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Pathology - CNS Flashcards

1
Q

Lipofuscin

A

Accumulation of complex lipids due to age in neurons cytoplasm and lysosomes

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2
Q

Gliosis and who does it?

A

Repair and scar formation in the CNS carried out by astrocytes

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3
Q

Ependyma cells

A

They line the ventricles

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4
Q

Choroid plexus

A

They produce CSF fluid

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5
Q

Cerebral edema

A

Excess fluid in brain parenchyma

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6
Q

Vasogenic edema

A

occurs when the BBB is disrupted so liquid goes from vascular part to extracellular parts

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7
Q

Cytotoxic edema

A

increase in intracellular fluid due to neuron or glial cell membrane damage:

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8
Q

Foramena Magendie and Luschka

A

Opening from the 4th ventricle to the subarachnoid

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9
Q

hydrocephalus

A

Accumulation of excess CSF within the ventricle system

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10
Q

non-communicating hydrocephalus

A

blockage in ventricular system flow by masses mainly in foramen Monroe or compressing the cerebral aqueduct

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11
Q

Communicating hydrocephalus

A

All the ventricles enlarged and caused by the reduced resorption

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12
Q

Hydrocephalus ex vacuo

A

Enlarged ventricles because of atrophy of brain parenchyme

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13
Q

Subfalcine herniation ( cingulate)

A

unilateral expansion of a cerebral hemisphere displaces the cingulate gyrus under the falx. This compresses the anterior cerebral artery

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14
Q

Transtentorial (uncinate) herniation

A

Medial aspect of temporal lobe is compressed against the tentorium. CN III is compressed. Posterior cerebral artery may be compressed also affecting the primary visual cortex

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15
Q

Kernohan’s notch

A

Compression of the peduncle against the tentorium causing hemiparesis ipsilateral to the side of herniation

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16
Q

Duret’s hemorrhages

A

Transtentorial (uncinate) herniation accompanied by linear or flame shaped hemorrhages in the midbrain or pons

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17
Q

Tonsillar herniation

A

displacement of the cerebral tonsils through the foramen magnum.

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18
Q

Which herniation is life threatening

A

Tonsillar herniation because it causes brain stem compression and compromises respiratory and cardiac centers in the medulla

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19
Q

Functional Ischemia

A

low partial pressure of oxygen e.g high altitude impairing oxygen carrying capacity

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20
Q

Ischemia

A

due to tissue hypoperfusion can be permanent or transient

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21
Q

Global Cerebral Ischemia

A

widespread ischemic hypoxia if pressure is below 50mmHg like in cardiac arrest, shock or hypotension

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22
Q

Most susceptible cells in the brain to hypoxia

A

Neurons

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23
Q

Most susceptible neurons

A

Pyramidal cells of hippocampus and neocortex and Purkinje cells of the cerebellum

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24
Q

Respirator brain

A

Irreversible brain damage thats now on mechanical ventilation and brainn undergoing autolysis

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25
Q

Histological changes in irreversible injury is in 3 categories

A

Early changes, Subacute changes and Repair

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26
Q

Early changes of irreversible injury

A

12-24hours. Red neurons, microvacuolization, cytoplasmic eosinophilia, nuclear pykosis and karyorrhexis. Also occurs in astrocytes and oligodendrocytes later

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27
Q

Subacute changes of irreversible injury

A

24hours-2weeks. Tissue necrosis, macrophages, vascular proliferation and reactive gliosis

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28
Q

Repair

A

> 2weeks. Removal of necrotic tisssue, loss of CNS structure, and gliosis

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29
Q

Border zone( Watershed infarcts)

A

wedge shaped areas that lie at the distal end of blood supply

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30
Q

What zone is at greatest risk for hypotensive episodes in the cerebral hemispheres

A

Zone between the anterior and middle cerebral artery

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31
Q

Focal Cerebral Ischemia

A

This is the first stage of cerebral artery occlusion.

