onset Long acting Prolonged post-op. recovery ANTEROGRADE AMNESIA NOT Analgesic |
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General IV Anesthetic High potency opioid Can be reversed w/naloxone Respiratory depression Analgesic Only anesthetic @ ↑ doses |
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General IV Anesthetic Rapid onset Rapid recovery Anti-emetic Respiratory depression Hypotension Most popular IV anesthetic Be proper, don't puke |
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General IV Anesthetic Rapid onset Rapid recovery Nausea & vomiting Pain (Minimal CV/repspiratory Depression) Not analgesic He tummy ache |
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General IV Anesthetic Blocks NMDA receptors CV stimulation: ↑HR, ↑BP, ↑CO ↑cerebral blood flow, ↑ICP Disorientation, illusions, vivid dreams Analgesic Amnesia Catatonia Ketamine = catatonic |
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First Generation H1 Receptor Antagonist Block H1 receptor → ↓ histamine ax Allergies Motion sickness Sedation Antiparkinsonian effects Anti-cholinergic effects Anti-serotonergic effects α receptor blocking Local anesthetic effects Rapidly absorbed orally Metabolized by CYP3A4 Ineffective in bronchial asthma (mediated by more than just ol' histamine) Seasonal allergic rhinitis Urticaria |
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First Generation H1 Receptor Antagonist Block H1 receptor → ↓ histamine ax Allergies Motion sickness Sedation Antiparkinsonian effects Anti-cholinergic effects Anti-serotonergic effects α receptor blocking Local anesthetic effects Strong sedation! OTOTOXICITY (newborns or ABX) Allergies Motion sickness Sedation (Benedryl) |
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First Generation H1 Receptor Antagonist Block H1 receptor → ↓ histamine ax Allergies Motion sickness Sedation Antiparkinsonian effects Anti-cholinergic effects Anti-serotonergic effects α receptor blocking Local anesthetic effects STRONG SEDATION! OTOtoxicity (newborns or ABX) Allergies Motion sickness Sedation |
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First Generation H1 Receptor Antagonist Block H1 receptor → ↓ histamine ax Allergies Motion sickness Sedation Antiparkinsonian effects Anti-cholinergic effects Anti-serotonergic effects α receptor blocking Local anesthetic effects Drug interax: CARDIOTOXIC w/ conazoles or macrolides Metabolized to fexofenadine (not cardiotoxic), if CYP3A4 inhibited, terfenadine accumulates Allergies |
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Second Generation H1 Receptor Antagonist Active Metabolite of Loratadine Long acting No significant side effects Block H1 receptor → ↓ histamine ax Allergies Little to NO sedation (Claritin) |
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Second Generation H1 Receptor Antagonist Metabolized to Desloratadine Long acting No significant side effects Block H1 receptor → ↓ histamine ax Allergies Little to NO sedation (Claritin) |
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Second Generation H1 Receptor Antagonist Block H1 receptor → ↓ histamine ax Little to NO Sedation Lower risk of arrhythmia Allergies (Allegra) |
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Degranulation Inhibitor Inhibit immunologically triggered mast cell degranulation Most Effective Ineffective after asthma attack has started Bronchial asthma (prophylaxis) |
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Degranulation Inhibitor Inhibit immunologically triggered mast cell degranulation Most Effective Ineffective after asthma attack has started Bronchial asthma (prophylaxis) |
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Antacid Weak base neutralizes secreted HCL Problems: Short duration of action, compliance, prevention of recurrence Relieve pain; Promote Healing |
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H2 Receptor Antagonist Competitive inhibitor of histamine (H2)- stimulated gastric HCl secretion Inhibits P450 system Drug interax: ↑chlordiazepoxide, EtOH, propranolol, theophylline, warfarin Diarrhea, muscle pain Headache, dizziness GYNECOMASTIA, impotence
Gastric/duodenal ulcers ZE syndrome GERD (Tagamet) |
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H2 Receptor Antagonist Competitive inhibitor of histamine (H2)- stimulated gastric HCl secretion 4-10x more effective than cimetidine DOES NOT interfere with P450 Less side effects than cimetidine No antiandrogenic effects Gastric/duodenal ulcers ZE syndrome GERD
