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COM II- Neuro Robbins > Chap 28 Morphology > Flashcards

Chap 28 Morphology Flashcards

1
Q

What is acute neuronal injury?

A
  • Involve “red neurons”

- Changes that occur from acute CNS hypoxia/ischemia

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2
Q

What are red neurons?

A
  • Seen in acute neuronal injury by 12 to 24 hours after irreversible hypoxic/ischemic insult
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3
Q

What are the morphologic features of irreversible hypoxic/ischemic insult?

A

shrinkage of cell body, pyknosis of the nucleus, disappearance of the nucleolus, and loss of Nissl structures with eosinophilia of the cytoplasm

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4
Q

What is subacute and chronic neuronal injury?

A
  • “degeneration”
  • Neuronal death occurring as a result of progressive disease
  • Ex. in neurodegenerative diseases (ALS and Alzheimers)
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5
Q

What are the histologic features of subacute and chronic neuronal injury?

A
  • Cell loss- involving functionally related groups of neurons
  • Reactive gliosis
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6
Q

What is the best indicator of subacute and chronic neuronal injury?

A

Associated reactive glial changes

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7
Q

What is an axonal reaction?

A

A change in the cell body during regeneration of the axon

*best seen in anterior horn of the spinal cord where motor axons are cut or damaged

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8
Q

What is the morphologic appearance of an axonal reaction?

A
  • Increased protein synthesis
  • Enlargement and rounding up of the cell body
  • Peripheral displacement of nucleus
  • Enlargement of the nucleolus
  • Central chromatolysis
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9
Q

What is central chromatolysis?

A

Dispersion of Nissl substance from the center to the periphery of the cell

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10
Q

What are neuronal inclusions and where are they seen?

A
  • Occur with aging

- Intracytoplasmic accumulation of complex lipids, proteins, or carbs

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11
Q

What viral infections can lead to abnormal intranuclear inclusions?

A
  • Herpetic infection: Cowdry body is seen

- Cytoplasmic inclusions: Rabies with Negri body

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12
Q

What degenerative diseases of the CNS are associated with neuronal intracytoplasmic inclusions?

A
  • Neurofibrillary tangles of Alzheimer Disease
  • Lewy bodies of Parkinson Disease
  • Abnormal vacuolization of perikaryon and neuronal cell processes in neuropil in Creutzfeldt-Jakob Disease
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13
Q

Appearance of a acute subdural hematoma

A
  • Collection of freshly clotted blood along brain surface without extension into the sulci
  • Subarachnoid space is clear
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14
Q

What is the sequence of a acute subdural hematoma?

A
  • 1 week: lysis of the clot
  • 2 weeks: growth of fibroblasts from dural surface into a hematoma
  • 1-3 months: early development of hyalinized connective tissue
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15
Q

What are chronic subdural hematomas?

A

Multiple recurrent episodes of bleeding from thin-walled granuloma tissue

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16
Q

When is the risk of repeat bleeding of a subdural hematoma most likely?

A

In the first few months after the initial hemorrhage

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17
Q

What are the histologic features of traumatic injury of the spinal cord at the level of the injury in the acute phase?

A

Hemorrhage, necrosis, and axonal swelling in surrounding white matter

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18
Q

What occurs at the time central areas of neuronal destruction in a spinal cord injury?

A

The areas become cystic and gliotic

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19
Q

What is the morphology of the brain during global ischemia?

A

Brain is edematous and swollen, widening of gyri, narrowing of sulci, poor demarcation of gray and white matter

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20
Q

Early microscopic features of infarction (ischemic injury)

A
  • Occur 12 -24 hours after insult

- Microvacuolization, eosinophilia in cytoplasm, nuclear pyknosis and karyorrhexis

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21
Q

Subacute microscopic changes of infarction

A
  • Occur 24 hours - 2 weeks

- Tissue necrosis, influx of macrophages vascular proliferation, and reactive gliosis

22
Q

Microscopic repair changes of infarction

A
  • Occur at 2 weeks

- Removal of necrotic tissue, loss of normal CNS architecture, and gliosis

23
Q

What is pseudolaminar necrosis and when is it seen?

