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Year 4 > Neuro & Medical Elderly > Flashcards

Neuro & Medical Elderly Flashcards

1
Q

Epileptic seizure types

A

Focal

  • with or without secondary generalisation
  • with or without loss of awareness

Generalised

  • Absence
  • Tonic
  • Clonic
  • Tonic Clonic
  • Myclonic
  • Atonic
  • Atypical absence
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2
Q

Epidemiology of epilepsy

A

5 per 1000
Childhood or over 60s
Learning disability
Family history

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3
Q

Aetiology of epilepsy

A

IDIOPATHIC most common

Vascular - Stroke, bleeds
Infection - meningitis, encephalitis
Trauma - head injury with unconsciousness >30 minutes
Autoimmune
Metabolic - hypoglycaemia, hypo/hyper natraemia, hypo/hyper calcaemia, uraemia
Neoplasm - brain cancer
Degenerative - Alzheimer’s, vascular dementia
Drugs - phenthiazines, isoniazid, alcohol, benzodiazepine or alcohol withdrawal, TCAs

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4
Q

Typical presentation of generalised seziures

A 
Disturbance in consciousness
Childhood or teenage onset
Seizures triggered by sleep deprivation or alcohol
Classically: TONIC --> CLONIC --> POSTICTAL
Associated with headache and drowsiness
Tongue biting 
Incontinence
Amnesia
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5
Q

Typical presentation of focal seizures

A

Aura
Focal motor activity
Automatisms

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6
Q

Investigations for epilepsy

A

Blood tests - glucose, electrolytes, calcium, renal function, LFTs, BCP

EEG - only to support diagnosis, only if history suggestive

  • Do after the second seizure
  • repeat only if epilepsy syndrome unclear

Imaging - MRI if focal or not controlled by medication

Polysomnography - if suspected sleep related epilepsy

ECG

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7
Q

Management principles of epilepsy

A

Comprehensive care plan
Advice - avoid sleep deprivation and alcohol
Epilepsy specialist nurses

Medications - AEDs
Single where possible
Only to be started by specialist
60% will achieve remission

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8
Q

Management of generalised tonic clonic seizures

A

Sodium valproate / Lamotrigine
Carbemazepine
+ clobazam, lamotrigine, levetiracetam, topiramate

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9
Q

Management of absence seizures

A
  1. Ethosuximide / sodium valproate / Lamotrigine
  2. Combine 2 of 3
  3. Add clobazam, clonazepam, levetriacetam, topiramate
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10
Q

Childhood absence epilepsy

A 
Frequent episodes of staring spells (up to 100 times per day, lasting 5-10 seconds)
Onset - 4-8 years
EEG - 3 per second spike and wave
Onset and termination is abrupt
Stops what they are doing are stares
40% develop GTCS, 80% remit in adulthood
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11
Q

Juvenile absence epilepsy

A 
Fewer absences than in childhood
Onset 10-15 years
EEG - polyspike and wave
80% seizure free in adulthood
80% develop GTCS
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12
Q

Juvenile myoclonic epilepsy

A

Early morning sudden myoclonic jerks (upper limbs)
Onset 15-20 years
GTCS, absence and myoclonic seizures on a morning
EEG - polyspike and wave with photosensitivity
90% remit with medication but recurs with removal

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13
Q

Dravet’s syndrome

A 
Severe myoclonic epilepsy of infancy with recurrent febrile or afebrile hemiclonic or generalised seizures in healthy infant
Onset before 15 months
Resistant to AEDs
Developmental arrest
Mortality 15% before 20
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14
Q

Management of acute seizure

A
  1. Remove patient from harmful situations, protect head
  2. ABCs - check glucose!
  3. If longer than 5 minutes benzos
    Buccal midazolam, rectal diazepam or IV lorazepam
    High flow O2
  4. Max 2 doses
  5. If doesn’t abate then IV phenobarbital or phenytoin.
    Give glucose
  6. If over 30 minutes - call anaesthetist and ITU
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15
Q

Investigations for acute seizure

A
  • Glucose
  • ABG
  • U&Es, LFTs, FBC, clotting
  • Calcium, magnesium
  • AED drug levels
  • Toxicology
  • CXR for ?aspiration
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16
Q

GCS

A 
Eyes 4
1 - No eye opening
2 - opens to pain
3 - opens to voice
4 - spontaneous eye opening

Voice 5
1 - No verbal response
2 - incomprehensible sounds
3 - inappropriate words / monosyllabic
4 - confused
5 - orientated

Motor 6
1 - no motor movements
2 - extension
3 - abnormal flexion (below clavicle)
4 - abnormal flexion (above clavicle)
5 - localises to pain
6 - obeys commands

Severe 3-8
Moderate 9-12
Mild 13-15

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17
Q

Definition of brain death

A
  • Patient deeply comatose (no hypothermia, no depressant drugs, no metabolic abnormality)
  • Patient on ventilator
  • Diagnosis of disorder firmly established
  • All brainstem reflex absent
  • Pupils fixed and dilated
  • No respiratory movement when ventilator switched off (PaCO2 must rise above 6.7kPa)

2 senior doctors = consultant + consultant/SPR
6-24 hours between assessments

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18
Q

Risk factors for delirium

A 
OVer 65
Male
Pre-existing cognitive deficit
Severe co-morbidity
Past delirium
Severe illness
Emergency surgery
Hip fracture
Drugs - benzos
Alcohol misuse
Hyper/hypothermia
Visual or hearing problems
Decreased mobility
Social isolation
Terminally ill
Stress
ICU admission
Moved to new environment
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19
Q

Aetiology of delirium

A

Vascular - stroke, MI, cardiac failure, SDH, SAH, vasculitis, cerebral venous thrombosis
Infection - any
Trauma - head injury
Autoimmune - vasculitis
Metabolic - hypo/hyperglycaemia, hypoxia, electrolyte abnormality (hyponatraemia, hypercalcaemia)
Iatrogenic - drugs
Neoplasm - primary brain, secondary mets, paraneoplastic
Endocrine - hypo/hyperthyroid parathyroid, hypopituitarism, Cushings, porphyria
Urinary retention
Faecal impaction

P ain
IN fection
C onstipation/retention
H ydration
M edication
E nvironmental
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20
Q

Presentation of delirium

A 
Acute or subacute
Fluctuating course
Poor concentration
Clouding of consciousness
Short term memory deficit
Abnormality of sleep wake cycle
Abnormality of perception - hallucinations/illusions
Agitation
Emotional lability
Psychotic ideas - simple content
Unsteady gait
Tremor
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21
Q

What is the confusion assessment method (CAM)

A

Used to assess delirium

Acute onset and fluctuating course AND
Inattention

AND EITHER

  • disorganised thinking
  • changed level of consciousness
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22
Q

Investigations for delirium

A

Bloods - FBC, U&Es, creatinine, glucose, calcium, magnesium, LFTs, TFTs, troponin, B12,

Urine dip and MSU
Blood cultures
ECG
Pulse ox and ABG
CXR

Septic screen!

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23
Q

Management of delirium

A

Treat underlying cause

Clear communication, reminders of day and time, familiar objects in room, staff consistency

Adequate sleep and space, control excessive noise, bright lights, adequate temperature

Adequate nutrition. Attention in incontinence,

Maintain competence. Don’t sedate for wandering

Medical - drugs can worsen, use with care
Haloperidol or olanzapine - lowest dose, shortest time

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24
Q

What drugs can cause delirium

A 
Benzos
Narcotic analgesia
Antispasmodics
Warfarin
first gen antihistamines
captopril
theophylline
dipyramidole
furosemide
lithium
TCAs
Cimetidine
Anti-arrhythmic
Statins
Digoxin
Beta blockers
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25
Q

Triad of normal pressure hydrocephalus

A

Incontinence
Frontal lobe symptoms
Gait instability

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26
Q

Cerebellar disease signs

A 
Vertigo
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonic/hyporeflexia
Exaggerated broad based gait
Dysdiadochokinesia
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27
Q

What are the geriatric giants?

A 
Categories of impairment in elderly
Incontinence
Instability
Immobility
Impaired cognition
Iatrogenic
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28
Q

Dorsal column medial lemnisucus

A

Ascending tract
In dorsum of spinal cord

Carries:
Fine touch
Proprioception
Vibration
2 point discrimination

Decussates at the medulla
Processed in the thalamus by the VPL (ventral posterior lateral nucleus)

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29
Q

Spinothalamic tract

A

Ascending tract
In anterolateral spinal cord

Carries:
Pain
Crude touch
Temperature

Decussates at the spinal level

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30
Q

Spinocerebellar traect

A

Ascending tract

Does not decussate - IPSILATERAL

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31
Q

Function of dorsal and ventral route of spinal cord

A 
Dorsal = sensory
Ventral = motor
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32
Q

Define epilepsy

A

Transient occurrence of signs or symptoms due to abnormal electrical activity in the brain leading to a disturbance in consciousness, behaviour, emotion, motor function or sensation.

Diseases of the brain with ANY 1 of:
- >2 unprovoked seizures occurring > 24 hours apart

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33
Q

Describe an absence seizure

A

Interruption to mental activity for < 30 seconds
3Hz spike and wave pattern on EEG
Rarely persists into adulthood

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34
Q

Symptoms of epilepsy

A

May have a cause that precipitates: decreased sleep, increased alcohol, medication (TCAs)

Possible seizure related symptoms:

  • Sudden falls
  • Blank spells
  • Involuntary jerking
  • Unexplained incontinence
  • Odd events occurring in sleep
  • Confusion with decreased awareness
  • Epigastric fullness
  • Deja vu
  • Premonition
  • Fear, elevation, depression
  • Inability to understand or express language
  • Loss of memory
  • Focal motor/sensory deficit
  • hallucinations
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35
Q

Café au lait spots

A

Neruofibromatosis

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36
Q

Port wine stains

A

Struge-Weber syndrome (associated with epilepsy)

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37
Q

Status epilepticus

A

Continuous seizure > 30 minutes or recurrent seizures without regaining consciousness > 30 minutes

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38
Q

Reflexes to be assessed to determine brain death

A 
Brainstem reflexes
Pupils fixed and unreactive
Corneal
Vestibulo-ocular reflex
Cranial nerve stimulation
Gag reflex
Suction in trachea - no reflex
No respiratory movement with off ventilator with PCO2 over 6.7
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39
Q

Define delirium and types

A

Abnormalities of thought, perception and levels of awareness

Hypoactive: apathy, quiet confusion. easily missed. can be confused with depression

Hyperactive: agitation, delusion, disorientation. can be confused with schizophrenia

Mixed

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40
Q

Complications of delirium

A

Hospital acquired infections
Pressure sores
Fractures
Residual cognitive impairment

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41
Q

Define coma

A

State of profound unconsciousness caused by disease, injury or poison.
Patient unresponsive

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42
Q

What to examine in coma patient at presentation

A 
Baseline obs
Skin - hyperpigmentation, sepsis, myxoedema, IVDU, anaemia, jaundice, purpura, cherry red discolouration
Emergency medical jewellery
Breath - ketones, solvents, alcohol
Neurological
- Pupils
- fundoscopy
- corneal reflex and gag reflex
- Plantars
- Respiratory pattern
Signs of head injury
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43
Q

Cherry red discolouration indicates what?