(Zantac) |
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H2 Receptor Antagonist Competitive inhibitor of histamine (H2)- stimulated gastric HCl secretion Not metabolized by P450 DON'T USE IN RENAL DISEASE Gastric/duodenal ulcers ZE syndrome GERD
(Pepcid) |
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H2 Receptor Antagonist Competitive inhibitor of histamine (H2)- stimulated gastric HCl secretion DON'T USE with salicylates Gastric/duodenal ulcers ZE syndrome GERD (Axid) |
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Proton Pump Inhibitor Active form irreversibly binds & inhibits proton pump in parietal cells Absorbed in alkaline SI pH Use >2 months not advisable Diarrhea, nausea Dizziness, headache Heals duodenal ulcers more rapidly than H2 blockers Gastric/duodenal ulcers ZE syndrome GERD (Prilosec) |
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Mucosal Protectant Aluminum salt of sucrose sulfate → binds plasma proteins in crater → protective barrier Short acting Drug interax: blocks tetracycline & PO4 absorption Constipation Nausea Additionally: inhibits pepsin & bile aciton Also: ↑ prostaglandin release Duodenal ulcer |
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Misoprostol Prostaglandin E1 analog → ↓ H+ ( ↓cAMP) ↑mucus & ↑bicarbonate secretion Nausea, diarrhea ABORTION IN PREGGOS Gastric/duodenal ulcers NSAID-induced damage |
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Definition
Inflammatory Bowel Disease Bacteria split azo bond → 5-ASA (& sulfapyridine) → ↓ inflammation 75% reaches colon 5-ASA = active metabolite Sulfapyridine = SEs Nausea, vomiting Headache Allergy Can cause ↓ folate absorption; Ulcerative colitis (85%) Colonic Crohn's Dz |
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Inflammatory Bowel Disease Infliximab Monoclonal antibody against TNF-α → ↓ inflammatory action Single IV infusion → remission Nausea Serum sickness Infections, autoimmunity, cancer; Crohn's disease |
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Definition
Guanine nucleoside analog Viral thymidine kinase produces analog → binds viral DNA polymerase & inactivates Valacyclovir −(rapidly)→ acyclovir Nausea, vomiting, diarrhea Headache, renal dysfx Resistance: altered/deficient viral thymidine kinase or viral DNA polymerase HSV VZV |
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Definition
Guanine nucleoside analog Viral thymidine kinase produces analog → binds viral DNA polymerase & inactivates MYELOSUPRESSION, neutropenia vision disturbances, carcinogenic CNS effects More toxic than acyclovir CMVertables are fos cars, cid so you ganci the road fomi CMV (retinitis) |
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Definition
Inorganic pyrophosphate analog Reversibly inhibits viral DNA & RNA polymerases Nausea, fever, headaches, hypocalcemia, hypomagnesemia, nephrotoxicity, anemia, GENITAL ULCER More toxic than gancyclovir CMV (retinitis) HSV (acyclovir resist.) |
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Viral Respiratory Infections Inhibits neuraminidase → ↓ release of virus → ↑ viral aggregates & ↓ viral spread Orally inhaled Used once taily to prevent flu Nasal/throat discomfort, headache, bronchospasm (asthmatics) Influenza A & B If taken within ~30 hrs of SX onset → ↓ duration & respiratory complications |
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Pyrimidine analog Cornea inflammation Tri flurting w/Kera's tits & HSV HSV (Keratoconjunctivitis) (Epithelial keratitis) |
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Definition
Antisense oligonucleotide Iritis, vitritis, ↑ intraocular pressure Vision changes Don't give to patients who have taken cidofovir in past month For herpes, tri giving acyclovir, doc (or dox)! CMV (retinitis) (in HIV patients unresp) |
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Viral Hepatitis Infection IFNα & IFNβ bind cellular receptors → activate JAK- STAT → ↑ 2,5-oligoadenylate synthetase & kinase → ↓ protein syn IM or SC injection Flu-like symptoms, BONE MARROW SUPRESSION, fatigue, infections, anorexia, diarrhea, depr, anxiety HPV Hepatits B & C Kaposi's sarcoma, MS |
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Definition
Viral Respiratory Infections Inhibits neuraminidase → ↓ release of virus → ↑ viral aggregates & ↓ viral spread Orally inhaled Used once taily to prevent flu Nausea, vomiting, headache If taken within ~30 hrs of SX onset → ↓ duration & respiratory complications Influenza A & B |
