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XXIII - The Nervous System Flashcards

1
Q

Acute hypoxic/ischemic injury(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 860

A

This pattern of neuronal cell injury leads to shrunken individual cell bodies and nuclei. They are prominently stained by eosin, leading to the term “red neurons.” SEE SLIDE 23.1.

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2
Q

Corpora amylacea (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

A

These are round, faintly basophilic, PAS-positive, concentrically lamellated aggregates of polyglucosans that range between 5 and 50 micrometers, and are located wherever there are astrocytic end processes, especially in the subpial and perivascular zones, seen more frequently with advancing age. SEE SLIDE 23.2.

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3
Q

Oligodendrocytes (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

A

Cells which produce myelin in the CNS.

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4
Q

Ependymal cells (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

A

Cells which line the ventricles, and are located in the region of the obliterated central canal of the spinal cord.

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5
Q

Choroid plexus (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

A

These are responsible for the secretion of CSF. It has a specialized epithelial covering with a fibrovascular stroma that may contain meningothelial cells.

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6
Q

Microglia (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

A

These are bone marrow-derived cells that function as the phagocytes of the CNS.

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7
Q

Cerebral Edema (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

A

It is the accumulation of excess fluid within the brain parenchyma. The brain is softer than normal and often appears to “overfill” the cranial vault. In generalized edema the gyri are flattened, the intervening sulci are narrowed, and the ventricular cavities are compressed.

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8
Q

Vasogenic edema (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

A

This occurs when the integrity of the normal blood-brain barrier is disrupted. With increased vascular permeability, fluid shifts from the vascular compartment into the intercellular spaces of the brain.

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9
Q

Cytotoxic edema(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

A

This is due to an increase in intracellular fluid secondary to neuronal, glial, or endothelial cell membrane injury, as might be encountered in an individual with a generalized hypoxic/ischemic insult or with exposure to some toxins.

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10
Q

Noncommunicating hydrocephalus (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

A

Refers to the accumulation of CSF leading to dilation of the ventricular system which resulted from an obstacle or disruption of flow seen most commonly at the foramen of Monroe or aqueduct of Sylvius.

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11
Q

Communicating hydrocephalus (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

A

Refers to the accumulation of CSF leading to dilation of the ventricular system due to reduced resorption of CSF. All of the ventricular system is enlarged.

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12
Q

Hydrocephalus ex vacuo (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

A

This refers to dilation of the ventricular system with a compensatory increase in CSF volume secondary to a loss of brain parenchyma, as may occur after infarcts or with a degenerative disease.

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13
Q

Subfalcine (cingulate) herniation(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

A

This ccurs when unilateral or asymmetric expansion of a cerebral hemisphere displaces the cingulate gyrus under the edge of falx. This may be associated with compression of branches of the anterior cerebral artery.

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14
Q

Transtentorial (uncinate) herniation (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

A

This occurs when the medial aspect of the temporal lobe is compressed against the free margin of the tentorium. As the temporal lobe is displaced, the third cranial nerve is compromised, resulting in pupillary dilation and impairment of ocular movements on the side of the lesion (“blown pupil”).

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15
Q

Tonsillar herniation (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

A

This refers to displacement of the cerebellar tonsils through the foramen magnum. This pattern of herniation is life-threatening, because it causes brain stem compression and compromises vital respiratory and cardiac centers in the medulla.

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16
Q

Duret hemorrhages(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

A

These linear or flame-shaped lesions usually occur in the midline and paramedian regions, which are hemorrhagic lesions that accompany transtentorial herniation. Presence of these lesion implies poor prognosis.

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17
Q

Global Cerebral Ischemia (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 863

A

In the setting of this condition, the brain is swollen, with wide gyri and narrowed sulci. The cut surface shows poor demarcation between gray and white matter. Results from generalized reduction of cerebral perfusion, usually below systolic pressures of less than 50mmHg.

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18
Q

Border zone (“watershed”) infarcts. Most at risk: border zone between anterior and middle cerebral artery. (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1264

A

These are wedge-shaped areas of infarction that occur in those regions of the brain and spinal cord that lie at the most distal fields of arterial perfusion. Usually seen after hypotensive episodes.

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19
Q

Liquefaction necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 863

A

Pattern of necrosis seen in nonhemorrhagic infarcts of the brain.

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20
Q

Saccular (berry) aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 866

A

The most frequent cause of subarachnoid hemorrhage. It is a thin-walled outpouching of an artery. At the neck of the aneurysm, the muscular wall and intimal elastic lamina stop short and are absent from the aneurysm sac itself; the sac is made up of thickened hyalinized intima. The adventitia covering the sac is continuous with that of the parent artery

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21
Q

Subarachnoid Hemorrhage (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 866

A

Patients with this type of intracranial hemorrhage complains of having “the worst headache I’ve ever had”/ thunderclap headache.

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22
Q

Anterior communicating artery in the Circle of WIllis (40%)(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 867

A

Most common location for berry/saccular aneurysms.

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23
Q

Cerebral amyloid angiopathy (CAA) (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 863

A

This is a disease in which amyloidogenic peptides are deposit in the walls of medium- and small-caliber meningeal and cortical vessels, which results in the weakening of the vessel wall and increases the risk of hemorrhage.

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24
Q

Lobar hemorrhages(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 863

A

Hemorrhages associated with cerebral amyloid angiopathy (CAA) due to involvement of the cerebral hemispheres?

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25
Q

Venous angiomas (varices) (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 868

A

A type of vascular malformation which are characterized by of ectatic venous channels.

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26
Q

Anterior communicating artery in the Circle of WIllis (40%)(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 867

A

Most common location for berry aneurysms.

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27
Q

Arteriovenous malformations (AVM)(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 868

A

The involved vessels in this condition resemble a tangled network of wormlike vascular channels. Microscopically, they are enlarged blood vessels separated by gliotic tissue, often with evidence of prior hemorrhage.

