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401 - Toxicology, Drug Abuse, Pharmacology > 10: Household Poisons > Flashcards

10: Household Poisons Flashcards

1
Q

APAP has what effects

A

analgesics, antipyretic, weak aniinflam

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2
Q

APAP effect on COX

A

nonselective inhibitor
COX 2> 1

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3
Q

APAP blocks production of prostaglandins by

A

reducing heme on peroxidases

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4
Q

APAP has evidence of analgesic effects by affecting

A

serotonergic, opioid, cannabinoid, and TRV 1 receptors

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5
Q

APAP is absorbed within ___, peaks at ___

A

abs 2hrs, peaks 4hrs

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6
Q

APAP metabolism includes

A

glucuronidation, sulfation, CYP2A1 oxidation

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7
Q

most APAP metabolism is _________, the rest is

A

most = hepatic conjugation
rest = oxidized by CYP2A1 to NAPQI

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8
Q

MOA of APAP toxicity

A

amount of NAPQI overwhelms glutathione and accumulates in hepatocytes = cell death by mitochondrial effects

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9
Q

describe stage 1 APAP toxicity

A

incubation (quiescent- might be missed)
Asymptomatic or nonspecific sx (N/V, malaise, diaphoresis)

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10
Q

describe stage 2 APAP toxicity

A

latent period
resolution/ improvement of stage 1 sx
Onset of hepatic injury (5% of patients who overdose), AST/ALT lab value abnormalities, elevated AST then ALT (1000IU/L)
Nephrotoxicity may occur as toxic metabolites are produced

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11
Q

describe stage 2 APAP toxicity

A

latent period
resolution/ improvement of stage 1 sx
Onset of hepatic injury (5% of patients who overdose), AST/ALT lab value abnormalities, elevated AST then ALT (1000IU/L)
Nephrotoxicity may occur as toxic metabolites are produced

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12
Q

describe stage 3 APAP toxicity

A

peak liver toxicity
Systemic sx reappear
Fulminant hepatic failure (encephalopathy, jaundice, coagulopathy, hypoglycemia)
Abnormalities in transaminase peak (3-4d), PT, INR, glucose, lactic acidosis
Highest risk of death

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13
Q

describe stage 4 APAP toxicity

A

resolution
Survivors make a complete recovery and/or death

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14
Q

what is the antidote for APAP toxicity

A

NAC

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15
Q

NAC must be administered within_____ of APAP OD

A

4-8hrs

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16
Q

NAC is given as a ____IV infusion or ____ oral schedule

A

24h IV
72hr oral

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17
Q

which is preferred? NAC iV or PO

A

IV preferred- faster, safer, rare ADRs
PO = strong smell, makes pt vomit, logically hard if unconscious

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18
Q

what is NAC?

A

a precursor for glutathione synthesis

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19
Q

NAC detoxifies NAPQI by (4)

A

Free radical scavenger
Increasing oxygen delivery/ microvascular tone
Increasing mitochondrial ATP production
Antioxidant effects

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20
Q

4 clinical tests for APAP OD

A

serum APAP
aminotransferases (ALT/AST)
INR
serum creatinine

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21
Q

traditionally, NAC IV is a ________ regimen

A

3 bag- AHS has new 2 step regimen

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22
Q

what is the Rumack- Matthew Nomogram used for

A

to see if NAC needs to be initiated in APAP toxicity

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23
Q

how is the slop of the Rumack-Matthew nomogram determined
1. clinical data
2. APAP half life
3. kinetics of hepatic failure
4. all of the above

A
  1. based on clinical data
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24
Q

what are some factors that impact interpretation of the RM nomogram

A

incorrect hx/ when they took it, multiple/ chronic ingestions, CYP inducers (ethanol), chronic alcohol use, extended release

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25
Q

what is the goal of the RM nomogram

A

to determine the risk of hepatotoxicity and need to initiate NAC tx

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26
Q

NAC reactions may be

A

anaphylactic or anaphylactoid

27
Q

anaphylactic reactions are ADR type ___, type ____ hypersensitivity reactions

A

type B, type 1 hypersens

28
Q

how do anaphylactic reactions happen

A

Cross linking allergen to specific IgE molecules (bound to mast cells and basophils)
Reexposure = degranulation release of histamine

29
Q

what is an anaphylactoid reaction? what happens after the drug triggers the reaction?

