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Clinical pharmacology and therapeutics > Toxicology > Flashcards

Toxicology Flashcards

1
Q

In general how do you recognise poisioning?

A

Non specific symptoms
High index of suspicion
Course that a poison runs - toxidromes
Toxicology screening only helpful in a few

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2
Q

Describe the clinical presentation of anticholinergics

A

Increased HR, BP, temp
Dilated pupils
Decreased bowel sounds and diaphoresis

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3
Q

Describe the clinical presentation of cholinergics

A

Constricted pupils

Increased bowel sounds and diaphoresis

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4
Q

Describe the clinical presentation of opioids

A

Decreased HR, BP, RR, temp, bowel sounds and diaphoresis

Constricted pupils

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5
Q

Describe the clinical presentation of sympathomimetics

A

Increased HR, BP, temp, bowel sounds and diaphoresis

Dilated pupils

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6
Q

Describe the clinical presentation of sedatives - hypnotics

A

Decreased HR, RR, BP, temp, bowel sounds and diaphoresis

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7
Q

What is acetyl choline made from?

A

Choline and acetyl CoA

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8
Q

What happens to acetyl CoA in the synaptic cleft?

A

Broken down by acetylcholinesterase to choline and acetyl CoA

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9
Q

List some drugs that cause bradycardia

A 
Beta blockers and opiates
Anticholinergics 
Calcium channel blockers
Ethanol 
Digoxin
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10
Q

List some drugs that cause tachycardia

A

Free base - cocaine
Anticholinergic
Sympathomimetic
Theophylline, thyroid hormones

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11
Q

List some drugs that cause hypothermia

A 
Carbon monoxide 
Opiates 
Oral hypoglycaemics, insulin 
Liquor 
Sedative hypnotics
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12
Q

List some drugs that cause hyperthermia

A

Nicotine
Antihistamines
Salicylates, Serotonin syndrome
Anticholinergics and antidepressants

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13
Q

List some drugs that cause hypotension

A 
Clonidine, calcium channel blockers (and beta blockers)
Reserpine (other antihypertensives)
Antidepressants
Sedative-hypnotics
Heroin (opiates)
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14
Q

List some drugs that cause hypertension

A 
Cocaine
Thyroid supplements
Sympathomimetic
Caffeine
Anticholinergic, amphetamines
Nicotine
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15
Q

List some drugs that increase respiratory rate

A

PCP
ASA, amphetamines
Non-cardiogenic pulmonary oedema
Toxin induced metabolic acidosis

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16
Q

List some drugs that decrease RR

A

Sedatives, strychnine, snakes
Liqour
Opiates, organophosphates
Weed

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17
Q

Which drugs can we perform lab assessments for?

A

Paracetamol levels, salicylate levels, alcohol, anti-epileptic drug levels

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18
Q

Which drugs does a urinary drug screen test for?

A

opiates, barbiturates, benzodiazepines, amphetamines, cocaine

19
Q

What is a normal anion gap?

A

Normal 12 ± 4 mEq/L

20
Q

Which drugs increase the anion gap

A

Ethylene glycol
Methanol
Salicylate poisoning

21
Q

What is a normal osmolal gap

A

Normal 5 ± 7 m osmol/kg

22
Q

Which drugs increase the osmolal gap?

A

Ethylene glycol
Methanol
Acetone, ethanol, isopropyl alcohol, propylene glycol

23
Q

What drugs is an ECG good at detecting

A

Digoxin toxicity
TCA overdose - sinus tachycardia, QT prolongation, increased QRS
Beta-blockers - conduction abnormalities

24
Q

What are the goals of toxicology treatment

A

Reduce absorption of the toxin (xenobiotic)

Enhance elimination

Neutralise toxin

25
Q

Describe the actions of paracetamol

A 
Analgesia
Relieves mild to moderate pain
Efficacy equivalent to salicylates
Inhibits brain prostaglandin synthetase
Blocks pain impulses peripherally

Antipyrexic
Efficacy similar to salicylates
Inhibits prostaglandin synthetase in the hypothalamus

26
Q

Describe the absorption of paracetamol

A

Rapidly absorbed from the GI tract
Peak concentration – between 60 and 120 minutes
Peak plasma levels - within 4 hours
Quicker with liquid preparations

