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Pathology Flashcards

1
Q

What are the two theories of ageing in the nervous system?

A
  1. slowly progressive decline

2. no change in normal ageing - NDDs result in decline

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2
Q

What are the common features of NDDs?

A
  • progressive
  • fatal
  • associated with ageing
  • increasing social burden
  • degeneration of neurons, dysfunction and cell death
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3
Q

What are the clinical classifications of NDDs? (5)

A
  1. cortical degeneration - alzheimers, dementia
  2. movement disorders - parkinson, huntington
  3. cerebellar ataxias
  4. diseases of motor systems - MND
  5. autonomic disorders
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4
Q

What are the two common presentations of NDDs?

A
  1. specific neurological syndrome - due to defined group of neurons
  2. dementia - due to widespread neuronal dysfunction or death
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5
Q

What is the pathogenesis of NDDs? (7)

A
  1. abnormal accum. of proteins
  2. genetic factors
  3. oxidative stress
  4. apoptosis
  5. neuroinflammation
  6. ubquitinin proteasome system
  7. mitochondrial failure
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6
Q

What is dementia and what are some causes?

A

Acquired progressive impairment in intellect, memory, personality (no change in consciousness)

  1. alzheimers
  2. dementia with lewy bodies
  3. vascular pathology
  4. Fronto-temporal lobar degeneration
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7
Q

What are the differences between the sporadic and familial forms of alzheimers?

A

sporadic - 90% cases, >65yrs, problem with removal of beta-amyloid due to E-e4 apolipoprotein allele
familial - 1-2%, 40-65 years, due to APP mutation or extra copy

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8
Q

What are the macroscopic and histopathological features of AD?

A

Macroscopic changes - cerebral atrophy, ventricular dilation, atrophy of hippocampi, medial temporal cortex, brain weight reduced
Histopathological - beta amyloid protein accumulation, Tau accumulation (NFT, plaque), loss of neurons and synapses

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9
Q

What is the amyloid hypothesis?

A
  • accum of beta-amyloid perpetuate neurotoxic events
  • A-beta cleaved from APP in neurons, and forms plaques in vessel walls as CAA
  • A-beta-42 particularly bad as it aggregates readily and forms cortical plaques
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10
Q

What is the diagnostic criteria for AD?

A
  • thal phase of amyloid plaques
  • Braak stage of NFT
  • CERAD stage of neuritic plaques
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11
Q

What are the 3 pathological causes of raised ICP?

A
  1. space occupying lesions - tumour, abscess, haemorrhage
  2. hydrocephalus - flow obstruction
  3. cerebral edema
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12
Q

What is communicating and non-communicating hydrocephalus?

A

Comm: full communication exists between ventricles, caused by XS CSF - overproduction, defective absorption (can do lumbar puncture)
Non-comm: CSF flow is obstructed resulting in non-communication (lumbar puncture is hazardous)

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13
Q

What are the causes of cerebral edema resulting in raised ICP?

A

TBI, Ischemic stroke, hypoxic or ischaemic encephalopathy, post op edema

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14
Q

What are the pathophysiological consequences of raised ICP?

A

Herniation syndromes:

  1. subfalcine/ transtentorial
  2. Central herniation
  3. Tonsillar herniation
  4. upward herniation - uncommon
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15
Q

Symptoms of raised ICP?

A

Headache worse lying down, nausea + vomiting, fatigue, focal deficits, confusion, loss of consciousness

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16
Q

Where is CSF produced, where does it flow and where is it resorbed?

A

Produced in choroid plexus, flows through ventricles, enters SA space via foramen of Luschka and Magendie, resorbed by arachnoid villi along dural venous sinus

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17
Q

What are contusions, coup contusions and contrecoup?

A

Contusion - focal mechanical injury to blood vessels
coup contusions - beneath the site of impact without fracture, damage to the brain
contrecoup contusions - damage to the brain where it has impacted on the skill

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18
Q

What is an extradural haematoma?

A

Blood between dura and skull commonly due to rupture of middle meningeal artery.
Usually associated with fracture
- lucid interval

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19
Q

What is a subdural haematoma?

A

Blood in subdural space (venous bleed = slow) either (1) related to contusions, lacerations or (2) rupture of bridging veins. Blood restricted by falx so confined to one hemisphere.