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Definition
Viral Hepatitis Infection Synthetic guanosine nucleoside analog Alters nucleotide pool → ↓ viral mRNA syn Conjunctiva irritation, wheezing, rash Anemia, BONE MARROW SUPRESSION TERATOGENIC Ribavirin blocks RNA of virin Hepatitis C RSV , Influenza, HIV Parainflu, Paramyxo |
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Definition
Nucleoside Reverse Transcriptase Inhibitor (AZT) Converted via human thymidine kinase → AZT-TP → incorporated into viral DNA → terminates chain elongation ↑ toxicity w: probenecid, tylenol, lorazepam, indomethacin, cimetidine Anemia, LEUKOPENIA, headaches, lactic acidosis, hepatic steatosis, lipoatropy, central fat, ↑lipids Protects fetuses from infection Resistance: mutated RT w/↓ affinity for AZT-TP Zitty Zal went nuclear & did stab a baby lamb he tends. HIV |
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Definition
Nucleoside Reverse Transcriptase Inhibitor Inhibits viral reverse transcriptase → terminates DNA chain elongation Given w/AZT or Lamivudine or protease inhibitor Hypersensitivity, fever, GI, malaise, rash Zitty Zal went nuclear & did stab a baby lamb he tends. HIV |
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Nucleoside Reverse Transcriptase Inhibitor (ddl) Inhibits viral reverse transcriptase → terminates DNA chain elongation Orally in buffered tablets ↑ toxicity w: stavudine PANCREATITIS (pot fatal), PAINFUL peripheral neuropathy Resistance: mutated RT Zitty Zal went nuclear & did stab a baby lamb he tends. HIV (AZT resistant) |
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Definition
Nucleoside Reverse Transcriptase Inhibitor (3-TC) Inhibits viral reverse transcriptase → terminates DNA chain elongation PANCREATITIS (pediatric patients) Resistance to AZT develops more slowly if you add lamivudine Zitty Zal went nuclear & did stab a baby lamb he tends. HIV Hepatitis B |
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Definition
Nucleoside Reverse Transcriptase Inhibitor (ddC) Inhibits viral reverse transcriptase → terminates DNA chain elongation Given w/AZT or alone (if can't tolerate AZT) Stomatitis, peripheral neuropathy, rash Resistance: mutated RT Zitty Zal went nuclear & did stab a baby lamb he tends. HIV |
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Nucleoside Reverse Transcriptase Inhibitor (d4T) Inhibits viral reverse transcriptase → terminates DNA chain elongation Peripheral neuropathy LACTIC ACIDOSIS (pot fatal), hepatic steatosis, lipoatropy, central fat, ↑lipids Zitty Zal went nuclear & did stab a baby lamb he tends. HIV |
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Definition
Non-Nucleoside RT Inhibitor Binds next to RT activation site → change conformation → inhibit RT activity Given w/AZT & lamivudine Dizziness, headache, insomnia, rash Nightmares, hallucinations ↓ [phenobarb, phenytoin, carbmzpne, methadone, rifabutin] Rifampin → ↓ efav Never ever tell a nun a lie. HIV |
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Definition
Non-Nucleoside RT Inhibitor Binds next to RT activation site → change conformation → inhibit RT activity Given w/didanosine & stavudine Rash, fever, nausea, HEPATOTOXICITY (pot fatal) ↓ [rifampin, ketoconazole, ethinyl estradiol (BC)] SJW → ↓ nevir Never ever tell a nun a lie. HIV |
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Definition
Nucleoside Reverse Transcriptase Inhibitor Inhibits viral reverse transcriptase → terminates DNA chain elongation Do not give w/didanosine, lamivudine, abacavir Flatulence Renal toxicity Zitty Zal went nuclear & did stab a baby lamb he tends. HIV Hepatitis B |
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Definition
Protease Inhibitor Interferes w/proteolysis of gag-pol viral protein precursor → nonfunctional virions Diarrhea, nausea, fatigue, headache, hyperlipidemia, hyperglycemia, altered body fat Administered together: Ritonavir inhibits CYP3A4 → ↑ Lopinavir Nel is a LIAR. She is a professional tease and will inhibit or slow your fost progress HIV |
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Definition
Protease Inhibitor Interferes w/proteolysis of gag-pol viral protein precursor → nonfunctional virions SJW lowers concentration Diarrhea, nausea, fatigue, headache, hyperlipidemia, hyperglycemia, altered body fat Administered together: Ritonavir inhibits CYP3A4 → ↑ Lopinavir Nel is a LIAR. She is a professional tease and will inhibit or slow your fost progress HIV |
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Definition
