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Sharon's Phase 3a > Geriatrics and Neurology > Flashcards

Geriatrics and Neurology Flashcards

1
Q

What is dementia?

A

Progressive decline in cognitive function affecting multiple domains including language , executive function, memory and social cognition.

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2
Q

Types of dementia

A

Neurodegenerative:

  • Alzheimer’s
  • Lewy body
  • Frontotemporal

Cerebrovascular:

  • Vascular

Reversible:

  • VItamin B12 deficiency
  • Hypothyroidism
  • Wernicke’s encephalopathy
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3
Q

Risk factors for dementia

A
  • Age
  • High BMI
  • Smoking
  • Type 2 diabetes
  • Hypertension
  • Low Education
  • Social isolation
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4
Q

What is the cause of Alzheimer’s disease?

A
  • Deposition of extracellular 𝛃-amyloid (senile plaques) and intracellular tau protein (neurofibrillary tangles) = neurotoxicity and reduced cholinergic transmission
  • 50 - 75%
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5
Q

Clinical features of Alzheimer’s

A
  • Characteristic order of language impairment: naming → comprehension → fluency
  • Memory impairment: 4As
  • Amnesia (recent memories lost first)
  • Aphasia (word-finding problems, speech muddled and disjointed)
  • Agnosia (recognition problems)
  • Apraxia (inability to carry out skilled tasks despite normal motor function)
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6
Q

Investigations for Alzheimer’s

A
  • Thorough history and neurological examination
  • Formal cognitive testing e.g. 6CIT
  • Bloods: FBC, U&Es, LFTs, glucose, calcium, TFT, vitamin B12, folate
  • CT head to exclude a structural lesion
  • MRI shows brain atrophy
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7
Q

Medical management for Alzheimer’s

A

Mild - moderate: AChE (Acetylcholinesterase) inhibitor: e.g. donepezil

Severe: AChE + Memantine

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8
Q

Conservative management for dementia

A
  • Support from memory service
  • Education: about dementia and adapting to changes
  • Advanced care plan
  • Cognitive stimulation therapy
  • Group reminiscence therapy
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9
Q

What is vascular dementia?

A
  • Up to 20%
  • Characterised by chronic, progressive and stepwise deterioration in cognitive function.
  • Caused by reduced blood flow to brain due to infarctions and small-vessel changes.
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10
Q

What are the clinical features of vascular dementia?

A

Stepwise deterioration in cognitive function and stroke-like symptoms, over months or years

  • Possible Hx of strokes
  • Visual disturbance
  • Sensory or motor symptoms
  • Difficulty with attention and concentration
  • Seizures
  • Memory disturbance
  • Gait/speech/emotional disturbance
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11
Q

Investigations for vascular dementia

A
  • Comprehensive history and exam
  • Cognitive tests e.g. 6CIT (6 item congitive impairment test), MMSE not used much anymore
  • Exclude organic causes: B12/folic acid deficiency, hypothyroidism
  • MRI head to visualise vascular changes
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12
Q

Management of vascular dementia

A
  • Manage CV risk factors such as hypertension, diabetes, hyperlipidemia, and smoking
  • Cognitive stimulation programmes, music and art therapy
  • Symptomatic treatment: cholinesterase inhibitors or memantine - if coexisting AD, Parkinson’s dementia, or dementia with Lewy bodies.
  • Advanced care plans
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13
Q

Difference between vascular and Alzheimer’s dementia

A

Alzheimer’s disease:

  • Predominant memory impairment
  • slower and continuous decline
  • Usually lack of significant vascular risk factors or cerebrovascular disease.

Vascular: stroke risk factors and/or symptoms, stepwise decline in visual skills, semantic (language) memory and executive functioning

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14
Q

What is Lewy-body dementia?

A

A type of progressive dementia caused by deposits of an abnormal protein, alpha-synuclein, which form inclusions (Lewy bodies) within brain cells, particularly in the substantia nigra

These aggregates disrupt normal cell functioning and eventually lead to neuronal death.

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15
Q

Clinical features of Lewy-body dementia

A
  • Fluctuating cognition
    Parkinsonism: Rigidity, bradykinesia, and postural instability
  • Visual hallucinations

High sensitivity to antipsychotics: induce or worsen parkinsonism.

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16
Q

How do you Lewy body dementia from parkinson’s disease dementia?

A

Cognitive impairment and parkinsonism develop <1 year of each other - likely LBD.

If diagnosed with PD and dementia develops >1 year later - Parkinson’s disease dementia

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17
Q

Investigations for Lewy body dementia

A
  • Clinical diagnosis with comprehensive history and physical exam
  • Dopamine transporter (DaT) scan: differentiate DLB from others.
  • Neuropsychological testing to assess cognitive functioning and fluctuations.
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18
Q

Medical management for Lewy body dementia

A

1st line: AChE (Acetylcholinesterase) inhibitor: donepezil or rivastigmine

Dopamine replacement if parkinsonism

Non-pharmacological interventions: cognitive stimulation, physical therapy, and occupational therapy.

Supportive care: progressive disease so palliative and end-of-life care consideration

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19
Q

What is frontotemporal dementia?

A

Progressive degeneration of the frontal and/or temporal lobes associated with Pick bodies.

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20
Q

Clinical features of frontotemporal dementia

A
  • Behavioural and personality changes, e.g. impulsivity
  • Memory impairment
  • Language impairment e.g. reduced fluency or comprehension
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21
Q

Management of frontotemporal dementia

A

AChE inhibitors and memantine are not recommended

Conservative management recommended e.g. behavioural management through counselling

  • SSRIs/antipsychotics (use carefully) to help control behavioural symptoms
  • Sppech and lanuage therapy , physio, OT to help manage impacts on daily functioning
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22
Q

Define stroke

A

Stroke is defined as an acute neurological deficit lasting more than 24 hours and caused by cerebrovascular compromise.

  • Ischaemic stroke
  • Haemorrhagic stroke
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23
Q

What is an ischaemic stroke?

A

Ischaemic stroke occurs when cerebral blood supply is critically reduced due to occlusion or critical stenosis of a cerebral artery.

~85% of stokes

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24
Q

Risk factors for ischaemic stroke

A
  • Hypertension
  • Age ≥55 years
  • Hx of TIA
  • Hx of ischaemic stroke
  • FHx of stroke at a young age
  • Smoking
  • Diabetes mellitus
  • Atrial fibrillation (3 - 5x risk)
  • Comorbid cardiac conditions
  • Carotid artery stenosis
  • Sickle cell disease
  • Dyslipidaemia
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25
Q

What is a haemorrhagic stroke?

A

Haemorrhagic stroke resulting from a vascular rupture in the brain, causing bleeding into the brain parenchyma > injury to the brain tissue

~ 15% stokes

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26
Q

Why is it important to differentiate between an ischaemic vs haemorrhagic stroke?

A

Because the treatment for ischaemic stroke can make the haemorrhage in a haemorrhagic stroke worse.

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27
Q

According to the Bamford classification, what are the different types of stroke?

A
  • Total anterior circulation stroke (TACS)
  • Partial anterior circulation stroke (PACS)
  • Lacunar stroke
  • Posterior circulation stroke
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28
Q

Clinical features of an ischaemic stroke

A
  • Unilateral weakness or paralysis in the face, arm or leg
  • Dysphasia
  • Ataxia
  • Visual disturbance
  • Risk factors
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29
Q

Ischaemic stroke: what symptom/signs indicate posterior circulation stroke?

A

Cerebellar syndrome:

  • Ataxia in absence of limb weakness
  • Problems with fine motor movements
  • Diplopia
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30
Q

Ischaemic stroke: what are the 3 cardinal signs of anterior circulation stroke?

A
  • Hemiplegia (unilateral paralysis)
  • Homonymous hemianopia (visual loss in same side of visual fields in both eyes)
  • Higher cortical dysfunction, such as dysphasia or neglect (ignores one side of the body)
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31
Q

What are the signs of partial anterior circulation stroke?

A

Two out of three of:

  • Hemiplegia
  • Homonymous hemianopia
  • Higher cortical dysfunction e.g. dysphasia or neglect
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32
Q

What are the clinical features of a Lacunar stroke?

A

A stroke that affects small deep perforating arteries supplying internal capsule or thalamus.

Presents as a pure motor stroke, pure sensory stroke, sensorimotor stroke or ataxic hemiparesis (weakness on one side of body)

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33
Q

Investigations for ischaemic stroke

A
  • CT head ≤ 1 hr of arriving in hospital to rule out haemorrhagic stroke
  • Blood glucose as hypoglycemia mimics stroke
  • U+E as hyponatremia mimics stroke + renal failure is contraindicated in some treatments
  • FBC
  • ECG (exclude AF)
  • Prothrombin time to exclude coagulopathy
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34
Q

Conservative measures to manage ischaemic stroke

A

Stabilise blood glucose levels

Maintain hydration status and temperature

O2 sats

Maintain BP and do not lower unless complications e.g. hypertensive encephalopathy.

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35
Q

Management for ischaemic stroke

A

ONCE and only when haemorrhagic stroke excluded:

  • Aspirin 300 mg immediately or 24hrs after thrombolysis (take for 2 weeks)
  • Thrombolysis with alteplase once haemorrhagic stroke excluded and ≤4.5 hr within onset
  • Mechanical thrombectomy within ≤ 6.5 hrs of onset
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36
Q

Secondary prevention of ischaemic stroke

A
  • 1st line: daily clopidogrel 75mg for life, after 2 weeks of aspirin 300mg
  • High-dose statin : such as atorvastatin 20-80mg 48 hours after
  • Manage hypertension , diabetes , smoking and other cardiovascular risk factors
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37
Q

Differentials for ischaemic stroke

A
  • Intracranial haemorrhage
  • TIA
  • Hypoglycemia
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38
Q

Clinical features of haemorrhagic stroke

A
  • Unilateral weakness or paralysis in the face, arm, or leg
  • Sensory loss (numbness)
  • Dysphasia
  • Dysarthria
  • Visual disturbance (e.g. homonymous hemianopia or diplopia)
  • Photophobia
  • Headache
  • Ataxia
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39
Q

Risk factors for intracranial haemorrhage (which can lead to haemorrhgic stroke)

A

MOST COMMON: uncontrolled hypertension

Older age

Drug use such as amphetamines and cocaine

FHx of ICH

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40
Q

Subtypes of haemorrhagic stroke

A
  • Intracerebral : bleeding within the brain parenchyma
  • Subarachnoid : bleeding into the subarachnoid space
  • Intraventricular : bleeding within the ventricles
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41
Q

Investigations for haemorrhgic stroke

A

Same as ischaemic stroke

  • Non-contrast CT head within 1 hour of arrival
  • Serum glucose
  • Serum electrolytes
  • Serum urea and creatinine
  • FBC

Plus

  • LFTs - to exclude liver dysfunction as cause
  • Clotting screen to exclude coagulopathy as cause
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42
Q

Management for hemorrhagic stroke

A
  • Admission to neurocritical care and neurosurgery
  • Raised intracranial pressure : consider intubation with hyperventilation, head elevation (30°) and IV hypertonic saline
  • BP control <140/80 mm Hg
  • Surgical intervention: decompression hemicraniectomy may be needed
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43
Q

Long-term management for haemorrhagic stroke

A

Rehabilitation: Physical, occupational, and speech therapy

Secondary prevention:

Blood pressure control, discontinuation of harmful substances (e.g., illicit drugs, alcohol), and management of coagulation disorders

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44
Q

Differentials for haemorrhagic stroke

A
  • Ischemic stroke: headache less common in IS than HS but rule out with NC-CT
  • Subarachnoid haemorrhage: sudden “worst headache of my life”
  • Brain tumor
  • Meningitis
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45
Q

Possible consequences from a stroke

A
  • Deep vein thrombosis : due to immobility
  • Aspiration pneumonia : due to dysphagia
  • Neurological sequelae : such as weakness, impaired mobility, middle cerebral artery syndrome and seizures
  • Requirement for nutritional support : such as nasojejunal feeding
    Depression
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46
Q

What is Parkinson’s Disease?

