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ICM > Toxicology > Flashcards

Toxicology Flashcards

1
Q

What would be your approach to toxicological emergencies?

A 
Resuscitation
Identify agent and quantify exposure
Drug manipulation to limit absorption
Specific antidotes
General supportive care
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2
Q

What is the anion gap?

A

AG is elevated by presence of unmeasured anions in plasma:

Na + K) - (Cl + HCO3
Normal is 10-14mmol/l

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3
Q

What causes a raised anion gap caused by drugs?

A 
Metformin & Methanol
Isoniazid
Cyanide
Ethylene glycol & Ethanol
Salicylate
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4
Q

What are the causes of a raised anion gap?

A

Cyanide
Alcohol ketoacidosis/ starvation ketoacidosis
Toluene

Metformin/ Methanol
Uraemia
DKA
Paracetamol/ Paraldehyde/ Propylene glycol
Isoniazid/ Iron
Lactic acidosis
Ethylene glycol
Salicylates
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5
Q

What is the osmolar gap?

A

Measured - Calculated Osmolality

2Na + K + Urea + Glucose

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6
Q

What is a normal osmolar gap?

A

<10mosm/l

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7
Q

What causes a raised osmolar gap?

A

A raised osmolar gap is >=10mosml

Benzodiazepines
Sorbitol
Mannitol/ methanol

Phenytoin
IVIg
TURPS (Glycine)
Ethylene glycol/ ethanol

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8
Q

What causes a normal anion gap acidosis?

A

Normal anion gap 10-14

Addisons/ Acetazolamide
Bicarbonate loss (GI / renal)
Chloride excess

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9
Q

What causes a low anion gap?

A 
Multiple myeloma (IgG)
Electrolytes (raised - you only get a medal if you score highly! - Na/ Ca/ Mg)
Dilutional
Albumin loss/ Amphotericin
Lithium
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10
Q

Where is ethylene glycol found?

A 
Anti-freeze
Coolant fluids
Detergents
Brake fluids
Plastics/ polymer industry
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11
Q

What drugs does activated charcoal NOT bind?

A

Heavy metals
Alcohol
Strong acids/ alkalis
Cyanide

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12
Q

What is forced alkaline diuresis?

A

Used to eliminate acidic drugs with a low pKa such as aspirin, methotrexate and phenobarbital

Infusion of IV Bicarbonate + IV diuretic to target urinary pH 7.5

The acidic drug molecules are converted to the ionic form in the glomerulus and so not reabsorbed

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13
Q

What are the properties of drugs removed by RRT?

A

Small molecules
Water soluble
Low protein binding
Small Vd

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14
Q

What drugs are removed by RRT?

A

Beta blockers
Dabigatran
Sodium valproate/ sotalol
Metformin/ methotrexate

Anticonvulsants (Phenytoin, carbamazepine, barbiturates)
Lithium

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15
Q

What are the features of a cholinergic toxidrome:

A 
Salivation
Lacrimation
Urination
Diarrhoea
Gastric cramping
Emesis

Confusion, decreased GCS, bradycardia, sweating, hypotension

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16
Q

What are the causes of a cholinergic toxidrome?

A 
Organophosphates
Nerve agents (Novichok)
Cholinesterase inhibitor overdose
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17
Q

What are the management principles of a cholinergic toxidrome?

A

Anti-cholinergics (atropine)
Anti-cholinesterase reactivator (pralidoxime)
Benzodiazepine

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18
Q

What are the features of an anti-cholinergic toxidrome?

A 
Dilated pupils
Delirium
Flushing
Fever
Tachycardia
Hypotension
Urinary retention
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19
Q

What are the causes of an anti-cholinergic toxidrome?

A 
Anti-histamines
Anti-depressants
Anti-Parkinsonian
Anti-psychotics
Atropine
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20
Q

What is the treatment of an anti-cholinergic toxidrome?

A

Supportive

  • Cool
  • Fluids
  • Benzos for seizures
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21
Q

What are the features of serotonin syndrome?

A

Triad of:

  • Altered mental status
  • Autonomic dysfunction
  • Neuromuscular hyperactivity (increased temp, seizures, rhabdomyolysis)

Hunters criteria (one of):

  1. Spontaneous clonus
  2. Inducible clonus and agitation
  3. Nystagmus and agitation
  4. Increased temperature and nystagmus or clonus
  5. Tremor and hyper-reflexia
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22
Q

What are the causes of serotonin syndrome?

A

SSRIs
Amphetamines
Ecstasy

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23
Q

What is the treatment of serotonin syndrome?

