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My Neurology > Pathology > Flashcards

Pathology Flashcards

1
Q

What is the best imaging for trauma of the head?

A

CT scan

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2
Q

What is the best vascular imaging?

A

CT angiogram

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3
Q

What is diffusion weighted imaging used for?

A

show cellular swelling in the brain when the brain tissue dies in stroke

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4
Q

What are the colours of the matter on a CT scan?

A
  • white matter = lower density = lighter

- grey matter = higher density = darker

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5
Q

What are the colours on the two types of MRI of the brain?

A
  • T1 MRI: fat is bright and water, air and cortical bone is dark
  • T2 MRI: water and fat is bright, air and cortical bone is dark (tWo- water)
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6
Q

What is a Chiari malformation?

A

cerebellar tonsils descend into the cervical canal

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7
Q

What are the most common cancers to metastasise to the brain?

A 
breast
lung
thyroid
colon
kidney
melanoma
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8
Q

What is the main division in location for child vs adult brain tumours?

A
  • children = infratentorial

- adults = supratentorial

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9
Q

What type of headache does a tumour cause?

A
  • worse lying down
  • worse first thing in the morning
  • associated with blurred vision and vomiting
  • causes patient to wake up due to pain
  • worse on coughing or leaning forward
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10
Q

What is aseptic meningitis?

A

no bacteria identified (can be viral from HSV 1 and 2 but not necessarily)

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11
Q

What is the difference between viral encephalitis and viral meningitis?

A
  • patient is confused, changes behaviour, speech difficulty

- because cerebral cortex is diffusely involved

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12
Q

What is red neuron?

A
  • lethal injury to the neuron
  • caused by hypoxia or ischemia
  • shrinking of nuclei
  • loss of nucleolus
  • very red cytoplasm
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13
Q

What is simple neuronal atrophy?

A

chronic degeneration causes shrunken neurons and cell bodies of functionally related neurons

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14
Q

What are inclusions and when are they added?

A

added with ageing eg Alzheimer’s disease has neurofibrillary tangles

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15
Q

What happens when oligodendrocytes are damaged?

A

demyelination and apoptosis so there is reduced conduction

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16
Q

What is gliosis?

A

scar forming process in the CNS done by astrocytes and is an indication of injury

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17
Q

What happens when microglia are damaged?

A

proliferate and form aggregates at the site of injury

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18
Q

What are the main causes of nervous system injury?

A
  • hypoxia
  • trauma
  • toxic insult
  • metabolic abnormalities
  • nutritional deficiency
  • infections
  • genetic abnormalities
  • ageing
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19
Q

What happens in terms of ATP in hypoxia?

A

ATP is consumed in a few minutes and no more can be made

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20
Q

What is cerebrovascular disease?

A

any abnormality of the brain caused by a pathological process of blood vessels

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21
Q

What are the main types of cerebrovascular disease?

A
  • brain ischaemia/infarction
  • haemorrhages
  • vascular malformation
  • aneurysms
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22
Q

What is the classification of cerebral ischaemia?

A
  • global (generalised due to cardiac arrest or hypotension)

- focal (vascular obstruction)

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23
Q

What can hypertension lead to the formation of?

A
  • micro-aneurysms (Charcot-Bouchard) which can rupture and lead to haemorrhage
    • lacunar infarcts which harm basal ganglia and can lead to dementia
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24
Q

What can severe hypertension lead to?

A

hypertensive encephalopathy which causes global cerebral oedema and herniation due to raised intracranial pressure

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25
Q

Where does intracerebral haemorrhage usually occur?

A
  • basal ganglia is most common
  • cerebellum
  • thalamus
  • white matter
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26
Q

What are the signs of an UMN lesion?

A

increased tone and hyperreflexia

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27
Q

What are the signs of a LMN lesion?

A

decreased tone, muscle wasting, fasciculation and diminished reflexes

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28
Q

What is Brown-Sequard syndrome?

A

cord hemisection where there is ipsilateral motor and dorsal column sensory but contralateral spinothalamic sensory

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29
Q

What is central cord syndrome?

A
  • common
  • caused by a hyperflexion or extension injury to neck
  • affects the upper limbs more than the lower limbs
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30
Q

What is the difference in presentation between chronic and acute spinal cord compression?

