Unconsciousness
Fluids
Substances
Overdose
Random
100

With a patient presenting with impaired consciousness, what would be a critical initial assessment?

A->Es 

Obs 

GCS!!!!! Pupils, BGL

100

A patient presents agitated and hyperthermic after cocaine use. Blood tests reveal hypernatremia.

Explain how stimulant intoxication may lead to hypernatremia.

Excess insensible water loss

  • Hyperthermia
  • Sweating
  • Tachypnoea

Reduced water intake

  • Agitation or altered mental state

Increased sympathetic activity

  • Vasoconstriction
  • Volume depletion

Result

  • Free water loss exceeds sodium loss
  • Plasma sodium concentration rises
100

What is the MOA of cocaine? 

  • Sympathomimetic (stimulant) 
  • Inhibits the reuptake of dopamine, serotonin, adrenaline & noradrenaline 
  • Blocks Na+ channels → slowed neuronal AP transmission → arrhythmias, local anaesthesia, myocardial infarction (vasospastic) 
100

What is the reversal agent for opioid overdose? 

Naloxone: competitive opioid receptor antagonist 

100

How do nerves and muscles contribute to the physiology of pupil constriction and dilation? 

Constriction (miosis)

  • Parasympathetic pathway
  • CN III → ciliary ganglion
  • Sphincter pupillae contracts
  • Pupil constricts

Dilation (mydriasis)

  • Sympathetic pathway
  • Dilator pupillae contracts
  • Pupil dilates
200

List the causes of unconsciousness 

Alcohol / Acidosis

Epilepsy / Electrolytes / Environment (e.g., hyper/hypothermia)

Insulin (hyperglycemia or hypoglycemia)

Overdose / Oxygen deficiency (hypoxia)

Uremia (kidney failure buildup)

Trauma / Temperature

Infection (e.g., sepsis, meningitis)

Psychiatric / Poisons

Stroke / Seizures / Shock / Syncope

200

A patient presents following a heroin overdose with reduced consciousness and respiratory depression. Blood tests later show hyponatraemia.

Explain how opioid overdose may contribute to hyponatraemia.

  • Opioids can stimulate ADH release
  • Increased ADH → increased water reabsorption in collecting ducts
  • Retained water dilutes plasma sodium

Clinical consequences

  • Confusion
  • Reduced consciousness
  • Seizures in severe cases
200

What receptors do opioids bind to and how does that binding cause an effect? 

Opiates are μ (mu) receptor agonists

Binding causes:

  • ↓ adenylate cyclase
  • ↓ cAMP
  • Opening of K⁺ channels → hyperpolarisation
  • Closing of presynaptic Ca²⁺ channels → ↓ neurotransmitter release

Net effect:

  • Reduced neuronal excitability
200

What are two tests you should do in every overdose? 


  • Serum paracetamol concentration, ECG (cardiotoxicity), BGL (reversible)
200

Explain how dysfunction of the reticular activating system (RAS), thalamus and cerebral cortex can each independently produce altered conscious states.


Reticular Activating System (RAS)

Role:

  • Maintains wakefulness and alertness
  • Located in brainstem/midbrain projections
  • Activates thalamus and cortex

RAS dysfunction:

  • Prevents cortical arousal
  • Produces reduced consciousness/coma
  • Can occur in:
    • Brainstem stroke
    • Compression/herniation
    • Sedative overdose

Thalamus

Role:

  • Sensory relay centre
  • Integrates cortical signalling
  • Important for awareness and consciousness

Thalamic dysfunction:

  • Disrupts cortical integration
  • Bilateral thalamic injury may cause coma
  • Metabolic/toxic states impair thalamic activity

Cerebral Cortex

Role:

  • Higher cognition
  • Awareness
  • Attention
  • Memory integration

Diffuse bilateral cortical dysfunction:

  • Causes impaired consciousness
  • Seen in:
    • Hypoxia
    • Hypoglycaemia
    • Drug overdose
    • Sepsis/metabolic encephalopathy
300

Define Delirium, consciousness, coma, brain death

Consiousness: Self-awareness, Access to memories, Ability to manipulate abstract ideas, Focus of attention

Delirium: Acute condition with altered mental state, organic basis, syndrome

Coma: Unrousable unresponsivenss, no response to pain

Brain death: Irreversible loss of brain death, no brainstem reflexes, **not in low temp/drugs**


300

A patient presents with severe vomiting, hypotension and tachycardia. Blood tests show hyponatraemia.

Explain why this patient activates both ADH secretion and the renin–angiotensin–aldosterone system (RAAS), and describe how these responses affect sodium and water balance.

  • Vomiting → loss of extracellular fluid volume
  • Reduced effective circulating volume sensed by:
    • Baroreceptors
    • Kidney afferent arteriole
  • Activates:
    • ADH release
    • RAAS
    • Sympathetic nervous system

ADH effects

  • Increases water reabsorption in collecting ducts
  • Produces concentrated urine
  • Preserves circulating volume

RAAS effects

  • Renin → angiotensin II → aldosterone
  • Aldosterone increases sodium reabsorption in distal nephron
  • Water follows sodium
300

What is the MOA of benzodiazepines? 

