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COM II- Neuro Robbins > Chap 28 Morphology 2 > Flashcards

Chap 28 Morphology 2 Flashcards

1
Q

Morphology of acute meningitis

A
  • Exudate is evident within the leptomeninges over the surface of the brain
  • Meningeal vessels are engorged and prominent
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2
Q

Where does H. influenzae meningitis usually occur?

A

Basal

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3
Q

Where does pneumococcal meningitis usually located?

A

Over the cerebral convexities near the sagittal sinus

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4
Q

What cell predominates the subarachnoid space in acute meningitis?

A

Neutrophils

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5
Q

What occurs during fulminant meningitis?

A

Inflammatory cells infiltrate the walls of the leptomeningeal veins and can extend into the brain

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6
Q

When does leptomeningeal fibrosis occur?

A

Following pyogenic meningitis and can cause hydrocephalus

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7
Q

What is chronic adhesive arachnoiditis and when does it occur?

A
  • Large quantities of polysaccharide of the organism produce gelatinous exudate that promotes arachnoid fibrosis
  • Occurs mostly in pneumococcal meningitis
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8
Q

What are abscesses?

A
  • Discrete lesions with central liquefactive necrosis surrounded by brain swelling
  • The outer margin of necrotic lesion has exuberant granulation tissue with neovascularization around the necrosis
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9
Q

What are the characteristics of meningoencephalitis?

A
  • Subarachnoid space contain gelatinous or fibrinous exudate
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10
Q

Microscopic exam of diffuse meningoencephalitis

A
  • Areas of mixed inflammatory infiltrates containing lymphocytes, plasma cells, and macrophages
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11
Q

What is a tuberculoma?

A

Well-circumscribed intraparenchymal mass that may be associated with meningitis

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12
Q

Appearance of a tuberculoma

A
  • Central area of caseous necrosis surrounded by granulomas
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13
Q

What is meningovascular neurosyphilis?

A
  • Chronic meningitis involving the base of the brain, cerebral convexities, and spinal leptomeninges
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14
Q

What causes paretic neurosyphilis?

A
  • Invasion of the brain by T. pallidum
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15
Q

What are the symptoms of paretic neurosyphilis?

A
  • Progressive cognitive impairment (mood alterations)

- “General paresis of the insane” –> dementia

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16
Q

Where is parenchymal damage in paretic neurosyphilis most common?

A

Frontal lobe

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17
Q

What are the characteristics of the lesions for paretic neurosyphilis?

A
  • Loss of neurons
  • Proliferation of microglia
  • Gliosis
  • Iron deposits
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18
Q

Why are there iron deposits in the lesions for paretic neurosyphilis?

A

From the small bleeds stemming from damage to the microcirculation

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19
Q

How does Tabes Dorsalis occur?

A

Damage to the sensory axons in the dorsal roots

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20
Q

What are the symptoms of Tabes Dorsalis?

A
  • Impaired join position sense
  • “Lightening pains”
  • Locomotor ataxia
  • Loss of pain sensation
  • Charcot joints- skin and join damage
  • Absence of deep tendon reflexes
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21
Q

Microscopic examination of Tabes Dorsalis

A
  • Loss of both axons and myelin in the dorsal roots

- Pallor and atrophy in dorsal columns in spinal cord

22
Q

Histology of encephalitides caused by arboviruses

A
  • Perivascular accumulation of lymphocytes
  • Multiple foci of necrosis of gray and white matter
  • Neuronphagia
  • Microglial nodules
23
Q

Neuronphagia

A

Single-cell neuronal necrosis with phagocytosis of debris

24
Q

Microglial Nodules

A

Microglial cells form small aggregates around foci of necrosis

25
Q

Where does HSV-1 encephalitis most severely involve?

A

Inferior and medial regions of the temporal lobes and orbital gyri of the frontal lobes

26
Q

What characteristics are present in HSV-1 encephalitis?

A
  • Necrotizing and hemorrhagic regions
  • Perivascular inflammatory infiltrates
  • Cowdry type A intranuclear viral inclusion bodies
27
Q

What does CMV in immunosuppressed individuals cause?

