Arnold Holmes

Question 1

Classification of head injury

Answer 1

mechanism
morphology 
fractures
concussion
haematomas
contusion 
severity

Question 2

difference between confusion and delirium

Answer 2

Confusion = the inability to think as clearly or quickly as you normally do. You may feel disoriented and have difficulty paying attention, remembering, and making decisions.

Delirium is defined as an acute confusional state – it is a transient global disorder of cognition and also a medical emergency. (it is basically a specific form of confusion brought on by acute illnesses)

Question 3

symptoms of confusion

Answer 3

Slurring words or having long pauses during speech

• Abnormal or incoherent speech
• Lacking awareness of location or time
• Forgetting what a task is while it’s being performed
• Sudden changes in emotion, such as sudden agitation

Question 4

causes of confusion

Answer 4

Alcohol or drug intoxication

• Brain tumour
• Head trauma or injury
• Fever
• Fluid and electrolyte imbalance
• Diseases such as dementia

Question 5

symptoms of delirium

Answer 5

Disorientation in time, space, person
- Impaired concentration and attention
- Altered cognitive state
- Impaired ability to communicate
- Insomnia
- Decreased cooperation in patient
- Exists in hypo- and hyperactive form
Hypoactive => withdrawn, sleepy and not interacting
Hyperactive => restless, agitated

Question 6

causes of delirium

Answer 6

PINCH’S ME

Pain, infection, nutrition, constipation, hydration (+urine retention), sleep, medication and electrolyte imbalance.

Question 7

RFs for epilepsy

Answer 7

Age: onset of epilepsy is most common in children and adults.
Family History
Head injuries
Stroke and vascular disease.
Brain infections: encephalitis
Babies born small for their age.
Babies who have seizures in the first month of their life.
Brain tumours
Cerebral palsy
Use of illegal drugs such as cocaine.
Having hyperexcitable neurones which get stimulated from triggers such as flashing lights, alcohol intake, alcohol withdrawal and sleep deprivation, mental exhaustion.

Question 8

ddx for epilepsy

Answer 8

syncope
cardiogenic/hypoT
hypoglycaemia 
sleep 
TIA

Question 9

Mx of epilepsy

Answer 9

General advice: Education to family members and individuals on how to recognise and manage seizures.
Advise to take showers, rather than baths.
Be cautious with swimming.
Be cautious with height
Be cautious with traffic
Be cautious when handling hot, heavy or electrical equipment.
Should inform the DVLA, they have seizures.
Avoid triggers.

As a general rule:
Sodium valproate, is used first line for patients with generalised seizures.
Carbamezapine, used first line for patients with partial seizures.
Can also have surgery.

Question 10

MICA diazepam

Answer 10

MOA: benzodiazepam. Bind to GABA receptors in the brain and spinal cord, which increases the inhibitory effects of the GABA neurons.
Indications: muscle spasm, tetanus, anxiety, insomnia associated with anxiety, acute alcohol withdrawal, sedation, status epilepticus, febrile convulsions, convulsions due to poisons, acute drug induced dystonic reactions, dyspnoea associated with anxiety in palliative care, pain of muscle spasm in palliative
CIs: neonates via injection, chronic psychosis in adults, CNS depression, compromised airway, hyperkinesis, respiratory depression
Adverse effects: abnormal appetite, impaired concentration, movement disorders, muscle spasms, palpitations, sensory disorder, vomiting, constipation, diarrhoea, hypersalivation, slurred speech.

Question 11

MICA phenytoin

Answer 11

M: Phenytoin is often described as a non-specific sodium channel blocker and targets almost all voltage-gated sodium channel subtypes. More specifically, phenytoin prevents seizures by inhibiting the positive feedback loop that results in neuronal propagation of high frequency action potentials.

I: tonic clonic seizures, focal seizures, prevention of seizures following surgery or head injury, status epilepticus

CI: 2d and 3rd degree heart block, SA block, sinus bradycardia

A: electrolyte imbalance, pneumonitis, vitamin D deficiency, arrhythmias, atrial conduction depression, cardiac arrest, hypoT

Question 12

MICA sandoK

Answer 12

M: KCl, prevention of K depletion

I: established hypoK, usually prescribed with sodium chloride because infusion of Chloride ions promotes retention of potassium in the serum, whereas glucose may promote insulin release with resultant stimulation of sodium potassium ATPase, shifting potassium into cells.

C: Patients with renal impairment or oliguria as they are more susceptible to hyperkalaemia.

A: Overcorrection leading to hyperkalaemia, and a resultant risk of arrhythmias.
If infused rapidly or in too high concentration it can become an irritant to veins.

