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Phase 2a medicine > Neuro > Flashcards

Neuro Flashcards

1
Q

What is the definition of a TIA?

A

Ischaemia caused by temporary blockage of the blood supply to the brain
Lasts less than 24hours, usually 5-15mins.

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2
Q

Risk factors for TIA?

A

Age, hypertension, smoking, diabetes, AF and combined oral contraceptive pill

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3
Q

What percentage of first strokes are preceeded by a TIA?

A

15%

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4
Q

What type of people are TIA’s more common in?

A

Males and black people

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5
Q

Where are atherothromboembolism’s from usually in TIA?

A

Carotid artery

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6
Q

What might be the cause of a cardioembolism?

A

Atrial fibrillation

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7
Q

Differential diagnoses for TIA?

A

Hypoglycaemia, Migraine aura, focal epilepsy, vasculitis

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8
Q

What are the presentations of a carotid territory TIA?

A

Amaurosis fugax, aphasia (speech difficulty), Hemiparesis, Hemisensory loss, Hemianopia visual loss

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9
Q

What types of symptoms would you see in a vertebrobasilar artery TIA?

A 
Cerebellar symptoms (as vertebral supply mostly cerebellum)
Vertigo, vomiting, choking, ataxia, hemisensory loss, hemi visual loss
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10
Q

What is Amaurosis fugax?

A

Unilateral sudden vision loss

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11
Q

What is usually the cause of amaurosis fugax?

A

Temporary occlusion of the retinal artery

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12
Q

What might a patient describe during amaurosis fugax?

A

Like a curtain descending

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13
Q

What risk score is used to predict a stroke after TIA?

A

ABCD2

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14
Q

What does ABCD2 stand for?

A 
Age 
Blood pressure 
Clinical features (unilateral weakness, speech disturbance)
Duration of TIA
DM
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15
Q

How to diagnose a TIA?

A 
Symptoms description 
Blood tests (glucose, FBC, ESR vasculaitis etc)
Brain imaging 
Carotid imaging (doppler ultrasound 
ECG 
Echo
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16
Q

Immediate management of TIA?

A

Aspirin, refer to a specialist

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17
Q

What would you do to control CV risk factors in TIA?

A

BP control, smoking cessation, statins, no driving for a month

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18
Q

Longterm management of TIA?

A 
Aspirin, clopidogrel, warfarin 
Carotid endartectomy (to reduce carotid stenosis)
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19
Q

What is a stroke?

A

Rapid onset neurological deficit lasting over 24 hours. Caused by infarction of cells.

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20
Q

What are the 2 types of stroke?

A

Ischaemia (blood clot)

Haemorrhagic (bleed in small vessel in the brain)

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21
Q

Risk factors for ischaemic stroke?

A

Age, male, HTN, smoking, diabetes, past TIA

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22
Q

General symptoms for ischaemic stroke

A

Contralateral sensory loss, contralateral hemiplegia, Facial weakness forehead sparing, dysphasia

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23
Q

What symptoms are you more likely to get with a stroke of the ACA?

A

Leg symptoms

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24
Q

What symptoms are you more likely to get with a stroke of the MCA?

A

Arm and face symptoms

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25
Q

What symptoms are you more likely to have if there is a brainstem infarct?

A

Quadriplegia, cerebellar signs, vertigo, N+V, locked in syndrome

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26
Q

What is a lacunar infarct?

A

Infarction of a small artery supplying a deep brain structure.

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27
Q

What investigations would you do for an ischaemic stroke?

A

CT scan (distinguish types), MRI scan (more sensitive), blood tests, ECG

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28
Q

What is the management of an ischaemic stroke?

A

Aspirin, warfarin

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29
Q

WHat should aspirin be swapped for long term in ischaemic stroke?

A

Clopidogrel

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30
Q

What drugs are used in thrombolysis?

A

IV alteplase

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31
Q

Within what time should you do thrombolysis in stroke?

A

4.5 hours

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32
Q

What is mechanical thrombectomy?

