CNS patho Flashcards

(43 cards)

1
Q

clinical presentations of patho of CNS

A
  • raised ICP
  • localising signs - sudden (hemorrhage), gradual (tumour)
  • neurodegenerative stage: cognitive/motor impairment
  • demyelinating diseases (problem w/ the myelin sheath)
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2
Q

CNS diseases

A

V: cerebrovascular disease, intracranial hemorrhage
I: infections
T: raised ICP from trauma
A: demyelinating disease
M: alcoholic encephalopathy, storage diseases
I: idiopathic
N: neoplastic (tumour)

C: congenital malformations
D: neurodegeneration

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3
Q

hydrocephalus

A

increase in CSF volume due to disturbances of formation/flow/absorption
- non-communicating: physical obstruction (tumour/mass, meningitis causing scarring)
- communicating: problem w/ venous drainage, defective absorption
subarachnoid hemorrhage -> block arachnoid villi in subarachnoid space
meningitis

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4
Q

cerebral herniation

A
  • subfalcine herniation: below falx cerebri
    can cause hemorrhage and necrosis -> compress cerebral artery -> infarction
    clinically silent
  • uncal herniation: medial temporal lobe
    loss of consciousness
    compress CN3 -> pupil fixed and dilated
    can cause displacement of the brainstem -> stretch the vessels -> hemorrhage
  • tonsillar herniation: through foramen magnum
    coning: compress pons and medulla -> affect respi and cardiac fn
    presents w/ neck stiffness
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5
Q

causes of cerebrovascular accidents

A
  • ischemia
  • hemorrhage

increases risk:

  • HTN -> lacunar infarcts; HT encephalopathy; HT intracerebral hemorrhage
  • DM
  • atherosclerosis
  • TIA (transient ischemic attack) - temp cerebrovascular insufficiency
  • atrial fibrillation
  • vascular malformations
  • coagulopathy
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6
Q

ischemia

A
  • thrombosis (pale infarct)
  • embolism (red hemorrhagic infarct)
    hemorrhagic infarct CANNOT use thrombolytics

micro appearance - liquefactive necrosis

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7
Q

hypertensive cerebrovascular disease (hemorrhagic)

A

effects:
- lacunar infarcts
multiple infarcts in basal ganglia/ white matter/ brainstem
- HT encephalopathy: diffuse cerebral dysfunction
can cause cerebral herniation (cause of the increased pressure)
- HT intracerebral hemorrhage: caused by atherosclerosis/ hyaline arteriolosclerosis/ aneurysms

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8
Q

hemorrhage within brain tissue

A
  • intraparenchymal - petechial hemorrhages (dislodged fat embolism, malaria, vasculitis, HT encephalopathy)
  • intraventricular

causes:

  • HTN
  • amyloid angiopathy
  • venous sinus thrombosis
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9
Q

hemorrhage outside tissue

A
  • subarachnoid: ruptured berry aneurysms (red) (high mortality)/ vascular malformations
  • subdural: tearing of bridging veins, can be by trauma. acute has high mortality - need urgent decompression, chronic good prognosis
  • epidural: caused by trauma: affects MMA
    lucid intervals, loss of consciousness, sudden deterioration
    immediate decompression surgery
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10
Q

CNS tumours presentation

A

raised ICP -> compression/herniation
headaches
seizures
focal neurological deficits

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11
Q

types of tumours

A

classification by age
children
- medulloblastoma
- ependymoma (ventricles/anywhere with CSF fluid)
- germ cell tumour (midline)
- pilocytic astrocytoma (arise from astrocytes)
adults: likely metastasis

site:

  • meninges: meningioma
  • parenchyma: neurons (neuroblastoma, medulloblastoma); glial cells (gliomas: astrocytoma/ oligodendroglioma/ ependomyoma)
  • ventricles: choroid plexus tumour, ependymoma
  • midline: pituitary tumour, germ cell tumour
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12
Q

meningioma

A

uniform ovoid cells
psammoma bodies
nuclear inclusions

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13
Q

astrocytoma (glial cells in parenchyma)

A
  • pilocytic astrocytoma (low grade) = hairy cell
    IDH1 mutant better prognosis than wild type
    in children
  • glioblastoma multiforme (high grade)
    aggressive
    ‘butterfly tumour’
    palisading necrosis (in a row)
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14
Q

oligodendroglioma (glial cells in parenchyma)

