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3a > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the most prevalent type of dementia in the UK?

A

Alzheimer’s

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2
Q

What is the peak incidence of Alzheimer’s?

A

70

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3
Q

What percentage of Alzheimer’s disease is inherited autosomal dominant?

A

5%

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4
Q

An amyloid precursor gene mutation causes Alzheimer’s; what chromosome is it found on?

A

Chromosome 21

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5
Q

A presenilin one gene mutation causes Alzheimer’s; what chromosome is it found on?

A

Chromosome 14

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6
Q

A presenilin two mutation causes Alzheimer’s; what chromosome is it found on?

A

Chromosome 1

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7
Q

What genetic condition is a risk factor for Alzheimer’s?

A

Downs syndrome

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8
Q

Describe the macroscopic changes seen in Alzheimer’s

A

Cerebral atrophy, particularly in the cortex and hippocampus

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9
Q

Describe the microscopic changes seen in Alzheimer’s

A
  • Cortical plaques
    -Deposition of A-beta amyloid protein
    -intraneuronal neurofibrillary tangles
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10
Q

What causes the neurofibrillary tangles seen in Alzheimer’s?

A

Abnormal aggregation of tau protein and hyperphosphorylation of tau is linked with AD

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11
Q

What neurotransmitter is in deficit in Alzheimer’s?

A

Acetylcholine

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12
Q

Describe the clinical features of Alzheimer’s

A

-Difficulties of daily living
- Onset is over months/years
-Cognitive impairment:
-Memory loss
-Difficulty learning new information
-Vague with dates
-Reasoning and communication
-Difficulty making decisions
-Dysphasia
-Behavioural/ psychological
-Depression
-agitation
-psychosis
-apathy
-disinhibition

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13
Q

Describe the non-pharmacological treatment of Alzheimer’s

A

-Social prescribing
-Group cognitive stimulation therapy (mild/ moderate cases)
-Group reminiscence therapy and cognitive inhibition

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14
Q

Describe the pharmacological treatment for mild-moderate Alzheimer’s

A

3 acetylcholinesterase inhibitors:
-donepezil
-galantamine
-rivastigmine

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15
Q

What is the contraindication for donepezil?

A

Bradycardia

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16
Q

What is the key side effect to remember for donepezil?

A

Insomnia

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17
Q

What drug is used in moderate Alzheimer’s intolerant of acetylcholinesterase inhibitors?

A

memantine

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18
Q

What drug is combined with acetylcholinesterase inhibitors when treating moderate/severe Alzheimer’s?

A

memantine

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19
Q

What drug is used as monotherapy in severe Alzheimer’s?

A

memantine

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20
Q

What type of drug is memantine?

A

NMDA

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21
Q

How can the non-cognitive symptoms of Alzheimer’s be treated?

A

-Antidepressants for depression
-Antipsychotics for those at risk of hurting themselves or others

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22
Q

Describe Parkinson’s disease

A

Progressive reduction in dopamine in the basal ganglia leads to movement disorders.

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23
Q

Describe the pattern of the movement disorder distribution seen in Parkinson’s disease

A

Asymmetrical, it affects 1 side of the body

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24
Q

What is the classic triad seen in Parkinson’s disease?

A

-Resting tremor
-Rigidity
-Bradykinesia

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25
Q

Describe the rigidity seen in Parkinson’s

A

-Resisting passive movement
-Cogwheel

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26
Q

Briefly describe the pathophysiology of Parkinson’s disease

A

-Dopamine is essential for the function of the basal ganglia
-The basal ganglia coordinate habitual movements such as walking
-The basal ganglia are involved in specific movement patterns

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27
Q

Describe the tremor seen in Parkinson’s

A

-worse on one side
- 4-6 hertz (4-6 cycles/ second)
-Pill rolling
-more noticeable at rest
-Better with voluntary movement
-worse when the patient is distracted
-Using the other hand exaggerates the tremor

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28
Q

Describe the features of bradykinesia seen in Parkinson’s

A

-Micrographia
-shuffling gait
-festinating gait
-difficulty initiating movement
-Lots of little steps when moving
-hypomimia

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29
Q

What are other features of Parkinson’s that are not associated with tremors or bradykinesia?

A

-Depression
-Sleep disturbance
-anosmia
-postural instability
-cognitive impairment
-memory problems

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30
Q

Describe a benign essential tremor

A
  • symmetrical
    -6-12 hertz
    -improves at rest
    -worse with intentional movement
    -no other Parkinson’s symptoms
    -improves with alcohol
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31
Q

Describe the Parkinson’s tremor

A

-Asymmetrical
- 4-6 hertz
- worse at rest
- improves with intentional movement
-other Parkinson’s features
- No change with alcohol

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32
Q

What condition may present mimicking Parkinson’s

A

-multiple system atrophy
- Multiple systems in the brain degenerate (including the basal ganglia, which can give a Parkinson’s presentation

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33
Q

In multiple system atrophy, how can autonomic dysfunction present?

A
  • Postural hypotension
    -constipation
    -Sexual dysfunction
    -abnormal sweating
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34
Q

In multiple systems atrophy, how can cerebellar dysfunction present?

A

ataxia

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35
Q

How is Parkinson’s disease diagnosed?

A
  • History and examination
    -UK Parkinson’s Disease Society Brain Bank clinical diagnosis criteria
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36
Q

What is the approach to managing Parkinson’s?

A

-Treating the symptoms as there isn’t a cure

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37
Q

What is the most effective treatment for Parkinson’s, and what is its caveat?

A

Levodopa (synthetic dopamine) it becomes less effective over time

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38
Q

What are the side effects of levodopa, and how are these managed?

A
  • dystonia
    -chorea (involuntary irregular movements)
    -athetosis (continuous, slow, writhing movements)
    Managed with amantadine (glutamate antagonist)
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39
Q

What drug are peripheral decarboxylase inhibitors combined with, and what do they do?

A
  • Levodopa
    -stop L-dopa being metabolised peripherally before it reaches the brain
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40
Q

Give two examples of peripheral decarboxylase inhibitors

A
  • Carbidopa
    -Benserazide
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41
Q

What are COMPT-inhibitors, how do they work and give an example of one?

A

-Catechol-o-methyl transferase inhibitors
-COMPT enzyme metabolises levodopa peripherally and centrally
-Entacapone, taken with levodopa to slow its breakdown

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42
Q

What are dopamine agonists, and how are they used?

A

-Mimic the action of dopamine in the basal ganglia
-less effective than L-dopa
- Used to delay the start of L-dopa and then used in combination with L-dopa

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43
Q

Name 3 dopamine agonists

A

-Bromocriptine
-Pergolide
-Cabergoline

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44
Q

What is the risk of taking dopamine agonists for a prolonged time?

A

Pulmonary fibrosis

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45
Q

What type of movements does a benign essential tremor affect?

A

All voluntary movement

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46
Q

What areas of the body are benign essential tremors most noticeable?

A

the hands, head, jaw and vocal cords

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47
Q

Describe the features of benign essential tremor

A
  • 6-12 hertz
    -symmetrical
    -improves with alcohol
    -more prominent with voluntary movements
    -worse with fatigue, stress or caffeine
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48
Q

What are the key differentials of benign essential tremors?