A

Endovascular removal of thrombus

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33
Q

What is an intracerebral haemorrhage?

A

Sudden bleeding into brain tissue due to rupture of a blood vessel within the brain

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34
Q

Risk factors for intracerebral haemorrhage?

A

HTN, age, anticoagulation, thrombolysis

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35
Q

How does hypertension cause intracerebral haemorrhage?

A

stiff brittle vessels more likely to rupture and cause microaneurysms.

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36
Q

What are the complications with increasing ICP?

A

Healthy tissue can die, CSF obstruction causing hydrocephalus, midline shift, herniation (putting pressure on your breathing centre and causing death)

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37
Q

Clinical presentation of an intracerebral haemorrhage than differentiate it from ischaemic?

A

Sudden loss of consciousness, severe headache, meningism, coma

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38
Q

Management of intracerebral haemorrhage?

A

Stop anticoagulants, control of BP, IV mannitol to reduce ICP

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39
Q

What is a subarachnoid haemorrhage?

A

Spontaneous bleeding into the subarachnoid space between pia and subarachnoid

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40
Q

Which arteries lie in the subarachnoid space?

A

Circle of Willis

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41
Q

Which blood vessels lie in the subdural space?

A

Bridging veins

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42
Q

Which arteries lie in the extradural space?

A

Middle meningeal artery

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43
Q

Epidemiology of SAH?

A

35-65, 50% of people die straight away

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44
Q

Risk factors for SAH?

A

HTN, Berry anneurysm, PKD, coarctation of aorta, EDS

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45
Q

What is the most common place for a berry aneurysm to occur?

A

Anterior communicating artery.

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46
Q

Pathophysiology of SAH?

A

Tissue ischaemia (from bleeding)
Raised ICP
Puts pressure on the brain
Irritates the meninges causing inflam

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47
Q

What are the clinical presentations of SAH?

A

THUNDERCLAP HEADACHE,

nausea, vomiting, collapse, loss of consciousness, seizures

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48
Q

Signs of SAH?

A

Neck stiffness, Kernig’s and Bridinskis sign

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49
Q

Differential diagnoses for SAH?

A

Migraine, meningitis

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50
Q

Investigations for a SAH?

A

Brain CT, LP (if ICP is normal), Xanthochromia (CSF looks yellow)

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51
Q

What would you see on CT in SAH?

A

A star shape sign on the CT

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52
Q

Management of SAH?

A

Refer to neurosurgeon, Nimodipine (reduces vasospasm), surgery to stop bleeding is the main treatment.

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53
Q

What is a subdural haematoma?

A

A big clot of blood in the subdural space

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54
Q

What is the cause of a subdural haematoma?

A

Rupture of a bridging vein

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55
Q

WHo is subdural haematoma most commonly seen in?

A

Babies (shaking baby syndrome), people with brain atrophy (dementia, elderly, alcoholics)

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56
Q

How long can the latent interval be in subdural haematoma?

A

Weeks/months as bleeding is slow and there is a gradual rise in ICP.

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57
Q

why do symptoms of subdural haematoma occur?

A

Haematoma starts to autolyse increasing oncotic pressure, drawing water in and therefore increasing ICP, leading to symptoms.

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58
Q

What are the symptoms of subdural haematoma?

A

Fluctuating levels of consciousness, drowsiness , headache, confusion.
Often cannot remember hitting head as it was months ago

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59
Q

Signs of subdural haematoma?

A

raised ICP, seizures

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60
Q

What does a subdural haematoma look like on CT?

A

Crescent shaped, looks like a banana

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61
Q

What is the management of subdural haematoma?

A

IV mannitol, surgery, address cause

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62
Q

What is an extradural haematoma?

A

Bleeding into extradral space caused by trauma to the temporal

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63
Q

Which artery is ruptured in extradural haematoma?

A

Middle meningeal artery

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64
Q

What is the latent interval in extradural haematoma?

