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MNI Drugs > Pathology of the Nervous system > Flashcards

Pathology of the Nervous system Flashcards

1
Q

The dura mater is made up of what kind of tissue?

A

Dense collagenous tissue

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2
Q

Arachnoid is made up of what kind of tissue? what lies beneath the arachnoid layer?

A

loose connective tissue

blood vessels

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3
Q

raised intracranial pressure, can be due to increased size of brain, blood and water. What is this doctrine called?

A

Munro-Kellie doctrine

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4
Q

Accumulation of excess fluid within brain parenchyma

A

cerebral edema

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5
Q

accumulation of excess CSF within ventricular system

A

hydrocephalus

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6
Q

Fluid from the vascular component goes to extracellular space of brain

A

vasogenic edema- ex meningitis, encephalitis, trauma and metastasis, paucity of lymphatics in CNS impairs resorption of excess extracellular fluid.

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7
Q

neuronal glial or endothelial cell membrane injury. there is an increase in intracellular fluid.

A

Cytotoxic edema: neuronal glial or endothelial cell membrane injury. there is an increase in intracellular fluid.
this can happen in generalized hypoxic/ischemic insult, metabolic damage, anything that injures the cell.

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8
Q

Pathology of hydrocephalus:

A

Impaired flow and resorption of CSF or increased production of CSF

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9
Q

Clinical features of hydrocephalus before and after suture fusion.

A

before sutures fuse- increase in head circumference due to available space

after they fuse: ventricular expansion and increased intracranial pressure

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10
Q

What kind of hydrocephalus is this?

Obstruction of flow of CSF in a part of the ventricle
Stricture of aqueduct of Sylvius or tumor in the 4th ventricle leads to interfered with or blocked normal CSF circulation from ventricles to subarachnoid space…

Results in only affected portion of the ventricles enlarges

A

non-communicating hydrocephalus

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11
Q

What kind of hydrocephalus is this?
You have poor absorption of CSF by arachnoid vili, it can be due to post meningitis, scarring, tumor, subarachnoid hemorrhage

This can also be caused by a choroid plexus papilloma causing overproduction of CSF

As a result the entire ventricular system is enlarged

A

Communicating hydrocephalus

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12
Q

What kind of hydrocephalus is this?
Patient has infarctions or neurodegenerative disorder. There is a loss of brain mass and volume.

Results in compensatory increase in CSF volume

A

Ex Vacuo

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13
Q

Normal pressure hydrocephalus is a type of communicating hydrocephalus characterized by abnormally enlarged ventricular size.
what are the clinical features associated with it?

A

dementia, gait disturbance, urinary incontinence

Wet, Wacky, Wobbly

differential diagnosis include Parkinsons and Alzheimer disease…

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14
Q

What is the treatment for normal pressure hydrocephalus?

A

lumbar puncture/ shunting.

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15
Q

Who typically gets a pseudo motor cerebri? ( benign intracranial hypertension)

A

overweight women of children bearing age.

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16
Q

What are the clinical features of pseudo motor cerebri (benign intracranial hypertension)?

A

increased intracranial pressure characterized by headache, papilledema, and vision loss

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17
Q

What is treatment for pseudo motor cerebri (benign intracranial hypertension)?

A

lumbar punctures, diuretics, steroids, shunt

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18
Q

Displacement of brain tissue past rigid dural folds (the falx and tentorium) or through openings in the skull because of increased intracranial pressure is called

A

cerebral herniation

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19
Q

displacement of cingulate gyrus under falx cerebri is what kind of cerebral herniation?

A

subfalcine ( cingulate) herniation

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20
Q

displacement of cerebellar tonsils through foramen magnum. what kind of cerebral herniation?

A

Tonsillar herniation

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21
Q

medial lobe of the temporal lobe compressed against margins of tentorium. what kind of cerebral herniation?

A

Transtentorial herniation

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22
Q

Subfalcine herniation compresses what?

