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Pathology > CNS > Flashcards

CNS Flashcards

1
Q

Order the neural tube defects In range of severity (mildest to most severe)

A

spina bifida occulta, meningocele, meningomyelocele, rachischisis

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2
Q

what’s the consequence of exposing the spinal canal in meningomyelocele?

A

Nerve roots become entrapped

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3
Q

What’s absent in holoprosencephaly? Is brain micro or macro cephalic?

A

Interhemispheric fissure; micro

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4
Q

When there is atresia of the aqueduct of sylvius, what findings are expected on a histologic exam of the midbrain?

A

Atretic channels or an aqueduct narrowed by gliosis

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5
Q

How much CSF is produced per day? Map out its flow

A

500 mL ; flows from its intraventricular origin to sites of reabsorption, principally through the arachnoid villi, into the dural sinuses.

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6
Q

What is transported in CNS? What CSF function is this related to?

A

Metabolites ; It serves as a medium for clearing metabolic waste. (irrelevant function: cushions”

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7
Q

Lissencephaly

A

congenital disorder in which the cortical surface of the cerebral hemispheres is smooth or has imperfectly formed gyri

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8
Q

Polymicrogyria

A

a congenital disorder in which the surface of the brain exhibits an excessive number of small, irregularly sized, randomly distributed gyral folds

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9
Q

Arrihnencephaly

A

absence of the olfactory tracts

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10
Q

Pachygyria

A

reduced number of gyri, usually broad

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11
Q

What chromosome abnormality is associated with holoprosencephaly?

A

Trisomies of chromosome 13-15 (rarely compatible with life beyond a few weeks to monnths)

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12
Q

Pathology of Tabes dorsales

A

posterior root of the spinal cord is constricted by chronic fibrosing meningitis from tertiary syphillis. Compression causes pain in extremities and impairs transmission of proprioceptive impulses

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13
Q

Usual lethal outcome of Alzheimer’s Disease

A

Bronchopneumonia

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14
Q

CJD has followed the administration of what substances?

A

Contaminated human pituitary Growth Hormone, Corneal Transplantation from a diseased donor, Insufficiently Sterilized Neurosurgical Instruments, and Surgical implanation of contaminated dura. (Spongiform encephalapothies are transmissable)

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15
Q

Prion proteins are normally found in what part of the cell?

A

Plasma Membrane. PrP (Prion gene product) is constitutively expressed and is a cell-surface glucoprotiend bound to the PM by a glycolipid anchor.

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16
Q

Hydrocephalus ex vacuo

A

enlargement of the ventricular system as a compensatory response to severe B/L symmetric brain atrophy unrelated to obstructive lesions.

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17
Q

In HD, what region of the brain is deteriorated?

A

The frontal cortex and the caudate nuclei. The FC is symmetrically and moderately atrophic; the caudate nucleus convex curvature is lost (causing enlargement of the lateral ventricles)

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18
Q

What chemicals are reduced in HD?

A

GABA and Glutamic acid decarboxylase (GAD- enzyme that catalyzes the decarboxylation of glutamate to GABA )

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19
Q

The Triplet Repeat Mutation Disorders (aka Trinucleotide Repeat Expansion Syndromes)

A

HD, Fragile X Syndrome, Friedreich Ataxia

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20
Q

Where is Frataxin most expressed?

A

Heart and Spinal Chord

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21
Q

What are common symptoms and systemic abnormalities seen in Friedrich’s Ataxia?

A

Dysarthria, Lower-limb areflexia, extensor plantar reflexies, sensory loss; Systemic Abnormalities: Scoliosis, DM, Hypertrophic Cardiomyopathy (causes death)

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22
Q

MS symptoms

A

sensory/motor deficits, sphincter weakness, tremosrs, loss of VF, blindness in 1 eye, diplopia, urinary incontinence, sexual dysfunction, bowel issues

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23
Q

MS end-stage lesions are featured by what findings?

A

Astrogliosis, thick-walled blood vessels, moderate perivascular inflammation, and a secondary loss of axons.

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24
Q

Where are Negri bodies found?

A

Rabies

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25
Q

What diseases are associated with whorled “myelin figures”

A

lysosomal storage of unmetabolized gangliosides in the nuerons of patients with Tay-Sachs

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26
Q

PD clinical features

A

Tremors at Rest, Muscular Rigidity, Expressionless Countenance, Emotional Liability, sometimes cognitive impairment late in the course

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27
Q

Although most Parkinsons cases are idiiopathic, what are some other primary causes (preceding illness)?

A

Viral encephalitis (von Economo encephalitis) and after intake of the toxic chemical methyl-phenyl-tetrahydropyridine

28
Q

What are pathologic features of Rabies encephalitis?

A

Perivascular cuffing by lymphocytes, neuronophagia, microglial nodules, and “Negri bodies”

29
Q

Councilman bodies

A

remnants of apoptotic hepatocytes seen in acute viral hepatitis

30
Q

What is a lethal cause of systemic dehydration?

A

Venous sinus thrombosis in brain which can lead to B/L hemorrrhagic infarctionso f the frontal lobe due to the venous obstruction / stagnation upstream to thrombosis of the sagittal sinus

31
Q

Gitter Cell

A

microglio cells that in response to necrosis become phagocytic, accumulate lipids and other cellular debris

32
Q

Rod Cells

A

Microglia that develop elongated nuclei

33
Q

What neurons would be experience functional paralysis due to a blow that deflects the head upward and posteriorly, often with a rotary component?