A

CO poisoning

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44
Q

Dolls head reflex

A

Roll head side to side

Eyes should move together in the opposite direction

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45
Q

Oculovestibular testing

A

20ml ice cold water in the ear
Psychogenic - move away from water + nystagmus
No response = brain stem lesion
Tonic conjugate movement = move towards water - intact pons therefore lesion above tentorium

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46
Q

Respiratory patterns and what they indicated in coma

A 
Deep breathing = acidosis
Regular shallow breathing = drug OD
Long cycle Cheyne-Stokes - diencephalon damage
Short cycle C-S = medulla damage
Yawining, vomiting, hiccups: brainstem
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47
Q

Cheyne-Stokes breathing

A

characterized by progressively deeper and sometimes faster breathing, followed by a gradual decrease that results in a temporary stop in breathing called an apnoea. The pattern repeats, with each cycle usually taking 30 seconds to 2 minutes.

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48
Q

Aetiology of coma

A

Trauma - DSH, SAH, depressed cranial #, intracerebral haemorrhage
Toxic - alcohol, drugs, sedatives, cocaine
Metabolic - hypo/hyper glycaemia, hypo/hyper natraemia, hypopituitarism, hypercapnia, hypoxia, hypothyroid, liver or renal failure
Neuro - epilepsy, raised ICP, hydrocephalus
Ischaemic - stroke, hypertensive encephalopathy, cerebral hypoperfusion (e.g. MI)
Infective - meningitis, encephalitis, sepsis, abscess, malaria, toxoplasmosis
Vasculitis
Space occupying lesion

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49
Q

Investigations for coma

A 
Blood glucose
ABG
Bloods - FBC, U&amp;Es, LFTs, CK, TFTs, troponin
Urine dip, culture, pregnancy test
Drug screen
Paracetamol and salicylate levels
Blood cultures
Ethanol levels
ECG
CXR
Head CT/MRI
EEF

Other - malaria film, LP, autoantibody screen

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50
Q

Management of coma

A

Resusciation - intubation and ventilation if needed
IV thiamine and glucose if cause unclear
Trial naloxone (opioids) and flumazenil (benzos)
Treat underlying cause
Mannitol if raised ICP
Fluids, nutrition, prevent bed sores

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51
Q

prognosis of coma

A

If > 6 hours and not due to head injury to drugs then 10% recovery

SAH or stroke < 5% recovery

Coma > 24 hours - 10% recovery
Coma > 1 week - 3% recovery

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52
Q

Persistent vegetative state

A

Lost cognition and external awareness but retain non-cognitive brain function and sleep wake cycle

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53
Q

Types of primary headaches

A

Tension type headache
Migraine
Cluster headaches

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54
Q

Causes of secondary headaches

A 
Stroke
Head and neck trauma
Substance or withdrawal of substance
Infection - meningitis, encephalitis
Space occupying lesion 
Psychiatric disorder
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55
Q

What should always be examined in a patient with a headache?

A 
Ophthalmoscopy - optic fundi for papilloedema
BP
Temporal artery palpation 
Full neurological exam
GCS and cognitive level
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56
Q

Red flags for headache

A 
New onset or change in over 50s
Under 5
Thunderclap
Headache on waking
Altered consciousness
Focal neurology
Jaw claudication or visual disturbance
Papilloedema
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57
Q

Types of tension type headache

A

Episodic - fewer than 15 days each month

Chronic - > 15 days per month, more likely to be medication induced

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58
Q

Epidemiology of tension type headaches

A

Most common headache type
Increased in young adults
More common in women
First onset after 50 RARE

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59
Q

Presentation of tension type headaches

A

Featureless, generalised headache
Pressure or tightness (vice or band like)
No photophobia, phonophobia or visual disturbance
May have mild nausea no vomiting
Gradual onset
more constant
Less severe

30 minutes to 7 days in duration

2 or more of the following

  • Bilateral or generalised of mild-moderate intensity
  • Fronto-occipital
  • Non pulsatile
  • No aggravated by physical activity
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60
Q

Causes of tension type headaches

A 
Anxiety
Depression
Poor posture
Poor sleep
Stress
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61
Q

Management of tension type headaches

A 
Reassurance that it is self limiting
Deal with any anxiety and stress
Increase exercise
Improve posture
1. Ibuprofen - then other NSAIDs
2. Amitriptyline if frequently occurring
Avoid codeine

Be aware of medication induced headaches

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62
Q

Classification of migraine

A

Migraine without aura
Migraine with aura
Hemiplegic migraine
Chronic migraine

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63
Q

Epidemiology of migraine

A 
6% of men, 18% of women
increased in women
Increased in boys
First attack is often in childhood, over 80% have first attack by 30
FHx common
If onset over 50 - look for pathology
Severity decreases with age
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64
Q

Presentation of migraine

A 
Paroxysmal headaches
Severe and unilateral (can be bilateral)
20-60% have premonitory phase
May have aura
May have photophobia
Vomiting
Tired, irritable, depressed, difficulty concentrating
Triggering factors:
- Stress, anxiety, depression
- trauma
- diet: cheese, chocolate, citrus fruit, missed meals
- dehydration 
- sleep deprivation
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65
Q

Aura in migraine

A

Occurs hours-days before headache
Highly variable presentation but tends to be constant for the patient
Visual disturbance - will start in one eye
- Fortification spectrum (scintillating scotoma)
- Geometric visual patterns
- Hallucinations

Sensory symptoms - paraesthesia, numbness.
It is unilateral and reversible, starts in hand and works up.

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66
Q

Migraine in children

A

Most commonly starts in children
Can have cyclical vomiting or abdominal migraine
Similar to adults but often bilateral and abdominal symptoms are more common

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67
Q

Management of migraine

A 
Identify trigger factors with diary
Prophylaxis if > 2 per months
- propranolol
- amitriptyline
- topiramate, sodium valproate

Simple analgesia +/- antiemetic if required

Triptans - eletriptan, sumatriptan

  • 5HT1 agonist
  • No used in HTN, CHD, coronary vasospasm
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68
Q

Define cluster headaches

A

Produces severe unilateral pain localised in and around the eye and accompanied by ipsilateral autonomic features

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69
Q

Classification of cluster headaches

A

Episodic - occurs in periods lasting from 7 days to 1 year. Separated by pain free periods lasting > 1 month
Cluster periods usually between 2 weeks and 3 months.

Chronic - occurring for 1 year without remissions or short lived remissions < 1 month

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70
Q

Epidemiology of cluster headaches

A

0.1%
Increased in males
Begins 20-40 years
Worse prognosis if head injury, smoking and alcohol.

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71
Q

Clinical features of cluster headaches

A

Bouts which last 6- 12 weeks
Often at the same time each year
Headaches often at night, 1-2 hours after falling asleep
Circadian pattern

Pain comes on rapidly < 10 minutes
Excrutiating, sharp, penetrating, constant
Pain centred around the eye or the temple
Unilateral
Attacks last 45-90 minutes
From 1-8 times daily
Restless - may hit head

Ipsilateral autonomic symptoms

  • lacrimation
  • nasal congestion
  • eyelid swelling
  • rhinorrhoea
  • facial sweating
  • flushing
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72
Q

Diagnostic criteria for cluster headaches

A 
5 attacks
Severe unilateral orbital pain lasting 15-180 minutes
Headache accompanied by at least one of:
- lacrimation
- nasal congestion +/- rhinorrhoea
- eyelid oedema
- forehead and facial swelling
- miosis and ptosis
- restlessness
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73
Q

Management of cluster headaches

A

Smoking cessation
Alcohol abstinence

Acute - SC sumitriptan
100% O2, up to 15 minutes, up to 5 times per day
Other options: ergotamine, anti-inflammatories, metoclopramide

Prophylaxis

  1. Verapamil
  2. Prednisolone
  3. Lithium
    - Melatonin
    - In chronic can use topiramate, sodium valproate
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74
Q

When to investigate headaches

A 
Worsening with fever
Sudden onset - thunderclap
Neurological deficit
Cognitive dysfunction
Change in personality
Decreased consciousness
Recent head trauma (<3months)
Orthostatic headache
Sx of temporal arteritis
Sx of acute closed angle glaucoma
<20 with history of malignancy
History of malignancy
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75
Q

Describe primary exertional headaches

A

Pulsating headache brought on by exercise
Lasts 5 minute - 48 hours
Occurs in hot weather and high altitude
Rule out acute mountain sickness and high altitude cerebral oedema

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76
Q

Describe primary sexual headache

A

Benign vascular headache or coital cephlagia
Precipitated by sexual activity
Starts during intercourse, peaks at orgasm
If explosive onset, rule out SAH

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77
Q

Hypnic headache

A

Dull headache that wakens from sleep
Occurs > 50% of the time lasting >15 minutes after waking
Over 50s only

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78
Q

Hemicrania continua

A

Persistent unilateral headache > 3 months
Daily and continuous
Moderate intensity with exacerbations
Autonomic symptoms - eye watering, ptosis
Responds completely to INDOMETHACIN

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79
Q

Cranial or vascular causes of headachees

A 
Stroke or TIA
SAH
Temporal arteritis
High or Low CSF
Cancer
epilepsy
chiari malformation
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80
Q

Epidemiology of SAH

A 
9 per 100,000
6% of first strokes are SAH
85% are due to intracranial aneurysms
10% non-aneurysmal haemorrhage
5% vascular - AV malformation, vasculitis

Mean age 50. 
Most are under 60
Increased in females
Increased in Blacks
Increased in Finland and Japan

RFs
Hypertension
Smoking
Cocaine
Alcohol
Marfan's, Ehler's Danlos, neurofibromatosis 1, polycystic disease
FHx
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81
Q

Presentation of sub arachnoid haemorrhage

A 
Sudden explosive headache
Like being hit on the back of the head
Most severe ever experienced
Diffuse headache
Pulsates towards occiput
Often lasts 1-2 weeks

Vomiting
Seizures
Acute confusional state
Signs of meninginism after 6 hours
Decreased consciousness
Hemiparesis

May have warning symptoms prior to event

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82
Q

Warning symptoms of SAH

A

10-15% of patients have warning symptoms
Due to sentinel bleeds or expansion of aneurysm
In preceding 3 weeks

Headache
Dizziness
Orbital pain
Sensory or motor disturbance
Seizures
Diplopia
Visual loss
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83
Q

Investigations for SAH

A

CT is first line

  • Without contrast
  • Hyper dense appearance of the blood in basal cisterns
  • correctly identified 98% within the first 24 hours

Angiography - immediately after confirmation to determine aneurysms

If CT scan is negative the LP
- After 12 hours to allows for sufficient lysis for bilirubin and oxyhaemoglobin

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84
Q

Management of SAH

A

Rebleeding is the most imminent danger
Occlusion of aneurysm with coiling (radiological) or clipping (neurosurgical)

Calcium antagonist to prevent vasospasm
No steroids
No antifibronolytics
Ventricular draining of hydrocephalus if present

Secondary prevention - smoking cessation, hypertension

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85
Q

Prognosis and complications of SAH

A 
Mortality 50%
cerebral ischaemia 
cardiac arrest
epilepsy
intra parenchymal haematomas
High risk of rebleed
hydrocephalus
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86
Q