A

a nonIgE medated response that does not require previous exposure
Drug triggers sudden and massive mast cell and basophil degranulation (release of histamine) in absence of imunoglobulins

30
Q

which of the following may be rechallenged
1. anaphylactic reactions
2. anaphylactoid reactions

A

2

31
Q

treatment for anaphylactoid reactions

A

antihistamines, beta 2 agonists, corticosteroids

32
Q

COX1 is

A

constitutive

33
Q

COX2 is

A

inducible

34
Q

ASA causes ____ inhibition of COX ____

A

irreversible inhibition of COX 1 and 2

35
Q

NSAIDs cause _____ inhibition of COX ___

A

reversible inhibition of COX 2

36
Q

prostacycline synthase produces _________ which are ___ inflammatory

A

prostacyclines
antiinflammatory

37
Q

thromboxane synthase produces _________ and ________ which are ___________

A

prostaglandins and thromboxanes
proinflammatory

38
Q

T or F: All NSAIDs have similar presentations in OD situations

A

T

39
Q

which of the following is false about NSAIDs
1. asymptomatic or nonspecific sx appear within 0-4hrs
2. there is no specific test to check for NSAID toxicity
3. treatment may include GI decontamination with charcoal
4. causes irreversible inhibition of COX 2 more than COX 1

A

4 - reversible

40
Q

sx of mod-severe NSAID toxicity include

A

coma, seizures, CNS depression, metabolic acidosis, hypotension, hypothermia, rhabdomyolysis, lethargy, unresponsiveness

41
Q

what labs should be ordered in NSAID OD

A

no spec test, but rec to check APAP levels

42
Q

Ts for NSAID OD includes

A

supportive care, antacids for GI upset, GI decont w/ charcoal for children that had >400mg/kg

43
Q

aspirin has 3 properties

A

analgesic, antiinglam, antipyretic

44
Q

aspirin is a _____ inhibitor of _____

A

irreversible inhibitor of COX 1 + 2

45
Q

platelets do not express COX

A

2

46
Q

ASA daily dose inhibits COX __ for the duration of the platelet’s lifespan (8-12d)

A

2

47
Q

ADME of aspirin

A

rapid absorption, highly protein bound, half life 15min-2-3h, hepatic metabolism, absorbed and excreted unchanged in urine

48
Q

in an aspirin OD, what happens to ADME?

A

decreased protein binding (runs out) = more into tissues = more SEs

49
Q

characteristics of patients more likely to have acute aspirin toxicity- list 3

A

younger, intentional, easily recognized (absent coingestion), no other diseases, suicidal ideation typical, marked elevations in serum concs, mortality uncommon when recognized and properly tx

50
Q

acute aspirin toxicity may see development of ___________ by impacting ___________

A

anion gap metabolic acidosis
impacting mitochondria

51
Q

worsening acute aspirin toxicity may result in

A

severe CNS toxicity

52
Q

characteristics of patients more likely to have acute aspirin toxicity- list 3

A

older, therapeutic misadventures/ iatrogenic, frequently undiagnosed, many underlying diseases (esp chronic pain), suicidal ideation not typical, intermediate elevation in serum concs, mortality more common due to delayed recognition

53
Q

mortality is more common with _____ aspirin toxicity due to __________

A

chronic
delayed recognition

54
Q

intermediate elevations in serum concs are more likely in ____ aspirin toxicity

A

chronic

55
Q

anion gap =

A

unmeasured cation – unmeasured anion = [Na+] – ([Cl- ] +[HCO3 - ]

56
Q

2 acronyms for poisons/ diseases that can increase anion gap

A

MUDPILES and GOLDMARK

57
Q

what does MUDPILES stand for

A

methanol/ metformin, uremia, DKA, paraldehyde, iron/ isoniazid/ ischemia, lactic acidosis (CO, CN), ethylene glycol, salicylates

58
Q

what does GOLDMARK stand for

A

glycols, 5-oxoproline, L-lactate, D-lactate, methanol, aspirin, renal failure, ketoacidosis

59
Q

metabolic acidosis may be due to ___________ or ___________

A

acid accumulation of HCO3 loss

60
Q

treatment for aspirin OD includes

A

supportive care- no true antidote
may use GI decontamination with activated charcoal
Cornerstone = shift salicylate out of brain and tissues in serum (alkalinization of serum and urine = ion trapping by adding serum IV sodium bicarbonate)
Hemodialysis: aims to remove salicylate from tissues but may not correct severe organ toxicity
Glucose supplementation (pts altered mental state)

61
Q

what is the cornerstone of treating aspirin OD

A

adding IV sodium bicarb to shift salicylate out of tissues into serum and urine by ion trapping it

62
Q

____ is produced by activated platelets and is prothrombotic

A

TxA2

63
Q

TxA2 increases platelet ______ (3)

A

aggregation, vasoconstriction, inflammation

64
Q

why do COXIBs result in an overall net inflammatory state

A

COXIBs only inhibit COX 2, but do not inhibit platelet COX 1 derived TxA2 = TxA2 effects are exaggerated while endothelial cell’s COX1/2 PGI2 process is inhibited = overall prothrombotic and hypertensive result

401 - Toxicology, Drug Abuse, Pharmacology (32 decks)

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