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28
Q

Capillary telangiectasias(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 868

A

A type of vascular malformation which are characterized by microscopic foci of dilated, thin-walled vascular channels separated by relatively normal brain parenchyma and occurring most frequently in the pons.

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29
Q

Charcot-Bouchard microaneurysms (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 868

A

Minute aneurysms in vessels that are less than 300 micrometers in diameter, associated with chronic hypertension.

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30
Q

Epidural Hematoma. SEE SLIDE 23.3. (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 870

A

This leads to accumulation of arterial blood between the dura and the skull. The expanding hematoma has a smooth inner contour that compresses the brain surface. Clinically, patients may experience a lucid interval between the moment of trauma and development of neurologic symptoms.

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31
Q

Primary angiitis of the CNS (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 868

A

This is an inflammatory disorder that involves multiple small to medium-sized parenchymal and subarachnoid vessels and is characterized by chronic inflammation, multinucleated giant cells and destruction of the vessel wall. Affected individuals manifest a diffuse encephalopathic clinical picture, often with cognitive dysfunction; improvement occurs with steroid and immunosuppressive treatment.

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32
Q

Concussion(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 869

A

This describes reversible altered consciousness from head injury in the absence of contusion. The characteristic transient neurologic dysfunction includes loss of consciousness, temporary respiratory arrest, and loss of reflexes.

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33
Q

Contrecoup injury(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 868

A

Injury which may occur from collision of the brain with the skull opposite the site of impact.

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34
Q

Contusions(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 868

A

These are wedge shaped lesions of the brain parenchyma which occur secondary to trauma. The broad base of the wedge spans the surface and centered on the point of impact.

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35
Q

Middle meningeal artery(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 870

A

Blood vessel involved in epidural hematoma.

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36
Q

Bridging veins(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 870

A

Blood vessels involved in subdural hemorrhage.

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37
Q

Myelomeningocele. SEE SLIDE 23.4. (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 872

A

This is an extension of CNS tissue through a defect in the vertebral column, most commonly in the lumbosacral region. both The meninges and spinal cord parenchyma are included in the cystlike structure visible just above the buttocks.

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38
Q

Meningocoele. SEE SLIDE 23.4. (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 872

A

Herniation of the meninges through a defect in the vertebral column.

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39
Q

Anencephaly. SEE SLIDE 23.5. (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 872

A

This is a malformation of the anterior end of the neural tube, with absence of the brain and top of skull.

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40
Q

Encephalocele. SEE SLIDE 23.5. (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 872

A

This is a diverticulum of malformed CNS tissue extending through a defect in the cranium. It most often involves the occipital region or the posterior fossa.

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41
Q

Polymicrogyria(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 872

A

Characterized by an increased number of irregularly formed gyri that result in an irregular bumpy or cobblestone-like surface.

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42
Q

Holoprosencephaly (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 872

A

Characterized by a disruption of the normal midline patterning. In severe forms the brain is not divided into hemispheres or lobes and may be associated with facial midline defects like cyclopia.

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43
Q

Arnold-Chiari malformation Type II(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 872

A

Consists of a small posterior fossa and a misshapen midline cerebellum with downward extension of vermis through the foramen magnum; hydrocephalus and a lumbar myelomeningocele are typically also present.

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44
Q

Arnold-Chiari malformation type I(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 872

A

Consists of low-lying cerebellar tonsils which extend through the foramen magnum at the base of the skull. This can lead to obstruction of CSF flow and compression of the medulla, resulting in symptoms of headache or cranial nerve deficits.

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45
Q

Dandy-Walker malformation (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 872

A

Cerebral malformation characterized by an enlarged posterior fossa. The cerebellar vermis is absent, and replaced by a large, midline cyst that is lined by ependyma and is contiguous with leptomeninges on its outer surface. SEE SLIDE 23.6.

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46
Q

Hydromyelia(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 873

A

Spinal cord abnormality characterized by a discontinuous or confluent expansion of the ependyma-lined central canal of the cord.

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47
Q

Increased pressureabundant neurophilsprotein - elevatedglucose - reduced(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 874

A

CSF findings in bacterial meningitis.

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48
Q

Meningitis (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 874

A

This is an inflammatory process of the leptomeninges and CSF within the subarachnoid space.

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49
Q

Acute meningitis(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 874

A

In acute cases of this condition, an exudate is evident within the leptomeninges over the surface of the brain. On microscopic examination, neutrophils fill the entire subarachnoid space in severely affected areas or may be found predominantly around the leptomeningeal blood vessels.

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50
Q

Tabes dorsalis (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 875

A

A form of neurosyphilis, resulting from damage to the sensory nerves in the dorsal roots producing impaired joint position sense and resultant ataxia, loss of pain sensation, leading to skin and “Charcot joints” (deformed bones). There is loss of both axons and myelin in the dorsal roots, with pallor and atrophy in the dorsal columns of the spinal cord.

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51
Q

Tuberculous meningitis (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 874

A

Presents with generalized symptoms of headache, malaise, mental confusion, and vomiting. The subarachnoid space contains a gelatinous or fibrinous exudate, most often at the base of the brain, obliterating the cisterns and encasing cranial nerves. There may be discrete white granules scattered over the leptomeninges. Obliterative endarteritis may be seen.

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52
Q

Moderate pleiocytosis - predominantly monocytesprotein - elevatedglucose - moderately reduced/normal(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 874

A

CSF findings in tuberculous meningitis.

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53
Q

Paretic neurosyphilis (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 874

A

Caused by invasion of the brain by Treponema pallidum and manifests as insidious but progressive loss of mental and physical functions with mood alterations (including delusions of grandeur), terminating in severe dementia.

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54
Q

Cytomegalovirus (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 877

A

This virus tends to localize in the paraventricular subependymal regions of the brain, which results in a severe hemorrhagic necrotizing ventriculoencephalitis and choroid plexitis.

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55
Q

Brain Abscesses (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 876

A

These are discrete lesions with central liquefactive necrosis and a surrounding fibrous capsule. On microscopic examination, there is exuberant neovascularization around the necrosis that is responsible for the marked edema and formation of granulation tissue. Outside the fibrous capsule is a zone of reactive gliosis.