A

a few hours

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65
Q

Epidemiology for extradural haematoma?

A

Young people, males, rare in children

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66
Q

Clinical presentation of extradural haematoma?

A

trauma then short episode of drowsiness, lucid interval for hours to days, rapid deterioration follows
Rapidly declinign GCS, headache, vomiting, seiures

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67
Q

What does an extradural haematoma look like on a CT scan?

A

Lemon, with midline shift

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68
Q

Management of extradural haematoma?

A

IV manitol, stabilise patient, Urgent surgery for clot evacuation

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69
Q

What is a migraine?

A

Recurrent throbbing headache often preceded by an aura and associated with nausea, vomiting and visual changes

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70
Q

What is the epidemiology of migraines?

A

More common in females, onset before 40

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71
Q

What are risk factors for migraines?

A

Genetics and family history, female, age (adolescence)

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72
Q

What mneumonic is used to remember the aetiology of migraines?

A

CHOCOLATE

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73
Q

What does chocolate stand for?

A 
Chocolate 
Hangovers
Orgasms
Cheese
Oral contraceptives 
Lie-ins 
Alcohol
Tumult 
Exercise
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74
Q

What is prodrome?

A

Before the migraine

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75
Q

What are symptoms of prodrome?

A

Yawning, cravings, mood sleep changes

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76
Q

What symptoms do people get in a migraine aura?

A

Visual disturbances (lines, dots, zigzags, somatosensory (pins and needles)

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77
Q

Clinical presentation of a migraine?

A

Unilateral pain, throbbing type pain, moderate to severe intensity, nausea, vomiting, photophobia

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78
Q

How to diagnose migraines?

A

Usually just made clinically, does not need extra tests unless red flags

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79
Q

What are the red flag symptoms for migraines?

A

Worst/ severe headache, change in pattern of migraine, abnormal neurological exam, onset older than 50, epilepsy, posterior located headache.

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80
Q

What tests would you do if there were red flags for migraines?

A

CRP/ESR, CT/MRI, LP

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81
Q

WHat is the first line treatment for migraines?

A

Triptans e.g. sumatriptan

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82
Q

How do triptans work?

A

Works on 5-HT receptors in the brain leads to vasoconstriction of the cranial vasculature

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83
Q

Other treatment options for migraines?

A

High dose NSAIDS (naproxen), antiemetics,

AVOID OPIOIDS

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84
Q

What can be used for the prevention of migraines?

A

Beta blockers (propranolol) , TCA’s such as amitriptyline

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85
Q

What is a cluster headache?

A

Episodic headaches lasting from 7days up to 1 year. HEadaches are extremely painful./

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86
Q

Clinical presentation of cluster headaches?

A

Rapid onset of excruciating pain, especially around the eye. Pain is localised to 1 area. crescendo of pain that lasts for around 30mins

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87
Q

Other features of cluster headaches

A 
Ipsilateral autonomic features:
Watery bloodshot eye 
Facial flushing
Rhinorrhoea 
Miosis (pupillary constriction) and ptosis (droopy eyelid)
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88
Q

Acute management of cluster headaches?

A

Analgesics are unhelpful.

Oxygen is really helpful, triptans

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89
Q

Prevention of cluster headaches?

A

Verapmil (CCB) 1st line prophylaxis, reduce alcohol consumption and stop smoking.

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90
Q

Triggers of tension headache?

A

Stress, sleep deprivation, bad posture, hunger, anxiety, eyestrain, noise

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91
Q

Clinical presentation of tension headache?

A

Bilateral, pressing tight, non pulsatile like an elastic band.
mild/moderate intensity
no aura

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92
Q

Symptomatic treatment of a tension headache?

A

Aspirin, paracetamol, ibuprofen

AVOID OPIOIDS

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93
Q

What is a secondary headache?

A

Has an underlying pathology

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94
Q

What might be the cause of a one sided headache in the temporal area?

A

Giant cell arteritis

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95
Q

What is the criteria for a diagnosis of epilepsy?

