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Neurology Flashcards

1
Q

What is parkinsons disease

A

progressive reduction in dopamine in the basal ganglia

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2
Q
  1. describe the typical patient that gets parkinsons
  2. what is the typical onset of parkinsons like
A

old man
gradual onset of symptoms

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3
Q

Is parkinsons symmetrical or asymmetrical?

A

asymmetrical

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4
Q

What is the triad of parkinsons

A

resting pill-rolling tremor (tremor worse at rest) 3-5Hz
cogwheel rigidity (resistance against passive movement in the form of jerky resistance)
bradykinesia (slow movement)

BRAT (bradykinesia, rigidity and tremor)

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5
Q

What are the other characteristics of parkinsons outside of the triad 5

A

shuffling gait
stooped posture
reduced arm swing on one side
smell (loss of)
facial masking (not using facial muscles as much to express themselves)

5 Ss

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6
Q

Does parkinsons tremor change with alcohol and what condition is the opposite of this

A

no change
benign essential tremor improves with alcohol

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7
Q

what are the three main parkinsons plus syndromes and what does this term mean?

A
  1. multiple system atrophy
  2. dementia with Lewy bodies
  3. parkinsonian dementia
    -> disorders with the triad of Parkinson’s disease but with additional features
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8
Q

What is the difference between lewy body dementia and parkinsonian dementia

A

When dementia is experienced within a year of the parkinsonian symptoms, a diagnosis of Lewy body is made
If longer than a period of a year, then it is Parkinsons dementia

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9
Q

what is multiple system atrophy as a parkinsons plus syndrome 4 and what is its pathophysiology 1

A

parkinsons symptoms eg bradykinesia and tremor PLUS autonomic dysfunction eg urinary incontinence and postural hypotension PLUS cerebellar dysfunction eg poor balance and gait PLUS reduced speech ability due to weakness

Damage of the nerves- no known causes

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10
Q

how is parkinsons diagnosed and how is this diagnosis regulated

A

clinical diagnosis with bradykinesia plus one of the following:
rigidity
resting tremor
posturla instability

6/12 month regular reviews of diagnosis

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11
Q

How can an essential tremor be clinically differentiated from parkinsonian if it is not clear from clinical hx/ examination

A

single photon emission computed tomography
will show reduced dopamine activity in parkinsons

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12
Q

what is the first line treatment for parkinsons where motor symptoms are affecting their life?

A

levodopa combined with benserazide or carbidopa
co- beneldopa /co-caroldopa

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13
Q

what is the first line treatment for parkinsons where motor symptoms are NOT affecting their life? 3

A

dopamine agonist/ levodopa/ MAO B inhibitors

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14
Q

What is the treatment for parkinsons where levodopa therapy has not worked and parkinsons has progressed

A

add dopamine agonist/ MOA B inhibitor/ COMT inhibitor

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15
Q

How does levodopa work?

A

it is a synthetic dopamine

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16
Q

What are 2 common combination drugs for Parkinsons and what is their mode of action and why is it combined?

A

co-beneldopa (levodopa and benserazide)
co-careldopa (levodopa and carbidopa)
carbidopa and benserazide are both peripheral decarboxylase inhibitors (which stop the metabolism of levodopa in the body before it reaches the brain)

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17
Q

What is the main side effect of levodopa?

A

dyskinesia (abnormal excess movements) eg dystonia (sustained muscle contration= noticeable abnormal postures) and chorea (discrete jerky movements)

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18
Q

What can mitigate the main side effect of levedopa and its mode of action?

A

amantadine
glutamate antagonist
which manages dyskinesia associated with levodopa

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19
Q

How do COMT inhibitors work for parkisons and give an example

A

inhibit catechol-o-methytransferase which metabolises levodopa in the body
eg entacapone

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20
Q

how do dopamine agonists work for parkinsons and give examples. How is it used in medicine and its main SE

A

mimic dopamine action by stimulating dopamine receptors
eg bromocriptine and cabergoline (ergot DA- never allowed to be first line according to NICE)
used with levodopa to reduce its dose required
SE: pulmonary fibrosis with long term use

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21
Q

How does MAOB inhibitors work for parkinsons and give examples.

A

blocks monoamine oxidase B enzymes and whose regular function is to breakdown dopamine= increase circulating dopamine
eg rasagiline or selegiline

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22
Q

What treatment should be given for parkinsons if symptoms are not controlled by medical therapy (NOT FIRST LINE)

A

deep brain stimulation via a electrical current

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23
Q

Complications of having parkinsons 2

A

recurrent falls due to motor issues
cognitive impairment

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24
Q

if cognitive impairement is identified early in parkinsons, what can help

A

Acetyl cholinesterase inhibitors eg rivastigmine or donepezil

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25
Q

What are the visible pathological changes for Alzheimer’s disease on an MRI 3

A

macroscopic: widespread cerebral atrophy
microscopic: deposition of beta amyloid protein plaques and increase of neurofibrillary tangles

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26
Q

What is the protein called that makes up the neurofibrillary tangles and what happens in Alzheimer’s

A

tau
excess phosphorylation of tau, impairing the normal function of tubulin in cetromeres

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27
Q

What are the 3 main clinical features of Alzheimer’s and explain characteristics of each

A

cognitive impairment: memory loss of more recent events, finds it hard to make decisions, nominal dysphasia (unable to identify objects/ people) but normal speech otherwise

dementia symptoms: agitation, apathy, depression

difficulties with ADLs: progresses from difficulty tasks to simple tasks like getting dressed

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28
Q

What is the non pharmacological treatment of Alzheimer’s 2

A

-> offer cognitive stimulation therapy
-> offer activities that the person prefers

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29
Q

What is the pharmacological treatment of Alzheimer’s disease?

A
  1. acetylcholinesterase inhibitors eg donepezil and rivastigmine for mild to moderate
  2. second line/ severe Alzheimer’s= add on NMDA receptor antagonist memantine
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30
Q

Should antidepressants and antipsychotics be given to Alzheimer patients according to NICE

A

antidepressants only for severe depression
antipsychotics only for patients at risk of harming themselves/ others or when hallucinations/ delusions cause severe distress because it can cause DEATH

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31
Q

SE and CI of donepezil for Alzheimer’s 1,1

A

SE= insomnia
CI= bradycardia

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32
Q

What is essential tremor and what demographic does it affect

A

a common neurological condition that can affect all ages and causes involuntary rhythmic shaking

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33
Q

What is the cause/risk factors of an essential tremor

A

genetic link, can pass from parents to child autosomal dominant
prevalence and severity increases with age (it is a progressive chronic condition)

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34
Q

what is the pathophysiology of essential tremor

A

increased activity of cerebello-thalamo-cortical pathway= rhythmic stimulation of neurones= rhythmic muscle contractions

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35
Q

What is the most common cause of intention tremor in adults?