A

Benzodiazepines

Cyproheptidine (serotonin antagonist)

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24
Q

What are the features of a sympathomimetic toxidome?

A 
Paranoia/ delirium
Hyper-reflex is
Tachycardia
Hypertension
Diaphoresis
Piloerection
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25
Q

What are the causes of sympathomimetic toxidrome?

A

Cocaine
Amphetamines
Salbutamol

26
Q

How is paracetamol metabolised?

A

Metabolised in the liver to gluconuride metabolites
Small amount metabolised by the P450 enzyme system to NAPQI (toxic)
NAPQI is bound to glutathione and renally excreted
In paracetamol OD the usual metabolism is overwhelmed, NAPQI production exceeds glutathione stores and NAPQI levels rise which results in toxicity

27
Q

What is the antidote for paracetamol and how does it work?

A

N-acetylcysteine works by binding NAPQI and stimulating glutothione production

28
Q

How does salicylate poisoning present?

A 
Fever
Tinnitus
Hypoglycaemia
Vertigo
Visual disturbance
Coagulopathy
Pulmonary oedema
Vomiting (activates CTZ)
Respiratory alkalosis
29
Q

What is the treatment of salicylate poisoning?

A

Forced alkaline diuresis

HD

30
Q

How does tricyclic antidepressant overdose present?

A
  1. Anti-cholinergic sydrome (SLUDGE)
  2. Na channel blockade
Seizures, coma
Tachycardia, Arrythmia prolonged QRS, hypotension
Respiratory depression
Dry mouth, prolonged gastric transit
Urinary retention
31
Q

What is the management of TCA overdose?

A
  • Activated charcoal
  • Sodium bicarbonate/ hyperventilation (to increase pH and reduced ionised free drug; NaHCO also increases Na load to overcome Na blockade)
  • Lipid emulsion
32
Q

What are the features of neuroleptic malignant syndrome?

A 
NMS is due to dopaminergic blockade
Triad of:
- Fever
- Rigidity
- Autonomic instability
Also:
- Increased CK
33
Q

What causes neuroleptic malignant syndrome?

A 
Anti-psychotics
Dopamine antagonists (metoclopramide)
Rapid withdrawal of dopamine agonists (levodopa)
34
Q

What is the treatment of neuroleptic malignant syndrome?

A 
Dantrolene
Bromocroptine (dopamine agonist)
35
Q

What are the toxic effects of alcohols? (Methanol and Ethylene glycol)?

A

Methanol:

  • Metabolic acidosis
  • Optic nerve toxicity (blindness)

Ethylene glycol:

  • Cerebral oedema
  • Metabolic acidosis
  • Renal failure
36
Q

What is the antidote for alcohol poisoning and how does it work?

A

Fomepizole

  • Key enzyme of alcohol metabolism is alcohol dehydrogenase
  • Fomepizole inhibits alcohol dehydrogenase so preventing the metabolism of alcohol to toxic products
37
Q

What is the pathophysiology of cyanide poisoning?

A

Cyanide reversibly binds to and inhibits cytochrome oxidase within the mitochondria, disrupting the electron transport chain and blocking aerobic respiration —> cytotoxic hypoxia

38
Q

What are the features of cyanide toxicity?

A
  • Confusion, seizures, tachypnoea, coma

- Lactic acidosis and raised ScvO2

39
Q

What is the management of cyanide toxicity?

A

CAUTION - can be absorbed through skin
Antidotes:
- Amyl nitrate: converts Hb to metHb for which cyanide has a higher affinity (can result in failure of oxygen delivery)
- Hydroxocobalamin: binds cyanide to form cyanocobalamin - excreted in urine
- Sodium thiosulfate: binds cyanide to form thiocyanite (slow)
- Dicobalt edetate: colabate binds cyanide (toxic - administer with glucose)

40
Q

What are the features of CO poisoning and why do they occur?

A

Features include:

  • Mild confusion to coma
  • Cherry red skin or cyanosed
  • COHb >40% = life threatening, >60% = fatal

CO binds to Hb with a higher affinity than O2, shifting the O2 dissociation curve to the left. It also binds cytochrome oxidase, uncoupling cellular respiration (Like cyanide)

41
Q

What are the features of paraquat poisoning?

A 
Abdominal pain
Vomiting
Local corrosive effects
Dyspnoea (due to pulmonary oedema —> pulmonary fibrosis - accelerated by oxygen)
Cardiac, renal and hepatic dysfunction

Paraquat is founds in pesticides and has a low fatal dose with rapid onset

42
Q

What is the management of paraquat poisoning?

