Toxicology Flashcards

1
Q

siallorhea, mydriasis, diaphoresis, hyperactive bowel sounds, hyperreflexia, increased muscle tone

A

Serotonin Syndrome

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2
Q

dry muycosa, hot red dry skin, mydriasis, normal reflexes and tone

A

anticholinergic

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3
Q

Lead pipe rigidity, bradyreflexia, normal pupils, fever, diaphoresis, delirium after DA agonist

A

NMS

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4
Q

Rigor mortis type of rigidity, hyporeflexia, normal pupils and mucosa, mottled skin and diaphoresis, temp very high

A

Malignant Hyperthermia

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5
Q

inherited sarcomere disorder that is triggered by inhalational anasthesia or succ shortly after surgery

A

Malignant Hyperthermia

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6
Q

Drugs that can lead to serotonin syndrome

A

SSRI, MOA, analgesics, antiemetics, linezolid

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7
Q

treatment for severe serotonin syndrome

A

benzos, cyproheptadine

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8
Q

NMS treatment

A

bromocrintpine- increase CNS dopamine

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9
Q

dantrolene use? MOA? when to use?

A

reduces excitation- contraction uncoupling in muscles

- can be used to tx hyperpyrexia in SS, NMS, MH

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10
Q

normal metabolism of acetaminophen?

A

most is glucoronidation to a non toxic metabolite by the liver. A small amount is by the CYP450 system into NAPQI which is toxic

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11
Q

MOA of acetaminophen toxicity?

A

large doses depletes glutathione and overwhelms the glucoronidation pathway shifting to more NAPQI formation

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12
Q

MOA of NAC?

A

replenishes glutathione stores

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13
Q

what is the Rumack Mathew nomogram?

A

plots serum concentation vs time after ingestion to determine whether or not to treat

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14
Q

when should you not use the Rumack Matthew nomogram?

A

taking acetaminophen chronically, chronic alcohol abuse, chronic liver disease, time of overdose is not reliable

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15
Q

Malignant Hyperthermia presentation

A

it is due to hypermetabolism and releasing a large quantity of calcium from the SR after triggering agent like succ
- inc CO2 production, inc O2 consumption, combined resp and metabolic acidosis, heat production, sympathetic upregulation, hyperkalemia, can see seizures but rare

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16
Q

tx of MH?

A

cooling, stop offending agent, dantrolene

17
Q

cyanide toxicity most common cause?

A

smoke from a building fire

18
Q

MOA of cyanide poisoning?

A

inihibits mitochondrial oxydative phosphorylation and shift to anaerobic metabolism leading to lactic acidosis

19
Q

treatment of choice for cyanide poisoning?

A

hydroxycobalamin- converts HCN to B12

20
Q

TOC of methemoglobinemia?

A

methylene blue-converts the MHG to hgb

21
Q

toxic metabolite of methanol?

A

formic acid

22
Q

toxic metabolite of ethylene glycol?

A

oxalic acid, glycolic acid

23
Q

where do you find ethylene glycol?

A

antifreeze, cleaning products

24
Q

where do you find methanol?

A

anti freeze, moonshine

25
Q

which toxic alcohol leads to blindness?

A

methanol

26
Q

what happens to the osmolar gap and AGAP over time in toxic alcohol ingestion?

A

osmol gap decreases and AGAP increases, some recommend to just check anion gap serially because osmol gap is not reliable

27
Q

when to start fomepizole?

A

high index of suspiscion wiht an AGAP tht continues to rise without another explanation

28
Q

lactate gap in ethylene glycol ingestion, explain?

A

glycolate that is a toxic metabolite in EG breakdown mimics lactate. So if there is a high lactate on blood gas machine because it measures lactate differently than lab assays

29
Q

reasons to start fomepizole?

A

ingestion history and very high anion gap without other cause

30
Q

why does fomepizole dosing need to be increased over the time iots being given?

A

it induces its own metabolism

31
Q

should you give bicarbonate to patient with toxic alcohol ingestion?

A

yes if they are acidotic.
- normalizing the pH can keep the toxic metabolites in their ionized state and thus less able to penetrate tissues such as brain and eye

32
Q

signs and sx of lithium toxicity

A

GI symptoms, prolonged QT interval

- chronic toxicity can lead to nephrogenic DI or chronic neuro sx, grand mal seizures

33
Q

osmol gap

calculated osmolality

A

measured- calculated normal <10

- (2xNa)+(glc/18)+(BUN/2.8)+(ethanol/3.7)

34
Q

how is isopropyl alcohol intoxication different than methanol and ethylene glycol?

A
  • no acidosis
  • breaks down into acetone so you will see extremely high ketones in the urine
  • but will still see a osmol gap