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56
Q

Creutzfeldt-Jakob Disease (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 880

A

The pathognomonic finding of this disease is a spongiform transformation of the cerebral cortex and deep gray matter structures (caudate, putamen); consists of a multifocal process that results in the uneven formation of small, empty, microscopic vacuoles of varying sizes within the neuropil and sometimes in the perikaryon of neurons. SEE SLIDE 23.7.

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57
Q

Herpes Encephalitis(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 876

A

Viral encephalitis which involves inferior and medial regions of the temporal lobes and the orbital gyri of the frontal lobes. Perivascular inflammatory infiltrates are usually present, and Cowdry type A intranuclear viral inclusion bodies can be found in both neurons and glia. SEE SLIDE 23.8.

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58
Q

Shingles / Herpes Zoster(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 876

A

Reactivation of varicella in adults manifests as a painful, vesicular skin eruption in the distribution of one or a few dermatomes.

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59
Q

Progressive Multifocal Leukoencephalopathy (PML) (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 877

A

This lesion caused by JC virus, consist of patches of irregular, ill-defined destruction of the white matter that enlarge. Each lesion is an area of demyelination, in the center of which are scattered lipid-laden macrophages and a reduced number of axons.

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60
Q

Meningiomas(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 885

A

These are predominantly benign tumors of adults, usually attached to the dura, and arising from the meningothelial cell of the arachnoid. Histologic patterns include syncitial, fibroblastic, psammomatous (SEE SLIDE 23.9), secretory and microcystic.

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61
Q

LungBreastSkin (melanoma)KidneyGIT(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 885

A

Five most common primary sites of carcinoma which may metastasize to the brain.

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62
Q

Oligodendrogliomas(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 883

A

These are infiltrative tumors that form gelatinous, gray masses, and may show cysts, focal hemorrhage, and calcification. On microscopic examination, the tumor is composed of sheets of regular cells with spherical nuclei containing finely granular chromatin (similar to normal oligodendrocytes) surrounded by a clear halo of cytoplasm. SEE SLIDE 23.10

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63
Q

Central pontine myelinolysis (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 889

A

A nonimmune process characterized by loss of myelin involving the center of the pons, most often after rapid correction of hyponatremia.

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64
Q

Leukodystrophies (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 889

A

These are inherited dysmyelinating diseases in which the clinical symptoms derive from either abnormal myelin synthesis or turnover.

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65
Q

Korsakoff syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 890

A

Profound memory disturbances as a result of thiamine deficiency.

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66
Q

Multiple Sclerosis (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 887

A

An autoimmune demyelinating disorder characterized by distinct episodes of neurologic deficits, separated in time, attributable to white matter lesions that are separated in space. Affected areas show multiple, well-circumscribed, slightly depressed, glassy, gray-tan, irregularly shaped lesions, termed “plaques”.

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67
Q

Wernicke encephalopathy(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 890

A

This condition occurs in the setting of thiamine deficiency and chronic alcoholism. Characterized by foci of hemorrhage and necrosis, particularly in the mammillary bodies but also adjacent to the ventricle, especially the third and fourth ventricles.

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68
Q

Hepatic encephalopathy (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 891

A

Characterized by “flapping” tremor, depressed levels of consciousness, which may lead to coma. Result of decreased hepatic function.

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69
Q

Alzheimer’s disease(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 893

A

It is the most common cause of dementia in the elderly, characterized by presence of plaques and neurofibrillary tangles, composed of tau proteins. SEE SLIDE 23.11.

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70
Q

GAA trinucleotide repeat (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 895

A

Mutation in Friedreich ataxia.

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71
Q

Parkinson disease (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 894

A

This is a clinical syndrome characterized by masked facies, stooped posture, slowness of voluntary movement, festinating gait rigidity, and a “pill-rolling” tremor. There are single or multiple, intracytoplasmic, eosinophilic, round to elongated inclusions that often have a dense core surrounded by a pale halo or “Lewy bodies”. SEE SLIDE 23.12.

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72
Q

Huntington Disease (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 894

A

It is an inherited autosomal dominant disease characterized clinically by progressive movement disorders and dementia, with degeneration of the striatum (caudate and putamen).

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73
Q

CAG trinucleotide repeats(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 895

A

Mutation in Huntington disease.

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74
Q

Friedreich ataxia (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 895

A

It is an autosomal recessive progressive illness, generally beginning in the first decade of life with gait ataxia, followed by hand clumsiness and dysarthria.

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75
Q

Amyotrophic Lateral Sclerosis (Motor Neuron Disease; Lou Gehrig’s Disease) (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 895

A

This is the most common form of neurodegeneration affecting the motor system. It is characterized by muscle atrophy and hypereflexia due to loss of both upper and lower motor neurons.

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76
Q

Guillain-Barre Syndrome (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 899

A

This is one of the most common life-threatening diseases of the peripheral nervous system. It may develop spontaneously or after a systemic infection (usually viral) or other stress. Usually presents with rapidly progressive, ascending motor weakness that may lead to death from failure of respiratory muscles.

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77
Q

Schwannomas (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 899

A

These are benign tumors arising from Schwann cells, which are well-circumscribed encapsulated, firm, gray masses but may also have areas of cystic and xanthomatous change.

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78
Q

Cutaneous neurofibroma. SEE SLIDE 23.13. (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 899

A

Present in the dermis and subcutaneous fat, these well-delineated but unencapsulated masses are composed of spindle cells. The stroma of these tumors is highly collagenized and contains little myxoid material.

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79
Q

Plexiform neurofibroma. SEE SLIDE 23.13. (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 899

A

These tumors may arise anywhere along a nerve, may be multiple, and is not easily separated from the nerve.

