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43 Cards in this Set
- Front
- Back
A pt presents w/ hypotension & bradycardia from a Ca2+ channel blocker overdose, what do you need to do to tx & prevent reflex tachycardia? |
Ca2+ Chloride infusion if CV contractility depressed--> glucagon (used for BOTH Ca2+ or Beta blocker ODs) |
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Erosives & caustic agents can cause rapid skin toxicity. The higher the _________, the faster the absorption. |
higher lipid solubility |
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In addition to antidotes, what else can be used to help remove toxic substances? (toxicology txs) *after tx, hold pt for 48 hrs to monitor for rebound toxicity! (goes into adipose & may redistribute rapidly) |
activated charcoal- slows absorption & spread of toxin, can cause N/V & constipation body surface irrigation- prevents further absorption Ionized diuresis- enhances excretion of weak acids & bases using sodium bicarb, ammonium Cl, Vit C, cranberry juice, etc urinary alkalinization- enhance elimination & excretion |
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What drugs undergo biotransformation & become more toxic (usually become active metabolites)? |
organophosphates (irreversible Ach inhibitor--> dumbells) acetaminophen benzos morphine (aspirin, iron, & acetaminophen are the mc household substances that cause toxicity) |
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What drugs cause photosensitivity? |
(antimicrobials- QSTs) Quinolone Sulfonamide Tetracycline |
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Q: Pt is recieving a drug w/ a clearance of 100 mL/min. If a target blood level is 1 mcg/mL & pt is going to be injected every 4 hrs, what dose should be injected (maintenance dose)? |
A: 24,000 mcg Maintenance dose = Clearance x concentration at steady state x time (minutes)** = 100 mL/min x 1 mcg/mL x 240 min (4 hrs) = 24,000 mcg (steady state conc = target blood level!) |
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________cause toxic neoplasm (cancer) |
nitrogen mustard |
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TCA's, cocaine, & amphetamine ODs can all cause __________ |
seizures |
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Furosamide diuretics & barium salt can cause toxic_________ |
HYPOkalemia |
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Spironolactone & ACE inhibitors can cause toxic________ |
HYPERkalemia |
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_______ OD causes toxic hepatic injury d/t accumulation of NAPQI (N-acetyl-para-benzoquinoneimine) in the liver What causes NAPQI to accumulate? |
acetaminophen glutathione depletion *acetaminophen undergoes glutathione conjugation & gets excreted, w/o glutathione, it undergoes CYT P450 metabolism & toxic NAPQI is produced *most likely to occur in acetaminophen OD d/t suicide attempt OR in alcoholic pts (alcohol induces glutathione pathway & causes incr NAPQI production) |
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Large stores of glutathione lead to delayed presentation of acetaminophen OD. How do pts present? |
No sx until initially 12-24 hrs--> N/V, bloody diarrhea, & GI shock 3-5 days--> RUQ tenderness, jaundice, hypoglycemia (liver damage) *CONFIRM w/ LFT & APAP testing!! |
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Acetaminophen OD must be tx ASAP!! __________ is given to replace glutathione, BUT there is no tx to reverse the hepatic damage that has already occurred, ONLY prevent worsening. *If recent OD, may give activated charcoal to prevent further drug absorption What else can be given for symptomatic relief? |
N-acetylcysteine (NAC)- glutathione precursor, helps replenish glutathione to prevent further NAPQI accumulation & damage Ondanestron (anti-emetic) can be given to relieve GI sxs |
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_________ OD causes rapid & toxic CNS depression--> diminished breathing, low body temp & skin reddening Tx: bicarbonate, why? |
barbiturates bicarbonate reduces proximal tubular reabsorption--> increases renal excretion |
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NSAID's & ethylene glycol OD's can cause ______ |
renal dysfunction |
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How do you reverse anuria from renal dysfunction? |
mannitol (osmotic diuresis) |
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Pt presents w/ CNS & respiratory depression, peripheral neuropathy, nephrotoxicity*, opthalmalogic & GI sx after consuming unknown liquid. Blood tests reveal anion gap & profound metabolic acidosis. Urine reveals oxalate crystals. What is the liquid? What antidote should be given to prevent fatal renal failure? |