A

At least 2 unprovoked seizures occurring more than 24 hours apart.

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96
Q

When is it most common for people to have seizures?

A

At the extremes of age , so in young people or old people

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97
Q

Causes of epilespy?

A

2/3 idiopathic, cortical scarring, tumours or space occupying lesions, family history

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98
Q

What do patients experience in an aura befroe a seizure?

A

Deja vu, strange smells, flashing lights, strange feelings in gut

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99
Q

What is a post ictal period?

A

The period after a seizure, headache, confusion, myalgia, sore tongue.

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100
Q

What are the main 2 types of seizure?

A

Primary generalized, partial (focal)

101
Q

WHat is a primary generalised seizure?

A

Spreads throughout the whole cortex, not just one part.
Always associated with loss of consciousness
bilateral and symmetrical motor manifestations.

102
Q

What is a partial seizure?

A

One single area in a singls lobe is affected. can progress to become generalised.

103
Q

What does tonic mean in a seizure?

A

tight, stiff rigid limbs

104
Q

What does clonic mean in a seizure?

A

Rhythmic muscle jerking

105
Q

What is a tonic-clonic seizure?

A

Mixture of tonic and clonic seizures, leads to characteristic shaking symptoms of a seizure.

106
Q

What is a myoclonic seizure?

A

Isolated jerking of a limb

107
Q

WHat is an atonic seizure?

A

Loss of muscle tone, go floppy

108
Q

What is a absence seizure>

A

Common in childhood, will go pale and stare blankly for a few seconds.

109
Q

What is a simple partial seizure?

A

No affect on consciousness or memory

110
Q

What is a complex partial seizure?

A

Patient has symptoms of a seizure and is not aware they are having them

111
Q

How to diagnose epilepsy?

A

Usually clinical, EEG (determine the type), Bloods to rule out underlying cause

112
Q

How to manage a seizure lasting over 5 mins?

A

Give benzodiazepines, either rectally or IV

113
Q

Drugs to manage epileps?

A

Sodium valproate unless female of childbearing potential.

Give lamotrigine

114
Q

Types of primary brain tumours?

A

Gliomas (astrocytoma)

115
Q

What are the most common origins for secondary brain tumours?

A

Non-small cell lung cancer

116
Q

What is Wernicke’s encephalopathy?

A

Depletion of vitamin B1

117
Q

What is the triad in Wernicke’s encephalopathy?

A

Confusion, ataxia, opthalmoplegia

118
Q

Who does Wernicke’s encephalopathy occur in?

A

Chronic alcoholism

119
Q

How to manage wernickes encephalopathy?

A

Pabrinex (IV b vitamins)

120
Q

What is the most common type of dementia?

A

Alzheimers

121
Q

Risk factors for alzheimers?

A

Down’s syndrome, over 65, depression and low mood, reduced cognitive activity

122
Q

What are the key pathological hallmarks for alzheimers?

A

Beta-amyloid plagues, tau tangles, atrophy of the centre of the brain

123
Q

Signs and symptoms for alzheimers?

A

Memory loss, particularly short term memory,
Difficulty understanding and finding words
Attention and concentration difficulties
Psychiatric changes
Disorientation

124
Q

Investigations and diagnosis of dementia?

A

MMSE (mini mental state exam), Bloods to check for other causes, memory clinic assessment, MRI

125
Q

Treatment for alzheimers?

A

No cure, supportive therapy with carers ar home,

Acetylcholinesterase inhibitors can help manage symptoms

126
Q

WHat is FT dementia?

A

More common in under 65, atrophy of the frontal and temporal lobes

127
Q

Signs and symptoms of FT dementia?

A 
Behavioural issues (loss of inhibition/empathy and compulsive behaviours)
Progressive aphasia 
Semantic dementia (loss of vocab and problems understanding)
128
Q

Treatment of FT dementia?

A

SSRI’s can help with behaviour symptoms, Levodopa if Parkinsons symptoms

129
Q

What is vascular dementia?

