Poisoning and Overdose Flashcards

Question

Is activated charcoal effective in iron poising?

Answer 1

* **Serum iron concentration** (peak levels occur 4-6 hours following iron ingestion) * Blood gas * Abdominal x ray (confirm ingestion) * LFTs. coag - hepatic failure * U&Es - renal failure

Answer 2

* A-E * Fluid resuscitation: boluses of 10-20 mL/kg crystalloid to prevent shock from gastrointestinal losses, vasodilation and third spacing **Whole bowel irrigation** is the decontamination procedure of choice - performed on all patients **presenting within 4 hours** who have** ingested > 60mg/kg elemental iron** or have **undissolved tablets** on abdominal x-ray. **Desferrioxamine** = antidote ## Footnote Activated charcoal = useless in iron overdose

Answer 3

* Patients taking **liver enzyme-inducing drugs** (**rifampicin**, phenytoin, **carbamazepine**, **chronic alcohol excess**, **St John's Wort**) * **Malnourished patients** (e.g. anorexia nervosa) or patients who have not eaten for a few days

Answer 4

* During an **overdose** the **conjugation system becomes saturated** leading to oxidation by P450 mixed function oxidases * This produces a **toxic metabolite** (**N-acetyl-B-benzoquinone imine** - **NAPQI**) * Normally glutathione acts as a defence mechanism by conjugating with the toxin * If **glutathione stores run-out**, the toxin forms covalent bonds with cell proteins, denaturing them and leading to **cell death**. This occurs not only in **hepatocytes** - but also in the **renal tubules** * **N-acetyl cysteine = first-line** → as it is a precursor of glutathione → hence can increase hepatic glutathione production ## Footnote This explains why there is a lower threshold for treating patients who take P450 inducing medications e.g. phenytoin or rifampicin

Answer 5

Symptoms: * Nausea & vomiting * Anorexia * Malaise * Abdominal pain * Altered mental status * Confusion Signs: * Asterixis * Bruising * Jaundice * Right upper quadrant pain * Oliguria/anuria * Tachycardia/hypotension * Coma

Answer 6

Diagnosis = made from pt or collateral history: * **Acute ingestion** (ingestion of a potentially toxic dose of paracetamol within one hour or less) * **Staggered ingestion** (excessive ingestion of paracetamol over a period longer than one hour, usually in the context of self-harm) * **Unknown time of ingestion** (should be treated as 'staggered overdose') * **Delayed presentation** (delay between the time of overdose and presentation to medical care) * **Unintentional** (unintentional use of excess paracetamol with the intent to treat an underlying problem (e.g. pain, fever) without intention of self-harm)

Answer 7

**Diagnosis of paracetamol overdose is based on the history** - but **investigations** are needed to assess for **complications**. * Full blood count * Urea & electrolytes * **Liver function tests** (esp. **INR** and **ALT**) * Bone profile * Venous/arterial blood gas (pH, bicarbonate, lactate) * Blood glucose * **Paracetamol levels** * Salicylates levels: should always be requested in acute overdose

Answer 8

The **paracetamol ingestion graph** or ‘**nomogram**’ ## Footnote Look at Pulse Notes for DETAILED management for paracetamol overdose

Answer 9

Therapeutic range: 0.4-1.0 mmol/L Toxicity: > 1.5 mmol/L ## Footnote Lithium has a long plasma half-life - being excreted primarily by the kidneys

Answer 10

* Dehydration * Renal failure * Drugs: diuretics (especially thiazides), ACE inhibitors/angiotensin II receptor blockers, NSAIDs and metronidazole.

Answer 11

CHAPS! * **C**oarse tremor (a fine tremor is seen in therapeutic levels) * **H**yperreflexia * **A**cute confusion * **P**olyuria * **S**eizure * Coma

Answer 12

* Mild-moderate: **IV fluids** with isotonic saline * Severe: **Haemodialysis** ## Footnote Monitor serum sodium closely if there is a concern of lithium-induced nephrogenic diabetes insipidus

Answer 13

* **CNS**: agitation, tremor, anxiety, confusion, somnolence, syncope, hallucinations, changes in perception, acute psychosis, nystagmus, convulsions and coma. * **Cardiac**: tachycardia, hypertension, chest pain, palpitations, ECG changes. * **Renal**: acute kidney injury. * **Muscular**: hypertonia, myoclonus, muscle jerking and myalgia. * **Other**: cold extremities, dry mouth, dyspnoea, mydriasis, vomiting and hypokalaemia

Answer 14

Cocaine = blocks the uptake of dopamine, noradrenaline and serotonin

Answer 15

**Cardiovascular** * Coronary artery spasm → myocardial ischaemia/infarction * Both tachycardia and bradycardia may occur * Hypertension * QRS widening and QT prolongation * Aortic dissection **Neurological** * Seizures * Mydriasis * Hypertonia * Hyperreflexia **Psychiatric effects** * Agitation * Psychosis * Hallucinations **Others** * ischaemic colitis is recognised in patients following cocaine ingestion. This should be considered if patients complain of abdominal pain or rectal bleeding * Hyperthermia * Metabolic acidosis * Rhabdomyolysis

