Neuro & Medical Elderly

Question 1

Epileptic seizure types

Answer 1

Focal

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

Generalised

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

Question 2

Epidemiology of epilepsy

Answer 2

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

Question 3

Aetiology of epilepsy

Answer 3

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

Question 4

Typical presentation of generalised seziures

Answer 4

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

Question 5

Typical presentation of focal seizures

Answer 5

Aura
Focal motor activity
Automatisms

Question 6

Investigations for epilepsy

Answer 6

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

Question 7

Management principles of epilepsy

Answer 7

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

Question 8

Management of generalised tonic clonic seizures

Answer 8

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

Question 9

Management of absence seizures

Answer 9

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

Question 10

Childhood absence epilepsy

Answer 10

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

Question 11

Juvenile absence epilepsy

Answer 11

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

Question 12

Juvenile myoclonic epilepsy

Answer 12

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

Question 13

Dravet’s syndrome

Answer 13

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

Question 14

Management of acute seizure

Answer 14

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

Question 15

Investigations for acute seizure

Answer 15

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

Question 16

GCS

Answer 16

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

Question 17

Definition of brain death

Answer 17

• 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

Question 18

Risk factors for delirium

Answer 18

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

Question 19

Aetiology of delirium

Answer 19

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

Question 20

Presentation of delirium

Answer 20

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

Question 21

What is the confusion assessment method (CAM)

Answer 21

Used to assess delirium

Acute onset and fluctuating course AND
Inattention

AND EITHER

• disorganised thinking
• changed level of consciousness

Question 22

Investigations for delirium

Answer 22

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!

Question 23

Management of delirium

Answer 23

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

Question 24

What drugs can cause delirium

Answer 24

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

Question 25

Triad of normal pressure hydrocephalus

Answer 25

Incontinence Frontal lobe symptoms Gait instability

Question 26

Cerebellar disease signs

Answer 26

``` Vertigo Ataxia Nystagmus Intention tremor Slurred speech Hypotonic/hyporeflexia Exaggerated broad based gait Dysdiadochokinesia ```

Question 27

What are the geriatric giants?

Answer 27

``` Categories of impairment in elderly Incontinence Instability Immobility Impaired cognition Iatrogenic ```

Question 28

Dorsal column medial lemnisucus

Answer 28

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)

Question 29

Spinothalamic tract

Answer 29

Ascending tract In anterolateral spinal cord Carries: Pain Crude touch Temperature Decussates at the spinal level

Question 30

Spinocerebellar traect

Answer 30

Ascending tract | Does not decussate - IPSILATERAL

Question 31

Function of dorsal and ventral route of spinal cord

Answer 31

``` Dorsal = sensory Ventral = motor ```

Question 32

Define epilepsy

Answer 32

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

Question 33

Describe an absence seizure

Answer 33

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

Question 34

Symptoms of epilepsy

Answer 34

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

Question 35

Café au lait spots

Answer 35

Neruofibromatosis

Question 36

Port wine stains

Answer 36

Struge-Weber syndrome (associated with epilepsy)

Question 37

Status epilepticus

Answer 37

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

Question 38

Reflexes to be assessed to determine brain death

Answer 38

``` 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 ```

Question 39

Define delirium and types

Answer 39

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

Question 40

Complications of delirium

Answer 40

Hospital acquired infections Pressure sores Fractures Residual cognitive impairment

Question 41

Define coma

Answer 41

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

Question 42

What to examine in coma patient at presentation

Answer 42

``` 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 ```

Question 43

Cherry red discolouration indicates what?

Answer 43

CO poisoning

Question 44

Dolls head reflex

Answer 44

Roll head side to side | Eyes should move together in the opposite direction

Question 45

Oculovestibular testing

Answer 45

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

Question 46

Respiratory patterns and what they indicated in coma

Answer 46

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

Question 47

Cheyne-Stokes breathing

Answer 47

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.

Question 48

Aetiology of coma

Answer 48

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

Question 49

Investigations for coma

Answer 49

``` Blood glucose ABG Bloods - FBC, U&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