Define temporal arteritis

A

Systemic immune mediated vasculitis affecting medium and large sized arteries
Particularly aorta and extracranial branches

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87
Q

Epidemiology of temporal arteritis

A

2 per 10,000
Increased in Northern European
Increased in females (3:1)

Associated with polymyalgia rheumatic
Increased in over 60s, peak 60-80

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88
Q

Presentation of temporal arteritis

A 
Headache
Temporal tenderness
Jaw claudication
Myalgia
Malaise
Fever
Visual disturbances - due to ischaemic optic neuritis
Blurred vision, amaurosis fugax, diplopia, visual loss
Anorexia, weight loss, fatigue
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89
Q

Features required for diagnosis of temporal arteritis

A

> 50 years
New headache or tenderness
Temporal artery abnormality at biopsy
ESR > 50

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90
Q

Investigations for temporal arteritis

A

FBC - Raised WCC
normocytic normochromic anaemia and thrombocytosis
Raised ESR or CRP
LFTs - raised ALP

Biopsy from symptomatic side

Colour duplex ultrasonography

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91
Q

Management of temporal arteritis

A

Treatment should not be delayed by investigations
High dose steroids - prednisolone 40mg daily
60mg if claudication
If visual problems - admit and give IV
Low dose aspirin and PPI
Osteoporosis prophylaxis

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92
Q

Complications of temporal arteritis

A 
Loss of vision
Aneurysms, dissections, stenotic lesions
CNS disease
Steroid related complications
- Osteoporosis
- Corticosteroid myopathy
- Bruising
- Emotional (insomnia, depression)
- HTN
- Diabetes
- high cholesterol
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93
Q

Presentation for space occupying lesion

A

Can have localised signs, generalised signs or false localising signs
Usually a gradual onset

Headache

  • New with features of raised ICP
  • Focal neurological symptoms
  • Blackout
  • Change in personality or memory
  • Past cancer or HIV diagnosis
  • new onset seizures
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94
Q

Generalised symptoms of space occupying lesion

A 
Vomiting
nausea
Change in mental status or behavioural change
Weakness
Ataxia
Disturbance of gait
Seizures
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95
Q

Symptoms of cerebellar space occupying lesion

A

Ataxia
Intention tremor
Dysdiadokinesis
Nystagmus

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96
Q

Symptoms of temporal lobe space occupying lesion

A

Most interesting collection of symptoms

  • Vague psychological symptoms
  • Depersonalisation
  • Emotional changes
  • Disturbance of behaviour
  • Temporal lobe epilepsy: hallucinations of smell, taste, sight and sound
  • Dysphasia
  • Visual field defect: contralateral upper quadrant
  • Forgetfulness
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97
Q

Symptoms of frontal lobe space occupying lesion

A

Loss of sense of small (anosmia)
Change in personality (indecent, indiscreet, dishonest)
Dysphasia if Broca’s area involved
Hemiparesis or fits on contralateral side

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98
Q

Symptoms of parietal lobe space occupying lesion

A

Hemisensory loss
Decreased 2 point discrimination
Astereognosis - inability to recognise objects in hand
Extinction - will only recognise one side of the body
Sensory inattention
Dysphasai
Gerstmann’s syndrome - agraphia, acalculia, L/R disorientation

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99
Q

Symptoms of occipital lobe space occupying lesion

A

Visual field defects

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100
Q

Symptoms of cerebellar pontine angle space occupying lesion

A

Most common is an acoustic neuroma

Tinnitus
hearing loss
nystagmus
Decreased corneal reflex
Facial and trigeminal nerve palsies
Ipsilateral cerebellar signs
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101
Q

Investigations for space occupying lesions

A

FBC, U&Es, LFTs
CT or MRI
Biopsy
Look for primary tumour (mammography or CXR)

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102
Q

Aetiology of space occupying lesion

A

Malignancy

  • mets, gliomas, meningiomas, adenomas, acoustic neuroma
  • astrocytoma, glioblastoma, oligodendrogliomas
  • Mets: Lung, breast, colon, melanoma
  • Haematoma
  • Hydrocephalus
  • Cerebral abscess
  • Cysts
  • Infection and lymphoma of CNS
  • Granuloma and tuberculoma
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103
Q

Define meningitis

A

Inflammation of leptomenings and underlying subarachnoid CSF

Can be due to bacteria, virus or non-infective causes

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104
Q

Epidemiology of meningitis

A

Increased in young children and elderly
Viral is the most common cause
Vaccines for - Haemophilus influenza B, Men C and B, pneumococcal disease

RFs

  • CSF shunts or dural defects
  • Spinal procedures/anaesthetics
  • Bacterial endocarditis
  • Diabetes
  • Alcohol, cirrhosis
  • Renal insufficiency
  • IV drug use
  • Malignancy
  • Splenectomy/ sickle cell
  • Crowding - military or students
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105
Q

Causes of meningitis in neonates

A

Group B strep
Listeria monocytogenes
E.Coli

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106
Q

Causes of meningitis in infants

A

Haemophilus influenza B (if not vaccinated)
Neisseria meningitis
Strep pneumoniae

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107
Q

Causes of meningitis in adults

A

Neisseria meningitis
Step pneumonia
Haemophilus influenza B

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108
Q

Causes of meningitis in elderly

A

Strep pneumonia
listeria
TB

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109
Q

RFs for neonatal meningitis

A 
Low birth weight
Premature
PROM
Traumatic delivery
Foetal hypoxia
Maternal group B strep carrier
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110
Q

Presentation of neonatal meningitis

A 
Raised or unstable temperature
Respiratory distress
Apnoea
Bradycardia
Hypotension
Feeding difficulty
Irritability
Decreased activity
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111
Q

Aseptic meningitis

A

CSF has cells but gram stain negative and no bacteria cultures

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112
Q

Causes of aseptic meningitis

A 
Partly treated bacterial meningitis
Viral - mumps, coxsackie, echovirus, HSV, herpes zoster, HIV, influenza
Fungal - rare but serious
- Atypical - TB, syphilis, lyme disease
- Kawasaki disease
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113
Q

Non infective causes of meningitis

A 
Malignancy - leukaemia, lymphoma
Intrathecal drugs
NSAIDs, trimethoprim
Sarcoidosis
SLE
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114
Q

Presentation for meningitis

A 
Fever 
Headache
Stiff neck, back rigidity, bulging fontanelle
Photophobia
Shock - tachycardia, hypotension
Altered mental state
Kernig's sign
Brudzinski's sign
Paresis
neurological deficit
Seizures

If meningococcal
- generalised petechial rash

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115
Q

Investigations for meningitis

A

SHOULD NOT DELAY TREATMENT

  • FBC - raised WCC
  • CRP
  • Coag screen
  • LP
  • CSF for culture and assessment
  • PCR of CSF
  • Blood glucose
  • ABG
  • Urine culture
  • MRI
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116
Q

Management of meningitis

A 
IV ABx ASAP - ceftriaxome
Supportive
- Fluids
- Antipyretics
- Antiemetics
- Nutritional support

If viral then acyclovir (herpetic)

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117
Q

Immediate complication of meningitis

A 
Septic shock
DIC
Coma
Cerebral oedema
Raised ICP
Septic arthritis
Pleural effusion
Haemolytic anaemia
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118
Q

Delayed complications of meningitis

A 
Decreased hearing
Seizures
Subdural effusions
Hydrocephalus
Intellectual deficits
Ataxia
Blindness
Peripheral gangrene
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119
Q

Causes of facial pain

A 
Sinusitis
URTI, nasal injury and foreign body
Otitis media
Mastoiditis
Dental abscess
Cellulitis
Trigeminal neuralgia
Mumps
Herpes zoster
Post-herpetic neuralgia
TMJ dysfunction
Glaucoma
Headaches
Temporal arteritis
Tumours
Idiopathic
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120
Q

investigations for facial pain

A 
FBC 
EST or CRP
X-rays dental
US if salivary gland pathology suspected
MRI/CT
Sialography if parotid conditions
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121
Q

Management for facial pain

A

Treat underlying cause

For atypical - amitriptyline, consider fluoxetine

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122
Q

Define trigeminal neuralgia

A

Chronic, debilitating condition resulting in intense extreme episodes of facial pain.
Episodes are sporadic and sudden electric shocks lasting seconds to minutes

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123
Q

Epidemiology of trigeminal neuralgia

A

50-60 years most common
Increases with age
27 per 100,000
Increased in females

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124
Q

Aetiology of trigeminal neuralgia

A

Caused by compression of trigeminal nerve by a loop of artery or vein
5-10% are due to tumours, MS, abnormalities of skull bases or AV malformations.

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125
Q

Presentation of trigeminal neuralgia

A

Sudden unilateral brief stabbing recurrent pain
Pain occurs in paroxysm which lasts from a few seconds to 2 minutes
Ranges up to 100 attacks per day
Periods of remission from months to years
May have triggers
May have preceding tingling or numbness
Shock like pain
One side of cheek or face
3-5% are bilateral

Provoked by - light touch to face, eating, cold winds, vibration, brushing teeth, wind

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126
Q

Atypical trigeminal neuralgia

A

Relentless underlying pain like a migraine with superimposed stabbing pain
May also have intense burning pain.

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127
Q

Red flags for trigeminal neuralgia

A 
Poor response to carbamazepine
Sensory changes, deafness
Hx or skin or oral lesions
Ophthalmic division
MS
Age < 40
Optic neuritis
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128
Q

Investigations for trigeminal neuralgia

A

Diagnosed clinically

MRI to rule out other causes of pain

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129
Q

Management of trigeminal neuralgia

A 
No definitive cure
Carbamazepine - very responsive
Normal analgesia does not work
Support and education 
Refer to pain clinic if needed

Surgery - damage trigeminal nerve or microvascular decompression

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130
Q

Define hydrocephalus

A

Increase volume of CSF in ventricles

Causes white matter damage

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131
Q

Classification of hydrocephalus

A

Non-communicating - CSF obstructed within ventricles or between ventricles and subarachnoid space

Communicating - problem outside of ventricular system

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132
Q

presentation of hydrocephalus

A

Acute - headache and vomiting.
papilloedema and impaired upward gaze

Gradual - unsteady gait, large head, 6th nerve palsy

Cognitive deterioration
Neck pain
Nausea and vomiting
Blurred or double vision
Incontinence
Infants - increased head circumference
Sun-setting sign - white above iris, eyes deviated down
Macewen's sign - cracked pot sounds on head percussion
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133
Q

Investigations for hydrocephalus

A

CT scanning

US in children

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134
Q

Management of hydrocephalus

A

LP for acute management if communicating
Furosemide can inhibit secretion of CSF from choroid plexus
Surgery - external drain insertion

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135
Q

Pathophysiology of subdural haematoma

A

Tearing of bridging veins from the cortex to one of the draining sinuses
Bleeding from damaged cortical artery

Usually due to blunt trauma but can be due to clotting disorder, AV malformations or aneurysms

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136
Q

Epidemiology of subdural haematoma

A 
Increased with age
1/3 of people with severe head injury
Alcoholics
Anti coagulated
Elderly due to cerebral atrophy providing vein tension
Infants
137
Q

Presentation of subdural haematoma

A

ACUTE

  • moderate to severe head injury
  • Can have LOC
  • Lucid interval with subsequent deterioration as haematoma forms

