Tox Flashcards
Antitodes to Acetampinophen
- 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
Viperidae
Copperhead, rattlesnakes, cotton mouths
- most often local tissue effects and coagulopathy
- crofab indicated with swelling crossing joints, coagulopathy, etc
Elapidae
coral and mamba snakes
- neurotoxic
- antivenom early
- red on yellow
source, results, and treatment of hydrofluoric acid exposure
- ruse removers, cleaners, insecticides
- hypocalcemia, hypomag, hyperK
- local tissue necrosis
- decon and calcium GLUCONATE (not chloride) near injury
Antitodes to Acetampinophen
- 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
5 treatments for CCB and BB overdose
- charcoal
- atropine
- Calcium (CCB)
- glucagon
- high dose insulin (ccb>bb)
high dose insulin
- CCB>BB overdose
- theoretically increases myocyte metabolism
- 1 unit/kg reg bolus then 1 unit/kg/hr
what enzyme is ccb metabolized by
cyp3A4
difference between CCB and BB overdose
CCB: hyperglycemia
BB: in peds may cause hypoglycemia
which beta blockers cause EKG changesm (4)
Propranolol- Na channel blockade, QRS
Sotalol - K blockade, QT prolonged
Carvedilol and acebutalol- Na channel blockade
why is propranolol uniqe
Na channel blockade
lipophilic -> crosses blood brain barrier and can cause seizures
Anti-arrhythmic Drug class
I: Na channel blocker
II: beta blocer
III: K channel blockade - prolongs APD
IV: CCB
Bupropion overdose
- QRS and QT prolongation due to gap junction inhibition
- seizures
Palytoxin
- where, mechanism, exposure
- 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
becaquerel
sievert
gray
- 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)
radiation injury labs
- trend ALC - predicts mortality
type of radiation
- 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
metabolic and laboratory changes with aspirin
EARLY respiratory alkalosis
metabolic acidosis- lactate and ketones
- hypokalemia
- hypoglycemia (very early hyperglycemia)
- falsely elevated chloride
- elevated INR
aspirin units (therapeutic, overdose)
mg/dcl
15-3o mg/dcl is therapeutic
early to late manifestations of aspirin toxicity
Early: GI/N/V and initius
progressing: tachypnea, fever
late: coagulopathy, cerebral edema and seizures
aspirin treatment (A-G and K)
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
indications for HD 2/2 aspirin
level nearing 100
level nearing 40 and pregnant
fluid restrictions - kidney, heart
AMS or seizure
therapies failing
Two tox exposures that are bad news for pregnancy
- aspirin: fetus more acidic environment
- CO: like fetal hemoglobin
Sulfonylurea toxicity management
- blocks K channels in pancreas -> insulin release regardless of BG
- ends in “ide” - glipizide, glimeperide
- one pill can kill peds
OCTREOTIDE 50-100mg SC
Cyclobenzarpine MOA and overdose
- NE and serotonin reuptake inhibition, centrally
- more sedating
- long half life 18h-33h
- ANTICHOLINERGIC effects
- NA channel blockade
Anticholinergic toxidrome
mad, blind, red, hot, dry
benadryl
cholinergic toxicity
dumbells- diarrhea, urination, miosis, bradycardia, emesis, lacrimation, lethargy, salivation
pesticides
acute and chronic lithium OD
acute: N/V
chronic: CNS -> rigidity, tremor, ataxia, slurred speech
Lithium therapeutic range
0.5 mEq/L - 1.5 mEq/L
Lithium toxic range and risk factors
> 1.5 (dialyze at 4)
- volume depletion (causes renal retention - renally excreted)
- CHF, CKD, ACEi/ARB or other diuretics
- age >60
Lithium toxicity management
- NACL (kidneys confuse Li and Na - giving NaCl helps prevent lithium retention
- agressive fluids
- discontinue ace/arb/diuretics
- HD at Li > 4mEq/L
what class of drugs is not dialyzable
antipsychotics
antipsychotic pyramidal side effects and management
- acute dystonia: benztropine, benadryl
- Akasthesia: B-CALM
B blocker, Clonazepam, Anticholinergic, cLonidine, Mirtazapine (5HT2A block) - Tardive dyskinesia: VMAT2 inhibitors
Clozapine, quetiapine (Seroquel), palperidone (invega) or aripiprazole?
granulocytopenia, sialorrhea, seizures (dose related), EKG changes
clozapine
Clozapine, quetiapine (Seroquel), palperidone (invega) or aripiprazole?
abuse causes euphoria with possible withdrawal, structurally simailar to TCA, bezoar formation
quetiapine
Clozapine, quetiapine (Seroquel), palperidone (invega) or aripiprazole?
metabolite of resperidone
prolonged tachycardia
required 24 hour obs
palperidone
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
aripiprazole
Diphenhydramine MOA
H1 blocker
- lipophilic: crosses BBB
At high doses - Na and K blockade -> QRS and QT prolongation
fatal dose of diphenhydramine
20-40mg/kg
diphenhydramine effects
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.
