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86 Cards in this Set
- Front
- Back
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APAP is anagesic/antipyretics its exact MOA is unknown
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YES
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APAP overdose is one of the most comon poisoning worldwide, death is unusual unless
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occurs with late presentation >24hrs
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The primary result of APAP overdose acute liver failure also could be
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renal insufficnecy
metabolic acidosis coma |
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APAP course of Toxicity is minimal symptoms early--as transaminases elveate, you have abd pain, N/V, they peak
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72-96 hrs have jaundice, coagulopathy INR >6, hypohlycemia, encephaloptahy
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When does hepatic function return in APAP overdose
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4-14 days in survivors or death
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The antidose for APAP, and why
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NAC--enchances GSH stoes-- and increases sulfation pathways
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How do you predict which pts who overdose on APAP will develop hepatoxicity
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Rumack-Matthew Nomogram
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Rumack Matthew Nomogram is based on, and what is a toxic level
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APAP concentration and hours since ingestion--->150 mcg/ml 4 hrs post ingestion
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The Rumack Matthew Nonogram DOES NOT apply if
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>1 ingestion
time of ingestion is unknown or <4hrs or >24 hrs |
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What is definiation of repeated supratherapeutic ingestion
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>4 grams of APAP >24hrs
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Repeat Supratherapteutic ingestion is often inadvertent--how to treat
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NAC if APAP >20mcg/ml, or Liver furction tests abnormal
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Alcoholics are NOT at an increased risk for hepatotoxcity
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NO
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What are various salicylate preparations, they are
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ASA
Methyl salicylate (oil wintergreen) Bismuth Subsalicutse Mesalamine, olsazaine, sulfasalzine) |
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Salicylate general metabolism, and in overdose situations
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95% liver, in overdose situations urinary excretion becomes importatn
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What is Salicylates mechanism of toxicity
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MIS U
uncouples oxidative phosphorlyation, stimulates respiratory center, inhibit cox, and alters capillary permeability |
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Clinical effect of Salcilate overdose
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ACCET HEN
ACID-BASE (both) Cerebral/Pulmonary edema CNS, Tinnitus, GI, Hematolgic, Endocrine, Neprhopaty |
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Acute overdose of ASA is often intentaional is better tolerated than chronic (Toxicity 80-100)
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YES
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Chornic ASA overdose is insidous onset, and severe toxicity at lower levels
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40mg/dl
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What is treatment of Salicylates
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Activated charcoal
Unrine alkalization with Bicarb Hemodialysis for severe cases |
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Urine alkalinization promotes increased elimination of
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Salicylate ion by "ion trapping" drug in urine--using bicarb
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Serum alkalinzaiton benefits
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prevent salicaltes into CNS
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CCB's block L-type voltage senstive ca channels, where BB block
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adrenegic recpetors
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What are primary effects of CCB toxicity
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hypotension, brady cardia,
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What are 2nd effects of CCB toxicity
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CNS depression, siezures, hyperglycemia
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BB toxicity is similar to CCB (hypotension,bradycardia, seziures), except has
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Bronchospasm, HYPOGLYCEMIA, and Hyperkalemia
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What is worst BB in overdose
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Proprnolol b/c it crosses BBB--leading to seziures
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What is inital mamagmetn of CCB and BB toxicity
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Fluid, and Atoprine for bradycardia
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What is first line therapy after fluids/atoprine for BB (ONLY)
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Glucagon
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Caclium is effective in both CCB and BB toxicity, what is perferred caclium
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CaCl perferred over Ca gluconate
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What is first line choice for treating CCB/BB with catecholamines
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Dopamine
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What is a new treatment in CCB/BB OD
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Insulin/Glucose
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Amrinone is PDE inhibitor rarely used for CC/BB OD but it an option
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YES
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Can you use intralipids 2nd for CCB or BB toxicity
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YES
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Digoxin has a large volume of distribution, narrow therapuetic index 1-2
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YES
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Digoxin follows 2 compartemtn model, when should you measure levels after ingestion
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6hrs
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What is MOA Diogxin
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Block Na+/K+ ATPase, cauing blocking of Na+ Ca+ exchanges increase intracellular Ca+ levels
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The increased amount of Ca+ in the cell (and sarcoplasmic reticumlum allow for
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more Ca+ available for contraction
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Digoxin also increases vagal tone--which
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Decreases SA/AV conduction
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Whta are toxic effects of Digoxin
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Vagal stimualtinon--bradycardia, PR prolongtion, nodal block
Increased intracellular Ca--increasing automaciity overall sinus/bradycarida/arrest, slowing of normal conduction |
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Acute toxicity of Digxoin is typicall intention, with N/V, HYPERKALEMIA, and really high DIG levels
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YES
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Chronic toxoicty occurs in elderly pts, renal function or other meds, signs
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N/V, low/normal K+, and minminally increase DIG levels