Answer 16

* First-line: **benzodiazepines** Chest pain: * Benzodiazepines + glyceryl trinitrate * MI → PCI Hypertension: Benzodiazepines + sodium nitroprusside ## Footnote Cocaine toxicity → BENZODIAZEPINES

Answer 17

* **Neurological**: agitation, anxiety, confusion, ataxia * **Cardiovascular**: tachycardia, hypertension * **Hyponatraemia** → this may result from either syndrome of inappropriate ADH secretion or **excessive water consumption** whilst taking MDMA * **Hyperthermia** * **Rhabdomyolysis**

Answer 18

* Supportive * **Dantrolene** may be used for **hyperthermia** if simple measures fail

Answer 19

* When inhaled, nitrous oxide acts as a **dissociative anaesthetic** → **blocking** the **NMDA receptors** → thus impairing the perception of pain → inducing a state of **euphoria + relaxation** * It also causes the **release** of **endogenous opioids** + **dopamine** → contributing to its **addictive potential**

Answer 20

Psychological symptoms: * euphoria * altered perception of reality * hallucinations * anxiety * paranoia Neurological symptoms: * dizziness * headache * incoordination * numbness * tremors Physiological effects: * hypoxia * hypothermia * elevated heart rate and blood pressure

Answer 21

* Vitamin B12 deficiency * Degeneration of the spinal cord → causing irreversible neurological impairments * Psychological issues: psychological dependcies → leading to mood disorders, anxiety etc * Physical harm: risk of lung damage, barotrauma and frostbite

Answer 22

* Heightening or distortion of sensory stimuli * Enhancement of feelings + introspection

Answer 23

Patients with LSD toxicity typically present following: * Acute panic reactions (known as bad trips) * Massive ingestions * Unintentional ingestions.

Answer 24

* Variable subjective experiences * **Impaired judgements** → which can lead to **injury** * Amplification of current mood → which leads to **euphoria** or **dysphoria** * **Agitation**, appearing **withdrawn** - especially in inexperienced users * **Drug-induced psychosis**

Answer 25

Somatic symptoms * Nausea * Headache * **Palpitations** * **Dry mouth** * Drowsiness * **Tremors** Signs * Tachycardia * Hypertension * **Mydriasis** * **Paresthesia** * Hyperreflexia * Pyrexia | Mydriasis = dilation of pupils

Answer 26

* Respiratory arrest * Coma * Hyperthermia * Autonomic dysfunction * Bleeding disorders

Answer 27

* Mainly diagnosis from history * Most urine drug screens do not pick up LSD

Answer 28

* Agitation → calm environment → benzos if needed * LSD-induced psychosis = may require antipsychotics * Massive amounts → respiratory support + intubation if needed; hypotension treated with fluids ## Footnote Because LSD is rapidly absorbed through the gastrointestinal tract, activated charcoal administration and gastric emptying are of little clinical value by the time a patient presents to the emergency department.

Answer 29

* Rhinorrhoea * Needle track marks * Pinpoint pupils * Drowsiness * Watering eyes * Yawning

Answer 30

* Viral infection secondary to sharing needles: HIV, hepatitis B & C * Bacterial infection secondary to injection: infective endocarditis, septic arthritis, septicaemia, necrotising fasciitis * Venous thromboembolism * Overdose may lead to respiratory depression and death * Psychological problems: craving * Social problems: crime, prostitution, homelessness

Answer 31

IV or IM **naloxone** (Has a rapid onset and relatively short duration of action)

Answer 32

* Needle exchange * Offer testing for HIV, hepatitis B & C

Answer 33

MAINTENANCE THERAPY or DETOXIFICATION First-line for **detoxification**: **Methadone** or **buprenorphine** Compliance = monitored using urinalysis Duration of opioid detoxification: * Inpatient/residental - up to 4 weeks * Community - up to 12 weeks

Answer 34

**Methadone** = **full agonist** of the **mu-opioid receptor** - binds to these receptors in the brain and fully activates them. * This action can relieve withdrawal symptoms and cravings. * Has a long half-life **Buprenorphine** = **partial agonist** of the **mu-opioid receptor** + an **antagonist** of the **kappa-opioid** * Partially activates mu-opipoid receptors in the brain → enough to alleviate cravings + withdrawal symptoms ## Footnote The binding of buprenorphine to the mu-opioid receptor is very strong, or 'high affinity,' meaning it can displace other opioids from these receptors and prevent them from exerting their effects. As a kappa-opioid receptor antagonist, buprenorphine may contribute to its ability to reduce symptoms of opioid withdrawal and potentially reduce depressive and dysphoric states.