A

affects cerebral cortex
mutation in the IDH1 gene and deletion of 1p and 19q
uniform round cells w/ fried egg appearance

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15
Q

neuronal tumour

A

neuroblastoma
supratentorial (above tentorial cerebelli)
rare, poor prognosis
affects children

medulloblastoma - better prognosis w/ treatment, more common
infratentorial
aggressive, spread via CSF
micro: sheets of small cells, high n/c, mitosis, “carrot shaped nuclei”, rosettes (canals)
treatment: surgery and radiotherapy
- loss of 17p

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16
Q

ependymoma (ventricle and tumour of glial cells in parenchyma)

A

young patients
can cause hydrocephalus -> raised ICP
micro: perivascular pseudorosettes and true rosettes (canals)

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17
Q

choroid plexus tumour

A
  • papilloma
  • carcinoma
    can cause hydrocephalus -> raised ICP
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18
Q

midline tumour

A

pituitary tumour: can compress optic chiasma -> visual field defects (bitemporal hemianopia)
- endocrine: adenoma (more common), carcinoma
- embryonal remnant: craniopharyngioma (benign)
—> micro: cysts lined by sse, calcification
good prognosis but possible recurrence

germ cell tumour ** (when there is a midline tumour, think GC tumour 1st)
affects children & males more
- teratoma: benign/malignant
- germinoma

pineal gland tumour

  • pineocytoma
  • pineoblastoma (high grade)
19
Q

lymphoma

A

B cell non-hodgkin lymphoma

affects immunosuppressed pts, esp AIDS pts

20
Q

peripheral nerve sheath tumours

A

benign:
- schwannoma: attached to nerve, well circumscribed & encapsulated
micro: spindled cells, nuclear palisading (arises from neural cells), hyalinised vessels
- neurofibroma: cutaneous (skin/nervous system), non-encapsulated
autosomal dominant
-> NF1 (neurofibromatosis)
can affect skin, CN8, spinal cord nerve roots. optic nerve lioma, hermartomas nodules
renal/musculoskeletal abnormalities
potential malignant transformation of neurofibromas
-> NF2
clinical diagnosis:
- bilateral vestibular schwannoma/
- 1st deg relative w/ NF2 + unilateral
- multiple meningiomas + unilateral
-> tuberous sclerosis
TSC1 and 2 gene alterations
presentation:
(brain) cortical tubers, hermartoma
(skin) lesions: thickened, elevated, pebbly skin on the lower back - contains a lot of fibrous tissue + lumps of fibrous tissue growth on nail bed
(lung) lesions
(renal) angiomyolipoma
-> von hippel-lindau disease (tumour in many organs)
hemangioblastoma (retinal, cerebellar)
cysts (renal, pancreatic, adrenal)
RCC
pheochromocytoma

malignant:
- neurofibromatosis

21
Q

CNS infections possible routes

A
  • trauma
  • blood borne: septicemia, infective emboli
  • peripheral nerves: rabies, HSV
  • sinusitis, otitis media, dental caries, facial infection (affecting venous sinuses)
22
Q

bacterial infection

A

can cause:

  • extradural abscess
  • meningitis
  • brain parenchyma abscess formation (localised)
23
Q

fungal infection

A

can cause:

  • meningitis
  • brain parenchyma abscess formation (localised)
24
Q

viral infection

A

can cause:

