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PATHOMA nervous system Flashcards

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USMLE® Step 1 flashcards
1
Q

what is the most common cause of hydrocephalus in newborns

A

cerebral aqueduct stenosis

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2
Q

where does CSF flow from the 4th ventricle

A

into the subarachdonic space via the forami=en of Lushka and Megendie

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3
Q

what is dandy walker syndrome

A

it is the absence of formation of the cerebral vermis. It presents as an enlarged (huge) 4th ventrice with the absence of the cerebellum

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4
Q

what is arnold chiari syndrome

A

it is the downward displacement if cerebellar vermis and tonsils into the foramen magnum

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5
Q

what is arnold chiari syndrome associated with

A
  1. Meningomyelocele

2. Syringomyelia

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6
Q

what is syringomyelia associated with

A

type I arnold chiari syndrome

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7
Q

what is a syrinx

A

it is the cyst in syringomyelia (damage to anterior white commissure from C8 - T1)

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8
Q

what happens if the syrinx expands (what tracts will be damaged)

A
  1. damage to anterior horn - lateral corticisoinal tract - LMN damage - negative babinski sign
  2. Lateral horn damage - hypothaloamosoinal tract - horners syndrome
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9
Q

what is damaged in poliomyelitis

A

anterior horn - flaccid paralysis, fasciculations, negative babinski sign, decreased reflexes, muscular weakness and muscular atrophy

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10
Q

what is Werdnig Hoffman disease

A

autosomal recessive damage to the anterior horn in a baby - floppy baby

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11
Q

what mutation is seen in familial ALS conditions

A

zinc-copper superoxide dismutase (SOD-1) mutation

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12
Q

what accumilates in fredrick ataxia

A

it tis the damage to spinal tarcts and to the cerebellum

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13
Q

what are the symptoms of fredrick ataxia

A

proprioception problems, muscular weakness in lower extremities, vibration damage and damage todeep tendon reflexed (DTR)

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14
Q

wht is frataxin useful for

A

it is used for mitochondrial iron regulation. It it is damaged, it’ll cause free radicle damage to hte nerves via phenytoin reaction

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15
Q

what are the associations of fredrick ataxia

A

hypertrophic cardiomyoathy

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16
Q

causes of meningitis in neonates

A

GBS, E.coli (both via birth canala) and Listeria

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17
Q

causes of meningitis in teenagers

A

N. meningitidis

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18
Q

causes of meningitis in unvaccinated people

A

H. influenza

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19
Q

causes of meningitis in adults and elderly people

A

Strep pneumoniae

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20
Q

causes of meningitis in immunocompromised people

A

fungal infections

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21
Q

characteristics of CSF in bacterial meningitis

A

high neutrophils with low glucose

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22
Q

characteristics of CSF in viral meningtis

A

high lymphocytes with high glucose

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23
Q

characteristics of CSF in fungal meningitis

A

high lymphocytes with low glucose

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24
Q

what is te classic triad of meningitis

A

headache, fever and nuchal rigidity…along with photophobia, vomiting and altered mental status

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25
Q

what is the sequale related to fibrosis after meningitis (bacterial)

A

hydrocephalus, hearing loss and seizures

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26
Q

what nucleotide is repeated in fredrick aatxia

A

nucleotide GAA is repeated in the frataxin gene

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27
Q

what are the causes for cerebrovascular diseases

A

ischemia (85%)and hemorrhage (15%)

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28
Q

how long does it take the neruron to undergo necrossis

A

3-5 minutes

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29
Q

etiology of global cerebral ischemia

A

low perfusion (atherosclerotic plaque), chrnoic hypoxia (ischemis), acute decrease in blood flow (cardiogenic shock) and repeated low glucose levels (insulinoma)

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30
Q

what does moderate global ischemia lead to

A
  1. Pyramidal cells infarction in 3rd, 5th and 6th layers if cortex( corticolaminar necrosis)
  2. Pyramidal cells in the hypothalamus in the temporal lobe (long term memory damage)
  3. Purkinjie cells in the cerebellum (integration between sensory and motor control is lost)
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31
Q

what are watershed areas

A

the areas of low perfusion between the anterior and middle cerebral arteries. They are the main areas of moderate global ischemia

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32
Q

what are the subtypes of ischemic stroke

A

thrombotic, ebolic and lacunar

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33
Q

where does the thrombotic infarct usually occur

A

bifurcation of internal carotid and middle cerebral artery in the anterior circle of willis