  • seen in falls and assaults
  • lucid interval then neuro degeneration
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20
Q

What is traumatic axonal injury?

A

Small foci to widespread brain damage (diffuse TAI is worst).
DAI - widespread damage including brainstem
- range from concussion to death

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21
Q

What is alcoholic dementia ?

A

AKA thiamine deficiency dementia - neuro impairment due to atrophy and ventricular enlargement
- changes due to nutritional deficiency rather than alcohol

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22
Q

What is alcoholic cerebellar degeneration?

A
  • acquired ataxia in alcoholic patients
  • atrophy of cerebellum
  • likely to be secondary to nutritional deficiency
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23
Q

What is the Wernicke-Korsakoff syndrome?

A

Malabsorption of thiamine due to GIT disease
Wernicke’s (acute) - vascular engorgement and haemorrhages
Korsakoff’s psychosis (chronic) - amnestic syndrome usually secondary to W. temporal sequence of memory is disrupted = confabulations

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24
Q

What are primary demyelinating diseases? and disorders in which demyelination may occur?

A

Primary - multiple sclerosis, acute disseminated encephalomyelitis, acute haemorrhagic leukoencephalopathy
Other disease: viral, metabolic, toxic

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25
Q

What is demyelination and how can it be detected?

A

Demyelination - loss of myelin sheath around nerve fibre, with the axon preserved
detected: MRI, slowed conduction, white matter becomes grey

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26
Q

What is multiple sclerosis? and clinical features?

A

MS: well circumscribed foci of demyelination (plaques) in the CNS
Onset: peak 20-40yrs
shows as grey discolouration in white matter

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27
Q

What are the variants of MS? (4)

A
  1. Classic/chronic - relapse and remissions and then progressive disability
  2. Acute: rapidly progressive and fatal
  3. Concentric - uncommon with large plaques
  4. Neuromyelitis
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28
Q

What are the 3 types of plaques in MS?

A
  1. acute plaques - active demyelination
  2. chronic plaques - most common at autopsy, complete myelin loss
  3. shadow plaques - remyelination has occurred
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29
Q

What is acute disseminated encephalomyelitis?

A

Rare disorder 7-10 days after URTI - immune mediated demyelination, usually recover

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30
Q

What is acute haemorrhagic leukoencephalopathy?

A

Petechial haemorrhages throughout white matter

  • fibrinoid necrosis of small BV
  • progressive and fatal
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31
Q

What is the difference between hypoxaemia and ischaemia?

A

Hypoxaemia - low oxygen in the blood

Ischaemia - reduction in blood supply

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32
Q

What are non-traumatic causes of subarachnoid haemorrhage?

A

Rupture of aneurysm, arteriovenous malformations

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33
Q

What are 4 pathological processes of cerebrovascular disease?

A
  1. occlusion from embolus or thrombus - ischaemia or hemorrhagic infarct
  2. rupture - haemorrhage
  3. altered permeability - vasculitis
  4. altered blood flow - hyper coagulable
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34
Q

What are the 2 types of cerebral ischaemic insult?

A
  1. focal cerebral ischaemia

2. global cerebral ischaemia

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35
Q

What is a thrombotic stroke?

A

Atheromatous plaques narrow the lumen and complete occlusion due to superimposed thrombus

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36
Q

In focal cerebral ischaemia, what does the damage look like?

A

Necrotic (dead) tissue surrounded by a low perfusion zone called a penumbra (may be salvaged)

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37
Q

What are some cardiac and non-cardiac causes of cerebral embolism?

A

Cardiac - AF, arrhythmia, endocarditis, valve prosthesis

Non-cardiac - atherosclerosis, thrombus, fat, tumour, air

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38
Q

What is spinal muscular atrophy?

A

Degeneration of motor neurons in the anterior horn of the spinal cord

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39
Q

What is meningitis? and what distinguishes it from encephalitis?

A

M - inflammation of the meninges, identified as abnormal WCC in CSF
M vs E - E has more neurological symptoms, altered mental status
However there is a lot of overlap and it doesn’t really change mgmt

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40
Q

What are normal CSF parameters? and what happens in infection?

