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Toxicology Flashcards

1
Q

Contrast the treatment of organophosphate or nerve gas poisoning with that of carbamate or herbicide intoxication.

A

organophosphate or malathion poisoning will inhibit acetylcholinesterase. some phosphastes target neuronal esterase and cause neurotoxicity/paralysis. Give atropine.

Sarin, Somin nerve gases should be treated with Pralidoxime (removes organophosphate from acetylcholinesterase)

Carbamate poisoning has short effects w/ spontaneous recovery

Herbicides (2,40dichlorophenoxyacetic) - GI symptoms, confusion, aggressiveness and metabolic acidosis. Give Sodium Bicarb to alkalinize. (control electrolytes like K and Ca loss)

Paraquat herbicide - free radical tissue damage. No antidote.

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2
Q

What is presentation of heavy metal poisoning?

A

Lead - decreased Ach release and Na/K ATPase inhibition. Low motiliity and water efflux. Slowed nerve conduction and lead anemia. Proximal tubule dysfunction. Encephalopathy.

Arsenic - derm changes, hyperpigmentation, palmar keratoses, malignant changes in all organs

Mercury - interstitial pneumonitis. Dequamative rash (acrodynia), paresthesias, nephrotic syndrome.

Iron - hematemesis, diarrhea, cellular toxicity to mitochond and low oxidative phosphorylation. Primarily affects liver, also heart, renal and lung, hematotox.

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3
Q

What is most frequent cause of intoxication?

A

took or given medication twice, followed by incorrect dosing and wrong medication taken/given.

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4
Q

What is most common therapy for intoxication?

A

decontamination only (almost 50% of the time)

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5
Q

What is general patient management for intoxication?

A

ABCDEFG
Airway, Breathing, Circulation, Disability-AVPU/Glasgow Coma scale, Dont Ever Forget Glucose, Get a set of basic observations

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6
Q

What is treatment for iron overdose?

A

deferoxamine

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7
Q

What is treatmetn for opiate overdose

A

naloxone

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8
Q

What is treatment for acetaminophen overdose?

A

N Aetylcysteine

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9
Q

What is treatment of digoxin overdose?

A

digibind + Mg

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10
Q

What is treatment of BNZ overdose?

A

flumazenil

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11
Q

What is essential when giving activated charcoal?

A

Protect the airway. Only give it if patient has ingested a potentially toxic amount of poison that is KNOWN to be absorbed by charcoal.

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12
Q

What is syrup of Ipecac?

A

emetic made from Cephaelis plant. Emesis withing 20 minutes that lasts 30-120 minutes.

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13
Q

What is ADE of ipecac?

A

drowsiness, abdominal pain, diarrhea.

High abuse potential and Chronic use causes cardiotoxicity

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14
Q

When should GI decontamination be used?

A

only when there is a life-threatening exposure

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15
Q

Patient comes in to ED with undifferentiated acute poisoning should you gastric lavage?

A

No. There is no benefit likely. Might cause GI perforation, hypoxia or aspiration. Likely the toxin has already passed duodenum

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16
Q

What can be used to clear toxic methanol, ethylene glycol, salicylates, lithium or sotalol levels from blood?

A

Hemodialysis. Only works for water soluble toxins with low molecular weight and low plasma protein binding.

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17
Q

What should be used to clear carbamazepine, phenobarbital, phenytoin or theophylline from blood?

A

hemoperfusion. Passage of blood thorugh absorptive cartridge that is usually charcoal. Good for substances highly bound to protein.

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18
Q

What is treatment for sympathomimetic overdose like cocaine, amphetamine, methamphetamine, decongestants (phenylpropanolamine, ephedrine, pseudoephedrine), caffeine, theophylline?

A

primary supportive.
Phentolamine, nitrates or Ca blockers for HTN
BNZ for agitation

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19
Q

What is absolutely contraindicated in someone who has OD on decongestants or other sympathomimetics?