A

-Parkinson’s
-MS
-Huntingtons chorea
-hyperthyroidism
-fever
-dopamine antagonists (antipsychotics)

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49
Q

How is benign essential tremor managed?

A

-doesn’t usually require intervention
-medications may improve symptoms:
Propanalol (non selective beta blocker)
Primidone (barbituarate anti-epileptic)

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50
Q

What is the 2nd most common type of dementia?

A

-Vascular dementia

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51
Q

Describe vascular dementia

A

A group of syndromes of cognitive impairment caused by mechanisms inducing ischaemia or haemorrhage secondary to cerebrovascular disease

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52
Q

List the RF for vascular dementia

A

-History of TIA
-AF
-Hypertension
-DM
-Hyperlipidaemia
-smoking
-obesity
-CHD
-FH of stroke of CVD

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53
Q

How can vascular dementia be inherited?

A

-CADASIL
-Cerebral autosomal arteriopathy with subcortical infarcts and leukoencephalopathy

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54
Q

How can vascular dementia be classified?

A
  • Stroke-related (multi-infarct or single-infarct dementia)
    -Subcortical (small vessel disease)
    -Mixed (VD and Alzheimer’s)
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55
Q

What is the timescale of deterioration in vascular dementia?

A

-months/ years

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56
Q

List the symptoms of vascular dementia

A

-Focal neurological abnormalities (visual disturbance, sensory or motor symptoms)
-Difficulty with attention and focus
-seizure
-memory disturbance
-Gait disturbance
-speech disturbance
-emotional disturbance

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57
Q

How is vascular dementia diagnosed?

A

-History and examination
-formal screen for cognitive impairment
-medical review to exclude prolonged medication use as a cause
-MRI

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58
Q

What are the MRI changes seen in vascular dementia?

A

-Infarcts
-White matter changes

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59
Q

How is vascular dementia treated?

A
  • Treat the symptoms
    -managed CVD RF
    -Cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
    -No pharmacological treatment for VD alone
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60
Q

Describe motor neurone disease

A

-Variety of specific diseases affecting motor nerves
-Progressive, eventually fatal, where motor neurons stop working
-No sensory signs

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61
Q

What is the most common type of MND, and what % of diagnoses does it account for?

A

-Amyotrophic lateral sclerosis
-50%

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62
Q

What is the distribution of disease seen in amyotrophic lateral sclerosis?

A

-LMN signs in the upper limbs
-UMN signs in the lower limbs

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63
Q

What chromosome is affected in amyotrophic lateral sclerosis with an inherited element, and what protein does it make?

A

-chromosome 21
-superoxide dismutase

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64
Q

What is the 2nd most common type of MND?

A

-Progressive bulbar palsy

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65
Q

Which type of MND has the worst prognosis?

A

-Progressive bulbar palsy

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66
Q

Describe progressive bulbar palsy

A
  • Affects muscles of talking and wallowing
    -due to loss of motor nuclei in the brainstem
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67
Q

Which type of MND has the best prognosis?

A

-Progressive muscular atrophy

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68
Q

Describe progressive muscular atrophy

A

-distal muscle affected before proximal muscles
-LMN signs only

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69
Q

Describe the pathophysiology of MND

A

-exact mechanism unknown

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70
Q

What % of MND is inherited?

A

5-10%

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71
Q

What factors is MND linked to?

A

-Smoking
-exposure to heavy metals
-exposure to pesticides

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72
Q

Describe the presentation of MND

A
  • 40-60 yr old
  • more commonly male
    -has an affected relative
    -Insidious, progressive asymmetrical muscle weakness affecting the limbs, trunk, face and speech
    -Weakness 1st noticed in the upper limbs
  • wasting of the small muscles of the hands and tibialis anterior
    -Increased fatigue when exercising
    -clumsiness, dropping things, tripping over
    slurred speech (dysarthria)
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73
Q

What is a late sign of MND?

A

sphincter dysfunction

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74
Q

Are there ever sensory signs in MND?

A

-No, there can be sensory symptoms (limb pain) early in the disease onset, however

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75
Q

How can the features of MND be used to rule out other diseases?

A
  • No external ocular muscle weakness like myasthenia gravis
  • No cerebellar signs
    -Abdominal reflexes maintained
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76
Q

Describe the UMN signs

A
  • Increased tone and spasticity
  • Brisk reflexes
  • upgoing plantar reflexes
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77
Q

Describe the LMN signs

A
  • Muscle wasting
  • decreased tone
  • Fasciculations (muscle twitching)
    -Decreased reflexes
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78
Q

How are alternative diagnoses excluded before diagnosing MND?

A
  • Nerve conduction studies will appear normal and will exclude neuropathy as the cause of symptoms
    -MRI excludes cervical cord compression and myelopathy
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79
Q

What test would indicate MND?

A

Electromyography will show reduced action potential and an increased amplitude

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80
Q

How well can MND currently be managed?

A

Not particularly well, no treatment halts or reverses the disease process

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81
Q

How does riluzole work, and for what type of MND is it prescribed?

A

-Prevents stimulation of glutamate receptors
- used mainly in ALS
-Extends life by 3 months

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82
Q

What support is given when respiratory muscles weaken?

A

-non-invasive ventilatory support (BIPAP)

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83
Q

How is symptom control managed in MND disease?

A
  • Baclofen is used in muscle spasticity
  • Antimuscarinics are used for excessive saliva production
    -Benzodiazepines to help with breathlessness exacerbated by anxiety
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84
Q

Describe multiple sclerosis

A

-Chronic
-autoimmune
demyelination of the CNS

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85
Q

How much more common is MS in women?

A

3x

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86
Q

What is the age that MS is most commonly diagnosed?

A

20-40

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87
Q

Describe the geographical distribution of MS

A

More common at higher latitudes (further from the equator)

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88
Q

What cells make myelin in the CNS?

A

oligodendrocytes

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89
Q

Which cells make myelin in the PNS?

A

Schwann cells

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90
Q

Describe the pathophysiology of MS

A

-Inflammation and immune infiltration damages the myeline, affecting the electrical signals
-Early in disease there is remyelination, causing symptom resolution
-Remyelination is incomplete later in the disease, so symptoms become permanent

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91
Q

Are all CNS lesions likely to cause symptoms?

A

NO, if someone has an MS attack, there are likely more lesions not causing symptoms throughout the CNS

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92
Q

What are the causes of MS?

A

-Multiple genes
-EBV
-Low vitamin D
-Smoking
-Obesity

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93
Q

Describe the duration of an initial MS attack

A
  • over more than 24 hours
    -lasts weeks or days
    -Resolves if it’s the 1st presentation
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94
Q

What is the most common presentation of MS?

A

-Optic neuritis

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95
Q

What causes optic neuritis?

A

demyelination of the optic nerve

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96
Q

Describe the symptoms of optic neuritis

A
  • Unilaterally reduced vision developing over hours-days
    -pain with eye movement
    -impaired colour vision
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97
Q

Describe the signs of optic neuritis

A

-Central scotoma (enlarged blind spot)
- Relative afferent pupillary defect

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98
Q

Describe the different ways there can be an afferent pupillary defect in MS

A

-Pupil in the affected eye constricts more when shining light in the contralateral eye than when shining directly
-Reduced response in the affected eye in direct pupillary response
-Normal response in the affected eye when testing consensual pupillary reflex

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99
Q

Other than MS, name 7 causes of optic neuritis

A
  • Sarcoidosis
    -SLE
    -measles
    -mumps
    -neuromyelitis optica
    -Lyme disease
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99
Q

What should be done if someone presents with optic neuritis

A

-Urgent ophthalmology review
-High-dose steroids
-MRI

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99
Q

When someone presents with optic neuritis, what can the MRI results indicate?