A

Normal: 0 White cells, <1 RBC
Protein: .23-.38 (increases in infection)
Glucose: .6 (reduction indicates bacterial or fungal)
Lactate: increased suggests bacterial over viral meningitis

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41
Q

What may affect the results of a lumbar puncture in detecting bacterial meningitis?

A
  1. Antibiotics taken >24 hrs before L.P

2. Traumatic LP - will have more RBC and WC - safest to just count #WC and disregard RBC

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42
Q

What are the 3 major routes of infection for bacterial meningitis?

A
  1. colonisation of nasopharynx blood stream
  2. direct entry into CNS from infection
  3. invasion following bacteraemia
43
Q

What are the main causative organisms of meningitis?

A
  1. S. pneumoniae
  2. N. Meningitidis
  3. H. Influenzae
  4. Listeria monocytogenes
    also group B strep
44
Q

What are the main viral causes of meningitis?

A

Enteroviruses
HSV-2
VZV

45
Q

Aseptic meningitis causes?

A

Syphilis, fungal infections, TB

46
Q

What are the clinical features of bacterial and viral meningitis?

A

Ill, fever, headache, mental status often altered, neck stiffness due to meningeal irritation

47
Q

What are the steps in diagnosing meningitis?

A
  1. Suspect Meningitis
  2. Get LP done within 30mins OR start on antibiotics
  3. Blood culture
48
Q

What is the empiric therapy for bacterial meningitis?

A
  1. Antibiotics - ceftriaxone/cefotaxime adults, cefotaxime/amoxycillin children
  2. dexamethasone to prevent neurological complications
    if HSV suspected - Acyclovir
    MRSA - vancomycin
49
Q

What are clinical signs of encephalitis?

A

Depressed or altered mood/consciousness >24 hrs, lethargy, irritability, fever, headache, seizures, focal neurological findings
- most people have increased WCC in CSF

50
Q

What is HSV encephalitis?

A

Virus remains dormant in DRG after primary infection, reactivation of trigeminal ganglia –> encephalitis, fever, headache, sore neck, maybe prodromal URTI symptoms

51
Q

What is a glioblastoma? macroscopically and microscopically

A

Grade IV astrocytoma that begins in the brain
macroscopic - expansile mass, irregular borders
microscopic - astrocytic cells (spindle shaped), apoptosis, necrosis

52
Q

What is the prognosis and management of glioblastoma?

A

prognosis - 100% at 3 months without treatment, with treatment 25% at 2 years
management - surgical debulking, chemo and radiotherapy

53
Q

What types of intracranial haemorrhage are commonly seen at autopsy?

A
  1. extradural haemorrhage
  2. subdural haemorrhage
  3. subarachnoid haemorrhage
  4. intracerebral haemorrhage
54
Q

What are common features associated with extradural haemorrhage?

A
  • lucid interval
  • often traumatic injury
  • middle meningeal artery
  • ovoid mass bleed
  • usually with fracture
55
Q

What are common features associated with subdural haemorrhage?

A
  • venous bleed - bridging veins
  • sudden onset headache, nausea, coughing exercise
  • midline shift and herniation
56
Q

What are common features associated with subarachnoid haemorrhage?

A
  • usually due to cerebral berry aneurysm/head trauma

- headache, dizziness, orbital pain

57
Q

Headache red flags

A 
Vascular - haemorrhage 
Infection - meningitis 
Vision - one eye 
ICP - raised 
D - progressive and getting worse
58
Q

Histopathological features of alzheimers disease

A

Beta amyloid protein accumulation
Tau accumulation - NFT, plaques, dystrophic neurites
Loss of neurons and synapses

59
Q

Fronto-temporal lobar degeneration macroscopic and microscopic changes

A

Macroscopic - pronto-temporal atrophy

Microscopic

  • thinned neocortical ribbon
  • microvacuolation of outer cortical layers
  • neuronal loss and astrocytosis
60
Q

Synucleopathies

A

Alpha synuclein is major component of cytoplasmic inclusions

  • lewy bodies in PD and DLB
  • glial cytoplasmic inclusions in MSA
61
Q

Where does degeneration occur in PD?

A
  • substantia nigra

- pigmented nucleus in dorsal pons

62
Q

What else may be seen in Parkinsons?

