Definitions, Tables, Facts

Question 1

Approach to overdose/toxic syndromes

Answer 1

1) resus and management of life threatening feature
2) identify drug and quantity
3) limit absorption/enhance removal
4) Antidotes
5) supportive care

Question 2

Investigations in poisoning

Answer 2

Urinalysis

Biochemistry —> renal and hepatic impairments

ABG

Anion gap (10-14)
	Elevated in ethanol, methanol, EG, metformin, cyanide, salicylate

Osmolar gap (2Na+K+urea+glucose). <10
	Ethanol, methanol and EG

ECG - TCA

Plasma drug levels

Question 3

Ways to limit absorption/force elimination

Answer 3

Induced emesis - NO

Gastric lovage - only within 1 hour. Do not do in corrosive agents

ACtivated charcoal - porous, large SA, binds
DOES NOT BIND - heavy metals, cyanide, alcohol, strong acids/all
1 hour unless slow emptying (opiates)
Entero-hepatic recirculating - carbamazepine, theophylline (4 hours)

Whole bowl irrigation - polyethylene glycol NG, rapid expulsions

Elimination
Forced alkaline diuresis —> iv Sodium bicarb with loop, urine pH>6.5
Acidic drugs are ionic and can’t be reabsorption
Aspirin, methotrexate

RRT if small, water soluble, low protein binding

Haemoperfusion - charcoal cartridge in HD

Question 4

Types of toxidrome

Answer 4

Cholinergic Organophosphates/fungi. Anti cholin-atropine, pralidoxime
Anticholinergic Antihistamines/depressants, Parkinson’s,—> supportive care
Opioid nalaxone

Hypno-sedative Benzos, barbiturates, Alcohiol

Serotinergic antidepressants, Amphet, ecstasy —> benzos and cypoheptadine

Sympatho Amphet, cockiness,salbutamol —> benzoes

Sympathomimetic

Question 5

Pathophys of paracetamol OD

Answer 5

Metabolised by sulphation and glucuronidation

Small part by cp450 to NAPQI

NAPQI detoxed by glutathione

OD - sulphate/gluc stopped

Switching to cp450 —> more NAPQI, glutathione depletes

Degree of toxicity is directly proportional to magnitude of overdose

Question 6

Factors aggregating a paracetamol OD

Answer 6

Pre-existing glutathione depletion —> eating disorder, chronic alcohol, CF, HIV

Induction of the cP450 system - phenytoin, rifampicin, carbamazepine

Question 7

Why does lactate rise in paracetamol OD

Answer 7

Impaired mitochondrial dysfunction —> anaerobic respiration

Due to hepatic failure

Question 8

How does NAC work

Answer 8

Provides reservoir of sulphydryl groups

Stimulates glutathione

Question 9

Side effects of NAC

Answer 9

Rash

Angiooedema

Bronchospasm

THESE ARE NOT A CI ….slow the rate, give an antihistamine

Question 10

Features of salicylate poisoning

Answer 10

Toxic level - CTZ activated, N&V. Resp centre activated—> resp alkalosis

High levels, uncouple cellular resp —> lactic acidosis

Fever
Tinnitus
Hypoglyc
Vertigo
Visual loss
Coag
Pulmonary oedema

Question 11

Management of aspirin oD

Answer 11

AC in one hour

Forced alkaline diuresis —> pH 7.40-7.50m urine to >6.5

HD

Question 12

Mechanism of TCA overdose

Answer 12

Cholinergic antagonisms

Na blockade

Question 13

Features of TCA OD

Answer 13

CVS - tachy, arrhymia, hypotension

Neuro - Dilated pupils, blurred vision, seizures

Resp - depression

GI - dry mouth, prolonged transit

Warm dry skin urine retention

Question 14

Key Ix of TCA OD

Answer 14

ECG, 12 lead and continuous monitor (wide WRS)

ABG

Question 15

Management of TCA od

Answer 15

ABCDE

Activated charcoal, and can be repeated

Intubation if low GCS

observe QRS and BP, (>100ms) increase pH
hyperventilate
iv sodium bicarbonate (also high sodium load to prevent blockade)

Arrhythmia - bicarb, magnesium, lidocaine

Care reports of lipid emulsions

Seizure - benzos