Protease Inhibitor Interferes w/proteolysis of gag-pol viral protein precursor → nonfunctional virions SJW lowers concentration Diarrhea, nausea, vomiting, lipodystrophy, hyperglycemia Nel is a LIAR. She is a professional tease and will inhibit or slow your fost progress HIV |
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Definition
Protease Inhibitor Interferes w/proteolysis of gag-pol viral protein precursor → nonfunctional virions Diarrhea, nausea, vomiting, lipodystrophy, hyperglycemia Nel is a LIAR. She is a professional tease and will inhibit or slow your fost progress HIV |
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Definition
Protease Inhibitor Interferes w/proteolysis of gag-pol viral protein precursor → nonfunctional virions Diarrhea, nausea, vomiting, lipodystrophy hyperglycemia Nel is a LIAR. She is a professional tease and will inhibit or slow your fost progress HIV |
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Definition
Protease Inhibitor Interferes w/proteolysis of gag-pol viral protein precursor → nonfunctional virions SJW lowers concentration Diarrhea, nausea, vomiting, lipodystrophy, hyperglycemia Nel is a LIAR. She is a professional tease and will inhibit or slow your fost progress HIV |
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Definition
Protease Inhibitor Interferes w/proteolysis of gag-pol viral protein precursor → nonfunctional virions Inhibits CYP34A (Rx toxicity) Rifampin induces CYP3A4 Diarrhea, nausea, vomiting, lipodystrophy hyperglycemia Although HIV cross-resistance occurs, most likely to still be Amprenavir susceptible Nel is a LIAR. She is a professional tease and will inhibit or slow your fost progress HIV |
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Fusion Inhibitor Binds viral envelope glycoprotein to prevent conformational change when binding host cell membrane Pain, erythema, nodules, cysts (at injection site) Injected twice a day Binds enfulope HIV |
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Definition
Partial & Generalized Tonic-Clonic Seizures Block Na+ channel (prolong inactive state) Enhance GABA activity Induces liver microsomes Produces active 10,11 epoxide metabolite Acute: stupor, coma, convulsions, irritability Chronic: diplopia, ataxia, GI, sedation, fluid reten Major: APLASTIC ANEMIA, AGRANULOCYTOSIS Accelerates metabolism: phenytoin, primadone, ethosuximide, valproate, BC Congener (oxcarb) less toxic, less potent Partial seizures Gen. tonic-clonic seizures Trigeminal neuralgia Bipolar Disorder (not absence) |
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Benzodiazepine Long Acting Bind α1γ2 on GABA-A receptor → ↑ GABA binding freq. → ↑ Cl- conductance → neuron hyperpolarizaiton → ↓ neuron activity ~ Anxiolytic-sedative Hypnotic Anesthesia Anticonvulsant Muscle relaxation Alcohol withdrawal Sedation, tolerance, withdrawal Absence seizures Myoclonic seizures Infantile spasms |
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Benzodiazepine Bind α1γ2 on GABA-A receptor → ↑ GABA binding freq. → ↑ Cl- conductance → neuron hyperpolarizaiton → ↓ neuron activity ~ Anxiolytic-sedative Hypnotic Anesthesia Anticonvulsant Muscle relaxation Alcohol withdrawal STATUS EPILEPTICUS |
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Generalized Seizures Block T-type Ca2+ channel (↓ threshold) ↓ rhythmic thalamic activity Good absorption orally (stomach irritation) 75% liver metabolized GI, lethargy, fatigue, rash, BONE MARROW SUPRESSION Phensuximide & methsuximide not as good Absence seizures |
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Partial & Generalized Tonic-Clonic Seizures (in conjunction) NMDA antagonist Enhance GABA APLASTIC ANEMIA SEVERE HEPATITIS Partial seizures (poorly controlled) |
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Definition
Partial & Generalized Tonic-Clonic Seizures (in conjunction) GABA analog (↑ release of GABA) Renal excretion of unchanged drug Somnolence, dizziness, ataxia NO LIVER INVOLVEMENT ALL RENAL! Partial seizures Neuropathic pain Alcoholism |
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Definition
Partial & Generalized Tonic-Clonic Seizures (in conjunction) Block Na+ channel (prolong inactive state) May block Ca2+ channel Headache, diplopia, rash, nausea, dizziness, ataxia Life-threatening rash in 1-2% of patients Partial seizures Generalized seizures Absence seizures Myoclonic seizures |