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34
Q

where does embolic stroke ususally occur

A

middle cerebral artery

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35
Q

In which conditions does hyaline arteriosclerosis occur

A

HTN and DM

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36
Q

where does lacunar stroke occur

A
  1. In the lenticulostriatal vessels from the middle cerebral artery in the deep poritons of the brain
  2. Internal capsule - motor lock
  3. Thalamus - sensory lock
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37
Q

what type of necrosis does ischemic stroke cause

A

liquefactive infarction

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38
Q

hematoma vs hemorrhage

A

hematoma is a solid collection that is clotted or in the process of clotting
hemorrhage is ongoing and active bleeding

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39
Q

where does intracerebral hemorrhage usualy occur

A

in the basal ganglia

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40
Q

causes for intracerebral hemorrhage

A

charcott bouchard microaneurysma - they occur due to HTN in lenticulostriatal vessels

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41
Q

presentation of intracerebral hemorrhage

A

headche, nausea, vomiting and eventually coma

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42
Q

where does a subarachnoid bleeding occur

A

at the base of the brain

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43
Q

causes of a subarachnoid aneurysm

A

berry aneurysms, anticoagulable state and AV malformations

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44
Q

why do berry aneurysms rupture easily

A

because they dont have medial (middle) layer in the blood vessel

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45
Q

where do berrry aneurysms uaually occur

A

in the anterior circle of willis in the branching point of anterior communicating artery

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46
Q

presentation of a subarachnoid hemorrhage

A

sudden headache (worst headache of life) with nuchal rigidity.LP has xanthochromia due to bilirubin breakdown

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47
Q

association of berry aneurysms

A

marfan syndrome and ADPKD

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48
Q

what do cerebral traumas cause

A

hematomas

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49
Q

Fracture of the skull usually causes rupture of which vessel

A

middle meningeal artery

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50
Q

how does an epidural hematoma presented on a CT

A

lens shaped

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51
Q

CT vs MRI

A

CT is used for hard tisue findings while MRI is used for soft tissue

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52
Q

what is the complication of an epidural hematoma

A

hermiation f thr brain due to increased intracranial pressure

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53
Q

talk and die syndrome

A

occurs in epidural hematoma due to sudden rupture of the hematoma nad sudden herniation of the brain

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54
Q

how does a subdural hematoma occur

A

due to breaking of the bridginf veins in the arachnoid space and also due to brain atrophy (as it pulls the brain vessels away frm the skull)

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55
Q

presentation ofsubdural hematoma on CT

A

cresent shaped

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56
Q

what is herniation of the brain

A

it is the diaplacement of the brain tissue due to mass effect or due to increased intracranial pressure in the brain (protruion of one part of thr brain into other part)

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57
Q

what is the lethal complication of subdural hemorrhage

A

brain herniation

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58
Q

what are the types of herniation

A
  1. subfalcime
  2. uncal
  3. tonsillar
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59
Q

what is subfalcine herniation and its result

A

it is the folding of the cingulate gyrus under the flax cerebri.It causes compression of the anteriot cerebral artery and leads to infarction

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60
Q

what is uncal herniation and its result

A

it is the downward displacement of the uncal part of th temporl love into the firamen magnum and it causes :

  1. compression of CN 3 - down and out eye
  2. duret (brainstem) hemorrhage due to compression of paramedian arteries
  3. posterior cerebral artery compression - contralateral homonymous hemianopsia
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61
Q

what is tonsillar herniation

A

downward displacement of the cerebral tonsils into the foramen magnum. It causes thecompression of brinstem and causes cardiopulmonary arrest

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62
Q

phases of ischemic stroke

A
  1. 12 hrs to 14 hrs - esinophilia with red nerons (dead neurons)
  2. 1-3 days :neutrophilic infiltration
  3. 4-7 days : nacrophage infiltration
    2-3 weeks : water filled cyst of necrotic area covered with gliosis
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63
Q

name the demyelinating disorders

A
  1. leukoencephalopathy
  2. Progressive multifocal leukodystrophy
  3. MS
  4. Subacute Sclerosing Panencephalitis.
  5. Central Pontine Myelinolysis
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64
Q

what is central pontine myelinolysis

A

focal degeneration of anterior braonstem (pons). It results in licken in syndrome

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65
Q

what is locked in syndrome

A

It is acute bilateral paralysis- paralysis of all the voluntary motor movements except eyes muscles as all the other motor nerves go down through the pons