A

essential tremor

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36
Q

Clinical features of essential tremor 3

A

-> intention tremor: exacerbated on intentional movements
-> bilateral but affects dominant side more
-> affects hands and arms first then progresses to head

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37
Q

What does the diagnostic criteria for essential tremor state

A

must be an absence of other neurological signs
greater than 3 years duration

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38
Q

What are soft neurological signs in essential tremor and give examples 2. If a patient has this how is their diagnosis changed?

A

other manifestations of disease
eg gait issues and cognitive impairment
essential tremor plus

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39
Q

Tests done for essential tremor 3

A

U&E- hypocalcaemia can cause tremor
TFT- exclude hypothyroidism as cause of tremor
NO brain imaging recommended unless other neurological findings suggesting other differentials to essential tremor (brain imaging is normal in essential tremor)

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40
Q

Treatment for essential tremor 4

A

1st line: propranolol or primidone
2nd line: gabapentin
surgical: deep brain stimultion into thalamus or botox injections into tremoring limbs

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41
Q

Typical prognosis and progression of essential tremor

A

the typicaly patient only experiences mild symptoms that don’t impact quality of life

however, tremor gets worse and can spread to other parts of body which impacts quality of life

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42
Q

What two things that are not medications that improve essential tremors

A

alcohol and rest

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43
Q

What are the 3 types of vascular dementia and explain each one

A

stroke related VD (single/ multi-infarct dementia)
subcortical VD (due to small vessel disease)
mixed dementia (VD plus alzhiemers)

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44
Q

What is vascular dementia?

A

Dementia caused by reduced blood flow to brain which causes major cognitive impairment

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45
Q

Typical progression of vascular dementia

A

sudden or stepwise deterioration of cognitive function over months or years

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46
Q

What symptoms can be included in vascular dementia 4

A

attention difficulties
problem-solving difficulties
gait issues
trouble with new information

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47
Q

How is vascular dementia diagnosed? 4

A
  1. presence of cognitive decline that affects ADL from clinical examination
  2. brain imaging/ neurological signs that show cerebrovascular disease
  3. stepwise or sudden decline
  4. dementia onset 3 months after a stroke
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48
Q

Management of vascular dementia 3

A
  1. address CV risk factors
  2. Non- Pharmacological: cognitive/ sensory stimulation or music/ animal assisted therapy
  3. Pharmacological: no specific treatment, only use Acetylcholinesterase inhibitors eg donepezil if comorbid with Alzheimers/ Lewy body/ Parkinsons
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49
Q

What is motor neuron disease?

A

neurological condition that presents with BOTH upper and lower motor neurone signs- it only involves motor symptoms so sensation will always be intact

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50
Q

What are the 4 types of motor neuron disease?

A

amytrophic lateral sclerosis
primary lateral sclerosis
progressive muscular atrophy
progressive bulbar palsy

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51
Q

How does amytrophic lateral sclerosis present

A

LMN signs in arms
UMN signs in legs

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52
Q

How does primary lateral sclerosis present

A

UMN signs only

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53
Q

How does progressive muscular atrophy present

A

LMN only
affects distal muscles then proximal

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54
Q

How does progressive bulbar palsy present and why

A

palsy of tongue, facial muscles and muscles of chewing/ swallowing
loss of function of brainstem motor nuclei

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55
Q

What symptoms suggest motor neurone disease?

A

fasciculations
mixtures of lower and upper motor neurone signs
wasting small hand muscles
abdominal reflexes intact and eye muscles preserved

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56
Q

Diagnosis/ investigations of motor neurone disease 3

A

clinical
nerve conduction studies will show normal motor conduction
electromyography shows reduced action potentials with increased amplitude

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57
Q

Management of motor neuron disease

A
  1. riluzole prolongs life for 3 months by preventing stimulation of glutamate receptors, usually for ALS
  2. non invasive ventilation BIPAP at night
  3. PEG for nutritional support
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58
Q

What is the most common presentation of ALS

A

asymmetric limb weakness

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59
Q

What are UMN signs 4

A

weakness/ paralysis
increased tone
increased reflexes and Babinski
NO muscle wasting

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60
Q

What are LMN signs 4

A

weakness/ paralysis
decreased tone
decreased reflexes and Babinski
rapid muscle wasting
LMN forehead sparring

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61
Q

What is multiple sclerosis and the official criteria for diagnosis

A

when immune system attacks myelin in CNS
McDonalds criteria: 2 episodes of autonomic neurological dysfunction separated in space and time

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62
Q

What are some risk factors of MS 3

A

female
smokers
family history

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63
Q

What is the histopathological character of MS 3

A

loss of oligodendrocytes
widespread demyelination
loss of axons in white matter

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64
Q

Symptoms of MS 12
demyelination

A

D-Diploplia
E-Eyes: painful movement and vision loss/ colour blindness
M-Motor: general weakness and high tone spasticity
Y-nYstagmus
E-Emotion: depression and anxiety mood disorders
L-Lhermitte’s phenomenon (neck flexion= shock radiating down spine)
I- Impotence (erectile dysfuction/ loss of libido)
N-Neuropathic pain
A-Ataxia
T-Talking slurred due to weak bulbar muscles and difficulty swallowing
I-Intention tremor of upper limb
O-Overactive bladder
N-Numbness

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65
Q

Types of MS 3

A
  1. relapsing remitting: acute attacks for 1/2 months followed by periods of remission, after each attack they’re never back to the same baseline
  2. secondary progressive: relapsing remitting patients develop into progressive primary patients with progressive deterioration and no relapses
  3. primary progressive: progressive deterioration from onset, less common, seen in older people, no remissions
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66
Q

Investigations for MS 5

A

1st line: bloods (NICE recommends FBC, inflammatory markers, LFTs, U&E, calcium, glucose, TFTs, B12, HIV serology)

when normal bloods and likely clinical picture of MS then:
1. refer to consultant neurologist
2. MRI brain
3. MRI spine to confirm MRI brain

CSF exam required when still not enough evidence, atypical MS demographic or atypical investigations: will show oligoclonal bands and increased igG synthesis

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67
Q

How is MS diagnosed for relapsing remitting

A

relapsing remitting:
-> MRI shows lesions disseminated in time and space AND hypotense T2 lesions

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68
Q

How is MS diagnosed for primary progressive

A

primary progressive:
1+ years of progression of disability AND two of the following:

1+ T2 hypertense lesions in brain
2+ T2 hyertense lesions in spinal cord
Presence of CSF-specific oligoclonal bands

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69
Q

how is MS acute relapse managed 1 and why 1. What does this drug not do 1

A

acute relapse: high dose IV/ oral meythlpred given for 5 days to shorten the duration of the relapse
change whether the px returns to baseline function

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70
Q

What drug reduces the risk of relapse in MS patients with relapsing remitting

A

IV natalizumab

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71
Q

how is fatigue in MS specifically treated 2

A
  1. amantadine
  2. CBT
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72
Q

how is spasticity in MS specifically treated 3

A

1st line: baclofen and gabapentin
physiotherapy is also very important alongside

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73
Q

how is bladder dysfunction in MS specifically treated 3

A
  1. US of bladder emptying
  2. if no significant residual volume, anticholinergics can improve urinary frequency eg oxybutynin
  3. if significant residual volume, intermittent self-catheterisation
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74
Q

complications of MS 3

A

recurrent UTIs
cognitive impairment
motor limitations

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75
Q

What is muscular dystrophy?