A

anterior cerebral artery that leads to infarct

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23
Q

Tonsillar herniation compresses what?

A

brain stem compression and compromise respiratory & cardiac centers= death

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24
Q

Transtentoral herniation compresses what?

A

Compresses oculomotor (third cranial nerve) → pupillary dilatation and impaired ocular movements on the side of the lesion
• Compresses posterior cerebral artery → infarct in the area supplied by it (includes the primary visual cortex)
• Pressure on midbrain and contralateral cerebral peduncle→hemiparesis (may be both ipsilateral as well as contralateral)
• Accompanied by linear flame shaped hemorrhages in midbrain and pons→“Duret hemorrhages”

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25
Q

A skull bone fracture is more likely if the head is….

A

stationary

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26
Q

An injury due to sudden momentum change with a rigid object to the head will cause what

A

a concussion

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27
Q

Signs of concussion

A
  • Loss of consciousness
  • Temporary respiratory arrest
  • Loss of reflexes
  • Amnesia often persists

multiple can cause CTE

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28
Q

Bruises to the brain are called

A

contusions

neuron damage, edema, pinpoint punctures or depressions and hemorrhaging

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29
Q

What is more serious a concussion or a contusion?

A

contusion

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30
Q

Coup vs contrecoup contusions

A
  • Coup: underneath the site of impact

* Contrecoup: at the opposite pole as a result of deceleration of the brain by the skull

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31
Q

Plaque Jaune

A

found on inferior surface of the brain with a yellow color

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32
Q

Damage to the deep white matter regions, cerebral peduncles, superior colliculi, and deep reticular formation in the brainstem are called

A

diffuse axonal injuries

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33
Q

What kind of injury in diffuse axonal injuries?

A

Commonly seen with rotational acceleration→shearing of axons as they are stretched beyond elastic point with rotational force → alterations in axoplasmic flow

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34
Q

diffuse axonal injury pathogenesis

A

Axonal swellings and focal hemorrhagic lesions
• Seen in around 50% of patients in coma after trauma; even without
contusions

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35
Q

Epidural hemorrhages tend to occur in what part of the brain?

A

skull fracture at temporal region

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36
Q

what artery is lacerated in epidural hemorrhages?

A

Middle Meningeal Artery

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37
Q

What area in reference to meninges has accumulation of blood for epidural hemorrhages?

A

between skull and dura mater

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38
Q

Which hemorrhage does not cross suture lines?

A

epidural

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39
Q

Which hemorrhage crosses sutural margins?

A

subdural

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40
Q

What is ruptured in a subdural hemorrhage?

A

Due to rupture of veins bridging arachnoid and dura

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41
Q

describe risk factors for subdural hemorrhage

A

In elderly due to brain atrophy→bridging veins get stretched out & brain has additional space to move.
In infants→bridging veins are thin-walled.

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42
Q

What hematoma is lens shaped?

A

epidural

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43
Q

what hematoma is crescent shaped

A

subdural

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44
Q

Stroke Caused by an embolus versus thrombosis. Can be both due to both focal or global hypoxia causing ischemia.

A

Ischemic stroke

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45
Q

Stroke Caused by vascular rupture and can be intracranial or subarachnoid.

A

hemorrhagic stroke

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46
Q

What kid of testing modality will show lesion within hours of onset of an ischemic stroke?

A

MRI

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47
Q

What kind of testing modality will appear negative for the first 24 hours after an ischemic stroke?

A

CT scan

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48
Q

What is the time frame of a positive CT and MRI for a hemorrhagic stroke?

A

immediately after onset

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49
Q

What are causes of global cerebral ischemia/hypoxia?

A

Severe systemic hypotension like in MI, shock or decreased O2 carrying capacity of the blood (CO poisoning)

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50
Q

What are the factors determining the outcome of a global cerebral ischemia/hypoxia?