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66
Q

wht does acute bilateral paraysis occur

A

It is due to rapid correction of hyponatremia in malnourished , alcoholics and in patietns with liver disease

67
Q

what is preogressive multifocal leukoencephalopathy and wht causes it

A

it is caused by JC virus.
Here, the oligodendrocytes are destroyed or damaged. The patient has fast neurological problems like dementia, vision loss and weakness. It can only cause this in immunocompromised state

68
Q

what is subacute sclerosing panencephalitis

A

it is caused by measels virus in childhood.It may lead to slow progresive neurological deficits and leads to death
Infection - infancy
panencephalitis - childhood (years later)

69
Q

wat is affected in subacute sclerosing panencephalitis

A

both grey mater (neurons) and white mater (myelin and axons)

70
Q

what are leukodystrophies

A

it is the dengeneration of white mater (defective enzymes that are necessary for myelin production)

71
Q

what are the types of leukodystrophies

A
  1. Metachromatic - damaged arylsulfatase :causes accumilation of sulfatides in lysosomes of oligodendrocytes…lysosomal storage disorders (autosomal recessive)
  2. Krabbes disease - galactocerebrocidase deficinecy…galactocerebrocides accumilate iin macrophages (autosomal recessive)
  3. Adrenoleukodystrophy - impaired coenzyme A attachment to long chani fatty acids.. fatty acids accumilation in the white mater and in the adrenal gland….X linked
72
Q

What is MS

A

it is degeneration of myelin and oligodendrocytes

73
Q

who does MS generally affect

A

younger people (20-30 yrs) , mostly women and people away from the equater

74
Q

which HLA is MS associated with

A

HLA-DR2

75
Q

How is MS presented

A
  1. optic nerve - blurred vision
  2. Spinal cord - lower extremity weakness or sesory loss
  3. Brainstem - vertigo and scannig speech similar to alcohol intoxication
  4. Internuclear opthalmoplegia - damaged MLF
  5. Cerebral white mater, usually periventricular - hemiparesis or inulateral sensation loss
  6. Autonomic system - sexual,bowel and bladder functions are affected
76
Q

Clinical featuress of MS

A

presents as recurrent neurological defects with rperiods of remission ( multple lesions in time and space)

77
Q

diagnosis of MS

A

MRI and LP

78
Q

features of MRI in MS

A

white plaques in white mater

79
Q

features of LP in MS

A

Oligoclonal IgG bands, increased lymphocytes, myelin basic protein and increased immunoglobulins

80
Q

Treatment of MS acute attacks

A

high dose steroids

81
Q

long term treatent ofMS

A

interferon beta slows the progression of the disease

82
Q

gross features of MS

A

grey plaques in white matter

83
Q

sources for brain metatastatic tumors

A

lung, breast and kidney

84
Q

name all the glial cells

A
  1. astrocytes (BBB)
  2. oligodendrocytes (myelination- schwann cells in PNS)
  3. ependymal cells (surround the ventricles)
  4. mesothelial cells (surround the ventricles)
85
Q

Adult brain tumor location

A

supratentorially

86
Q

Child brain tumors location

A

infratentorially

87
Q

most common primary brain tumors in adults

A

glioblastoma multiforme
schwannoma
meningioma

88
Q

most common primary brain tumors in children

A

pilocytic astrocytoma,
ependymoma
medulloblastoma

89
Q

what is meningioma

A

it is benign tumor od arachnoid cells in adults

90
Q

who is suseptible to meningioma

A

females, as meningioma has estrogen receptors

91
Q

imaging of meningioma

A

round tumor attached to the dura

92
Q

histology of meningioma

A

it has whorled cells , also may have psammoma bodies

93
Q

presentation of meningioma

A

it compresses the brain but doesnt invade (and so causes seizures)

94
Q

wht is GFAP

A

Glial Fibrillary Acidic Protein - it is a types III intermediate filament in the brain cells usually in the astrocytes and in the ependymal cells during development
It is encided by GFAP gene

95
Q

what is glioblastoma multiforme (GBM)

A

It is the malignant tumor of astrocytes in adults

96
Q

histology of GBM (glioblastoma multiforme)

A

It has pseudopallisading around necrotic tissue, endothelial cells proliferation and is GFAP positive