Question 50

Management of coma

Answer 50

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

Question 51

prognosis of coma

Answer 51

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

Question 52

Persistent vegetative state

Answer 52

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

Question 53

Types of primary headaches

Answer 53

Tension type headache Migraine Cluster headaches

Question 54

Causes of secondary headaches

Answer 54

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

Question 55

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

Answer 55

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

Question 56

Red flags for headache

Answer 56

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

Question 57

Types of tension type headache

Answer 57

Episodic - fewer than 15 days each month Chronic - > 15 days per month, more likely to be medication induced

Question 58

Epidemiology of tension type headaches

Answer 58

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

Question 59

Presentation of tension type headaches

Answer 59

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

Question 60

Causes of tension type headaches

Answer 60

``` Anxiety Depression Poor posture Poor sleep Stress ```

Question 61

Management of tension type headaches

Answer 61

``` 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

Question 62

Classification of migraine

Answer 62

Migraine without aura Migraine with aura Hemiplegic migraine Chronic migraine

Question 63

Epidemiology of migraine

Answer 63

``` 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 ```

Question 64

Presentation of migraine

Answer 64

``` 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 ```

Question 65

Aura in migraine

Answer 65

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.

Question 66

Migraine in children

Answer 66

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

Question 67

Management of migraine

Answer 67

``` 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

Question 68

Define cluster headaches

Answer 68

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

Question 69

Classification of cluster headaches

Answer 69

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

Question 70

Epidemiology of cluster headaches

Answer 70

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

Question 71

Clinical features of cluster headaches

Answer 71

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

Question 72

Diagnostic criteria for cluster headaches

Answer 72

``` 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 ```

Question 73

Management of cluster headaches

Answer 73

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

Question 74

When to investigate headaches

Answer 74

``` 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 ```

Question 75

Describe primary exertional headaches

Answer 75

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

Question 76

Describe primary sexual headache

Answer 76

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

Question 77

Hypnic headache

Answer 77

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

Question 78

Hemicrania continua

Answer 78

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

Question 79

Cranial or vascular causes of headachees

Answer 79

``` Stroke or TIA SAH Temporal arteritis High or Low CSF Cancer epilepsy chiari malformation ```

Question 80

Epidemiology of SAH

Answer 80

``` 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 ```

Question 81

Presentation of sub arachnoid haemorrhage

Answer 81

``` 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

Question 82

Warning symptoms of SAH

Answer 82

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 ```

Question 83

Investigations for SAH

Answer 83

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

Question 84

Management of SAH

Answer 84

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

Question 85

Prognosis and complications of SAH

Answer 85

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

Question 86

Define temporal arteritis

Answer 86

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

Question 87

Epidemiology of temporal arteritis

Answer 87

2 per 10,000 Increased in Northern European Increased in females (3:1) Associated with polymyalgia rheumatic Increased in over 60s, peak 60-80

Question 88

Presentation of temporal arteritis

Answer 88

``` 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 ```

Question 89

Features required for diagnosis of temporal arteritis

Answer 89

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

Question 90

Investigations for temporal arteritis

Answer 90

FBC - Raised WCC normocytic normochromic anaemia and thrombocytosis Raised ESR or CRP LFTs - raised ALP Biopsy from symptomatic side Colour duplex ultrasonography

Question 91

Management of temporal arteritis

Answer 91

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

Question 92

Complications of temporal arteritis

Answer 92

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

Question 93

Presentation for space occupying lesion

Answer 93

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

Question 94

Generalised symptoms of space occupying lesion

Answer 94

``` Vomiting nausea Change in mental status or behavioural change Weakness Ataxia Disturbance of gait Seizures ```

Question 95

Symptoms of cerebellar space occupying lesion

Answer 95

Ataxia Intention tremor Dysdiadokinesis Nystagmus

Question 96

Symptoms of temporal lobe space occupying lesion

Answer 96

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

Question 97

Symptoms of frontal lobe space occupying lesion

Answer 97

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

Question 98

Symptoms of parietal lobe space occupying lesion

Answer 98

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

Question 99

Symptoms of occipital lobe space occupying lesion

Answer 99

Visual field defects

Question 100

Symptoms of cerebellar pontine angle space occupying lesion

Answer 100

Most common is an acoustic neuroma ``` Tinnitus hearing loss nystagmus Decreased corneal reflex Facial and trigeminal nerve palsies Ipsilateral cerebellar signs ```

