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PGY2 EM > Tox > Flashcards

Tox Flashcards

1
Q

Antitodes to Acetampinophen

A
  • NAC: 150mg/kg IV then 15mg/kg/hr x23 hours (or 140mg/kg po load)
  • Fomepizole: if cross product >10,000 - - give 15mg/kg (blocks cytochrome 2E1)
    Vit K
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2
Q

Viperidae

A

Copperhead, rattlesnakes, cotton mouths
- most often local tissue effects and coagulopathy
- crofab indicated with swelling crossing joints, coagulopathy, etc

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3
Q

Elapidae

A

coral and mamba snakes
- neurotoxic
- antivenom early
- red on yellow

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4
Q

source, results, and treatment of hydrofluoric acid exposure

A
  • ruse removers, cleaners, insecticides
  • hypocalcemia, hypomag, hyperK
  • local tissue necrosis
  • decon and calcium GLUCONATE (not chloride) near injury
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5
Q

Antitodes to Acetampinophen

A
  • NAC: 150mg/kg IV then 15mg/kg/hr x23 hours (or 140mg/kg po load)
  • Fomepizole: if cross product >10,000 - - give 15mg/kg (blocks cytochrome 2E1)
    Vit K
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6
Q

5 treatments for CCB and BB overdose

A
  • charcoal
  • atropine
  • Calcium (CCB)
  • glucagon
  • high dose insulin (ccb>bb)
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7
Q

high dose insulin

A
  • CCB>BB overdose
  • theoretically increases myocyte metabolism
  • 1 unit/kg reg bolus then 1 unit/kg/hr
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8
Q

what enzyme is ccb metabolized by

A

cyp3A4

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9
Q

difference between CCB and BB overdose

A

CCB: hyperglycemia
BB: in peds may cause hypoglycemia

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10
Q

which beta blockers cause EKG changesm (4)

A

Propranolol- Na channel blockade, QRS
Sotalol - K blockade, QT prolonged
Carvedilol and acebutalol- Na channel blockade

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11
Q

why is propranolol uniqe

A

Na channel blockade
lipophilic -> crosses blood brain barrier and can cause seizures

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12
Q

Anti-arrhythmic Drug class

A

I: Na channel blocker
II: beta blocer
III: K channel blockade - prolongs APD
IV: CCB

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13
Q

Bupropion overdose

A
  1. QRS and QT prolongation due to gap junction inhibition
  2. seizures
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14
Q

Palytoxin
- where, mechanism, exposure

A
  • produced by algae
  • binds Na/K ATPase pump and locks it open
  • dermal: irritation, pain, edema, erythema
    inhalation: parasthesia, dysguesia, HTN, respiratory depression and coma
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15
Q

becaquerel
sievert
gray

A
  • Becquerel: amount of radiation from decayed matter
  • Sievert: equivalent absorbed radiation dose adjusted by area of body exposed
  • Gray = absorbed energy (J)/mass of part receiving radiation (kg)
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16
Q

radiation injury labs

A
  • trend ALC - predicts mortality
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17
Q

type of radiation

A
  • Alpha (particles): 1-2 cm, does not penetrate skin; highly ionizing, very dangerous to DNA if ingested or injected
  • Beta (particles): penetrates a few layers of skin
  • gamma and xrays (photon): passes all layers of skin; gamma rays tx cancer
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18
Q

metabolic and laboratory changes with aspirin

A

EARLY respiratory alkalosis
metabolic acidosis- lactate and ketones
- hypokalemia
- hypoglycemia (very early hyperglycemia)
- falsely elevated chloride
- elevated INR

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19
Q

aspirin units (therapeutic, overdose)

A

mg/dcl
15-3o mg/dcl is therapeutic

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20
Q

early to late manifestations of aspirin toxicity

A

Early: GI/N/V and initius
progressing: tachypnea, fever
late: coagulopathy, cerebral edema and seizures

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21
Q

aspirin treatment (A-G and K)

A

A: alkilinization- BICARB: goal urine pH 8: a few amps bicarb and then 3 amps in 1L with 40 KCl
B: breathing is fast, avoid intubation
C: charcoal - bezoars possible
D: dialysis
E: electrolytes: K >4
F: frequent labs
G: hypglycemia
K: Vit K if INR >2

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22
Q

indications for HD 2/2 aspirin

A

level nearing 100
level nearing 40 and pregnant
fluid restrictions - kidney, heart
AMS or seizure
therapies failing

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23
Q

Two tox exposures that are bad news for pregnancy

A
  • aspirin: fetus more acidic environment
  • CO: like fetal hemoglobin
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24
Q

