2.16 Neuropathology: CNS Atherosclerosis Flashcards Preview

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Flashcards in 2.16 Neuropathology: CNS Atherosclerosis Deck (40):
1

What are the four vascular malformation of the CNS?

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

2

What is a Telangiectasia?

• A focal aggregate of uniformly small vessels, with intervening neural parenchyma
• May initiate seizures, but rarely ruptures

3

What is a venous angioma?

•Consists of a few enlarged veins distributed randomly in the spinal cord or brain
•The lesion is generally asymptomatic.

4

What are Arteriovenous malformations (AVM)?

- It evolves during embryonic development which permits direct communication between cerebral arteries and veins, which gradually enlarges.

5

Where are arteriovenous malformations?

-The resultant conglomeration of abnormal vessels is usually located in the cerebral cortex and the contiguous underlying white matter.

6

What is the end result of arteriovenous malformations?

-Seizures, subarachnoid and intracerebral hemorrhages can occur in the 2nd or 3rd decades.

7

What is a Cavernous angioma?

Composed of large vascular spaces compartmentalized by prominent fibrous walls.

8

What is the end results of Cavernous angioma?

-Most remain asymptomatic, although a minority of patients have intracranial bleeding, epilepsy, or focal neurologic disturbances

9

What are the four types of cerebral aneurysms?

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

10

Define berry aneurysm and it causes?

They are caused by arterial defects that originate during embryonic development, when the bifurcation of an artery creates Y-shped configuration

11

Where do 90% of all berry aneurysms occur?

-Circle of Willis
1. Anterior Cerebral Artery and the Anterior Communicating Artery.
2. The complex of the Internal Carotid Artery-Posterior Communicating Artery-Anterior Cerebral Artery.
3. The trifurcation of the Middle Cerebral Artery.

12

Explain the pathology of berry aneurysms?

-The bloodstream from the parent vessel exerts relentless pressure on the crotch of the Y, and with time, the endothelium and internal elastic membrane degenerates and fragments.

13

Large aneurysms of the internal carotid complex can cause palsies in which cranial nerves?

Large aneurysms of the internal carotid complex can produce palsies of the 3rd, 4th, and 6th cranial nerves and seizures initiated by the compression of the medial aspect of the temporal lobe.

14

How do berry aneurysms present clinically?

•A sudden severe headache heralds the onset of the SAH and may be followed by coma.
•Patients who survive for 3-4 days often manifest a progressive decline in consciousness, due to arterial spasm and consequent cerebral ischemia and infarction.
•Survivors of the initial episode may rebleed, in which case the prognosis is worse.

15

Where are atherosclerotic aneurysms located?

Usually localized to the larger cerebral vessels (vertebral, basilar, and internal carotid arteries).

16

What is a atherosclerotic aneurysms?

-There is fibrous replacement of the media and destruction of the internal elastic membrane weaken the arterial wall and permit aneurysmal dilatation.

17

What is the general characteristics of an atherosclerotic aneurysms?

-Are characterisically fusiform, and elongates the vessel as they enlarge.

18

What are the clinical features of an atherosclerotic aneurysms?

-They rarely rupture, but the major complication is thrombosis, leading to strokes.

19

What is a mycotic aneurysm?

-Infections of the arterial walls that results from septic emboli, usually from an infected cardiac valve (endocarditis) that lodges itself in a branch of the middle cerebral artery.

20

What is Charcot-Bouchard aneurysms?

Aneurysms, associated with long-standing HTN

21

Where do Charcot-Bouchard aneurysms normally occur?

Occurs in a geographic distribution that closely corresponds to the pattern of intercerebral hemorrhage

22

What are Hypertension-Associated Aneurysms?

-The integrity of small interparenchymal cerebral arterioles is compromised by hypertension through the deposition of lipid and hyaline material in their walls (lipohyalinosis).

23

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

-The resulting weakening of the walls leads to the formation of Charcot-Bouchard aneurysms, small fusiform dilatations located on the trunk of a vessel, rather than at a bifurcation, and are predisposed to rupture, causing hypertensive cerebral hemorrhage

24

Where are hypertensive hemorrhages?

- The Basal Ganglia Thalamus (75%)
- The Pons (15%)
- The Cerebellum (10%)

25

What are the clinical features of intercerebral hemorrhages?

-Onset of symptoms is abrupt and weakness usually dominates.
-Death occurs within hours to days.
-Causes death by transtentorial herniation

26

What happens if a rupture of a small vessel into ventricle (intrventricular)?

-Ventricle rapidly distends the entire lateral ventricular system with blood, with expansion of the 3rd and 4th ventricle.
-The rush of blood through the ventricular system seemingly
-Causes death by distention of the 4th ventricle and the compression of vital centers in the medulla.

27

What is a cerebellar hemorrhages?

-Bleeding into the cerebellum causes abrupt ataxia, with occipital headache and vomiting.
-Compression of medulla via herniation of the cerebellar tonsils through foramen magnum

28

What is a cerebral ischemia?

Inadequate perfusion of the brain may result from extra cerebral events, such as shock or cardiac arrest.

29

What are the two types of cerebral infarcts?

Hemorrhagic or bland

30

What are hemorrhagic cerebral infarcts?

In general, infarcts caused by embolization are the sites of hemorrhage

31

What are bland cerebral infarcts?

-Whereas those initiated by thrombotic occlusion are largely ischemic and therefore bland.

32

How do acute infarcts present histologically?

-Acute infarct of the brain transforms the cerebral tissue into a liquefactive, necrotic putty-like debris with Neutrophils

33

How do healed infarct present?

-Cerebral infarcts are not repaired by fibroblasts, and as an early response, capillaries and astrocytes proliferate at the margin of the lesion and become numerous by the 5th day. (Gliosis)
-Within months, the necrotic area is excavated by phagocytosis and a permanent cyst is formed, and at the same time the neovascularity regresses.

34

What types of infarctions are localized in the middle cerebral artery?

-Is a favored site not only for the lodgement of emboli
-Also for atherosclerosis, which promotes thrombosis in-situ.

35

What type of deficits for cerebral cortex?

-This deprives the cerebral cortex of circulation and produces motor and sensory deficits, as well as aphasias, when the dominant hemisphere is involved.

36

What vessels are involved in lacunar infarcts?

Parenchymal Arteries and Arterioles

37

What are lacunar infarcts?

These vessels are not predisposed to atherosclerosis like the larger arteries, but they can become damaged by hypertension and become stenotic because of secondary arteriolosclerosis, the narrowing causing small ischemic lesions called lacunar infarcts.

38

What does lunar infarcts cause?

These minute infarcts can impair cognition and create the entity termed multi-infarct dementia.

39

What are fat embolism?

-Small emboli, composed of fat, can occlude capillaries in the brain and lungs, as a result of traumatic leg bone fractures

40

What happens when fat emboli lodge?

Their semifluid consistency creates a major barrier to blood flow. The distal capillary endothelium becomes hypoxic and permeable, and petechiae develop, restricted to the white matter.