Question 101

Investigations for space occupying lesions

Answer 101

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

Question 102

Aetiology of space occupying lesion

Answer 102

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

Question 103

Define meningitis

Answer 103

Inflammation of leptomenings and underlying subarachnoid CSF | Can be due to bacteria, virus or non-infective causes

Question 104

Epidemiology of meningitis

Answer 104

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

Question 105

Causes of meningitis in neonates

Answer 105

Group B strep Listeria monocytogenes E.Coli

Question 106

Causes of meningitis in infants

Answer 106

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

Question 107

Causes of meningitis in adults

Answer 107

Neisseria meningitis Step pneumonia Haemophilus influenza B

Question 108

Causes of meningitis in elderly

Answer 108

Strep pneumonia listeria TB

Question 109

RFs for neonatal meningitis

Answer 109

``` Low birth weight Premature PROM Traumatic delivery Foetal hypoxia Maternal group B strep carrier ```

Question 110

Presentation of neonatal meningitis

Answer 110

``` Raised or unstable temperature Respiratory distress Apnoea Bradycardia Hypotension Feeding difficulty Irritability Decreased activity ```

Question 111

Aseptic meningitis

Answer 111

CSF has cells but gram stain negative and no bacteria cultures

Question 112

Causes of aseptic meningitis

Answer 112

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

Question 113

Non infective causes of meningitis

Answer 113

``` Malignancy - leukaemia, lymphoma Intrathecal drugs NSAIDs, trimethoprim Sarcoidosis SLE ```

Question 114

Presentation for meningitis

Answer 114

``` 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

Question 115

Investigations for meningitis

Answer 115

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

Question 116

Management of meningitis

Answer 116

``` IV ABx ASAP - ceftriaxome Supportive - Fluids - Antipyretics - Antiemetics - Nutritional support ``` If viral then acyclovir (herpetic)

Question 117

Immediate complication of meningitis

Answer 117

``` Septic shock DIC Coma Cerebral oedema Raised ICP Septic arthritis Pleural effusion Haemolytic anaemia ```

Question 118

Delayed complications of meningitis

Answer 118

``` Decreased hearing Seizures Subdural effusions Hydrocephalus Intellectual deficits Ataxia Blindness Peripheral gangrene ```

Question 119

Causes of facial pain

Answer 119

``` 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 ```

Question 120

investigations for facial pain

Answer 120

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

Question 121

Management for facial pain

Answer 121

Treat underlying cause | For atypical - amitriptyline, consider fluoxetine

Question 122

Define trigeminal neuralgia

Answer 122

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

Question 123

Epidemiology of trigeminal neuralgia

Answer 123

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

Question 124

Aetiology of trigeminal neuralgia

Answer 124

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.

Question 125

Presentation of trigeminal neuralgia

Answer 125

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

Question 126

Atypical trigeminal neuralgia

Answer 126

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

Question 127

Red flags for trigeminal neuralgia

Answer 127

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

Question 128

Investigations for trigeminal neuralgia

Answer 128

Diagnosed clinically | MRI to rule out other causes of pain

Question 129

Management of trigeminal neuralgia

Answer 129

``` 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

Question 130

Define hydrocephalus

Answer 130

Increase volume of CSF in ventricles | Causes white matter damage

Question 131

Classification of hydrocephalus

Answer 131

Non-communicating - CSF obstructed within ventricles or between ventricles and subarachnoid space Communicating - problem outside of ventricular system

Question 132

presentation of hydrocephalus

Answer 132

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 ```

Question 133

Investigations for hydrocephalus

Answer 133

CT scanning | US in children

Question 134

Management of hydrocephalus

Answer 134

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

Question 135

Pathophysiology of subdural haematoma

Answer 135

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

Question 136

Epidemiology of subdural haematoma

Answer 136

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

Question 137

Presentation of subdural haematoma

Answer 137

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

Question 138

Investigations for subdural haematoma

Answer 138

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

Question 139

Management of subdural haematoma

Answer 139

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

Question 140

Complications of subdural haematoma

Answer 140

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

Question 141

Epidemiology of extradural haematoma

Answer 141

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

Question 142

Aetiology of extradural haematoma

Answer 142

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

Question 143

Presentation of extradural haematoma

Answer 143