A

A neurodegenerative disorder characterised by loss of dopaminergic neurones within the substantia nigra pars compacta (SN PC ) of the basal ganglia (nigrostriatal pathway).

This leads to loss of communication between the basal ganglia, thalamus, and motor cortex, resulting in impaired control of voluntary movements .

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47
Q

What is the histological hallmark for PD?

A

Inclusion bodies consisting of misfolded α-synuclein in the dopaminergic neurones of the SN PC called Lewy bodies

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48
Q

What are the clinical features of PD?

A

According to NICE, a diagnosis should be suspected in a patient who has bradykinesia and at least one of the following:

  • Tremor (Resting ‘pill-rolling’ (4-6Hz) tremor)
  • Rigidity
  • Postural instability
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49
Q

Non-motor symptoms of PD

A
  • Anosmia
  • Sleep disturbance (REM)
  • Depression, anxiety, dementia
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50
Q

Investigations for PD

A
  • Clinical diagnosis

Consider

  • MRI brain: exclude other neurological diseases
  • SPECT (DaT scan): show reduced dopamine uptake in the basal ganglia
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51
Q

Management of PD

A

NICE recommends referral to movement disorders specialist (e.g. care of elderly physician) for diagnosis and review every 6-12m

Motor symptoms affecting QoL:

  • Levodopa + decarboxylase inhibitor e.g. co-beneldopa (stops Levodopa from being metabolised in the body before it reaches the brain)

Motor symptoms not affecting QoL:

  • Dopamine agonist e.g. ropinirole or as above
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52
Q

What are some side-effects of antiparkinsonian medication?

A

Motor fluctuations:

symptoms are initially well-controlled (on period) but then re-emerge prior to the next dose (off period).

Freezing: sudden stoppage of movement

Dyskinesia: (excessive involuntary movements) levodopa use

Non-motor complications:

  • Impulse control disorders
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53
Q

Causes of secondary parkinsonism

A
  • Lewy Body Dementia
  • Meds e.g. antipsychotics, lithium
  • Wilson’s disease
  • Encephalitis
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54
Q

Define transient ischaemic attack

A

A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction

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55
Q

Key clinical features of TIA

A
  • Sudden onset and brief duration of symptoms (mins)
  • patient/witness report of focal neurological deficit e.g. unilateral weakness or paralysis, dysphasia, sudden transient loss of vision in one eye (amaurosis fugax)
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56
Q

Risk factors for TIA

A
  • Increasing age
  • Hypertension
  • Smoking
  • Diabetes
  • Hypercholesterolaemia
  • Atrial fibrillation
  • Carotid stenosis
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57
Q

Investigations for TIA

A
  • Blood glucose - hypo can cause sudden-onset neuro symptoms
  • FBC and platelet count
  • ECG (AF)
  • Lipid profile
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58
Q

Management of TIA

A
  • Antiplatelet therapy - aspirin 300mg
  • Statin e.g. atorvastatin
  • Anticoagulant (warfarin/DOAC) if AF
  • Referral to TIA clinic within 24hrs
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59
Q

What is osteoporosis?

A

Osteoporosis is the reduction in trabecular bone mass/density and disruption of bone architecture , resulting in porous bone with increased fragility and fracture risk.

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60
Q

What causes osteoporosis?

A

It is caused by prolonged imbalance of bone remodeling where resorption ( osteoclastic activity) exceeds formation ( osteoblastic activity).

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61
Q

Risk factors for osteoporosis

A

Fight Me!

  • Female
  • Post-Menopausal

SHATTERED

  • Steroids
  • Hyper/hypothyroidism
  • Alcohol + smoking
  • Thin (low BMI)
  • Testrosterone (low)
  • Early menopause (decreased oestrogen)
  • Renal/liver failure
  • Erosive/inflammatory disease (IBD)
  • DMT1 or malabsorption
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62
Q

Investigations for osteoporosis

A

1st line + gold standard: Dual X-ray absorptiometry (DEXA) - T- and Z-score
Diagnosis = T-score ≤-2.5

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63
Q

Clinical features of osteoporosis

A

Asymptomatic until fragility fractures occur: pain and inability to bare weight.

Common sites include NOF, wrist and vertebrae

Back pain and kyphosis indicate vertebral fracture.

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64
Q

What is the FRAX score?

A

Risk score tool for estimating 10-year risk of osteoporotic fractures in untreated patients

Personal information: ABFS (Asian baby femaleS)

  • Age
  • BMI
  • Femoral bone density
  • Sex - female increased risk

PMH (P.S.R - pumpkin spice Rosa)

  • Previous fractures
  • Secondary osteoporosis - CKD, diabetes type 1, IBD, hyperthyroidism, hyperparathyroidism
  • Rheumatoid arthritis

Drug history

  • Glucocorticoids

Social history

  • Smoking
  • Alcohol 3 units or more per day

Family history

  • Parental previous fractures
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65
Q

Conservative management for osteoporosis (also prevention of fragility fractures)

A
  • Weight-bearing exercise
  • Increase dietary vitamin D and calcium
  • Smoking cessation
  • Reduce alcohol consumption
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66
Q

Medical management for osteoporosis

A
  • Bisphosphonates e.g. alendronic acid
  • VitD and calcium supplement e.g. adcal D3
  • Denosumab for post-menopausal women at high risk of fractures
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67
Q

Differentals for osteoporosis

A
  • Osteopenia if -2.5 < T-score < -1
  • Multiple myeloma (bone pain with anaemia & renal failure
  • Osteomalacia
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68
Q

Types of urinary incontinence

A
  • Stress
  • Urge
  • Mixed
  • Overflow
  • Functional
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69
Q

What is stress incontinence?

A

Involuntary urine leakage during increased abdominal pressure, such as coughing, sneezing, or exercise.

Caused by weakened pelvic floor muscles or an impaired urethral sphincter

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70
Q

What is urge incontinence?

A

Involuntary leakage with strong, sudden need to urinate, usually due to overactive bladder muscle contractions.

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71
Q

What is overflow incontinence?

A

Involuntary, constant leakage of urine caused by an inability to completely empty the bladder leading to excess urine retention often due to an obstruction or poor bladder muscle function.

Caused by neurological damage or outlet obstruction.

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72
Q

What is mixed incontinence?

A

A combination of two or more types of incontinence, stress and urge incontinence most common.

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73
Q

What is functional incontinence?

A

Inability to reach the toilet in time due to physical or cognitive impairments, despite normal bladder function.

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74
Q

Risk factors for urinary incontinence

A
  • Age
  • Female gender
  • Previous pregnancies and deliveries: stress incontinence due to weakness of the pelvic floor
  • Obesity
  • Menopause
  • Urinary tract infections
  • Certain medications: e.g. diuretics
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75
Q

Reversible causes of incontinence

A

DIAPPERS

D - Delirium

I - Infection

A - Atrophic vaginitis or urethritis

P - Pharmaceutical (medications)

P - Psychiatric disorders

E - Endocrine disorders (e.g. diabetes)

R - Restricted mobility

S - Stool impaction

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76
Q

Investigations for urinary incontinence

A

Physical exam: pelvic and neurological

Questionnaire: assess symptoms and severity

Bladder diary: record fluid intake, frequency, incontinence over 3-7 days

Urinalysis: exclude infection

Post-void residual urine (PVR): uses US or catheterisation to assesses bladder emptying

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77
Q

When should women be referred onto 2WW for bladder cancer?

A

≥ 45 with unexplained visible haematuria without UTI or persistent/recurrent visible haematuria after UTI treated

≥ 60 with unexplained non-visible haematuria and dysuria or raised WCC on a blood test

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78
Q

Management for stress incontinence

A
  • Weight loss, smoking cessation, fluid management and avoiding caffeine
  • 1st line: pelvic floor muscle training
  • Duloxetine (SNRI) if not effective
  • Surgery: gold standard is mid-urethral sling which helps closure of urethra during increased abdo pressure
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79
Q

Management of urge incontinence

A

Bladder training: Scheduled voiding with gradually increasing intervals to distend and improve bladder control

Antimuscarinic drugs such as oxybutynin to improve detrusor muscle activity

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80
Q

Management of mixed incontinence

A

Treatment focused on the most bothersome component of symptoms.

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81
Q

Define pressure ulcer

A

Localised damage to the skin and underlying soft tissue usually over a bony prominence as a result of pressure or related to a medical or other device.

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82
Q

Risk factors of pressure ulcers

A
  • Immobility
  • Age >70 years
  • Recent surgery or ITU stay
  • Malnutrition.
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83
Q

Category/grade/stage 1 pressure ulcer

A

Intact skin with a localised area of non-blanchable erythema, or a darker area on dark skin

Non-blanchable erythma

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84
Q

Category 2 pressure ulcer

A

Partial-thickness skin loss with exposed dermis.

The wound bed is viable, pink/red, moist, and may present as an intact or ruptured serum-filled blister

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85
Q

Category 3 pressure ulcer

A

Full-thickness skin loss, and adipose (fat) visible in ulcer. Granulation tissue and epibole (rolled wound edges) often present.

Slough and/or eschar may be visible.

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86
Q

Category 4 pressure ulcer

A

Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone in the ulcer.

Slough and/or eschar may be visible.

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87
Q

Management of pressure ulcers

A
  • Pressure relief through repositioning (ideally every 2 hours) and support surfaces e.g. seat cushions, wheelchairs, mattress
  • Cleansing + dressing
  • Pain relief (e.g. paracetamol, ibuprofen, codeine)
  • Dietitian to optimise nutrition intake
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88
Q

Differentials of pressure ulcers

A
  • Venous ulcers: usually lower legs near ankles; accompanied by skin staining.
  • Arterial ulcers - usually feets, toes, heels
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89
Q

Which age group is more likely to fall?

A

over 65s

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90
Q

Neuropsychiatric causes of falls in the elderly

A
  • Visual impairment
  • Peripheral neuropathy
  • Vestibular dysfunction, particularly benign paroxysmal positional vertigo (BPPV)
  • Fear of falling can increase risk of fall
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91
Q

Cardiovascular causes of falls in the elderly

A
  • Syncope
  • Orthostatic hypotension
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92
Q

MSK causes of falls in the elderly

A
  • Joint buckling/instability/poor mechanical mobility: may be due to prior injury or arthritis
  • Deconditioning: insufficient exercise and prolonged periods of immobility leading to reduced muscle tone and function.
  • Sarcopenia/ osteosarcopaenia: muscle weakness, muscle and/or bone mass loss
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93
Q

Medications that increase risk of falls in the elderly

A
  • Benzodiazepines, antidepressants, and anxiolytics
  • Insulin
  • NSAIDS, opioids
  • Polypharmacy: ≥ 5 meds
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94
Q

Environmental causes of falls in the elderly

A

Loose rugs or tiles, poor lighting, clutter etc.

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95
Q

What is involved in a falls-risk assessment?

A

An assessment that identifies the causes of a fall and implements strategies to prevent future falls.

Areas that are assessed (NICE):

  • Falls history
  • Cognitive impairment and neurological examination
  • fear relating to falling
  • visual impairment
  • Cardiovascular examination
  • Motor: gait, balance and mobility, and muscle weakness
  • osteoporosis risk
  • urinary incontinence
  • home hazards
  • Medications review
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96
Q

What is involved in multifactorial intervention for fall prevention?