A

genetic disease that causes progressive weakness and degeneration of skeletal muscles

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76
Q

What are the three types of muscular dystrophy

A

Beckers, Duchennes and myotonic

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77
Q

What is the genetics for beckers and duchennes muscular dystrophy

A

x-linked recessive disorder (affects mostly males)
mutation of gene coding for dystrophin on chromosome 21
duchenne= framshift mutation= severe form
becker= non frameshift insertion= milder form

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78
Q

What is the symptoms of duchenne/ beckers muscular dystrophy 4

A
  1. proximal muscle weakness
  2. gait abnormalities
  3. motor milestones delayed
  4. Gower’s sign: child uses arms to stand up from a squatted position
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79
Q

What age does duchennes and beckers muscular dystrophy occur

A

3-5 years= Duchennes
10-15 years= Beckers

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80
Q

Ix for duchennes and beckers muscular dystrophy 2

A

CK (usually raised)
genetic testing to confirm diagnosis

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81
Q

Mx of duchennes and beckers muscular dystrophy 1

A
  1. oral pred to improve muscle function
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82
Q

Prognosis for duchennes and beckers muscular dystrophy 1

A

Many patients now live into their 30s.

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83
Q

What is the genetics of huntingtons inheritence and what mutation is this and what chromosome

A

autosomal dom
trinucleotide repeat of CAG, chromosome 4

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84
Q

What is the pathophysiology of Huntingtons

A

mutation causes degeneration of cholinergic and GABAnergic neurones in the striatum of basal ganglia

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85
Q

What are the symptoms of huntingtons 5

A

chorea (involuntary jerking movements)
personality changes (irritability and apathy)
intellectual impairment
dystonia (uncontrollable painful muscle spasms)
saccadic eye movements

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86
Q

What is the prognosis 1 of huntingtons

A

familial- anticipation where disease presents at earlier age going thorugh generations and with increasing severity

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87
Q

What is the mx of huntington patients

A

MDT
tetrabenazine for chorea
SSRI for depression

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88
Q

How is huntingtons diagnosed 3

A

combination of:
genetic testing (for CAG repeats 36+ is definately Huntingtons)-> definitive diagnosis
family history
can do neuro MRI to see if there is striatial atrophy but this is not specific to huntingtons only)

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89
Q

What is a brain abscess

A

pus filled pocket in the brain

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90
Q
A
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91
Q

What are the casues of brain abscesses 3

A

sepsis
neurosurgery
trauma

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92
Q

What are the clinical features of brain abscesses 4

A

headache (dull and progressively worsening, localised to site of abscess)
focal neurological deficits
fever
symptoms of raised ICP: nausea, seizures, papilloedema

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93
Q

Why is it hard to identify a brain abscess based on its symptoms 2

A

Non specific symptoms
Symptoms can mimic other neurological conditions

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94
Q

How are brain abscesses diagnosed 1

A

MRI with contrast

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95
Q

What is contraindicated for a brain abscess and why

A

LP- due to risk of brain herniation

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96
Q

What is the management for a brain abscess

A
  1. craniotomy + abscess drained
  2. IV antibiotics: ceftrioxone + metronidazole 9metronidazole convers for anaerobic species)
  3. intracranial pressure management: e.g. dexamethasone
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97
Q

What is the risk of craniotomy for draining brain abscesses

A

the abscess may reform because the head is closed following abscess drainage.

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98
Q

What are the complications of brain abscesses 4

A

seizures
meningitis
hydrocephalus
herniation

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99
Q

What is Guillain Barre syndrome

A

immune mediated demyelination of peripheral nervous system after an infection- usually campylobacter jejuni

100
Q

what is the pathophysiology of Guillain Barre

A

antibodies to current infection react with the gangliosides in the peripheral nervous system
Type 4 reaction
anti-GM1 antibodies found in 25% patients

101
Q

Symptoms of guillain barre

A

-progressive weakness of all four limbs, affecting the legs first and in a proximal to distal pattern
-mild sensory symptoms eg distal paraesthesia
-can be autonomic involvement eg urinary retention, respiratory muscle weakness and cranial nerve involvement eg oropharyngeal weakness

102
Q

What is important to ask the patient in guillain barre 1

A

history of gastroenteritis/ diarrhoeal illness a few weeks before onset of symptoms

103
Q

Investigations for guillain barre syndrome 2

A
  1. lumbar puncture (CSF has normal WCC and high protein found in 2/3 of cases)
  2. Nerve conduction studies show decreased motor nerve conduction velocity due to demyelination

guillain

104
Q

What is the management for guillain barre 3 What is not useful for management

A
  1. plasma exchange or IV immunoglobulins
  2. FVC spiromtery to monitor respiratory function
  3. ventilatory support if needed

steroids have not proven to be beneficial in the managment of guillain barre

steroids for MG, patients with guillain barre get better (GB) without steroids

105
Q

What are the risk factors for poor prognosis of guillain barre syndrome 3

A

over 40 years
Hx of a diarrhoeal disease
need for ventilatory support

106
Q

What is meningitis and what is encephalitis

A

meningitis= inflammation of the meninges (3 membranes around the brain and spinal corod)
encephalitis= inflammation of the brain

107
Q

What are the symptoms of meningitis (including triad 3) 2

A

triad:
neck stiffness
photophobia
severe headache
general symptoms: fever, rash

108
Q

What is important to remember about acute meningitis and encephalitis

A

must be reported to Public Health England

109
Q

Who is at risk of each cause of bacterial meningitis

A
  1. listeria monocytogenes: pregnant, neonates, elderly
  2. staph aureus: all ages
  3. strep pneumonia/ nissesria meningitidis: children, adults, elderly
  4. group B strep agalactaie: neonates from mother’s genital tract
  5. cyrtococcus neoformans: immunocompromised
110
Q

What are the causes of meningitis 2, 6

A

viral:
enterovirus eg Coxsackie virus
herpes virus

bacterial:
listeria monocytogenes, staph aureus, S pneumoniae, N meningitidis, group B strep, cyrococcus neoformans

111
Q

Who is most at risk of chronic meningitis 1 and what does this appear as on imaging 1

A

immunocompromised eg TB
brain covered with green grey exudate

112
Q

compare symptoms of viral and bacterial meningitis

A

bacterial: suddent onset, papilloedema, reduced GCS, vomiting
viral: self limiting 1 week and headache for months after

113
Q

investigations for meningitis 3

A
  1. blood cultures
  2. black and green throat swabs
  3. lumbar puncture within an hour in order to give abx within an hour timeframe (IF no signs of raised ICP)
114
Q

