Cerebrovasculat

Question 1

Compare vasogenic & cytotoxic edema

Answer 1

V, integrity of BBB is disrupted resulting in inc vascular permeability, may be local adjacent to inflammation or generalized
C, inc IC fluid 2ry to neuronal & glial cell membarne injury, e.g. generalized hypoxic/ischemic insult or exposure to some toxin

Question 2

Describe gross features of cerebral edema

Answer 2

Edematous brain is softer, overfill cranial cavity, in generalized edema gyri are flattened against dura & skull, sulci are narrowed, ventricles are compressed.

Question 3

Enumerate causes of global cerebral ischemia

Answer 3

Cardiac arrest, shock, severe hypotension (below 50 mmHg)

Question 4

Compare outcomes of mild & severe global cerebral ischemia

Answer 4

M, transient postischemic confusion state with eventual complete recovery
S, widespread neuronal death, patients who servive remain severely impaired neurologically in vegetative state, in some patient—> brain death, mechanical ventilation & eventual brain autolysis “respirator brain”

Question 5

Describe morphology of generalized cerebral ischemia

Answer 5

Brain is swollen with wide gyri & narrowed sulci, poor demarcation between white & grey matter. “Pseudolaminar necrosis”: some layers are devastated others preserved, “watershed infarcts” at most distal areas of arterial territories,

Question 6

Thrombotic arterial occlusion is mostly due to….

Answer 6

Atherosclerosis

Question 7

Mention a cause in which venous occulsion may be common

Answer 7

In cancer due to inc predisposition to thrombosis, superior sagittal thrombosis may occur leading to multiple bilateral parasagittal hemorrhagic infarcts

Question 8

Mention G&M changes of cerebral infarction in each of the following:
1. 0-12 hrs
2. 12-24 hrs
3. 24-48 hrs

Answer 8

1. No changes, minimal or no change
2. Minimal changes, red (hypereosinophilic) neurons with pyknotic nuclei
3. Indistinct gray-white matter junction, neutrophilic infiltrate

Question 9

Mention G&M changes of cerebral infarction in each of the following:
1. 2-10 days
2. 2-3 weeks

Answer 9

1. Friable tissue with marked edema, histiocytic infiltrate+ neurons disapear
2. Liquefied tissue. Liquefactive necrosis, histiocytes filled with myelin breakdown products

Question 10

Mention G&M changes of cerebral infarction in each of the following:
1. 3w-1mon
2. Years

Answer 10

1. Fluid-filled cavity surrounded by gliotic scar. Fluid-filled cavity, reactive astrocytes, lipid-laden macrophages
2. Old cyst surrounded by gliotic scar. Astrogliosis surrounding a cyst.

Question 11

Mention causes of (1)intraparenchymal & (2)subarachnoid hemorrhages

Answer 11

1. HTN/cerebral amyloid angiopathy, structural lesions (AVM, cavernous m.), tumours
2. Structural vascular abnormalities commonly aneurysm also AVM

Question 12

Berry aneurysm affect….., they cause……, associated with……

Answer 12

Circle of Willis
Subarachnoid hemorrhage
Polycystic kidney disease

Question 13

Describe etiology of congenital aneurysms

Answer 13

Congenital defects of media at arterial bifurcation
Focal destruction of internal elastic lamina due to hemodynamic alterations
Collagen subset abnormality

Question 14

Describe etiology & common sites of following aneurysms:
1. Mycotic
2. Atherosclerotic

Answer 14

1. Due to subacute bacterial endocarditis/polyarteritis nodosa, the artery is weakened by mild infection. MCA
2. Cerebral atherosclerosis, fusiform in shape. ICA & basilar

Question 15

Minute microaneurysmd in vessels less than 300 um is……..

Answer 15

Charcot-Bouchard microaneurysms

Question 16

Describe effects of cerebral aneurysms

Answer 16

1. Inc ICT
2. Rupture & hemorrhage
3. Hydrocephalus
4. Thrombosis & calcification

Question 17

AVM is most common in…..

Answer 17

MCA