A

The result of multiple small infarcts over time

130
Q

Signs and symptoms for vascular dementia?

A

Characterised by stepwise progression (stable followed by jump in progression),
Visual disturbances, UMN signs, muscle weakness etc

131
Q

Investigations and diagnosis for vascular dementia ?

A

Full history, ask about previous stroke/TIA, Cognitive impairment screen, medication review , MRI to look for previous infarcts

132
Q

How to treat vascular dementia?

A

Supportive therapy, SSRI’s or anti-psychotics to control symptoms.

133
Q

What is dementia with Lewy bodies?

A

Lewy bodies found in the brainstem and neocortex

On a spectrum with dementia and Parkinsons

134
Q

Signs and symptoms of Lewy body dementia?

A

Dementia presented initially, may also present with parkinsonism (tremor, rigidity, change in gait)

135
Q

How to diagnose Lewy body dementia?

A

Presence of dementia with 2 of : fluctuating attention and concentration, hallucinations, spontaneous parkinsonism

136
Q

How to treat dementia with Lewy bodies?

A

Refer to a specialist, supportive therapy, cholinesterase inhibitors to treat cognitive decline

137
Q

Typical age of onset of parkinsons?

A

55-65 years

138
Q

Aetiology of parkinsons?

A

Too little dopamine,

139
Q

What is the Parkinson’s triad?

A

Bradykinesia, rigidity, resting tremor

140
Q

What are common clinical signs of parkinsons?

A

Impaired dexterity, fixed facial expressions, foot drag

141
Q

Associated symptoms of parkinsons?

A

Dementia, depression, urinary frequency, constipation, sleep disturbances

142
Q

How is Parkinson’s diagnosed?

A
  1. diagnosis of parkinsonian syndrome
  2. exclusion criteria
  3. supportive criteria (unilateral onset, rest tremor present)
143
Q

How to treat parkinsons?

A

MDT care, Levodopa, COMT inhibitor,

144
Q

What is huntingtons?

A

neurodegenrative disease causing hyperkinesia, lots of uncontrolled movement.

145
Q

What penetrance does huntingtons have?

146
Q

What is the classical triad in huntingtons?

A

Chorea, dystonia and incoordination

147
Q

Other symptoms of huntingtons?

A

psychiatric issues, depression, cognitive impairment

148
Q

Investigations for huntingtons?

A

MRI/CT loss of striatal volume
Genetic testing,
Tests for SLE, thyroid disease, WIlsons and dementia

149
Q

Treatment of huntingtons?

A

Can only manage, no effect on the progression of the condition.
Benzodiazepines for chorea, SSRI for depression, haloperidol for psychosis

150
Q

Causes of spinal cord compression?

A

Trauma, tumours, central disc protrusion, epidural haematoma, infection,

151
Q

Signs and symptoms of spinal cord compression?

A

Loss of bladder or bowel function, UMN signs in the lower limbs, LMN signs in the upper limbs
Dependant on injury site, paraplegia, pain, paasthesia etc.

152
Q

Investigations for spinal cord compression?

A

X ray wole spine, MRI, renal function, haemoglobin to monitor blood loss

153
Q

How to treat spinal cord compression?

A

Dexamethasone until treatment plan confirmed, catheterisation, analgesia, surgical decompression

154
Q

What is brown-sequard syndrome?

A

Hemi section of the spinal cord, ipsilateral hemiplegia

155
Q

Signs and symptoms of brown sequard?

A

Ipsilateral loss of position, light touch and vibration sensation at the level of the lesion.
Contralateral loss of pain and temparature below the level of the lesion.

156
Q

Investigations and diagnosis for brown sequard?

A

Plain radiographs for penetrating or blunt trauma, MRI to determine extent of injury

157
Q

Treatment of brown sequard

A

Spine immobilisation, steroids to decrease swelling, physical therapy and occupational therapy

158
Q

What is the cauda equina?