A
  • Strength and balance training
  • Home hazard assessment and intervention
  • Vision assessment and referral
  • Medication review with modification/withdrawal
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97
Q

Differential diagnoses for a fall

A
  • Stroke
  • Transient ischaemic attack
  • Joint buckling/instability/mechanical gait disorders
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98
Q

What is frailty?

A

Frailty is a distinctive health state related to the ageing process in which multiple body systems gradually lose their in-built reserves.

Results in increased vulnerability to stressors. Even “minor” changes like new med, infections or surgery can cause a drastic deterioration in health state, taking the person from independent to dependent.

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99
Q

Biggest risk factor for developing frailty

A

Age, although frailty is not an inevitable consequence of ageing.

Also, co-morbidities increase the risk of developing frailty:

  • Cognitive impairment
  • Depressive symptoms
  • Diabetes
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100
Q

Define polypharmacy

A

Taking multiple medicines or drugs (usually 4/5+)

the risk of problems such as side effects increases as the number of drugs increases.

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101
Q

Medication interactions

A

Warfarin + NSAIDs = increased bleeding risk

Warfarin + macrolide

Omeprazole + clopidogrel

SSRI + NSAID = increased bleeding risk

ACEi + Spironolactone = AKI risk and hyperkalaemia

Statin + Macrolide = increased statin effect

Statin + grapefruit = increased statin effect

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102
Q

Clinical tools to assess frailty

A
  • Clinical frailty scale ( 1 is very active to 9 (terminally ill))
  • Gait speed test > 5 seconds to walk 4 metres indicates frailty
  • PRISMA-7 questionnaire ≥3 = frailty
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103
Q

Ways to prevent frailty

A
  • Optimise diet and nutrition
  • Exercise: ≥ 150 min moderate intensity or ≥ 75 min vigorous + 2 days of strength
  • Eye + hearing care
  • Psychological wellbing - screnning and treat depression
  • Prevent cognitive decline - active, healthy diet, reduce alcohol and smoking, socialising + groups
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104
Q

What are parkinson-plus syndromes?

A

They are 4 syndromes that present as Parkinsonism (triad of resting tremor, hypertonia, and bradykinesia) with additional clinical features.

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105
Q

Parkinson-plus syndrome: define progressive supranuclear palsy

A

Parkinsonism and vertical gaze palsy

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106
Q

Parkinson-plus syndrome: define multiple system atrophy

A

Parkinsonism and early autonomic clinical features such as: postural hypotension, incontinence, and impotence.

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107
Q

Parkinson-plus syndrome: define cortico-basal degeneration

A

Parkinsonism and involves spontaneous activity by an affected limb, or akinetic rigidity of that limb.

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108
Q

Parkinson-plus syndrome: define lewy body dementia

A

Parkinsonism and fluctuations in cognitive impairment and visual hallucinations, often before Parkinsonian features occur.

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109
Q

Define syncope

A

Syncope is the transient loss of consciousness due to disruption of blood flow to the brain that often leads to a fall, sometimes called a vasavagal episode or fainting.

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110
Q

Causes of primary syncope

A

Primary syncope (simple fainting):

  • Dehydration
  • Missed meals
  • Extended standing in a warm environment
  • Vasovagal response to a stimuli, such as sudden surprise
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111
Q

Secondary causes of syncope

A
  • Hypoglycaemia
  • Dehydration
  • Anaemia
  • Infection
  • Anaphylaxis
  • Arrhythmias
  • Valvular heart disease
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112
Q

How to distinguish between an episode of syncope and seizure?

A

Vasovagal syncope: clear trigger, blurring/clouding of vision, sweating and dizziness, no postictal period

Seizures: lateral tongue biting, urinary incontinence, long postictal period, residual focal neurological deficit, and seizure activity (tonic-clonic or focal seizures).

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113
Q

What are the investigations for syncope?

A
  • ECG - arrhythmia, long QT syndrome
  • 24hr ECG - ?paroxysmal arrhythmia
  • Echocardiogram - ?structural heart disease
  • Bloods: FBC (anaemia), electrolytes (arrhythmias and seizures) and blood glucose (diabetes)
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114
Q

Management of primary syncope

A
  • Avoid dehydration
  • Avoid missing meals
  • Avoid standing still for long periods
  • If prodromal symptoms such as sweating and dizziness, sit or lie down, eat something until feel better
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115
Q

Management of syncope if secondary

A

Otipmise management of underlying cause.

If waiting for confirmation of underlying cause:

  • Unexplained syncope: 6 months off driving and inform DVLA.
  • Advise showers over baths.
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116
Q

What is a deprivation of liberty safeguard (DoLS)?

A

An application made by a hospital or care home for patients who has been assessed as lacking capacity to allow them to provide care and treatment. Whilst in hospital, or a care home, the patient is under control and is not able to leave. This means they are “deprived of their liberty” and require a legal framework to protect them.

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117
Q

What is power of attorney?

A

A simple legal document that allows an adult to consent for another adult to conduct financial affairs on their behalf. It is only valid as long as the donor has capacity.

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118
Q

What is a lasting power of attorney?

A

A document whereby a person legally nominates a person of their choice to make decisions on their behalf if they lack mental capacity. LPA only comes into effect if the patient lacks the capacity to decide for themselves. It does not give the person with LPA control over a decision if they can still make that decision themselves.

Can be put in place when the donor has capacity.

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119
Q

What is an advanced directive?

A

A patient-led medical decision, made when patient is competent and designed for when the patient becomes incompetent.

Advance refusals of treatment are legally binding if:

  • The person is an adult
  • Was competent and fully informed when making the decision
  • The decision is clearly applicable to current circumstances
  • There is no reason to believe that they have since changed their mind
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120
Q

What is malnutrition?

A

A state in which a deficiency of energy, protein, and/or other nutrients causes measurable adverse effects on the body’s form, composition, function and clinical outcome.

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121
Q

Causes of malnutrition

A
  • Decreased nutrient intake (starvation)
  • Increased nutrient requirements (sepsis or injury)
  • Inability to utilise ingested nutrients (malabsorption)
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122
Q

Tool used to assess malnutrition

A

Malnutrition universal screening test (MUST)

  1. BMI
  2. Unintentional weight loss past 3 - 6m
  3. Establish acute disease effect and score
  4. Add score from 1,2 & 3 to obtain overall malnutrition risk
  5. Management plan according to local guidelines
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123
Q

According to the MUST tool, what is considered a diagnosis of malnutrition?

A

Score:
- 1= low risk
- 2 = med risk
- 3 = high risk

  • BMI <18.5kg/m2
  • Unintentional weight loss >10% last 3-6mths
  • BMI <20kg/m2 AND unintentional weight loss >5% within last 3-6mths
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124
Q

What is refeeding syndrome?

A

Metabolic disturbances as a result of reintroduction of nutrition to patients who are starved/severely malnourished.

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125
Q

What are the biochemical features of refeeding syndrome?

A
  • Hypophosphatemia
    -Hypocalcemia
  • Thiamine deficiency
  • Abnormal glucose metabolism
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126
Q

Complications of refeeding syndrome?

A

Cardiac arrhythmias, Coma, Convulsions, Cardiac failure

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127
Q

Management of refeeding syndrome

A
  • Monitor blood biochemistry (phosphate, K+, Mg)
  • Monitor glucose and Na levels
  • Carefully commence re-feeding with guidelines
  • Supportive care, and refer to nutritional support team/dietician
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128
Q

Risk factors for constipation

A

Advanced age, inactivity, low calorie intake, low fibre diet, medications, female sex

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129
Q

What is the bristol stool chart?

A

A chart used to document stool frequency and consistency over a period of time.

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130
Q

What are the clinical features needed for a diagnosis of constipation?

A

Rome IV critieria - constipation may involve some or all:

  • <3 bowel movements per week
  • Hard stool > 25% of bowel movements (BMs)
  • Tenesmus (sense of incomplete evacuation) in > 25% BMs
  • Excessive straining in more than 25% BMs
  • Manual evacuation of bowel movements
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131
Q

Causes of constipation

A

Primary constipation:

  • No organic cause

Secondary constipation:

  • Can be due to diet, medications, metabolic, endocrine or neurological disorders or obstruction
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132
Q

Dietary and behavioural causes of constipation

A

Dietary factors, such as inadequate fibre or fluid intake.

Behavioural factors, like inactivity (common in inpatients) or avoidance of defecation.

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133
Q

Example of electrolyte imbalance that can cause constipation

A

Hypercalcaemia

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134
Q

MEdications that can cause constipation

A
  • Opiates, calcium channel blockers and some antipsychotics
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135
Q

Neurological disorders that can cause constipation

A

Spinal cord lesions, Parkinson’s disease, and diabetic neuropathy

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136
Q

GI causes of constipation

A

Colon diseases, like strictures or malignancies.

Bowel obstruction can cause complete constipation (obstipation)

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137
Q

What bedside investigations are carried out for constipation?

A
  • PR exam
  • Stool culture
  • FIT testing (if accompanied with new rectal bleeding and signs suggestive of colorectal cancer)
  • Faecal calprotectin (IBD)
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138
Q

What other investigations are carried out for constipation?

A
  • Bloods: FBC (may show an anaemia), U+Es (including calcium), TFTs
  • Abdominal x-ray if ?secondary cause of constipation such as obstruction
  • Barium enema if suspicious of impaction or rectal mass
  • Colonoscopy if suspicious of lower GI malignancy
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139
Q

Management of constipation

A
  1. Exclude underlying causes including colorectal cancer
  2. Conservative: improve diet, exercise
  3. Enema if faecal impaction
  4. Medical: laxatives (many different types)
  • Bulk laxatives e.g. ispaghula husk
  • Stool softeners e.g. sodium docusate, macrogol

Osmotic laxative e.g. lactulose,

Stimulant laxatives e.g. senna

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140
Q

Define heart failure

A

The inability of the heart to deliver blood and thus oxygen at a rate that matches the requirements of the body.

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141
Q

Clinical features of acute heart failure

A

Suspect acute HF in patients with:

  • Breathlessness
  • Ankle swelling
  • Reduced exercise tolerance
  • Fatigue
  • Nocturnal cough

On lung auscultation: coarse bi-basal crackles

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142
Q

Risk factors of acute HF

A
  • Previous cardiovascular disease - CHD most common cause of HF
  • Older age
  • Prior episode of heart failure
  • Diabetes mellitus
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143
Q

Give some causes of acute HF

A
  • MI
  • High-output state e.g. sepsis
  • Infective endocarditis
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144
Q

Investigations for acute HF

A
  • FBC : anaemia can cause HF

U&Es : renal failure can cause HF

Troponin

BNP >100 pg/ml or NT‑proBNP >300 pg/ml

ECG : arrhythmias and MI (ST elevation)

CXR
Transthoracic echocardiogram : systolic and diastolic function, and ejection fraction

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145
Q

What are the features seen on CXR for a patient with acute/chronic HF?