What does a non blanching purpuric rash indicate for meningitis

A

meningococcal septicaemia caused by N meningitis/septicaemia

115
Q

What is the treatment for meningitis 5

A

-community: IM/IV benxylpenicillin then bring into hospital ASAP
-hospital: IV cefotaxime (+ vancomycin in travellers, + amoxicillin in neonates and elderly)
-then IV dexamethasone to prevent neurological complications
-anyone in contact with in past 7 days should be given single dose oral ciprofloxacin prophylaxis
-if penecillin allergy, give chloramphenicol

116
Q

Compare the LP results for bacterial, viral and fungal/TB microorganisms

A

bacterial: cloudy, low glucose, high protein, neutrophils, high opening pressure
viral: clear, normal/ raised protein, high glucose lymphocytes
fungal/TB: clear, low glucose, high protein, lymphocytes

117
Q

What are the normal values for CSF

A

appearance: clear
opening pressure 90-180
WBC <8
protein 15-45
glucose 50-80

118
Q

What are the symptoms of encephalitis 4 and what is its onset like 1
compare to meningitis sx

A

fever, headache, altered mental status/ personality change, neurologial focal features eg aphasia in HS1 (HS1 usually affects temporal lobes)
gradual onset
vs meningitis: no photophobia, more likely to have AMS, onset is more gradual, commonly associated with seizures

119
Q

Investigations for encephalitis 3

A

PCR of CSF for HSV 1
CT/ MRI: medial temporal and inferior frontal changes (petechial haemorrhages )
CSF: high lymphocytes, high protein
EEG: lateralised periodic discharges at 2 Hz

main cause is HSV1, so testing mainly for this, otherwise VZV is another cause

120
Q

treatment for encephalitis 1

A

IV acyclovir in suspected encephalitis

121
Q

What is the main cause of encephalitis 1

A

Herpes simplex virus 1

122
Q

What is chickenpox caused by and what type of infection is this

A

primary infection with varicellar zoster

123
Q

How can chickenpox be spread and who from

A

respiratory droplets
from both people with chickenpox and shingles

124
Q

When is someone with chickon pox infective

A

infective 4 days before rash appears to 5 days after rashes first appeared

125
Q

What is the incubation period of varicella zoster in chickenpox

A

21 days

126
Q

what are the symptoms of chickenpox 3

A

fever
itchy rash on head/ trunk then spreading
rash: macular-> papular-> vesicular-> crusting over

127
Q

Management for chickenpox 4

A
  1. conservatively at home (kids shouldn’t go to school until lesions crusted over!!)
  2. calamine lotion and chlorphenamine for itching
  3. aciclovir if severe
  4. varicella zoster immune globulin vaccine for prophylaxis of close contacts who are immunocompromised (if they get chickenpox then start acyclovir)
128
Q

Management for chickenpox in immunocompromised 2

A

varicella zoster immunoglobulin vaccine for prophylaxis of close contacts who are immunocompromised (if they get chickenpox then start acyclovir)

129
Q

Complications of chickenpox

A

in paeds: secondary bacterial infection of lesions, causing cellulitis or group A strep invasion causing necrotizing fasciitis
in adults: viral pnuemonia

130
Q

What is shingles and its presentation

A

rash caused by reactivation of the Varicella Zoster Virus

characteristic single dermatome distribution

131
Q

Compare age epidemiology for chickenpox and shingles

A

shingles: 70+
chickenpox: 6-15

132
Q

where does varicella zoster lay dormant until reactivation into shingles 2

A

dorsal root or cranial nerve ganglia

133
Q

What type of virus is varicella zoster

A

double stranded DNA herpes virus

134
Q

Explain the symptoms of shingles throughout its difference stages

A

PRODROME:
2-3 days long
acute neuralgia (nerve pain=tingling/ burning/ itching)
INFECTIOUS STAGE:
10-12 days
rash: across single dermatome, unilateral, macular-> papular-> vesicular-> pustular-> crusting
pain: around rash area
RESOLUTION:
crusted lesions take 1 months to disappear

135
Q

Management of shingles 3

A
  1. analgesia: paracetamol/ ibuprofen first line and go up pain ladder (step up and use amitryptyline or gabapentin/ pregabalin instead)
  2. calamine lotion
  3. oral aciclovir antiviral within 72 hours rash onset (can be considered up to a week) alongside corticosteroids- only taken for 2 weeks (only if bad pain, immunocompromised, over 50 years old or affects limbs/ face)
136
Q

What are the complications of shingles 4

A
  1. post-herpetic neuralgia: persistant pain where rash was despite resolution
  2. herpes zoster opthalmicus: CN5 involvement involves CN5- opthalmic branch palsy and causes a rash on eye and potentially vision loss
  3. Ramsey Hunt syndrome: CN7 involvement causes lesions in ear and facial paralysis
  4. encephalitis
137
Q

Tell me about the shingles vaccine 3

A

offered above 70-79 years old
live attenuated so CI for immmunosuppressed

138
Q

What are the most commonly affected dermatomes in shingles

A

T1 to L2 (torso and front groin area)

139
Q

What causes malaria and how is this spread

A

Palsmodium protozoa
female Anopheles mosquito

140
Q

What are the four species of plasmodium, which is the most common and which is the most severe

A

Plasmodium falciparum
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
common: vivax
severe: falciparum

141
Q

What are the protective factors for malaria 2

A

sickle cell
G6PD deficiency

142
Q

What is the pathophysiology of malaria plasmodium 6

A
  1. mosquito bite injects sporozoites into the bloodstream
  2. sporozoites go to liver where they asexually reproduce and mature in schizonts
  3. schizonts rupture from liver cells and release merozoites
  4. merozoites infect RBC, multiply and burst out of them
  5. both male and female gametocytes are produced
  6. mosquito picks gametocytes when taking a blood meal and these sexually reproduce in the mosquito

(sexual reproduction via male and female gametocytes which releases sporozoites- only occurs in mosquito)

143
Q

Which two species of plasmodium remain dormant and how

A

vivax and ovale
lay hyponozoites in liver which remain dormant for many years

144
Q

What are the symptoms for malaria 6

A
  1. fever patterns accompanied by chills
  2. GI symptoms: nausea, vomiting, diarrhoea, abdo pain
  3. neuro: altered mental state
  4. GI organs: splenomegaly and AKI
  5. jaundice
  6. non specific symptoms: headache and fatigue

Malaria Fights GNASTY
mental state altered
fever plus chills
gi sx
non specific: headache
aki
splenomegaly
tiredness
yellowing (jaundice)

145
Q

Investigations for malaria 3

A

GS: blood film
-> thick for sensitivity to malaria
-> thin to determine species
bloods: normocytic anaemia, thrombocythaemia (high platelets)