A

absolutely no BB w/o alpha blocker. There will be unopposed alpha-stimulation

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20
Q

What is treatment for BB toxicity?

A

activated charcoal.
For bradycardia and hypoTN, give IV glucagon
For cardiotoxicity use high dose insulin and dextrose
Can give Na bicarbonate to correct membrane depression (from TCA poisoining)
Lipid emulsions

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21
Q

What is treatment of Ca channel blocker toxicity?

A 
activated charcoal
for hypoTN and bradycardia give IV Ca chloride or Ca gluconate to get Ca levels to 2x normal. (most useful because of its negative inotropic effects)
Give epinephrine and glucagon
Or High dose insulin +dextrose
Lipid emulsion also
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22
Q

How does insulin and dextrose work for BB or CaB toxicity?

A

promotes uptake of lgucose, shifts K intracellularly, improves inotropy,
Increases myocardial metabolism and decreases FFA metabolism

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23
Q

What is toxidrome of isoniazid?

A

acute reduction in brain pyridoxal 5-phosphate, active Vitamin B6.
Results in low GABA levels and seizures.
Inhibits hepatic conversion of lactate to pyruvate causing lactic acidosis (compounds with seizures)

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24
Q

What is treatment for isoniazid overdose?

A

vitamin B6 (pyridoxine)

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25
Q

What are the phases of acetaminophen?

A

Phase 1 - 30min-4hrs patient will appear normal (minor anorexia, pallor, N/V, diaphoresis)
Phase 2- 24-48hrs Recovery, Right UQ pain from hepatic damage. PT time increased and decraesed renal function.
Phase 3 (3-5days) - hepatic necrosis, coag defects, jaundice, renal failure, hepatic encephalopathy, centrilobar necrosis
Phase 4- (4days-2weeks) - death or resolution

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26
Q

What can be used to determine extent of acetaminophen toxicity?

A

Rumack-Matthew Nomogram

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27
Q

What is toxidrome for salicylate poisoining?

A

uncoupled cellular oxidative phosphorylation.
Anaerobic metabolisma nd excessive production of lactic acid and heat that interfere with Krebs cycle enzymes.
Brainstem stimulted causing tachypnea.
Respiratory alkalosis, metabolic acidosis
Tachycardia, tinnitus, agitation, confustion, seizures, pulmonary edema, hyperthermia

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28
Q

What is metabolism of salicylates?

A

zero-order metabolism

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29
Q

How do you diagnose salicylate poisoining?

A

NOT by presentation. Must measure blood levels and high anion gap.

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30
Q

WHat is treatment for salicylate poisoining?

A

charcoal 10:1 weight ratio.
Glucose to prevent cerebral hypoglycemia
For metabolic acidosis give IV Na Bicarb
Alkinalize the urine to enhance renal excretion.
Add potassium chloride to IV
Hemodialysis if severe metabolic acidosis or altered mental status

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31
Q

Which drugs cause high anion gap acidosis?

A

MUDPILES CAT
methanol/metformin, Uremia, DKA, Iron, INH, Ibuprofen, LActic acidosis, ehtylene glycol, salicylates, cyanide, alcohol or acids (valproate), toluene ror theophylline

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32
Q

What is cyproheptadine?

A

antihistamine with anti-serotonin activity

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33
Q

What is presentation of CO poisoining?

A

headache, dizziness, N/V, seizures, coma

34
Q

What is treatment of CO poisoning?

A

100% O2

35
Q

What is presentation of irritant intoxication like chlorine, ammonia, sulfur dioxide?

A

stridor, wheezing, pneumonia

36
Q

What is treatment for chlorine, ammonia or sulfor dioxide irritants?

A

humidified O2 and bronchodilators

37
Q

How is cynaide toxic? How does it present?

A

it blocks O2 binding to cytochrome C.

HEadache, N/V, syncope, seizures, coma

38
Q

How is hydrogen sulfide toxic? How does it present?