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80
Q

Type 1 Neurofibromatosis (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 901

A

This autosomal dominant disorder is characterized by neurofibromas (plexiform and solitary), gliomas of the optic nerve, pigmented nodules of the iris (Lisch nodules), and cutaneous hyperpigmented macules (cafe au lait spots).

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81
Q

Type 2 Neurofibromatosis (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 901

A

This is an autosomal dominant disorder in which patients develop a range of tumors, most commonly bilateral vestibular (acoustic) schwannomas and multiple meningiomas.

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82
Q

Tuberous Sclerosis (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 901

A

An autosomal dominant syndrome characterized by the development of hamartomas and benign neoplasms involving the brain and other tissues. The lesions are firm areas of the cortex that, in contrast to the softer adjacent cortex, have been likened to potatoes, hence the appellation “tubers.” SEE SLIDE 23.14.

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83
Q

von Hippel-Lindau Disease (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 901

A

An autosomal dominant inherited disease in characterized by development of hemangioblastomas within the cerebellar hemispheres, retina, and less commonly the brain stem and spinal cord. A cerebellar capillary hemangioblastoma, is the principal neurologic manifestation of the disease.

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84
Q

Inflammation of peripheral nerve, manifested as perivenular and endoneurial infiltration by lymphocytes, macrophages, and a few plasma cells. SEE SLIDE 23.15. (TOPNOTCH)

A

What is the dominant histopathologic finding in Immune mediated neuropathies like Guillain- Barre Syndrome?

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85
Q

Symmetric neuropathy that involves distal sensory and motor nerves (TOPNOTCH)

A

What is the most common type of peripheral neuropathy seen in adult-onset DM?

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86
Q

Axonal neuropathy (TOPNOTCH)

A

In patients with peripheral neuropathy, what is the predominant histologic findings?

87
Q

Dermatomyositis. SEE SLIDE 23.16. (TOPNOTCH)

A

Morphology: Perifascicular Atrophy

88
Q

Inclusion body myositis (TOPNOTCH)

A

Morphology: presence of rimmed vacuoles within myocytes and are highlighted by basophilic granules at their periphery. In addition, the vacuolated fibers may also contain amyloid deposits that stain with Congo Red.

89
Q

Spinal Muscular Atrophy (Infantile Motor Neuron Disease. SEE SLIDE 23.17. (TOPNOTCH)

A

Morphology: Panfascicular atrophy

90
Q
  1. Variation in fiber diameter 2. Increased numbers of internalized nuclei 3. Degeneration, necrosis, and phagocytosis of muscle fibers 4. Regeneration of muscle fibers 5. Proliferation of endomysial connective tissue. SEE SLIDE 23.18 (TOPNOTCH)
A

What are the 5 histopathologic abnormalities common to Duchenne Muscular Dystrophy and Becker Muscular Dystrophy?

91
Q

Duchenne Muscle Dystrophy (TOPNOTCH)

A

Morphology: In later stages of this disease, all muscles eventually become almost totally replaced by fat and connective tissue

92
Q

Enlarged, rounded, hyaline fibers that have lost their normal cross striation, believed to be hypercontracted fibers (TOPNOTCH)

A

What is the histologic pathology that is usually seen in Duchene muscle dystrophy and is rare in Becker Muscle Dystrophy?

93
Q

Myotonic Dystrophy. SEE SLIDE 23.19 (TOPNOTCH)

A

Morphology: Ring fiber ( subsarcolemmal band of cytoplasm that appears distinct from the center of the fiber) and Sarcoplasmic mass

94
Q

Myasthenia Gravis (TOPNOTCH)

A

Morphology: Disuse changes with Type 2 fiber atrophy, post synaptic membrane is simplified, with loss of AChRs from the region of the synapse. Immune complexes as well as the MAC of the complement cascade can be found along the post synaptic membrane as well

95
Q

Inclusion body myositis (TOPNOTCH)

A

Electron Microscopy: tubular and filamentous inclusions are seen in the cytoplasm and the nucleus, and they are composed of B-amyloid or hyperphosphorylated tau.

96
Q

Dermatomyositis (TOPNOTCH)

A

Grotton lesions (scaling erythematous eruption or dusky red patches over the knuckles, elbows, and knees) are seen in what disease entity? SEE SLIDE 23.20.

97
Q

Mitochondrial Myopathies (Oxidative phosphorylation Disease) (TOPNOTCH)

A

Morphology: the most consistent pathologic findings in skeletal muscle are aggregates of abnormal mitochondria that stain with modified Gomori Trichrome and fiber appears irregular on cross section “ragged red fibers” and on electron microscope, they contain “parking lot inclusions” SEE SLIDE 23.21.

98
Q

Axonal degeneration (TOPNOTCH)

A

This is general reaction of the motor unit which is a result of primary destruction of the axon, with secondary disintegration of its myelin sheath.

99
Q

Segmental demyelination (TOPNOTCH)

A

This general reaction of the motor unit occurs when there is dysfunction of the Schwann cell or damage to the myelin sheath; there is no primary abnormality of the axon

100
Q

Peripheral Neuropathy in DM Type 2 (TOPNOTCH)

A

Morphology: Endoneurial arterioles show thickening, hyalinization, and intense PAS positivity in their walls and extensive reduplicaton of the basement membrane. SEE SLIDE 23.22

101
Q

Myotonic Dystrophy (TOPNOTCH)

A

Of all the dystrophies, this type is the only one that shows pathologic changes in the intrafusal fibers of muscle spindles, with fiber splitting, necrosis and regeneration.

102
Q

Lipid Myopathies (TOPNOTCH)

A

Morphology: the principal morphologic characteristic is accumulation of lipid within myocytes. The myofibrils are separated by vacuoles that stain with oil red O or Sudan black

103
Q

Small cell carcinoma of the lungs (TOPNOTCH)

A

Lambert Eaton Myasthenic Syndrome is a paraneoplastic process which commonly develops in what type of carcinoma?