A

A - Alveolar oedema (batwing opacities)
B - Kerley B lines
C - Cardiomegaly
D - Dilated upper lobe vessels
E - Pleural Effusion

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146
Q

Acute management of acute HF

A
  • Treat underlying cause (e.g. MI)
  • Stabilise the patient : O2 for SpO 2 ≥94%

Fluid restriction : usually <1.5L/day

  • IV diuretic : furosemide
  • Inotropes or vasopressors to increase BP if haemodynamically unstable e.g. dobutamine
  • Non-invasive ventilation (NIV)
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147
Q

Surgical management of acute HF

A
  • If HF caused by aortic stenosis - aortic valve replacement
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148
Q

Long-term management of acute HF

A

1st line : ACE-inhibitor and cardioselective β-blocker
e.g. Ramipril + bisoprolol

Fluid restriction : usually <1.5L/day

Loop diuretic e.g. furosemide

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149
Q

DIfferent types of chronic HF

A
  • Heart failure with preserved ejection fraction (HFpEF) = LVEF ≥ 50%
  • Heart failure with reduced ejection fraction (HFrEF) = LVEF ≤ 50%
  • Left-sided HF
  • Right-sided HF
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150
Q

Risk factors for chronic HF

A
  • Myocardial infarction (MI)
  • Hypertension
  • Diabetes mellitus
  • Dyslipidaemia
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151
Q

Clinical features of left-sided HF

A

Symptoms:

  • SOB
  • Fatigue and weakness
  • Cough (frothy white/pink sputum)

Signs:
- Bilateral basal crackles (sounding “wet”)

  • Hypotension if severe (cardiogenic shock)
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152
Q

Symptoms and signs of right-sided HF

A
  • Ankle swelling (peripheral pitting oedema)
  • Distended abdo (ascites)
  • Fatigue and weakness
  • Hepatosplenomegaly
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153
Q

Investigations for chronic HF

A
  • NT-proBNP or BNP
  • ECG: broad QRS complexes + LVH
  • CXR
  • Transthoracic echocardiogram: LVEF, diastolic function, valve abnormalities
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154
Q

Conservative management for chronic HF

A
  • Weight loss if BMI >30
  • Smoking cessation
  • Salt and fluid restriction - improves mortality
  • Supervised exercise-based group rehabilitation programs
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155
Q

Medical management for chronic HF

A

1st line = ACE-I and beta-blocker (e.g. ramipril + bisoprolol)

Mortality improvement in HFrEF but not HFpEF

SGLT2 inhibitors (e.g., dapagliflozin, empagliflozin) for HFpEF

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156
Q

Differentials for HF

A
  • COPD
  • ARDS
  • Renal failure
  • Liver failure
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157
Q

Define migraine

A

A chronic, episodic neurological disorder characterised by recurrent, unilateral, throbbing headaches.

Typical migraine aura (reversible visual, sensory or speech symptoms) that precede the headache only occurs in 15 - 30% patients.

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158
Q

Risk factors for migraines

A
  • Family history of migraine
  • Female sex
  • Menstruation
  • Stressful life events
  • Obesity
  • Sleep disorders
  • Medication overuse.
159
Q

Triggers for migraines

A

CHOCOLATE

  • CHocolate
  • Oral Contraceptive
  • Alcohol + Anxiety
  • Travel
  • Exercise

Others: tiredness, lack of food, dehydration, menstruation, red wine and bright lights

160
Q

Key features of migraine

A
  • Prolonged headache ( 4 - 72 hrs if untreated)
  • Nausea (most commonly associated)
  • Reduced ability to function
  • Headache worse on activity (unlike tension headaches)
  • Photophobia
161
Q

Investigations for migraine

A

Clinical diagnosis - fulfils ICHD-3 criteria for migraine

Criteria
A - At least five attacks fulfilling criteria B-D
B - Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated)

C - Headache has at least two of the following four characteristics:

  1. Unilateral location
  2. Pulsating quality
  3. Moderate to severe pain intensity
  4. Aggravation by or causing avoidance of routine physical activity

D - During headache, at least one of the following:

  1. Nausea and/or vomiting
  2. Photophobia and phonophobia

E - Not better accounted for by another ICHD-3 diagnosis

162
Q

Acute management of migraine

A
  • Triptans (e.g. sumatriptan)
  • NSAIDS and/or paracetamol
  • Anti-emetics if needed (e.g. metoclopramide)
  • High-flow O2
163
Q

Prophylactic management of migraine

A
  • Avoid triggers
  • Propranolol
  • Amitriptyline
  • Topiramate
164
Q

Why should females with migraines avoid the COCP?

A

Significantly increases risk of ischaemic stroke

165
Q

Triptans: routes, side effects and contraindications

A

5HT1 (serotonin) receptor agonists

Routes: oral, nasal, subcutaneous

Side effects: flushing, tingling, chest and throat tightness (may mimic angina)

Contraindicated in IHD or cerebrovascular disease

166
Q

Differentials for migraine

A
  • Tension headache (usually bilateral and non-throbbing)
  • Cluster headaches (most common in men, severe pain around one eye, ≤3 hrs)
167
Q

Define cluster headache

A

Sudden onset severe headache affecting the periorbital area unilaterally.

168
Q

Key differentiating symptoms of cluster headaches

A
  • Watery and bloodshot eye
  • Lacrimation
  • Rhinorrhoea
  • Ptosis
  • Lid swelling
169
Q

Duration of a cluster headache

A

15 minutes to 3 hours

170
Q

Investigation for cluster headache

A

Brain and pituitary MRI with and without contrast.

  • Normal in cluster headache
  • Abnormal indicates secondary cause e.g. tumour
171
Q

Management of cluster headache

A
  • Avoid triggers,
  • Prophylaxis = Verapamil (calcium channel blocker for vasodilation)
  • Acute attacks = 100% oxygen via non-rebreather mask and triptan
172
Q

Key differentiating symptoms of tension headaches

A
  • Bilateral, non-pulsatile headaches
  • Tightness sensation, like a band around the head
  • Scalp muscle tenderness
173
Q

Management of tension headaches

A

Analgesia according to the WHO pain ladder (paracetamol or NSAID)

  • Address stress as a common precipitating factor
174
Q

Define Giant Cell Arteritis (GCA)

A

Vasculitis affecting extracranial branches of the carotid artery.

Common in > 50

175
Q

Key symptoms/signs of GCA

A
  • Headache
  • Scalp pain or tenderness (particularly when brushing hair)
  • Temporary blindness that can progress to irreversible blindness
176
Q

Management of GCA

A

Oral prednisolone

177
Q

Define raised intracranial pressure

A

Increase in the pressure within the skull, with normal levels <20mmHg

178
Q

What is Cushing’s triad?

A

Late-stage symptoms of raised intracranial pressure:

  • Bradycardia
  • Hypertension
  • Irregular respirations
179
Q

Key symptoms of raised intracranial pressure

A
  • Headache
  • Nausea
  • Vomiting
  • Confusion
180
Q

Signs of raised intracranial pressure

A
  • Papilloedema (optic disc swelling) on fundoscopy
  • Altered consciousness
181
Q

Investigations for ICP

A

1st line:

  • CT head to identify tumours or haemorrhage
  • Fundoscopy: to identify papilloedema
182
Q

Medical management of ICP

A
  • ABCDE
  • Elevate head 15 - 20 degree
  • Hypertonic saline/mannitol to osmotically reduce cerebral oedema
  • Dexamethasone if brain abscess or tumour
183
Q

Management of underlying causes of ICP

A
  • Antibiotics: if meningoencephalitis or brain abscess (ceftriaxone)
  • Ventriculo-peritoneal (VP) shunts for hydrocephalus
  • Surgical excision of tumours
184
Q

Define epilepsy

A

Epilepsy is a neurological condition characterised by recurrent seizures.

Seizures are paroxysmal alteration of neurological function as a result of excessive, hypersynchronous firing of neurons within the brain

185
Q

Types of epileptic seizures

A
  • Focal
  • Generalised
  • Focal to bilateral
  • Unknown

Important to know origin as it determines treatment

186
Q

Three key features to classify seizures

A
  1. Where the seizures began
  2. Level of awareness during the seizure
  3. Other features of the seizure e.g. motor
187
Q

Focal seizures: clinical features of temporal lobe seizures (most common)

A
  • Automatism: lip smacking, picking
  • Automatic behaviour: running, walking
  • Auras: déjà vu, unpleasant smells
188
Q

Focal seizures: clinical features of frontal lobe seizures

A

Predominantly motor symptoms: pelvic thrusting, bicycling, tonic posturing

189
Q

Focal seizures: clinical features of parietal lobe seizures

A
  • Parasthesias
  • Visual hallucinations
  • Visual illusions
  • More subjective and difficult to diagnose than other areas
190
Q

Focal seizures: clinical features of occipital lobe seizures

A
  • Visual hallucinations
  • Amaurosis fugax
  • Rapid and forced blinking
  • Movement of head or eyes to the opposite side
191
Q

How are focal seizures classified in terms of awareness?

A
  • Focal aware
  • Focal impaired awareness
192
Q

Investigations for focal and generalised seizures

A
  • Bedside: FBC, blood glucose, electrolyte screen, tox screen if drugs suspected, LP and CSF analysis if infection suspected
  • CT head (1st line)
  • MRI brain (gold standard)
  • Electroencephalography (EEG)

All adults must be referred to specialist via “first fit” clinic.

Diagnosis usually after 2 unprovoked seizures or 1 if abnormal EEG

193
Q

Medical management for focal seizure

A

Lamotrigine or Levetiracetam

194
Q

Define generalised seizures

A

Generalised seizures affect both hemispheres and always impair awareness. They can be classified as motor or non-motor.

195
Q

Types of generalised seizures

A
  • Tonic-clonic
  • Tonic
  • Clonic
  • Myoclonic
  • Atonic
196
Q

Generalised seizures: clinical features of tonic-clonic seizures

A

Stiffening of limbs (tonic) with rhythmic jerking (clonic) simultaneously

197
Q

Generalised seizures: clinical features of tonic seizures

A

Sudden stiffness or tension in muscles of arm, legs or trunk

198
Q

Generalised seizures: clinical features of clonic seizures

A

Repeated jerking movements of arms or legs on one or both sides of the body

199
Q

Generalised seizures: clinical features of myoclonic seizures

A

Some or all of the body suddenly twitches. Usually lasts less than a second.

Can be generalised or focal

200
Q

Generalised seizures: clinical features of atonic seizures

A

Sudden loss of muscle strength. Might cause a person to drop to the ground

Can be generalised or focal

201
Q

Conservative management for seizures

A

Education - avoiding triggers, safety measures

Stop driving and inform the DVLA:

  • First unprovoked seizure with normal EEG: 6-month suspension
  • First unprovoked seizure with a structural abnormality or epileptiform activity on EEG: 12-month suspension
  • Established epilepsy: can apply for a license if seizure-free for 12-months or 5 years if an HGV driver
202
Q

What are absence seizures?

A

They are generalised non-motor seizures which involve brief changes in awareness, staring or repeated movements like lip-smacking.

203
Q

Medical management for generalised seizures

A
  • Sodium valproate - highly teratogenic so avoid in women of childbearing age
  • Lamotrigine/Levetiracetam in women of childbearing age
  • Absence seizure: Ethosuximide
204
Q

What areas should hx for an epileptic seizure focus on?

A

Before, during and after seizure, eye-witness account is important.

Pre-ictal

  • Risk factors for epilepsy
  • Seizure triggers: e.g. alcohol
  • Aura: subjective feeling of warning pre-seizure

Ictal

  • Length of the seizure
  • Appearance: jerking suggests tonic-clonic, behavioural arrest suggests absence
  • Progression: e.g. jacksonian march - seizure spreads from the distal part of the limb toward the face
  • Consciousness
  • Injury: tongue biting, head injury
  • Urinary incontinence

Post-ictal

  • Drowsiness, headaches, amnesia, confusion around 30 minutes
  • Neurology: e.g. Todd’s paresis (weakness/paralysis in body after seizure)
205
Q

Define status epilepticus

A

Status epilepticus (SE) is a single, continuous seizure lasting >5 minutes or two or more seizures within five minutes without regaining consciousness in between.

It is a medical emergency.