146
Q

What are the types of malaria categorisation and explain each 6,4

A

complicated:
- severe malaria that can cause organ failure
- usually associated with P falciparum
-Parasitaemia >2%
- schizonts in blood smear
-complications
-patient not walking

uncomplicated:
-no fever
-no complications
-walking patient -Parasitaemia <2%

147
Q

What is the treatment for uncomplicated malaria 1

A

6 doses artemether + lumefantrine

148
Q

Why are there many complications in complicated malaria and give examples 3

A

due to adherence of schizonts and sequestration of erythrocytes to the vascular endothelium
= DIC, AKI, severe anaemia

149
Q

What is the treatment for complicated malaria 1

A

IV artesunate
then once stable: artemether + lumefantrine

150
Q

What are the 2 drugs for malaria prophylaxis and how are they taken, any contraindications, SE

A

atovaquone +proguanil (malarone) start 2 days before travel and end 7 days after travel
taken OD
avoid in pregnancy
SE: GI upset

doxycycline
start 2 days before adn end 4 weeks after
taken OD
avoid in under 12
SE: oesophagitis

151
Q

What can be used to repel mosquitos and has shown to repel up to 100% mosquitos if used correctly 1
what is the advantage of this 1

A

DEET containing spray
can be used for children over 2 months old

152
Q

What are migraines and features 2,3,2

A

Unilateral Recurrent, severe headaches
Prodrome: Aura (zigzag lines/ flashing lights), mood swings
ictal: severe unilateral headache +/- photophobia, N+V
post ictal: drowsy and fatigue

153
Q

What are the triggers of migraine 9

A

MIGRAINED:
menstruation, insufficient sleep, glare (bright lights), red wine, anxiety and stress, irregular/ skipping meals, nitrates, chEEse and chocolatE, dehydration

154
Q

What is the management for migraines

A

acute: sumitiptan combined with either NSAID or paracetomol
prophylaxis: propranolol or topiramate if asthmatic (topiramate avoided in pregnant women so pregnant asthmatic women give amitryptylline)

155
Q

What are tension headaches

A

recurrent, bilateral headaches like a tight band

156
Q

What is the management for tension headaches

A

acute: aspirin/ paracetomol/ NSAID
prophylaxis: amitriptyline

157
Q

What are cluster headaches

A

Each attack is around 15 min to 3 hours
Intense pain around one eye + lacrimation, lid swelling

158
Q

What is the treatment for cluster headaches

A

Acute: high flow O2 + subcut triptan
Prophylaxis: Verapamil (Cluster=CCB)

159
Q

Temporal/ Giant cell Artritis features 4 and what is it

A
  1. Unilateral headache
  2. Jaw claudication (pain caused by chewing/ speaking, goes down when not using jaw)
  3. Tender scalp + palpable temporal artery
  4. in an elderly pt

medium and large vessel vasculitis

160
Q

What are the ix and mx for temporal artritis

A

ix: raised ESR, GS= temporal artery biopsy
mx: URGENT glucocorticosteroids (prednisolone) + ophthalmology review (because they can quickly loose all of their sight)

161
Q

What is trigeminal neuralgia

A

Unilateral electric shock pains
Evoked by light touch

162
Q

What is the mx for trigeminal neuralgia

A

Carbamazepine

163
Q

Define seizure

A

Seizure: sudden, uncontrolled and disorganised electrical activity in the brain that can cause temporary changes in behavior, muscle tone, and awareness

164
Q

Define epilepsy

A

Epilepsy: a neurological disorder that causes a person to experience recurring seizures

165
Q

What is the first line management for a patient who presents with an unprovoked seizure and normal bloods/ CT 2

A

arrange EEG
neurology referral

166
Q

What is status epilepticus 2 and management 5

A
  1. Single seizure lasting more than 5 minutes
  2. 2 or more seizures within a 5 minute period

MX:
1. A to E
2. Pre-hospital: PR diazepam/buccal midazolam or if in hospital: IV lorazepam
3. if not resolving, give another dose of BZD after 5-10 min
4: 2nd line agent if ongoing status IV phenytoin or levetiracetam, sodium valproate
5. If reached refractory status (no response 45 mins after onset), induce general anaesthesia to achieve control of seizure activity

167
Q

What seizure characteristics correspond with different lobes of the brain

A

Frontal lobe: Jacksonian march, head/leg movements
Parietal lobe: Paraesthesia
Occipital lobe: Floaters/Flashers
Temporal lobe: Automatisms, aura

168
Q

What are the seizure characteristics with different seizure types 5

A

Tonic : Tensing, clenching
Atonic: Complete loss of tone, collapse
Clonic: rhythmic jerking
Myoclonic: brief muscle twitching
Tonic + clonic: rigidity then jerking (grand mal)
Absence seizure: zoning/spacing out + post-ictal confusion (petit mal)

169
Q

What are the treatments for different types of epilepsy (M/F)

A

Focal
M Levetiracetam
F Levetiracetam

Generalised tonic-clonic
M Sodium Valproate
F Levetiracetam

Myoclonic
M Sodium Valproate
F Levetiracetam

Tonic/Atonic
M Sodium Valproate
F lamotrigine

Absence
M Ethosuximide
F Ethosuximide

generalised= encompasses Tonic, clonic, myoclonic, absence

males: sodium valproate
females: levetiracetam
except ethosuximide for absence and lamotrogine for tonic/ atonic in females

focal= seizure starts in one part of brain so lobe based symptoms, unilateral, complete/ partial awareness during seizure

levetiracetam

170
Q

What is a stroke and two types

A

a sudden interruption in the vascular supply of the brain
ischaemic: vessel blockage
haemorrhagic: vessel bursting and bleeding

171
Q

define a TIA

A

a transient episode of neurologic dysfunction caused by focal (brain, spinal cord, or retinal) ischaemia, without acute infarction

172
Q

compare stroke and tia

A

TIA= sx for less than 24 hours
stroke= more than 24 hours

173
Q

What are the features of a stroke/ TIA 5

A
  1. facial drooping
  2. UNILATERAL weakness/ sensory loss
  3. Slurred speech
  4. Swallowing problems
  5. Visual field defects: homonymous hemianopia/ amaurosis fugax

FUSSY (Y being a V)

174
Q

Explain stroke localisation for ACA and what it supplies

A

Frontal + parietal lobes

Contralateral weakness and sensory loss in lower limbs
(remember this by drawing a stickman with A as its legs)

175
Q

Explain stroke localisation for MCA and what it supplies and where this clot comes from

A

Temporal + parietal
Contralateral weakness (hemiparesis) and sensory loss in upper limbs
Aphasia if it affects broccas area in temporal lobe

from internal carotid artery (as this directly conencts to middle cererbal artery and the clot will go down the path of least resistance with the blood flow)= this means it is the most common type of stroke

(remember this by drawing a stickman with M as its arms and yelling out YMCA- to remember this causes aphasia)

176
Q

Explain stroke localisation for PCA and what it supplies

A

Occipital + thalamus (thalamus processes visual information)
Contralateral homonymous hemianopia with macular sparing
Visual agnosia (seeing a picture of a cat, recognising its a cat but unable to say that it’s a cat)