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Partial & Generalized Tonic-Clonic Seizures Block Na+ channel (prolong inactive state) Prolongs GABA-A channel activity Block AMPA receptor Sedation, ataxia, respiratory depression, rash, nystagmus, porphyria, tolerance, withdrawal Congeners (mephobarbital & primidone) Partial seizures Gen. tonic-clonic seizures (not absence) |
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Partial & Generalized Tonic-Clonic Seizures Block Na+ channel (prolong inactive state) Admin: oral / IV (status epilepticus) 90% protein bound First order (low) → Zero order (high) Displaced by other protein-bound Rx Acute: nystagmus, diplopia, ataxia, GI, conf. Chronic: GINGIVAL HYPERPLASIA, hirsutism, osteomalacia, rash, AGRANULOCYTOSIS, megaloblastic anemia High IV: arrhythmia, CNS depression Congeners (mepheny/etho-toin) more toxic Phenacemide very toxic (refractory partial) Fosphenytoin = more soluble (injection) ↓ BC effectiveness & birth defects Partial seizures Gen. tonic-clonic seizures Status epilepticus (not absence) |
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Definition
Partial & Generalized Tonic-Clonic Seizures (in conjunction) Block Na+ channel (prolong inactive state) Enhance GABA activity Somnolence, dizziness, fatigue, cognitive slowing, weight loss USED FOR WEIGHT LOSS Partial seizures Gen. tonic-clonic seizures |
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Generalized Seizures Block Na+ channel (prolong inactive state) ↑ GABA (↑ GAD) ↓GABA-T activity Block T-type Ca2+ channel Well absorbed 90% protein bound Liver metabolized Nausea, vomiting, GI, hepatotoxicity, TERATOGEN, Sedation (w/phenobarbital) Preferred over ethosuximide if absence + generalized tonic-clonic seizures Absence seizures Myoclonic seizures Atonic seizures Partial seizures |
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Alternative Medicines Proposed immune stimulant Flu-like, hepatitis, asthma, rash, nausea, urticaria, anaphyaxis May contain organocholine pesticides URI or "Colds" |
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Definition
Alternative Medicines Contains ephedrine (sympathomimetic) Stroke, arrhythmias, hypertension 16x risk of hemorrhagic stroke (w/phenylpropanolamine) Weight loss Energy |
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Alternative Medicines Effective anti-nausea Inhibit thromboxane synthase Contraind: anti-coagulants (may inhibit platelet aggregation) As effective as antihistaminics in nausea Motion sickness Morning sickness |
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Alternative Medicines Inhibit 5α-reductase → ↓DHT Block α1 receptors Headache, GI, hypertension, ↓libido Trad. > Saw palmetto > placebo BPH |
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Definition
Alternative Medicines Enhances GABA activty Dry flaking skin, puffy face, red eyes, weakness, oral tingling, GI, SOB, EKG abnormalities Can cause serious cirrhosis & LIVER FAILURE! Anxiety Insomnia |
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Definition
Alternative Medicines Stimulate cartilage cells → GAG & proteoglycans Gi discomfort, nausea, photosensitivity, systolic HTN, proteinuria Osteoarthritis Wound healing |
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Dopamien Agonists Dopamine agonist (→ DA) L-DOPA −(AADC)→ DA ↑ DA in striatum C-DOPA: ↓ peripheral AADC L-DOPA → DA (AADC) DA (MAO-B, DBH, COMT) Periph: N/V, OH, arrhythmia CNS: On-off, wear-off, dyskin Psych: hallucin, delusion, sleep Peak-Dose: grimace/writhe Neuroleptic malignant syndrome ↑ SNS tone peripherally N/V/anorexia via CTZ stimulation Tubero-infund DA → ↓ prolactin Parkinson's Disease |
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Potent Non-Ergot Dopamine Agonists Dopamine agonist Used in "frozen" cases (Reverses "off" state) Advanced PD on ↑ dose L-DOPA Parkinson's Disease |
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Ergot-Der. Dopamine Agonists B: D2 agonist / D1 antagonist P: D2 agonist / D1 agonist B: short half-life P: better w/L-DOPA (D1 & lipophilic) Nausea/vomiting, somnolence, dry mouth, edema, insomnia, postural/OH, recalled due to heart valve regurg Peak-dose, on-off, depr., anxiety, hallucinations Bromo only works in pts resp. to L-Dopa; causes CARDIAC ARRHYTHMIA Pergolide allows ↓ L-DOPA dose Parkinson's Disease |
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Definition
MOA-Inhibitor Inhibits MAO-B → ↑ striatal DA Used when L-DOPA effects are starting to decline or in early mono-therapy Insomnia; Dyskinesia; Nausea; Headache; Cardiac Arrhythmia; Hypertension; Contra-indicated w/ SSRI's and Tricyclics Parkinson's Disease |