A

The nerve roots caudal to the spinal cord termination

159
Q

Causes of cauda equina syndrome?

A

Herniation at L4/5 or L5/S1 levels, tumours, trauma, infection, AS

160
Q

Signs and symptoms of cauda equina syndrome>

A

Sudden onset, saddle paraesthesia, bladder/bowel dysfunction, sexual dysfunction, motor problems, lower back pain,

161
Q

Investigations for cauda equina syndrome?

A

Rectal exam, loss of anal tone and sensation,
MRI spine
This is a medical emergency

162
Q

WHat is the treatment for cauda equina syndrome?

A

Surgical decompression, immobilise spine, give anti inflammatories, antibiotics if infection, chemo if indicated.

163
Q

What is carpal tunnel syndrome?

A

Compression of the median nerve within the carpal tunnel

164
Q

Which areas of the hand does the median nerve supply?

A

Thumb, index finger, middle finger and half of the ring finger

165
Q

Who most commonly presents with carpal tunnel?

A

people in their late 50’s and 70’s; pregnant women

166
Q

Signs and symptoms of carpal tunnel?

A

Pins and needles (middle and index fingers tend to be affected first.
Pain in fingers that can reach to the shoulder, numbness in the same areas, weakness and loss of grip of the fingers, symptoms typically worse at night

167
Q

What investigations for carpal tunnel?

A

Clinical diagnosis based on symptom presentation.

Nerve conduction test if unclear, USS or MRI if nerve damage suspected.

168
Q

How to treat carpal tunnel?

A

Most cases will resolve, rest the wrist and try to avoid gripping, squeezing actions.
Steroid injections and surgery if severe.

169
Q

What is foot drop?

A

Difficulty in lifting the front part of the foot resulting in dragging of the toes. This can be permeant or temporary

170
Q

What is foot drop caused by?

A

Damage to the common peroneal nerve.

171
Q

What causes of foot drop?

A

Injury, tumour, hip replacement, cauda equina, MS

172
Q

Signs and symptoms of foot drop

A

Unilateral symptoms, complaint of one foot dragging across the floor when walking, tripping, numbness and weakness in the same side

173
Q

Investigations for foot drop?

A

Find underlying cause:
X-ray, USS, CT, MRI
Nerve conduction study.

174
Q

Treatment for foot drop?

A

Brace or splint, physio, specialised shoes, surgery, nerve stimulation.

175
Q

What is Charcot Marie Tooth?

A

An inherited peripheral neuropathy.

176
Q

What is Duchenne’s muscular dystrophy?

A

X-linked recessive condition, progressive muscle wasting and weakness, damage to the dystrophin gene.

177
Q

What is the function of dystrophin?

A

Strengthen muscle fibres and protect from injury.

178
Q

Signs and symptoms of duchennes muscular dystrophy?

A 
Presents in childhood, proximal muscular dystrophy, pseudohypertrophy of the calves 
Major milestones delayed 
Can't hop, run or jump,
recurrent falls
speech delay
fatigue
179
Q

Investigations for duchennes?

A

Serum creatinine kinase very high, genetic analysis, muscle biopsy with assay for dystrophin protein, muscle strength test, gait assessment.

180
Q

Complications of Duchennes?

A

Joint contractures, resp failure , cardiomyopathies and HF, gastric dillation, learning difficulties, constipation, osteoporosis and hypertension

181
Q

How to treat Duchennes?

A

MDT care, Immunisations, physio, vit D and bisphosphonates, corticosteroids, mobility help , nutritional care.

182
Q

What is the most common form of MND?

183
Q

What is Riluzole?

A

A life prolonging MND drug

184
Q

How does ALS present?

A

signs of degeneration of upper and lower motor neurons, asymmetric onset, positive babinski sign, fasiculations of the tonuge.

185
Q

What is the Babinski sign>

A

Stroking the sole of the foot, causing your big toe to move upwards and your toes to spread out.

186
Q

What age should you have a positive Babinski sign?