A

severity and duration of the insult, type of cell involved ( neurons&raquo_space; glia, ex pyramidal cells on hippocampus and neocortex, Purkinje cells of the cerebellum

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51
Q

What are the causes of focal cerebral ischemia?

A

embolization from a distant source, in situ thrombosis, or various vasculitides.

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52
Q

In a focal cerebral ischemia what helps in limiting the damage?

A

collateral blood flow, circle of willis ( supplemented by external carotid-ophthalmic artery collaterals)

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53
Q

Where do watershed infarct occur?

A

at the most distal reaches of the arterial blood supply.

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54
Q

What border has the greatest risk of infarction of the watershed areas?

A

cortical border zone between ACA and MCA

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55
Q

When are watershed infarcts seen?

A

usually after a hypotensive episode/ usually after resuscitating patients after cardiac arrest

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56
Q

Sickle shaped/wedge shaped band of necrosis over the cerebral convexity is seen in watershed infarcts in what area?

A

few centimeters lateral to the inter-hemispheric fissure. often bilateral.

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57
Q

What is the source of an embolic infarction?

A

cardiac mural thrombus or carotid atheromatous plaque

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58
Q

What are the predisposing factors of an embolic infarction?

A

atrial fibrillation, valvular disease, Myocardial dysfunction

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59
Q

What kind of infarcts can a thrombotic occlusion lead to?

A

small lacunar infarcts- occlusion of penetrating arteries usually due to hypertension.

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60
Q

When a venous emboli crosses over to the arterial side due to the presence of a right to left shunt it can lead to ischemia on the systemic side ( stroke)

A

Paradoxical emboli

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61
Q

What consists of a right to left shunt to help diagnose a paradoxical embolus?

A

patent foramen ovale, atrial and ventricular septal defect

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62
Q

Morphology of an infarct

A

swollen brain with wide gyro and narrowed sulk. Poor demarcation between gray and white matter, Tissue liquifies leaving a fluid filled cavity “ destruction of cortex and gloss”

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63
Q

What happens during the acute stage of an infarct? ( <24 hours)

A

Microvacuolation, cytoplasmic eosinophilia, nuclear pyknosis and karyorhexis.. First in neurons, astrocytes and oligodendroglia… then neutrophilic infiltration.

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64
Q

What happens during the subacute stage of ( 24 hours to 2 weeks) of an infarct?

A

Tissue necrosis, influx of macrophages, vascular proliferation, and reactive gliosis

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65
Q

What happens during the Repair stage ( after 2 weeks) of an infarct?

A

Gliosis with removal of necrotic tissue

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66
Q

What intraparenchymal hemorrhages are due to hypertension?

A

Primary intraparenchymal hemorrhage, Hyaline arteriolar sclerosis, Slit hemorrhages, Lacunar infarcts.

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67
Q

What intraparenchymal hemorrhages are not due to hypertension?

A

cerebral amyloid angiopathy, arteriovenous malformation, coagulopathy, cortical vein or dural sinus thrombosis, Tumor hemorrhage

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68
Q

A subarachnoid hemorrhage is caused by

A

a saccular berry aneurysm

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69
Q

What are the locations of primary intraparenchymal hemorrhage ? ( hypertensive)

A

it is due to rupture of small intraparenchymal vessel.

locations are basal ganglia, thalamus, pons, and cerebellum

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70
Q

If you have a small versus large primary intraparenchymal hemorrhage what occurs?

A

small- silent

large or in ventricles= death

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71
Q

Hyaline arteriolar sclerosis is seen in deep penetrating arteries and arterioles that supply what?

A

basal ganglia, brainstem, hemispheric white matter

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72
Q

What kind of hypertensive intraparenchymal hemorrhage contains Charcot Bouchard aneurysm and what is it?

A

small micro aneurysms on vessel walls vulnerable to rupture found in Hyaline arteriolar sclerosis

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73
Q

What kind of hypertensive intraparenchymal hemorrhage has rupture of small caliber penetrating vessels?