``` 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 ```

Question 144

Investigations for extradural haematoma

Answer 144

``` Baseline FBC, U&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 ```

Question 145

management of extradural haematoma

Answer 145

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

Question 146

Complications of extradural haematoma

Answer 146

``` Neurological deficits Post-traumatic seizures Post-concussion syndrome Inability to concentrate Mortality 30% ```

Question 147

Aetiology of raised ICP

Answer 147

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

Question 148

Presentation of raised ICP

Answer 148

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

Question 149

Investigations for raised ICP

Answer 149

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

Question 150

Management of raised ICP

Answer 150

``` 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

Question 151

Rinnes test

Answer 151

512 Hz External auditory meatus Then on mastoid process Which is louder Normal - louder in air Conductive - louder on bone Sensorineural - louder in air

Question 152

Weber's test

Answer 152

512 Hz Centre of forehead, which ear is loudest Normal - equal in both Conductive - louder in affected ear Sensorineural - louder in unaffected ear

Question 153

Causes of perforated tympanic membrane

Answer 153

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

Question 154

Treatment for perforated tympanic membrane

Answer 154

Watchful waiting - may heal spontaneously | Tympanoplasty if persisting - keep ear dry

Question 155

Symptoms of perforated ear drum

Answer 155

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

Question 156

Levels of hearing loss

Answer 156

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

Question 157

Epidemiology of deafness in children

Answer 157

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 ```

Question 158

Aetiology of deafness in children

Answer 158

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

Question 159

Presentation of deafness in children

Answer 159

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

Question 160

Screening for deafness in new born

Answer 160

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

Question 161

Investigations for hearing problems in children

Answer 161

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

Question 162

Management of deafness in children

Answer 162

``` 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)

Question 163

Epidemiology of otitis media with effusion

Answer 163

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

Question 164

RFs for otitis media with effusion in adults

Answer 164

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

Question 165

Acute otitis media

Answer 165

Acute inflammation of middle ear. | Bacterial or viral

Question 166

Acute suppurative otitis media

Answer 166

Pus in middle ear | 5% perforates

Question 167

Chronic otitis media

Answer 167

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

Question 168

Conditions included under otitis media

Answer 168

``` Acute OM Chronic OM Acute suppurative OM OM with effusion (glue ear) Mastoiditis Cholesteatoma ```

Question 169

Presentations of otitis media with effusion

Answer 169

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

Question 170

Examination findings in otitis media with effusion

Answer 170

``` 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 ```

Question 171

Presentation of otitis media with effusion in adults

Answer 171

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

Question 172

Investigations for otitis media with effusion

Answer 172

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

Question 173

Management of otitis media with effusion

Answer 173

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

Question 174

Epidemiology of deafness in adults

Answer 174

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

Question 175

Causes of conductive hearing loss | OCCLUSION

Answer 175

cerumen foreign body impaction oedema exostosis

Question 176

Presentation of conductive hearing loss in OCCLUSION

Answer 176

Painless loss of hearing, usually sudden

Question 177

Management of conductive hearing loss in OCCLUSION

Answer 177

If no perforation, past surgery or infection then can irrigate cerumen Soften with olive oil in preceding days Treat any cause of oedema

Question 178

Exostosis

Answer 178

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

Question 179

Presentation of conductive hearing loss in INFECTION

Answer 179

Sudden painful loss of hearing | Media - red, immobile tympanic membrane

Question 180

Most common causes of otitis externa

Answer 180

pseudomonas aeruginosa | Staph aureus

Question 181

What condition is associated with bilateral schwannomas

Answer 181

Neurofibromatosis type 2

Question 182

Causes of conductive hearing loss

Answer 182

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

Question 183

Otosclerosis

Answer 183

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

Question 184

Myringosclerosis

Answer 184

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

Question 185

TMJ syndrome

Answer 185

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

Question 186

Causes of sensorineural hearing loss

Answer 186

``` 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 ```

Question 187

Noise induced hearing loss

Answer 187

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

Question 188

Causes of ototoxic hearing loss

Answer 188

``` Aminoglycosides cis-platinum Salicylates Quinine Some loop diuretics ```

Question 189

Ototoxic hearing loss

Answer 189

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.