A

similar to cyanide. it blocks O2 binding to cytochrome C.

HEadache, N/V, syncope, seizures, coma

39
Q

How does nitrogen oxide cause toxicity?

A

causes methemoglobinemia. Presents as dyspnea, cyanosis, seizures, coma

40
Q

How should exposure to oxidizing agents like nitrogen oxide be treated?

A

give methylene blue to reverse methemoglobinemia

41
Q

What is a cyanide kit?

A

amyl nitrite followed by IV sodium nitrite convert a portion of hemoglobin into methemoglobin (ferrous to ferric). Cyanide binds to it to form cyanmethemoglobin.
Sodium thisulfate and cyanmethamoglobin become thicyanate which is renally eliminated.

42
Q

What is toxidrome for hydrocarbons?

A

coughing, gagging, choking within 30 minutes to hours. Headache, lethargy, decreased mental status, dyspnea, syncope, myocardial sensitization to catecholamines, hepato toxicity, renal toxicity, local reactions.

43
Q

What is treatment for hydrocarbon toxicity?

A

decontaminate + ABCs.
Magnesium and K for arrhthmia
Lidocaine or BB for V-fib
Charcoal DOES NOT WORK!

44
Q

What is likely to be inhibited by an insectiside? What will side effects be?

A

acetylcholinesterase, causing SLUDGEBBB

Salivation, lacrimation, urination, defecation, GI, emesis, bronchorrhea, bronchospasm, bradycardia

45
Q

What is treatment for insectisie or organophosphate poisoining?

A

atropine

46
Q

What is treatment for sarin or nerve gas?

A

pralidoxime IV

47
Q

What is treatment of nicotine OD?

A

symptomatic support / control seizures

48
Q

What is toxidrome of pyrethrum?

A

Botanical insectiside. CNS toxicity by voltage sensitive Na, Ca, Cl channels. Excitation, convulsions, tetanic paralysis.
Contact dermatitis

49
Q

What is toxidrome for rotenone?

A

botanical insectiside. GI irritaiton, rhinitis, pharyngitis, dermatitis

50
Q

What is toxidrome for Herbicides?

A

Much more GI» pulmonary
Breath odor, vomiting, diarrhea, headache, confusion, aggressiveness, coma, metabolic acidosis, elevated CPK, myoglobinuria

51
Q

What is treatment for herbicide (2,4-dichlorophenoxyacetic) poisoining?

A

IV lfuids and alkalkine diuresis
Na bicard to accelerate urine excretion
Control K and Ca losses and correct

52
Q

What is toxidrome for paraquat?

A

slow free-radical tissue damage.
Acute pain and swelling of mouth/throat, N/V, abdominal pain, bloody diarrhea.
Slow onset of liver, kidney and heart failure
Lung scarring, pulmonary edema
CNS toxicty

53
Q

What is treatment for paraquat herbicide?

A

NO antidote. Support

54
Q

What is MOA of causitc acid damage?

A

tissue injury by coag necrosis, replaced by granulation tissue. Stomach most common.
Pharynx and esophagus resistant.

55
Q

What is MOA of caustic alkali damage?

A

tissue injury by liquefactive necrosis. Damage to epithelium of oropharynx, hypopharynx, and esophagus (most common).
Immediate tissue edema can obstruct airways.
Eventual granulation tissue –> strictures

56
Q

What is treatment for acid or alkali ingestion?

A

Gastric lavage using large bore tube
Nasogastric tube suction of liquids
If an alkaline solid, dilute. IF ACID DO NOT DILUTE
NO charcoal, NO dilution, NO neutralization

57
Q

Toxidrome of lead?

A

colic and constipation
Decreased Ach release and Na/K-ATPase inhibition decreases motility and water flux
Slowed nerve conduction and demyelination
Lead anemia (either micro or normocytic hypochromic with reticulocytosis)
Proximal renal tubule impairment causes aminoaciduria, glycosuria and hyperphosphaturia.
CNS encephalopathy.