A

slit hemorrhages

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74
Q

Small cavitary infarct secondary to thrombosis of a vessel with arteriolosclerosis changes of a single penetrating branch/ due to hypertension

A

Lacunar infarcts ( lacunes)

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75
Q

What is the etiology of arteriovenous malformation/ a non hypertensive intraparenchymal hemorrhage ?

A

more in males, age 10-30

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76
Q

What are the clinical features of arteriovenous malformation/ a non hypertensive intraparenchymal hemorrhage ?

A

seizures, intracerebral hemorrhage or even a subarachnoid hemorrhage

In newborns with large AVM’s there is a high output congestive heart failure because blood shunts from arteries to veins

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77
Q

Vascular malformations are included in the non-hypertensive intraparenchymal hemorrhage, AVM and what are the others?

A

cavernous malformation, capillary telangiectasis, Venous angioma

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78
Q

How does Arteriovenous malformation (AVM) look grossly?

A

tangled network of worm-like vascular channels

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79
Q

How does Arteriovenous malformation (AVM) look microscopically?

A

enlarged blood vessel separated by gliotic tissue, often with evidence of a previous hemorrhage

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80
Q

Where do berry aneurysms occur?

A

at the anterior circulationof the circle of willis

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81
Q

Aneurysms are a defect of what part of the artery?

A

tunica media

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82
Q

There is increased risk of aneurysm in patient with…

A

autosomal dominant polycystic kidney disease, Ehler Danlos syndrome, those who smoke and with hypertension

83
Q

A thin walled outpouching of an artery…

A

Saccular (sac like) aneurysm

84
Q

In a subarachnoid hemorrhage, beyond the neck what is absent?

A

the muscular wall and the internal elastic lamina

85
Q

The sac of an a saccular/berry aneurysm is lined by

A

thickened hyalinized intima and a covering of adventitia

86
Q

The extravasated blood from a saccular aneurysm, berry enters what area?

A

the subarachnoid space.

87
Q

What causes a berry aneurysm?

A

a lot of straining precipitated by acute increase in intracranial pressure such as straining of stool or sexual orgasm

88
Q

What Is the most common clinical signs of a berry aneurysm?

A

thunderclap headache, loss of consciousness, neck stiffness, and photophobia=== poor prognosis

89
Q

You have a patient with a high number of RBCs and xanthochromia after a lumbar puncture what do they have?

A

Berry aneurysm…

xanthochromia means. yellowish CSF due to bilirubin after RBC lysis

90
Q

What are the complications of a Berry aneurysm?

A

rebleed, vasospasm ( in early period of hemorrhage), Hydrocephalus ( due to healing and meningeal fibrosis== abstruct flow of CSF or its absorption)

91
Q

__________ disorders are characterized by progressive death of neurons and accumulation of protein aggregates (misfiled/abnormal)

A

neurodegenerative disorders

92
Q

_________ is characterized by Impaired higher intellectual function, memory impairment, altered mood and behavior, impaired cognition, overtime aphasia and disorientation

A

Alzheimer disease

93
Q

The _______ systems are usually intact in Alzheimer disease.

A

sensory and motor

94
Q

When is Alzheimers diagnosed?

A

mental status examination, but realistically only confirmed during autopsy.

95
Q

What is the typical cause of death of Alzheimer’s disease?

A

Intercurrent pneumonia or other infections

96
Q

Abeta amyloid mutation confers an elevated risk for Alzheimer’s… Aggregates of these leads to what is called _________

A

Plaques

97
Q

Neurofibillary tangles found in Alzheimer’s are aggregates of _______ that develop intracellularly and persist extracellular after neuronal death

A

tau

98
Q

Mutation of tau protein is associated with Alzheimer’s and also_______

A

frontotemporal lobar degeneration

99
Q

APP ( amyloid precursor protein is associated with chromosome ______.