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32
Q

Which structures have no collateral blood flow

A

thalamus, basal ganglia and deep white matter

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33
Q

Embolic or thrombosis infarction more common

A

Embolic

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34
Q

Factors for cardiac mural thrombi

A

MI, Valve disease, Atrial fibrillation

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35
Q

Most common cerebral artery affected by embolic infarction

A

middle cerebral artery

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36
Q

Superimposed thrombotic occlusions on atherosclerosis places in the cerebral

A

Carotid bifurcation, origin of middle cerebral artery and basilar artery

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37
Q

Non hemorrhagic infarcts

A

acute occlusion that can be treated with thrombolytic

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38
Q

Hemorrhagic infarcts

A

reperfusion of infarcted tissue producing petechial hemorrhages

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39
Q

Non contributors to the healing process of infarction

A

Pia and arachnoid

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40
Q

Most common cause of subarachnoid hemorrhage

A

Ruptured aneurysms from HTN

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41
Q

Sites of HTN intraparenchymal hemorrhages

A

Basal ganglia, thalamus, pons, cerebellum

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42
Q

Cerebral Amyloid Angiopathy

A

amyloid peptides depositing in meningeals and cortical vessels. It stains with Congo Red. Weakens vessel to cause hemorrhages

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43
Q

Location of Cerebral amyloid angiopathy

A

CErebral cortex ( lobar hemorrhages)

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44
Q

Most common cause of non-traumatic subarachnoid hemorrhage

A

saccular (berry) aneurysm

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45
Q

The worst headache I have ever felt and becomes unconscious

A

Subarachnoid hemorrhage

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46
Q

Location of most saccular aneurysms

A

Anterior circulation

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47
Q

Who had increased risks for aneurysms

A

ADPKD

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48
Q

What layers are present in aneurysm

A

Hyalinized intima

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49
Q

Most common location for a atherosclerotic aneurysms

A

basilar artery involvement

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50
Q

Vascular malformations

A

Arteriovenous malformations, Cavernous malformations, Capillary telangiectasia, Venous angiomas

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51
Q

Whats the most common vascular malformations

A

Arteriovenous malformation

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52
Q

Arteriovenous malformations presentation

A

10-30, seizures, intracranial or subarachnoid hemorrhage

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53
Q

What genetic defect is seen in most multiple Arteriovenous malformations

A

Herediatary hemorrhagic telangiectasia

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54
Q

Cavernous malformation occurences

A

Cerebellum, pons and subcortical regions

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55
Q

Capillary telangiectasis

A

Pons (no bleed)

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56
Q

Venous angiomas

A

venous channels

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57
Q

Lacunar infarcts

A

small infarcts due to occlusion of a single penetrating branch of a large cerebral artery occurring in the deep gray matter- basal ganglia, thalamus, internal capsule, deep white matter and pons

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58
Q

Acute HTN encephalopathy

A

when diastolic pressure is >130mmHg

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59
Q

Causes of Primary angiitis of the CNS

A

chronic inflammmation, giant cells and destruction of vessel walls

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60
Q

Coup injury

A

Injury occurring at the site of of head impact

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61
Q

Contrecoup injury

A

Injury to the opposite side of where the head was hit

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62
Q

Contusion

A

Rapid tissue displacement, disruption of vascular channels and then hemorrhage, tissue injury and edema

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63
Q

What brain part most susceptible to traumatic brain injury

A

Crest of gyri

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64
Q

Concussion

A

Reversible altered consciousness from head injury without contusion

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65
Q

Epidural Hematoma

A

Middle meningeal artery from skull fractures

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66
Q

Subdural Hematoma

A

Rapid movement of brain during trauma can tear the bridging veins spilling into the subdural space. Higher rates in older people because bridging veins strethced out and children because theirs is thin-walled

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67
Q

Most common site for a subdural hemorrhage

A

Lateral aspects of the cerebral hemisphere and can be bilateral

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68
Q

Most frequent type of CNS malformation

A

Neural tube defect at the posterior end, where spinal cord forms

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69
Q

Anencephaly

A

malformation of anterior end of neural tube, leads to absence of brain and top of skull

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70
Q

Encephalocele

A

Diverticulum of malformed CNS tissue extending through the cranium defect

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71
Q

Microencephaly more common than macro. Causes

A

fetal alcohol syndrome, HIV acquired in utero, chromosome issues

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72
Q

Lissencephaly ( agyria)

A

Absent gyration leading to smooth brain surface

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73
Q

Holoprosencephaly

A

disruption of normal midline dividing due to sonic hedgehog mutations

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74
Q

Arnold Chiari malformation Type II

A

small posterior fossa with mishapen midline cerebellum with vermis through foramen magnum, hydrocephalus and lumbar myelomeningocele