A
  • decreased # pigmented neurons
  • EC neuromelanin
  • Lewy bodies in some remaining neurons
  • reactive astrogliosis
63
Q

What is dementia with LB and what can be seen?

A

Fluctuating cognitive impairment, visual hallucinations, parkinsonism

  • macro like AD
  • micro like PD and additional LB in cortex on IHC
64
Q

What is vascular dementia caused by and what can be seen macro and microscopically

A

Cause - additive effects of multiple episodes of vascular insufficiency
Macro - small vessel disease in white matter
Micro - changes in infarction

65
Q

What are the 4 human prion diseases?

A
  1. Creutzfeldt-Jakob (CJD) - vacuolation of grey matter, neuronal loss and gliosis
  2. Gerstmann-straussler-scheinker disease - mutation in PRP and cerebellum involved
  3. Fatal familial insomnia - mutation in PRP and involvement of thalamus
  4. Kuru - cannibalism
66
Q

Prion hypothesis

A
  • Prp (c) is normal protein
  • Prion disease = abnormal PRP (sc) protein which aggregates in ECS and causes spongiform change
  • the abnormal protein has different conformation
  • common polymorphism at codon 129
67
Q

Accumulation of PRP due to:

A
  • catalytic conversion from c to sc
  • host PRP c with abnormal AA sequence
  • rarely sporadic change from c to sc
68
Q

Causes of hydrocephalus in raised ICP

A
  • aqueductal stenosis
  • subarachnoid haemorrhage
  • space occupying lesion
69
Q

What is compressed during uncal/transtentorial herniation

A
  • stretch and damage to CN III
  • fixed dilated pupil
  • compression of post. cerebral artery
  • midbrain compression
70
Q

Cerebellar tonsillar herniation

A
  • cerebellar tonsils through foramen magnum
  • vital medullary centres compromised
  • CONING
71
Q

Subfalcine herniation

A
  • side to side

- ACA compression

72
Q

Central herniation

A
  • downward shift of brain stem/diencephalon
  • coma
  • bilaterally blown pupils
  • bilateral midbrain and PCA compression
73
Q

Raised ICP symptoms

A
  • headache worse lying down/coughing
  • relieved by vomiting
  • fatigue
  • nausea and vomiting
  • focal deficits - VI palsy
74
Q

Glasgow coma scale

A 
E4
- spontaneous
- to speech 
- to pain
V5
- oriented
- confused 
- inappropriate words
M6
- obeys commands
- localises to pain 
- withdraws from pain
75
Q

Managing raised ICP

A
  • head up
  • maintain MAP >90mmhG
  • normothermia
  • glucocorticoids in patients with brain tumour
  • Avoid hypoxia
  • avoid hyperventilation hyporthermia, hyperglycaemia, steroid
  • sedatives, analgesic
76
Q

In communicating hydrocephalus, where is the obstruction?

A

Sub arachnoid space

77
Q

Common obstruction location in non-communicating hydrocephalus

A

Foramen of monroe
aqueduct of sylvius
exit foramen of 4th ventricle

78
Q

What is a strong predictor of response to chemo/radiation in oligodendroglioma?

A

1p and 19q deletions

79
Q

Stereotypic features of meningiomas

A
  • whorls
  • syncytial arrangment
  • nuclear pseduoinclusions
  • psammoma bodies
  • stromal calcification
80
Q

Schwannoma

A

Benign sheet covering nerve

81
Q

EDH cause

A

Commonly rupture of middle meningeal artery which forms ovoid mass

82
Q

Cause of SDH

A
  • venous bleed = slow
  • related to contusion/laceration OR rupture of bridging veins
  • seen in falls and motor vehicle accidents
83
Q

What causes Foetal alcohol syndrome?

A
  • ethanol consumption during pregnancy
  • alcohol/nutritional deficits are teratogenic
  • microcephaly is most common feature
84
Q

What can cause alcoholic dementia?

A
  • thiamine deficiency
  • ## neuropsychological impairment and atrophy (reversible)
85
Q

What is alcoholic cerebellar degeneration?