A

Neurons of the reticular formation

34
Q

What prevents lateral movement of the cerebral hemispheres (such as a blow to the temporoparietyal area that doesn’t cause a concussion)?

A

Falx

35
Q

Kernig Sign

A

Classic sign of meningitis : knee pain with hip flexion

36
Q

Brudzinski sign

A

Classic sign of meningitis: knee/hip flexion when the neck is flexed

37
Q

What immunoglobulins are needed for neutralization

A

IgM

38
Q

TORCH syndrome

A

Fetal or neonatal infection symptoms from Toxoplasmosa, Rubella, CMV, HSV and Other (Syphillis, VZV, Parvovirus, HIV) . Symptoms include CNS LESIONS (encephalitis w/ necrosis and calcification, micro/hydro/porencecephaly , microgyria, missing olfactory bulbs), also: OCULAR defects, CARDIAC anomalies

39
Q

How are CMV particles demonstrated in neurons and astrocytes

A

Intranuclear and intracytoplasmic inclusions

40
Q

How does hydrocephalus develop in CMV induced encephalitis?

A

lesions iin embryonic CNS predominate in the periventricular areas near third ventricle and the aqueduct and leads to hydrocephalus

41
Q

What are some key characteristics of crytococcus?

A

They reproduce by budding. They are opportunistic. They are visible with India Ink ( you see clear halos about the encapsulated organism)

42
Q

How does a Berry Aneurysm form?

A

It’s a Congenital Defect that develops during embryogenesis. The blood vessel when forming may fail to interdigitate at a bifurcation branch point causing a congential muscular weakness bridged only by endothelium, the int elastic membrane, and a thin adventitia.

43
Q

What are the most likely areas to find a Berry Aneurysm?

A

Circle of Willis, Junction of 1. anterior cerebral and ant.. Communicating arteris, 2. Int. Carotid- Post. Communicating-ant cerebral-anteriar choroidal arteries, 3. Trifurcation of the MCA

44
Q

Apoplexy

A

Cerebral hemmorrhage causes stroke

45
Q

What causes necrosis of pyramidal neurons of Sommer’s sector in the hippocampus?

A

Global Anoxia

46
Q

In the CNS, which cells are infected by HIV? What is the consequence of their infection?

A

Macrophages and Microglial cells; Macrophages release cytokines or other neurotoxic factors that injure strocytes and neurons. Most common clinical manifesation of AIDS encephalopathy, ranges from mild to severe cognitive impairment, with paralysis and loss of sensory functions.

47
Q

Which patient population is more likely to get JC virus induced PML?

A

Immunosuppressed such as those treated for cancer or Lupus Erythematosus, Organ transplant patiens, and persons with AIDS.

48
Q

What do Adrenoleukodystrophy, Gaucher disease, and Metachromatic leukodystrophy have in common?

A

They are inborn errors of metabolism.

49
Q

What are the key features and outcomes of inadequately treated TB meningitis?

A

TB meningitis is more often seen at the base of the brain. TB meningitis whn not treated is prone to infarction of the brain due to arteritis and also meningeal fibbrosis and communoicating hydrocephalus.

50
Q

What clinical manifestations are associated with central pontine myelinolysis?

A

Quadriparesis, pseudobulbar palsy, severe depression of consciousness (pseudocoma)

51
Q

Which nuerons are especially sensitive to a lack of oxygen?

A

Cerebellar Purkinje cells, Hippocampus’ pyramidal neurons of Sommer’s sector

52
Q

What kind of emboli occlude capillaries?

A

Samll, especiallly those composed of fat or air

53
Q

How do petechiae develop in the white matter?

A

When capillaries become hypoxic and permeable, petechiae develop

54
Q

Which motor neurons are affected in ALS?

A
  1. Anterior horn cells (SC) 2. Motor Nuclei (Brainstem) 3. UMNs (cerebral cortex)
55
Q

What is defining histologic change in ALS?

A

Loss of large motor neurons accompanied by mild gliosis

56
Q

What is the beginning clinical manifestations of ALS?

A

Weakness and wasting of the hand muscles

57
Q

What are the main findings in Alexander disease?

A

GFAP mutation leading to aggregates of fibrous structures

58
Q

How is hepatic encephalopathy manifested clinically? Morphologically?

A

As delirium, seizures, and coma; altered astroglia (Alzheimer Type II Astrocytes)

59
Q

Characterize the cells of medulloblastomas?

A

small, hyperchromatic cells, and rare neuroblastic rosettes

60
Q

What are the most common sites for a Meningioma?

A

parasagittal regions of the cerebral hemispheres, the olfactory groove and the lateral spheroid wing..

61
Q

Where do Craniopharyngiomas originate>?

A

Rathke Pouch epithelium- from the embryonic nasopharynx which becomes the anterior lobe of the hypophysis.

62
Q

What symptoms are first seen in craniopharyngiomas?

A

Visual deficits and headaches. Later, pituitary failure including DI may occur

63
Q

Where are Craniopharyngiomas located?

A

Above the sell turcica

64
Q

What are Kayser-Fleischer rings?

A

Ocular Lesions that represent deposition of copper in Descement membrane in the iris

65
Q

Neurofibromatosis Type 2

A

A syndrome defined by B/L tumors of CN8 (Acoustic Neuromas= Intracranial schwannomas restricted to CN8) and commonly by meningiomas and gliomas

Pathology (30 decks)

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