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75
Q

Dandy Walker malformations

A

Enlarged posterior fossa, non-cerebellar vermis, large midline cysts and Joubert syndrome

76
Q

Joubert syndrome

A

No vermis so eye movement problems

77
Q

Cerebral palsy

A

Non-progressive neurological motor deficits featuring spasticity, dystonia, ataxia or athetosisand paresis

78
Q

Most common injuries that occur in perinatal periods are

A

hemorrhages and infarcts

79
Q

Routs of reaching Nervous System by microbes and most common one

A

hematogenous( most common), direct, local extension( air sinuses), peripheral nerves

80
Q

Meningitis

A

Inflammation of the leptomeninges within the subarachnoid space

81
Q

Acute Pyogenic Meningitis ( Bacterial Meningitis)

A

Neonates: E.coli, Group B Strep,
Adolescents and Young Adults: N. meningitis, (most common),
Older: Strep pneumococcus and Listeria mening

82
Q

Signs of Meningitis

A

Headache, photophobia, irritability, clouded consciousness and neck stiffness

83
Q

Aseptic meningitis ( viral meningitis)

A

Self limiting, lymphocytes, normal glucose levels,

84
Q

Features of TB chronic meningitis

A

lymphocytes, plasma cells and macrophages

85
Q

Location of Neurosyphilis

A

Base of brain

86
Q

Aseptic meningitis with facial palsy, polyneuropathies

A

Lyme disease by Borrelia burgdorferi

87
Q

Increased intracranial pressures with progressive focal deficits

A

Brain abscess

88
Q

Viral spread range in brain abscess

A

Diffuse

89
Q

Bacterial spread range in brain abscess

A

Localized

90
Q

Abscess

A

Discrete lesion with central liquified necrosis surrounded by a fibrous capsule

91
Q

How does center of abscess look like

A

Granulomatous tissue with exuberant vascularization and a zone of reactive gliosis

92
Q

Meningoencephalitis

A

Viral encephalitis

93
Q

Alterations in mood, memory and behavior

A

Herpes virus in the CSF

94
Q

HIV encephalitis H&E slide feature

A

multinucleated giant cell due to infecting microglial cells causing an innate immune response

95
Q

Loss of motor neurons and paralysis of respiratory muscles

A

Polio virus

96
Q

Headache, malaise, fever, slight touch is painful sensation, and convulsions to mania and stupor progressing to coma

A

Rabies from a bat

97
Q

Oligodendrocyte demyelination in immunocompromised person, focal and progessive neurological symptoms, ring forming lesions in the hemisphere

A

Progressive multifocal leukoencephalopathy (PML) caused by JC virus a polyomavirus

98
Q

Triad of chorioretinitis, hydrocephalus and intracranial calcifications

A

Toxoplasmosis

99
Q

Meningitis in immunocompromised person,”soap bubble appearance” and India Ink is used

A

Cryptococcus neoformans

100
Q

Cysticercosis in the brain and subarachnoid space, causing seizures

A

Tenia solium

101
Q

Rapidly fatal necrotizing encephalitis from swimming in nonflowing warm freshwater

A

Naegleria spp

102
Q

Chronic granulomatous meningoencephalitis

A

Amoeba

103
Q

> 70 years old, Rapidly progressing dementia illness

Spongioform transformation of cerebral cortex and deep gray matter

A

Creutzfeldt-Jakob disease

104
Q

Young adultsSlowly progressive dementia, spongioform encephalitis ( cattle), abundant cortical amyoid plaques

A

Variant-CJD

105
Q

Distinct episodes of neurological deficits, separated in time and space, oligoclonal bands seen in brain

A

MS

106
Q

MS players

A

CD4, Th 17, Th1, CD8, B cells, IL-2, IL-7

107
Q

Acute disseminated encephalomyelitis

A

Develop a week or 2 after infection, headache, lethargy and coma. Non localizing findings

108
Q

Acute necrotizing hemorrhagic encephalitis

A

similar to MS but affecting young adults and children

109
Q

Neuromyelitis optica

A

Inflammatory demyelinating disease of the eyes and spinal cord

110
Q

Diagnostic text for Neuromyelitis optica

A

Antibody to aquaporin 4

111
Q

Central Pontine Myelinolysis

A

Non-immune loss of myelin involving the pons after a rapid correction of hyponatremia causing rapidly evolving quadriplegia