A

Changes on the MRI can help predict which patients will go on to develop MS

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100
Q

Lesions to which cranial nerves cause diplopia and nystagmus?

A

CN3, CN4 and CN6

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101
Q

What is oscillopsia?

A

The visual sensation that the environment is moving and is unable to create a stable image

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102
Q

What are the signs of internuclear ophthalmoplegia?

A

-Impaired adduction in the ipsilateral eye
-nystagmus in the quadrilateral eye

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103
Q

In internuclear ophthalmoplegia, where is the lesion?

A

The medial longitudinal fasciculus
-Connects the cranial nerve nuclei that control eye movements, meaning that they are unable to coordinate movements

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104
Q

A lesion to which cranial nerve causes conjugate lateral gaze disorder?

A

-CN4

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105
Q

Describe how conjugate lateral gaze disorder presents

A

When the person is attempting to look laterally to the side affected, the unaffected eye will look medially and the affected eye will look straight on

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106
Q

Describe 4 different focal neurological symptoms that MS may present with

A

-Incontinence
-Horner’s syndrome
-facial nerve palsy
-limb paralysis

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107
Q

Describe 4 focal sensory symptoms that MS may present with

A

-trigeminal neuralgia
-numbness
-paraesthesia
-Lhermitte’s sign

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108
Q

What is Lhermitte’s sign?

A

-Sensation of electric shock which travels down the spine and into the limbs when flexing the neck

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109
Q
A
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109
Q

Describe the pathology behind Lhermittes spine

A

Disease in the cervical spine in the dorsal column, the demyelinated dorsal column is stretched

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110
Q

What is the word to describe sensory ataxia?

A

pseudoathetosis

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111
Q

What causes sensory ataxia?

A

loss of proprioception, possibly by a lesion in the dorsal columns

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112
Q

What causes cerebellar ataxia?

A

a cerebellar lesion

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113
Q

What test would indicate sensory ataxia?

A

a positive Romberg’s test

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114
Q

What is the most common disease pattern for MS?

A

mild relapsing-remitting

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115
Q

Describe the relaxing-remitting MS pattern

A

-symptoms are inn different areas with each episode
-Active: new symptoms, new lesion
-Inactive: no new symptoms, no new lesions
-Worsening: Overall worsening of disability over time
- Not worsening: no overall worsening over time

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116
Q

Describe clinically isolated syndrome MS

A

-1st episode of demyelination, neurological signs and symptoms
- may never have another episode or may develop MS

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117
Q

In clinically isolated syndrome, what makes someone more likely to develop MS?

A

A lesion being found on MRI

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118
Q

Describe the primary progressive disease pattern of MS

A

the disease and neurological symptoms worsen from the initial episode

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119
Q

describe the secondary progressive disease pattern of MS

A

the disease is initially relapsing-remitting, but then symptoms worsen and progress with incomplete remission, becoming more permanent

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120
Q

How is MS diagnosed?

A

-MRI scan for lesions
-LP

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121
Q

What findings on an MRI indicate MS?

A

-Periventricular plaques
- Dawson fingers

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122
Q

What are Dawson fingers?

A

Hyperintense lesions perpendicular to the corpus collosum

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123
Q

What lumber puncture findings would indicate MS?

A

-Oligoclonal bands in the CSF, however not in the serum
-Increased intrathecal IgG

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124
Q

Describe the basic management of MS

A
  • DMARDS to induce long-term remission
    -relapses are treated with 500mg oral steroids (methylprednisolone) 5 days or 1g daily 3-5 days
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125
Q

What is an indicator for IV steroids over oral steroids in MS relapses?

A

-Previous failure with oral or a very severe relapse

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126
Q

What is the use of steroids in treating MS relapses?

A
  • shortens the length of an acute relapse, doesn’t alter the disease progression
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127
Q

Describe symptomatic management of MS

A

-Exercise to maintain activity and strength
-fatigue: amantadine, modafinil or SSRI’s
-Neuropathic pain: amitriptyline or gabapentin
-Depression: SSRI’s
-urge incontinence: antimuscarinics (solifenacin)
-spasticity: Baclofen or gabapentin
-Oscillopsia: gabapentin or memantine

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128
Q

What are the indications for DMARD’s in someone with a relapsing-remitting MS pattern

A

2 relapses in 2 years, walks 100m unaided

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129
Q

What are the DMARD’s indications in secondary-progressive MS?

A

2 relapses in 2 yeras, able to walk 10m unaided

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130
Q

What DMARD is used 1st line in MS?

A

Natalizumab

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131
Q

Describe the action of natalizumab in ms?

A

-inhibits migration of leucocytes across the endothelium in the blood brain barrier
- strongest evidence for preventing relapses
- IV

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132
Q

Describe how ocrelizumab is used in MS management

A
  • Humanised anti- CD20 monoclonal antibody
  • High efficacy, can be used 1st line
  • IV
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133
Q

Describe how fingolimod can be used in MS treatment

A
  • sphingosine 1-phosphate receptor modulator
  • prevents lymphocytes leaving lymph nodes
  • oral option
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134
Q

Name 2 older drugs used in MS management

A
  • beta interferon
    -glatiramer acetate
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135
Q

What is the most common type of muscular dystrophy and what is it’s inheritance pattern?

A

-Duchennes muscular dystrophy
-X-linked

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136
Q

Describe the mutation in Duchenne’s muscular dystrophy

A

-defective dystrophin gene due to a frameshift mutation which leads to a blockage of one or both binding sites
-the dystrophin gene helps to hold muscles together at a cellular level

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137
Q

How are females affected by Duchenne’s muscular dystrophy?

A
  • X-linked disease, females have 2 copies of the dystrophin gene so are rarely symptomatic but are carriers, there’s a 50% chance of a daughter being a carrier and a 50% chance of a son having the disease
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138
Q

When does Duchenne’s muscular dystrophy present?

A

3-5 years

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139
Q

How does Duchenne’s muscular dystrophy present?

A
  • pelvic girdle weakness
    -progressive, eventually all muscles are affected
  • Gower’s sign
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140
Q

What is Gower’s sign?

A
  • demonstrates proximal muscle weakness
    -child can’t stand up without assistance from arm muscles
    -crouching dog position, shifts weights onto legs
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141
Q

when do boys with Duchenne’s muscular dystrophy usually become reliant on wheelchair use?

A

by teenage years

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142
Q
A
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143
Q

what is the life expectancy of someone with Duchenne’s muscular dystrophy?

A

25-35 years, with goof management of cardiac and respiratory complications

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144
Q

What treatments can improve Duschenne’s muscular dystrophy?

A

-Steroids: can slow the progression by 2 years
-Creatinine: can give slight improvement of muscle strength

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145
Q

What sign of Duchenne’s muscular dystrophy may be observed in the calves?

A

pseudohypertrophy

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146
Q

What percentage of boys with Duchenne’s muscular dystrophy have an intellectual impairment ?