CHRONIC

  • 2-3 weeks post head trauma
  • Symptoms are gradually progressive
  • History of anorexia, nausea and vomiting
  • Gradually evolving neurological deficit
  • Accompanying progressive headache
138
Q

Investigations for subdural haematoma

A

Bloods - FBCs, U&Es, LFTs, coag screen, CRP, group and save
Imaging - CT best for acute
- Crescenteric bleed that crosses sutures

139
Q

Management of subdural haematoma

A

ABCs and trauma team
Priority imaging of the head
Refer to neurosurgery
Mannitol or hypertonic saline for raised ICP
Surgery - emergency craniotomy and clot evacuation

140
Q

Complications of subdural haematoma

A 
Death - cerebellar herniation
Raised ICP
Cerebral oedema
Recurrent haematoma
Seizures
Meningitis from wound infection
Permanent neurological deficit
Coma
Persistent vegetative state
141
Q

Epidemiology of extradural haematoma

A 
2% of head injuries
60% acute
30% subacute
10% chronic
Increased in men (4:1)
Increases with age due to dura adherent
142
Q

Aetiology of extradural haematoma

A

Most often due to fractured temporal or parietal bone damaging the middle meningeal artery or vein
Caused b trauma to temple or tear in dura venous sinuses
If it is in the spinal column, can be due to LP or epidural

143
Q

Presentation of extradural haematoma

A 
History of head injury and loss of consciousness
CLASSICALLY - lucid interval then deterioration 
Headache
Nausea and vomiting
Seizures
Bradycardia and hypertension
CSF otorrhoea or rhinorrhoea
Altered GCS
Unequal pupils
May have focal neurology
144
Q

Investigations for extradural haematoma

A 
Baseline FBC, U&amp;Es, coag screen
Plain skull xray for #
Cervical spine xray to exclude injury
CT - haematoma or air pockets
Lentiform bleed - doesn't cross sutures 
Avoid LP
145
Q

management of extradural haematoma

A

ABCs and trauma team
IV mannitol or hypertonic saline for raised ICP
Burrhole may be required
Surgical evacuation of haematoma

146
Q

Complications of extradural haematoma

A 
Neurological deficits
Post-traumatic seizures
Post-concussion syndrome
Inability to concentrate
Mortality 30%
147
Q

Aetiology of raised ICP

A

Subdural, extradural haematoma
Cancer - mets or primary
Abscess
Focal oesdema from trauma
Obstructive hydrocephalus or communicating
Obstruction to major venous sinuses due to depressed # or central venous thrombosis
Diffuse brain oedema from encephalitis, meningitis, head injury, SAH, Reye’s syndrome
Idiopathic intracranial HTN

148
Q

Presentation of raised ICP

A

Headache - nocturnal, on waking, worse on coughing or moving
Vomiting - in early stages no nausea but becomes projectile
Papilloedema
Lethargy, irritability
Pupil changes
Fundoscopy - blurring of disc margins, disc hyperaemia, flame shapes haemorrhages
Unilateral ptosis to 3rd and 6th nerve palsies

Hypertension
Bradycardia
Widened pulse pressure

149
Q

Investigations for raised ICP

A

CT or MRI for underlying lesion
Monitor blood glucose, renal function, U&Es, osmolality

Monitor ICP

150
Q

Management of raised ICP

A 
Avoid pyrexia
Manage seizures
CSF drainage 
Elevate head of bed to lower ICP
Analgesia and sedation - GA
Mannitol
Hyperventilation
Some evidence for hypertonic saline

2nd line

  • Barbituate coma
  • Hypothermia to 35oC
  • Decompressive craniotomy
151
Q

Rinnes test

A

512 Hz

External auditory meatus
Then on mastoid process
Which is louder

Normal - louder in air
Conductive - louder on bone
Sensorineural - louder in air

152
Q

Weber’s test

A

512 Hz

Centre of forehead, which ear is loudest

Normal - equal in both
Conductive - louder in affected ear
Sensorineural - louder in unaffected ear

153
Q

Causes of perforated tympanic membrane

A

Infection - acute otitis media or chronic
Trauma - to temporal bone or tympanic membrane
Iatrogenic - from myringotomy

154
Q

Treatment for perforated tympanic membrane

A

Watchful waiting - may heal spontaneously

Tympanoplasty if persisting - keep ear dry

155
Q

Symptoms of perforated ear drum

A 
Sudden hearing loss (or muffled hearing)
Ear pain
Itching
Fluid leaking from ear
Fever > 38
Tinnitus
156
Q

Levels of hearing loss

A

Mild 25-39 dB loss - cannot hear whispers
Moderate 40-69 - cannot hear conversational speech
Severe - 70-94 cannot hear shouting
Profound > 95 loss, cannot hear sounds that are painful to normal

157
Q

Epidemiology of deafness in children

A

50% of deaf children are born deaf
Temporary deafness is common

RFs
FHx
Infection - rubella, mumps, meningitis
Ototoxic meds
Decreased birth weight, prematurity
Craniofacial abnormalities
Severe neonatal hyperbilirubinaemia
Head injury
Neurodegenerative disorders
158
Q

Aetiology of deafness in children

A

50% genetic - including Turner’s and Klinefelter’s

Intrauterine (8%) - congential infection (TORCH), HIB, maternal drugs (streptomycin, alcohol, cocaine)

Perinatal (12%) - prematurity, low birth weight, birth asphyxia, severe hyperbilirubinaemia or sepsis

Post natal (30%) - child hood infection (meningitis, encephalitis), head injury

20-30% unknown cause

159
Q

Presentation of deafness in children

A 
Depends on degree
If congenital and profound may present at 6-9 months
Language delay
Behavioural problems
Chronic infections - cholesteatoma
160
Q

Screening for deafness in new born

A

Automated Otoacoustic Emissions Test (AOAE)
At birth - tests reflections from tympanic membrane, pass or fail

Automated Auditory Brainstem Response test (AABR)
Detects brain activity from sound, tests cochlea and nerve supply.
Done in any failed AOAE or NICU patients

If both failed then refer within 4 weeks for audio logical assessment

161
Q

Investigations for hearing problems in children

A

Normal screening
Tympanometry
MRI or CT for underlying cause
Chromosomal studies for genetic causes

162
Q

Management of deafness in children

A 
Family support advice and information
Communication support
- hearing aids/cochlea implants
- Lip reading
- British Sign Language
- Finger spelling
School support

If conductive - grommet insertion and/or adenoidectomy, autoinflation of Eustachian tube or surgery (if cholesteatoma)

163
Q

Epidemiology of otitis media with effusion

A

Glue ear
Most common cause of acquired hearing loss in children
1-6 years old
20% of 2 year olds
Most will have a single episode before 10
Increased in boys

RFs

  • Winter
  • Acute otitis media
  • Craniofacial malformations
  • Downs
  • Allergic rhinitis
  • CF
  • Day care attendance
  • Frequent URTI
  • Decreased socioeconomic group
  • Smokers
164
Q

RFs for otitis media with effusion in adults

A

Eustachian tube dysfunction - sinusitis, chronic allergy
Tumours
Barotrauma - diving or flying
Radiation to the head and neck

165
Q

Acute otitis media

A

Acute inflammation of middle ear.

Bacterial or viral

166
Q

Acute suppurative otitis media

A

Pus in middle ear

5% perforates

167
Q

Chronic otitis media

A

Long standing suppurative middle ear infection usually with persistent perforated tympanic membrane

168
Q

Conditions included under otitis media

A 
Acute OM
Chronic OM
Acute suppurative OM
OM with effusion (glue ear)
Mastoiditis
Cholesteatoma
169
Q

Presentations of otitis media with effusion

A

Hearing loss
- Mishearing, difficulty communicating in group
- Lack of concentration, withdrawal
- Impaired speech and language development
- Impaired school progress
Mild intermittent ear pain with fullness or popping
Hx of recent ear infection, URTI or nasal obstruction
Occasionally balance problems

170
Q

Examination findings in otitis media with effusion

A 
Opacification of drum,
Drum in tact
In inflammation or discharge
Loss of light reflex
Drum indrawn, retracted or concaved
Decrease drum motility
Bubbles or fluid level
171
Q

Presentation of otitis media with effusion in adults

A 
Aural fullness
hearing loss
Crackling or popping tinnitus
Mild diffuse pain
Foreign body sensation
Vague unsteadiness
172
Q

Investigations for otitis media with effusion

A

Hearing assessment

  • pure tone audiometry in > 4
  • McCormick toy test in < 4
  • Shows mild conductive loss
  • Repeat after 3 months

In adults assess for head and neck tumours as will be present in 5%
Refer to ENT if anything suspicious

173
Q

Management of otitis media with effusion

A

Reassure. 90% have complete resolution. Self-limiting
No benefit from any treatments
Slow, clear, loud speech.
Surgery if bilateral and lasted longer than 3 months or significant hearing loss > 30dB : grommets
Hearing aids if surgery not suitable

174
Q

Epidemiology of deafness in adults

A

1 in 6 have some hearing loss
Increases with age
Sharp rise after 50
Increased in males (slightly)

RFs
Excessive noise
Specific to causes e.g. trauma, infection

175
Q

Causes of conductive hearing loss

OCCLUSION

A

cerumen
foreign body impaction
oedema
exostosis

176
Q

Presentation of conductive hearing loss in OCCLUSION

A

Painless loss of hearing, usually sudden

177
Q

Management of conductive hearing loss in OCCLUSION

A

If no perforation, past surgery or infection then can irrigate cerumen
Soften with olive oil in preceding days

Treat any cause of oedema

178
Q

Exostosis

A

Benign bony growth in the external auditory canal, sometimes precipitated by cold water swimming

179
Q

Presentation of conductive hearing loss in INFECTION

A

Sudden painful loss of hearing

Media - red, immobile tympanic membrane

180
Q

Most common causes of otitis externa

A

pseudomonas aeruginosa

Staph aureus

181
Q

What condition is associated with bilateral schwannomas

A

Neurofibromatosis type 2

182
Q

Causes of conductive hearing loss

A 
Occlusion (wax or foreign body_
Infection
Exostosis
Perforation
Growths
Cholesteatoma
Adenoids
Otosclerosis
Otospongiosis
Myringosclerosis
TMJ syndrome
183
Q

Otosclerosis

A

Abnormal bone deposition at the base of the stapes preventing normal ossicular vibration
Increased in middle aged white women
Positive family history
Painless, progressive, bilateral hearing loss
Mainly managed with hearing aids

184
Q

Myringosclerosis

A

Deposition of irregular white calcium patches on tympanic membrane
Generally OK unless causes tympanic sclerosis

185
Q

TMJ syndrome

A

Pain in jaw, face and head especially around the ears.
Clicking or popping in jaw and ears
pain opening mouth
Can be associated with bilateral hearing loss

186
Q

Causes of sensorineural hearing loss

A 
Presbyacusis
Noise induced hearing loss
Ototoxic eharing loss
Acoustic neuroma
Meniere's disease
Immune conditions
Idopathic unilateral sudden sensorineural hearing loss
Perilymph fistula
Other
- Inflammation and infection (meningitis etc.)
- Scarlet fever, typhoid, varicella zoster,
- trauma: fracture of temporal bone
- Pyrexia
- Auditory neuritis
- Diabetes
- MS
- Muscular dystrophies
- Paget's
187
Q

Noise induced hearing loss

A

Exposuire to excessive sounds produces a temporary shift int eh stimulus threshold of the outer hair cells in the middle ear
Sufficiently intense or repreat exposiure causes a permanent shift
- Occupational. Military. Social. Fireworks
High frequencies are first to be affected

presentation:
Gradual hearing loss (unless sudden e.g. explosion), tinnitus in 60%. bilateral, symmetrical.