(drawing two Ps as sunglasses on a stickman)

177
Q

Explain stroke localisation for Webers syndrome, what it supplies and who is affected

A

PCA branches supply the mid brain, sepcifically the Cerebral peduncle

Ipsilateral CN III palsy AND
Contralateral weakness in arm and leg

178
Q

Explain stroke localisation for Posterior Inferior Cerebellar Artery and what it supplies

A

Brainstem + cerebellum

Ataxia, nystagmus (any cerebellar signs)
Pain and temperature loss: ipsilateral for face, contralateral for limbs (spinothalamic tract)

ipsilateral horners

179
Q

Explain stroke localisation for Anterior Inferior Cerebellar Artery and what it supplies

A

Brainstem + cerebellum + **dura of internal acoustic meatus **

Ataxia, nystagmus
Pain and temperature loss: ipsilateral for face, contralateral for limbs (spinothalamic tract)

Deafness +
Facial paralysis (branches can compress the facial nerve)

180
Q

Explain stroke localisation for ophthalmic artery, where does the artery come from and what it supplies

A

branch of hte internal cortid artery

supplies Optic nerve

blockage= Amaurosis fugax (darking of vision in one eye)

181
Q

Explain stroke localisation for Basilar artery and what it supplies

A

Ventral pons of the brainstem (neuronal pathways between your cerebrum, spinal cord and cerebellum)

Locked-in syndrome- paralysis of all muscles except for eyes

182
Q

What is a lacunar stroke and features

A

occurs when an artery that supplies blood to the deeper portions of the brain ie subcortex (thalamus, basal ganglia)

sensory loss/ weakness BUT intact awareness and speech
the sensory loss/ weakness will be one of the following
pure motor stroke (C/L weakness but no sensory defecit)
pure sensory stroke (C/L sensory loss but no motor weakness- involves thalamus as this processes sensory information, thalamus= THenTHory information)
sensorimotor stroke= C/L sensory loss and weakness of arms and legs

183
Q

What is the Oxford Bamford classification

A

System that classifies strokes based on the initial systems
LOOK SPEAK MOVE:
Homonymous hemianopia
Dysphasia (or other higher cognitive dysfunction)
Weakness/sensory loss

All 3 = total anterior infarct (anterior + middle cerebral arteries)
⅔ = partial anterior infarct
ONLY weakness/ONLY sensory loss = lacunar infarct

ONLY homonymous hemianopia = posterior circulation infarct

184
Q

What are the first ix for stroke in the ER

A
  1. Rosier’s tool for stroke (in ER) (U/L face, arm, leg, speech issues and vision issues all +1 point and LOC and seizure activity -1 each) a score of greater than 0 indicates stroke
  2. non contrast CT head 1st line
185
Q

How is a TIA managed?

A

*Step 1: exclude hypoglycaemia and haemorrhage with MRI imaging *

Step 2: When did the suspected TIA occur?

Within 7 days→
*300mg aspirin * + specialist assessment within 24h
-> This involves carotid artery doppler imaging within 24 hours- if intervention needed then carotid endarterectomy done within 7 days
More than 7 days ago → specialist assessment within 7 days

Step 3: Secondary prevention
Initial 21 days: dual antiplatelet therapy with aspirin 75 + clopidogrel 75 (PLUS PPI!)
Long-term prevention: clopidogrel
If AF: DOAC
+ high-dose statin 80mg

Driving:
Single TIA: don’t drive for 1 month, no need to inform DVLA
Multiple TIAs: don’t drive for 3 months, notify DVLA
Stroke: don’t drive for 1 month, no need to inform DVLA

186
Q

How is a stroke managed

A

Step 1: Rule out haemorrhage with CT (hyperdense collection meaning lighter on CT)
Step 2: aspirin 300mg IF AFTER 24 hours
Step 3: Is patient presenting within 4.5h of stroke?
If YES → thrombolysis IV alteplase
If NO → no thrombolysis unless CT shows potential to salvage brain tissue, in which case, thrombolysis allowed within 9 hours of sx onset
Step 4: Is patient presenting within 6h of stroke?
Perform CT/MR angiography: if proximal anterior circulation occlusion confirmed → mechanical thrombectomy
Step 5: Is patient presenting within 24h of stroke?
Perform CT/MR angiography: if proximal circulation occlusion confirmed AND potential to salvage brain tissue → mechanical thrombectomy
Step 6: Is stenosis in carotid artery >50% ?
** consider carotid endarterectomy**

Step 7: secondary prevention
Clopidogrel 75mg OD (this is postponed to 24 hours after any alteplase/ mechanical thromebctomy is done to reduce the risk of bleeding)
simvaastatin high dose 80mg
If AF → DOAC
T2DM control, HTN control

187
Q

What is mononeuritis multiplex and appropriate mx

A

stand alone episodes of neuropathy involving both sensory and motor function (including being isolated to nerve palsies) in different areas with no pattern and gradual recovery taking a few weeks

mx= tends to be in diabetics so tighter glucose control to reduce the risk of future episodes happening and otherwise physiotherapy of affected limbs

188
Q

What shape are extradural haemorrhages, location, artery affected, way of presentation, management

A

half lemon= lentiform (lemonform)
location: between dura and skull but cannot cross suture lines
meningeal artery (usually middle meningeal artery)
LOC (often a contact injury) then short lucid interval (improvement in condition) then LOC- in younger
Craniotomy + evacuation of haematoma

189
Q

What shape are subdural haemorrhages, location, artery affected, way of presentation, management

A

crescent shaped
location: between dura and arachnoid- can cross suture lines
Bridging veins (veins)
hx head trauma then lucid interval (can be acute or chronic) then decreasing consciousness- in older
Conservative/surgical decompression with burr hole evacuation

190
Q

What shape are subarachnoid haemorrhages, location, artery affected, way of presentation, management 3

A

outline of edge of entire skull shape- acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.

location: between arachnoid and pia mater
Berry aneurysms in cerebral artery (MC MCA)
Thunderclap occipital headache, meningisms (n/v, neck stiffness)
Oral nimodipine to prevent vasospasm + coil, VTW prophylaxis

191
Q

what is the investigation for subarachnoid management 3

A
  1. non-contrast CT
  2. if CT head done after 6 hours of sx onset and is normal= do LP at least 12 hours after sx to allow the development of xanthochromia (breakdown of RBC) CSF findings= xanthochromia, normal/ raised opening pressure, raised bilirubin
  3. 3.if CT shows SAH evidence, urgent referral to neurosurgery and CT intracranial angiogram to identify the lesion
192
Q

A 52 year old man comes in complaining of a sudden severe headache that started 12 hours ago. There is no significant past medical history. He is unsure of his family history.
On examination he is in significant pain and distress. He is not confused and neurological assessment is unremarkable. An urgent CT head is requested. It came back normal and a lumbar puncture was requested.
Given the most likely diagnosis, what are you likely to see in the LP results?