104
Q

Gliosis(TOPNOTCH)

A

The most important histopathological indicator of CNS injury, regardless of etiology

105
Q

Myoclonic Epilepsy(TOPNOTCH)

A

Lafora bodies

106
Q

Spat-apoplexie (Delayed post traumatic hemorrhage) (TOPNOTCH)

A

A syndrome of sudden, deep intracerebral hemorrhage that follows even minor head trauma by an interval of 1-2 weeks

107
Q

48 hours(TOPNOTCH)

A

Subdural hematomas most often become manifest approximately how many hours after the injury?

108
Q

mechanical forces damage the integrity of the axon at the node of Ranvier, with subsequent alterations in axoplasmic flow(TOPNOTCH)

A

The most widely accepted explanation for diffuse axonal injury

109
Q

Diffuse axonal injury(TOPNOTCH)

A

Morphology: wide asymmetric distribution of axonal swellings that appear within hours of the injury and are best demonstrated with silver impregnation techniques or with immunoperoxidase stains for AB protein

110
Q

1 week(TOPNOTCH)

A

How long does it take for the clot to lyse in subdural hematomas?

111
Q

2 weeks(TOPNOTCH)

A

How long does it take for fibroblasts to grow from the dural surfaces into the hematoma after subdural hematoma/

112
Q

1-3 months(TOPNOTCH)

A

How long does it take for the development hyalinized connectice tissue in SDH

113
Q

12-24 hours(TOPNOTCH)

A

In the setting of global ischemia, early histological changes are seen after how many hours after the insult?

114
Q

24 hours to 2 weeks(TOPNOTCH)

A

In the setting of global ischemia, subacute changes are seen after how many hours after the insult?

115
Q

2 weeks(TOPNOTCH)

A

In the setting of global cerebral ischemia, repair is seen after approximately how many weeks?

116
Q

Repair(TOPNOTCH)

A

In the setting of global ischemia, this is characterized by eventual removal of all necrotic tissue, loss of normally organized CNS structure, and gliosis

117
Q

Subacute changes(TOPNOTCH)

A

In the setting of global ischemia, this is characterized by necrosis of tissue, influx of macrophages, vascular proliferation and reactive gliosis

118
Q

Early change(TOPNOTCH)

A

In the setting of global ischemiaThis is characterized by acute neuronal cell damage

119
Q

Poliomyelitis(TOPNOTCH)

A

Morphology: Mononuclear cell perivacular cuffs and neuronophagia of the anterior horn motor neurons of the spinal cord. SEE SLIDE 23.23.

120
Q

Subacute encephalitis(TOPNOTCH)

A

In the immunosuprressed individual, the most common pattern of involvement in viral meningitis is:

121
Q

Paraventricular subependymal regions(TOPNOTCH)

A

Although any type of cell within the CNS can be infected with CMV, the virus tends to localize at what particular area in the brain?

122
Q

Cerebellar capillary hemangioblastoma(TOPNOTCH)

A

What is the principal neurologic manifestation of Von Hippel Lindau Disease?

123
Q

Schwannoma. In Antoni A areas, cells align to produce nuclear palisading, with alternating bands of nuclear and anuclear areas called VEROCAY BODIES. (TOPNOTCH) Robbins Basic Pathology, 9th ed, p 807.

A

Antoni A and Antoni B patterns of growth are seen in what tumors of the CNS? SEE SLIDE 23.24.

124
Q

Glioblastoma multiforme(TOPNOTCH)

A

Morphology: Histologic appearance similar to anaplastic astrocytoma with the additional feature of necrosis and vascular or endothelial cell proliferation. SEE SLIDE 23.25

125
Q

Glioblastoma multiforme(TOPNOTCH)

A

Pseudopalisading. SEE SLIDE 23.25

126
Q

Glioblastoma multiforme(TOPNOTCH)

A

Glomeruloid body

127
Q

Medial dorsal nucleus of the thalamus(TOPNOTCH)

A

Lesion of what area of the brain appear to be the best correlate of the memory disturbance and confabulation seen in Korsakoff syndrome?

128
Q

Friedreich Ataxia(TOPNOTCH)

A

The spinal cord shows loss of axons and gliosis in the posterior columns, the distal portions of the corticospinal tracts, and the spinocerebellar tracts.

129
Q

Ataxia Telangiectasia(TOPNOTCH)

A

The abnormalities are predominantly in the cerebellum,with loss of Purkinje and granule cells; there is also degeneration of the dorsal columns, spinocerebellar tracts and anterior horn cells and a peripheral neuropathy

130
Q

Parkinson Disease(TOPNOTCH)

A

Gross morphology: pallor of the substantia nigra and locus ceruleus

131
Q

Pick Disease(TOPNOTCH)

A

Gross morphology: the brain shows pronounced, frequently asymmetric, atrophy of the frontal and temporal lobes with conspicuous sparing of the posterior two thirds of the superior temporal gyrus

132
Q

Neuritic/Senile PlaquesNeurofibrillary tanglesAmyloid angiopathy. SEE SLIDE 23.11. (TOPNOTCH)

A

What are the 3 major microscopic abnormalities of Alzheimer disease?

133
Q

Dementia(TOPNOTCH)

A

What is the principal clinical manifestation of Alzheimer disease?

134
Q

Alzheimer Disease(TOPNOTCH)

A

What is the most common cause of dementia in the elderly?

135
Q

Alzheimer Disease(TOPNOTCH)

A

Gross morphology: Variable degree of cortical atrophy with widening of the cerebral sulci that is most pronounced in the frontal, temporal, and parietal lobes with compensatory ventricular enlargement (hydrocephalus ex vacuo)

136
Q

AB peptide(TOPNOTCH)

A

Neurotic plaques are focal, spherical collection of dilated, tortuous, silver staining neuritic processes often around a central amyloid core, which may be surrounded by clear halo, and can be stained with Congo red. SEE SLIDE 23.11. What is the most predominant component of this plaque core?

137
Q

Tau proteins(TOPNOTCH)

A

Neurofibrillary tangles are bundles of filaments in the cytoplasm of the neurons that displace or encircle the nucleus. SEE SLIDE 23.11. What is the major component of this structure?