A
  • Pattern of injury

- When the cerebral neocortex has uneven neuronal loss and gliosis and preservation or destruction of different layers

24
Q

Gross Appearance of a Nonhemorrhagic Infarct

A
  • varies with time
  • 6 hours- little change
  • 48 hours- tissue becomes pale, soft, swollen, and corticomedullary junction becomes indistinct
  • 2-10 days- brain becomes gelatinous and friable
  • 10 days- 3 weeks- tissue liquefies, leaving a fluid filled cavity that expands until tissue is dead
25
Q

Microscopic tissue reaction of nonhemorrhagic infarct after first 12 hours

A
  • Ischemic neuronal change (red neurons)
  • Cytotoxic and vasogenic edema
  • Endothelial and glial cells swell
  • Myelinated fibers disintegrate
26
Q

Microscopic tissue reaction of nonhemorrhagic infarct up to 48 hours

A
  • Neutrophilic emigration increases and then falls
  • Phagocytic cells are prominent until 2-3 weeks
  • Macrophages filled with myelin breakdown products or blood
27
Q

When are reactive astrocytes seen in nonhemorrhagic infarcts?

A
  • As early as 1 week after the insult

- As liquification and phagocytosis proceeds, astrocytes enlarge, divide, and develop extensions

28
Q

Microscopic tissue reaction of nonhemorrhagic infarct after several months

A

Astrocytic response recedes, leaving behind a dense meshwork of glial fibers mixed with capillaries and connective tissue

29
Q

What occurs during hemorrhagic infarctions?

A

Same as ischmeic infarctions with the addition of blood extravasation and resorption

30
Q

When are spinal cord infarctions seen?

A
  • In the setting of hypoperfusion or after traumatic interruption of branches leading to the aorta
31
Q

Where can hypertensive intraparenchymal hemorrhages originate?

A

Putamen, thalamus, pons, cerebellar hemispheres

32
Q

What are the characteristics of an acute hemorrhage?

A

Extravasation of blood with compression of the adjacent parenchyma

33
Q

What is the appearance of an old hemorrhage?

A

Area of cavitary destruction of brain with a rim of brownish discoloration

34
Q

What do early lesions of hypertensive intraparenchymal hemorrhages look like?

A

Central core of clotted blood surrounded by a rim of brain tissue showing anoxic neuronal and glial changes and edema

35
Q

What occurs in the later stages of a hypertensive intraparenchymal hemorrhage?

A

Edema is resolved, hemosiderin and lipid-laden macrophages appear and proliferation of reactive astrocytes is seen at periphery of the lesion

36
Q

What vascular abnormalities are usually associated with cerebral amyloid angiopathy (CAA)?

A
  • Leptomeningeal and cerebral cortical arterioles and capillaries
  • Dense and uniform deposits of amyloid
37
Q

What is a distinguishing factor between cerebral amyloid angiopathy and arteriolar sclerosis?

A

In CAA there is no fibrosis but arteriolar sclerosis has fibrosis

38
Q

What is an unruptured saccular aneurysm?

A

Thin-walled outpouching

*Usually in Circle of Willis

39
Q

What is the usual size of a saccular aneurysm?

A

2-3 cm

40
Q

Appearance of a saccular aneurysm

A

Red, shiny surface and a thin, translucent wall

41
Q

What part of a saccular aneurysm does a rupture usually occur?

A

Arterial wall adjacent to the neck of the aneurysm

42
Q

What is the aneurysm sac of a saccular aneurysm made up of?

A

Thickened hyalinized intima and covering of adventitia

43
Q

What vessels are involved in arteriovenous malformation?

A

Vessels in the subarachnoid space or in the brain or both

44
Q

What are some characteristics of arteriovenous malformations?

A
  • Composed of greatly enlarged blood vessels separated by gliotic tissue
  • Some arteries are duplicated and have fragmented internal elastic lamina
  • Some arteries show thickening or partial replacement of the media by hyalinized connective tissue
  • High flow channels
45
Q

What are the components of a cavernous malformation?

A

Distended, loosely organized vascular channels arranged back to back with collagenized walls

  • No parenchyma between vessels
  • Low-flow channels
46
Q

Where are cavernous malformations most common?

A

Cerebellum, pons, and subcortical regions

47
Q

What are capillary telangiectasias?

A

Microscopic foci of dilated, thin-walled vascular channels separated by relatively normal brain parenchyma

48
Q

Where are capillary telangiectasias usually found?

A

In the pons

49
Q

Components of venous angiomas (varices)

A

Aggregates of dilated venous channels

50
Q

What is Foix-Alajoyanine disease (angiodysgenetic necrotizing myelopathy)?

A
  • Venous angiomatous malformation of the spinal cord and overlying the meninges
  • Commonly associated with ischemic injury to the spinal cord and slowly progressive neurologic symptoms
51
Q

Where is Foix-Alajoyanine disease mostly located?

A

lumbosacral region

COM II- Neuro Robbins (8 decks)

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