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NMSK-B II > Pathology 2.16 > Flashcards

Pathology 2.16 Flashcards

1
Q

What are the four major Vascular Malformations of the CNS?

A

1) Arteriovenous Malformation (AVM)
2) Cavernous Angioma
3) Telangiectasia
4) Venous Angioma

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2
Q

What is arteriovenous malformation?

A
  • most common congenital vascular malformation

- dilated vascualr channels in the brain

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3
Q

What is the cause of arteriovenous malformation and where are they located?

A
  • cerebral arteries, veins
  • central cortex and contiguous white matter
  • hemorrhage (subarachnoid, intracerebral) 2nd and 3rd decade
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4
Q

What is cavernous angioma?

A
  • congenital vascular malformation
  • large vascular spaces compartmentalized by prominent fibrous walls
  • most asymptomatic; some IC bleeding, epilepsy, nero deficet
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5
Q

What is Teleangiectasia?

A
  • focal aggregate of uniformally small vessels
  • w/ intervening neural parenchyma
  • may initiate seizures, rarely ruptures
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6
Q

What is venous angioma?

A
  • few enlarged veins in spinal cord/brain
  • distributed randomly
  • generally asymptomatic
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7
Q

What are cerebral aneurysms?

A

intravascular pressure exploits weakness in arterial walls and causes saccular dilations

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8
Q

What are the causes of cerebral aneurysms?

A

1) Developmental defects- Berry Aneurysms
2) Atherosclerotic Aneurysms
3) Bacterial infections- Mycotic Aneurysms
4) Hypertension-associated which induces interparenchymal Charcot-Bouchard Aneurysms

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9
Q

What are the causes of berry aneurysms?

A
  • arterial defects at arterial bifurcation (Y-shaped)
  • muscular layer of vessel weakened
  • vessel bridged only endothelium and elastic lamina
  • *90% in circle of willis**
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10
Q

How do berry aneurysms evolve?

A
  • bloodstream pressure on bifurcation point
  • endothelium and elastic membranes degrade
  • saccular aneurysm evolves; wall formed only by adventitia
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11
Q

Where are berry aneurysms typically located?

A

1) anterior cerebral artery
2) junction of:
a. internal carotid artery
b. posterior communicating artery
c. anterior cerebral artery
3) trifurcation of middle cerebral artery

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12
Q

What is the most feared complication of berry aneurysms?

A
  • rupture causing subarachnoid hemorrhage

- large aneurysms can create palsies of CN III, IV, VI

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13
Q

How do berry aneurysms present clinically?

A
  • sudden severe headache heralds onset of SAH followed by coma
  • progressive decline in consciousness
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14
Q

Where are atherosclerotic aneurysms?

A

-larger cerebral vessles (vertebral, basilar, internal carotid arteries)

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15
Q

What is the cause atherosclerotic aneurysms?

A
  • fibrous replacement of media and destruction of internal elastic membrane
  • weakened arterial wall
  • prevents aneurysmal dilatation
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16
Q

What are the shapes of artherosclerotic aneurysms?

A

fusiform and elongate the vessel as they enlarge

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17
Q

What is the major complication of atherosclerotic aneurysms?

A

thrombosis leading to stroke

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18
Q

What is mycotic aneurysms?

A
  • arterial wall infection
  • etiology: endocarditis causes septic emboli to lodge in middle cerebral artery
  • inflammation causes rupture
19
Q

What are hypertension-associated aneurysms?

A

lipid and hyaline material deposits in walls of small interparenchymal cerebral arterioles

20
Q

What happens to the thin walls deep inside the brain of a hypertension-associated aneurysm?

A

Charcot-Bouchard aneurysms [small fusiform dilatations] form on trunk rather than bifurcation

21
Q

Where do hypertensive intercerebral hemorrhages occur?

A

1) basal ganglia-thalamus* (75%)
2) pons
3) cerebellum

22
Q

How does a patient present with a hypertensive intracerebral hemorrhage?

A
  • weakness [abrupt onset of symptoms]

- death occurs within hours to days

23
Q

What is meant by interventricular hemorrhage?

A
  • rupture of a small vessel into a ventricle rapidly distends entire lateral ventricular system with blood
  • 3rd and 4th ventricle expand
  • causes death by compressing vital centers in medulla
24
Q

What is characteristic clinically about cerebellar hemorrhages?

A
  • bleeding into cerebellum causes abrupt ataxia
  • severe occipital headache and vomiting
  • acute life threatening through medulla compression and tonsil herniation through foramen magnum
25
Q

What is cerebral ischemia?

A

inadequate perfusion of brain

26
Q

What are the causes of cerebral ischemia?

A

extracerebral events (shock, cardiac arrest)

27
Q

What does a generalized decrease in cerebral blood flow cause in cerebral ischemia?

A
  • global ischemia

- hypoxic events (CO poisoning, near-drowning)

28
Q

What do vascular obstructions cause in cerebral ischemia?

A
  • regional ischemia

- localized infarct

29
Q

What are cerebral infarcts?

A

??

30
Q

What are the causes of cerebral infarcts?

A
  • cerebrovascular occlusive disease

- atherosclerosis predisposes to vascular thrombosis and embolic events

31
Q

How are cerebral infarcts designated pathologically?

A
  • “hemorrhagic” or “bland”
  • infarcts caused by embolization are the sites of hemorrhage
  • infarcts caused by thrombotic occlusion are largely ischemic and bland
32
Q

How does an embolus cause hemorrhage acutely?

A
  • occludes vascular flow abruptly
  • ischemic region undergoes rapid necrosis
  • blood vessels in area become necrotic and leak blood into region
33
Q

How does an thrombus cause bland infarcts?

A
  • slow progressing

- collateral vessels also thrombose and guard against secondary hemorrhage

34
Q

How do cerebral infarcts present histologically?

A
  • cerebral tissue becomes a liquefactive, necrotic putty-like debris with neutrophils
  • later is phagocytized by macrophages
35
Q

What happens to cerebral infarcts as they heals?

A
  • NOT repaired by fibroblasts
  • capillaries and astrocytes proliferate at margin of lesion (gliosis)
  • permenant cyst formed after months of healing and neovascularity regresses
36
Q

Do different cerebral vessel occlusions cause different deficits?

A

Yes, localized neurologic deficits are produced by the occlusion of different cerebral vessels

37
Q

What results from artherosclerosis and thrombosis of striate arteries?

A

(origin at proximal middle cerebral artery)

-transect internal capsule and produce hemiparesis or hemiplegia

38
Q

What is the preferred location for the lodgement of emboli and atherosclerosis?

A

trifurcation of the middle cerebral artery

39
Q

What is the most common site of large artery occlusion leading to infarction?

A

common carotid artery

40
Q

What is characteristic of parenchymal arteries and arterioles?

A
  • not predisposed to artherosclerosis

- can become damaged by HTN and become stenotic from secondary artherosclerosis

41
Q

What is multi-infarct dementia?

A

multiple minute infarcts in parenchymal arteries impair cognition

42
Q

What is Hypertensive Encephalopathy?

A

-CNS manifestation of malignant HTN
EX: fibrinoid necrosis of small arteries and arterioles with petechiae
-cerebral edema and resulting papilledema may complicate the vascular pathology

43
Q

How does hypertensive encephalopathy present clinically?

A
  • headache
  • vomiting
  • progression to lethergy
  • possible coma and death
44
Q

What is fat embolism syndrome?

A
  • small emboli (composed of fat) occlude capillaries in brain and lungs as a result of traumatic leg bone fractures
  • emboli carried through cerebral vessels and lodges to create barrier to blood flow

NMSK-B II (15 decks)

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