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Definition
Non-Ergot Dopamine Agonist D2 agonist Nausea, somnolence, dry mouth, edema, insomnia, postural/OH Peak-dose, on-off, depr., anxiety, hallucinations Reduce on-off in late PD, most effective in early-mono therapy; Pramipexole can delay L-DOPA by 2 years Parkinson's Disease |
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Definition
Anticholinergic Treats influenza A & hepatits C May: alter DA release/reuptake Block NMDA receptors Block mACh receptors Restlessness, agitation, insomnia, confusion, hallucinations, OH No effect on tremor Parkinson's Disease Bradykinesia & Rigidity or L-Dopa induced motor side-effects, no effect on Tremor |
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COMT-Inhibitors Inhibits COMT → ↑ DA in cleft Produce 2x ↑ in bioavailability & half-life of L-DOPA Tolcapone: FATAL HEPATOTOXICITY & CNS activity Competes w/L-DOPA → BBB Attenuates the "wearing off" time Prim in pts who have received long L-Dopa trx with motor side-effects Parkinson's Disease Adjunctive therapy in late stage after 5/7 yrs of L-Dopa; used to amelorate "Freezing" and peak-dose dyskinesia |
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Definition
Anticoagulant HMW binds Antithrombin III and catalytically accelerates (~1000-fold) interaction w/ thrombin forming inactive 1:1 ratio (also inhibits XIIa, IXa, VIIa, and Xa), LMW heparin fractions inhibit activated factor X but have much less effect on coagulation in general. Highly electronegative acidic mucopolysaccharides 1/3 of molecules in Heparin have catalytic effect Anti-compliment Anti-histiminic (slight) Inhibit BOTH in vivo/in vitro clotting Metabolism follows ZERO-ORDER KINETICS Does NOT cross placenta/breast milk Contraindicated in bleeding, hemophilia, GI ulcerative lesions, severe hypertension, brain, spinal cord, eye surgery, viceral carcinoma, threatened abortion. osteoporosis + fractures (long term) Special caution renal or hepatic dysfunction. Synergistic with oral anti-coag Protamine sulfate neutralizes in vivo STOPS CLOTTING |
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Definition
Coumarin Anti-coagulant Blocks gamma-carboxylation of glutamate residues in prothrombin (II) and coag factors VII, IX, and X; proteins C and S Blocks an epoxide reductase essential in regenerating active form of Vit. K → prevents hepatic synthesis of clotting factors 8-12 hr onset; acts ONLY IN VIVO Second-most-likely drug after Insulin to send pts to the emergency room Very narrow therapeutic window Variations in CYP2C9 (liv metab) and VKORC1 (Vit K) genes account for variability in pts Warfarin metabolism Extensively bound to plamsa albumin and crosses placenta/breast milk readily → hemorrhagic event in fetus TERATOGENIC - messes with bone formation hydroxylated in liver, elim feces/urine Synergistic with Pyrazolones (augment antithrombosis, peptic ulcer disease) Barbs and Rifampin induce liver CYP enzymes, lower warfarin effect Aspirin, hepatic disease, and hyperthyroidism augment warfarin effect Vit. K, Chlorthalidone/Spironolactone, and hypothyroidism reduce effects of Warfarin |
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*IRREVERSIBLY binding to COX *Prevents activation of thromboxane A2 (a potent stimulator of platelet aggregation) *Inhibits platelet aggregation and platelet content release *Prolongs bleeding time *Prevention of MIs (low dose , 325mg daily) *Excessive bleeding , GI bleeding , PUD |
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Definition
Antiplatelet *IRREVERSIBLE inhibition of ADP-mediated platelet aggregation *NO effect on prostaglandin metabolism *Prevention of ischemic events *Fewer SE than ticlopidine *~1% LEUKOPENIA *Thrombotic thrombocytopenia purpura |
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Definition
Thrombolytic *Human enzyme produced by the kidney that converts plasminogen to plasmin *Plasmin then functions to break up the clot by dissolving fibrin *IV for mutiple pulmonary emboli , central deep venous thrombosis *Management of acute MIs *t-PA (Altepase) is also utilized for patients with acute stroke symptoms (shown to decrease disability 1-year post CVA). *Excessive bleeding , cerebral hemorrhage |
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Definition
Thrombolytic *Unmodified tissue plasminogen activator (t-PA) *Converts fibrin-bound plasminogen to plasmin (CLOT SELECTIVE) *IV for mutiple pulmonary emboli , central deep venous thrombosis *Management of acute MIs *t-PA (Altepase) is also utilized for patients with acute stroke symptoms (shown to decrease disability 1-year post CVA). *Excessive bleeding , cerebral hemorrhage |