A

Subacute encephalitis with are associated with CMV inclusion-bearing cells

28
Q

Where does CMV in immunosuppressed patients localize?

A
  • Paraventricular subependymal regions of the brain

- Results in severe hemorrhagic necrotizing ventriculoencephalitis and a choroid plexitis

29
Q

Microscopy of CMV infection

A

Prominent enlarged cells with intranuclear and intracytoplasmic inclusions

30
Q

Appearance of acute cases of poliomyelitis

A

Show mononuclear cell perivascular cuffs and neuronophagia of anterior horn motor neurons of the spinal cord

31
Q

Brain examination of patient with Rabies

A
  • Intense edema

- Vascular congestion

32
Q

Microscopic appearance of Rabies

A
  • Widespread neuronal degeneration and inflammatory reaction most severe in the brainstem
  • Negri bodies
33
Q

What are Negri bodies?

A
  • Found microscopically in Rabies

- Cytoplasmic, round/oval eosinophilic inclusions found in hippocampus and Purkinje cells

34
Q

What is HIV encephalitis?

A

Chronic inflammatory reaction associated with microglial nodules that contain multinucleared giant cells

35
Q

Where are microglial nodules found in HIV encephalitis?

A

Near small blood vessels which are prominent in endothelial cells and perivascular foamy or pigment laden macrophages

36
Q

What cells can HIV be detected in?

A

CD4+ mononuclear and multinucleated macrophages and microglia

37
Q

What occurs with cryptococcal infection?

A

Chronic meningitis affecting the basal leptomeninges which are thickened by connective tissue that can obstruct outflow of CSF causing hydrocephalus

38
Q

Where is CSF obstructed in cryptococcal infection from the connective tissue?

A

Foramina of Luschka and Magendie

39
Q

What are soap bubbles and where are they found?

A
  • Found in subarachnoid space during cryptococcal infection, particularly the basal ganglia
  • Small cysts within the parenchyma
40
Q

What do the parenchymal lesions in cryptococcal infections consist of?

A
  • Organisms within expanded perivascular spaces (Virchow-Robin)
41
Q

What occurs in Toxoplasmosis?

A

CNS brain abscesses mostly in cerebral cortex and deep gray nuclei

42
Q

Characteristics of acute lesions of toxoplasmosis

A

Central necrosis, petechial hemorrhages surrounded by acute and chronic inflammation, macrophage infiltration, and vascular proliferation

43
Q

What is the appearance of the lesions of toxoplasmosis after toxoplasmosis?

A

Large, well-demarcated areas of coagulative necrosis surrounded by lipid-laden macrophages

44
Q

What is the pathognomonic finding in classic CJD?

A

Spongiform transformation of the cerebral cortex and deep gray matter structures (caudate and putamen)

45
Q

Result of spongiform transformation in CJD

A

Small, empty microscopic vacuoles of varying sizes within the neuropil

46
Q

What are kuru plaques and where are they seen?

A
  • Extracellular deposits of abnormal protein

- Seen in cerebellum with normal CJD and cerebral cortex for vCJD

47
Q

What is multiple sclerosis?

A

A white matter disease in the brain and spinal cord

48
Q

Appearance of MS lesions in the early state

A

Firm, surrounded by white matter (sclerosis) , well circumscribed, and appear depressed, glassy, with irregularly shaped plaques

49
Q

What are active plaques and when are they seen?

A
  • Seen microscopically in MS on small veins

- Is ongoing myelin breakdown associated with macrophages

50
Q

What are inactive plaques and when are they seen?

A
  • Microscopically in MS after lesions become quiescent
  • Have little to no myelin and a reduced number of oligodendrocyte nuclei
  • Astrocytic proliferation and gliosis are prominent
51
Q

What are shadow plaques and when are they seen?

A
  • Microscopically in MS

- Have abnormally thinned out myelin sheaths

COM II- Neuro Robbins (8 decks)

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