A

30%

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147
Q

Describe the mutation in Becker’s muscular dystrophy

A

non- frameshift mutation, both binding sites are preserved

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148
Q

when does Becker’s dystrophy present?

A

8-12 years old

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149
Q

When may patients with Becker’s muscular dystrophy require wheelchair assistance?

A

-late 20’s or 30’s
-may be able to walk with assistance into adulthood

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150
Q

How is Becker’s muscular dystrophy managed?

A

similarly to Duchenne’s muscular dystrophy

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151
Q

How common is intellectual impairment in Becker’s muscular dystrophy?

A

Not very common

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152
Q

When does myotonic muscular dystrophy present?

A

in adulthood

153
Q

How is myotonic muscular dystrophy characterised?

A
  • progressive muscle weakness
    prolonged muscle contractions (unable to let go after a handshake/ after holding a door handle)
    -cataracts
    -cardiac arrhythmias
154
Q

When does facioscapulohumeral muscular dystrophy present?

A

-childhood

155
Q

How does facioscapulohumeral muscular dystrophy present?

A
  • weakness around the face, progressing to the shoulders and arms
156
Q

what are 3 signs of facioscapulohumeral dystrophy?

A
  • sleeping with eyes slightly open
    -weakness pursing lips
    -unable to blow out cheeks without letting air out of the mouth
156
Q

How does oculopharyngeal muscular dystrophy present?

A

-bilateral ptosis
-restricted eye movement
-swallowing problems
-muscles around the limb girdles are affected differently

156
Q

when does oculopharyngeal muscular dystrophy present?

A
  • in late childhood
157
Q

When does limb girdle weakness present?

A

teenage years

158
Q

When and how does Emery-Dreifuss muscular dystrophy present?

A

-Childhood
- Contractures
-progressive weakness and wasting of muscles

159
Q

What is the inheritance pattern of Huntington’s disease?

A

Autosomal dominant

160
Q

What are the chances of the child of someone with Huntington’s disease developing the condition?

A

50%

161
Q

Describe the pathology of Huntington’s disease

A

-Trinucleotide repeat disorder
-Mutation on the HTT gene on chromosome 4 which codes for the huntingtin protein
-Degeneration of cholinergic GABAergic neurons in the striatum of the basal ganglia

162
Q

When do symptoms usually start for people with Huntington’s disease?

A

30-50 years

163
Q

Name 4 other trinucleotide disorders other than Huntington’s disease

A
  • Myotonic dystrophy
    -Fragile X-syndrome
    -Spinocerebellar ataxia
    -friedreich ataxia
164
Q

Describe the concept of genetic anticipation

A
  • progressive generations have more trinucleotide repeats
    -early onset of symptoms and more severe disease
165
Q

Describe the presentation of Huntington’s disease

A

-Insidious onset of psychiatric, cognitive and mood problems followed by movement disorders

166
Q

What movement disorders may come with Huntington’s disease?

A
  • Chorea: involuntary, random, irregular and abnormal movements
  • Dystonia and irregular posture due t dystonia
    -rigidity: resistance to passive movement
    -dysarthria
    -dysphagia
167
Q

How is Huntington’s disease diagnosed?

A

Genetic testing

168
Q

What is the treatment for Huntington’s disease?

A

There currently is no treatment to change alter the disease progression

169
Q

How may Huntington’s disease be managed?

A

MDT approach
-genetic counselling
-physiotherapy
-SALT
-Advanced directive’s
-End of life care

170
Q

What drugs may be used in Huntington’s disease management?

A

-SSRI’s for depression
-Tetrabenazine, for chorea symptoms

171
Q

What is the prognosis for Huntington’s disease?

A

10-20 years after diagnosis

172
Q

Describe the pathogenesis of a brain abscess

A

-Focal intracranial infection that begins as a localised area of cerebritis and evolves into a collection of puss surrounded by a well vascularised capsule

173
Q

Which types of organisms may cause abscesses?

A

-Streptococcus
-staphylococcus
-anaerobes
-fungi
-parasites

174
Q

What may cause brain abscesses?

A

-Secondary to infections elsewhere in the body
-direct inoculation from trauma or surgery
-complication of meningitis

175
Q

I what demographic are brain abscesses most common?

A

males aged 20-30

176
Q

Why can diagnosing a brain abscess be difficult?

A

-Vague symptoms
-mimics other neurological conditions

177
Q

What are the risk factors for a brain abscess?

A

-immunosuppression
-recent neurosurgery
-chronic ear or sinus infections
-systemic infection and new onset neurological symptoms

178
Q

How will the presentation of a brain abscess differ in someone who is immunosuppressed?

A

-Symptoms will be more subtle

179
Q

What type of headache would a brain abscess present with?

A

-dull
-constant
-progressively worse
-localised (to the area where the abscess is)

180
Q

What percentage of patients with a brain abscess have focal neurological symptoms and what may these be?

A

-50%
-hemiparesis
-language/speech disorders
-visual field defects (oculomotor or abducens nerve palsy)

181
Q

What percentage of patients with brain abscesses present with fever?

A

50%

182
Q

What non-specific features may indicate a brain abscess?

A

-lethargy
-altered mental status
-seizures

183
Q

When are seizures more likely from a brain abscess?

A
  • When the abscess is in the cerebral cortex due to cortical irritation
184
Q

Name 4 features of someone presenting with a brain abscess

A

-headache
-non-specific features
-focal neurological symptoms
-fever

185
Q

What contrast agent is used in MRI when scanning for an abscess and what may it show?

A

-gadolinium
-early cerebritis

186
Q

What complications may be indicated by a CT when scanning a brain abscess?

A

-hydrocephalus
-herniation

187
Q

What situations should you order a CT before a LP?

A

if raised intracranial pressure is suspected

188
Q

Why is a LP contraindicated in a suspected brain abscess?

A

Herniation risk

189
Q

What technique may provide diagnostic information and treatment for a brain abscess?

A

stereotactic needle aspiration

190
Q

Describe the management for a brain abscess

A

-Surgery: craniotomy for cavity debridement, the abscess may come back after the head is closed
-IV antibiotics: 3rd generation cephalosporin and metronidazole
- Dexamethasone for raised ICP

191
Q

List 6 bacteria that cause meningitis

A

-Neisseria meningitidis
-streptococcus pneumoniae
-Haemophilus influenzae
-Group B streptococcus (streptococcus agalactiae)
-Listeria monocytogenes
-Escheria coli

192
Q

What type of bacteria are neisseria meningitidis?

A

Gram negative diplococci

193
Q

Name 3 bacteria that neonates in particular are susceptible to causing meningitis

A

-Group B streptococcus (streptococcus agalactiae, it colonises the vagina)
-Listeria monocytogenes
-E. coli

194
Q

Which pathogen causes the typical non-blanching rash associated with meningitis?

A

-Neisseria meningitidis, when it causes meningococcal septicaemia

195
Q

Compared with bacterial, how quick is the onset of viral meningitis?

A

more gradual

196
Q

Compared with bacterial, describe the prognosis of viral meningitis

A

-good
-often patients are fully recovered in 7-10 days and need little treatment

197
Q

Name 5 viruses which may cause meningitis

A

-Enteroviruses (coxsackie virus)
-Herpes simplex virus
-Varicella zoster virus
-Arboviruses
-mumps
-HIV

198
Q

Which viruses causing meningitis should be treated with acyclovir?

