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ED Primary Exam > Week 20 Pharmacology - Toxicology > Flashcards

Week 20 Pharmacology - Toxicology Flashcards

1
Q

What effect does large volume of distribution have on ability for drug to be cleared via dialysis?

A

Large Vd = not readily cleared by dialysis

i.e. antidepressants, amphetamines, benzodiazepines, CCB, digoxin, beta blockers, opioids

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2
Q

What drugs have low Vd and are well cleared via dialysis?

A

Salicylates, ethanol, lithium, phenytoin, valproate, phenobarbital

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3
Q

What is the RRISDEAD acronym?

A

Resuscitation
Risk assessment
Supportive care
Investigations
Decontamination
Enhanced elimination
Antidotes
Disposition

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4
Q

What does the risk assessment in toxicology assessment entail?

A

What drug, coingestions
Time since ingestion
Amount taken
Formulation/route

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5
Q

What drug/toxin should be suspected with tachycardia, hypertension?

A

Amphetamines
Cocaine
Anticholinergic drugs

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6
Q

What drug/toxin should be suspected with bradycardia, hypotension?

A

CCBs
Beta blockers
Clonidine
Sedative hypnotics

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7
Q

What drug/toxin should be suspected with tachycardia and hypotension?

A

TCAs
Beta-agonists
Quetiapine
Vasodilators (I,e, GTN, hydralazine)

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8
Q

What ingestions can cause miosis?

A

Opioids
Clonidine
Cholinesterase inhibitors

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9
Q

What ingestions can cause mydriasis?

A

Amphetamines
Anticholinergic drugs

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10
Q

What ingestion classically causes tachypnoea and respiratory alkalosis?

A

Salicylates

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11
Q

What are common causes of prolonged QT interval in overdose?

A

TCAs, antipsychotics, lithium, anti-arrhythmic, macrolides

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12
Q

What is the most common cause of death in overdose?

A

Airway compromise, due to respiratory depression, loss of airway protective reflexes, aspiration of gastric contents, obstruction with flaccid tongue

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13
Q

What are the causes of mortality in overdose RE cardiovascular system?

A
  1. CVS collapse/toxicity due to cardiac depression, hypovolaemia due to vomiting, blockade of peripheral alpha 1 receptors
  2. Cardiac arrhythmia: VT or VF secondary to either cardiac active drugs (adrenaline, amphetamines, cocaine, digoxin) and non CVS drugs (TCA, antidepressants, anti-histamines)
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14
Q

What agents can causes seizures?

A

Antidepressants
Amphetamines
Ioniazid
Withdrawal from EtOH

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15
Q

What is the toxic effect of paraquat?

A

Generation of reactive oxygen species, causing alveolar fibrosis , poor prognosis

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16
Q

What is the pathway of metabolism of paracetamol, and what are the toxic metabolites?

A

95% of Paracetamol is metabolised via glucouronidation and sulfation reactions into harmless metabolites.

5% is metabolised via YP450-dependent metabolic pathway, which generates NAPQI + superoxide anions. Normal conditions, NAPQI is rapidly conjugated with glutathione. Superoxide anions can cause oxidative stress.

Where in excess, glutathione stores are exhausted and NAPQI concentration increases.

17
Q

How does NAPQI cause toxic effect?

A

Uncoupling of oxidative phosphorylation via inhibition of cytochrome enzymes, lactic acidosis, release of intracellular calcium stores and apoptosis –> massive liver injury and cell death

18
Q

What is the approach to treatment of methamphetamine induced seizure, hyperthermia, rhabdomyolysis?

A

IV benzodiazepines, cooling techniques for hyperthermia

19
Q

What is anticholinergic syndrome?

A

Red as a beet
Hot as a hare
Dry as a bone
Mad as a hatter
Blind as a bat

20
Q

What are common features of clinical findings for someone with anticholinergic poisoning?

A

Sinus tachycardia
Mydriasis
Urinary retention
Agitated delirium

21
Q

What are general principles of anticholinergic poisoning management?

A

Supportive cares
Benzodiazepines
Urinary catheterisation

+/- consideration of anticholinesterase inhibitor (physostigmine)

22
Q

What are the general principles of managing anti-depressant overdose? (TCA in particular)

A

MoA = anticholinergic, antihistamine, Na+ channel blockage

Supportive therapy = mainstay, important to obtain ECG and administer sodium bicarbonate if widening QRS

If hypotension, IVF and consideration of noradrenaline

23
Q

What is a toxic dose of aspirin/salicylate?

A

> 200mg/kg

24
Q

What is the mechanism of toxicity in aspirin?

A

Uncoupling oxidative phosphorylation, metabolic disruption.

25
Q

How does aspirin overdose present?

A

Initially increased RR and respiratory alkalosis, followed by profound metabolic acidosis and lactaemia

26
Q

What form of enhanced elimination can be considered in aspirin overdose?

A

Sodium bicarbonate to increase urinary alkalisation and trap salicylic acid in ionic form.

Also haemodialysis can be effective in severe cases.

27
Q

Are beta blockers selective for B1/B2 in high doses?

A

No, lose selectivity

28
Q

What physical observations and ECG findings are associated with beta blocker OD?

A

Bradycardia
Hypotension
Wide QRS complex on ECG

29
Q

What is the treatment for ethylene glycol/methanol OD?

A

IV Fomepizole, an alcohol dehydrogenase inhibitor

Less commonly, IV ethanol

30
Q

What does activated charcoal NOT work for?

A

Anything on the periodic table! Also corrosive mineral acids and alkali

31
Q

What time frames would be considered for administering activated charcoal?

A

2 hours immediate release, 4 hours modified

32
Q

Using ADME framing, what are pharmacokinetic changes associated with ageing?

A

A: minimal (can be altered by antacid, laxative use, nutritional habits, changes in gastric emptying)

D: Reduced lean body mass, body water, and have increased fat percentage. Reduced serum albumin, usually = increased free drug circulating

M: Liver capacity decines with age (reduced clearance of benzos, barbiturates, propranolol, theophylline) - greatest impact on phase I reactions (P450)

E: Age related decline in creatinine clearance

33
Q

What are the criteria for classification of a teratogen?

A

1) Result in characteristic set of malformations
2) Exert effect at particular stage of foetal development
3) Dose dependent incidence

34
Q

What are some examples of drugs unsafe in pregnancy?

A

ACEi –> renal injury
Warfarin
NSAIDs
Phenytoin
Valproate
Carbamazepine
Lithium

35
Q

What syndrome is precipitated by lack of VitB1?

A

Wenicke’s Encephalopathy –> Thiamine

36
Q

What is pellagra caused by?

A

Vit B3 deficiency (Niacin)

Dementia
Diarrhoea
Dermatitis
Death

37
Q

What is the clinical triad of serotonin syndrome?

A
  1. Mental state changes: agitation, anxiety, delirium
  2. Autonomic changes/instability: inc. temp, tachycardia, HTN, diaphoresis
  3. Neuromuscular abnormalities: hyperreflexia, clonus
38
Q

What is neuroleptic malignant syndrome precipitated by?

A

Dopamine antagonism:
- Antiemetics: metoclopramide, promethazine
- Antipsychotis: haloperidol, chlorpromazine, clozapine, risperidone

39
Q

What are the features of NMS?

A

Muscle rigidity/bradykinesia
Febrile
Tachycardia

ED Primary Exam (46 decks)

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