A

same but in chronic the motor signs will predominate

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31
Q

What are the causes of acute spinal cord compression?

A

trauma, tumours, infection or spontaneous haemorrhage

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32
Q

What are the causes of chronic spinal cord compression?

A

degenerative spondylosis, tumours or RA

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33
Q

What are the features of trauma, tumours and spinal canal stenosis relating to spinal cord compression?

A
  • Trauma: high energy injury, cervical
  • Tumours: metastasis usually extradural, meningioma, schwannoma, astrocytoma and ependymoma, this can be chronic or acute with sudden collapse or haemorrhage
  • Spinal canal stenosis: osteophytes, bulging of discs, subluxation or facet joint hypertrophy
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34
Q

What are the features of infection and haemorrhage relating to spinal cord compression?

A
  • Infection: epidural abscess, surgery and trauma

- Haemorrhage: due to trauma, bleeding diathesis, anticoagulant or AV malformations

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35
Q

What is the treatment for spinal cord compression for trauma, tumours and infections?

A
  • Trauma: CT, decompress and stabilise
  • Tumours: mets- surgery if life expectancy >6m, dexamethasone, chemo or radio…primary- surgery
  • Infection: antimicrobial therapy, surgical drainage, stabilisation if needed
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36
Q

What is the treatment for spinal cord compression for haemorrhage and degenerative disease?

A
  • Haemorrhage: reverse anticoagulation, decompression

- Degenerative disease: surgical decompression and stabilisation

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37
Q

What are the clinical signs of raised ICP?

A
  • papilloedema
  • headache
  • reduced consciousness
  • nausea + vomiting
  • neck stiffness
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38
Q

What are the two types of injury in terms of head trauma?

A
  • Primary injury: injury to neurons at the time which is irreversible
  • Secondary injury: haemorrhage, oedema etc which is potentially treatable
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39
Q

What is a coup and contra-coup injury?

A
  • coup = at the site of the impact

- contra-coup = at the site opposite from the impact, can be worse than coup

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40
Q

What is diffuse axonal injury?

A
  • occurs at the moment of injury

- affects central areas and causes reduced consciousness and coma

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41
Q

What is the pathogenesis behind head trauma?

A

disrupt the BBB –> oedema and swelling –> hypoxia and ischemia –> glutamate release/oygen free radical formation/lipid membrane disruption –> Ca2+ influx –> apoptosis and necrosis

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42
Q

What is the most common traumatic haematoma?

A

intradural

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43
Q

What is the difference in recovery between a seizure and syncope?

A

seizures have a longer recovery than syncope

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44
Q

What is the one investigation that you always do for collapse?

A

ECG so you never miss long QT

45
Q

What are EEGs good for?

A

determining if a patient is in non-convulsive status or encephalopathy

46
Q

What are the side-effects of sodium valproate?

A
  • weight gain
  • teratogenicity
  • hair loss
  • fatigue
47
Q

What drug interactions does carbamazepine have?

A
  • contraceptive pill so never use progesterone only or an implant
  • higher dose of morning after pill needed
  • alters the work of chemotherapy
48
Q

What are the main pitfalls of epilepsy drugs?

A
  • increase pregnancy complications

- teratogenic

49
Q

What is involved in functional localisation history taking?

A
  • where the lesion is (date of onset, nature of main symptoms eg weakness, associated symptoms and exacerbating/relieving factors)
  • what the condition is (evolution and recurrence)
50
Q

What are the main CNS issue symptoms?

A
  • Hemiplegia / paraplegia
  • Heaviness
  • Spasms associated
  • Sensory symptoms are possible
  • Cognitive and sphincter involvement
51
Q

What are the main PNS issue symptoms?

A
  • Peripheral or localised area
  • Positional or ascending weakness
  • Associated twitching
  • Sensory issues possible
  • Loss of grip, tripping
52
Q

What is seen on examination of a PNS issue?

A
  • Wasting or fasciculation OE
  • Decreased tone
  • Distal weakness which can be specific to a plexus or named nerve
  • Decreased reflexes
  • Glove and stocking decreased sensation
53
Q

What are the main NMJ issue symptoms?