Bilirubin
Light chain and raised protein
Oligoclonal bands and Bence-Jones proteins
Oligoclonal bands and low glucose
Normal LP

A

Bilirubin
most likely diagnosis is subarachnoid haemorrhage= bleed in brain
blood will get broken down= bilirubin

193
Q

What is a glioblastoma and what is it and effect and mx

A

aggressive cancer of CNS/ brainstem

solid tumours with central necrosis and a rim that enhances with contrast

Disrupts the blood-brain barrier and therefore are associated with vasogenic oedema- treated with dexamethasone

194
Q

What is vestibular schwannoma and Sx 2

A

cancer of vestibulocochlear nerve CN8

Sx: ipsilateral hearing loss + facial nerve palsy CN 7

195
Q

What is the most common cancer in children and sx 5

A

astrocytoma

Sx: increased ICP sx n/v, weakness/ gait/ visual disturbance (similar to stroke symptoms in a kid)

(Increase ICP cushings triad- bradycardia, bradypnoea and hyPERtension)

do MRI as LP is CI here- 48 hour referral

196
Q

What is Meniere’s disease and its features

A

fluid build up in inner ear

  1. recurrent episodes of vertigo, tinnitus and hearing loss from minutes to hours
  2. starts off unilateral sx then after years becomes bilateral
197
Q

What is the Mx for Meniere’s disease 4

A
  1. ENT assessment for diagnosis
  2. patient to inform DVLA and do not drive during episodes
  3. for acute attacks give buccal/ IM prochlorperazine (pro chlorine pair of (swimming trunks) zine= like seine river)
  4. for prevention betahistine and vestibular rehabilitation

(Bad Ears Don’t Process Voices)

198
Q

What is narcolepsy and what are its associations 2

A

early onset of REM

HLA DR2 (also causes MS and hayfever)
low levels of orexin (protein that is responsible for controlling sleep patterns)

199
Q

What are the features of narcolepsy

A
  1. hypersomnolence (excessive daytime sleepiness)
  2. cataplexy (sudden loss of muscle tone often triggered by emotion)
  3. sleep paralysis
  4. vivid hallucinations on going to sleep or waking up

medical student tired in lectures goes to sleep (excessive daytime sleepiness)
gets hallucination of monster chasing her (vivid hallucinations on going to sleep/ waking up)
cannot run away (sleep paralysis)
when she wakes up, lecturer tells her off but she gets angry because narcolepsy is not her fault and collapses (cataplexy)

200
Q

bel

What is the ix and mx for narcolepsy

A

ix: multiple sleep latency test (EEG that monitors brain activity whilst taking naps)
mx: daytime modafinil to keep you awake and at night sodium oxybate

201
Q

What is neurofibromatosis, how is it inherited and what is the mutation in both types

A

genetic condition that causes benign tumours to grow along nerves
chromosome 17 mutation in type 1
chromosome 22 mutation in type 2
autosomal dominant

202
Q

What are the features of neurofibromatosis 1/2

A

type 1: cafe au lait spots, axillary/ groin freckles, phaechromocytoma, iris hamartomas (ocular hamartomas)

C: café-au-lait spots (greater than six seen during one year)
A: axillary or inguinal freckling
F: fibromas (neurofibroma (two or more) or plexiform neurofibroma (one))
E: eye hamartomas (Lisch nodules)
S: skeletal abnormalities, e.g. sphenoid wing dysplasia, leg bowing
P: positive family history
OT: optic tumour (optic nerve glioma)

type 2: bilateral vestibular schwanommas

203
Q

What is normal pressure hydrocephalus and who presents with this

A

hydrocephalus due to reduced CSF absorption at the arachnoid villi
elderly patients with dementia (reversible cause of dementia)

204
Q

What are the features of normal pressure hydrocephalus 4

A

wet (urinary incontinence)
wacky (dementia)
wobbly (wide gait- can be similar to Parkinsons)
symptoms develop over several months

205
Q

What is the ix 1 and mx 1 for normal pressure hydrocephalus

A

ix: CT: shows enlarged fourth ventricle and not proportionate sulcal enlargement
mx: ventriculoperitoneal shunting

206
Q

What is the peripheral neuropathy caused by diabetes and management 3

A

glove and stocking distribution of lower leg sensory loss, which may also be painful
mx:
first line is amitriptyline, duloxetine, gabapentin or pregabalin
if first line dose not work then try one of the other 3
neuropathic pain exacerbation= tramadol short term

207
Q

What are the causes of cauda equina 3

A
  1. central disc prolapse occurs at L4/5 L5/S1
  2. tumours
  3. trauma

these all can compress ther nerves at cauda equina

208
Q

What are the features of cauda equina 3

A
  1. lower back pain
  2. bilateral sciatica (tingling/ numbness + pain in buttocks
  3. urinary dysfunction (incontinence, loss of urge to void)

leaning down to get something= ow (lower back pain)
feels tingling and numbness + pain in buttocks= oh
wets themself= (oh) no

209
Q

What are the Ix and mx for cauda equina

A

ix: urgent MRI spine
mx: surgical decompression

210
Q

What are the mc for spinal cord compression

A

mc cause is extradural compression from vertebral body metastases (cancers)

211
Q

features of spinal cord compression and how to located site of lesion

A
  1. back pain worse on lying down and coughing
  2. lower limb weakness
  3. sensory loss
  4. neurological signs
    -> lesion above L1= UMN signs in legs and sensation
    -> lesion below L1= LMN signs in legs and perianal numbness
    -> tendon reflexes increased below level of lesion and absent at level of lesion

imagine princess and pea (pea symbolises spinal cord compression)
-> princess realises back pain is worse when lying down/ coughing
-> she tries to get up but her legs won’t move (weakness LL)
-> she picks up one leg to swing it over to the side but realises she can’t feel it (sensory loss)
(((((neuro signs: tries to get up before 1am- LMN signs in legs + perianal numbeness so she decides to rest and try again. tries to get up after 1am, UMN signs in legs and can feel sensation)))))

212
Q

What are the ix and mx for spinal cord compression

A

Ix: urgent MRI spine
Mx: high dose oral dexamethasone and urgent oncological assessment for consideration of radiotherapy/ surgery

213
Q

What level is cauda equina

A

L1

214
Q

What are the two ascending tracts, what information do they carry

A

ascending tracts carry sensory info from body to brain

dorsal column: fine touch, vibration, proprioception

spinothalamic tract: pain and temp

215
Q

What is the most important descending tract

A

corticospinal tract (main motor pathway for voluntary movement)

216
Q

What level of spinal cord lesions do the following symptoms indicate:
respiratory difficulties
autonomic dysfunction
all four limbs
legs only

A
  1. C3-C6
  2. T1- L2
  3. cervical C1-7
  4. thoracic T1 and below
217
Q

What are the causes of anterior/ posterior cord syndrome

A
  • external metastatic mass
  • anterior or posterior spinal artery blockage
218
Q

What is anterior cord syndrome and features

A
  1. bilateral loss of pain and temp (spinothalamic)
  2. bilateral paralysis and UMN (corticospinal)
  3. all symptoms occur below the level of the lesion
219
Q

What is spinal stenosis and features and what is the most common part of spine to be affected and ix 2 and ddx

A

spinal canal narrowing which compresses the spinal cord
presents with glute/ leg pain on walking/ standing and is relieved by forward flexion or sitting
lumbar spine
MRI, ABPI to rule out intermittent claudication
ddx: peripheral arterial disease

only spinal compression presentation that gets better with position

220
Q

What is posterior cord syndrome and features and causes

A
  1. bilateral loss of fine touch, proprioception and vibration below side of lesion (dorsal column)
  2. poor co-ordination/ unsteady walking (due to lack of proprioception)
  3. all symptoms occur below the level of the lesion
221
Q

What is syringiomyelia? How can you differentiate between this and other spinal cord conditions?

