Toxicology

Front 1

AEIOU

TIPS

Back 1

Alcohol, Endocrine, Encephalopathy, Electrolytes, Insulin, Oxygen, Opiates, Uremia

DIFFERENTIAL FOR ALTERED MENTAL STATUS

Toxins, Temperature, Trauma, Infection, Psychiatric, Porphyria, Space-Occupying Lesion, Subarachnois Hemorrhage, Stroke, Shock, Sugars

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Mechanisms of Toxic Death

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Metabolic, Cardiac, CNS

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Metabolic Toxic Death

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Body cannot properly metabolize, or use oxygen, or carry out normal metabolic function because of drug toxicity.

Ex: Salicylates and Cyanide

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Cardiac Toxic Death

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Disrupts heart rate, rhythm, or cardiac output to the point --> body not receiving adequate blood flow --> organ system collapse

Ex: Digoxin (?)

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CNS Toxic Death

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CNS stimulation leads to seizures
CNS depression leads to apnea

Stimulation Ex: INH and tricyclic antidepressants

Depression Ex: Heroine

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Glascow Coma Scale

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Scale from 3-15
Eyes, Motor, Speech (EMS)
GCS<8 = coma/intubation

AVPU conversion: A:15, V:13, P:8, U:3

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Toxidromes

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Toxic Syndromes
Opioid
Cholinergic
Sympathomimetic
Anticholinergic

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Opioid Toxidrome

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Coma, bradypnea (slow breathing), pinpoint pupils (miosis), bradycardia

Ex: heroine overdose

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Cholinergic Toxidrome

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DUMBBELS
Defecation, Urination, Miosis, Bradycardia, Bronchorrhea, Emesis, Lacrimation, Salivation

SLUDGE - Salivation, Lacrimation, Urination, Defecation, GI, Emesis

Ex: Sarin OD (Nerve gas)

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Sympathomimetic Toxidrome

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HTN, Tachycardia, Dilated Pupils, Anxiety, DIAPHORESIS (Sweating!)

Diaphoresis differentiates from anticholinergic

Ex: cocaine, methamphetamine OD

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Anticholinergic Toxidrome

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Red, Dry, Blind, Mad, Hot, Seizing

(Red as a Beet, Dry as a Stone, Blind as a Bat, Mad as a Hatter, Hot as Hell, Seizing like a Squirrel) --> Dry differentiates from Sympathomimetic.

Ex: Jimson Weed (Atropine Nightshade), Antihistamines

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Salicylate Overdose

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Signs of toxicity: nausea, tinnitus, diaphoresis, low-grade fever

Syndrome: Acid/Base disturbance --> Respiratory Alkalosis and Metabolic Acidosis. Metabolic Acidosis predominates.

Level: >30 mg/dL is considered toxic 50-90 mg/dL is considered severe.

Tx: Moderate: Urinary Alkalization
Severe: Hemodialysis

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Acetominophen Overdose (Tylenol)

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Most common cause of acute fulminant hepatic failure in US

Doesn't have toxidrome. Tylenol not toxic, but CYP in liver metabolizes to NAPQI which is toxic.


Level: 4 hour level >150 mg/dL is toxic. (~10-20 is therapeutic dose)

Syndrome: centrilobular necrosis. Zone 3. Indicative of tylenol overdose.

Tx: N-acetylcysteine (NAC) or Mucomist

Rumack-Matthew Nomogram useful for telling you who needs to be treated. Valid only for acute, single OD.

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Tricyclic Antidepressants

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Anticholinergic Toxidrome (Red, Dry, Blind, Mad, Hot, Seizing)

Syndrome: Widening in QRS --> dysrhythmia

Tx: Sodium Bicarbonate

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Toxic levels for Tylenol

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150 mg in 4 hours

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Ethylene Glycol

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Found in Antifreeze (sugar alcohol)
Binds Calcium, creates dihydrate crystals which cause ATN and renal failure. Acidosis.

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Methanol

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Metabolized to formaldehyde then to formic acid* (toxic to retina, causes acidosis)
Blurred vision, sluggish, swelling of optic disk and possible hemorrhage.

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Isopropyl Alcohol

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Rubbing alcohol (non-streak addition to Windex)
Metabolized to acetone. Dipstick urine test. (UKet test)

Front 19

Which takes less to become lethally toxic a 10kg patient?
Ethylene glycol or methanol

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Ethylene glycol
(though both are considered one sip toxic agents)

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Most common source of cyanide?
Primary mechanism of toxicity?

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House fires (cushions)
Reason of airplane fire moralities

Blocks cytochrome oxidase (which is essential for ox phos)

CN and CO are synergistic

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Alcohols are not toxic. What enzyme converts it to a toxic intermediate?