97
Q

characteristics of GBM brain tumor

A

It has poor prognosis and invades the corpus callosum and goes to the other hemisphere. And so it is called as a BUTTERFLY LESION

98
Q

what is schwannoma

A

It is a benign tumor od schwann cells in adults

99
Q

staning for schwannoma

A

s-100

100
Q

what is affected in schwannoma

A

the cranial and spinal neurins inside the cranium, but largely CN VIII is affected in the cerebellopontine angle causing tinnitis and heairng loss

101
Q

associations of schwannoma

A

bilateral schwannoma is associated with neurofibromatosis II

102
Q

what is an oligodendroglioma

A

it is a malignant tumor of oligodendrocytes in aduts

103
Q

oligodendroglima imaging

A

It looks as a calcifies tumor on the frontal lobe

104
Q

histology of oligodendroglima

A

it has fried eggs imaging

105
Q

where does oligodendroglima usually occur and what are its presentations

A

it occurs in the frontal lobe and it causes seizures

106
Q

what is pilocytic astrocytoma and where does it occur

A

it is a benign tumor in children and it occurs in the cerebellum

107
Q

imaging of pilocytic astrocytoma

A

it looks like a cyctic lesion with a mural nodule

108
Q

histology of pilocytic astrocytoma

A

it is GFAP positive, it has rosenthal cells and has edinophilic granular cells in histology

109
Q

wht is a medulloblastoma

A

It is a malignant tumor of granular cells of the cerebellum (neuroectoderm) in children

110
Q

how and where does a medulloblastoma spread

A

it is highly spreading and has drop metastasis to cauda equina via the CSF

111
Q

histology of medulloblastoma

A

it has small blue round cells called as Horner Wright rosette

112
Q

what is an ependymoma

A

It is a malignant tumor of ependymal cells in children

113
Q

ependymoma histology

A

It has periventricular pseudorosette on histology

114
Q

location of ependymoma

A

it is located in the 4th venetricle and may cause a hydrocephalus

115
Q

whatis a craniopharyngeoma

A

It is a benign tumor derived from the epithelial cells of rathkes pouch in children

116
Q

how does a craniopharyngeoma present as

A

It compresses the optic nerve and causes blurred vision and it may also cause seizures

117
Q

medulloblastoma imaging

A

It look like a calcified tooth on imaging

118
Q

which brain tumors are GFAP positive

A

Glioblastoma multiforme

pilocytic astrocytoma

119
Q

what are the malignant brain tumors in children

A

ependymoma

medulloblastoma

120
Q

what are the malignant brain tumors in adults

A

Oligodendroglioma

Glioblastoma multiforme

121
Q

which brain tumors arise from the cerebellum

A

Pilocytic astrocytoma

Medulloblastoma

122
Q

What leads to movement problems

A

degeneration of brainstem and basal ganglia

123
Q

what leads to dementia

A

degeneration of cortical grey mater

124
Q

what is associated with increased risk of sporadic alzheimers

A

Epsilon 4 allele of apolipoprotein E (APOE)

125
Q

what is associated with decreased risk of sporadic alzheimers

A

Epsilon 2 allele of apolipoprotein E (APOE)

126
Q

what is the most common cause of demetia

A

alzheimers

127
Q

wht is the cause of death (COD) in alzheimers

A

infections in bed-ridden patients

128
Q

what are the clinical features of alzheimers

A
  1. behavioral changes and
  2. loss of cholinergic stimulation from the basal nucleus of meynert
  3. slow onset dementia and progressive disorientation
  4. lossof learned motor skills and language
129
Q

when is early onset alzhemiers seen

A
  1. Down syndrome patients

2. familial cases witl presinilin 1 ans presinilin 2 mutation (mostly presenilin 1)

130
Q

how is down syndrome associated with alzheimers

A

Epsilon 4 allele of APOE is on chromosom 21 and down syndrome is trisomy 21. Epsilon 4 allele causes increased production of AB amyloid and since down syndrome patietns hav trisomy, it increases the conversion and it leads to early onset alzheimers

131
Q

what are the morphological features of alzheimers

A
  1. Cortical degeneration with narrowing of gyrus , widening of sulsi and hydrocephalus ex vacuo
  2. Neurofibrillary tangles
  3. Neuritic plaques
132
Q

how are AB amyloid formed and wht do they result in

A

Every neuron has amyloid precursor protein (APP) and the action of alpha-secretase causes degeration and recycling of the APPs. But when beta-secretase acts on APPs, it formes beta pleated configurated AB amyloids which cant degrade and hence deposit in the brain and cause alzheimers