A

-Herpes simplex virus
-varicella zoster virus

199
Q

Name 3 non-infective causes of meningitis?

A

-Malignancies: leukemia or metastatic cancers
-Drugs: NSAIDs, some antibiotics (trimethoprim-sulfamethoxazole), intrathecal therapies
-Autoimmune conditions: SLE, Behet’s disease, sarcoidosis

200
Q

Which ages are most susceptible to meningitis?

A

Under 5’s and over 60’s

201
Q

Name 5 risk factors for meningitis

A

-Age
-Immunocompromised
-Crowded living conditions
-splenectomy or spleen dysfunction

202
Q

What is the classic triad for meningitis?

A

-Fever
-Neck stiffness
-altered mental state

203
Q

How may meningitis present?

A

-Fever
-neck stiffness
-altered mental state
-vomiting
-headache
-photophobia
-seizures

204
Q

what non-specific symptoms in neonates may indicate meningitis?

A

-Hypotonia
-poor feeding
-lethargy
-hypothermia
-bulging fontanelle
-high pitched cry

205
Q

When would you LP a child?

A

-under 1 month, fever
-1-3 months, unwell with a high/low WCC

206
Q

Which tests would you perform which may indicate if someone has meningitis?

A

-Kernig’s test
-Brudzinski’s test

207
Q

Describe Kernig’s test

A

patient supine, hip and knee flexed to 90 degree’s, slowly straighten the knee whilst keeping the hip flexed, this creates stretch in the meninges
+ve if there’s spinal pain or resistance to moving

208
Q

Describe Brudzinki’s test

A

patient supine, lift head and neck of the bed and flex the chin the the chest
+ve if involuntary flexion of hips and knees

209
Q

Where does the spinal cord end?

A

L1-L2

210
Q

Where is the needle inserted in an LP?

A

L3-L4 or L4-L5

211
Q

What tests are performed on CSF obtained via LP?

A

-Bacterial culture
-Viral PCR
-Cell count
-Protein
-Glucose

212
Q

Why should a blood glucose be performed when doing an LP?

A

to compare the blood glucose to the CSF glucose, CSF glucose will be about 40% CSF glucose in bacterial meningitis

213
Q

Describe CSF findings in bacterial meningitis

A

-Cloudy
-high protein
-low glucose
-high neutrophils
-+ve culture

214
Q

Describe CSF findings in viral meningitis

A

-Clear
-protein mildly high or normal
-glucose normal
-high lymphocytes
-Ve culture

215
Q

If a child presented to primary care with suspected meningitis, what would the correct course of action be ?

A

-IM/IV benzylpenicillin
- if true penicillin allergy, don’t delay hospital transfer to find alternative
-Don’t delay transfer for ABx

216
Q

What are the dosages of benzylpenicillin in primary care for suspected meningitis?

A

-Under 1= 300mg
-1-9 = 600mg
-over 10 =1200mg

217
Q

In hospital which antibiotics are used to treat meningitis?

A

-Under 3 months ceftriaxone and amoxicillin to cover listeria
-above 3 months cefotaxime
-acyclovir if viral meningitis is suspected

218
Q

What investigations should be done in someone with suspected meningitis?

A
  • Blood cultures and LP before antibiotics if possible without delaying AbX administration
    -Meningococcal PCR, it’s quicker than cultures
219
Q

What treatment is given to close contacts of people with meningococcal meningitis?

A

a single dose of ciprofloxacin ASAP

220
Q

List 5 complications of meningitis

A

-Hearing loss
-seizures and epilepsy
-cognitive impairment and learning disability
-memory loss
-focal neurological deficits (limb weakness or spasticity)

221
Q

In the context of the pathology of meningitis, what are the 3 stages in the Invasion stage?

A

-colonisation
-invasion
-crossing the blood brain barrier

222
Q

in the context of pathology in meningitis, describe colonisation

A
  • Nasopharynx
  • usually by the causative bacteria ( Neisseria meningitidis, streptococcus pneumoniae, haemophilus influenzae)
223
Q

in the context of pathology in meningitis, describe invasion

A

-Pathogens invade the blood stream
- This bacteriaemia transient or sustained

224
Q

in the context of pathology in meningitis, describe the 3 methods of crossing the BBB

A

1) transcellular penetration (directly through endothelial cells)
2) paracellular (between endothelial cells)
3) Trojan horse mechanism (via infected phagocytes)

225
Q

in the context of pathology in meningitis, what are the 3 stages involved in survival and replication in the host?

A
  • Evasion of host immune response
  • Bacterial proliferation and inflammation
    -Tissue damage
226
Q

in the context of pathology in meningitis, describe evasion of host immune response

A

-antigenic variation
-inhibition of complement system
-intracellular survival inside phagocytes
-biofilms
-immunomodulatory molecules

227
Q

Where do bacteria multiply in the CNS in meningitis, why do they do it here and what is the overall effect?

A
  • Subarachnoid space
    -there’s a lack of effective immune response in this space
  • raised ICP
228
Q

Describe the inflammatory response of the host during meningitis

A

-cell wall components trigger an inflammatory response
-cytokines and chemokines are released, inflammatory cells are recruited to the site

229
Q

How is tissue damage sustained during meningitis?

A

-Inflammation
-damages neuronal tissue and the BBB

230
Q

What are the clinical manifestations of the BB being damaged during meningitis?

A

-headache
-fever
-neck stiffness
-neurological deficits

231
Q

Which group of patients are at risk of fungal meningitis?

A
  • Immunocompromised
232
Q

What pathogens may cause fungal meningitis?

A

-Cryptococcus neoformans
-cryptococcus immitis

233
Q

List 3 parasites which may cause meningitis?

A
  • Toxoplasma gondii
    -taenia solium
    -amoebae
234
Q

What does primary meningitis mean?

A

CNS infection, no concurrent or prior infection

235
Q

what does secondary meningitis mean?

A

Infection latter to neurosurgery or penetrating head trauma

236
Q

What does acute meningitis mean?

A

symptoms develop over hours to 2 days

237
Q

What does subacute meningitis mean?

A

symptoms develop over 1-2 weeks

238
Q

What does chronic meningitis mean?

A

symptoms persist for more than 4 weeks

239
Q

What are the 3 most likely differential diagnoses of meningitis?

A

-Encephalitis
-subarachnoid haemorrhage
-Brain abscess

240
Q

What features differentiate encephalitis to meningitis?

A
  • encephalitis is inflammation of the brain parenchyma, which causes fever, headache and altered mental state
    -focal neurological signs (hemiparesis or aphasia) are more common in encephalitis
    -neck stiffness is less common
    -seizures at onset of illness are more indicative of meningitis
241
Q

How may a subarachnoid haemorrhage present similarly to meningitis

A

-sudden, severe headache
-nausea
-vomiting
-photophobia

242
Q

How may a subarachnoid haemorrhage present differently to meningitis?

A
  • SAH, loss of consciousness at onset is less common
    -SAH, no fever
    -SAH LP findings: xanthochromia due to the breakdown of RBC’s if performed 12hr+ after onset
243
Q

How may a brain abscess present similarly to meningitis?