112
Q

Arylsulfatase A deficiency

A

Metachromatic leukodystrophy

113
Q

Galactocerebroside beta galactosidase deficiency

A

Krabbe disease

114
Q

Peroxisome dects: elevated very long fatty acid chains

A

Adrenoleukodystrophy

115
Q

Aspartoacylase deficiency

A

Canavan disease

116
Q

Proteolipid protein mutation

A

Pelizaeus-Merzbacher dx

117
Q

Translation initiation factor

A

Vanishing white matter

118
Q

GFAP mutations - Glial fibrillary acidic protein

A

Alexander dx

119
Q

Abrupt onset of confusion, abnormal eye movements, ataxia. Mammaory body necrosis with preservation of the neurons

A

Wernicke-Korsakoff syndrome in alcoholics due to thiamine deficiency

120
Q

What brain structure mostly affected by hypoglycemia

A

hippocampus neurons

121
Q

Why hyperglycemia bad

A

Intracellular dehydration, onfusion, stupor and death

122
Q

Elevated ammonia, Flapping tremor, inflammation and hyponatremia

A

Hepatic encephalopathy

123
Q

Protein inclusion and location in Alzheimer

A

Abeta and tau. Extracellular neurons

124
Q

Protein inclusion and location in Frontotemporal lobar degeneration

A

Tau, TDP-43. Neurons

125
Q

Protein inclusion and location in Progressive Supranuclear palsy and Corticobasal degeneration

A

Tau. Glial and neurons

126
Q

Protein inclusion and location in Parkinsons

A

alpha-synuclein and neurons

127
Q

Protein inclusion and location in Multiple System Atrophy

A

alpha-synuclein and neurons and glial

128
Q

Protein inclusion and location in Amyotrophic lateral sclerosis

A

TDP-43, SOD-1 and neurons

129
Q

Protein inclusion and location in Huntington Disease

A

Huntingtin and neurons

130
Q

Spinocerebellar ataxias

A

Ataxins and neurons

131
Q

Elderly, > 65 loss or memory, altered mood and behavior,, disorientation and memory loss and aphasia. In 5 to 10years becomes mute and immobile

A

Alzheimer disease. Abeta plaque accumulation causes the chain of events.

132
Q

Risk factors for Alzheimer disease

A

Downs syndrome (Trisomy 21), ApoE4, Abeta plaques cause inflammation causing cell injury and hyperphosphorylation of Tau which then forms tangles

133
Q

What forms tangles in Alzheimer disease

A

Taus that were overphosphorylated by Abeta plaques. Taus cause neural dysfunction and death

134
Q

Diagnosis of Alzheimer

A

Plaques with neurofibrillary tangles

135
Q

Frontotemporal Lobar degeneration difference from Alzheimer

A

Behavior changes/language defects precedes memory ( dementia) deficits.

136
Q

Mutations in Frontotemporal Lobar degeneration

A

Smooth round inclusions9Pick bodies)-Picks disease

Aggregates of DNA/RNA binding -TDP-43 ( frontal lobe impairment)

137
Q

Tremor, Rigidity, bradykinesia and instability

A

Parkinsons

138
Q

Cause of Parkinsons

A

Damage to dopaminergic neurons from the substantia nigra to the striatum

139
Q

Diagnostic of Parkinsons

A

Lewy bodies- an inclusion containing alpha-synuclein

140
Q

Diseases with alpha-synuclein

A

Parkinson, Multiple System atrophy, Progressive supranuclear palsy, and corticobasal degenration

141
Q

Lewy body dementia

A

Dementia with hallucinationsarising within one year of motor symptoms

142
Q

Degeneration of the striatum- caudate and putamen, choreiform-dancelike, increased voluntary jerky movements. Progressive disease and death after 15 years

A

Hungtinton

143
Q

Cause of Huntington

A

CAG trinucleotide repeat expansions on Ch 4. Anticipation involved, Atrophy of caudate nucleus,

144
Q

Friedreich Ataxia

A

GAA repeat in gene for frataxin, leads to mitochondrial dysfunction and increased oxidative damage

145
Q

Features of Friedreich Ataxia

A

<10. Gait ataxia, Hand clumsiness, dysarthria, pes cavus, kyphoscoliosis, cardiac disease and diabetes