Ethylene glycole (anti-freeze) antidote: fomepizole (competitive ADH inhibitor) if unavailable, infuse ethanol up to 100 mg/dL |
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Ethylene glycole forms a toxic metabolite ____________ that accumulates in the kidney & leads to serious nephrotoxicity--> renal failure How should pts be tx if severe nephrotoxicity occurs or if pts become unresponsive? |
calcium oxalate hemodialysis for severe poisoning & unresponsive pts |
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_______ presents similarly to Ethylene Glycol OD, w/ peripheral neuropathy, ocular damage (--> permanent blindness*), & GI sxs. Metabolic acidosis & tissue injury occurs occurs d/t formation of toxic formic acid. How is metabolic acidosis tx? (for any cause*) |
Methanol (found in paint thinner & moonshine) Tx: infusion of sodium bicarbonate--> keep pH at 7.2 or above |
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How do you tx peripheral neuropathy caused by ethylene glycol or methanol OD? |
ethylene glycol: pyridoxine + thiamine methanol: leucovorin |
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Delayed toxicity usually arises d.t redistribution (esp in fat). Delayed toxicity of __________ is very severe & presents w/ pulmonary fibrosis & smurf skin |
Amiodarone |
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Q: Pt on digoxin therapy suddenly develops toxicity w/ a plasma level of 4 ng/mL. Renal function is normal & half-life of digoxin is 1.5 days. How long should you withhold digoxin in order to reach a safer therapeutic dose (1 ng/mL is preferred, toxic about 2)? |
A: 4.5 days (3 half lives--> 4--> 2--> 1) |
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Pt who works on a farm presents w/ Diarrhea, Urination, Myosis, Bradycardia, Bronchoconstriction, Excitation, Lacrimation, Salivation, & Sweating (DUMBBELSS). Pt begins to experience muscular paralysis. What toxic compound has he been exposed to? What is the MOA? |
Organophosphate (insecticides, etc) MOA: irreversible acetylcholinesterase inhibitor--> High lipophilicity, forms covalent irreversible phosphate bond w/ AchE--> Ach overstimulation--> desensitized nicotinic receptors at NMJ--> neuromuscular paralysis |
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Organophosphate poisoning must be tx ASAP to prevent respiratory failure! _________ is given as an antidote, but MUST be given quickly to work. Why? |
Pralidoxime (2-PAM) *breaks covalent bonds btwn organophosphate & AchE, but bonds get stronger w/ time "aging process" & 2-PAM no longer works |
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__________ can be given to reverse the systemic effects of Ach. *There is no tx to reverse the neuromuscular paralysis (will reverse on own w/i 24 hrs). Why? |
Atropine -competitive inhibition of Ach muscarinic receptors *Can't reverse desensitization of nicotinic receptors, need to wait for new receptors to form |
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_________ toxicity caused hypertension, tachycardia, fever, dry mouth, urinary retention, hallucinations, confusion "dry as bone, red as a beet, hot as a pistol, blind as a bat, & mad as a hatter!" how do you tx? |
Anticholinergics: Antihistamines (1st gen- diphenhydramine) TCA's (meperidine) Jimson weed, mushrooms tx: Physostigmine (AchE inhibitor, that crosses BBB*) |
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Pt presents w/ tachycardia, hypertension, increased muscle tone, horizontal & frontal nystagmus & is action very agitated & aggressive. What drug toxicity? Tx? |
PCP tx: Benzos (sedation), antipsychotics (haloperidol), beta blockers, activated charcoal (if recent) |
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______ toxicity; abdominal cramping, seizures, anemia, neuropathy, fatigue--> encephalopathy, GI shock & bleeding *inhibits heme biosynthesis Tx? |
Lead toxicity (metal contaminants, house dust, occupational exposure) Tx: antidote= dimecaprol w/ EDTA (chelation therapy) Benzo for seizures mannitol & corticosteroids if Incr ICP |
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_______toxicitiy: Garlic breath & rice water stools* severe abdominal pain, NV--> GI hemorrhage--> Hypotension, shock--> convulsions, delirium, polyneuropathy *disrupts oxidative phosphorylation Tx? |
Arsenic toxicity (insecticides) Tx: antidote = Dimecaprol (ASAP!) Gastric lavage O2 & electrolyte support |