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Fibrinolytic Inhibitor *Inhibits fibrinolysis via inhibition of plasminogen activation *Treatment of acute bleeding episodes in hemophilia and other bleeding disorders. *Prophylaxis for rebleeding from intracranial aneurysms *Intravascular thrombosis , Hypotension , Myopathy , Abdominal discomfort , Diarrhea *CI: DIC , Genitourinary bleeding of the upper tract (kidneys , ureters) => potential for excessive clotting |
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Confers Biological Activity upon Prothrombin (II), VII, IX, and X *Supplementation of naturally endogenous substance responsible for the carboxylation of coagulation factors VII , IX , X , II (prothrombin) *Treatment of vitamin K-deficient states seen in newborns , elderly , ICU pts *Given to ALL newborns prophylacticly *Reversal of warfarin overdose *Rapid IV infusion can cause dyspnea , chest and back pain , or death |
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IRON *Parenteral *Used only for the treatment and prevention of iron deficiency anemia *Increased iron requirements-- infants , rapid growth in children, pregnancy and lactation , elderly populations , chronic kidney disease (may lose or form rbc's 2ary to hemodialysis and erythropoietin treatment) *In men and postmenopausual women presume Fe deficiency is from blood loss until proven otherwise *Inadequate iron absorbtion-- Inadequated GI absorbtion *Inadequate GI Fe absorbtion and advanced kidney disease = parenteral iron *Dextran hypersensitivity: urticaria , fever , phlebitis , arthralgieas , bronchospasm. Anaphylaxis and death (both rarely). *Should perform test for Iron Dextran toxicity *CI: Pts w Fe overload , idiopathic hemchromatosis , thalassemia major , transfusion hemosiderosis. |
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IRON *Ferrous more efficiently absorbed *Used only for the treatment and prevention of iron deficiency anemia *Increased iron requirements-- infants , rapid growth in children, pregnancy and lactation , elderly populations , chronic kidney disease (may lose or form rbc's 2ary to hemodialysis and erythropoietin treatment) *In men and postmenopausual women presume Fe deficiency is from blood loss until proven otherwise *Inadequate iron absorbtion-- Inadequated GI absorbtion *Normal GI absorbtion = oral preparations prefered *SE are directly related to bioavailability *Acute oral iron toxicity in children : necrotizing gastroenteritis w/ vomitting , bloody diarrhea , lethargy and dyspnea. Followed by severe metabolic acidosis , coma , and death *Treatment of toxicity: whole bowel irrigation (eliminate unabsorbed Fe in GI Tract) ; Iron-Chelating agent , Deferoxamine sulfate (Desferal) to sequester and excrete already absorbed Fe ; Supportive therapy *As little as 400 mg Fe can cause death in children *200-400mg Fe given daily to correct deficency rapidly (3-6 months) *50-100mg Fe can be incorporated into hemoglobin daily for Fe deficient individual. *CI: Pts w Fe overload , idiopathic hemchromatosis , thalassemia major (cooley's anemia , 2ary to numerous transfusions) , transfusion hemosiderosis. |
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Cyanocobalamin/Hydroxocobalamin |
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Definition
Vitamin B12 *Vitaminer of the B12 family (somehow related to B12??) *Pernicous anemia and malabsorbtion *Vit B12 Def (seru cobalamin levels < 200 pM/L . Macroovalocytosis and reduced hemogobin levels occur in late stages of disease) *IM or SC |
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*Vit B12 Def (serum cobalamin levels < 200 pM/L . Macroovalocytosis and reduced hemogobin levels occur in late stages of disease) *Normoblasts w/in 6-8 hours , Psychiatric problems relieved w/in 24 hours , Neurological damage requires more slow recovery because of need for myelin regeneration , failure of reversal after 12 - 18 months indicate that neurological damage is irreversible *Injection (parenteral???) *Anaphylaxis possible *Overly rapid correction of anemia can produce circulatory overload. |
