Chap 28 Morphology 2 Flashcards

(51 cards)

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
Where does HSV-1 encephalitis most severely involve?
Inferior and medial regions of the temporal lobes and orbital gyri of the frontal lobes
26
What characteristics are present in HSV-1 encephalitis?
- Necrotizing and hemorrhagic regions - Perivascular inflammatory infiltrates - Cowdry type A intranuclear viral inclusion bodies
27
What does CMV in immunosuppressed individuals cause?
Subacute encephalitis with are associated with CMV inclusion-bearing cells
28
Where does CMV in immunosuppressed patients localize?
- Paraventricular subependymal regions of the brain | - Results in severe hemorrhagic necrotizing ventriculoencephalitis and a choroid plexitis
29
Microscopy of CMV infection
Prominent enlarged cells with intranuclear and intracytoplasmic inclusions
30
Appearance of acute cases of poliomyelitis
Show mononuclear cell perivascular cuffs and neuronophagia of anterior horn motor neurons of the spinal cord
31
Brain examination of patient with Rabies
- Intense edema | - Vascular congestion
32
Microscopic appearance of Rabies
- Widespread neuronal degeneration and inflammatory reaction most severe in the brainstem - Negri bodies
33
What are Negri bodies?
- Found microscopically in Rabies | - Cytoplasmic, round/oval eosinophilic inclusions found in hippocampus and Purkinje cells
34
What is HIV encephalitis?
Chronic inflammatory reaction associated with microglial nodules that contain multinucleared giant cells
35
Where are microglial nodules found in HIV encephalitis?
Near small blood vessels which are prominent in endothelial cells and perivascular foamy or pigment laden macrophages
36
What cells can HIV be detected in?
CD4+ mononuclear and multinucleated macrophages and microglia
37
What occurs with cryptococcal infection?
Chronic meningitis affecting the basal leptomeninges which are thickened by connective tissue that can obstruct outflow of CSF causing hydrocephalus
38
Where is CSF obstructed in cryptococcal infection from the connective tissue?
Foramina of Luschka and Magendie
39
What are soap bubbles and where are they found?
- Found in subarachnoid space during cryptococcal infection, particularly the basal ganglia - Small cysts within the parenchyma
40
What do the parenchymal lesions in cryptococcal infections consist of?
- Organisms within expanded perivascular spaces (Virchow-Robin)
41
What occurs in Toxoplasmosis?
CNS brain abscesses mostly in cerebral cortex and deep gray nuclei
42
Characteristics of acute lesions of toxoplasmosis
Central necrosis, petechial hemorrhages surrounded by acute and chronic inflammation, macrophage infiltration, and vascular proliferation
43
What is the appearance of the lesions of toxoplasmosis after toxoplasmosis?
Large, well-demarcated areas of coagulative necrosis surrounded by lipid-laden macrophages
44
What is the pathognomonic finding in classic CJD?
Spongiform transformation of the cerebral cortex and deep gray matter structures (caudate and putamen)
45
Result of spongiform transformation in CJD
Small, empty microscopic vacuoles of varying sizes within the neuropil
46
What are kuru plaques and where are they seen?
- Extracellular deposits of abnormal protein | - Seen in cerebellum with normal CJD and cerebral cortex for vCJD
47
What is multiple sclerosis?
A white matter disease in the brain and spinal cord
48
Appearance of MS lesions in the early state
Firm, surrounded by white matter (sclerosis) , well circumscribed, and appear depressed, glassy, with irregularly shaped plaques
49
What are active plaques and when are they seen?
- Seen microscopically in MS on small veins | - Is ongoing myelin breakdown associated with macrophages
50
What are inactive plaques and when are they seen?
- 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
What are shadow plaques and when are they seen?
- Microscopically in MS | - Have abnormally thinned out myelin sheaths