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_________ toxicity: severe N/V*, diarrhea, hematemesis--> GI strictures, bowel perforation--> CNS depression--> Coma *disrupts oxidative phosphorylation--> mitochondrial damage (free radicals)--> shift to anerobic metabolism |
Iron toxicity |
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How is iron toxicity tx? *Tx ASAP to prevent renal failure |
antidote = deferoxamine mesylate (chelates iron, makes it wate soluble) Bowel irrigation |
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__________ toxicity: tissue ischemia & hypoxia--> Decreased Cardiac Output--> tachycardia, hypertension--> MI, seizures, metabolic acidosis--> coma *displaces O2 & forms carboxyhemoglobin (COHgb) Tx: |
Carbon monoxide (CO) (car generators, left on) Tx: Hyperbaric O2 chamber Benzo for seizures |
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Rapid infusion of ________ may cause cyanide poisoning. *cyanide inhibits formation of ATP--> CV, CNS, & respiratory depression How is cyanide poisoning tx? |
nitroprusside tx: amyl nitrite pearls (if unconscious) or sodium nitrite (cyanide binds methemoglobulin & forms cyanomethemoglobulin)--> then give sodium thiosulfate (breaks bond creating less toxic thiocyanate which is excreted & methemoglobulin)--> followed by methylene blue (if d/t nitroprussimide*)(generates oxyhemoglobin) |
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__________toxicity---> Sustained rapid eye movement, shivering, diarrhea, fever, seizures = ___________ Tx? |
Antidepressant toxcicity * occurs w combos w/ St. John Wort & Meperidine, buproprion = Serotonin syndrome Tx: Benzos for seizures bowel irrigation if sustained release buproprion |
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______ toxicity----> anticholinergic effects reflex tachycardia (alpha antagonist) postural hypotension Tx? |
TCA toxicity tx: IV saline w/ vasopressors for hypotension |
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________ toxicity---> tachycardia, hypertension--> HA, N/V, abdominal cramps, delirium--> rhabdomyolsis, MI UA: benzoylecgonine Tx? |
Cocaine toxicity *benzoylecgonine is metabolite, remains in urine up to 5 days after use Tx: nitroglycerin or phentolomine (for severe HTN, NEVER give beta-blocker) Benzos (for agitation, anxiety, seizures) Endoscopic removal (if d/t body packing) O2, dextrose, thiamine |
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Combining alcohol w/ cocaine, leads to ___________ production--> CV shock--> death***** |
cocaethylene *VERY toxic metabolite |
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Corrosive acids & alkalies (bleach, sulfuric acid, ammonia, etc) are EXTREMELY toxic--> tissue burns--> rapid perforation--> hemorrhage (skin, GI, any body part in contact) Tx? |
Tx: Endotracheal intubation (for respiratory distress) Gastric lavage (stomach irrigation, NOT w/ emesis) Dilution ASAP (milk or water) Corticosteroids + Abx* |
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Toxic__________, can lead to stinging, burning--> blistering, swelling (histamine release)--> N/V, weakness, muscle fasciculations--> hypotensive shock & CV collapse Tx: |
Toxic Crotaline snake bite (venom) (rattlesnakes, copperheads, cottonmouths) tx: Crotaline polyvalent Fab (antivenom) + Prednisone (Corticosteroids) IV fluids (hypotension) Anti-histamines, Antiinflammatories *instruct pt to remain as still as possible to prevent further venom spread, further degranulation of mast cells & histamine spread |
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What type of antagonist interacts DIRECTLY w/ an agonist & NOT at all w the receptor? |
Physiological antagonist (Ex: vasodilators & vasoconstrictors, don't share receptors) |
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A pt taking warfarin following a recent heart valve surgery develops a UTI & is given Trimethoprim-sulfamethoxazole (bactrum). In addition to checking prothrombin time, what else needs to be done? |
Reduce warfarin dose* warfarin is highly bound--> sulfonamides (bactrum) displaces warfarin--> toxicity (need to reduce) |
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A multiple myeloma pt is taking vincristine, cisplatin, bleomycin & methotrexate. They develop declining renal fxn. What drug is responsible? |
Cisplatin ^alkylating agent, prevents DNA cross-linking, causes nephrotoxicity |
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________ would be responsible if the multiple myeloma pt presented w/ peripheral nephrotoxicity |
Vincristine ^mitotic spindle inhibitor, strips axon sheaths--> peripheral neuropathy |