diphenhydramine treatment
- bicarb for EKg changes
- foley placement and temp management
- benzos for seizures
- physostigmine for delirium
physostigmine in benadryl OD
- 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
metformin toxicity
GI symptoms → lethargy → seizure and CV collapse → coma
metformin OD management
- causes lactic acidosis via inhibition of gluconeogenesis and mitochondrial complex
charcoal
bicarb
HD (decreased mortality if dialysis <6 hrs)
osmolar gap formula
2Na + (BUN/2.8) + (glucose / 18) + (EtOH / 4.6)
Toxic alcohol management, indications, dosing (4)
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
windshield wiper fluid
methanol
methanol toxic metabolite
formic acid
methanol presentation
mild intoxication with long slow elimination
HAGMA
snowfield vision
basal ganglia toxicity / parkinsonism
ethylene glycol toxic metabolites
Glycolic acid
oxalic acid
antifreeze
ethylene glycol
propylene glycol
ethylene glycol presentation
Antifreeze
intoxication with more rapid (RENAL) elimination
- nephrotoxicity
- urine fluorescence
- lactate gap (False VBG lactate)
wallpaper or paint stripper
diethylene glycol - similar to ethylene glycol just two molecules
isopropyl alcohol toxic metabolite
acetone
rubbing alcohol
isopropyl alcohol
isopropyl alcohol presentation
ketosis without acidosis
significant inebriation with AMS, resp depression, obtunded
propylene glycol toxic metabolite
lactate
methanol vs ethylene glycol vs isopropyl alcohol
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
absinthe made from and contains?
wormwood
contains thujone
what determines where in respiratory tract will be irritated by irritant gas?
water solubility
high: eyes and mucus membranes
low solubility: lower airway
management for irritant gas exposure
- remove source
- humidified O2 or PEEP if hypoxic
- HCO3 of chlorine expected
4 can consider nebs or cxr
which irritant gas has special management
chlorine gas- nebulized bicarb
difference between irritant gas and asphyxiants
irritant gases irritate
asphyxiants prevent O2 absorption or distribution (CO and CN)
when to expect CO
smoke inhalation, summer or winter with generators, family members
- ZAMBONI or METHYLENE chloride
3 mechanisms of CO
- hgb shift to left
- myoglobin binding- decreased cardiac contractility
- displaces NO -> hypotension
diagnosis and treatment of CO
- VBG with CO-ox which will give % carboxyhemoglobin
- hyperbarics a discussion with >25% or 15 if pregnant
- 100% FIO2 via NRB or HFNC x 4 hours for goal <3%
when to actually consider hyperbarics with CO
“>25% or 15 if pregnant”
put on 100% for 4 hours
do cerebellar walk test
whats the benefit of hyperbaric with CO?
prevents delayed neurologic sequelae
sources of CN
Cyanide salts
B17/amydalin supplements
fruit seeds
fire- burning of furniture - hydrogen CN
MOA CN toxicity
sudden collapse in fire -> from burning of furniture
blocks cytochrome oxidase -> lactic acidosis
presentation of CN
SUDDEN collapse
fire victims
options for management of CN
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
whats the problem with traditional hydrogen cyanide kit
- 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.
hydroxycobalamin dose and results
5g over 15 min / 70 mg/kg in kids
binds to CN -> B12 -> excreted
raises BP and turns things red
what is the toxin in castor beans, MOA and toxicity
ricin
inhibits RNA synthesis - cell death
inhaled (pulm issues), injected (MSK death), ingested (GI organ injury)
stages of iron toxicity
GI upset
AGMA/lactate and shock
Hepatic failure
GI mucosal healing- scarring and strictures
toxic dose of iron
> 60 mg/kg
20 - 60 mg/kg
toxic iron levels
@4 hours
<300 mcg/dl = asymptomatic
300 - 500 = GI symp, TREAT
> 500 = shock and bad news
iron toxicity treatment and dose
Deferoxamine (11mg binds 8.5mg elemental iron)
5-15 mg/kg/h
side effects of deferoxamine (3)
Anaphylactoid, ARDS, yersinia infection
often take holiday after 24 hours and reassess
safe in pregnancy
3 iron formulations and percentage of elemental iron
Fumarate 33%, sulfate 20%, gluconate 12%
Digoxin
- indications
- MOA
- therapeutic range
- excretion and interactions
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
Other sources of digitalis toxicity
foxglove, lily of the valley, yellow oleander, colorado river and cane toad, squill
Presentation of Dig toxicity
Nonspecific: fatigue, confusion, N/V, HA, anorexia
CARDIAC: anything, bradycardia, heart block, v tach, hypotension
HyperK, Hypomag, renal failure
Pathognomonic - bidirectional V tach
electrolyte derangements with dig toxicity
HyerK
HypoMag
Renal failure
Indications to give digoxin fab
Dysrhythmia
Hypo, brady
K >5 in acute (>5.5 portends bad prognosis)
Chronic with AMS, dysrhythmia or GI symptoms
K of what portends bad prognosis in dig toxicity
> 5.5
dig tox treatments (and contraindicated!) besides dig fab
Charcoal (multi-dose)
magnesium
?atropine
?Class IB antiarrhythmics like phenytoin or lidocaine
Calcium contraindicated (stone heart)
No pacing
HD (Vd too big)
Digoxin Fab MOA and dosing
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
formulas to decide how much dig fab to give in acute and chronic ingestions
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!