133
Q

what are neurofibrillary tangles

A

They are abnormal elongated tau proteins (microtubular associated proteins) due to hyperphosphorylation of tau protein

134
Q

how is alzheimers diagosed

A

by clinical features

135
Q

how is alzheimers confirmed

A

post-mortem brain autopsy

136
Q

what does amyloid deposition around or in the brain vessels cause

A

it causes CEREBRAL AMYLOID ANGOPATHY which causes weakening of the blood vessels and leads to hemorrhage

137
Q

what is the 2nd most cause of dementia

A

vascular dementia

138
Q

what is vascular dementia

A

it is due to degeneration of pyramidalcells in the cortical 3rd, 5th and 6th layers and the pyramidal cells in the hippocampus

139
Q

Name the degenerative disorders of the brain

A
  1. Alzheimers
  2. Vascular dementia
  3. Parkinsons disease
  4. Norma pressure hydrocephalus
  5. Spongiform encephalitis
  6. Huntingtons disease
  7. Picks disease
140
Q

what is picks disease

A

It is selective frontal and temporal cortical degeneration

141
Q

clnical features of picks disease

A

early onset behavioral and language symptoms and progresses to dementia

142
Q

what is seen on histology for picks

A

round tau proteins aggregates (pick bodies) in the cortex

143
Q

what is masked face

A

It is the less expressive fase in parkinsons patients due to facial muscle rigidity

144
Q

what is parkinsons disease

A

it is the degeneration of substancia niagra pars compacts (SNPC) in the basal ganglia that leads to deteriorated nigostraiatal pathway

145
Q

causes of parkinsons disease

A

unknown, byt rarepy, MPTP exposure can lead to parkinsons

146
Q

what are the clinical features of parkinsons disease

A

TRAP

  1. Tremor - pill rolling tremor of the fingers and hands that reduced with movement
  2. Rigidity - cogwheel rigidity of the expremities
  3. Akinesia/bradykinesia - masked face and slowing of voluntary movements
  4. Postural instability and gait problems
147
Q

histology of parkinsons disease

A

lewy bodies in the basal ganglia and degraded substantia nigra in the basal ganglia

148
Q

what are lewy bodies

A

round esinophilic inclusions with aphla synergin

149
Q

what is huntungtons disease

A

It is the degeneration of GABA in the caudate nucleus

150
Q

what is the clinical finding in Huntingtons disease

A

repeated trinucleotide sequence accumilation of CAG in the caudate nucleus

151
Q

how is huntingtons transmitted

A

the CAG is added to the spem in every spermatogenesis and is autosomal dominant in trnasmission

152
Q

presentation of huntingtons disease

A

presents with chorea and progresses to dementia and depression

153
Q

CODin huntingons disease

A

suicide from depression

154
Q

what are the clinical features of normal pressure hydrocephalus

A

triad of urinary incontinence, dementia nd gait problems

155
Q

Rx of normal pressure hydrocephalus

A

VP shunt for excess CSF or repeated lumbar punctures

156
Q

what is spongiform encephalitis

A

It is a prion disease in humans. Every neuro had normal prio protein PrPc (alpha form).

157
Q

how is spongiform encephalitis transmitted

A
  1. Sporadic form
  2. Familial form
  3. Trasmitted form
158
Q

what are the features of spongiform encephalitis

A

When alpha form of PrPc changes to PrPsc of beta pleated configuration, an abnormal prion protein is formed and it cant be degraded and it leads to accumilstion of this abnormal protein in the cytoplasm of the neuron which forms spongy spaces in the white mater of the brain

159
Q

how does CJD occur

A

it can occur with a retinal or human growth hormone tranplant from a pron infected donor

160
Q

what is the most common form of spongiform encephalitis

A

creutzfeldt-jakob disease

161
Q

whar are the features of CJD

A

progressivedementia , rapid ataxia (due to cerebellum involvement) and startle myoclonus (exacerbated muscular movement with minimal stimulus)

162
Q

what is variant CJD

A

It is a form of CJD that occurs with beef consumption of a cow with mad cow disease

163
Q

what are the EEG features of CJD

A

periodic sharp waves

164
Q

What is familial fatal insomnia

A

It is a form of spongiform encehalitis characteried by severe insomnia and exacerbated startle response

usmle step 1 (3 decks)

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