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Alcohol Dehydrogenase (rate limiting step)

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Nitroprusside

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5 CN molecules, toxic with kidney insufficiency. Used in hypertensive emergencies.

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CN antidote?

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Lilly Antidote Kit
New: activated B12

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CN toxicity clinical signs?

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Dysfunction of oxygen sensitive organs (brain, heart)

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Hemoperfusion

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dialysis with activated charcoal (little to gain now)

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When do you use Dialysis?

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mostly with toxic alcohols
(also treated with Ethanol or 4MP)

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Antidote for cyclic anti depressants

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sodium bicarbonate

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Anion Gap formula

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Na-(Cl+HCO3)
Normal ~ 12 +/- 4

CAT MUD PILES

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Most common cause of Anion gap

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Lactic acid, renal failure

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Most commonly missed factor in the difference between calculated and measured osmotic gap?

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Ethanol (therefore, most cases are not in toxic crisis)

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TIBC and serum iron concentration. Implications of Fe toxicity?

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TIBC is normally much greater than serum iron concentration. In toxicity you would expect Serum Iron Concentration to be greater than Total Iron Binding Capacity. Actually, the TIBC is an erroneous measure in this situation. The comparison cannot be used.

Front 32

Iron Toxicity
4 stages

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1. Direct corrosive effect on GI. Fe levels after 6 hours are unreliable.
2. 12-24 hours. Quiescent, "redistributive" phase. Reassuring...
3. Shock and metabolic acidosis develops
4. Weeks later: recuperative. secondary scarring

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TIBC and serum iron concentration. Implications of Fe toxicity?

Back 33

TIBC is normally much greater than serum iron concentration. In toxicity you would expect Serum Iron Concentration to be greater than Total Iron Binding Capacity. Actually, the TIBC is an erroneous measure in this situation. The comparison cannot be used.

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Does Iron bind to activated charcoal?

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NO. deferoxamine - scavenges free iron. (chelation)

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Iron Toxicity
4 stages

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1. Direct corrosive effect on GI. Fe levels after 6 hours are unreliable.
2. 12-24 hours. Quiescent, "redistributive" phase. Reassuring...
3. Shock and metabolic acidosis develops
4. Weeks later: recuperative. secondary scarring

Front 36

Does Fe toxicity harm a fetus?

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Fe does not appear to cross the placenta barrier. Fetal demise is likely due to maternal shock/toxicity. TREAT MOM.

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Does Iron bind to activated charcoal?

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NO. deferoxamine - scavenges free iron. (chelation)

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Two most common toxicities in Pregnant women?

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Tylenol and Iron (though Iron does not cross placental barrier)

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Does Fe toxicity harm a fetus?

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Fe does not appear to cross the placenta barrier. Fetal demise is likely due to maternal shock/toxicity. TREAT MOM.

Front 40

Arsenic: what form is toxic?

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Organic (elemental) is insoluble in water. Therefore it is non-toxic. The inorganic forms are soluble and therefore can be absorbed and are toxic

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Two most common toxicities in Pregnant women?

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Tylenol and Iron (though Iron does not cross placental barrier)

Front 42

Acute toxicity in Arsenic

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Diarrhea (rice-water, cholera like)
sinus tachycardia
shock QTc Prolongation
SEVERE: Encephaopathy, seizures

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Arsenic: what form is toxic?

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Organic (elemental) is insoluble in water. Therefore it is non-toxic. The inorganic forms are soluble and therefore can be absorbed and are toxic

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Organic Arsenic is concentrated in what foods?

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Seafood (therefore urine poison test will test positive)

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Acute toxicity in Arsenic

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Diarrhea (rice-water, cholera like)
sinus tachycardia
shock QTc Prolongation
SEVERE: Encephaopathy, seizures

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Chelation

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binds to metal and forms a ring
(Greek for lobster)

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Organic Arsenic is concentrated in what foods?

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Seafood (therefore urine poison test will test positive)

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First step in Metal poisoning?

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Remove the person from the source (even if its the job)

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Chelation

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binds to metal and forms a ring
(Greek for lobster)

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Normal Lead amount in the body?

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None. there is no biological need for it.

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First step in Metal poisoning?

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Remove the person from the source (even if its the job)

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Normal Lead amount in the body?

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None. there is no biological need for it.

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Manifestation of Lead poisoning in the CNS?

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Overt neurotoxicity classically manifests as encephalopathy.

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Manifestation of Lead poisoning in the CNS?

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Overt neurotoxicity classically manifests as encephalopathy.