206
Q

Acute management of status epilepticus

A

ABCDE approach:

  • Securing the airway
  • Giving high-concentration oxygen
  • Checking blood glucose levels
  • Gaining IV access (inserting a cannula)
207
Q

Medical management of status epilepticus after ABCDE management

A

1st line: benzodiazepine (e.g. IV lorazepam 4mg or diazepam 10mg or buccal midazolam 10mg)

Repeat after 5-10 minutes if the seizure continues

If ineffective then IV levetiracetam, phenytoin or sodium valproate

Call on-call anaesthetist if still ineffective

208
Q

Investigations for status epileptius

A
  • Glucose,
  • ECG: cardiac arrhythmias can precipitate seizures
  • ABG
  • FBC, U&Es and LFTs
  • Sodium, calcium, magnesium
  • Inflammatory markers: identify possible infection
209
Q

What is multiple sclerosis?

A

Multiple sclerosis (MS) is a demyelinating central nervous system condition clinically defined by two episodes of neurological dysfunction (brain, spinal cord, or optic nerves) that are separated in space and time.

210
Q

Risk factors for epilepsy

A
  • Family history
  • Previous CNS trauma or infection
  • Previous history of seizures
211
Q

Risk factors for MS

A
  • Female
  • 20 - 40
  • Family history (HLA-DR2)
  • Northern latitude
212
Q

Types of MS

A

Relapsing-remitting (85%)

  • Episodic flare-ups lasting days - months with periods of remission
  • 60% progress to secondary progressive

Secondary progressive

  • Begins with a relapsing-remitting course but progressively worsens with no periods of remission

Primary progressive (10%)

  • Symptoms get progressively worse from disease onset with no periods of remission
213
Q

Key clinical features of MS

A
  • Blurred vision and red desaturation (optic neuritis) - most common presentation
  • Weakness/tingling/numbness
  • Symptoms worsen after hot bath/shower (Uhtoff’s phenomenon)
214
Q

Investigations for MS

A

Diagnosis made by a neurologist based on the clinical picture and symptoms suggesting lesions that change location over time. Other causes for the symptoms need to be excluded.

McDonald criteria

2 or more relapses with either:

  • Objective clinical evidence of 2 or more lesions

OR

  • Objective clinical evidence of one lesion WITH a reasonable history of a previous relapse

Consider
MRI - periventricular white matter lesions

CSF analysis = oligoclonal bands

215
Q

Management of acute relapse in MS

A

Methylprednisolone IV or oral

216
Q

Maintenance management of relapsing-remitting MS

A

Disease-modifying therapy e.g. Interferon beta, glatiramer acetate

217
Q

Define subarachnoid haemorrhage (SAH)

A

SAH is a type of intracranial haemorrhage characterised by blood within the subarachnoid space. It is most commonly caused by trauma (traumatic SAH).

218
Q

Common causes of SAH

A
  • Trauma (e.g. head injury)
  • Berry aneurysm (80% of spontaneous SAH)
219
Q

Risk factors for SAH

A
  • Increasing age: >50
  • Hypertension
  • Smoking
  • Family history
  • Autosomal Dominant Polycystic
    kidney disease (PKD)
  • Alcohol excess
220
Q

Clinical features of SAH

A
  • Severe sudden-onset headache (peaks within 1-5 mins and lasts > 1 hour)
  • Vomiting
  • Depressed consciousness/loss of consciousness
  • Neck stiffness and muscle aches (meningismus)
221
Q

Investigations for SAH

A
  • Urgent non-contrast CT head
  • Diagnostic if hyperdense appearance of blood in the subarachnoid space/basal cistern
  • Lumbar punture if normal CT, NICE recommend LP > 12 hours after symptom onset, because bilirubin takes time to accumlate in CSF

SAH on CSF will show:

  • Raised red cell count
  • Xanthochromia (a yellow colour to the CSF caused by bilirubin)

CT angiography to confirm source of SAH

222
Q

Management of SAH

A
  • Urgent referral to neurosurgery
  • Call the anaesthetist (UK)
  • Medical: 1st line is nimodipine (calcium-channel blocker) to prevent vasospasm
  • Surgerical: 1st line is endovascular coiling of aneurysm
223
Q

DIfferentials for SAH

A
  • Migraine (can be severe headache but often previous hx)
  • Intracerebral haemorrhage (ICH)
  • Meningitis (fever present)
224
Q

Define meningitis

A

Inflammation of the meninges, the membranes covering the brain and spinal cord

Most commonly caused by bacteria or viruses

225
Q

Most common causes of viral meningitis

A
  • Herpes simplex virus (HSV, HSV-1 in Western world)
  • Enterovirus e.g. coxsackie virus
  • Varicella zoster virus (VZV).
226
Q

Risk factors for viral meningitis

A

Age (infants, young children, young and older adults) and exposure to insect vectors.

227
Q

Clinical features of viral meningitis

A
  • Headache
  • Photophobia
  • Neck stiffness
  • Fever
  • Nausea and vomiting
228
Q

Special tests for meningitis

A
  • Kernig’s sign: flexed hip and the knee at 90°, extension of knee = pain
  • Brudzinski sign: severe neck stiffness causes the hips and knees to flex when the neck is flexed
229
Q

Investigations for meningitis

A
  • Blood tests: FBC, U+E, clotting, blood glucose
  • Arterial Blood Gas
  • Blood cultures
  • CT Head
  • Lumbar puncture for CSF analysis - bacterial culture, viral PCR, cell count, glucose, protein
230
Q

Management for viral meningitis

A

Suspected meningitis, unknown cause: empirical antibiotics and follow local guidelines

Confirmed viral: supportive care

  • Analgesia/antipyretic (pain ladder)
  • Anti-emetics (e.g., ondansetron) if vomiting
  • IV fluids if needed
  • Stop empirical antibiotics
231
Q

CSF analysis: bacterial meningitis results

A

Appearance = Cloudy

Protein = High (>1g/L)

Glucose = Low (<50% serum glucose)

White Cell Count = High - 10-5000/mm3 (neutrophils)

Culture = +ve for bacteria

232
Q

CSF analysis: viral meningitis results

A

Appearance = Clear

Protein = Mildly raised/normal (<1g/L)

Glucose = High (>60% serum glucose)

White Cell Count = High 1000/mm3 (lymphocytes)

Culture = Negative

233
Q

Most common causes of bacterial meningitis

A

Children + adults
N. meningitidis aka meningococcus

S. pneumoniae aka pneumococcus

Neonates
Group B streptococcus (GBS)

234
Q

Which is more serious: bacterial or viral meningitis?

A

Bacterial! It is a life-threatening inflammation of the meninges! Needs urgent empirical antibiotics

235
Q

Clinical features of bacterial meningitis

A
  • Headache
  • Neck stiffness
  • Fever
  • Altered mental status

Children with meningococcal meningitis can have a non-blanching rash

236
Q

Risk factors for bacterial meningitis

A
  • Advanced age (over 60s)
  • Crowded places (e.g. student halls)
  • Exposure to causative microorganisms
  • Immunocomprising conditions e.g. diabetes
237
Q

Management for bacterial meningitis

A

Community:

  • Empirical antibiotics: signle dose IM/IV benzylpenicillin or ceftriaxone
  • Hospital admission/transfer

Hospital:

  • Follow local guidelines and seek guidance from micrology
  • Under 3 months – cefotaxime plus amoxicillin (amoxicillin is to cover listeria)
  • Above 3 months – ceftriaxone
238
Q

DIfferntials for meningitis

A

Encephalitis

239
Q

Define encephalitis

A

Encephalitis describes inflammation of the brain parenchyma.

240
Q

Most common cause of encephalitis

A

HSV-1 - 95% cases

241
Q

Risk factors for encephalitis

A
  • Under 1 or over 65 years
  • Immunodeficiency
  • Body fluid exposure: HIV,
  • Organ transplantation
  • Animal or insect bites (mosquito bites for West Nile virus)
242
Q

Clinical features of encephalitis

A
  • Altered mental state
  • Fever
  • Rash
  • Focal neurological deficit (e.g. ataxia, aphasia)
  • Behavioural changes (e.g. withdrawal, personality changes, psychosis
243
Q

Investigations for encephalitis

A
  • Blood tests: FBC, CRP, U&Es, LTFs
  • Viral throat swab
  • CT or MRI (preferred) head - HSV affects temporal lobes and bilateral multifocal haemorrhage seen

CSF analysis:

  • lymphocytosis + raised protein if viral
  • PCR for HSV and other common viral causes
  • Blood cultures
244
Q

Management for encephalitis

A

Aciclovir for HSV-1

245
Q

Differentials for encephalitis

A
  • Hypoglycaemia
  • Hepatic encephalopathy
  • Diabetic Ketoacidosis (DKA)
246
Q

What are brain tumours?

A

An abnormal growth occurring in any tissue within the cranium, including the brain, cranial nerves, meninges, skull and pituitary gland.

  • Benign or malignant
  • Primary or secondary (metastatic)
247
Q

EXAM TIP!

A

A common exam scenario is an unusual change in personality and behaviour, which indicates a frontal lobe tumour. The frontal lobe is responsible for personality and higher-level decision-making.

248
Q

Clinical features of brain tumours

A

Usually asymptomatic when small, progressive focal neurological deficits as they grow bigger.

Symptoms and signs of raised intracranial pressure (ICP)

249
Q

Clinical features of raised intracranial pressure

A
  • Headache: red flags are constant, worse in morning, nocturnal, vomiting

Other clinical features

  • Altered mental state
  • Visual field defects
  • Seizures (particularly partial seizures)
  • Unilateral ptosis (drooping upper eyelid)
  • Third and sixth nerve palsies (eye down and out, can’t abduct)
250
Q

What would be the finding on fundoscopy in ICP?

A

Papilloedema - swelling of optic disc secondary to ICP

251
Q

What is a giloma?

A

Tumours of the glial cells in the brain or spinal cord. Glial cells surround and support neurons. Glial cells include astrocytes, oligodendrocytes and ependymal cells.

252
Q

Classification of gliomas

A

Grades 1 to 4.

Grade 1 = most benign

Grade 4 = most malignant (e.g., glioblastoma multiforme).

253
Q

Main types of gliomas

A
  • Most aggressive: astrocytoma (the most common and aggressive form is glioblastoma)
  • Oligodendroglioma
  • Least aggressive: Ependymoma
254
Q

What are meningiomas?

A

Tumours originating from cells of the meninges

Usually benign but they take up space and the “mass effect” can lead to ICP and neurological symptoms.

255
Q

What cancers most commonly metastate to the brain?

A
  • Lung
  • Breast
  • Renal cell carcinoma (Kidney)
  • Melanoma
256
Q

What are pituitary tumours?

A

Usually benign, but can press on optic chiasm if grows large enough

Visual field defect = bitemporal hemianopia

Causes hypo/hyperpituitarism, causing:

  • Acromegaly (excessive growth hormone)
  • Hyperprolactinaemia (excessive prolactin)
  • Cushing’s disease (excessive ACTH and cortisol)
  • Thyrotoxicosis (excessive TSH and thyroid hormone)
257
Q

Management for pituitary tumours

A
  • Trans-sphenoidal surgery (through the nose and sphenoid bone)
  • Radiotherapy
  • Bromocriptine to block excess prolactin
  • Somatostatin analogues (e.g., octreotide) to block excess growth hormone
258
Q

What are acoustic neuromas?

A

Benign tumours of the Schwann cells that surround the auditory nerve (vestibulocochlear nerve).