Question 13

define DT

Answer 13

severe form of alcohol withdrawal that usually occurs 6-12hrs after their last drink

Question 14

DDx for DT

Answer 14

sympathomimetic intoxication, encephalitis, meningitis, hypoglycaemia, Wernicke’s encephalopathy, benzodiazepine withdrawal, opioid withdrawal, thyrotoxicosis, schizophrenia

Question 15

clinical features of DT

Answer 15

agitation, global confusion, disorientation, hallucinations, fever, high blood pressure, diaphoresis, and autonomic hyperactivity (tachycardia and hypertension

Question 16

pathophysiology of DT

Answer 16

Ethanol predominantly targets the GABA type A receptor, where the persistent stimulation of inhibitory receptors results in downregulation of the GABA type A receptor/Cl- channel complex. The adaptive downregulation of GABA type A receptors also contributes to the development of tolerance by allowing alcohol users to maintain a level of consciousness despite the presence of a sedative ethanol concentration.

The presence of a persistent blood ethanol concentration primarily affects the expression of the post-synaptic NMDA receptor-Ca+2 channel complex. In contrast to GABA type A receptor agonism, ethanol inhibits the NMDA receptor (glutamate receptor) function by competitively binding to the glycine binding site on the NMDA receptor. This inhibitory effect causes a compensatory upregulation of NMDA receptors on the post-synaptic membrane.

Abstinence from alcohol in the alcohol-dependent patient leads to a disequilibrium between NMDA and GABA type A receptor function due to decreased blood ethanol concentration from the previously maintained steady-state level. As a result, excessive glutamatergic stimulation with diminished inhibitory (GABA) activity leads to the development of clinical symptoms of alcohol withdrawal syndrome (AWS), including autonomic hyperactivity, tremors, hallucinations, and seizures

Question 17

Ix for DT

Answer 17

Investigations: full hx and exam, VBG, BM, FBC, U&E, blood cultures, CT head, CXR, ECG

Question 18

Tx of DT

Answer 18

oral lorazepam or IV lorazepam or haloperidol

Question 19

causes of wernicke’s encephalopathy

Answer 19

thiamine deficiency

Question 20

Symptoms of wernicke’s encephalopathy

Answer 20

mental slowing, impaired concentration, and apathy, frank confusion, gaze palsies, sixth nerve palsies, and impaired vestibulo-ocular reflexes, gait dysfunction, delirium, acute psychosis, tachycardia, hypoT

Question 21

acute tx of wernicke’s encephalopathy

Answer 21

1st line –

stabilisation/resuscitation + thiamine + magnesium + multivitamins

Question 22

MICA of haloperidol

Answer 22

M: it exerts its antipsychotic effect through its strong antagonism of the dopamine receptor (mainly D2), particularly within the mesolimbic and mesocortical systems of the brain. It acts primarily on the D2-receptors and has some effect on 5-HT2 and α1-receptors, with negligible effects on dopamine D1-receptors. The drug also exerts some blockade of α-adrenergic receptors of the autonomic system.13

I: nausea and vomiting, schizophrenia, psychoses, mania, agitation and restlessness in the elderly

C: CNS depression, comatose states, dementia with Lewy bodies, history of ventricular arrhythmia, parkinsons, recent acute MI, uncorrected hypoK

A: depression, eye disorders, headache, hypersalivation, nausea, postural hypoT, vomiting, weight loss

Question 23

MICA chlordiazepoxide

Answer 23

Mechanism:
It is a benzodiazepine which targets GABAa receptors. GABAa is a chloride channel that opens in response to binding by GABA which is the main inhibitory neurotransmitter in the brain. The influx of chloride makes cells more resistant to depolarisation. Benzos facilitate and enhance binding of GABA to GABAa. This has a widespread depressant effect on synaptic transmission.
It is also called Librium. Has a long half-life.

Indications:
First line for seizures and status epilepticus
First line for alcohol withdrawal reactions
Sedation for interventional procedures

Contraindications:
Best avoided in patients with respiratory impairment or neuromuscular disease e.g. myasthenia gravis.
Also in liver failure as it can precipitate hepatic encephalopathy.

Adverse effect:
Dose-dependent drowsiness, sedation and coma

There is relatively little cardiorespiratory depression in q QM overdose but loss of airway reflexes can lead to airway obstruction and death.
Dependency if used for more than a few weeks. Abrupt cessation will produce withdrawal symptoms similar to that seen with alcohol

Question 24

difference between delusions and hallucinations

Answer 24

A delusion is a false belief that persists in spite of evidence. A hallucination is a false perception of objects or events and is sensory in nature. a delusion is defined as a false idea or belief, sometimes originating in a misinterpretation of a situation

Question 25

factors to consider when assessing a homeless patient

Answer 25

physical needs
social needs
emotional and mental health needs
psychological and behavioural needs