A
  • most common form of acquired ataxia in alcoholic patients
  • M>F
  • selective atrophy of anterior portion of vermis of cerebellum
  • probably secondary to nutritional deficiency
86
Q

Wernicke Korsakoff syndrome

A 
Thiamine deficiency due to GIT disease (alcoholic)
Wernicke encephalopathy (Acute)
- vascular engorgement and haemorrhages 
- loss of myelin
Korsakoff psychosis (chronic)
- amnestic syndrome 
- structural abnormalities
- temporal memory impaired = confabulations
- high morbidity
87
Q

Primary and secondary causes of demyelination

A 
Primary 
- multiple sclerosis
- acute disseminated encephlomyelopathy 
- acute hemorrhagic leukoencephalopathy
Secondary 
- Viral 
- Metabolic/nutritional 
- Toxic
88
Q

Detection of demyelination

A

Neuroimaging - MRI
Visual evoked response - demyelination slows conduction
Macro - white matter turns grey
Micro - IHC for myelin proteins

89
Q

Clinical features of MS

A
  • focal lesions in CNS
  • peak onset 20-40
    F&raquo_space;>M
  • chronic disease that has relapse and remission in early years then progresses in later years
90
Q

Variants of MS

A
  1. Classic/chronic (charcot) - relapse and remission then progressive later years
  2. Acute (Marburg) - rapidly progressive, fatal in a few months
  3. Concentric sclerosis (balo) - uncommon with large plaques that have concentric ring of alternating demylenation and myelin preservation
    ?4. neuromyelitis optica
91
Q

What are the three types of plaques in MS?

A
  1. Acute - extensive active demyelination, lymphocytes, plasma cells and indirect axonal damage
  2. Chronic plaques - well circumscribed and complete myelin loss, axons demyelinated, little inflammation
  3. Shadow plaques - chronic plaque in which demyelination has occurred = thinly myelinated axons
92
Q

Demyelination

A

Loss of myelin sheath of a nerve fibre, with preservation of axon
Diagnosis - loss of myelin is not sufficient, need to demonstrate preserved axon to distinguish from other process like infarction

93
Q

What is acute disseminated encephalomyelitis?

A
  • Rare monophonic self limiting disorder onset 7-10 days after URTI
  • Immune demyelination due to production of antibodies which cross react with CNS myelin proteins
  • Multifocal demyelination and inflammation scattered throughout white matter
    Macro - edema and vascular congestion
    Micro - cuffing of small BV
94
Q

Petechial haemorrhages throughout white matter, fibrinoid necrosis of small blood vessels and perivascular demyelination … usually fatal

A

Acute hemorrhagic leukencephalopathy

95
Q

What is spinal muscular atrophy?

A
  • degeneration of MN in anterior horn of spinal cord
  • 2nd most common NM disorder
    SMA1 - infantile/intruterine death <18months
    SMA2 - onset 18 months, death 4-16yrs
    SMA3 - loss of motor function by 15-20yrs
96
Q

Diagnosis of Duchenne muscular dystrophy disease

A 
CK > 2000U/L
Myopathic EMG
Muscle wasting on MRI
Cardiomyopathy on ECG
Reduced lung function 
IHC on muscle biopsy 
genetic testing
97
Q

Causes of nosocomial meningitis

A
  • gram -ve bacilli
  • streptococci
  • staph. aureus
  • coagulase -ve straphylococci
  • anaerobes
98
Q

Examination for meningeal irritation

A
  1. Nuchal rigidity - can’t touch chin to neck
  2. Brudzinski - spontaneous flexion of hips during passive flexion of neck
  3. Kernig sign - intolerance to knee extension when the hip is flexed at 90
99
Q

What investigations do you ask for on a lumbar puncture?

A
  1. microscopy - gram stain and cell count
  2. culture
  3. PCR - HSV, enterovirus
100
Q

Lumbar puncture contraindications

A
  • anticoagulant
  • evidence of localised infection like epidural abscess
  • raised ICP
  • Herniation signs
  • decreased cellular immunity
101
Q

Treatment of encephalitis

A

Acyclovir - and if HSV is resistant, then use foscarnet or cidofovir

102
Q

What grade of astrocytoma is a glioblastoma and what are some positive prognostic factors?

A

IV

+VE FACTORS: age <60, location of tumour, ability to tolerate chemo/radiation, IDH-1/2 mutation

103
Q

What does the ovoid bleed in epidural haematoma cause?

A

Midline shift, compression of ipsilateral ventricle

NEURO (5 decks)

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