A
  • Ocular and bulbar tracts
  • Fatigable weakness worse at the end of the day
  • Swallowing, speaking, eye issues, SOB
  • No sensory issues
54
Q

What is seen on examination of a NMJ issue?

A
  • Ptosis OE
  • No change in tone
  • Fatiguability
55
Q

What are the main muscle issue symptoms?

A
  • Proximal and symmetrical
  • Aching or insidious
  • Myalgia associated
  • No sensory issues
  • Getting up from low chairs is difficult
56
Q

What is seen on examination of a muscle issue?

A
  • Proximal wasting and weakness OE
  • No change in tone
  • Myotonia is failure of relaxation
57
Q

How is fatiguability of muscles demonstrated?

A
  • counting out loud (bulbar)
  • fixed horizontal gaze (ocular)
  • fixed upgaze (ptosis)
  • repetitive movements (limb)
58
Q

What are the progressions of severity in inflammatory, vascular and SOL issues?

A
  • Inflammation: relapsing and remitting pattern
  • Vascular: huge incline and then gradual improvement
  • SOL: problem will only get worse
59
Q

What is the most common NMJ pathology?

A

Myaesthenia Gravis which will also present with ocular issues too and will have positive antibody testing

60
Q

What is acute peripheral polyneuropathy suggestive of?

A

Guillain-Barre syndrome and most patients are positive for anti-ganglioside antibodies

61
Q

What is a psychogenic non-epileptic attack?

A

functional attack that patients have no control of which can be related to traumatic events, sexual or physical abuse or stress

62
Q

How do you diagnose a psychogenic non-epileptic attack?

A

seizure description and EEG monitoring during attack

63
Q

What can functional attacks present with?

A
  • prominent motor activity
  • collapse with no movement
  • abreactive attacks (hyperventilation etc)
  • attacks last 10-20 minutes which is longer than seizures
64
Q

What are psychogenic non-epileptic attacks treated with?

A

counselling and do not give anticonvulsant or anti-epileptic drugs

65
Q

What is the classification of movement disorders?

A
  • hypokinetic: too little movement eg Parkinson’s

- hyperkinetic: too much movement

66
Q

What types of movements do hyperkinetic disorders include?

A
  • tics
  • tremor
  • chorea
  • myoclonus
  • dystonia
  • athetosis
67
Q

What are the features of tremor?

A
  • occur at rest, postural or kinetic

- rhythmic oscillations of a body part

68
Q

What are the features of dystonia?

A

sustained or intermittent muscle contractions causing twisting movements and abnormal postures

69
Q

What are the features of chorea?

A

irregular purposeless movements that flit between body parts eg restlessness and fidgeting

70
Q

What are the features of myoclonus?

A

brief electric shock like jerks caused by activation of a group of muscles

71
Q

What are the features of tics?

A

repetitive stereotyped movements which can be suppressed but this causes the patient anxiety

72
Q

What is an essential tremor?

A
  • common
  • postural tremor
  • holding the hands outstretched
  • can run in families autosomal dominant
73
Q

What are the two presynaptic neuromuscular junction issues?

A
  • botulinum

- lambert eaton myasthenic syndrome

74
Q

How is muscle strength graded?

A

MRC muscle power grading from 0 no movement to 5 normal strength

75
Q

What are the muscle investigations?

A

blood tests, muscle biopsy and MRI of muscle tissue

76
Q

What is the main drug that can cause myopathy?

A

statins which can be myalgia or necrotising myopathy

77
Q

What is rhabdomyolysis?

A

dissolution of muscle and a cascade of events causing myalgia, muscle weakness and myoglobinuria

78
Q

What is the main difference between large and small fibre neuropathies?

A

large fibre causes a loss of reflexes but small fibre doesn’t

79
Q

What are the two main demyelinating neuropathies?

A

Guillan Barre

CIDP

80
Q

What is the common type of neuropathy if the patient is young?

A

hereditary neuropathy

81
Q

What are two signs of hereditary neuropathy?

A
  • champagne bottle deformity

- very high arched foot

82
Q

What are the parts of the GCS score?

A
  • Eye opening- spontaneously, to speech, to pain, none (4)
  • Motor- oriented, confused, inappropriate, incomprehensible, none (5)
  • Verbal- obeying, localising, flexing, abnormal flexing, extending, none (6)
83
Q

What are the main types of brain herniation?