A
  • Minimise oxygen
  • Cyclophosphamide/ methylprednisolone
  • Palliative care
43
Q

What is the management of beta blocker/ calcium channel blocker overdose?

A
  • Fluids
  • Atropine
  • Inotropes/ vasopressors
  • Electrical pacing
  • Calcium chloride infusion
  • Glucagon: increases intracellular cAMP (positive inotrope)
  • HDIT
  • VA-ECMO
44
Q

What are the risk factors for digoxin toxicity?

A
  • Drug interactions: amoxicillin, clarithromycin, amiodarone,quinine
  • Reduced excretion: AKI
  • Electrolyte abnormalities: hypoMg, hypoK, hyperNa, hyperCa
45
Q

How does digoxin toxicity present?

A
  • Bradycardia, hypotension

- ECG change: AV block, paroxysmal tachycardia with AV block, sinus Brady, ventricular tachycardia

46
Q

What is the management of digoxin toxicity?

A
  • AC
  • Electrolyte correction
  • Atropine
  • Digibind (antibody fragments which bind digoxin)
47
Q

What are the features of lithium toxicity?

A

Neurological: ataxia, dysarthria, tremor, seizures, coma
GI: N+V, diarrhoea
Renal: Polyuria, AKI

48
Q

What is the management of lithium toxicity?

A
  • HD

- Keep Na raised as impedes renal clearance

49
Q

What is the pathophysiology of propofol infusion syndrome?

A

Prolonged infusion of high dose propofol (>4mg/kg/h)

Impaired mitochondrial function

50
Q

How does propofol infusion syndrome present?

A

Metabolic acidosis
Rhabdomyolysis
Bradyarrythmias
Myocardial dysfunction

51
Q

What is DRESS syndrome?

A

Drug Related Eosinophilia and Systemic Symptoms

A severe drug reaction with ~10% mortality

52
Q

What are the causes of DRESS syndrome?

A

Anticonvulsants: Phenytoin, carbamazepine, sodium valproate
Antibiotics: Cefotaxime, Linezolid, Metronidazole, Vancomycin
Antidepressants: Fluoxetine
Antihypertensives: Amlodipine, Captopril
Allopurinol
Antiinflammatories: NSAIDs

53
Q

How does DRESS syndrome present?

A

A delayed response - 2-6 weeks after exposure

  • Fever
  • Rash
  • Lymphadenopathy
  • Haematological and hepatic are most common systemic complications

**Eosinophilia only present in 30% of cases, however leukocytosis is common

54
Q

What are the differentials for DRESS syndrome?

A

Steven-Johnson Syndrome/ Toxic Epidermal Necrolysis: Commonly with bullae and epidermal necrosis; faster onset of 1-3 weeks

Also consider: chemical/ toxins, GVHD, toxic shock syndrome (staph scalded skin)

55
Q

What is the management of DRESS syndrome?

A

Withdraw the offending agent
Steroids
Supportive care
Consider referral to a burns centre

56
Q

What is Steven Johnson Syndrome and TENs

A

Steven Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are rare, acute and potentially lethal reactions that result in epidermal detachment and mucosal loss

SJS has <10% TBSA involvement
TEN has >30% TBSA involvement

They are immune mediated hypersensitivity reactions that are usually caused by drugs (75%) but also infection (25%)

57
Q

What are the risk factors for SJS/ TEN?

A

Antibiotics: Co-trimoxazole (thus increased risk in HIV patients treated prophylactically)
Anticonvulsants: Carbamazepine, Phenytoin, Sodium Valproate
Bacterial infections: Mycoplasma pneumonia
Viral infections: Herpes, EBV, CMV
Other drugs: Paracetamol, NSAIDs, steroids (thus increased risk in patients with conditions such as SLE)
Radiotherapy
Genetic predisposition

58
Q

What are the clinical features of SJS/ TEN?

A 
Prodromal flu like illness
Skin rash
Mucosal ulceration
Macular skin rash progressing to blistering
Desquamation
Epidermal detachment with pressure
59
Q

What is the management of SJS/ TEN?

A

Withdraw any offending agent
Refer to dermatology and plastic surgeons
If >10% should be transferred to burns centre
Fluid resuscitation
Heat preservation
Treat as a burns patient
Strict barrier nursing
Eye care
Oral hygiene/ nutrition support
Analgesia (avoid NSAIDs, consider procedural sedation)

60
Q

Why does Albumin effect the anion gap?

A

It is a negatively charged protein, a fall in albumin will result in an overestimation in anion gap

For every 1g, subtract .25

ICM (16 decks)

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