Toxicology and Posioning Flashcards

1
Q

4 ways to prevent absorption

A

emesis, gastric lavage, chemical absorption, osmotic cathartics

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2
Q

2 drugs for inducing emesis

A

Ipecac and apomorphine

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3
Q

when does ipecac make you vom,can you repeat, how does it work, what concern do you have with other overdose problems

A

throwup in 15-30 minutes, can repeat in 20 minutes, works by local irritation and CMS stimulation of CTZ, MUST be given before activated charcoal

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4
Q

apomorphine how does it work and major concern

A

dopamine agonist that produces emesis by stimulating CTZ , causes respiratory depression and is toxic in kids

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5
Q

5 contraindications of emetic agent

A

comatose, ingestion of corrosive poisons, ingestion of CNS stimulant, ingestion of petroleum distillate, or pgenancy category C

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6
Q

Pros/Cons of gastric lavage and when do you need to do it

A

PRO: most rapid and complete method to empty stomach but CON alvage and emesis only empties 30% of oral poisons, do it within 60 minutes

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7
Q

Activated charcoal - how does it work, what does it bind, what can it do, how do you administer it and what challenges do you face

A

binds drug in the gut to limit absorption and can bind through back diffusion of drug with ion trapping in stomach to reduce elimination half life…. also binds ipecac…. give 10:1 ratio of charcoal:toxin and do it every 4 hours.. hard to administer and kids don’t do well with it

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8
Q

purpose of osmotic cathartics, 4 indicated uses

A

decrease time of toxin in the GI tract like a laxative, do it if the drug was ingested >60 minutes ago, if the toxin is enteric coated tablet or if the toxin is a hydrocarbon

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9
Q

4 drugs that do osmotic cathartics

A

sorbitol 70%, magnesium citrate or sulfate, sodium sulfate, or polyethylene glycol

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10
Q

what do you give with sorbitol 70%

A

charcoal

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11
Q

whats recommended for osmotic cathartics

A

sorbitol 70%

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12
Q

magnisum citrate or sulfate should be avoided when

A

in renal disease or with nephrotoxic agents

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13
Q

sodium sulfate gets avoided when

A

CHF or HTN

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14
Q

when do you use PEG for osmotic cathartics

A

poisonings with sustained release drugs, metal ions, or drug packets

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15
Q

differences between hemodialysis vs hemoperfusion

A

hemodialysis is good for a drug with a small Vd and hemoperfusion is good for drugs with a high MW with a poor water solubility

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16
Q

2 means of enhancing renal excretion

A
  1. forced diuresis (protects kidney) 2. block reabsorption from kidney by altering urinary pH
17
Q

2 ways that chelation works

A

enhances elimination and inactivates toxin

18
Q

in 70-80% of the time with acetametophin metabolism, what phase metabolizes it and what do adults and kids do differently

A

phase 2 conjugation adults- glucuronic acid, kids- sulfate

19
Q

5-10% of the time with acetametophin (or in overdoses), how does it get metabolized

A

phase 1 cytochrome p450 oxidation with CYP2E1–> NAPQI or Ac* that then bind proteins or get detoxed by GSH-Transferase and are excreted as mercaptourate

20
Q

2 predisposing factors to hepatic injury from acetametophin injury

A

increase in CYP2E1 and decrease in hepatic glutathionine (both are also symptoms of alcohol overdose)

21
Q

4 stages of acetametophin toxicity

A

1 (0-24 hours), 2 (24-48 hours) 3(72-96 hours) 4 (7-8 days)

22
Q

stage 1 of acetametophin toxicity symptoms

A

not reflective of severity, expect nausea vomitting and abdominal pain

23
Q

stage 2 of acetametophin toxicity is important why and what do you see

A

see liver damage, increase in plasma aminotransferases and increase in prothrombin time

24
Q

stage 3 of acetametophin toxicity is important why

A

peak liver toxicity

25
Q

stage 4 of acetometophin toxicity - what happens

A

if you had gotten good treatment in quickly, recovery. 10% have severe liver damage and 10-20% end up dying

26
Q

2 treatments of acetametophin toxicity and timeframe

A
  1. activated charcoal and gastric lavage in 4 hours and 2. 12-36 hours use N-acetylcysteine
27
Q

loading dose, maintenance dose, and method for using Nacetylcysteine

A

LD= 140 mg/kg+ 70 mg/kg an hour for 17 doses, give via IV

28
Q

methanol and ethylene glycol pathway of metabolism and rate limiting enzyme

A

first organic acids (nontoxic) and then gets metabolized to formic acid and oxalic acid, alcohol dehydrogenase is the rate limiting enzyme

29
Q

formic acid is toxic to what and oxalic acid is toxic to what

A

FA= retinas–> blindness, OA–> acute renal failure

30
Q

what does fomepizole do

A

inhibits alcohol dehydrogenase so good inhibitor of methanol and ethylene glycol overdose

31
Q

symptoms of methanol and ethylene glycol toxicity

A

severe metabolic acidosis in 4-12 hours, methanol–> visual disturbances “snowstorm” and ethylene glycol–> deposits calcium oxalate crystals that cause acute renal failure

32
Q

2 ways to inhibit alcohol dehydrogenase

A

1) infuse EtOH to keep blood alcohol at 0.1% as a competitive inhibitor to saturate the enzyme or 2) fomepizole (better because it doesn’t cause CNS depression)

33
Q

besides alcohol dehydrogenase inhbition, how else can you treat methanol and ethylene glycol toxicity

A

hemodialysis to correct for metabolic acidosis