A

subfalcine, transtentorial and cerebellar tonsillar

84
Q

What is the medical management of raised ICP?

A
  • sedation
  • head of bed tilt (30 degrees)
  • ensure neck collars aren’t too tight so venous drainage is working
  • CO2 control
  • osmotic diuretic eg mannitol or hypertonic saline
  • CSF release
85
Q

What is the essence of a brainstem death declaration?

A

cranial nerve exam

86
Q

What is seen on CNS issue examination?

A
  • Limb posture OE
  • Increased tone velocity dependent so spasticity or clonus
  • Pyramidal pattern of weakness so in arms ex more than flex, legs flex more than ex
  • Increased reflexes
  • Abnormal extensor plantar response
  • Hemisensory disturbance for a brain injury or a sensory level disturbance for a spinal cord issue
87
Q

What is syringomyelia?

A

fluid filled cyst or cavity in the spinal cord

88
Q

What is a sudden onset 10/10 headache with vomiting, neck stiffness and photophobia?

A

subarachnoid haemorrhage until proven otherwise

89
Q

What are the features of chronic regional pain syndrome?

A
  • one limb
  • allodynia (things that shouldn’t hurt do)
  • hyperalgesia
  • welling
  • colour change
  • hair and nail changes
  • osteopenia
90
Q

What is nociceptive pain?

A

pain from injury relayed through a normal nervous system

91
Q

What is neuropathic pain?

A

pain generated within the nervous system eg post herpetic neuralgia, surgery, trauma, diabetic neuropathy, amputation

92
Q

What is the main treatment options for neuropathic pain?

A

tricyclic antidepressants and anticonvulsant

93
Q

What are the main primary demyelination disorders?

A
  • MS
  • acute disseminated encephalomyelitis
  • acute hemorrhagic leukoencephalitis
94
Q

What are the main secondary demyelination disorders?

A
  • viral eg progressive multifocal leukoencephalopathy
  • metabolic eg central pontine myelinolysis
  • toxic eg CO, solvents or cyanide
95
Q

What is transient global amnesia?

A

once off issue with amnesia which can be triggered by emotion or temperature but the pathophysiology is unknown

96
Q

What is transient epileptic amnesia?

A

forgetfulness and repetitive questioning which is short-lived due to seizures

97
Q

What is functional cognitive impairment?

A

everyday forgetfulness which impacts on functioning which fluctuate but is just patient’s having a higher expectation of what things they should be able to remember

98
Q

What is Prion disease?

A

eg CJD is a very aggressive dementia which causes death due to strange folding of proteins

99
Q

What is limbic encephalitis?

A

inflammatory condition causing short term memory deficits sometimes associated with a tumour

100
Q

What is the main cause of all dementias?

A

neurodegenerative proteinopathies

101
Q

What does narcolepsy involve?

A
  • daytime sleepiness
  • cataplexy which is loss of muscle tone related to an onset of emotion
  • sleep paralysis
  • hallucinations at sleep onset
  • patients go into REM very quickly
102
Q

What are watershed infarcts?

A
  • hypotension
  • outside areas of the brain die
  • areas of small vessel overlap not large vessel supply
103
Q

Where does metastasis tend to occur in the brain?

A

small bits lining where the grey and white matter meets

104
Q

What does darkness in the white matter mean?

A

white matter = myelin so the darkness means demyelination ie MS

105
Q

What are the red flags for headache?

A
  • New onset headache >55
  • Known or previous malignancy
  • Early morning headache
  • Immuno-suppressed
  • Exacerbation by valsalva
106
Q

What is the equation for cerebral perfusion pressure?

A

MAP - ICP = CPP

usually around 80mmHG in a normal person

107
Q

What is cerebral auto regulation?

A

the body keeps cerebral blood flow constant despite BP changing with pressure and metabolic autoregulation

108
Q

What are the causes for raised ICP?

A
  • mass effect
  • brain swelling
  • increase in central venous pressure
  • problems with CSF flow
109
Q

What is the point of decompensation in ICP?

A

pressure will increase but ICP will remain stable until this point when it will begin to rise exponentially

My Neurology (6 decks)

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