A

fluid filled cyst forms in the spinal cord which can press on nerve fibres in and spinal cord

syringiomyelia: affects upper limbs first and dorsal root column not affected, unlike other spinal cord conditions

syringio= like syringe to draw up injections and injections go into the arm= upper limb affected first + inject DNA= dorsal

222
Q

What is Brown sequard syndrome presentation

A
  1. Ipsilateral paralysis below the level of the lesion
  2. Ipsilateral loss of fine touch, proprioception and vibration sense (dorsal)
  3. Contralateral loss of pain and temperature sensation (spinothalamic)- contralateral as the spinothalamic tract is the only tract who’s fibres decussate as they enter the spinal cord and ascend contralaterally
223
Q

What is the presentation of long thoracic nerve injury?

A

medial winging of scapula

224
Q

What is the presentation of radial nerve injury? What nerve endings? Cause?

A

wrist drop
C5-T1
midshaft humerous fracture

225
Q

What is the presentation of common peroneal nerve injury? Nerve ending? Cause?

A

foot drop and weak eversion with absent ankle jerk
L4-5
fibular head fracture

226
Q

What is the presentation of posterior tibial nerve injury?

A

pain and numbness in the plantar foot and heel

227
Q

What is the presentation of ulnar nerve injury? What nerve endings? Cause?

A

claw hand (flexion of last two digits and extension of others)
C8-T1
Medial Epicondyle fracture

228
Q

What is the presentation of median nerve injury, nerve endings, sx, dx, mx, causes

A

carpal tunnel: tingling in palm with thenar muscle wasting, pts often wake up at night due to symptoms and shake their hand around (wake and shake)

C6-T1

dx tinel (tap) and phalen (prayer sign in reverse) test positive, nerve conduction studies in hand show decreased conductivity

mx splints, last resort is surgery

causes: acromegaly, repetitive overuse, RA, pregnancy

229
Q

What is the presentation of horners syndrome

A

anhydrosis (loss of sweating on affected side)
myosis (on affected side of face)
ptosis (on affected side of face)
ipsilateral

230
Q

What is the pathophys of myasthenia gravis and what type of hypersensitivity is it

A

autoimmune condition with insufficiency functioning acetylcholine receptors of skeletal muscle
T2

231
Q

astrocyt

What are the features of myasthenia gravis

A

muscle weakness worse with activity and improve with rest

  1. muscle weakness starting from head to lower body
  2. weak eye muscles= diplopia + ptosis
  3. face: myasthenic snarl (difficulty smilling), speech fatiguability (=slurred speech), jaw fatiguability (tired after chewing)

HEAD-> EYE-> MOUTH/JAW

232
Q

What are the causes of myasthenia gravis

A
  1. thyomas (thymus gland tumour)
  2. thymic hyperplasia
  3. autoimmune conditions: pernicious anaemia, autoimmune thyroid disorders, RA, SLE
233
Q

What are the ix for myasthenia gravis 3

A
  1. single fibre electromyography= repetitive stimulation= redeuced muscle actiona potentials
  2. Abx testing: Anti Ach-R (1st line) and Anti- MuSK (2nd line)
  3. CT thorax of thymus to look for thymoma

myasthenia

234
Q

What is the management for myasthenia gravis 3

A
  1. acetylcholinesterase inhibitors eg pyridostigmine first line
  2. immunosuppression eg pred
  3. thymectomy/ thymic hyperplasia if thyomas is the cause, generally can cause long term benefits even in pts without thyoma
235
Q

What is the sx and management for a myasthenic crisis 2

A

sx: acute worsening of sx + respiratory failure
tx: plasma exchange, IVIG

236
Q

What does C5+6 innervate

A

skin: lateral forearm + thumb + index
muscle: elbow flexion, shoulder abduction and flexion (like a guy flexing his biceps in the mirror)
reflex: bicep jerk, C6 supinator

237
Q

What does C7 innervate

A

skin: middle finger
muscle: wrist flexion, finger and elbow extension (like showing an engagement ring to someone)
reflex: tricep

238
Q

What does C8 +T1 innervate

A

skin: medial forearm + lateral 2 fingers
muscle: C8 finger flexion, T1 finger add and abd

239
Q

What does L5 innervate

A

skin: big toe and dorsum
muscle: dorsiflexion of foot

240
Q

What does S1 innervate

A

skin: heel and sole
muscle: plantarflexion of foot
reflex: ankle

241
Q

What innervates the knee jerk

A

L4

242
Q

Ix for DVT

A

if wells 2+ then proximal leg vein US
if wells 1- then do d-dimer
whenever proximal leg vein US cannot be done within 4 hours, give LMWH

243
Q

treatment for DVT

A

DOAC apixiban (LMWH if renally impaired) for 3 months if provoked (and event that provoked is no longer a rfx) or 6 months if unprovoked

244
Q

investigations for PE (4)

A

if wells >4 then CTPA (diagnostic)
if wells <4 then D-dimer

ECG: sinus tachycardia, new RBBB, S1Q3T3 (large S wave in lead 1, Q wave in lead 3, inverted T wave in lead 3)

245
Q

What is the wells criteria

A

Active cancer/ tx within 6 months

Bedridden recently >3 days or major surgery within 12 weeks

Calf swelling >3 cm compared to the other leg (Measured 10 cm below tibial tuberosity)

Collateral (non varicose) superficial veins present

Entire leg swollen

Localized tenderness along the deep venous system

Pitting edema, confined to symptomatic leg

Paralysis, paresis, or recent plaster immobilization of the lower extremity

Previously documented DVT

Alternative diagnosis to DVT as likely or more likely

(each is +1 point, except last one is -2)

246
Q

how do you identify the cause of a bitemporal hemianopia?

A

bitemporal hemianopia with mostly lower quadrants affected= craniopharyngioma, causing superior optic chiasm obstruction
bitemporal hemianopia with mostly upper quadrants affected= pituitary tumour,
causing inferior optic chiasm obstruction
(second one= UP= upper quadrants affected, pituitary tumour)

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