Question 190

Presentation of immune related hearing loss

Answer 190

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

Question 191

Idiopathic unilateral sudden sensorineural hearing loss

Answer 191

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

Question 192

Perilymph fistula

Answer 192

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

Question 193

Functional hearing loss

Answer 193

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

Question 194

Management of hearing loss generally

Answer 194

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

Question 195

Types of tinnitus and causes

Answer 195

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

Question 196

Epidemiology of tinnitus

Answer 196

1 in 10 people | Increased in men

Question 197

Presentation of tinnitus

Answer 197

``` Ringing Buzzing Hissing Whistling Humming ``` 22% unilateral 34% bilateral and equal 50% bilateral but one side dominant

Question 198

Investigations for tinnitus

Answer 198

Thorough examination hearing tests Exclude acoustic neuroma with MRI if unilateral

Question 199

Management of tinnitus

Answer 199

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

Question 200

Define presbyacusis

Answer 200

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

Question 201

Aetiology of presbyacusis

Answer 201

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

Question 202

Epidemiology of presbyacusis

Answer 202

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

Question 203

Presentation of presbyacusis

Answer 203

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

Question 204

Investigations for presbyacusis

Answer 204

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

Question 205

Management of presbyacusis

Answer 205

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

Question 206

Define acoustic neuroma

Answer 206

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

Question 207

Epidemiology of acoustic neuroma

Answer 207

8% of all intracranial tumours 80% of cerebellar pontine angle tumours RFs - neurofibromatosis - high dose radiation

Question 208

Presentation of acoustic neuroma

Answer 208

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

Question 209

Investigations for acoustic neuroma

Answer 209

Audiology assessment | MRI is imaging of choice

Question 210

Management of acoustic neuroma

Answer 210

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

Question 211

Complications of surgery for acoustic neuroma

Answer 211

- Meningitis and CSF leak - Stroke, epilepsy - Facial paralysis - Hearing loss - balance impairment - Persistent headache

Question 212

Define cholesteatoma

Answer 212

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

Question 213

Classification of cholesteatoma

Answer 213

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

Question 214

presentation of cholesteatoma

Answer 214

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

Question 215

Investigations for cholesteatoma

Answer 215

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

Question 216

Managemnt of cholesteatoma

Answer 216

Medical - only if surgery declined or contraindicated Regular ear cleaning or treatment of infections Surgery - preferable - GA + removal

Question 217

Indications for LP

Answer 217

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

Question 218

Contraindications for LP

Answer 218

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

Question 219

Signs of raised ICP

Answer 219

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

Question 220

Complications of LP

Answer 220

Post LP headache Infection Bleeding Cerebral herniation

Question 221

Indications for EEG

Answer 221

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

Question 222

Define vertigo

Answer 222

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)

Question 223

Aetiology of vertigo

Answer 223

``` 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 ```

Question 224

Epidemiology of vertigo

Answer 224

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

Question 225

Assessment of vertigo (questions)

Answer 225

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

Question 226

Romberg's test

Answer 226

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)

Question 227

Head impulse test

Answer 227

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

Question 228

Unteberger's test

Answer 228

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

Question 229

Central vertigo symptoms

Answer 229

``` 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&V less than in peripheral Hearing loss unusual No sensation of pressure in ear Head impulse test negative ```

Question 230

Peripheral vertigo symptoms

Answer 230

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.

Question 231

Investigations for vertigo

Answer 231

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

Question 232

Management of vertigo

Answer 232

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

Question 233

Define Meniere's

Answer 233

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

Question 234

Aetiology of Meniere's

Answer 234

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

Question 235

Presentation of Meniere's

Answer 235

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%)

Question 236

Stages of Meniere's

Answer 236

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.

Question 237

Diagnostic criteria for Meniere's

Answer 237

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

Question 238

Investigations for Meniere's

Answer 238

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

Question 239

Management of Meniere's

Answer 239

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

Question 240

BPPV pathophysiology

Answer 240

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

Question 241

Epidemiology of BPPV

Answer 241

2% Most common in over 50s Increased in females (x2) RFs Meniere's Anxiety disorders migraine

Question 242

Aetiology of BPPV

Answer 242

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

Question 243

Presentation of BPPV

Answer 243

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

Question 244

Investigations for BPPV

Answer 244

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

Question 245

Management of BPPV

Answer 245

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

Question 246

Define stroke

Answer 246

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

Question 247

Epidemiology of stroke

Answer 247