A
  • fever
    -headache
    -change in mental status
244
Q

What is Guillain-Barre syndrome?

A

-Acute polyneuropathy affecting the peripheral nervous system
- causes acute, symmetrical ascending weakness and sensory symptoms
- usually triggered by an infection

245
Q

What infections are associated with Guillain-Barre syndrome?

A

-campylobacter jejuni
-cytomegalovirus
-EBV

246
Q

There are 2 potential mechanisms for Guillain-Barre syndrome, name them

A

-Molecular mimicry
-Bystander activation

247
Q

Describe the mechanism of molecular mimicry

A

B cells make antibodies that correspond with the antigens of the triggering pathogen. These antibodies also correspond with the antigens of the peripheral nervous system, either the myelin sheath or the nerve axon itself.

248
Q

Describe the mechanism of bystander activation

A

Non-specific immune system activation which attacks peripheral nerves. Thought to be more likely in GBS triggered by viral infection.

249
Q

How does GBS present?

A
  • symptoms begin within 4 weeks of a triggering infection and peak within 2-4 weeks
    -history of gastroenteritis
    -Symmetrical ascending weakness (lower limbs affected first, however proximal muscles more likely to be affected before distal)
  • reduced reflexes
    -peripheral loss of sensation
    -neuropathic pain
250
Q

Why may facial weakness be a symptom of GBS?

A

if the peripheral neuropathy affects the cranial nerves

251
Q

How may autonomic dysfunction in GBS manifest?

A

-Urinary retention
-Ileus
-arrhythmias

252
Q

What criteria is used to diagnose GBS?

A

The Brighton criteria

253
Q

Outline the 5 points in the Brighton criteria for diagnosing GBS

A

-Flaccid limb weakness
-Areflexia
-A monophasic course of less than 28 days
-albuminocytological dissociation in the CSF
-Suggestive findings in nerve conduction studies
-Absence of alternative diagnosis

254
Q

What LP results would indicate GBS?

A
  • High proteins (albuminocytological dissociation)
    -Normal cell count
    -glucose
255
Q

Outline the management of GBS

A
  • Supportive care
    -VTE prophylaxis
    -Iv immunoglobulins
    -plasmapheresis if IVIG inappropriate
    -Severe cases may develop respiratory failure and require intubation and ventilation and ICU admission
256
Q

Describe the prognosis of GBS

A

-Recovery months- years
-function may return up to 5 years later
-Full recovery or minor persistent symptoms for most
- 20% left with a significant disability
5% mortality due to respiratory/ cardiovascular complications

257
Q

Why does GBS cause respiratory complications?

A

Diaphragmatic weakness

258
Q

Name 3 risk factors for GBS

A

-Infections
-Vaccinations (very small risk)
-surgery

259
Q

Give 3 differentials for GBS

A
  • Acute transverse myelitis
    -Chronic inflammatory demyelinating polyneuropathy
    -Botulism
260
Q

How may acute transverse myelitis present similarly to GBS?

A
  • rapid spinal cord dysfunction, which may mimic the ascending weakness seen in GBS
261
Q

How does acute transverse myelitis differ from GBS?

A

-ATM has a clear spinal level
-bladder/ bowel dysfunction is more common in ATM
-MRI findings in ATM show a T2 weighted image with hyperintense lesions on the spinal cord

262
Q

How is chronic inflammatory demyelinating polyneuropathy similar to GBS?

A
  • they’re both peripheral polyneuropathies
263
Q

How does chronic inflammatory demyelinating polyneuropathy differ from GBS?

A

-CIDP develops over at least 2 months, BGS more acute
-CIDP responds well to immuno-supression and may require long term treatment, GBS is usually self limiting

264
Q

How does botulism differ from GBS?

A
  • eyelid ptosis and fixed pupils are early signs of clostridium botulinum poisoning but not GBS
    -History of ingesting food which has been canned at home, preserved or fermented
    -Descending pattern f paralysis
265
Q

What are the 2 different causes of encephalitis?

A

-infective
- autoimmune

266
Q

What is the most common cause of encephalitis in children in the UK?

A

-HSV-1
- from cold sores

267
Q

What is the most common cause of encephalitis in neonates in the UK?

A

HSV-2
-genital herpes, contracted during birth

268
Q

Other than HSV, what other viruses can cause encephalitis?

A

-Varicella zoster virus
-Cytomegalovirus
-Epstein-barr virus
-enterovirus
-adenovirus
-influenza virus
-Polio, measles, mumps, rubella if unvaccinated

269
Q

Which antibodies are associated with autoimmune encephalitis?

A

-anti-NMDA receptor antibodies

270
Q

How can autoimmune encephalitis be treated?

A

-corticosteroids
-immune therapies

271
Q

How may encephalitis present?

A

-altered consciousness
-altered cognition
-unusual behaviour
-acute onset of neurological symptoms
-acute onset of focal seizures
-fever above 38
-severe, persistent, diffuse headache
-meningeal irritation

272
Q

What Investigations should be performed in suspected encephalitis?

A

-LP
-CT if LP contraindicated
-MRI after LP
-EEG if mild/ ambiguous symptoms
-Nasal and throat swabs
-HIV testing

273
Q

What are the contraindications of LP?

A

-GCS below 9
-Haemodynamically unstable
-active seizures
-post ictal
- Signs of raised ICP

274
Q

What would the CSF show in encephalitis?

A
  • High lymphocytes
    -viral DNA
275
Q

Describe the management of encephalitis

A

-Acyclovir for HSV or VZV
-Ganciclovir for CMV
-Repeat LP’s for test of cure before stopping antivirals

276
Q

List the complications of encephalitis

A

-Lasting fatigue and prolonged recovery
-change in personality or mood
-changes to memory or cognition
-Learning disability
-headaches
-chronic pain
-movement disorders
-sensory disturbance
-seizures
-hormonal imbalance

277
Q

Roughly, there are 3 phases in the pathophysiology of encephalitis, what are these phases?

A

-entry of pathogen
-neuronal tissue invasion
-inflammatory response

278
Q

What are the 2 possible mechanisms of pathogen entry in encephalitis?

A

-Haematogenous
-Neuronal retrograde transmission

279
Q

Describe neuronal retrograde transmission and give an example of a virus which does this.

A
  • Varicella zoster virus
    -neurotropic virus enters the peripheral nerves and travel to the CNS
280
Q

Describe neuronal tissue invasion in encephalitis pathophysiology.

A

-Viral replication inside neurons and glial cells induces cellular damage, causes necrosis and apoptosis of cells, causing neurological dysfunction
- Cytotoxic T-cells recognise and destroy infected cells, contributing to tissue damage

281
Q

Describe the inflammatory response in encephalitis

A

-cytokines and chemokines released from affected cells trigger the acute immune response, macrophages and lymphocytes are recruited into the CNS
-The cerebral oedema causes raised ICP

282
Q

Name 2 neurological complications which may arise from raised ICP

A

-coma
-seizures

283
Q

How is meningitis similar to encephalitis?

A

-Fevere, headache, altered mental state, signs of meningeal irritation

284
Q

What are the 3 differential diagnoses for encephalitis?

A

-Brain abscess
-stroke
-Brain abscess

285
Q

What is more specific to meningitis than encephalitis?