A

21/ Down syndrome and is present on neuronal membranes containing Abeta peptide

100
Q

Plaque with dystrophic neuritis surrounding amyloid core is evidence of__________.

A

Alzheimer’s disease

Plaque core and surrounding region are immunoreactive for Abeta= brown= positive

101
Q

_____ is a microtubule associated protein present in axons.

A

Tau

102
Q

What is the pathogenesis with tau in Alzheimers?

A

Abeta oligomers activate kinases that hyperphosphorylate tau and it loses its ability to bind microtubules…. when it aggregates it form Neurofibrillary tangles inside cells…

103
Q

Early onset alzhiemers is associated with amyloid precursor protein on chromosome ______ and Abeta amyloid formation

A

21

104
Q

Early onset Alzheimer’s is associated with chromosome 21 and Prensenilin genes on chromosome ___ and _____ and _____ enzyme

A

chromosome 1 and 14 and gamma secretase enzyme

105
Q

Late onset Alzheimer’s is associated with _____ protein

A

tau

106
Q

Late onset Alzheimer’s is associated with tau protein, ApoE genotype on chromosome _____

A

19.

3 allelic forms e2,e3,e4,,, e4 homozygous is greatest risk .

107
Q

How does the brain look on gross with Alzheimer’s disease?

A

atrophy in frontal, temporal and parietal lobes.
widening of cerebral sulk
may lead to compensatory ventricular enlargement hydrocephalus ex vacuo

108
Q

How does the brain look microscopically with Alzheimer’s disease?

A

Neuronal loss in cerebral cortex, Gliosis ( astrocyte proliferation and hypertrophy), Neurofibrillary tangles ( intracellular) and neuritic plaques ( extracellular)

109
Q

What is the difference between Alzheimer’s and Frontotemporal Lobar Degeneration?

A

FTLD- present in younger people and memory loss is last in comparison to Alzheimer’s where it is first, also in alzhiemers the frontal, parietal and temporal are affected. in FTLD It is just Frontal and Temporal. but also an accumulation of tau

110
Q

What are the clinical features of Frontotemporal Degeneration?

A

Progressive behavioral changes, or language problems depending on the lobe affected. primarily memory disturbances occur later. in younger person than in Alzheimer’s

111
Q

You have a younger patient with cytoplasmic inclusions containing TDP43 protein and they also have atrophy of the temporal cortex with relative preservation of the frontal cortex What do they have?

A

Frontotemporal Degeneration

112
Q

Patient has hypokinetic, movement disorder due to loss of dopaminergic neurons from the substancia nigra. what do they have?

A

Parkinson’s disease

113
Q

patient has triad of tremor, muscle rigidity and braykinesia, or akinesia. what do they have ?

A

Parkinson’s disease

114
Q

Mutation of the _______ gene is seen in Autosomal Dominant Parkinson.

A

a-synuclein gene - protein involved in synaptic transmission

115
Q

Depigmented substantia nigra is seen in what disorder?

A

Parkinson’s

116
Q

The remaining neurons of substantia nigra in Parkinson’s have _________

A

Lewy bodies, single or multiple cytoplasmic and eosinophilic inclusions

117
Q

A Dementia that involves with fluctuating course and hallucinations within 1 year of motor symptoms is called

A

Lewy body dementia

118
Q

Asymmetric pill rolling, bradykinesia (shuffling), Cogwheen rigidity, postural instability masked facies, hypokinetic, dysarthria, micrographia, sleep disorders, Dementia… characterizes what disorder?

A

Parkinson

119
Q

Progression of Parkinson is typically of

A

10-15 years

120
Q

Death of Parkinson typically occurs due to:

A

aspirational pneumonia or trauma from fall with poor stability.