138
Q

Alzheimer’s disease (TOPNOTCH)

A

Hirano bodies. SEE SLIDE 23.11

139
Q

Cerebellar capillary hemangioblastoma(TOPNOTCH)

A

What is the principal neurologic manifestation of Von Hippel Lindau Disease?

140
Q

Renal Cell Carcinoma(TOPNOTCH)

A

Patients with Von Hippel Lindau Disease has the propensity to develop what type of carcinom?

141
Q

Cortical hamartomas or “tubers’ of Tuberous Sclerosis (TOPNOTCH)

A

These are firm areas of the cortex that, in contrast to the softer adjacent cortex, have been likened to potatoes and are composed of haphazardly arranged neurons that lack the normal laminar organization of neocortex.

142
Q

Neurofibromatosis Type 1(TOPNOTCH)

A

Malignant Peripheral Nerve Sheath Tumor (MPNST, Malignant Schwannoma) is strongly associated with what type of Familial Tumor Syndrome?

143
Q

Lung, breast, Melanoma, Kidney, and GIT. (TOPNOTCH)

A

What are the 5 most common carcinoma that metastasize to the brain?

144
Q

Primary CNS Lymphoma(TOPNOTCH)

A

What is the most common CNS neoplasm in immunosuppressed patients, including those with AIDS and immunosuppression after transplantaion?

145
Q

Well differentiated fibrillary astrocytomas(TOPNOTCH)

A

Morphology: Characterized by amild to moderate increase in the number of glial cell nuclei, somewhat variable nuclear pleomorphism, and an interveing feltwork of fine, GFAP positive astrocytic cell processes that give the background a fibrillary appearance.

146
Q

Ependymoma(TOPNOTCH)

A

Morphology: Perivascular pseudorosettes SEE SLIDE 23.26

147
Q

Amyotorphic Lateral Sclerosis(TOPNOTCH)

A

Morphology: The anterior roots of the spinal cord are thin; the precentral gyrus may be atrophic and demonstrates a reduction the number of anterior horn neurons throughout the length of the spinal cord with associated reactive gliosis. Remaining neurons often contain Bunina bdoies and PAS positive cytoplasmic inclusions.

148
Q

Pilocytic Astrocytoma (TOPNOTCH)

A

Morphology: composed of bipolar cells with long, thin “hairlike” processes that are GFAP- Positive; Rosenthal fibers, eosinophilic granular bodies, and microcysts are often present. SEE SLIDE 23.27.

149
Q

Desmoplastic variant of Medulloblastoma(TOPNOTCH)

A

Morphology: Characterized by areas of stromal response with collagen and reticulin deposition and nodules of cells forming “pale islands” that have more neuropil and lack the reticulin deposition

150
Q

Huntington Disease(TOPNOTCH)

A

Gross morphology: the brain is small and shows striking atrophy of the caudate nucleus and the putamen. The globus pallidus may be atrophied secondarily, and the lateral and third ventricles are dilated.

151
Q

Glioma and Meningioma (TOPNOTCH)

A

What are the two most common primary tumors of the optic nerve?

152
Q

Idiopathic orbital inflammation (TOPNOTCH)

A

Morphology: characterized histologically by chronic inflammation and replacement of orbital fat by fibrosis

153
Q

Basal cell carcinoma (TOPNOTCH)

A

What is the most common malignancy of the eyelid?

154
Q

Keratoconus (TOPNOTCH)

A

Morphology: histological hallmark is the thinning of the cornea with breaks in the Bowman’s layer

155
Q

Calcific Band keratopathy (TOPNOTCH)

A

Morphology: deposition of calcium in Bowmans layer

156
Q

Actinic band keratopathy (TOPNOTCH)

A

This type of keratopathy develops in patients who are exposed chronically to high levels of ultraviolet light

157
Q

Fuchs dystrophy (TOPNOTCH)

A

Morphology: numerous drop like excrescences - guttata- protrude downward from Descemet’s membrane

158
Q

Phthisis Bulbi (TOPNOTCH)

A

Also known as the End-Stage Eye

159
Q

Glaucomatous optic nerve damage (TOPNOTCH)

A

Morphology: diffuse loss of ganglion cells and thinning of the retinal nerve fiber layer, in advanced cases, the optic nerve is both cupped and atrophic

160
Q

Retinoblastoma (TOPNOTCH)

A

Flexner Wintersteiner Rosettes

161
Q

Age related macular degeneration (TOPNOTCH)

A

Morphology: A neovascular membrane is positioned between the retinal pigment epithelium and Bruchs membrane

162
Q

Retinitis Pigmentosa (TOPNOTCH)

A

“Waxy pallor” of the optic disk. SEE SLIDE 23.28

163
Q

Retinitis Pigmentosa (TOPNOTCH)

A

In this condition, both rods and cones are lost to apoptosis

164
Q

Malignant hypertension (TOPNOTCH)

A

Elschnig’ spots

165
Q

Thickening of the BM of the epithelium of the pars plicata of the ciliary body (TOPNOTCH)

A

What is known to be a reliable histological marker of diabetes mellitus in the eye?

166
Q

Hypertension (TOPNOTCH)

A

Cytoid bodies

167
Q

Malignant hypertension (TOPNOTCH)

A

Macular star

168
Q

Sympathetic ophthalmia (TOPNOTCH)

A

Morphology: Characterized by diffuse granulomatous inflammation of the urea. Plasma cells are typically absent, but eosiophils may be identified in the infiltrate

169
Q

Metastasis to the uvea, typically to the choroid (TOPNOTCH)

A

What is the most common intraocular malignancy in adults?

170
Q

Uveal melanoma (TOPNOTCH)

A

What is the most common primary intraocular malignancy in adults?

171
Q

Microglia (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1254

A

These are the resident monocyte-lineage population of CNS that proliferate and accumulate in response to injury.

172
Q

Anterior cerebral artery(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1255

A

Subfalcine(cingulate) herniation leads to compression of what blood vessel?