A

Under the age of 2

187
Q

Is it normal to have a positive Babinski sign in adulthood?

A

No, this indicates neurological issues.

188
Q

What are the corticobulbar signs that indicate a worse prognosis in ALS?

A

Brisk jaw reflex, dysarthria, dysphagia, sialorrhoea (excess salivation)

189
Q

Investigations for ALS?

A 
Diagnosis via the El escorial criteria
Nerve condiction studies
EMG 
CT/MRI of the brain 
Bloods
Muscle biopsy
190
Q

Treatment for ALS?

A

MDT care
Quinine/baclofen for cramps
Hyoscine for sialorrhoea
PEG tube for nutrition

191
Q

What is progressive bulbar palsy?

A

Involves the brain stem, the part of the brain required for swallowing, speaking, chewing and other functions

192
Q

Pathophysiology of PBP?

A

Its in the origin of the cranial nerves 9-12 and so this can lead to a much worse prognosis than ALS

193
Q

signs and symptoms of PBP?

A

First affected muscles are those used for talking, chewing and swallowing
Palsy of the tongue, difficulty swallowing and palsy of facial muscles

194
Q

Diagnosis of PBP?

A

The same as ALS

195
Q

Treatment of PBP?

A

Same as ALS

196
Q

What does Primary lateral scelrosis involve?

A

UMN of the arms legs and face

197
Q

What does progressive muscular atrophy involve?

A

Progressive degeneration of only the LMNs

198
Q

Which form of MND involves genes?

199
Q

What is MS?>

A

An autoimmune condition resulting in the loss of the myelin sheath in the CNS

200
Q

Which cells produce myelin in the CNS>

A

Oligodendrocytes

201
Q

Which cells produce myelin in the peripheries?

A

Schwann cells

202
Q

What happens in MS?

A

SLows or blocks transmisson to the CNS

203
Q

What people are more commonly affected with MS?

A

Females more common than males, younger 20-30

204
Q

What is relapsing and remitting MS?

A

Symptoms come and go, periods of good health followed by sudden symptoms>

205
Q

What is secondary progressive MS?

A

Follows relaxing remitting, gradually worsening symptoms with fewer remissions

206
Q

WHat is primary progressive MS?

A

From the beginning of the disease symptoms gradually get worse, has the worst prognosis.

207
Q

Pathophysiology of the remission in MS?

A

Remyelinating of nerve cells in-between relapses

208
Q

Symptoms of MS/

A

Upper limb extensions and lower limb flexors are weaker, spastic paraparesis, changes in sensation causing numbness and tingling, fatigue

209
Q

Signs of MS?

A

Symptoms worse with heat, Lhermitte sign (electric jolt down the neck when flexing spine), UMN signs, loss of colour vision, optic neuritis

210
Q

What is optic neuritis?

A

Damage to the optic nerve causing pain with eye movement and temporary vision loss in one eye

211
Q

What are the investigations for MS>

A

Symptoms must be spaced apart, MRI gold standard, LP,
Use Macdonald criteria
Bloods to rule out other causes

212
Q

How to treat MS?

A

MDT care, notify DVLA,
Steroids in acute
Interferon beta, fingolimod and Natalizumab

213
Q

What is Guillain Barre syndrome?

A

Acute polyneuropathy caused by rapid damage of the peripheral nerves. Demyelination and axonal degeneration.

214
Q

How does GBS most commonly present?

A

Commonly, 6 weeks post GI infection. Increased incidence in males, peak ages 15-35 and 50-75

215
Q

What are the signs and symptoms of GBS?

A

Toes to nose weakness, starts at the feet and works its way up.
Absent reflexes, sensory loss in the lower extremities.

216
Q

Investigations of GBS?

A

Bloods, LP (raised protein, normal white cells), Spirometry to monitor lung function, ECG to identify abnormalities and monitor

217
Q

Treatment for GBS?