If still present after 3 days, refers for audiology testing.
NOT PROGRESSIVE
If prolonged then permanent damage, if short then full recovery

188
Q

Causes of ototoxic hearing loss

A 
Aminoglycosides
cis-platinum
Salicylates
Quinine
Some loop diuretics
189
Q

Ototoxic hearing loss

A

Presentation:
Hearing loss, tinnitus, balance problems following drug exposure. Feeling of pressure. Often insidious

Management:
Avoid drugs in pregnancy. lowest dose, shortest time. Consider alternatives. hearing aids.

190
Q

Presentation of immune related hearing loss

A

Often only diagnosed when hearing loss improves when treating autoimmune condition with steroids

Rapidly progressing, possibly fluctuating, bilateral hearing loss
OR attacks of hearing loss or tinnitus (resembles Meniere’s)
50% have dizziness
Responds well to prednisolone

191
Q

Idiopathic unilateral sudden sensorineural hearing loss

A

Sudden sensorineural hearing loss > 30bB within 3 days
May be associated with tinnitus, vertigo and aural fullness
May have history of URTI in last month
Refer urgently as better prognosis
Oral steroids within 3 weeks

192
Q

Perilymph fistula

A

Abnormal connection between perilymphatic space of inner ear and middle ear cavity.
Can be acquired (trauma) or congenital
Presentation: sudden unilateral hearing loss associated with vertigo and tinnitus
Management: 3-6 weeks bed rest. may require surgery

193
Q

Functional hearing loss

A

Deafness from psychological or emotional factors
Signs: inconsistent response to tuning forks, hearing appears better than described
Manage sensitively

194
Q

Management of hearing loss generally

A

Hearing aids for all with hearing difficulties

  • Externally worn
  • Analogue or digital (more digital now)
  • Behind ear, in ear, in canal or completely in canal
  • only behind ear available on NHS unless specific reasons

Cochlear implant
- microphone and speech processor worn behind ear and transmitter coil on side of head
- Stimulator implanted on mastoid bone and wire into cochlea
- Translates electrical signals to stimulate auditory nerve
Criteria
- Unilateral: profound deafness not experiencing benefit from hearing aids for 3m
- Bilateral: children with severe profound bilateral deafness, or adults with additional impairment e.g. sight

Supportive devices:

  • Hearing loops
  • Vibrating pagers
  • Special alarm clocks
  • Visual trigger units

Support groups

195
Q

Types of tinnitus and causes

A

OBJECTIVE
There is noise to be heard generated in the head
- Pulsatile: movement of blood e.g. carotid stenosis, vascular abnormalities, high output states
- Muscular or anatomical: spasm of tympanic muscles, palatial myoclonus
- Spontaneous: optoacoustic emissions

SUBJECTIVE
No acoustic stimulus
- Otological: noise induced, presbyacusis, otosclerosis, impacted cerumen, infection, Meniere’s
- Neurological: vestibular schwannoma, tumour, MS, head injury
- Infection: meningitis, encephalitis
- drugs: salicylates, NSAIDs, aminoglycosides, loop diuretics, cytotoxics
- TMJ dysfunction

196
Q

Epidemiology of tinnitus

A

1 in 10 people

Increased in men

197
Q

Presentation of tinnitus

A 
Ringing
Buzzing
Hissing
Whistling
Humming

22% unilateral
34% bilateral and equal
50% bilateral but one side dominant

198
Q

Investigations for tinnitus

A

Thorough examination
hearing tests
Exclude acoustic neuroma with MRI if unilateral

199
Q

Management of tinnitus

A

Reassure that it is non progressive
Relation - association between tinnitus and stress
Tinnitus retraining therapy
Masking devices - low level white noise
SSRIs may decrease tinnitus and treat depression

Treat underlying causes

Microvascular decompression of auditory nerve - controversial

200
Q

Define presbyacusis

A

Progressive, usually bilateral, sensorineural hearing loss that occurs in people as they age

201
Q

Aetiology of presbyacusis

A

A number of auditory factors play a role

  • Decrease auditory sensitivity to sounds
  • Deterioration in understanding of speech
  • Decreased central auditory processing

Intrinsic factors

  • Neuronal loss
  • Loss of cochlear outer hair cells
  • Atrophy of vascular stria in lateral cochlear wall
  • Oxidative stress causing DNA mutation and damage
  • Inflammation
  • Metabolic and systemic disease

Extrinsic factors:

  • Noise
  • ototoxic drugs
  • Raised BMI
  • HTN
  • Diet
  • Alcohol
  • Diabetes
  • FHx
  • Smoking
202
Q

Epidemiology of presbyacusis

A

Increases with age
70% over 70 have some hearing loss
Increased in males

203
Q

Presentation of presbyacusis

A

Slow insidious onset
Gradual progression
Usually first noticed in noisy environments
Difficulty understanding speech is often first (higher pitch)
Friends/relatives may notice
Discrimination of t, p, k, f, s and ch becomes harder
Difficulty in groups or with background noise
May have tinnitus

204
Q

Investigations for presbyacusis

A

Pure tone audiometry

  • worse at higher frequencies
  • measures threshold for air and bone conduction to determine if conductive or sensorineural

No neuroimaging unless clinical suspicion of pathology

205
Q

Management of presbyacusis

A

Communication, courtesy, environmental noise manipulation
- Clear, unhurried speech, face to face
Reassurance and education
Hearing aids
Assistive listening devices - flashing light alarms - smoke and door.
Speech and lip reading

206
Q

Define acoustic neuroma

A

Vestibular schwannoma - tumours of vestibulocochlear nerve arising from Schwann cells of nerve sheath

Most arise from vestibular portion not cochlear

benign and slow growing.
Causes symptoms through mass effects and pressure on local structures
Can grow up to 4cm in cerebellopontine angle
Tumours in internal auditory canal will cause symptoms earlier

207
Q

Epidemiology of acoustic neuroma

A

8% of all intracranial tumours
80% of cerebellar pontine angle tumours

RFs

  • neurofibromatosis
  • high dose radiation
208
Q

Presentation of acoustic neuroma

A

Consider in all with unilateral of asymmetrical hearing loss or tinnitus, impaired facial sensation or loss of balance

Classically

  • Unilateral progressive hearing loss
  • Vestibular dysfunction
  • Tinnitus
  • As the tumour spreads, increased hearing loss and disequilibrium
  • Facial pain or numbness (from trigeminal involvement)
  • Facial weakness (uncommon)
  • Earache
  • Ataxia
  • Severe brainstem compression can cause hydrocephalus with visual loss and persistent headache
209
Q

Investigations for acoustic neuroma

A

Audiology assessment

MRI is imaging of choice

210
Q

Management of acoustic neuroma

A

Growth pattern is variable.
75% have no growth but cannot predicts

Conservative - if small with preserved hearing - annual MRI to monitor

Surgery

  • Microsurgery
  • Stereotactic radiosurgery
211
Q

Complications of surgery for acoustic neuroma

A
  • Meningitis and CSF leak
  • Stroke, epilepsy
  • Facial paralysis
  • Hearing loss
  • balance impairment
  • Persistent headache
212
Q

Define cholesteatoma

A

3D collection of epidermal and connective tissues in the middle ear
It grows independently and can be locally invasive and destructive
- Bone erosion occurs by pressure
- Release of osteolytic enzymes
- Osteolytic activity is increased by presence of infection

213
Q

Classification of cholesteatoma

A

Congenital - occurs when squamous epithelium becomes trapped within temporal bone during embryogenesis

Primary acquired - chronic negative middle ear pressure causes retraction of tympanic membranes. Erosion of lateral wall causes slow expanding defect

Secondary acquired - insult to tympanic membrane e.g. perforation, infection, trauma. Squamous epithelium inadvertently implanted

214
Q

presentation of cholesteatoma

A

Unilateral progressive painless hearing loss
Associated with multiple episodes of glue ear
As it grows it can erode into adjacent structures
- Vertigo
- Headache
- Facial nerve palsy
May have discharge

Congenital

  • Presents 6m to 5 years
  • Pearly white mass on intact tympanic membrane
  • Found on tympanic membrane

Acquired

  • frequent or unremitting episodes of painless discharge - may be foul smelling
  • Recurrent otitis media
  • Progressive unilateral conductive hearing loss
  • 90% perforated tympanic membrane
  • OR tympanic membrane retracted
  • Pus filled canal with granulation
215
Q

Investigations for cholesteatoma

A

Audiological testing
CT imaging can assess subtle bony defects
MRI if soft tissue concerns

216
Q

Managemnt of cholesteatoma

A

Medical - only if surgery declined or contraindicated
Regular ear cleaning or treatment of infections

Surgery - preferable
- GA + removal

217
Q

Indications for LP

A

Suspected meningitis
- >90% of bacterial have raised WCC
Suspected intracranial bleeding & SAH
- If CT or MRI does not confirm diagnosis
- within first 6-12 hours hard to determine bleed from traumatic LP

To establish a diagnosis

  • Confusional state
  • Meningeal malignancies
  • Demyelinating disorders
  • CNS vasculitis
  • MS

To administer thecal therapy

  • Chemotherapy
  • neuromodulation in spasticity and dystonia

To treat

  • communicating hydrocephalus
  • Benign intracranial hypertension
218
Q

Contraindications for LP

A 
Signs suggesting raised ICP
Shock
Extensive or spreading purpura
Convulsions (until stabilised)
Coagulation abnormalities
Superficial infection over LP site
Respiratory insufficiency
219
Q

Signs of raised ICP

A

Decreased or fluctuating level of consciousness
Bradycardia and hypertension
Focal neurology
Abnormal posture
Unequal, dilated or poorly responsive pupils
Abnormal dolls eye movement
Tense, bulging fontanelle

220
Q

Complications of LP

A

Post LP headache
Infection
Bleeding
Cerebral herniation

221
Q

Indications for EEG

A 
Altered consciousness
Seizure disorders
Tumours
Head trauma
Headache
Behavioural disorders
MH - anxiety and panic disorder, OCD, bipolar
Restless legs
222
Q

Define vertigo

A

False sensation that oneself or surroundings are moving or spinning
Often accompanied by nausea and loss of balance
Mismatch between vestibular, visual and somatosensory systems

Can be central - cortex, cerebellum, brainstem
- stroke, migraine, MS, acoustic neuroma, diplopia, alcohol
Or peripheral - BPPV, Meniere’s, motion sickness, ototoxicity, herpes Zoster (Ramsay Hunt syndrome)

223
Q

Aetiology of vertigo

A 
Vestibular neuritis and labyrinthitis
BPPV
Vertebrobasilar ischaemia
Meniere's disease
Chronic otitis media
Drugs - aminosalicylates, quinine, aminoglycosides
Vestibular migraine
Acoustic neuroma
Epilepsy - likely if LOC
Nasopharyngeal carcinoma
MS
Cerebellar tumours
Stroke
Post head injury
224
Q