Sulfonylurea toxicity management

A
  • blocks K channels in pancreas -> insulin release regardless of BG
  • ends in “ide” - glipizide, glimeperide
  • one pill can kill peds

OCTREOTIDE 50-100mg SC

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25
Q

Cyclobenzarpine MOA and overdose

A
  • NE and serotonin reuptake inhibition, centrally
  • more sedating
  • long half life 18h-33h
  • ANTICHOLINERGIC effects
  • NA channel blockade
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26
Q

Anticholinergic toxidrome

A

mad, blind, red, hot, dry
benadryl

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27
Q

cholinergic toxicity

A

dumbells- diarrhea, urination, miosis, bradycardia, emesis, lacrimation, lethargy, salivation
pesticides

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28
Q

acute and chronic lithium OD

A

acute: N/V
chronic: CNS -> rigidity, tremor, ataxia, slurred speech

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29
Q

Lithium therapeutic range

A

0.5 mEq/L - 1.5 mEq/L

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30
Q

Lithium toxic range and risk factors

A

> 1.5 (dialyze at 4)
- volume depletion (causes renal retention - renally excreted)
- CHF, CKD, ACEi/ARB or other diuretics
- age >60

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31
Q

Lithium toxicity management

A
  • NACL (kidneys confuse Li and Na - giving NaCl helps prevent lithium retention
  • agressive fluids
  • discontinue ace/arb/diuretics
  • HD at Li > 4mEq/L
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32
Q

what class of drugs is not dialyzable

A

antipsychotics

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33
Q

antipsychotic pyramidal side effects and management

A
  • acute dystonia: benztropine, benadryl
  • Akasthesia: B-CALM
    B blocker, Clonazepam, Anticholinergic, cLonidine, Mirtazapine (5HT2A block)
  • Tardive dyskinesia: VMAT2 inhibitors
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34
Q

Clozapine, quetiapine (Seroquel), palperidone (invega) or aripiprazole?

granulocytopenia, sialorrhea, seizures (dose related), EKG changes

A

clozapine

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35
Q

Clozapine, quetiapine (Seroquel), palperidone (invega) or aripiprazole?

abuse causes euphoria with possible withdrawal, structurally simailar to TCA, bezoar formation

A

quetiapine

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36
Q

Clozapine, quetiapine (Seroquel), palperidone (invega) or aripiprazole?

metabolite of resperidone
prolonged tachycardia
required 24 hour obs

A

palperidone

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37
Q

Clozapine, quetiapine (Seroquel), palperidone (invega) or aripiprazole?

effects on dopamine, serotonin, H1 and a1 adrenergic receptor; odd presentation of biphasic light somnolence, dystonia, orthostatic hypotension, anticholinergic toxidrome; tx= supportive care; 10h obs in OD

A

aripiprazole

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38
Q

Diphenhydramine MOA

A

H1 blocker
- lipophilic: crosses BBB
At high doses - Na and K blockade -> QRS and QT prolongation

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39
Q

fatal dose of diphenhydramine

A

20-40mg/kg

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40
Q

diphenhydramine effects

A

antimuscarinic effects, it can produce blurred vision, dry mouth, urinary retention, tachycardia, nausea, and constipation. EKG changes can occur including widening of QRS from sodium channel blockade and tachycardia.

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41
Q

diphenhydramine treatment

A
  • bicarb for EKg changes
  • foley placement and temp management
  • benzos for seizures
  • physostigmine for delirium
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42
Q

physostigmine in benadryl OD

A
  • Reversible ACh-ase inhibitor that crosses BBB; onset 3-8 min, works for 30-90 min
  • Contraindications: bradydysrhythmias, AV block, TCA/Na blocker toxicity, seizures, asthma or bronchospasms
  • 2 g over 5 min IV
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43
Q

metformin toxicity

A

GI symptoms → lethargy → seizure and CV collapse → coma

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44
Q

metformin OD management

A
  • causes lactic acidosis via inhibition of gluconeogenesis and mitochondrial complex
    charcoal
    bicarb
    HD (decreased mortality if dialysis <6 hrs)
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45
Q

osmolar gap formula

A

2Na + (BUN/2.8) + (glucose / 18) + (EtOH / 4.6)

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46
Q

Toxic alcohol management, indications, dosing (4)

A

Fomepizole
Osm Gap / HAGMA with toxic alcohol >20 or high suspicion
15 mg / kg followed by 10 mg/kg q12h