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*Deficiency usually results from increased requirements : liver disease , GI abnormalities , alcoholism , drugs *Rapid response , bone marrow pathology back to normal in hours , brisk reticulocytosis in 2-5 days *Alcoholics may have impaired hepatic storage and/or increased folic acid release (even w adequate dietary intake) *Increased Folic Acid requirement during pregnancy , deficiency can cause neural tube defects , spina bifida , anencephaly *Parenteral : critically ill , GI disorders (limiting folate absortion) *Oral : Folic acid supplements , Pregnant , Liver disease , Alcoholism , Hemodialysis *DI: methotrexate (inhibit dihydrofolate reductase) , anti-convulsants , some anti-malarial drugs *Long term use of following drugs may increase need for folate : some oral contraceptives , steroids , analgesics , sulfsalazine *Large doses of folate can mask pernicous anemia and lead to irreversibe neurologic damage *Present in many common foods (fruits , vegetables , meats) , Used to fortify enriched grains in America *Increased requirements or inadequate intake may lead to folate deficiency: pregnancy and lactation , children w poor diets , critical illness , severe infections , hemolytic anemia , hemodialysis , chronic diseases (eg. renal failure ,inflamation , neoplasia) |
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Iron Chelating Agent Treats Iron Overdose |
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*Erythropoietin stimulates erythroid proliferation and differentiation by interacting with specific erythropoietic receptors , member of JAK/STAT cytokine receptor superfamily , on RBC progenitor cells *For anemia of chronic renal failure since kidneys are unable to produce enough hormone. *Can actually prevent the need for blood transfusion *ruHuEPO , Epoetin Alpha not cleared by dialysis *In selected patients , primary bone marrow disorders , aplastic anemia , secondary anemias (AIDS , chronic malignancies , chronic inflamation) *Accelerate erythropoiesis after phlebotomies to treat hemochromatosis (or maybe some other blood loss) *SE: Rapid increase in hemoglobin-- hypertension , thrombotic complications *PTS w bone marrow disorders , nutritional and secondary anemia have high levels of endogenous erythropoietin. Positive response to this treatment is less likely *Failure to respond to this teatment can often be easily resolved by adding iron or folic acid if either of these are deficient *Normally produced in the peritubilar interstitial cells of the kidney in response to tissue hypoxia *Increased erythropoietin reverses anemia provided there is normal bone function , sufficient iron , Vitamin B12 , Folic Acid *Normal levels : 20 IU/L , Moderately severe anemia : 100-500 IU/L , Severe anemia : 1000's of IU/L |
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Granulocyte Colony Stimulating Factor (GCS-F) (filgrastim) |
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Definition
*Synthesized w recombinant DNA technology *Stimulate proliferation and differentation of their respective cell lines *React with specific receptors of various myeloid progenitor cells . Recpetors are associated wuith cytoplasmic tyrosine kinases in JAK/STAT pathway *Neutrophil lineage *Use in autologous / allogenic (same species) hematopoietic stem cell transplantation. *Chemotherapy-induced neutropenia *Chronic neutropenia *IV *Bone pain *Better tolerated than GM-CSF |
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Granulocyte Macrophage Colony Stimulating Factor (GM-CSF) (Sargramostim) |
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Definition
*Synthesized w recombinant DNA technology *Stimulate proliferation and differentation of their respective cell lines *React with specific receptors of various myeloid progenitor cells . Recpetors are associated wuith cytoplasmic tyrosine kinases in JAK/STAT pathway *Multi-potential hematopoietic growth factor *Use in autologous / allogenic (same species) hematopoietic stem cell transplantation. *Chemotherapy-induced neutropenia in acute myeloid leukemia *IV *Fever , arthralgias , malaise |
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Megakaryocye Growth Factor: Interleukin 11 (Oprelvekin) |
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Definition
*Acts through a specific cell surface cytokine receptor , stimulated the growth of multiple lymphoid and myeloid cells. *Increase number of peripheral platelets and neutrophils. *Thrombocytopenia *Prevent thrombocytopenia in patients receiving chemotherapy for nonmyeloid cancer. *SE: Fatigue , HA , CV effects , anemia , dyspnea (fluid retention) *Reversible upon drug discontinuation. |
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