121
Q

An autosomal dominant disorder associated with degeneration of the striatum ( caudate and putamen)

A

Huntington chorea/disease

122
Q

Patient has involuntary jerky movements (chorea), writhing movements of the extremities (athetosis), cognitive changes range from forgetfulness to dementia

A

Huntington chorea

123
Q

What mutation does Huntington have?

A

polyglutamate trinucleotide repeat expansion disorder

CAG repeats=Glutamine 6-35 repeats is normal, abnormal = 39-250

124
Q

the GOF related to the polyglutamine in Huntington interferes with _______

A

nucleic acid and protein regulation ( disrupts protein degradation and mitochondrial function, sequester transcription factors)

125
Q

More repeats in Huntington is proportional to ________

A

earlier onset of disease

126
Q

When do repeat expansions occur? (Like CAG in HT)

A

during spermatogenesis, paternal transmission is associated with earlier onset AKA ANTICIPATION

127
Q

The more degenerated the striatum is the more severity of _____ symptoms
The more cortical neuronal loss the more _______

A

motor…

dementia

128
Q

On Gross of HT disease you can see

A

marked atrophy of the caudate nucleus and putamen, dilated lateral and third ventricles

129
Q

Pt has severe loss of neurons from striatum with gliosis, in the remaining neurons present there are intranuclear inclusions of ubiquiniated huntingtin protein… what disease?

A

Huntington

130
Q

Neurodegenerative disease due to death of lower motor neurons in spinal cord and brain stem and upper motor neurons in the motor cortex

A

ALS/ Lou Gehrig’s disease/ Motor Neuron disease

131
Q

Etiology of ALS:

A

males>females, 5th decade or later, life expectancy 2-5 years after onset, sporadic… familial are AD.

132
Q

You have a chromosome 9 hexanucleotide repeat and superoxide dismutate gene mutation. what disorder is it?

A

ALS. may be due to abnormal RNA and/or protein processing.

133
Q

Pt has distal asymmetric extremity weakness

loss of lower Motor neurons:muscle atrophy, weakness, fasciculations

Loss of upper motor neurons: paresis, spasticity, hyperreflexia, babinski sign and degeneration of cortical spinal tract in lateral portions of the spinal cord.

A

ALS

134
Q

What is spared in a patent with ALS?

A

intellect, sensation, sphincter control, and eye movements

135
Q

What is the typical cause of death of ALS?

A

recurrent pulmonary infections

136
Q

Gross of ALS:

A

found on anterior roots of spinal cord

137
Q

What disease presents with a reduction of anterior horn cell neurons throughout the spinal cord? skeletal muscles have neurogenic atrophy

A

ALS

138
Q

What disease is associated with reactive gliosis and loss of anterior root myelinated fibers?

A

ALS

139
Q

________ are the dominant component of white matter

A

myelinated axons

140
Q

What are examples of acquired conditions with damage to previously normal myelin? ( demyelination)

A

MS, and post-infectious/ immune (ADEM,AHEM), Myelinolysis

141
Q

what is an example of a disorder with improper myelin formation? ( dysmyelination)

A

leukodystrophy

142
Q

what is the disorder that describes autoimmune demyelinating disorder characterized by episodes of disease activity, separated in time that produces white matter lesions?

A

MS

143
Q

Who gets MS most often? what are the risk factors?

A

females, smoking, low vitamin D, White, Infection with EBV, Genetic susceptibility HLA DR, maternal family Hx, moving to endemic area before puberty

144
Q

What cells cause demyelination in MS?

A

TH1 and TH17 T cells react against myelin antigens— secrete cytokines—- recruitment and activation of leucocytes

145
Q

What are the genetic factors for MS ?

A

15X risk if 1st degree relative affected
150X risk if monozygotic affected
HLA DR associated
IL2 and IL17 receptor gene associated

146
Q

What are the environmental factors for MS ?