NaHCO3 (most useful in methanol)
Folic acid (methanol)
Thiamine (B1) and pyridoxine (B6) and Mg (ethylene glycol)

HD: definitive

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47
Q

windshield wiper fluid

A

methanol

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48
Q

methanol toxic metabolite

A

formic acid

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49
Q

methanol presentation

A

mild intoxication with long slow elimination
HAGMA
snowfield vision
basal ganglia toxicity / parkinsonism

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50
Q

ethylene glycol toxic metabolites

A

Glycolic acid
oxalic acid

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51
Q

antifreeze

A

ethylene glycol
propylene glycol

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52
Q

ethylene glycol presentation

A

Antifreeze
intoxication with more rapid (RENAL) elimination
- nephrotoxicity
- urine fluorescence
- lactate gap (False VBG lactate)

53
Q

wallpaper or paint stripper

A

diethylene glycol - similar to ethylene glycol just two molecules

54
Q

isopropyl alcohol toxic metabolite

A

acetone

55
Q

rubbing alcohol

A

isopropyl alcohol

56
Q

isopropyl alcohol presentation

A

ketosis without acidosis
significant inebriation with AMS, resp depression, obtunded

57
Q

propylene glycol toxic metabolite

A

lactate

58
Q

methanol vs ethylene glycol vs isopropyl alcohol

A

methanol: windshield wiper fluid, AGMA, mild and prolonged intoxication, snowfield vision

ethylene glycol: antifreeze, AGMA, quicker and renally elimination intoxication

isopropyl alcohol: rubbing alcohol, ketosis without acidosis, obtundation

59
Q

absinthe made from and contains?

A

wormwood
contains thujone

60
Q

what determines where in respiratory tract will be irritated by irritant gas?

A

water solubility

high: eyes and mucus membranes
low solubility: lower airway

61
Q

management for irritant gas exposure

A
  1. remove source
  2. humidified O2 or PEEP if hypoxic
  3. HCO3 of chlorine expected
    4 can consider nebs or cxr
62
Q

which irritant gas has special management

A

chlorine gas- nebulized bicarb

63
Q

difference between irritant gas and asphyxiants

A

irritant gases irritate
asphyxiants prevent O2 absorption or distribution (CO and CN)

64
Q

when to expect CO

A

smoke inhalation, summer or winter with generators, family members

  • ZAMBONI or METHYLENE chloride
65
Q

3 mechanisms of CO

A
  1. hgb shift to left
  2. myoglobin binding- decreased cardiac contractility
  3. displaces NO -> hypotension
66
Q

diagnosis and treatment of CO

A
  1. VBG with CO-ox which will give % carboxyhemoglobin
  2. hyperbarics a discussion with >25% or 15 if pregnant
  3. 100% FIO2 via NRB or HFNC x 4 hours for goal <3%
67
Q

when to actually consider hyperbarics with CO

A

“>25% or 15 if pregnant”

put on 100% for 4 hours
do cerebellar walk test

68
Q

whats the benefit of hyperbaric with CO?

A

prevents delayed neurologic sequelae

69
Q

sources of CN

A

Cyanide salts
B17/amydalin supplements
fruit seeds
fire- burning of furniture - hydrogen CN

70
Q

MOA CN toxicity

A

sudden collapse in fire -> from burning of furniture
blocks cytochrome oxidase -> lactic acidosis

71
Q

presentation of CN

A

SUDDEN collapse
fire victims

72
Q

options for management of CN

A

Hydroxycobalamin (cyanokit): standard, more severe cases

Hydrogen cyanide kit: amyl nitrate, sodium nitrite and sodium thiosulfate (traditionally - but causes methemoglobinemia and worsens hypotension)

Nithiodote: amyl nitrate, sodium nitrite and sodium thiosulfate

Sodium thiosulfate- only option available or for less severe cases

73
Q

whats the problem with traditional hydrogen cyanide kit

A
  • amyl nitrate, sodium nitrite and sodium thiosulfate.
  • They cause methemoglobinemia which has high affinity for cyanide -> forms complex + thiosulfate -> complex that can be excreted (often pts have CO too…)
  • Nitrites also cause hypotension.
74
Q

hydroxycobalamin dose and results

A

5g over 15 min / 70 mg/kg in kids

binds to CN -> B12 -> excreted

raises BP and turns things red

75
Q

what is the toxin in castor beans, MOA and toxicity

A

ricin
inhibits RNA synthesis - cell death
inhaled (pulm issues), injected (MSK death), ingested (GI organ injury)

76
Q

stages of iron toxicity

A

GI upset
AGMA/lactate and shock
Hepatic failure
GI mucosal healing- scarring and strictures