173
Q

CN III and Posterior Cerebral artery(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1255

A

Transtentoria(uncinate) herniation compress what structures?

174
Q

Transtentorial (uncinate) herniation/CN III compression (TOPNOTCH)

A

Patient X who had a moderate traumatic injury presented with lethargy. 12 hours later it he progressed rapidly to having dilated pupils and impairment of ocular movements. This is most likely due to:

175
Q

Lissencephaly(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1257

A

A malformation characterized by reduction in the number of gyri, agyria in extreme cases

176
Q

Perventricular leukomalacia(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1259

A

Infarcts in the supratentorial periventricular white matter in premature infants presenting with chalky yellow plaques consisting of discrete regions of white matter necrosis and calcification

177
Q

Frontal and temporal lobes(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1260

A

Most common site of contusions in the brain

178
Q

Subdural hematoma(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1262

A

Vascular injury presenting with slowly evolving neurologic symptoms, often with a delay from the time of injury(most often within 48 hours of injury) Grossly, it appears as a collection of freshly clotted blood along the brain surface, without extension into the depths of sulci.

179
Q

Above C4(TOPNOTCH)

A

After a vehicular crash, patient presented with quadriplegia and respiratory distress. Spinal cord injury was suspected. This can be due to damage to what level of vertebra?

180
Q

Neurons(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1264

A

CNS cells most sensitive to ischemia

181
Q

Acute hypertensive encephalopathy(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1268

A

Clinicopathologic syndrome arising in the setting of malignant hypertension, characterized by diffuse cerebral dysfunction, including headaches, confusion, voming, and convulsion, and sometimes leading to coma

182
Q

Hypertension(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1268

A

Risk factor most commonly associated with deep brain parenchymal hemorrhages.

183
Q

Neisseria meningitidis(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1272

A

Most common cause of bacterial meningitis in adolescents and young adults.

184
Q

Increased WBC, increased protein, normal glucose(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1273

A

Typical CSF findings in brain abscess

185
Q

Arachnoid fibrosis(producing hydrocephalus) and Obliterative endarteritis(causing arterial occlusion and infarction)(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1274

A

Most serious complications of chronic TB meningitis

186
Q

Viral Encephalitis(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1275

A

Morphology: perivascular accumulation or lymphocytes and/or neutrophils, multiple foci of necrosis of gray and white matter, single-cell neuronal necrosis with phagocytosis of debris, microglial nodules

187
Q

Toxoplasmosis of the CNS(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1280

A

It produces brain abscess, most ofen in the cerebral cortex and deep gray nuclei, central necrosis, petechial hemorrhages surrounded by acute and chronic inflammation, macrophage infiltration, and vascular proliferation; CT and MRI studies may show multiple ring enhancing lesions. SEE SLIDE 23.29.

188
Q

Plasmodium falciparum(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 1280

A

A rapidly progressive encephalitis, cerebral malaria, is the complication with the highest mortality caused by what etiologic agent?

189
Q

Temporal lobe(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1281

A

HSV-1 infection has predilection to what part of the brain?

190
Q

Prion diseases(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1281

A

This group of degenerative disorders is caused by “spreading” of misfolded proteins, allowing a pathogenic protein to acquire many of the characteristics of an infectious agent. Accumulation of PrPSC in neural tissue seems to the cause of pathologic changes in these diseases.

191
Q

Creutzfeldt-Jakob Disease (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1283

A

The most common prion disease that manifest clinically as a rapidly progressive dementia.

192
Q

Alzheimers Disease(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1288

A

The fundamental abnormality in this disease is the accumulation of A-beta and tau in specific brain regions.

193
Q

Kearns-Sayre syndrome(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1245

A

Syndrome caused by deletions in mitochondrial DNA, characterized by ophthalmoplegia, pigmentary degeneratation of the retina, and complete heart block

194
Q

Leigh syndrome(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1245

A

Mitochondrial disoder caused by mutations in either mtDNA or the nuclear genome causing subacute necrotizing encephalopathy

195
Q

hippocampus and cerebellum (TOPNOTCH) Robbins Pathologic Basis of Disease 8th ed

A

A 12 year old student presents with lethargy, fever, and headaches. These progress to irritability, anxiety, and confusion, with difficulty in swallowing. He refuses any drink being offered. A few days later, he slips into a coma, and dies. On history, he was bitten by a stray dog 4 months ago. At autopsy, where would the characteristic infected neurons with cytoplasmic inclusions most likely be found? (A) frontal and parietal cerebral cortex (B) hippocampus and cerebellum (C) globus pallidus and medulla (D) pineal gland and pituitary

196
Q

temporal lobes (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 876

A

A 19 year old male presents with fever and changes in mood and behavior. His neck is supple, and shows no lateralizing signs, or cranial nerve defects. Memory is impaired. A lumbar tap is performed with a slight lymphocytosis and protein elevation. Bacterial cultures were negative. On PCR, herpes simplex virus I was detected. THe histologic changes of necrotizing inflammation and Cowdry Type A bodies would most likely be found in (A) temporal lobes (B) occipital lobes (C) cerebellar vermis (D) parietal lobes

197
Q

amyloid (Alzheimer disease) (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 893

A

A 78 year old woman in a nursing home is found dead in her bed. She has had a 5 year history of progressive disorientation, memory loss, and alteration of mood and behavior. In her final year, she was mute and could not perform activities of daily living without assistance. Her relatives requested an autopsy, and her brain showed cortical atrophy with widening of the sulci. Histology showed multiple plaques and neurofibrillary tangles. The plaques are collections of neuritic processes with a central core of extracellular (A) amyloid (B) tau protein (C) glycogen (D) sphingomyelin

198
Q

loss of pigmented catecholaminergic neurons in his midbrain (pallor of substantia nigra in Parkinsonism) (B - Huntington disease; C - Wernicke encephalopathy; D - Lewy body dementia/disease) (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 893-894