A

IV ig for 5 days, plasmapheresis, DVT prophylaxis (low molecular weight heparin)
AVOID CORTICOSTEROIDS

218
Q

What is lambert eaton syndrome?

A

Impaired presynaptic release of acetyl choline, caused by an autoimmune attack of voltage gated calcium channels

219
Q

Symptoms of Lambert eaton?

A

Proximal muscle weakness, depressed tendon reflexes , gait changs, dry mouth, impotence in males, eyelid ptosis,

220
Q

How to differentiate Lambert Eaton from myasthenia gravis?

A

Detection of ACh receptor antibodies indicate MG

221
Q

Investigations for lambert eaton?

A

Nerve stimulation, serum test for VGCC

222
Q

Which cancer is associated with lambert eaton?

A

Small cell lung cancer.

223
Q

How to treat lambert eaton?

A

Treat any cancers, acetylcholinesterase inhibitors, amifampridine for muscle strength, immunosuppression in severe cases.

224
Q

What is myastenia gravis?

A

Binding of autoantibodies to the neuromuscular junction

225
Q

When do women commonly present with MG?

226
Q

Signs and symptoms of MG?

A

Muscle weakness that is worse on exertion and gets better with rest, occular manifestations (drooping eyelid etc)
No muscle weakness
can be seizures

227
Q

Investigations of MG?

A

Diagnosis is mostly clinical , thyroid function tests, detection of ACH receptor antibodies.

228
Q

What is the crushed ice test for MG?

A

Ice is applied to the ptosis for 3 mins, if it improves its likely to be MG

229
Q

How to treat MG?

A

ACh esterase inhibitors, pyridostigmine can control symptoms

230
Q

What is amaurosis fugax usually a complication of?

A

Giant cell arteritis

231
Q

What is the most common cause of peripheral neuropathy?

232
Q

Sensory symptoms for peripheral neuropathy?

A 
Loss of touch, proprioception, temperature/pain sensation, paraesthesia
Romberg test (cannot stand with feet together and eyes closed)
233
Q

What are the motor symptoms for peripheral neuropathy?

A

Tripping, difficulty opening jars, difficulty climbing stairs, muscle wasting

234
Q

How to treat peripheral neuropathy?

A

Treat cause

Can give pregabalin, gabapentin for pain

235
Q

What is meningitis?

A

Inflammation of the meninges

236
Q

What can bacterial meningitis be caused by?

A

E.coli, listeria, HIB, s.pneumoniae, klebsiella. TB

237
Q

Viral causes of meningitis?

A

HIV, influenza, measles, enteroviruses

238
Q

Risk factors for meningitis?

A

Immunosuppression, smoking, CSF shunts, DM, IVDU,

239
Q

Symptoms for meningitis?

A 
Stiff neck 
Photophobia 
Non-blanching rash 
Kernigs sign 
Raised ICP
Fever, headache, vomiting, nausea, lethargy, irritability, muscle pain, chills, sore throat
240
Q

Investigations for meningitis?

A

Bloods (cultures) ABG, LP (contraindicated in ICP and shock)

241
Q

Treatment for meningitis?

A

Antibiotics (IV cefotaxime or IV benzyl penicillin)

242
Q

What is encephalitis?

A

Inflammation of the brain parenchyma due to a viral infection.

243
Q

Triad of symptoms in encephalaitis?

A

Fever , headache, and altered mental status

244
Q

Treatment for encephalitis?

A

Aciclovir ASAP, IV benzylpenicilin immediately.

245
Q

What is herpes zoster?

A

More commonly known as shingles, painful rash caused by the reactivation of a nerve infection caused by the varicella zoster virus

246
Q

How does herpes zoster present?

A

Red, painful rash, stabbing or burning pain, fever, headache, fatigue and itching.

247
Q

Investigations for herpes zoster?

A

PCR test, CSF analysis, bloods

248
Q

Treatment for herpes zoster?

A

Antiviral therapy (Acyclovir) analgesia and antipyretics

Phase 2a medicine (14 decks)

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