Epidemiology of vertigo

A

5% have vertigo
1.6% have BPPV
increased in over 60s (30%)

225
Q

Assessment of vertigo (questions)

A

Check is pre-syncope or lightheadedness

Associated symptoms

  • hearing loss, discharge, tinnitus
  • headache, diplopia, visual disturbance, dysarthria, dysphagia, paraesthesia, ataxia, weakness
  • Nausea and vomiting, sweating, palpitations
  • aura

Relevant PMH

  • Recent URTI, ear infection
  • history of migraine
  • head trauma or recent labyrinthitis (BPPV)
  • anxiety and depression (can aggravate)
  • CV RFs
  • Drugs
  • Alcohol
226
Q

Romberg’s test

A

Determine if instability is peripheral or central

Stand up with arms outstretched
Shut eyes
Positive if cannot maintain balance
FALL TO SIDE OF LESION

Positive if vestibular or proprioception (peripheral)

227
Q

Head impulse test

A

Determines if vertigo is peripheral or central
- Assess normal neck rotation first
- Sit upright - fix gaze on examiner
- Rapidly turn head to 20 degrees to one site
POSITIVE if corrective abnormal movements
Positive indicated problems with ipsilateral semi-circular canal

228
Q

Unteberger’s test

A

Identifies damage to labyrinth
March on spot for 30s with eyes closed
Observe for lateral rotation
If POSITVE will rotate towards the side of the damaged labyrinth

229
Q

Central vertigo symptoms

A 
Persistent, severe, prolonged
New onset headache
Focal neurology
Central type nystagmus (vertical)
Abnormal response to Dix-Hallpike
Prolonged severe imbalance with inability to stand with eyes open
N&amp;V less than in peripheral
Hearing loss unusual
No sensation of pressure in ear
Head impulse test negative
230
Q

Peripheral vertigo symptoms

A

Vertigo induced by changing head position (BPPV), lasts for seconds
Can persist for days but gradually improves (vestibular neuritis)

Vestibular neuronitis - no hearing loss or tinnitus

Labyrinthitis - sudden hearing loss and vertigo. may have progressive tinnitus. no fullness in ear.

Meniere’s - spontaneous episodes of vertigo lasting 30mins - 1hour. Tinnitus, hearing loss and fullness.

231
Q

Investigations for vertigo

A

None in primary care
Audiometry for cochlear function
Vestibular function - electronystagmograpohy
CT or MRI for possible neurological cause
EEG for epilepsy
LP and ? MS

232
Q

Management of vertigo

A

Treat underlying condition

  • Do not drive when dizzy or likely to have event
  • Measures to decrease the risk of falling
  • Prochlorperazine (stematil), cinnarizine, cyclizine, promethazine

vestibular rehabilitation

Surgery - if Meniere’s

233
Q

Define Meniere’s

A

Disorder of inner ear caused by a change in the fluid volume in the labyrinth
Progressive distension of the membranous labyrinth resulting in ENDOLYMPHATIC HYDROPS
This may injure the vestibular system causing vertigo or cochlear causing hearing loss

234
Q

Aetiology of Meniere’s

A 
Multifactors
RFs include:
- Allergy e.g. food allergy
- Autoimmunity: APL antibodies, RA, lupus
- Genetic susceptibility
- Metabolic disturbances
- Migraine
- Viral infection
235
Q

Presentation of Meniere’s

A

Vertigo
Tinnitus
Hearing Loss
Aural pressure

Acute attacks last 2-3 hours
Acute episodes occur in clusters of 6-11 per year
Remission of symptoms can last months

Initially UNILATERAL can become bilateral

Drop attacks - sudden unexplained falls without LOC or vertigo (4%)

236
Q

Stages of Meniere’s

A

Early stage - predominantly vertigo attacks, sudden and unpredictable. Hearing worsens, tinnitus increased. Good recovery between attacks

Middle stage - continuing episodes of vertigo. Progression of tinnitus. periods of remission vary

Late stage - increased hearing loss. Vertigo lessens. balance may be difficult especially in the dark. Tinnitus persists.

237
Q

Diagnostic criteria for Meniere’s

A

Vertigo - at least 2 episodes lasting > 20 minutes
Tinnitus - and/or perception of aural fullness
Sensorineural hearing loss

238
Q

Investigations for Meniere’s

A

FBC, ESR, TFTs, syphilis screen, glucose, U&Es, lipids

Audiometry - if hearing loss transient then may not catch it

Video nystagomemtry

Brain stem auditory evoked potentials

Electrocochleography

MRI advised if unilateral

239
Q

Management of Meniere’s

A

Inform DVLA of vertigo

Acute - prochlorperazine, cinnarizine, cyclizine, promethazine

Prophylaxis - low salt diet, avoid caffeine, chocolate, alcohol and tobacco.
- Consider betahistine

Supportive measures

  • Avoid heights and heavy machinery
  • Vestibular rehab programs
  • maintain mobility
  • hearing support

Local gentamicin to damage the sensorineural epithelium
Local steroid injection
Surgery

240
Q

BPPV pathophysiology

A

benign paroxysmal positional vertigo
Due to inner ear dysfunction
Otoliths become detached from the macula in the semicircular canals

  • 85-90% are posterior semi-circular canal
  • 10% inferior semi-circular canal
  • Rarely anterior semi-circular canal

hair cells in otoliths are stimulated as they are moved by flow of endolymph through semicircular canals following head movement.
Stops when head movement stops.
Vertigo occurs due to conflicting sensation from sensory inputs

241
Q

Epidemiology of BPPV

A

2%
Most common in over 50s
Increased in females (x2)

RFs
Meniere’s
Anxiety disorders
migraine

242
Q

Aetiology of BPPV

A 
Most are idiopathic (60%)
Head trama
Spontaneous degeneration of labyrinth
Post-viral illness (viral neuronitis)
Complications of stapes surgery
Chronic middle ear disease
243
Q

Presentation of BPPV

A

Episodes of vertigo provoked by head movements
- rolling over in bed/lying down/ sitting up/ leaning forward
Sudden attacks lasting 20-30s
Worse when head tilted to one side
Rapid resolution with stillness
Normal brief latency between vertigo and movement
Nausea is common
Vomiting is rare
No tinnitus
No hearing loss
May present as a fall

244
Q

Investigations for BPPV

A

Dix-Hallpike
will confirm posterior canal BPPV
- Eyes open, look straight ahead
Start with head turned 45 degrees to left while sitting
Quickly lie down in that position - head 30 degrees below couch level
Observe for nystagmus then return to upright
Repeat on other side
POSITIVE = vertigo and nystagmus (rotary) < 30 seconds

No imaging required as no imaging can detect otoliths

245
Q

Management of BPPV

A

Epley’s manoeuvre
- As D-H but hold in first position, head at 45 degrees for 30s-1min, then rotate to other side for 30-60s then roll onto side, hold, sit up

  • Symptoms are self-limiting and will resolve
  • Get out of bed slowly, minimise head movements
  • Inform DVLA
  • Vestibular rehabilitation
  • No medication or surgery advised
  • High spontaneous remission
246
Q

Define stroke

A

A cerebrovascular event - a clinical syndrome caused by disrupted blood supply to the head

  • Rapidly developing sings of focal or global disturbance of cerebral function
  • Lasting > 24 hours or causing death
247
Q

Epidemiology of stroke

A 
150,000 per year
70% are cerebral infarction
15% primary haemorrhage
5% SAH
Increased in men
Increased with age
Increased Fhx - CADASIL

HTN
Smoking
Diabetes
IHD, valve disease
AF
Post-TIA
Peripheral vascular disease
Polycythaemia
COCP
Carotid occlusion or bruit
Hyperlipidaemia
Alcohol
Clotting disorders
248
Q

Aetiology of stroke

A 
Thrombosis in situ
Athero-thromboembolism (from carotids)
Heart emboli (AF, endocarditis, MI)
CNS Bleed (HTN, head injury, aneurysm)
SAH
Vasculitis (temporal arteritis) 
Venous sinus thrombosis
Sudden drop in BP > 40mmHg
Carotid artery dissection
Thrombophilia
249
Q

Presentation of a cerebral hemisphere infarct

A 
50% of strokes
Contralateral hemiplegia
Flaccid initially then spastic
Contralateral sensory loss
Homonymous hemianopia
Dysphasia
250
Q

Presentation of brainstem infarction

A

25%
Quadriplegia
Disturbance of gaze or vision
Locked in syndrome

lateral medullary occlusion of vertebrobasiliar
- vertigo, N&V, decreased consciousness, headache, visual disturbance, ataxia, speech disturbance, contralateral motor weakness

251
Q

Todd’s paresis

A

Episode of paralysis following a seizure
Can range from weakness to complete paralysis
Usually resolves within 48 hours

252
Q

Investigations for stroke

A 
FBC - polycythaemia, anaemia, thrombocytopaenia
ESR - temporal arteritis
Glucose
lipid profile
BP
CXR
ECG

Brain imaging - CT ASAP

253
Q

Management of stroke

A

If haemorrhage

  • Manage supportively
  • Surgery if GCS <8 or large bleed
  • Reverse INR

If ischaemia

  • Thombolysis: alteplase within 4.5 hours (must exclude haemorrhagic first)
  • Decompressive hemicraniotomy if MCA within 48 hours if decreased GCS and under 60
  • AFTER:
  • Anticoagulation: 300mg aspirin within 24 hours
  • Then clopidogrel
Supplemental O2 if sats low
Control BP < 185/110 only if:
- Aortic dissection
- Hypertensive encephalopathy, nephropathy or MI
- Pre-eclampsia
- Haemorrhagic stroke

If non disabling = carotid imaging and surgery if >50% occlusion

Increase mobility - REHAB

254
Q

Complications of stroke

A

Increase risk of further strokes
increase MI and other vascular events
Dysphagia
VTE, pneumonia, incontinence, constipation, bed sores

Mortality 20% at 1 months
Most will survive first stroke but will have significant morbidity

255
Q

Define TIA

A

Transient ischaemic attack
Temporary inadequacy of the circulation in part of the brain.
Gives a similar picture to stroke except it is TRANSIENT and REVERSIBLE.
Deficit no longer than 24 hours.
Generally ~30 minutes

256
Q

Epidemiology of TIA

A 
50 per 100,000
Increased in Men
Increased in Blacks
Increases with age
FHx

RFs
Smoking 
Hypertension
Diabetes
Heart disease
Peripheral arterial disease
Polycythaemia vera
COCP
Carotid artery occlusion
Hyperlipidaemia
Alcohol excess
Clotting disorders
257
Q

Polycythaemia vera

A

Also called Vaquez disease, Osler-Vaquez disease, polycythaemia rubra vera

Neoplasm in which bone marrow produces too many RBCs.
Generally asymptomatic
Signs and symptoms include:
Itching, particularly after exposure to warm water
Gouty arthritis

258
Q

Aetiology of TIA

A

Usually embolic
May be thrombotic
Occasionally haemorrhagic

Most common emboli: carotids, usually at bifurcation
Can be from AF, mitral valve disease, aortic valve disease
Vertebrobasilar arteries may be a source