A

incidence higher in areas away from the equator , low vitamin D ( longer winters, less sun)

147
Q

Gross finding of what?: Mutlifocal white matter disease, patchy loss of myelin: grey white matter, characteristic plaque: discrete, slightly depressed, glassy- appearing, gray-tan… Plaques commonly seen adjacent to the ventricles in optic nerves, chiasm, brainstem, tracts

A

MS

148
Q

What kinds of plaques are these in MS? Abundant macrophages and myelin breakdown,… perivascular lymphocytic inflammation

A

Active plaques

149
Q

What kinds of plaques are these in MS? inflammation disappears without any myelin and replaced by astrocytic proliferation and gliosis

A

inactive plaques

150
Q

What is found on lab analysis of CSF of MS patient?

A

elevated protein with increased Immunoglobulins ( oligoclonal bands) moderate pleocytosis

151
Q

What disorder? Immune mediated demyelination that occurs following number of systemic infectious illnesses including mild viral disease

A

post infectious demyelination

152
Q

what is the etiopathogenesis of post infectious demyelination?

A

may occasionally occur following a vaccine, mechanism possibly include cross-reacting antibodies that result in myelin damage.

153
Q

state the pattern name of the demyelinating disease: Non-localizing symptoms, over 1-2 weeks, preceded by infection, rapid progression, potentially fatal

A

Post infectious demyelination: acute disseminated encephalomyeltitis (ADEM)

154
Q

state the pattern name of the demyelinating disease: occurs in children and young adults and is most divesting compared to the other form

A

Post infectious demyelination: Acute hemorrhagic encephalomyelitis (AHEM)

MAHEM

155
Q

Patient had correction of hyponatremia that resulted in a rapidly evolving quadriplegia what disease?

A

Central pontine myelinolysis: this occurs due to non-immune damage to oligodendrocytes

156
Q

Central pontine myelinolysis is associated with hyponatremia. what are examples of conditions that cause hyponatremia?

A

renal and hepatic disease, severe vomiting or diarrhea, congestive HF, SIADH

157
Q

Wernicke encephalopathy is due to deficiency in what?

A

thiamine

158
Q

what is the triad of a thiamine deficiency?

A

encephalopathy and confusion, ocular palsies, ataxia

159
Q

What are the risks for thiamine deficiency?

A

chronic alcoholism and gastric disorders

160
Q

What occurs with delayed treatment of a thiamine deficiency?

A

irreversible memory disturbance called Korsakoff’s syndrome

161
Q

Location of pathological features due to thiamine deficiency

A

foci of hemorrhage and necrosis in maxillary bodies, thalamus, periaqueductal gray matter.

162
Q

CNS focal effects:

A

seizures, compression of nerve or vessel

163
Q

CNS Diffuse effect:

A

increased intracranial pressure, confusion, ataxia, nausea and vomiting, urinary incontinence, headache worsened by straining

164
Q

What is the most common location in children of brain tumors?

A

infratentorial or posterior fossa ( cerebellum)

165
Q

what are the most common tumors in children?

A

piloytic astrocytoma, medulloblastoma, and ependymommas

166
Q

what is the most common location for tumors in adults?

A

supratentorial or anterior fossa

167
Q

What are the most common tumors in adults?

A

astrocytoma, glioblastoma, oligodendrogliomas, metastatic tumors, and meningiomas

168
Q

What is the location of the pilocytic astrocytoma? what is the mutation and who do they affect?

A

cerebellum, BRAF translocations,

169
Q

what tumor has this in gross appearance? cystic lesion with mural nodule

A

pilocytic astrocytoma

170
Q

What tumor has bipolar cells with think hair like processes in fibrillary meshwork with eosinophilic rod like structures called Rosenthal fibers

A

pilocutic astrocytoma

171
Q

what grade is a pilocytic astrocytoma ?

A

I

172
Q

where is the location of a glioblastoma? what is the mutation and who does it affect?

A

cerebral hemispheres, IDH wild or mutant, found in adults.

173
Q

Infiltrating tumor with hemorrhage and necrosis and crossing the midline… what tumor is it?