58
Q

Why would lead levels decrease and then rise after chelation therapy?

A

initial drop from chelation, then increase as more lead is mobilized from tissues.

59
Q

What should be given for mild lead cases? Severe?

A

succimer (DMSA) for mild

Dimercaprol for severe

60
Q

Which lead chelator must be given with another and why?

A

Ca EDTA must be given with dimercarprol because EDTA alone can increase CNS lead levels.

61
Q

Toxidrome for arsenic poisoining?

A

accumulation in liver, kidney, heart and lungs.
Derm changes (hyperpigment and palmar keratoses) common in chronic.
Malignant change in almost every organ.
Risk of CV disease, respiratory disease, DM and neutropenia

62
Q

What is treatment for arsenic poisoning?

A

dimercaprol (BAL in Oil) - risk of hypersensitivity and G6Pd deficiency. Give iron supplements.
May be nephrotoxic and cause abscesses at injection site.

Succimer - for childs

63
Q

What is Toxidrome for mercury?

A 
interstitial pneumonitis from vapors.
Intention tremor
gum inflammation, excessive salivation
Psych symptoms
acrodynia (desquamative rash)
paresthesia (especially around mouth)
Dose-dependent nephrotoxicity
64
Q

What is treatment for mercury?

A

chelation therapy via
Dimercaprol (BAL) and succimer (DMSA)
Exchange transfusion as last resort

65
Q

MOA of penicillamine

A

copper, lead and mercury chelator

66
Q

ADE of penicillamine?

A

fatal thrombocytopenia, agranulocytosis, aplastic anemia, pancytopenia, sideroblastic anemia
Exertional dyspnea
Renal failure
Neurologic effects
tinnitus, neorpathy, optic neruitis, agitation
N/V, anorexia, diarrhea

67
Q

Toxidrome for iron?

A

corrosive to mucosa. Hematemesis and diarrhea–> hypovolemic shock.
Cellular toxicity to mitochondria decrease oxidative phosphorylation and cell death.
Affects heart, renal, lung, hematologics
GI toxicity
60 mg/kg lethal
metabolic acidosis

68
Q

MOA of deferoxamine

A

only works for iron. Excreted in urine and bile. Gives urine red color.

69
Q

ADE of deferoxamine

A 
red urine.
Tachycardia, hypotension, shock
Cardiovascular collapse in combo with the iron.
abdominal discomfort
flushing/fever
70
Q

What is CroFAB

A

small antibody fragments used as a snake bite antivenom. Given when reapid progression of swelling, significant coagulation defects, neuromuscual paralysis, CV collapse

71
Q

MOA of brown recluse venom

A

endothelial damage, platelet aggregation and RBC lysis causes small vessel occlusion and necrosis

72
Q

MOA of black widow venom

A

neurotransmitter dysregulator. Erythema –> cramping, headache, restlessness.

73
Q

Treatment for black widow venom

A

antispasmodics like BNZ and opiates.

Black widow antivenin (latrodectus mactans antivenin)

74
Q

MOA of atropine

A

muscarinic antagonist used to treat acetylcholinesterase inhibitor toxicity

75
Q

MOA of dimercaprol

A

chelator for mercury, arsenic, lead, and copper

76
Q

MOA of EDTA

A

removes mercury, lead and iron from body.

MUST use with dimercaprol to prevent metal level spikes in CNS

77
Q

MOA of flumazenil

A

GABA receptor antagonist

78
Q

MOA of hydroxycobalamin

A

treatment for cyanide poisoning

79
Q

MOA of nalmefene

A

opioid receptor antagonist similar to naltrexone but with longer half-life and no dose-dependent liver toxicity. opiod toxicity

80
Q

USE of octreotide

A

sulfonylurea toxicity

81
Q

USE of physostigmine

A

cholinesterase inhibitor.

Used for anticholinergic toxicity

82
Q

USE for protopam

A

organophosphate and carbamate toxicity

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