Schwann cells provide myelin sheath of the PNS

Usually unilateral, bilateral associated with neurofibromatosis type 2

Management options include:

Conservative management with monitoring may be used if there are no symptoms or treatment is inappropriate
Surgery to remove the tumour (partial or total removal)
Radiotherapy to reduce the growth

259
Q

What would a typical patient with acoustic neuromas present with>

A

40 - 60, gradual onset of:

  • Unilateral sensorineural hearing loss (often the first symptom)
  • Unilateral tinnitus
  • Dizziness or imbalance
  • Sensation of fullness in the ear
  • Facial nerve palsy (if the tumour grows large enough to compress the facial nerve)
260
Q

Management options for acoustic neuromas

A
  • Conservative: active monitoring if no symptoms or treatment not suitable
  • Surgery to remove the tumour (partial or total removal)
  • Radiotherapy to reduce the growth
261
Q

Investigations for brain tumour

A

1st line: MRI head

Biopsy to confirm histological diagnosis, taken during surgical removal

262
Q

Management for brain tumours

A

Depends on type and grade and is guided by MDT, main options are:

  • Surgery
  • Chemotherapy
  • Radiotherapy
  • Palliative care
263
Q

Define spinal cord compression (SCC)

A
  • Injury to the spinal cord as a result of external pressure
  • Causes damage to white matter and grey matter resulting in partial or complete loss of sensory modalities and motor function.
  • Can lead to acute, sub-acute or chronic spinal cord injury
264
Q

Common cause of SCC

A

Trauma: e.g. car accident

Vertebral compression fractures: e.g. osteoporosis

Intervertebral disc disease: disc herniation

Tumours: e.g. metastatic disease

Infection: discitis, TB (Pott’s disease)

265
Q

RIsk factors for SCC

A
  • High-risk sporting activity: e.g. horse-riding
  • High-risk occupation: construction
  • Malignancy: particularly breast, prostate, renal, lung, multiple myeloma metastasis
  • Age
  • Immunosuppression or IVDU: osteomyelitis, discitis, epidural abscess
266
Q

Clinical features of SCC

A
  • UMN signs: hyperreflexia, spasticity, and a positive Babinski’s sign.
  • Sensory disturbance (temp, fine touch, vibration): typically below lesion level
  • Deep and localized back pain
  • Radicular sensory disturbance: stabbing sensation at the level of the lesion.

Bladder and bowel incontinence or retention.

267
Q

Investigations for SSC

A
  • Full neuro exam: tone, power, reflexes, sensation, proprioception
  • Urgent whole spine MRI, aim to surgically decompress within 48 hours
268
Q

Management for acute traumatic SSC

A
  • Immediate immobilisation
  • Surgical spinal cord decompression and stabilisation
269
Q

Management of malignant SSC

A
  • Dexamethasone: reduce inflammation

Radiotherapy: palliative

Surgery: depending on the impact of radiotherapy, age and prognosis

270
Q

Management of infective SSC (e.g. epidural abscess

A
  • IV antibiotics
  • Surgery: spinal cord decompression or CT-guided needle aspiration if abx ineffective
271
Q

Differentials for SCC

A
  • MS
  • Peripheral neuropathy
272
Q

Define cauda equina syndrome

A

Cauda equina syndrome (CES) is caused by compression of the lumbosacral nerve roots of the cauda equina below the spinal cord

Neurological emergency!

273
Q

Risk factors for CES

A
  • Lumbar disc herniation: the most common cause of CES
  • Trauma
  • Spinal tumour
274
Q

Clinical features of CES

A
  • Bladder dysfunction (overflow incontinence, less awareness of full bladder)
  • Lower limb weakness - absent reflexes too
  • Saddle anaesthesia - red flag
  • Lower back pain & sciatica
275
Q

Investigations for CES

A
  • Gold-standard - non-contrast MRI spine - lesions and compression od neural structures
276
Q

Management of CES

A
  • Urgent surgical decompression, 48-hour window remains controversial as some studies showed that it can affect prognosis.
  • VTE prophylaxis
  • PPI (e.g. omeprazole) to prevent gastric stress ulcer
  • Bladder/bowel management (catheter, laxatives, manual evacuation)
277
Q

DIfferentials for CES

A
  • Spinal stenosis
  • Spinal epidural abscess (fever often present)
  • Sciatica
278
Q

Define myasthenia gravis

A

Myasthenia gravis is a chronic autoimmune disorder of the postsynaptic membrane at the NMJ of skeletal muscle.

Autoantibodies against the nicotinic acetylcholine receptor (AChR) and sometimes muscle-specific kinase (MuSK)

Fewer available binding sites for acetylcholine (Ach), resulting in weakness.

279
Q

Risk factors for myasthenia gravis

A
  • Female gender: 2:1
  • Family history
  • Other autoimmune conditions: personal or FHx e.g. SLE, RA
  • Thymoma or thymic hyperplasia
280
Q

Symptoms of myasthenia gravis

A
  • Muscle weakness worse at end of the day
  • Double vision
  • Droopy eyelids
  • Dysphagia (chewing/swallowing)
  • SOB - might indicate myasthenic crisis
281
Q

Signs of myasthenia gravis

A
  • Muscle strength fatigability, might have diurnal pattern (better in morning than evening)
  • Unilateral/bilateral ptosis
  • Myasthenia snarl - “snarling” expression when smiling
282
Q

What medications can exacerbate myasthenia?

A
  • Beta-blockers
  • Lithium
  • Penicillamine
  • Gentamicin
  • Quinolones
  • Phenytoin
283
Q

Investigations for myasthenia gravis

A

1st line: Acetylcholine receptor (AChR) antibody analysis

Muscle-specific tyrosine kinase (MuSK) antibodies if above -ve

Serial pulmonary tests

Chest CT for thymoma or thymic hyperplasia

-Repetitive nerve conduction studies: decremental muscle response

284
Q

What is a myasthenic crisis?

A

Complication of myasthenia gravis due to weakening of the respiratory muscles and is often provoked by infections or medications.

Presents with SOB which can progress to respiratory failure

285
Q

Management of myasthenic crisis

A
  • IV immunoglobulin or plasmapheresis
  • Intubation: if severe respiratory compromise
  • Corticosteroids as an adjunct
286
Q

Maintenance management of myasthenia gravis

A

First-line: pyridostigmine which is an acetylcholinesterase inhibitor

287
Q

Differential for myasthenia gravis

A

Lambert-Eaton syndrome, usually as a result of SCLC, improves with exercise unlike MG

288
Q

Define motor neuron disease (MND)

A

Motor neuron disease (MND) is a disorder of both upper and lower motor neurons mostly present ≥ 40.

Amyotrophic lateral sclerosis (ALS) most common ~50%

289
Q

What is ALS?

A

A neurodegenerative disorder characterised by progressive muscle weakness that can start in limb, axial, bulbar, or respiratory muscles and then generalises relentlessly, causing progressive disability and ultimately death, usually from respiratory failure.

290
Q

Clinical features of ALS

A

Both UMN and LMN symptoms

  • Upper extremities weakness - difficulties with e.g. brushing teeth, dressing due to mix of UMN and LMN
  • Difficulties arising from sitting - LMN causing lower limb weakness
  • Difficulties with swallowing (dysphagia)
  • Difficulties with speech (dysarthria)
  • Hyperreflexia - UMN
  • Fasciculations, especially on the tongue
  • Muscle wasting: particularly of small hand muscles and tibialis anterior
291
Q

What features are characterisedly absent in MND?

A

No sensory abnormalities

No extraocular involvement

No cerebellar involvement

292
Q

Investigations for MND/ALS

A

Clinical diagnosis

Consider:

  • Electromyography: fibrillation potential (action potentials generated by recently denervated muscle fibres)
  • Nerve conduction studies: reductions in amplitude
  • MRI spine: exclude spinal pathologies that mimic MND e.g. cervical cord compression
  • Pulmonary function tests: risk of respiratory failure
293
Q

Management for ALS

A
  • Riluzole: prolongs survival in ALS by 2-4m
  • Respiratory support: non-invasive ventilation at home, usually BiPAP, prolongs life by 7m

Supportive treatment:

  • Antispasmodics: such as baclofen
  • Feeding support: often PEG tube
  • Speech and language therapy
  • Physiotherapy
294
Q

Complications of ALS

A
  • Aspiration pneumonia
  • Respiratory failure: often in advanced disease when respiratory muscles have been affected
  • Most patients die within 3- 5 years from onset of symptoms from respiratory complications
295
Q

Define muscular dystrophy

A

Muscular dystrophy is an umbrella term for genetic conditions that cause gradual weakening and wasting of muscles.

Main type is Duchenne’s muscular dystrophy (DMD-exams)

296
Q

What is Duchenne’s muscular dystrophy?

A

X-linked recessive muscular dystrophy caused by a defective gene for dystrophin on the X-chromosome.

Dystrophin is a protein that provide structural stability to muscles at a cellular level.

Women who are carriers don’t usually notice the symptoms, her offsprings have:

  • 50% chance of carriers if female
  • 50% chance of the condition if male
297
Q

What is Gower’s sign?

A

Children with proximal muscle weakness get on their hands and knees and push into a “downward” dog position and slowly stand up legs first and walk their hands up as
the muscles around the pelvis are not strong enough to get their upper body erect without the help of their arms.

298
Q

Investigations for DMD

A
  • Serum creatinine kinase - elevated CK levels are characteristic of DMD, levels of over 20,000 international units/L not common.
  • 50-100 times normal level consistent with DMD
  • Genetic testing
299
Q

Management for DMD

A

No cure

Aims to improve QoL

MDT: doctors, nurse, OT, Physio

Medical appliances e.g. wheelchairs, braces

Medical management of complications e.g. spinal scoliosis and HF

300
Q

Define Guillian-Barre syndrome (GBS)

A

GBS is an acute paralytic polyneuropathy that affects the peripheral nervous system.

It causes acute, symmetrical, ascending weakness and can also cause sensory symptoms.

Usually triggered by a preceding infection, associated with:

  • Campylobacter jejuni
  • Cytomegalovirus (CMV)
  • Epstein-Barr virus (EBV).
301
Q

Pathophysiology of GBS

A
  • Autoimmune condition
  • Due to a process called molecular mimicry.
  • The B cells of the immune system create antibodies against the antigens on the triggering pathogen.
  • These antibodies also match proteins on the peripheral neurones.
  • They may target proteins on the myelin sheath (demyelinating form) or the nerve axon (axonal form).
302
Q

Clinical features of GBS

A

Required features:

  • Symmetrical ascending weakness that begins in the feet
  • Hyporreflexia/arflexia

Supprotive of diagnosis:

  • Peripheral loss of sensation, neuropathic pain or/and autonomic dysfunction (urinary retention, heart arrhythmias).

Symptoms start within 4 weeks of the triggering infection.

Symptoms peak within 2-4 weeks

Recovery period of months to years

303
Q

Investigations for GBS

A

Clinical diagnosis with Brighton criteria supported by investigations:

Nerve conduction studies - reduced signal through the nerves
Lumbar puncture for CSF analysis - raised protein with a normal cell count and glucose

304
Q

Management of GBS

A
  • 1st line: IV immunoglobulin, or plasmapheresis (plasma exchange)
  • Supportive care
  • VTE prophylaxis (pulmonary embolism is a leading cause of death)
  • Severe cases with respiratory failure may require intubation, ventilation and admission to the ITU
305
Q

Differentials for GBS

A
  • Myasthenia gravis
  • Lambert-Eaton myasthenic syndrome (LEMS)
  • Botulism
306
Q

Define diabetic neuropathy

A

Diabetic peripheral neuropathy (DPN) refers to a variety of peripheral nerve disorders caused by diabetes.

Mainly caused by chronic hyperglycaemia.