77
Q

toxic dose of iron

A

> 60 mg/kg
20 - 60 mg/kg

78
Q

toxic iron levels

A

@4 hours
<300 mcg/dl = asymptomatic
300 - 500 = GI symp, TREAT
> 500 = shock and bad news

79
Q

iron toxicity treatment and dose

A

Deferoxamine (11mg binds 8.5mg elemental iron)

5-15 mg/kg/h

80
Q

side effects of deferoxamine (3)

A

Anaphylactoid, ARDS, yersinia infection

often take holiday after 24 hours and reassess

safe in pregnancy

81
Q

3 iron formulations and percentage of elemental iron

A

Fumarate 33%, sulfate 20%, gluconate 12%

82
Q

Digoxin
- indications
- MOA
- therapeutic range
- excretion and interactions

A

A fib with low BPs, HFrEF failing GDMT, peds HF

NA/K ATPase inhibition -> increase Ca and contractility

0.5-1 ish : NARROW

RENAL excretion. Many interactions including amiodarone and macrolides

83
Q

Other sources of digitalis toxicity

A

foxglove, lily of the valley, yellow oleander, colorado river and cane toad, squill

84
Q

Presentation of Dig toxicity

A

Nonspecific: fatigue, confusion, N/V, HA, anorexia

CARDIAC: anything, bradycardia, heart block, v tach, hypotension
HyperK, Hypomag, renal failure

Pathognomonic - bidirectional V tach

85
Q

electrolyte derangements with dig toxicity

A

HyerK

HypoMag

Renal failure

86
Q

Indications to give digoxin fab

A

Dysrhythmia
Hypo, brady
K >5 in acute (>5.5 portends bad prognosis)
Chronic with AMS, dysrhythmia or GI symptoms

87
Q

K of what portends bad prognosis in dig toxicity

A

> 5.5

88
Q

dig tox treatments (and contraindicated!) besides dig fab

A

Charcoal (multi-dose)
magnesium
?atropine
?Class IB antiarrhythmics like phenytoin or lidocaine

Calcium contraindicated (stone heart)
No pacing
HD (Vd too big)

89
Q

Digoxin Fab MOA and dosing

A

binds digoxin with higher affinity and is excreted in urine

each vial is 40mg and binds 0.5 mg

oral bioavailability 80%

Number of vials in Acute = (mg ingested x 0.8.) / 0.5 = 1.6 x mg ingested

Imminent arrest: 5-10 vials

Chronic = (serum dig x weight) / 100

90
Q

formulas to decide how much dig fab to give in acute and chronic ingestions

A

Number of vials in Acute = (mg ingested x 0.8.) / 0.5 = 1.6 x mg ingested

Imminent arrest: 5-10 vials

Chronic = (serum dig x weight) / 100

round up!

91
Q

serotonin syndrome VS NMS

A
  • serotonin: rapid- tremor, seizures, myoclonus, hyperreflexia. treat with benzos and cyproheptadine
  • NMS: gradual- bradykinesia, lead pip rigidity, hyperthermia. treat with benzos, bromocriptine, levodopa
92
Q

presentation of SSRI/SNRI OD

A

GI
CNS- drowsy tremulous, seizures, ataxia
CV: sinus tach, NA channel blockade and QRS prolongation, QT prolongation

93
Q

EKG finding and management of TCA overdose

A

widened QRS
terminal R wave in avR
Na bicarb
intralipid

94
Q

treatment of TCA OD

A

Na bicarb
- intralipis

95
Q

Alkali caustic examples and results

A

hydroxide, hydrogen peroxide

liquifactive necrosis

96
Q

Acidic caustic examples and results

A

Hydrochloric, sulfuric, hydrofluoric acid

coagulative necrosis

97
Q

ingestion of caustic, worrisome clnical signs

A

stridor by itself
drooling and vomiting

predictive of esophageal injury

98
Q

which caustic has unique dermal decon

A

phenol: use propranolol or isopropranolol

visible metals- wipe off

99
Q

in caustic ingestion, who gets scope?