259
Q

Presentation of TIA

A

Acute neurological symptoms that resolve in 24 hours
- need 300mg aspirin and full stroke assessment
Usual duration is 10-15 minutes
Symptoms depend on affected area

Carotids

  • Unilateral, generally motor area
  • unilateral weakness
  • may have dysarthria
  • may have dysphasia or sensory symptoms
  • Amaurosis fugax

Vertebrobasilar

  • homonymous hemianopia
  • hemiparesis, hemi sensory symptoms, diplopia, vertigo
  • vomiting, dysarthria, ataxia
  • drooping face, gait, confusion
260
Q

Investigations for TIA

A 
Urine for glucose
FBC + ESR
U&amp;Es 
Lipids
LFTs
TFTs
ECG - AF or MI
Specialist review within 24 hours
If likely AF then echo and ECG
Doppler studies of carotid
CT or MRI of brain for decreased slow or infarct
261
Q

Assessing risk of stroke after TIA

A 
ABCD2
A - age > 60
B - BP > 140/90
C - clinical features
- 2: unilateral weakness
- 1: speech disturbance, no weakness
D - duration
2. > 60 minutes
1. 10-59 minutes
D - Diabetes

> 4 points is high risk of stroke

262
Q

Management of TIA

A

Calculate risk for stroke ABCD2

Lifestyle: smoking cessation, weight loss, alcohol, diet, exercise

Clopidogrel
Atorvastatin
Antihypertensive
Carotid endarterectomy if occlusion >50%

263
Q

CT appearance of ischaemic stroke

A

Non contrast CT
Hyperacute - visualisation of the clot (hyperdense artery) and early parenchymal changes
- See filling defect on CT angiography
Loss of grey-white matter differentiation

264
Q

CT appearance of haemorrhagic stroke

A

Acute blood is hyperdense compared to brain parenchyma

265
Q

Functions of the frontal lobe

A 
Attention and concentration
Planning
Organisation
Personality
Expressive language - Broca's area
Motor planning and initiation
Inhibition of behaviour
Problem solving
266
Q

Functions of the temporal lobe

A 
Memory
Receptive language - Wernicke's area
Sequencing 
hearing
Organisation
267
Q

Functional of the parietal lobe

A

Sensation - touch, pressure, pain, temperature, texture
Spatial positioning perception
Differentiation of sizes, shapes and colours
Visual perception

268
Q

Functions of occipital lobe

A

Vision

Visual processing

269
Q

Functions of brainstem

A 
Breathing
Arousal and consciousness
Attention and concentration
HR
Sleep wake cycles
270
Q

Functions of limbic system

A 
Attention
Sensory gateway
Rage
Aggression
Sexuality
Appetite and thirst
271
Q

Functions of cerebellum

A

Balance
Skilled motor activity
co-ordination
Visual perception

272
Q

Functions of basal ganglia

A

Modifies movement on minute by minute basis
Inhibits movement
Co-ordination
Cortical relay

273
Q

Symptoms of middle cerebral artery occlusion

A 
Contralateral lower facial weakness
Contralateral hemiplegia
Contralateral hemianaesthesia
Ataxia
Speech impairments (left brain)
Perceptual impairments (R brain)
Visual defects
274
Q

Symptoms of anterior cerebral artery occlusion

A 
Weakness of foot and leg
Sensory loss of foot and leg
Ataxia
Incontinence
Slowness and lack of spontaneity
275
Q

Symptoms of posterior cerebral artery occlusion

A 
Midbrain syndrome: 3rd nerve palsy and contralateral hemiplegia
Chorea
Hemiballismus
Visual field defects
Visual halluincations
Memory problems
276
Q

Aetiology of sore throat

A

Viral infection: adenovirus, Coxsakie, Rhinovirus, Parainfluenza, EBV
Bacterial: Group A beta haemolytic strep, other streps
TB
Candidiasis
Chemical irritation

Chronic

  • Smoking
  • Poor inhaler technique
  • Allergy
  • Chemicals
277
Q

Criteria for bacterial sore throat

A

CENTOR criteria

3 or 4 out of 4 = 60% bacterial
Antibiotic therapy by be beneficial
Due to group A beta haemolytic strep

  • Tonsillar exudate
  • Tender anterior cervical nodes
  • Absence of cough
  • Hx of fever
278
Q

Blood test to show bacterial sore throat

A

ASO

Antistreptolysin O titre will be positive

279
Q

Symptoms of streptococcal sore throat

A 
Scarlet fever like rash
- Prominent in skin creases, red punctate skin eruption
Flushed face
Circumoral pallor
Strawberry tongue
280
Q

Symptoms of Infectious mononucleosis

A 
Low grade fever
Fatigue
prolonged malaise
Tronsilalr enlargement, uvular oedema
Fine macular non-pruritic rash (rapidly disappears)
Lymphadenopathy
Nausea. Anorexia. Myalgia
Hepato and splenomegaly
281
Q

Cause of infectious mononucleosis

A

EBV - Epstein Barr Virus

282
Q

Test for infectious mononucleosis

A

Positive Paul Bunnel Test
Positive Monospot test
EBV antibodies

283
Q

Causes of coryza

A

80% rhinovirus

20% coronavirus

284
Q

Symptoms of coryza

A 
Nasal discharge
Nasal obstruction
Sneezing
Sore throat
Decreased smell and taste
Pressure in ears
Cough
Mild fever
285
Q

Symptoms of influenza

A

Uncomplication

  • Fever
  • Coryza
  • Headache
  • myalgia
  • GI symptoms
  • Pyrexia

Complicated

  • LRTI
  • Hypoxaemia
  • SOB
  • Lung infiltrate
286
Q

Epiglottis

A 
Rare
Caused by H influenzae
Common in 2-5 years or 40-50s
Sore throat
Odynophagia
Drooling
Muffled voice
Fever
Tachycardia
Lymphadenopathy

In severe = life threatening EMERGENCY

  • Stridor
  • SOB
  • Dysphagia
  • Respiratory distress
287
Q

Tonsillitis

A 
Common in 5-10 years and 15-25 years
Due to infection of the tonsils
Very severe main, headache, voice changes
Can have abdominal pain
Fever
Lymphadenopathy
Swollen tonsils with pus coating
Rapid antigen test for group A strep
Treat with antibiotics if > 3 centor criteria
288
Q

Laryngitis - causes

A

Viral: rhinovirus, adenovirus, influenza, parainfluenza, HIV, Coxsackie
Bacterial: HiB, strep pneumonia, group B strep, S. aureus
Candidiasis
Trauma
Allergy
Reflux
Smoking
meds: ACEi, steroids (increased risk of fungal infection)

289
Q

Symptoms of laryngitis

A 
Feeling of lump in throat
myalgia 
Fever
Cough
Rhinitis
Dysphagia
Fatigue
290
Q

Symptoms associated with dysphagia

A 
Feeling of food sticking
Discomfort/pain
Regurgitation
Vomiting
coughing
Choking
Weight loss + worsening dysphagia = MALGINANCY
291
Q

Aetiology of dysphagia

A

OBSTRUCTION

  • GORD with stricture
  • Oesophagitits
  • Cancer
  • Oesophageal rings
  • Foreign body

NEURO

  • Stroke
  • Achalasia
  • Spasm
  • Myasthenia gravis
  • MS
  • MNS
  • Parkinson’s
  • Chaga’s disease

OTHER

  • Pharyngeal pouch
  • Globus hystericus
  • External compression
  • CREST syndrome
  • Amyloidosis
  • Tonsillitis, laryngitis
292
Q

Investigations for dysphagia

A 
FBC and ESR
Barium swallow or endoscopy with biopsy
Videofluoroscopy
Oesophageal motility studies
Endoscopic US or MRI for carcinoma
293
Q

Define epistaxis

A

Bleeding from the nose
Can be anterior or posterior

Anterior: bleeding source visible in 95%, usually from nasal septum and Little’s area

Posterior: from deeper structures of the nose. Increased in elderly

294
Q

Epidemiology of epistaxis

A

Very common
Peak 2-10 years and 50-80 years
Equal in both sexes
Increased in children with migraines

295
Q

Aetiology of nose bleeds

A

Usually benign, self-limiting and spontaneous
Trauma - nose picking, excessive blowing, foreign body
Disorders of platelet function = thrombocytopaenia, splenomegaly, leukaemia,
Drugs - aspirin, anticoagulants
Abnormal blood vessels
hereditary haemorrhagic telangiectasia
Malignancy of the nose
Cocaine use
Wegener’s granulomatosis

296
Q

Investigations for epistaxis

A

Unnecessary in most cases
Recurrent or severe may require FBC, coag studies, group and save
Any suspicion of malignancy = ENT referral
Then CT scan and/or nasopharyngoscopy

297
Q

Management of epistaxis

A

ABCDE
Sit upright, squeeze bottom (not bridge) of nose for 10-20 mins
Breathe through mouth
Cautery - electro or more commonly, chemically with silver nitrate
If bleeding continues packing
Topical transexamic acid
Ligation of external carotid artery as last resort

298
Q

Epidemiology of otitis externa

A

10% will have an episode in their lifetime

RFs
Hot and humid climates
Diabetes
Swimming
Narrow external meatus
Increased age
Obstruction - foreign body, hearing aid
Immunocompromised
Insufficient wax (over cleaning)
Wax build up
Eczema, dermatitis
Trauma from cotton buds
Radiotherapy
Past tympanostomy
299
Q

Basic anatomy of otitis externa

A

Outer 1/3 is cartilage
Inner 2/3 is bone
Cerumen is composed of epithelial cells, lysozymes and oily secretions

300
Q

Aetiology of otitis externa

A 
Disturbance of lipid/ acid balance of the canal
- Infection: 90% bacterial 10% fungal. 
Most S.aureus or P.aeroginosa
Fungal: 90% aspergillosis 10% candida
Or herpes zoster (ramsay hunt syndrome)
301
Q

Presentation of otitis externa

A 
Pain 
Itching
Discharge
\+/- hearing loss
Ear canal with erythema, oedema and exudate
Mobile tympanic membrane
Pain with movement of tragus
Lymphadenopathy
Fever
302
Q

Ramsay Hunt syndrome

A 
Reactivation of herpes zoster in geniculate ganglion
Triad of:
- Ipsilateral facial paralysis
- Ear pain
- vesicles on the face or ear.

Can present with deafness, vertigo and pain.

303
Q

Hutchinson’s sign

A

Vesicles on the tip of the nose or on the side of the nose which precede the development of ophthalmic herpes zoster infection.

Occurs as the nasociliary branch of the trigeminal nerve supplies both the cornea and lateral and tip of nose.