  • Bind GABA-A receptor
  • Increase frequency of Cl⁻ channel opening
  • Potentiate GABA inhibition

Effects:

  • Sedation
  • Anxiolysis
  • Muscle relaxation
300

What are the reversible causes of unconsciousness? 

1. Hypovolaemia, hypoxia, H+ (acidosis), hyper./hypokalaemia, hypoglycaemia, hypothermia 

2. Toxins, tamponade, tension pneumothorax, thrombosis, trauma 

300

A patient opens their eyes to a painful stimulus, speaks using inappropriate words, and withdraws their arm when you apply pain. What is their GCS score and how is it written?

GCS = 9 E2V3M4




400

Explain why hypoglycaemia causes altered conscious state.


  • Brain relies on glucose for ATP production
  • Neuronal dysfunction occurs rapidly
  • ↓ cerebral energy supply
  • Leads to confusion, seizures, coma 
400

Explain why hypernatremia causes neurological symptoms and compare this mechanism with neurological dysfunction in hyponatraemia.

Key comparison

  • Hypernatremia → cellular dehydration/shrinkage
  • Hyponatraemia → cellular swelling/oedema
400

What are four effects of opioids in the CNS? 

  • Analgesia
  • Sedation
  • Respiratory depression
  • Euphoria
400

Compare and contrast opioid toxicity, benzodiazepine toxicity and serotonin syndrome with reference to receptor pharmacology, neurotransmitter effects and clinical manifestations.



Opioid toxicity results from μ-opioid receptor agonism causing inhibition of neuronal activity through reduced cAMP production, potassium efflux and decreased neurotransmitter release, producing profound respiratory depression, miosis and reduced consciousness. Benzodiazepine toxicity occurs through potentiation of GABA-A receptor activity by increasing the frequency of chloride channel opening, leading predominantly to sedation, anxiolysis and CNS depression, with less severe respiratory depression unless combined with other sedatives such as opioids. In contrast, serotonin syndrome is caused by excessive serotonergic activity at 5-HT receptors, producing a hyperactive state characterised by agitation, hyperthermia, hyperreflexia and clonus rather than the sedative features seen in opioid or benzodiazepine overdose.

400

At follow up the patient reports back pain and is prescribed tramadol. What is the main drug interaction you would be worried about with this patient? 

  • Serotonin syndrome

Why:

  • Tramadol increases serotonin
  • Combined with escitalopram/mirtazapine

Features:

  • Agitation
  • Hyperreflexia
  • Clonus
  • Hyperthermia

Other concern:

  • Seizures

500

An unconscious patient is brought to the emergency department after suspected polysubstance overdose. Initial assessment reveals hypotension, tachycardia, dry mucous membranes and hypernatremia.

Explain the pathophysiological mechanisms contributing to the patient’s hypernatremia and reduced level of consciousness.

  • Hypernatremia usually indicates a free water deficit
  • In unconscious patients:
    • Reduced ability to access water
    • Impaired thirst response
    • Possible vomiting and insensible fluid losses
  • Water loss exceeds sodium loss → increased plasma osmolality
  • Hypovolaemia activates:
    • ADH secretion
    • Renin–angiotensin–aldosterone system
    • Sympathetic nervous system
  • These mechanisms attempt to conserve sodium and water
  • Despite compensation, ongoing water deficit causes hypertonic extracellular fluid
  • Increased extracellular osmolality causes water to move out of brain cells by osmosis
500

A patient with SIADH is hyponatraemic despite having normal total body sodium.

Explain the mechanism responsible for hyponatraemia in SIADH and why the patient is usually clinically euvolaemic.

  • Excess ADH causes inappropriate water reabsorption
  • Retained water dilutes plasma sodium
  • Hyponatraemia is due to excess water, not sodium deficiency

Why euvolaemic?

  • Mild extracellular volume expansion occurs initially
  • This suppresses:
    • RAAS
    • Aldosterone
  • Promotes natriuresis
  • Sodium excreted until near-normal volume restored
500

What is the management for Alcohol use disorder? 

1. Motivational enhancement (MET)
2. Psychotherapy referral (CBT)

3. Motivational interviewing (Using FLAGS) 

4. Meds: Disulfiram, naltrexone 

500

Explain why co-ingestion of opioids and benzodiazepines significantly increases mortality in overdose patients compared with either drug alone.



Opioids and benzodiazepines both depress central nervous system activity but act through different receptor systems, producing synergistic rather than merely additive respiratory depression. Opioids suppress medullary respiratory centres through μ-opioid receptor agonism, reducing respiratory rate and responsiveness to carbon dioxide, while benzodiazepines potentiate GABA-A receptor activity, further depressing neuronal excitability, consciousness and airway protective reflexes. Together, these effects markedly increase the risk of hypoventilation, hypoxia, aspiration, coma and death, particularly because sedation may delay recognition of respiratory compromise until severe cerebral hypoxia has already developed.




500

What are some symptoms of burn-out that doctors may experience (2marks)

What are three things a junior doctor's supervisor can do to help with this burnout? (1.5 marks)

1. Emotional exhaustion, depersonalisation, diminished sense of self worth. Primarily driven by workplace stressors and excessive workload

Actions 

1. Workload modifications, rest breaks 

2. Mentorship & well-being check ins. Clinical supervisor 

3. Refer to EAP (employee assistant program) 

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