A
  • intentional ingestion
    -AMS or baseline behavioral
  • stridor
  • vomiting and drooling

not needed if unintentional, no symptoms x8 hours and tolerating PO

100
Q

treatment post endoscopy of caustic ingestons

A
  • IF 2B -> methylpred

abx only for perf
PPI theoretical

101
Q

MOA, presentation, treatment methemoglobinemia

A

Fe2+ -> Fe 3+ -> left shift and thus functional anemia and los SpO2

methylene blue reduces it: 1-2 mg/kg over 5 min

102
Q

causes methemoglobinemia

A

amyl nitrate, silver nitrate, local anesthetics, abx, phenazopyridine, phenacetin, oxides

103
Q

presentation and management of hydrofluorocarbon

A
  • CNS depressant and asphyxiant
  • sudden sniffing death 2/2 tachydysrhythmias from catecholamine surge
  • NO EPI
  • propranolol or eosmolol
104
Q

pyrethrins/pyrethroids, where are they and MOA, treatment

A
  • mosquito netting, topical for scabies and life
  • Na channal openers -> tremors, seizures, ataxia, cardiac effects
  • Vit E, benzos
105
Q

MOA HF acid

A

rapid release of hydrogen ions and subsequent tissue dehydration and coagulation necrosis, binds up all your calcium and causes vasospasm
the release of the highly reactive free fluoride ion, F– (liquefactive necrosis)

106
Q

acids and alkali type of necrosis

A

Acids: coagulative necrosis
alkali: liquefactive necrosis.

107
Q

deforoximine ??mg binds???

A

100 mg binds 8.5 mg

108
Q

symptoms CN

A

headache, seizure, coma, resp failure, tachycardia followed by bradycardia, AGMA
cherry red skin is late finding

109
Q

VPA: MOA, level, presentaiton, treatment

A
  • inreased GABA, impairs mitochondrial beta oxidation, depletes carnitine stores and disrupts urea cycle
  • acute ingestion>200 mg/kg
  • sx: n/v, pancreatitis, CNS depression, AGMA, hyperammonemia, hypotension, pancytopenia
    get serial levels
  • tx: L-carnitine for encephalopathy with hyperammonemia (VPA 450 mg/L), meropenem, HD (VPA > 850 mg/L, cerebral edema)
110
Q

Tessalon MOA and treatment

A

NA channel blockade - seizures and dysrhythmias

  • inralipid, bicarb, benzos
111
Q

cyclopeptide mushrooms example and phases

A

amanita phalloides with amatoxin- inhibits RNA polymerase II

Phase 1 (5-24h) terrible GI sx; phase 2 (12-36h) minimal symptoms that can be falsely reassuring; phase 3 (2-6d) hepatic/renal failure, death

112
Q

gyromitra mushroom / false morel

A

False Morel- BRAINS< PYRIDOXINE

Gyromita toxin: metabolized to monomethylhydrazine which acts like isoniazid to deplete B6 → no glutamate to make GABA → refractory seizures

Consider pyridoxine for seizures (you need like 50 vials)

113
Q

muscarine mushrooms

A

Ivory tunnel
CHOLINERGIC - NO BBB cross

114
Q

amanita smithiana
- contains?
- preentation?

A

BREAKS 6 HOUr RULE

  • contains crotylglycine and allenic norleucine
    R- apid N/V <6h (breaks the 6h rule), delayed renal failure with peak Cr @ 2-7d
115
Q

foxglove

A

digitalis

116
Q

jimson weed

A

anticholinergic

117
Q

phytolaccatoxin

A

GI syjptoms

118
Q

hallucinogenic plants

A

Morning glory/nutmeg/claviceps, hawaiian baby wood rose, kava kava, kratom, salvia

119
Q

convulsant plants

A

water hemlock/strychnos

120
Q

Na channel blocking plants

A

rhododendron/false hellebore/death camus/monkshood/yew (& Ca+ channel blocker)

121
Q

Trazodone MOA

A

Alpha 1 agonist, H1 and 5HT2A/2C antagonist, 5HT1 agonist → CNS depression, hypotension

122
Q

fresh mown hay

A

phosgene
akasthesia
benzo, propranolol 20 mg BID to 80 mg/day, clonidine 0.1 mg TID, 5HT2A antagonist (mirtazapine, cyproheptadine)

123
Q

which SSRI’s are cardiotoxic

A

citalopram/escitalopram

124
Q

organophosphate available at lowes

A

carbomyl

125
Q

colchicine plant

A

antimitotic (tubulin) -> multiorgan failure

autumn crocus and glory lily
highest concentration in bulb

126
Q

what heavy metal causes torsades

A

aresenic

127
Q

what lead level is toxic

A

500 at 4 hours

128
Q

4 ways NAC works

A

▪ Limits further formation of NAPQI
▪ Acts as precursor for glutathione
▪ Improves microvascular blood flow/oxygen delivery
▪ Increases capacity to detoxify NAPQI

PGY2 EM (2 decks)

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