A

Glioblastoma/ butterfly glioma

174
Q

what tumor has microvascular proliferation with areas of pseudo palisading necrosis?

A

glioblastoma

175
Q

what is the grade of a glioblastoma?

A

IV

176
Q

what form of astrocytoma is found in adults?

A

Diffused infiltrating astrocytoma ( IDH mutation) grade II and III

177
Q

Glial timmors are positive for what immunohistochemistry?

A

GFAP ( Glial fibrillary acidic protein)

178
Q

what are the clinical features of an oligodendroglioma

A

this is found in adults of 4th and 5th decade. patients have several years of antecedent neurological symptoms especially seizures prior to this.

179
Q

What is the most common site of oligodendroglioma?

A

cerebral hemispheres especially frontal and temporal lobes.

180
Q

What is the genetic mutation for oligodendroglioma?

A

Codeletion of 1p and 19q, IDH mutation= good prognosis

181
Q

what tumor has this on gross: gray masses often with cysts, focal hemorrhage and calcification.

A

Oligodendroglioma

182
Q

what tumor has this: Microscopic: cells with round nuclei, clear cytoplasm forming halos ( fried egg appearance) and thin walled capillaries

A

Oligodendroglioma

183
Q

Cancer in children consisted of ependymal cells lining ventricular cavity including central canal of spinal cord

A

ependymoma

184
Q

In adults, where do ependymoma present? and what genetic feature associated with them?

A

Neurofibromitosis-2, spinal cord.

185
Q

What tumor has regular cells with round to oval nuclei and abundant granular chromatin.. cells form rosettes with long delicate processes into lumen called canals.

A

ependymoma

186
Q

what tumor has small round cells and consists of remnants of the normal progenitor cells during embryology

what is the most common one?

A

embryonal tumors

medulloblastoma pediatric brain tumor

187
Q

what is the most common site of a medulloblastoma?

A

cerebellum, posterior fossa

188
Q

where does metastasis from a medulloblastoma go?

A

CSF to cauda equina

189
Q

what are the genes associated with medulloblastoma?

A

WNT-b catenin pathway, MYC overexpression

190
Q

What grade are medulloblastomas?

A

IV they are highly malignant.

191
Q

what is the prognosis of medulloblastoma?

A

usually poor but better if b catenin pathway involved

192
Q

On microscopy what tumor is this: sheets of small round blue anaplastic cells. Hyperchomatic nuclei, abundant mitosis, scant cytoplasm and rosettes ( homer wright rosettes in classic type)

A

medulloblastoma

193
Q

On gross well circumscribed, grey friable may involve leptomeninges

A

medulloblastoma

194
Q

Tumor of arachnoid meningothelial ells attached to dura matter

A

meningioma

195
Q

what is the age and location of meningioma?

A

mostly adults, external surface of brain or ventricular system

196
Q

A person that has multiple meningiomas + 8th nerve schwannoma or glial tumor is associated with______________.

A

Neurofibromatosis type 2

197
Q

What are the genetics associated with meningioma?

A

Chromosome 22q

198
Q

Histo: whorled tight clusters of cells without visible cell membrane that may show psammoma bodies is what kind of tumor?

A

meningioma

199
Q

benign encapsulated tumor that may occur in soft tissues internal organs or spinal nerve roots.

A

schwannoma

200
Q

_______ contains dense pink Antoni A areas and loose pale atoni B areas and hyalinized Blood vessels

A

Schwannomas

the rows of Antoni A are called Verocay bodies

201
Q

what is the most commonly affected CN with a schwannoma? and what chromosome is typically affected?

A

CN8 Chromosome 22q

202
Q

on gross this tumor is a circumscribed mass abutting an adjacent nerve

A

schwannoma

203
Q

secondary tumor sites are….

A

lung breast skin kidney GIT

MNI Drugs (4 decks)

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