``` 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 ```

Question 248

Aetiology of stroke

Answer 248

``` 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 ```

Question 249

Presentation of a cerebral hemisphere infarct

Answer 249

``` 50% of strokes Contralateral hemiplegia Flaccid initially then spastic Contralateral sensory loss Homonymous hemianopia Dysphasia ```

Question 250

Presentation of brainstem infarction

Answer 250

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

Question 251

Todd's paresis

Answer 251

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

Question 252

Investigations for stroke

Answer 252

``` FBC - polycythaemia, anaemia, thrombocytopaenia ESR - temporal arteritis Glucose lipid profile BP CXR ECG ``` Brain imaging - CT ASAP

Question 253

Management of stroke

Answer 253

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

Question 254

Complications of stroke

Answer 254

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

Question 255

Define TIA

Answer 255

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

Question 256

Epidemiology of TIA

Answer 256

``` 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 ```

Question 257

Polycythaemia vera

Answer 257

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

Question 258

Aetiology of TIA

Answer 258

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

Question 259

Presentation of TIA

Answer 259

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

Question 260

Investigations for TIA

Answer 260

``` Urine for glucose FBC + ESR U&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 ```

Question 261

Assessing risk of stroke after TIA

Answer 261

``` 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

Question 262

Management of TIA

Answer 262

Calculate risk for stroke ABCD2 Lifestyle: smoking cessation, weight loss, alcohol, diet, exercise Clopidogrel Atorvastatin Antihypertensive Carotid endarterectomy if occlusion >50%

Question 263

CT appearance of ischaemic stroke

Answer 263

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

Question 264

CT appearance of haemorrhagic stroke

Answer 264

Acute blood is hyperdense compared to brain parenchyma

Question 265

Functions of the frontal lobe

Answer 265

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

Question 266

Functions of the temporal lobe

Answer 266

``` Memory Receptive language - Wernicke's area Sequencing hearing Organisation ```

Question 267

Functional of the parietal lobe

Answer 267

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

Question 268

Functions of occipital lobe

Answer 268

Vision | Visual processing

Question 269

Functions of brainstem

Answer 269

``` Breathing Arousal and consciousness Attention and concentration HR Sleep wake cycles ```

Question 270

Functions of limbic system

Answer 270

``` Attention Sensory gateway Rage Aggression Sexuality Appetite and thirst ```

Question 271

Functions of cerebellum

Answer 271

Balance Skilled motor activity co-ordination Visual perception

Question 272

Functions of basal ganglia

Answer 272

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

Question 273

Symptoms of middle cerebral artery occlusion

Answer 273

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

Question 274

Symptoms of anterior cerebral artery occlusion

Answer 274

``` Weakness of foot and leg Sensory loss of foot and leg Ataxia Incontinence Slowness and lack of spontaneity ```

Question 275

Symptoms of posterior cerebral artery occlusion

Answer 275

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

Question 276

Aetiology of sore throat

Answer 276

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

Question 277

Criteria for bacterial sore throat

Answer 277

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

Question 278

Blood test to show bacterial sore throat

Answer 278

ASO | Antistreptolysin O titre will be positive

Question 279

Symptoms of streptococcal sore throat

Answer 279

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

Question 280

Symptoms of Infectious mononucleosis

Answer 280

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

Question 281

Cause of infectious mononucleosis

Answer 281

EBV - Epstein Barr Virus

Question 282

Test for infectious mononucleosis

Answer 282

Positive Paul Bunnel Test Positive Monospot test EBV antibodies

Question 283

Causes of coryza

Answer 283

80% rhinovirus | 20% coronavirus

Question 284

Symptoms of coryza

Answer 284

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

Question 285

Symptoms of influenza

Answer 285

Uncomplication - Fever - Coryza - Headache - myalgia - GI symptoms - Pyrexia Complicated - LRTI - Hypoxaemia - SOB - Lung infiltrate

Question 286

Epiglottis

Answer 286

``` 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

Question 287

Tonsillitis

Answer 287