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What are other sources of Digoxin toxicity
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toad, Heart remedeny, Aphrodiiacs (love stone)
flowers |
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What reverse the toxic effects of ditlais, digitoxn, plany glycosides, bufotxin
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Digibind
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When are effects seen with Digibind, and complete
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seens 1 hrs after administration, and complete reversal 4-6hrs
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What is MOA of Digibind
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Purified Fab fragment from immunized sheeep, that binds and inactivtea cardiac glycosides
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What are digibind indications
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hemodyamic compromise, ventricular dyshrymias, serum K >5
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Ingestion of Digoxen indictated Digibind
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>4 grams in child
>10 grams in adults |
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What is empiric dose for Digibind for acute toxicity
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10-20 vials
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Dosing of Digibind is based on amt ingested, and steady-state levles
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amt ingest number of vial= amt ingest X.48
steady-state--serum level X IBW/100 |
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2-5 vials are needed in chronic toxicity, and is only based on serum levels=
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Serum level X IBW/100
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Digibind should be reconsituted in 4cc of water, by GENTLY ROLLOING, a bolus is given for unstable pts
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Stable pts receive IV
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Main concern of Digibind is allergic reactions to
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sheep protein
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Some pts are dpenedent on digoxin (HF or A-fib), withdrawl of the digoxin effect
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may worsen CHF or A-Fib
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What should you not give with Digoxin toxicity
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Ca_
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How do you treat Digoxin toxicity with NO DIGIBIND
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Phenytoin, Magnesium, Atropine or Magnesim
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Hypokalemia sensitizes heart to digoxin, keep K+ levels
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4.5-5 in chornicn toxicity
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There are only 35 antidoites available, most have no antidotes--how can you survive without antidote
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good supportive care
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What is an antidote
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remedy that stop or controls effects of a specific poison
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When is Naloxone indicated
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Opitate/opoid toicity WITH respiraotry depression
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What is Mechanism of Naloxone
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competitive antagoism of Mu receptros
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B/c Naloxone competive antagoinism of the Mu receptors what is an adverse effect
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withdrawl
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Naloxone has HIGH 1st pass effect so how is it given
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IV, IM, SQ, or SL
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What is use of Flumazenil,
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Benzodiazepine toxicity AND oversedation
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MOA of Flumazenil
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binds to BZD receptor on GABA--ihbiting CL- channel
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Adverse effects of Flumzenil
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withdrawl of BZD
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Contraindications of Flumzenil
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unknown coma, seizure HXx, long term BZD use
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Flumazenil does NOT consiisentl reverse BZD induced resp depression, and has a shorter half-life, which it icnreased risk for
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resedation
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What are indications of Physostigmine
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Reverse anticholingeric meds
diagonis of anticholinergic sydrom |
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Physosigmine is a theriary amine carbamate that MOA
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inbhit Achetlycholinesterase--which increases Ach in the synpase
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Cyanide kit is for Cyanide poisoning from strucutal fires, nitoprusside, pitted fruits arifical nail remover
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YES
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What are components of Cynadie Kit
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Amyl nitrite/sodium nitrite
Soium thiosulfate |
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WHat is other drug that reverses cyanide posioning
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Hydroxcolamin
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What is MOA Hydroxocobalamin,
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bind cyanide and fro Vitamin B12 precurocon
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What is the B12 precursor
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cyancobalamin--which is excreted in urine
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What are adverse effects of hydroxocobalamin
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skin disocolation, transient HTN, interferes with colorimetic assay
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What drug treats Insonizid toxicity
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Pyridoxine (B6)
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Pyridoxine increases GABA leading to improved symptoms
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YES
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What dosing Pyridoxine
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gm for gm repalce
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What is indiciation of Methylene Blue
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Methemoglobinemia >20% or if symtpoms
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What is indication for methnaol, etheleen glycol toxicity
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ADH INHIBITIORS
alcohol dehydronense inhibitors |
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What are alcohol dehydrongenase inhibitors
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Fomepizole adn Ethanol
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What is indication of Octreotide
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hypoglycemia due to overdose, sulfonlurea or quinine
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What is MOA of Octreotide
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inhibitts pancretatic insulin secretion
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Warfarins antidote is Vit K, and Heparin is Protamine Sulfate
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YES
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CroFab is used for rattlesnakes bites, MOA
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Fab fragment that bind venmon--same dose in adults/kids
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CroFab is NOT need for mild symtpoms
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NO
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