304
Q

Acute diffuse otitis externa

A

Also referred to as swimmers ear
Temp > 38. Lymphadenopathy
Slight thick discharge that can become bloody
Commonly bacterial from water stasis in the ear canal

305
Q

necrotising malignant otitis externa

A

Life threatening extension into mastoid and temporal bones

Usually pseudomonas aeruginosa or staph aureus

306
Q

Management of otitis externa

A

Acute: topical drops, removal of debris, oral abx is cellulitis or lymphadenopathy, systemic symptoms = same day ENT referral

Acetic acids
Topical abx = neomycin or clioquinol
Topical steroids - betamethasone, hydrocortisone, prednisolone, dexamethasone (all only given WITH Abx)
Ear wick impregnated with Abx

307
Q

prevention of otitis externa

A 
Keep ears dry
Ear plugs when swimming
Avoid swimming in stagnant water
Dry ears with towel or hairdryer
Don't use cotton swabs
Olive oil to decrease wax build up
308
Q

Define diabetic retinopathy

A

Chronic, progressive, potentially sight threatening disease of retinal microvasculature associated with prolonged hyperglycaemia of diabetes

309
Q

Eye conditions associated with diabetes

A 
Diabetic retinopathy
Cataracts
Rubeosis iridis
Glaucoma
Ocular motor nerve palsies
310
Q

Rubeosis iridis

A

Medical condition of the iris
New abnormal blood vessels (neovascularisation) on surface of iris

Due to ischaemia (mediated by VEGF)
Blood vessels close the angle of the eye preventing fluid leaving, causing raised IOP
Neovascular glaucoma

311
Q

Characteristic features of diabetic retinopathy

A

Microaneursyms - physical weakening of capillary walls causing leakage

Hard exudates - precipitates of lipoprotein/protein from retinal vessels

Haemorrhages - rupture of weakened capillaries.

  • Small dots or larger blots
  • Flame haemorrhages along nerve fibre bundles

Cotton wool spots - axonal debris build up from poor axonal metabolism at margin of infarct

Neovascularisation - attempt to revascularise hypoxia retina

312
Q

Classification of diabetic retinopathy

A

MILD - BACKGROUND NON-PROLIFERATIVE
At least 1 microaneurysm

MODERATE - NON-PROLIFERATIVE DR
Microaneurysms or intraretinal haemoarrhages
+/- cotton wool spots, venous beading, intraretinal microvascular abnormalities

SEVERE to V. SEVERE NON PROLIFERATIVE DR
(Pre-proliferative)
As above.
Minimum numbers in minimum number of quadrants

NON HIGH RISK PROLIFERATIVE
New vessels on disc or without one disc diameter or new vessels elsewhere

HIGH RISK PROLIFERATIVE
Large new vessels on disc or presence of pre-retinal haemorrhage.
Can have retinal detachment

313
Q

Define diabetic maculopathy

A

Focal or diffuse macular oedema - leakage well circumscribed or diffuse

Ischaemic maculopathy - decreased visual acuity and ischaemia on fluorescein angiography

Clinically significant macular oedema = thickening of retina + hard exudates

314
Q

Epidemiology of diabetic retinopathy

A

Diabetes is the most common cause of severe sight impairment

Type 1 -25% have microaneurysms at 5 years, 50% at 10 years
Nearly all by 20 years
Increased in type 2s as increased time with uncontrolled hyperglycaemia

RFs

  • Increased severity and time with hyperglycaemia
  • HTN and other vascular risk factors
  • Renal disease
  • Pregnancy
  • Ethnic minorities
315
Q

Symptoms of diabetic retinopathy

A

Painless gradual decrease in CENTRAL vision
Sudden onset dark painless floaters (haemorrhage)
Painless visual loss (severe haemorrhage blocking vitreous)
Acute pain if rubeosis iridis and glaucoma

316
Q

Signs of diabetic retinopathy

A

Decreased VA
Spots in red reflex (vitreous haemorrhage)
Little red dots (small aneurysms)
Irregular notching (venous beading)
Thinner disorganised vessels
Demarcated creamy/yellow lesions (hard exudates)
Pale lesions with poorly defined edges (cotton wool spots)

317
Q

Investigations for diabetic retinopathy

A 
Dilated retinal photography
Ophthalmoscopy
Fluorescein angiography
Optical coherence tomography
Glucose control

Screening

318
Q

Screening for diabetic retinopathy

A

Eye screening at diagnosis then annually

  • Midriasis with tropicamide for retinal photography
  • Test visual acuity

Refer if

  • New vessel formation
  • maculopathy (exudates, retinal thickening)
  • Retinopathy (cotton wool spots, venous beading, dot/blot haemorrhages)
  • Any large decrease in VA
319
Q

Management of diabetic retinopathy

A

Primary prevention

  • Optimise glycaemic control
  • BP control
  • Lipid control
  • Smoking cessation

Laser treatemtn

  • Induces regression of new vessels and decreases macular thickening
  • Can arrest progression but will not restore vision
  • Can be focal or total peripheral (panrentinal photocoagulation)
  • If both retinopathy and maculopathy, treat maculopathy first

Intravitreol steroids

Anti-VEGF (expensive)

Surgery - vitrectomy if large haemorrhage

320
Q

Retinal layers

A 
- Vitreous
Internal limiting membrane
nerve fibre layer
Ganglion cell layer
Ineer plexiform
Inner nuclear
Outer plexiform
Outer nuclear
External limiting membrane
Rod and cone outer segments
Retinal pigment epithelium
321
Q

Blood supply to retina

A

Outer retinal pigment epithelium (RPE) and photoreceptors - POSTERIOR CILIARY ARTERIES

Inner neural retina = central retinal artery

322
Q

Define hypertensive retinopathy

A

Microvascular abnormalities and persisntently high BP

  1. Copper wiring / arterial narrowing
  2. Vascular leakage
  3. Arteriosclerosis
323
Q

Presentation of hypertensive retinopathy

A

Decrease vision
Bilateral attenutation of vells (copper/silver wiring)
Arteriovenous nipping - where arteries cross veins
Eventually haemorrhages and exudates
Chronic HTN > 140/90

324
Q

Hypertensive retinopathy in malignant hypertension (>180/100) signs and symptoms

A 
Headache
Decreased vision
Hard exudates (macular star)
Disc swelling
Cotton wool spots
Flame Haemorrhage
Arterial or venous occlusions
325
Q

Define papilloedema

A

Optic disc swelling that occurs due to raised ICP

Almost always bilateral

326
Q

Pathophysiology of papilloedema

A

Raised ICP is transmitted to the subarachnoid space around the optic nerve
Increased pressure prevents axonal flwo back causing swelling and protrusion

Time course for development depends on cause
If optic atrophy then no papilloedema even if raised ICP

327
Q

Symptoms of papilloedema

A

Symptoms of raised ICP

Headache - worse on waking, bending
Nausea and vomiting
Hypermetropia (long sighted)
- If chronic = blurring or complete visual loss
Visual acuity not usually impaired unless severe
If CN 6 palsy then diplopia

328
Q

Examination findings in papilloedema

A 
Disc swelling bilaterally
Venous engorgement
Absent venous pulsation
Haemorrhages over or adjacent to optic disc
Blurring of optic disc margins
Elevation of optic disc
Radial retinal lines - Parton's lines
Visual field defect - enlarged blind spot
Impaired colour vision- red desaturation
329
Q

Classification of papilloedema

A 
Stage 0 to 5
with increased obscuration of borders
Increasing diameter of optic nerve head
Peri-papillary halo
Elevated nerve head
Obliteration of optic cup
330
Q

Causes of papilloedema

A

35% - non arteritis anterior ischaemic optic neuropathy
31% optic neuritis
14% intracranial pathology

Causes of raised ICP
- tumour/trauma. SDH/ cerebral inflammation/ infection/ abscess/ idiopathic intracranial hypertension/ respiratory failure / cerebral oedema/ medication (tetracycline and lithium)

Optic neuritis

Vascular - retinal vein or artery occlusion, malignant hypertension, ALL

Globe - glaucoma, pan or posterior uveitis, posterior scleritis, CO2 retention, uraemia, inflammation

331
Q

Epidemiology of cataracts

A 
Age related
Increases with age
Increased in women
Lower age of onset in Indian and Bangladeshi
World's leading cause of blindness

RFs
- Smoking
- Diabetes
- Systemic corticosteroids
Eye trauma
Uveitis
UV exposure
Poor nutrition
decreased socioeconomic class
Dehydrating illness crisis
Galactosaemia
Genetics
Inflammation and degenerative eye disease
Alcohol
332
Q

Pathophysiology of cataracts

A

Lens continues to grow after birth, new secondary fibres are added to outer layers
New fibres are made from lens epithelium

Lens has 3 parts

  • Capsules: collagen
  • Epithelium: anterior between capsule and fibres, lays down new fibres
  • Fibres - long thin and transparent. Arranged length wise from posterior to anterior poles and are stacked in concentric layers (crystallins)

Disruption of crystalline fibres affects the integrity and causes protein aggregation
Protein is deposited and causes clouding, light scattering and obstruction of vision

333
Q

Presentation of cataracts

A 
Depends on size, location and whether bilateral
Gradual, painless loss of vision
Difficulties with reading
Failure to recognise faces
Problems watching TV
Diplopia in one eye
haloes

Nuclear sclerosis - cataract formed by new layers of fibre compressing nucleus of lens

  • Decreased contrast
  • Decreased colour intensity
  • Reading OK

Cortical - new fibres added to outside of the lens. causing cortical spokes

  • Light scatter from opacities
  • Glare driving at night
  • Difficulty reading

Posterior subcapsular - in central posterior cortex. in younger patients.

  • Glare
  • Deterioration in near vision
  • Visually disabling
334
Q

Signs of cataracts

A

Defects in red reflex - brown or white

Check pupil reactions and VA

335
Q

Management of cataracts

A

No prevention or medical treatment

Surgery - lens extraction and replacement

  • Done under local
  • Remove anterior capsules, lens and cortex
  • Post-op topical antibiotics and steroids
336
Q

Complications of cataract surgeyr

A

Most common - capsular rupture with vitreous loss
Poor vision
- Inadequate correction of refractive error post op
- Failure to detect pre-existing eye disease
- Post-op complications

EARLY
Protruding or broken sutures
Trauma to iris
Wound gape or prolapse of iris
Anterior chamber haemorrhage <1%
Vitreous haemorrhage <1%
Choroidal haemorrhage <1%
Endopthalmitis - devastating 0.05%
Refractory uveitis
LATE
Posterior capsule opacifdication
Uveitis
Retinal detachment (increased in myopia)
Glaucoma
Increased risk of macular degeneration 
Dysphotopsias
337
Q

Endophalmitis

A

Inflammation of interior of the eye
Complication of all intraocular surgery, esp cataracts

Hx

  • Recent surgery or penetrating injury
  • Severe pain
  • loss of vision
  • Redness of conjunctiva and episclera
  • Hypopyon

Causes:

  • most commonly staph epidermidis
  • N. meningitides, S. aureus, S. pneumonia
  • Herpes simplex
  • Candida

Treated as emergency with intravitreal injection of potent antibiotics e.g. vancomycin

338
Q

Define glaucoma

A

Group of eye conditions that lead to damage to the optic nerve head with progressive loss of retinal ganglion cells and their axons

  • Progressive loss of visual field
  • Usually raised IOP
339
Q

Types of glaucoma

A

Primary

  • Congenital or acquired
  • Open or closed
  • Closed can be acute, chronic, intermittent or superimposed

Secondary

  • Inflammatory e.g. with uveitis
  • Phacogenic e.g. caused by lense
  • Neovascular (rubeosis iridis)
  • Ocular tumours
  • 2y to intraocular haemorrhage
  • Traumatic
  • Steroid induced

Year 4 (7 decks)

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