146
Q

Amyotrophic Lateral Sclerosis

A

Loss of upper and lower motor neurons. with hyperreflexia, babinski sign

147
Q

Cause of Amyotrophic Lateral Sclerosis

A

SOD-1 on Ch 21 mutation, DNA/RNA binding protein, TDP-43

148
Q

Most CNS tumor location in children

A

Posterior fossa

149
Q

Most CNS tumor location in adults

A

Supratentorial

150
Q

Gliomas are

A

astrocytomas, oligodendrogliomas and ependymomas

151
Q

Diffuse gliomas

A

astrocytomas, oligodendrogliomas and mixed

152
Q

Solid masses glioma

A

Ependymomas

153
Q

40s - 60s, seizures, headaches and focal neurological deficits

A

Diffuse astrocytoma

154
Q

Diagnosis of Diffuse astrocytoma

A

GFAP +, IDH1

155
Q

Child, young adult, tumor in cerebellum, 3rd ventricle involvement, Rosenthal fibers with eosinophil granular bodies

A

Pilocytic Astrocytoma

156
Q

Mutations in Pilocytic Astrocytoma

A

serine-threonine kinase BRAF, V600E, IDH1

157
Q

Frontal or temporal lobe masses, focal hemorrhage, calcifications round nuclei surrounded by white halo

A

oligodendrogliomas

158
Q

Cause of oligodendrogliomas

A

deletion of 1p, 19q, responsive to chemotherapy and radiotherapy

159
Q

Tumor arising by ventricular system,

A

Ependydoma

160
Q

Most common location of Ependydoma in adults

A

Spinal cord

161
Q

Most common location of Ependydoma in first 2 decades

A

Near the 4th ventricle

162
Q

NF2 associated with what tumor

A

Ependydoma

163
Q

Features of Ependydoma

A

Rosette canals

164
Q

Most common primitive neuroectodermal tumor (PNET)

A

Medulloblastoma

165
Q

Location of medulloblastoma tumor in child

A

midline

166
Q

Location of medulloblastoma tumor in adult

A

Lateral tumor

167
Q

Which medulloblastoma have good outcomes

A

WNT

168
Q

Which medulloblastoma have good outcomes

A

MYC

169
Q

Most Common Primary CNS tumor in immunocompromised

A

Diffuse large B cell lymphoma with Epstein Barr virus

170
Q

Most common primary CNS germ cell tumor

A

germinoma

171
Q

Multiple meningiomas with 8th nerve schwannomas or glial tumors think

A

NF2 on ch 22

172
Q

Features of meningiomas

A

Psammoma bodies, synctial whorled clusters of cells like keratin

173
Q

Most common primary sites of metastatic tumors

A

Lung, breast, skin, kidney and GI

174
Q

Benign neoplasms, hamartomas in brain

A

Tuberous sclerosis

175
Q

Associations with Tuberous Sclerosis

A

renal angiomyolipomas, retinal glial hamartomas, pulmonary lymphangiomyomatosis and cardiac rhabdomyomas

176
Q

Tuberous sclerosis

A

a normal tissue growing at the same rate as neighbors but growing in an irregular pattern

177
Q

von Hippel-Lindau disease association

A

Hemangioblastomas within the cerebellar hemispheres, retina. Renal cell carcinoma

178
Q

Role of VHL genes

A

Encodes protein thats part of ubiquitin ligase complex. that targets hypoxia induced factor for degradation. Mutation causes high HIF which causes VEGF, growth factors, erythropoietin to form paraneoplastic polycythemia

179
Q

Role of HIF

A

causes VEGF, growth factors, erythropoietin to form paraneoplastic polycythemia

180
Q

Most often nerve affected with Schwannomas

A

CN VIII

181
Q

Bilateral vestibular schwannomas

A

NF2 with loss of function on Ch 22

182
Q

NF2 mutation at risk for

A

Schwannomas, Meningiomas and ependydomas

183
Q

NF1 origin

A

Ch 17, regulator of Ras

184
Q

NF2 origin and role

A

Ch 22 and its Merlin gene is a tumor suppressor of E-cadherin mediated contact inhibition

185
Q

Features of NF1 mutation

A

learning disability, seizures, skeletal deformities, arterial stenosis, pigmented iris, pigmented skin lesions (axillary freckling and cafe au lait spots)

Wrap Up (11 decks)

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