A

-Neck stiffness
-photophobia

286
Q

What is more specific to encephalitis than meningitis?

A

focal neurological deficit’s like aphasia or hemiparesis

287
Q

What is more specific to a stroke than encephalitis?

A

-deficits related to specific vascular territories
-no systemic symptoms

287
Q

How may a stroke present similarly to encephalitis?

A

focal neurological deficits

288
Q

How may a brain abscess present similarly to encephalitis?

A

-Headache
-fever
-focal neurological deficits

289
Q

What is the peak age of contracting chickenpox?

A

6-15

290
Q

Is the herpes zoster virus different to the herpes simplex virus?

A

Yes

291
Q

What 5 illnesses does the herpes zoster virus cause?

A

-Chicken pox
-shingles
-herpes zoster ophthalmicus
- Ramsay-Hunt syndrome
-Eczema herpeticum

292
Q

Describe the rash seen in chickenpox

A

-Widespread
-erythematous
-vesicular
-blistering
-spreads outwards from trunk and face
-spreads over 2-5 days

293
Q

At what stage will the rash in chickenpox indicate that the child is no longer infectious?

A

when it scabs over

294
Q

How is chickenpox spread?

A

-Direct contact with lesions
- droplet

295
Q

What illness other than chickenpox may someone come into contact with and then develop chickenpox?

A

Shingles

296
Q

How long after coming into contact with herpes zoster will someone become symptomatic of chickenpox?

A

10 days- 3 weeks

297
Q

When is chickenpox most infectious?

A

1-2 days before the rash appears

298
Q

Name 4 signs and symptoms of chickenpox

A

-rash
-fever
-itch
-general malaise and fatigue

299
Q

Name 5 possible complications of chickenpox

A
  • Bacterial superinfection
    -dehydration
    -conjunctival lesions
    -pneumonia
    -encephalitis
  • Reactivation of virus as shingles or Ramsay Hunt syndrome
300
Q

What makes developing a bacterial superinfection more likely in chickenpox?

A

using NSAIDs

301
Q

How would encephalitis as a complication of chickenpox present?

A

Ataxia

302
Q

If a pregnant lady has had chickenpox previously, is she at risk of developing antenatal chickenpox if exposed to herpes zoster?

A

No she would be immune

303
Q

What can be used to protect pregnant women who aren’t immune to chickenpox but have come into contact with it?

A

Varicella zoster immunoglobulins

304
Q

Until what week of gestation is someone at risk of developing congenital varicella syndrome?

A

28 weeks

305
Q

What can be a consequence of a mother having chickenpox during delivery?

A

-life threatening neonatal infection
-Treat with acyclovir and varicella zoster immunoglobulins

306
Q

Describe the management of chickenpox

A

-Usually self limiting and requires no support in generally healthy children
-acyclovir given in immunocompromised, adult (over 14 presenting within 24 hours of rash onset) and neonatal patients at risk of complications
-calamine lotion for itching
-keep cool and trim nails

307
Q

What is the peak age of incidence for shingles?

A

70+ yrs

308
Q

Is it possible for someone to have shingles without having had chickenpox previously?

A

Yes but it’s incredibly unlikely
-This is thought to be because the triggers of reactivation are so numerous it may be caused by a different process

309
Q

Briefly describe the pathophysiology of shingles

A
  • Initial infection
  • varicella zoster remains dormant in the dorsal root or cranial nerve ganglia
    -Trigger
    -Virus multiplies along the affected sensory nerve until it reaches the skin
    -The inflammation and destruction of the nerve leads to rash and neuropathic pain
310
Q

List the possible triggers of the reactivation of the herpes zoster virus in shingles

A
  • emotional stress
    -immunosuppression via chemo or high dose steroids
    -recent illness or surgery
    -skin injury via sunburn or taruma
311
Q

What are the 3 stages of the clinical features of shingles?

A

-Prodrome
-Infectious rash
-Resolution

312
Q

Describe the clinical features seen in the prodrome stage of shingles

A
  • Acute neuralgia
    -non-specific symptoms
    -enlarged lymph nodes
313
Q

How long does the infectious rash last in shingles?

A

7-10 days

314
Q

Describe the infectious rash seen in shingles

A

-single dermatome with a band like distribution
-Unilateral
-erythematous to macular to erythematous papules to vesicles and bullae by day 7
- vesicles become haemorrhagic or pustular near the end before crusting over
-pain in affected region

315
Q

How long may crusted lesions in shingles take to crusts over?

A

up to 1 month

316
Q

Name 5 differentials of shingles

A

-herpes simplex virus
-impetigo
-dermatitis herpetiformis
-drug eruptions
-contact dermatitis

317
Q

How may herpes simplex present similarly to shingles?

A

may be recurrent, individual lesions may appear similar

318
Q

How may you differentiate herpes simplex virus form shingles?

A

shingles: single band like distribution
herpes: clusters

319
Q

How may impetigo present similarly to shingles?

A

initially erythematous sores which blister and burst

320
Q

How may impetigo be differentiated from shingles?

A

Impetigo: painless, itchy, school children, mouth and nose

321
Q

How may dermatitis herpetiformis present similarly to shingles?

A

Both are small, clustered papules and vesicles

322
Q

How can you differentiate shingles from dermatitis herpetiformis?

A

dermatitis herpetiformis: symmetrical and bilateral (elbows, knees, buttocks, back and scalp< usually symmetrical and bilateral

323
Q

How can rashes caused by drug eruptions be differentiated from shingles?

A

for drug related eruptions there will be a causative agent such as NSAID ABx, anti-epileptics
- This rash may be symmetrical and bilateral

324
Q

How can a rash caused by contact dermatitis be distinguished from a rash caused by shingles?

A

Contact dermatitis: not painful but severely itchy

325
Q

Describe the management for shingles

A

-Analgesia (for mild pain paracetamol, paracetamol+/- codeine, paracetamol +/- NSAID) (moderate-severe pain: amitriptyline, duloxetine gabapentin, pregabalin)
-Calamine lotion
-topical capsaicin
-cool compress
- Possibly antivirals

326
Q

Describe antiviral therapy in shingles

A
  • Give within 72hrs of rash onset if immunocompromised, non-truncal, moderate-severe pain
  • Consider if 50+ to reduce risk of post herpetic neuralgia
    -oral acyclovir, famciclovir, valaciclovir
    give corticosteroids if giving antivirals in immunocompromised adults with severe, localised symptoms
327
Q

Describe prevention for shingles

A

-Vaccination
-70+ yrs or earlier if predisposing condition
-single subcut dose
-contraindicated in immunocompromised, pregnancy and children as it’s a live vaccine

328
Q

Describe what causes herpes zoster ophthalmicus

A

-Reactivation of the Varicella zoster virus in the opthalmic branch of the trigeminal nerve

329
Q

Why is herpes zoster ophthalmicus concerning?

A

-Vision threatening infection

330
Q

How does herpes zoster ophthalmicus present?

A
  • Preherpetic neuralgia
    -vesicular rash in the 1st division of the trigeminal nerve
331
Q

What are the complications of herpes zoster ophthalmicus?

A

-Keratitis
-Uveitis
-glaucoma
-retinal necrosis

332
Q

How is herpes zoster ophthalmicus diagnosed?

A

-fluorescent antibody testing
-Viral PCR

333
Q

What is the management of herpes zoster ophthalmicus?