27
Q

Describe the distribution of paracetamol

A

Approximately 20% plasma protein bound - may increase to 50% in overdose
Has been reported to cross the placenta

28
Q

Describe paracetamol metabolism

A

Occurs via several pathways in the liver

52% by sulfation
42% by glucuronidation
2% excreted unchanged in the urine
4% biotransformed by C-P450 MFO system

29
Q

Describe paracetamol excretion

A

metabolic products are excreted by the kidneys

minimal excretion into breast milk

30
Q

Describe the conjugation of paracetamol

A

In a healthy individual, about 95% of paracetamol is conjugated with glucuronide and excreted in the urine. Most of the remainder is conjugated with glutathione.

31
Q

What is the toxic dose of paracetamol

A

Adults > 150 mg/kg in acute dose
Adults > 7.5 Grams in 24 hours (chronic)
Children (<10 yrs): > 200 mg/kg

32
Q

Describe phase 1 paracetamol toxicity

A

30mins - 4 hrs

Within a few hours after ingestion, patients experience anorexia, nausea, pallor, vomiting, and diaphoresis. Malaise may be present.

Patient may appear normal

33
Q

Describe phase 2 paracetamol toxicity

A

24-48 hrs

may seem like a period of recovery

right upper quadrant pain may be present due to hepatic damage

blood chemistry becomes abnormal with elevations of liver enzymes

prothrombin times may be prolonged

renal function may begin to deteriorate

34
Q

Describe phase 3 paracetamol toxicity

A

3-5 days

characterized by symptoms of hepatic necrosis
coagulation defects/ jaundice/ renal failure
hepatic encephalopathy
hepatic biopsy - centrilobular necrosis
nausea and vomiting may reappear
death is due to hepatic failure

35
Q

Describe phase 4 paracetamol toxicity

A

Complete resolution or death

36
Q

What is the antidote for paracetamol toxicity

A

N-acetylcysteine (NAC/ Parvolex)

glutathione substitute

37
Q

Describe the mechanism of action of N-acetylcysteine

A

Prevents toxicity if administered in the acute setting

Acts as a precursor for the synthesis of glutathione
Acts intracellularly as a glutathione substitute
Directly binds to NAPQI intracellularly
Enhances reduction of NAPQI to a non-toxic substance

Modifies toxin induced inflammatory response later in clinical course

Increases Nitric Oxide synthesis & EDRF
Acts as antioxidant thus improving oxygen delivery and extraction in extrahepatic organs – brain/ heart/ kidney

38
Q

When is a liver transplant needed for a paracetamol overdose patient?

A 
pH < 7.3 after resuscitation
INR > 6.5 
Creatinine >300mmol/l
Lactate > 3 mmol/l after resuscitation
encephalopathy grade III/IV)
39
Q

List some class A drugs

A

Heroin/ cocaine/ crack/ MDMA (“ecstasy”)/ methamphetamine/ LSD/ psilocybin mushrooms

40
Q

Name some class B drugs

A

Amphetamine/ cannabis/ codeine/ methylphenidate

41
Q

Name some Class C drugs

A

GHB/ ketamine/ diazepam/ flunitrazepam/ and most other tranquillisers/ sleeping tablets/ benzodiazepine as well as anabolic steroids

42
Q

Describe sympathomimetic syndrome

A

CVS tachycardia/ hypertension/ chest pain/ MI

CNS nistagmus/ tremor/ headache/ seizures

Psych. anxiety/ paranoia/ psychosis / hallucinations

Resp. tachypnea/ dyspnea

Metabolic lactic acidosis/ hyper-K/ hypo-Na/ high CK

Ocular mydriasis/ blurred vision/ retinal hemorrhages

GI nausea/vomiting/ diarrhoea/ abdominal pain

43
Q

Describe the management of serotonin syndrome

A

Supportive
Cold IV fluids/ other methods of cooling
Diazepam for agitation and seizures
Metoprolol for Narrow Complex Tachycardia
GTN for hypertension
Close monitoring of the CK – rhabdomyolysis is common

Clinical pharmacology and therapeutics (27 decks)

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