307
Q

Risk factors for diabetic neuropathy

A
  • Poorly controlled hyperglycaemia
  • Older age (e.g., >70 years),
  • Prolonged duration of diabetes (e.g., >10 years), and tall stature.
308
Q

Most common type of diabetic neuropathy and clinical features of it

A
  • Distal Symmetrical Sensory Neuropathy
  • Resulting from loss of large sensory fibres.

Clinical features

  • Sensory loss in a ‘glove and stocking’ distribution, typically affecting touch, vibration and proprioception.
309
Q

Investigations for diabetic neuropathy

A

Neurological exam - assess extent of sensory and motor deficits

Clinical diagnosis with bloods to exclude differentials:

  • Fasting blood glucose
  • HbA1c
  • Serum TSH
  • U+E (renal disease)
  • B12 (exclude deficiency)
  • LFTs
  • FBC +ESR (anaemia, inflammatory diseases)
310
Q

Management of diabetic neuropathy

A

Glycemic control and supportive measures

Diet and exercise effective in type 1 and 2

Multiple insulin injections are more effective in type 1 than type 2

Proper foot and wound care

311
Q

Differentials for diabetic neuropathy

A
  • Vitamin B12 deficiency: peripheral neuropathy, typically in a glove and stocking distribution. May also feature megaloblastic anemia
  • Alcohol-induced peripheral neuropathy: presents similarly to DPN but may also have accompanying signs of chronic alcohol misuse.
312
Q

Define Charcot arthropathy

A

A chronic, progressive condition characterised by painful or painless bone and joint destruction in the limbs that have lost sensory innervation. The condition primarily affects patients with peripheral neuropathy, usually from long-standing diabetes.

313
Q

Clinical features of Charcot arthropathy

A

6Ds (some are imaging features)

  • Destruction of bone and joint
  • Deformity
  • Degeneration
  • Dense bones
  • Debris of bone fragments
  • Dislocation
314
Q

What joints do Charcot arthropathy classically affect?

A

Tarsometatarsal joints, but it can involve any joint in a limb that has lost sensation due to neuropathy.

315
Q

Investigations for Charcot Arthropathy

A

Clinical diagnosis with imaging:

1st line = X-ray - shows bone destruction, debris, sclerosis (dense bones), and dislocation.

316
Q

Management for Chorcot arthropathy - conservative

A

Prolonged off-loading, often involving special footwear or plaster casts, to allow healing and prevent further damage.

Long-term use of orthotics for prevention of recurrences.

317
Q

Medical management for Charcot arthropathy

A
  • Bisphosphonates - slows down bone destruction
  • Gabapentin or pregabali for paiin
  • Topical anesthetics
318
Q

Surgical management of Charcot arthropathy

A

Resection of bony prominences to prevent ulcers or improve fitting of footwear.

Amputation if severe or concurrent uncontrolled infection.

319
Q

Define carpal tunnel syndrome

A
  • Most common mononeuropathy
  • It is a collection of symptoms and signs caused by compression of the median nerve in the carpal tunnel.
320
Q

What is the carpal tunnel?

A

In the wrist, there is a fibrous band called the flexor retinaculum that runs across the palmar side of the wrist.

The carpal bones lie underneath. The carpel tunnel is a passage, from the forearm to the hand. that runs between the flexor retinaculum and the carpal bone.

It contains the median nerve and the forearm flexor tendons.

321
Q

What causes carpal tunnel syndrome?

A

Compression of the contents of the carpal tunnel (causing carpal tunnel syndrome) is the result of either:

Swelling of the contents (e.g., swelling of the tendon sheaths due to repetitive strain)
Narrowing of the tunnel

322
Q

What structures does the palmar digital cutaneous branch of the median nerve innervate?

A

It passes through the carpal tunnel, and is responsible for sensory innervation of the palmar aspects and full fingertips of the:

  • Thumb
  • Index and middle finger
  • The lateral half of ring finger
323
Q

What muscles does the median nerve innervate?

A

Thenar muscles motor function

  • Abductor pollicis brevis (thumb abduction)
  • Opponens pollicis (thumb opposition)
  • Flexor pollicis brevis (thumb flexion)
324
Q

Risk factors for carpal tunnel syndrome

A

Most commonly idiopathic

Key risk factors:

  • Repetitive strain
  • Obesity
  • Perimenopause
  • Rheumatoid arthritis
  • Diabetes
  • Acromegaly
  • Hypothyroidism
325
Q

Clinical features of carpal tunnel syndrome

A

Gradual onset, worse at night

Sensory symptoms: numbness, paraesthesia, burning sensation and pain in the distribution of the palmar digital cutaneous branch of the median nerve (see above)

Motor symptoms affect thenar muscles

  • Weakness of thumb movements
  • Weakness of grip strength
  • Difficulty with fine movements involving the thumb
  • Wasting of the thenar muscles (muscle atrophy)
326
Q

Special tests for carpel tunnel syndrome

A
  • Phalen’s
  • Tinel’s
327
Q

Investigations for carpel tunnel

A
  • Hand exam with special tests

Carpal tunnel questionnaire: the Kamath and Stothard carpal tunnel questionnaire (CTQ)

It scores based on questions such as:

  • Do symptoms wake you at night?
  • Do you have trick movements (e.g., shaking the hand) to improve symptoms?
  • Is your little finger affected? (Answering yes scores negatively, making carpal tunnel syndrome less likely)

High score = more likely to be carpal tunnel syndrome

  • Electromyography (EMG): to assess the electrical activity of the muscles at rest and during contraction.

Gold standard:
- Nerve Conduction Studies (NCS): to measure the speed and strength of signals traveling through the median nerve.

328
Q

Management of carpal tunnel syndrome

A
  • Rest and altered activities
  • Wrist splints for a minimum of 4 weeks
  • Steroid injections
  • Surgery

Surgery:

  • Day case under local anaesthetics
  • Open or endoscopic
  • The flexor retinaculum is cut to release the pressure on the median nerve.
329
Q

Differentials for carpal tunnel syndrome

A
  • Cubital tunnel syndrome
  • Ulnar nerve compression at the elbow
  • Cervical nerve root entrapment
330
Q

Define radiculopathy

A

Radiculopathy is a condition where a nerve root in the spinal column becomes inflamed or compressed, causing pain, numbness, or weakness radiating along the nerve root’s pathway.

331
Q

Common causes of radiculopathy

A
  • Herniated discs
  • Spinal stenosis
  • Degenerative disc disease
332
Q

Classification of radiculopathy

A
  • Cervical radiculopathy: neck and upper limbs
  • Thoracic radiculopathy: mid-back and torso

Lumbosacral radiculopathy: lower back and lower limbs

333
Q

Risk factors for radiculopathy

A

Age: most common 30 - 50

Occupational factors: heavy lifting or repetitive movements

Osteoarthritis: cervical radiculopathy can arise from osteoarthritic changes in the C-spine

334
Q

What is a dermatome?

A

A dermatome is a patch of skin that receives sensory nervous supply from a single spinal nerve root (e.g. T1).

335
Q

Clinical features of radiculopathy

A

Symptoms:

  • Radiating pain originating in neck or back
  • Paraesthesia or numbness
  • Muscle weakness

Signs:

  • Positive straight leg raise test = places stress on L2 -L4 and sciatic nerve, lumbar radiculopathy
  • Sensory deficits in a dermatomal distribution
  • Reduced muscle power
336
Q

Distinguishing L5 radiculopathy from a common peroneal nerve injury is a common exam question. What are the overlapping clinical features and differences?

A

Overlapping clinical features

Weakness of foot dorsiflexion

Weakness of toe extension

Differences

L5 radiculopathy: Weakness during foot inversion

Common peroneal nerve injury: Weakness during foot eversion

L5: Lower limb tendon reflex changes present

Common peroneal: no changes to lower limb reflexes

L5: L5 dermatomal distribution of sensory loss

Common peroneal: sensory loss over the anterior aspects of foot and leg

337
Q

Investigations for radiculopathies

A
  • MRI: level and cause of nerve root compression if severe
  • Nerve conduction studies: to assess the speed of nerve signal transmission.
  • Electromyography (EMG): measures electrical activity in muscles and identifies the affected nerve root.
338
Q

Management of radioculopathies

A

First-line:

NSAIDs: ibuprofen

Physiotherapy to relieve pressure on affected nerve root

Second-line:

Epidural steroid injections: if severe to reduce inflammation

Surgery: laminectomy or discectomy if conservative and medical treatment not effective

339
Q

What are the red flag features in a new acute-onset headache that warrants referral to the emergency room or urgent referral to secondary care?

A
  • Sudden-onset severe headache reaching maximum intensity within 5 minutes:
  • Subarachnoid haemorrhage

New-onset headache in a person aged over 50 years:

  • Temporal arteritis
  • Space-occupying lesion

Progressive or persistent headache or headache that has changed dramatically:

  • Space-occupying lesion
  • Subdural haematoma

Headache worse on standing or sitting: raised ICP e.g. space-occupying lesion

  • Headache worse on waking - raised ICP

Recent head trauma <3m: subdrural haematoma

340
Q

Define brain metastases

A

Brain metastases occur when cancer cells spread from their primary location to the brain via haematogenous spread (via blood).

341
Q

What is the tentorium cerebelli and how is used in the classification of brain metastases?

A

A membrane that extends from the dura mater that invaginates to separate the occipital and temporal lobes (superiorly) from the cerebellum and brain stem (inferiorly).

Used to categorise brain metastases as it affects treatment.

  • Supratentorial
  • Infratentorial
342
Q

Most common primary cancers that metastate to the brain

A
  • Lung cancer
  • Breast cancer
  • Melanoma
  • Colorectal cancer
  • Renal cell carcinoma
343
Q

Symptoms of brain metastases

A
  • Headache that is worse on lying flat e.g. at night and first thing in the morning
  • N+V
  • Reduced consciousness
  • Seizure
  • Blurred vision
344
Q

Signs of brain metastases

A
  • Focal neurological deficits: determined by site of brain metastasis
  • ICP: e.g. papilloedema (optic disc swelling) on fundoscopy
  • Cushing triad: hypertension, bradycardia and irregular respirations
  • Hemiparesis
345
Q

Investigations for brain metastases

A

MRI brain: Gold standard as detailed and can identify even small metastases

CT brain: less sensitive than MRI but more available in emergencies

346
Q

Acute management for brain metstates

A

Corticosteroids: dexamethasone to reduce oedema

347
Q

Ongoing management for brain metastases

A
  • Radiotherapy: whole brain radiotherapy (WBRT) for multiple metastases
  • Stereotactic radiosurgery : delivery of a high dose of radiation focally to the tumour
  • Surgery: if solitary tumour or as a diagnostic tool if primary unknown
  • Chemotherapy: drugs with good CNS penetration, such as temozolomide, topotecan, and irinotecan

Targeted therapies and immunotherapy: immune checkpoint inhibitor (ICI), ipilimumab effective in recurrent brain metastases

348
Q

Rehabilitation after treatment for brain metastases

A

Physical therapy can help regain lost motor skills or muscle strength.

Occupational therapy: help patients return to their normal daily activities, including work

Speech therapy if difficulties with speech

349
Q

Define normal pressure hydrocephalus (NPH)

A

A rare condition that occurs when the ventricles of the brain become enlarged due to an increase in CSF in the brain space, without a concomitant increase in the CSF opening pressure on a lumbar puncture.