A

-Systemic antiviral therapy
-topical treatments
-possibly steroids

334
Q

What is Ramsay Hunt syndrome also known as?

A

Zoster oticus

335
Q

Describe what causes Ramsay Hunt syndrome

A

Reactivation of the varicella zoster virus in CN 7

336
Q

What age is Ramsay Hunt syndrome likely to happen in?

A

70+yrs

337
Q

How may Ramsay HUnt syndrome present?

A

-Severe otalgia
-Sudden ipsilateral facial paralysis (partial or complete)
-altered taste perception in ant. 2/3s tongue
-reduced lacrimation
-hyperacusis
-vestibular disturbances (vertigo or tinnitus)

338
Q

Describe the otalgia seen in Ramsay Hunt syndrome

A

-Vesicular rash in the external auditory canal, auricle or mucous membrane of the oropharynx

339
Q

What are the 3 differentials of Ramsay Hunt syndrome?

A

-Bell’s palsy
-Herpes simplex herpeticus
-Acute peripheral facial palsy

340
Q

How is Bell’s palsy similar to Ramsay Hunt Syndrome?

A

Sudden onset unilateral facial paralysis

341
Q

How is Bell’s palsy different to Ramsay Hunt syndrome?

A

-No otalgia
-No vesicular eruptions
-Quicker onset of symptoms

342
Q

How is herpes simplex oticus similar to Ramsay Hunt syndrome?

A

-otalgia
-facial paralysis

343
Q

How is herpes simplex oticus different to Ramsay Hunt syndrome?

A

-No vesicular eruptions in the auditory canal or auricle
-Systemic signs

344
Q

How is Ramsay Hunt syndrome similar to acute peripheral facial palsy?

A

-sudden unilateral facial weakness/paralysis

345
Q

How is Ramsay Hunt syndrome different to acute peripheral facial palsy?

A

Peripheral facial palsy:
-No rash
-ipsilateral ear pain

346
Q

How is Ramsay Hunt syndrome managed?

A

-oral acyclovir
-corticosteroids

347
Q

what was eczema herpeticum previously known as?

A

kaposi varicelliform eruption

348
Q

What most commonly causes eczema herpeticum?

A

HSV-1

349
Q

What is eczema herpeticum commonly associated with?

A

cold sores and patients with pre-existing skin conditions

350
Q

Describe the presentation of eczema herpeticum

A

-Widespread painful, vesicular rash
-systemic symptoms
lymphadenopathy

351
Q

Describe the rash seen in eczema herpeticum

A
  • painful
    -vesicular
    -whole body
    -itchy
    -pustular
    -contain fluid
    -when it bursts it leaves small punched out ulcers with a red base
352
Q

how is eczema herpeticum managed?

A

viral swabs
-acyclovir

353
Q

What type of organism causes malaria?

A

Protozoa

354
Q

What are the 4 different types of malaria?

A

-P. falciparum
-P. ovale
-P. vivax
-P. malariae

355
Q

What is the most common and most severe type of malaria?

A

P.falciparum

356
Q

Describe the general lifecycle of malaria sporozoites to schizonts

A

-Spread by female anopheles mosquitoes
-Mosquito feeds on an infected person and the parasites reproduce in the GIT of the bug, making sporozoites
-The mosquito bites someone else and injects them with sporozoites which travel to the liver
-The sporozoites reproduce asexually for 10 days in the liver, maturing into schizont

357
Q

Describe the life cycle of malaria schizonts to merozoites

A

-Schizont become merozoites when they emerge from the liver

358
Q

Describe the life cycle of malaria as merozoites

A

-merozoites spread from the liver to the blood, infecting the RBC’s
-Merozoites reproduce in RBC’s causing RBC rupture and releasing more merozoites

359
Q

Which types of malaria can stay dormant for 4 years and through what mechanism do they do this?

A

-P. ovale and P. vivax
-They become hypnozoites in the liver and are not affected by normal antimalarial drugs

360
Q

Which part of the parasites life cycle in malaria causes haemolytic anaemia?

A

The merozoites rupturing RBC’S

361
Q

Each type of malaria has a different rupture and release cycle, how long is the rupture and release cycle of P. ovale and P. vivax, and what type of fever does this cause?

A

-48 hours
-tertian malaria

362
Q

Each type of malaria has a different rupture and release cycle, how long is the rupture and release cycle of P. falciparum, and what type of fever does this cause?

A
  • more frequent but irregular
    -subtertian fever
363
Q

Each type of malaria has a different rupture and release cycle, how long is the rupture and release cycle of P. malariae, and what type of fever does this cause?

A

-72 hours
-quartan

364
Q

Who should you suspect of having malaria?

A

-Anyone who has travelled to an endemic area, incubation is usually 1-4 weeks however p.ovale and p. vivax can be dormant for up to 4 years

365
Q

What may prolong the presentation of someone with malaria?

A

-partial immunity
-antimalarial prophylaxis
-symptoms may be gradual or abrupt

366
Q

What are the symptoms of someone with malaria?

A

-Fever up to 41 degrees
-sweats
-rigors
-fatigue
-myalgia
-headache
-nausea
-vomiting
-headache

367
Q

What are the signs of someone with malaria

A

-pallor
-hepatosplenomegaly
-jaundice

368
Q

How is malaria diagnosed, and what do the results of this investigation tell us?

A

-Blood film
-Type of parasite and concentration

369
Q

What stain is used in a blood film for malaria?

A
  • Giesma
370
Q

Which blood collection bottle is used to send a sample for a blood film?

A

-EDTA
-same as for FBC

371
Q

What type of blood film is used when diagnosing malaria?

A
  • thick (sensitive to malaria)
    -Thin ( determines species)
372
Q

How many blood films must be done to exclude malaria?

A

-3 on 3 consecutive days due to the cyclical nature of merozoite eruption

373
Q

What is the most likely treatment for malaria?

A
  • admission
    -if complicated admission to ICU or HDU
    -Artesunate 1st line
    -Iv quinine dihydrochloride
374
Q

What is a common side effect of artesunate?

A

haemolysis

375
Q

List the complications of malaria

A

-Cerebral malaria
-seizures
-reduced consciousness
-AKI
-pulmonary oedema
-DIC
-Severe haemolytic anaemia
-multi-organ failure
-metabolic acidosis

376
Q

What precautions should someone take when traveling to a malaria endemic area?

A
  • mosquito spray
    -mosquito nets and barriers
    -seek medical advice if symptomatic
    -antimalarial medication
377
Q

Name 4 antimalarial medications

A

-Progranulin with atovaquone
-doxycycline
-mefloquine
-chloroquine with proguanil

378
Q

How is progranulin with atovaquone taken as prophylaxis and what are its pros and cons?

A
  • 2days before travelling 7 days after
  • most expensive
    -least side effects
379
Q

How is doxycycline taken as prophylaxis for malaria and what are it’s cons

A
  • 2 day -4 weeks after travel
    -increased sunlight sensitivity
    -diarrhoea and thrush
380
Q

How is mefloquine used as prophylaxis and what are its cons

A
  • once a week for 2 weeks before - 4 weeks after travelling
  • depression, anxiety, abnormal dreams, seizures of psychosis
381
Q
A

3a (3 decks)

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