``` 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 ```

Question 288

Laryngitis - causes

Answer 288

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)

Question 289

Symptoms of laryngitis

Answer 289

``` Feeling of lump in throat myalgia Fever Cough Rhinitis Dysphagia Fatigue ```

Question 290

Symptoms associated with dysphagia

Answer 290

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

Question 291

Aetiology of dysphagia

Answer 291

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

Question 292

Investigations for dysphagia

Answer 292

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

Question 293

Define epistaxis

Answer 293

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

Question 294

Epidemiology of epistaxis

Answer 294

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

Question 295

Aetiology of nose bleeds

Answer 295

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

Question 296

Investigations for epistaxis

Answer 296

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

Question 297

Management of epistaxis

Answer 297

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

Question 298

Epidemiology of otitis externa

Answer 298

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 ```

Question 299

Basic anatomy of otitis externa

Answer 299

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

Question 300

Aetiology of otitis externa

Answer 300

``` 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) ```

Question 301

Presentation of otitis externa

Answer 301

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

Question 302

Ramsay Hunt syndrome

Answer 302

``` 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.

Question 303

Hutchinson's sign

Answer 303

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.

Question 304

Acute diffuse otitis externa

Answer 304

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

Question 305

necrotising malignant otitis externa

Answer 305

Life threatening extension into mastoid and temporal bones | Usually pseudomonas aeruginosa or staph aureus

Question 306

Management of otitis externa

Answer 306

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

Question 307

prevention of otitis externa

Answer 307

``` 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 ```

Question 308

Define diabetic retinopathy

Answer 308

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

Question 309

Eye conditions associated with diabetes

Answer 309

``` Diabetic retinopathy Cataracts Rubeosis iridis Glaucoma Ocular motor nerve palsies ```

Question 310

Rubeosis iridis

Answer 310

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

Question 311

Characteristic features of diabetic retinopathy

Answer 311

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

Question 312

Classification of diabetic retinopathy

Answer 312

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

Question 313

Define diabetic maculopathy

Answer 313

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

Question 314

Epidemiology of diabetic retinopathy

Answer 314

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

Question 315

Symptoms of diabetic retinopathy

Answer 315

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

Question 316

Signs of diabetic retinopathy

Answer 316

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)

Question 317

Investigations for diabetic retinopathy

Answer 317

``` Dilated retinal photography Ophthalmoscopy Fluorescein angiography Optical coherence tomography Glucose control ``` Screening

Question 318

Screening for diabetic retinopathy

Answer 318

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

Question 319

Management of diabetic retinopathy

Answer 319

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

Question 320

Retinal layers

Answer 320

``` - 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 ```

Question 321

Blood supply to retina

Answer 321

Outer retinal pigment epithelium (RPE) and photoreceptors - POSTERIOR CILIARY ARTERIES Inner neural retina = central retinal artery

Question 322

Define hypertensive retinopathy

Answer 322

Microvascular abnormalities and persisntently high BP 1. Copper wiring / arterial narrowing 2. Vascular leakage 3. Arteriosclerosis

Question 323

Presentation of hypertensive retinopathy

Answer 323

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

Question 324

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

Answer 324

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

Question 325

Define papilloedema

Answer 325

Optic disc swelling that occurs due to raised ICP | Almost always bilateral

Question 326

Pathophysiology of papilloedema

Answer 326

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

Question 327

Symptoms of papilloedema

Answer 327

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

Question 328

Examination findings in papilloedema

Answer 328

``` 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 ```

Question 329

Classification of papilloedema

Answer 329

``` 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 ```

Question 330

Causes of papilloedema

Answer 330

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

Question 331

Epidemiology of cataracts

Answer 331

``` 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 ```

Question 332

Pathophysiology of cataracts

Answer 332

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

Question 333

Presentation of cataracts

Answer 333

``` 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

Question 334

Signs of cataracts

Answer 334

Defects in red reflex - brown or white | Check pupil reactions and VA

Question 335

Management of cataracts

Answer 335

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

Question 336

Complications of cataract surgeyr

Answer 336

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 ```

Question 337

Endophalmitis

Answer 337

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

Question 338

Define glaucoma

Answer 338

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

Question 339

Types of glaucoma

Answer 339

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