Produces a rapidly progressing dementia-like picture with gait disturbances not responsive to levodopa

350
Q

Causes of NPH

A
  • Mostly idiopathic

Secondary causes:

  • Subarachnoid haemorrhage
  • Intracerebral haemorrhage
  • Severe meningitis
  • Brain tumour
  • Head trauma
351
Q

Clinical features of NPH

A

Classic triad (Hakim’s triad) of:

  • Mental impairment (poor conc, poor memory, increasing confusion),
  • Urinary incontinence
  • Gait disturbance (shuffling + “magnetic” like feet stuck to floor)
352
Q

Investigations for NPH

A
  • CT/MRI head: key diagnostic features include ventriculomegaly; absence of macroscopic obstruction to CSF flow
  • Levodopa challenge - give levodopa if PD suspected to confirm
353
Q

Management of NPH

A

1st line

Ventriculo-peritoneal shunting (VPS): permanent CSF diversion from the ventricular system to the peritoneum via shunt surgery.

354
Q

DIfferentials for NPH

A
  • Parkinson’s disease
  • Parkinson-plus syndromes
  • Alzheimer’s
355
Q

Define hydrocephalus

A

Hydrocephalus is a neurological disorder characterized by an excessive accumulation of CSF within the brain’s ventricular system, leading to ventricular enlargement or ventriculomegaly. This increase in CSF results in raised intracranial pressure.

356
Q

Clinical features of hydrocephalus

A

Symptoms often relate to ICP:

  • Early morning headaches
  • Nausea and vomiting
  • Lethargy
  • Vision disturbances
  • Balance problems
  • Cognitive difficulties

Investigations and management are the same as NPH

357
Q

DIfferentials for hydrocephalus

A
  • Brain tumours
  • Subdural haematoma
  • Benign intracranial hypertension
358
Q

Define Huntington’s disease

A

Huntington’s disease is an autosomal dominant genetic condition that causes progressive neurological dysfunction.

It is a trinucleotide repeat disorder involving a mutation in the HTT gene on chromosome 4, causing an excessive repetition of the CAG trinucleotide (>38 repeats)which codes for the huntingtin (HTT) protein.

359
Q

Clinical features of Huntington’s

A

Insidious, progressive worsening of symptoms.

Initially, cognitive, mood, and psychiatric symptoms e.g. concentration impairments, personal hygiene changes, personality changes such as irritability, and temper outbursts.

Later onset:

  • Chorea (involuntary, random, irregular and abnormal body movements)
  • Dystonia (abnormal muscle tone, leading to abnormal postures)
  • Rigidity (increased resistance to the passive movement of a joint)
  • Dysarthria (speech difficulties)
  • Dysphagia (swallowing difficulties)
360
Q

Investigations for Huntington’s

A

Clinical diagnosis supported by:

  • Genetic testing i.e. CAG repeat testing:
  • Positive result = ≥ 40 CAG repeats on 1 of the 2 alleles - certain development of HD in lifetime
  • Intermediate result = 36 to 39 repeats - may/ may not develop HD
  • CT or MRI - caudate or striatal atrophy in moderate-severe disease
361
Q

Management of Huntington’s

A
  • Behavioural and genetic counselling for patient, carer and family
  • Tetrabenazine - chorea symptoms
  • MDT input to improve QoL
  • Physiotherapy to improve mobility, maintain joint function and prevent contractures
  • Speech and language therapy
  • Antidepressants (e.g., SSRIs)
  • Advanced directives to document their wishes as the disease progresses
  • End-of-life care
362
Q

Common exam scenario regarding Huntington’s

A

You have to counsel a child of someone with HD, 50% chance of inheritance.

Must be 18 before deciding

Your job is to provide info for the patient to make an informed decision, not to advise them to have a test or not

Usual outcome - patient to think about it further and return if they have further questions.

363
Q

What is the prognosis of Huntington’s?

A

A progressive condition, life expectancy is around 10 - 20 years from symptom onset.

As disease progresses, patients become more frail and susceptible to illness (e.g., infection). Death = aspiration pneumonia or suicide.

364
Q

DIfferentials for Huntington’s

A
  • Parkinson’s disease
  • Wilson’s disease
365
Q

Define essential tremor

A

Essential tremor (ET), is a progressive tremor affecting predominantly the upper limb. I

Absent at rest, occurs in posture and movement (i.e. action tremor). Typically without additional neurological signs or symptoms.

366
Q

Risk factors for essential tremor

A
  • Advanced age: >50% of cases in patients >70
  • Family history
  • Caucasian ancestry
  • Exposure to environmental toxins: organochlorine pesticides, lead, mercury
367
Q

Clinical features of essential tremor

A

Tremor:

  • Upper limb (hands, somestimes voice/head tremor)
  • Worse on movement and posturing
  • Bilateral

Improvement with drugs that affect gamma-aminobutyric acid (GABA)-ergic systems:

  • Alcohol
  • Benzodiazepines
  • Gabapentin
368
Q

Assessment of essential tremor

A

Movement Disorder Society on tremor criteria:

  • Isolated tremor syndrome of bilateral upper limb action tremor
  • At least 3 years’ duration
  • With or without tremor in other locations (e.g., head, voice, or lower limbs)
  • Absence of other neurological signs, such as dystonia, ataxia, or parkinsonism.
369
Q

Investigations for essential tremors

A

Urine

  • 24-hour urinary copper: Wilson’s disease

Bloods

  • TFTs: hyperthyroidism
  • U&Es: electrolyte disturbance
  • LFTs: hepatic failure
  • Serum caeruloplasmin: Wilson’s disease

Imaging

  • MRI head: exclude structural cause
  • SPECT (dAT) scan: Parkinson’s disease
370
Q

What medication can cause tremors and must be excluded in the investigations for essential tremor?

A

Lithium

371
Q

Management for essential termors

A

Depends on severity and effects on ADLs

  • Mild disease: Observation
  • Moderate disease: first-line (medical) is propranolol
  • Treatment-resistant disease: surgery: deep brain stimulation or
    MRI-guided thalamotomy
372
Q

Define extradural haemorrhage (EDH)

A

Bleeding into the potential space between the skull and the dura mater.

The blood collection is called extradural haematoma (EDH).

373
Q

Causes of EDH

A

Most common is trauma e.g. blunt force. Causes middle meningeal artery rupture

Non-trauma:

  • Haemorrhagic tumour
  • Coagulopathy
  • Infection
374
Q

Clinical features of EDH

A

Initial brief loss of consciousness followed by a lucid interval (~20% patients)

Then subsequent deterioration of neurological status and reduced GCS

Often accompanied by physical evidence such as bruising, Battle’s sign (bruising behind mastoid process), periorbital haematoma (racoon eyes), Bleeding from one/both ears

375
Q

What score is used to assess a patient with traumatic brain injury (TBI) which can be caused by head injury?

A

Glasgow coma score (GCS)

3 (completely unresponsive) to 15 (responsive)

Mild TBI: GCS 13-15; mortality 0.1%

Moderate TBI: GCS 9-12; mortality 10%

Severe TBI: GCS <9; mortality 40%.

376
Q

Investigations for EDH

A

Non-contrast CT head - EDH appears as a hyperdense biconvex collection often below temporal bone.

377
Q

Acute management for EDH

A

Urgent neurosurgery opinion

Aim to reduce ICP

Bed position so head at 30 degrees

Intubation if reduced GCS

Oxygen (15L 100% through non-rebreather mask)

Hypertonic saline/mannitol to reduce ICP

Maintain perfusion (= MAP - ICP) via
inotropes (increase cardiac contractility) and vasopressors (increase MAP)

378
Q

Surgical management for EDH

A

Definitive management

  • Craniotomy and haematoma evacuation if ≥ 30cm 3 regardless of the GCS score

Serial CT and observation ONLY if:

  • < 30cm 3
  • < 15mm thickness
  • < 5mm midline shift
  • GCS > 8 without focal deficit
379
Q

Complications of head injury

A
  • If TBI then mortality risk increases as GCS decreases.
  • Neurological deficits such as gait, mobility, muscle weakness dysarthria, dysphasia
  • Cognitive deficits e.g. memory and concentration
  • Intracranial lesions such as extradural haematoma
  • Depression
  • PTSD
380
Q

Define cerebral palsy (CP)

A

Cerebral palsy (CP) is an umbrella term for a non-progressive disease of the brain originating during the antenatal, perinatal or early postnatal period.

Results in motor and postural disorders, 80% have spasticity

381
Q

Causes/risk factors for CP

A

Antenatal (80%):

  • Premature birth: 35% of babies born before 26 weeks will develop CP
  • Maternal infections: chorioamnionitis, and TORCH infections

Perinatal:

  • Asphyxia
  • Birth trauma

Postnatal (10%):

  • Neonatal sepsis
  • Meningitis
382
Q

Clinical features of CP

A

Spastic: (70 - 90%)
- Due to damage to pyramidal pathways
- Hypertonia and hyperreflexia
- “Scissor” gait due to tight adductor muscles

Dyskinetic:

  • Damage to basal ganglia (involved in inhibition of movement)
  • Dystonia (random, slow movements in limbs/trunk)
  • Chorea (random “dance-like” movement)

Ataxic
- Damage to cerebellum
- Uncoordinated movements
- Signs of cerebellar lesion

383
Q

Differentials for CP

A
  • Muscular dystrophies - progressive weakness and loss of muscle mass
  • Metabolic disorders: developmental delay, sezures, failure to thrive
  • Juvenile idiopathic arthritis - joint inflammation, stiffness, pain and swelling
384
Q

Investigations for CP

A

Clinical diagnosis with supporting tests:

  • Imaging - MRI head - periventricular leuko- (white matter) malacia (softening), congenitial malformations, stroke/haemorrhage, cystic lesions
385
Q

Management of CP

A

MDT - physiotherapy (mobility, strength training), OT (adaptive equipment), speech therapy, dietitian

Medical: Baclofen or botulinum toxin as muscle relaxant

386
Q

Define delirium

A

Delirium (sometimes called ‘acute confusional state’) is an acute , fluctuating, clinical syndrome characterised by inattention ,an impaired level of consciousness and disturbed cognitive function

387
Q

Types of delirium

A
  • Hyperactive delirium: agitation, hallucinations, restlessness, combativeness
  • Hypoactive delirium: associated with lethargy , reduced activity and concentration
  • Mixed delirium with symptoms and signs of both hyper- and hypoactive delirium
388
Q

Risk factors for delirium

A
  • Advancing age
  • Co-morbidities
  • Dementia
  • Current hip fracture
  • Increased time in hospital
389
Q

Precipitating factors for delirium

A

PINCH ME

Pain
Infection
(Ma)lNutrition
Constipation
(De)Hydration
Medication
Environment (change)

390
Q

Shared symptoms of hyper and hypoactive delirium

A
  • Disorganised thinking and cognitive disturbance
  • Memory impairment , language disturbance
  • Disorientation + confusion
  • Loss of awareness of surroundings
  • Reversal of sleep-wake cycle
391
Q

Screening for delirium

A

4AT

Alertness

AMT4 (adderviated mental test 4) - age, date of birth, place, current year

Attention (months of the year backwards)

Acute changes/fluctuating course

392
Q

Investigations for delirium

A

Depends on clinical picture

  • ECG
  • Urinalysis
  • Urine or sputum culture: infection
  • Bloods: FBC, BM, LFT, bone profile, TFT, U+E, folate and B12
393
Q

Management for delirium

A
  • Most patients = hospital admission

DOLS if needed

1st line:

  • treat precipitating factors,
  • optimise management of co-morbidities
  • Reorientation methods e.g. accurate, easily readable calendars and clock

Sedation: avoid unless patient is a risk to themselves and others, de-escalation technique first. Haloperidol 0.5mg if sedation needed

394
Q

Five key principles of the Mental Capacity Act 2005

A
  • Capacity is assumed, it needs to be proven otherwise
  • Enabling people to make their own decisions
  • Unwise decisions
  • Best interests
  • Least restrictive option

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