A

A 45 year old actor begins to experience hand tremors, and eventually develops a shuffling gait, a stooped posture, and diminished facial expressions. His mental faculties are intact. What is the expected histologic change in his brain? (A) loss of pigmented catecholaminergic neurons in his midbrain (B) loss of neurons in the striatum (C) foci of hemorrhage and necrosis in the mamillary bodies (D) multiple Lewy bodies in his cerebral cortex

199
Q

her kidney disease is heritable, in an autosomal dominant fashion (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 569-570, 866-867

A

A 30 year old saleslady has untreated hypertension. While at work, her colleagues heard her complain of an excruciating headache then lose consciousness a few seconds later. She was pronounced dead at the ER. An autopsy is performed, which showed massive subarachnoid hemorrhage, and a ruptured aneurysm at the right anterior cerebral artery. Her kidneys were markedly enlarged, with multiple 3-4 cm diameter cysts. Which of the following is accurate? (A) the aneurysm is neoplastic (B) the aneurysm was likely present at birth (C) her kidney disease is heritable, in an autosomal dominant fashion (D) her kidney disease more commonly manifests in early childhood

200
Q

raw pork (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 880

A

A 26 year old backpacker presents with seizures. On imaging, there are four 1-2 cm cysts in his cerebral cortex. He undergoes surgery, where two were removed. Histopathology showed an ovoid structure with a tegument, underlying smooth muscle, three oval suckers, all surrounded by an intense inflammmatory infiltrate of plasma cells, lymphocytes, and eosinophils. The surrounding brain tissue is gliotic. The patient acquired this infection by ingesting (A) raw pork (B) raw beef (C) ova from cat litter (D) raw freshwater crabs

201
Q

a meningioma (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 886

A

A 33 year old woman has been having intermittent headache for 3 years. She develops a seizure. Imaging studies show a 4 cm well circumscribed intracranial mass at the convexity of the right cerebral cortex, compressing the adjacent brain. The tumor is surgically excised, and histopathology showed cells in syncytial whorls, some in fascicles. There are occasional concentric calcifications interspersed. There is no significant mitosis, necrosis, pleomorphism, or brain invasion. Her tumor is (A) a metastasis from a thyroid primary (B) a primary lymphoma (C) a glioma (D) a meningioma

202
Q

all of the above (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 882

A

A 40 year old lawyer presents with seizures and loss of consciousness. On imaging, there is a contrast-enhancing, intracranial mass straddling the corpus callosum, with a “butterfly” appearance. An open biopsy is performed, which showed a densely cellular tumor of with astrocytic cell processes, foci of necrosis with surrounding pseudo-palisading of tumor cell nuclei, vascular proliferation, and numerous mitoses. His tumor (A) is a glioma (B) is poorly circumscribed (C) confers a dire prognosis (D) all of the above

203
Q

Astrocytes. When activated, they enlarge and develop multiple stout, ramifying processes (Gemistocytic astrocyte). In long-standing gliosis, they begin to shrink, with cellular processes becoming more tighly interwoven (Fibrillary astrocyte with Rosenthal fibers) (TOPNOTCH)Robbins Basic Pathology, 9th ed., p 812

A

Principal cells that are responsible for repair and scar formation in the brain (Gliosis)

204
Q

Rosenthal fibers (TOPNOTCH)Robbins Basic Pathology, 9th ed., p 812

A

Thick, elongated, brightly eosinophilic protein aggregates seen in astrocytic processes in CHRONIC GLIOSIS and in some LOW-GRADE GLIOMAS. SEE SLIDE 23.27.

205
Q

Acute. 12-24 hours. (TOPNOTCH)Robbins Basic Pathology, 9th ed., p 815

A

Irreversible ischemic injury category (Early, Subacute, or Repair): Red neurons

206
Q

Subacute. 24 hours to 2 weeks. (TOPNOTCH)Robbins Basic Pathology, 9th ed., p 815

A

Irreversible ischemic injury category (Early, Subacute, or Repair): Necrosis, influx of macrophages, reactive gliosis

207
Q

Repair. More than 2 weeks. (TOPNOTCH)Robbins Basic Pathology, 9th ed., p 815

A

Irreversible ischemic injury category (Early, Subacute, or Repair): Removal of necrotic tissue, gliosis (pseudolaminar necrosis)

208
Q

Alpha-Synuclein. An inclusion containing alpha-synuclein is called a LEWY BODY. (TOPNOTCH)Robbins Basic Pathology, 9th ed., p 836

A

Protein inclusion seen in Parkinson disease

209
Q

Beta amyloid and Tau protein(TOPNOTCH)Robbins Basic Pathology, 9th ed., p 836

A

Protein inclusion seen in Alzheimer disease

210
Q

Plaque. SEE SLIDE 23.11. (TOPNOTCH)Robbins Basic Pathology, 9th ed., p 838

A

Alzheimer-related lesions. PLAQUE, TANGLE or TAU PROTEIN: Focal spherical collections of neuritic processes, often around a central amyloid (Beta-amyloid) core. Found in the hippocampus and amygdala usually.

211
Q

Tangle. SEE SLIDE 23.11. (TOPNOTCH)Robbins Basic Pathology, 9th ed., p 838

A

Alzheimer-related lesions. PLAQUE or TANGLE: Bundles of paired helical filaments visible as basophilic fibrillary structures. A major component is an abnormally hyperphosphorylated TAU protein. Not specific for Alzheimer’s.

212
Q

Interesingly, it appears first in the medulla, and then the pons, before involvement of the substantia nigra. (M>P>S in alphabetical order) (TOPNOTCH)Robbins Basic Pathology, 9th ed., p 839

A

In Parkinson’s Disease, where are Lewy bodies appear first?

213
Q

Medulloblastoma (TOPNOTCH)Robbins Basic Pathology, 9th ed., p 845

A

Often located midline in the cerebellum in children, and lateral in adults. On histology, lesion is extremely cellular with sheets of anaplastic (small blue) cells.

New Pathology TN (24 decks)

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