  • meningitis
  • encephalitis
  • meningoencephalitis
25
prion disease (misfolded proteins)
can cause: | - encephalitis
26
meningitis
clinical presentation: - headache - fever - neck stiffness, kernig's sign (stiffness of leg doesnt allow extension of knee) - photophobia bacterial: - neonates: e.coli, listeria - infants: h.influenza - adolescent: n.menigitidis - adults: s.pneumonia
27
encephalitis
clinical presentation: altered mental state usually caused by viral infection: - acute: HSV, measles, HIV, CMV, rubella - delayed: VZV, measles - prion disease HSV, rabies -> affect neuron/glial cells polio, enterovirus -> motor neurons VZV -> DRG HIV -> microglia
28
parenchyma abscess
clinical presentation: - swinging fever - raised ICP -> vomitting/ fluctuating conscious level - localising signs causes: - single abscess: local source (otitis media/ sinusitis/ trauma) - multiple: from septic emboli of infective endocarditis - organisms (bacteria): strep, s.aureus, e.coli
29
subdural empyema (pus)
from skull/air infection | cause: thrombophlebitis (clotting of blood) of bridging veins -> infarction
30
extradural abscess
cause: local - sinusitis | if it infects the spinal cord -> cord compression (emergency)
31
diagnostic method for infections
- imaging: localise the infection - sterile samples: CSF/blood - EEG: detect prion disease
32
HSV infection
affect neuron/glial cells - temporal lobe abscess think HSV clinical: alteration in mood/memory/behavior micro: necrotising, perivascular lymphocytic infiltrates, intranuclear inclusions
33
rabies
affect neuron/glial cells edema, congestion location: basal ganglia, midbrain, 4th ventricle, spinal cord, DRG micro: (hippocampus) cytoplasmic oval eosinophilic inclusion (cerebellum) purkinje cells symptoms: early - (nonspecific) malaise, fever, headache advanced - CNS excitability: painful touch, violent motor response, spasms, convulsions
34
HIV infection
cause menigitis, encephalitis micro: multinucleated giant cell, microglial nodules (elongated nuclei), perivascular cuffing if it infects spinal cord: vacuolar myelopathy (holes in myelin sheath) of posterior column presentation: progressive painless leg weakness/stiffness; sensory loss; imbalance
35
neurosyphilis
affects (brain) neuronal loss -> dementia (meninges) granulomatous meningitis, subintimal vessel thickening (spinal cord) demyelination of post cord -> damage skin and joints
36
fungal infection
affects immunocompromised pts - candida - Cryptococcus neoformans cause vasculitis and thrombosis -> infarction, hemorrhage meningitis (crypt) parenchymal invasion
37
parasitic infection
protozoa: - malaria - toxoplasma - amoeba - trypanosoma helminths - echinococcus - taenia solium
38
prion disease pathogenesis
usually genetic cause, affects males more can also be transmissible - contaminated transplant tissue/ food spread of misfolded proteins -> causes spongiform encephalopathy -> neuronal death CJD: rapidly progressive dementia; abnormal muscular coordination (jerks, myoclonus); personality changes (impaired memory, depression) variant CJD affects young adults slower progress; prominent behavioral changes micro: spongiform transformation (cerebral cortex, deep grey matter) amyloid deposits and plaques
39
CNS malformations
causes - prenatal insult: folate def/ radiation/ infections/ drugs - genetic types: - neural tube defects: neural tube fail to close folate def -> spina bifida (spine) (causes LL weakness/paralysis; bladder and bowel dysfunction, UTIs; clubbed feet, hip dilocation) (brain) anencephaly (born w/o parts of brain/skull cause forebrain development got disrupted); encephalocele (outpouching of membrane into skin) - forebrain anomalies polymicrogyria: seizures, mental retardation, hemi/quad paresis (paralysis) microencephaly: difficulty swallowing, seizures, psychomotor retardation - post fossa anomalies 1. Arnold chiari (chirai type 2) malformation*: displacement of cerebellar tonsils through foramen magnum -> headaches, muscle weakness, fatigue severe: brainstem damage 2. dandy walker syndrome: enlarged post fossa -> enlargement of skull raised ICP - vomitting, irritability poor coordination of eye and facial muscles affects females & infants (slow motor development) more
40
Alzheimer's disease
pathology: mutation of chromosome 21 (amyloid precursor protein) -> production and deposition of beta amyloid peptides (in hippocampus, amygdala, neocortex) -> neuronal damage frontal and parietal lobes affected + brain atrophy micro: amyloid deposits; intracellular tau protein
41
parkinson disease
``` pathology: loss of nerve cells from midbrain -> reduced dopamine lewy bodies (contain a-synuclein gene) ``` gross: substantia nigra (basal ganglia) becomes pale
42
metabolic/toxic diseases
``` vit B1 (thiamine) def = wernicke encephalopathy: thiamine def -> damage medial thalamus and mammillary bodies -> cerebral atrophy vit B12 def = degeneration of spinal cord ``` storage diseases: niemann pick, tay-sachs disease hepatic encephalopathy CO poisoning: diffuse cortical necrosis
43
alcohol affecting CNS
- fetal alcohol syndrome: growth retardation, cerebral malformation of baby - acute intoxication -> respiratory depression - chronic: cerebral cortical atrophy cerebellar atrophy wernicke encephalopathy (cause of b1 def) -> korsakoff psychosis