serotonin syndrome VS NMS
- serotonin: rapid- tremor, seizures, myoclonus, hyperreflexia. treat with benzos and cyproheptadine
- NMS: gradual- bradykinesia, lead pip rigidity, hyperthermia. treat with benzos, bromocriptine, levodopa
presentation of SSRI/SNRI OD
GI
CNS- drowsy tremulous, seizures, ataxia
CV: sinus tach, NA channel blockade and QRS prolongation, QT prolongation
EKG finding and management of TCA overdose
widened QRS
terminal R wave in avR
Na bicarb
intralipid
treatment of TCA OD
Na bicarb
- intralipis
Alkali caustic examples and results
hydroxide, hydrogen peroxide
liquifactive necrosis
Acidic caustic examples and results
Hydrochloric, sulfuric, hydrofluoric acid
coagulative necrosis
ingestion of caustic, worrisome clnical signs
stridor by itself
drooling and vomiting
predictive of esophageal injury
which caustic has unique dermal decon
phenol: use propranolol or isopropranolol
visible metals- wipe off
in caustic ingestion, who gets scope?
- intentional ingestion
-AMS or baseline behavioral - stridor
- vomiting and drooling
not needed if unintentional, no symptoms x8 hours and tolerating PO
treatment post endoscopy of caustic ingestons
- IF 2B -> methylpred
abx only for perf
PPI theoretical
MOA, presentation, treatment methemoglobinemia
Fe2+ -> Fe 3+ -> left shift and thus functional anemia and los SpO2
methylene blue reduces it: 1-2 mg/kg over 5 min
causes methemoglobinemia
amyl nitrate, silver nitrate, local anesthetics, abx, phenazopyridine, phenacetin, oxides
presentation and management of hydrofluorocarbon
- CNS depressant and asphyxiant
- sudden sniffing death 2/2 tachydysrhythmias from catecholamine surge
- NO EPI
- propranolol or eosmolol
pyrethrins/pyrethroids, where are they and MOA, treatment
- mosquito netting, topical for scabies and life
- Na channal openers -> tremors, seizures, ataxia, cardiac effects
- Vit E, benzos
MOA HF acid
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)
acids and alkali type of necrosis
Acids: coagulative necrosis
alkali: liquefactive necrosis.
deforoximine ??mg binds???
100 mg binds 8.5 mg
symptoms CN
headache, seizure, coma, resp failure, tachycardia followed by bradycardia, AGMA
cherry red skin is late finding
VPA: MOA, level, presentaiton, treatment
- 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)
Tessalon MOA and treatment
NA channel blockade - seizures and dysrhythmias
- inralipid, bicarb, benzos
cyclopeptide mushrooms example and phases
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
gyromitra mushroom / false morel
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)
muscarine mushrooms
Ivory tunnel
CHOLINERGIC - NO BBB cross
amanita smithiana
- contains?
- preentation?
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
foxglove
digitalis
jimson weed
anticholinergic
phytolaccatoxin
GI syjptoms
hallucinogenic plants
Morning glory/nutmeg/claviceps, hawaiian baby wood rose, kava kava, kratom, salvia
convulsant plants
water hemlock/strychnos
Na channel blocking plants
rhododendron/false hellebore/death camus/monkshood/yew (& Ca+ channel blocker)
Trazodone MOA
Alpha 1 agonist, H1 and 5HT2A/2C antagonist, 5HT1 agonist → CNS depression, hypotension
fresh mown hay
phosgene
akasthesia
benzo, propranolol 20 mg BID to 80 mg/day, clonidine 0.1 mg TID, 5HT2A antagonist (mirtazapine, cyproheptadine)
which SSRI’s are cardiotoxic
citalopram/escitalopram
organophosphate available at lowes
carbomyl
colchicine plant
antimitotic (tubulin) -> multiorgan failure
autumn crocus and glory lily
highest concentration in bulb
what heavy metal causes torsades
aresenic
what lead level is toxic
500 at 4 hours
4 ways NAC works
▪ Limits further formation of NAPQI
▪ Acts as precursor for glutathione
▪ Improves microvascular blood flow/oxygen delivery
▪ Increases capacity to detoxify NAPQI
