Block 4 - Cerebrovascular Disease

Front 1

Low inspired partial pressure of O2

Impaired O2 carrying capacity

Inhibition of O2 use by tissue

Back 1

"Functional Hypoxia"

Front 2

What 2 conditions can cause cerebral ischemia?

Back 2

Reduction in perfusion pressure (hypotension)

vessel obstruction

Front 3

Upon what does the survival of ischemic brain tissue depend?

Back 3

Availablity of collateral circulation

Duration of Ischemia

Magnitude and rapidity of the reduction of flow

Front 4

Which brain cells are the most sensitive to ischemia and hypoglycemia?

Back 4

neurons

Front 5

What can be caused by ischemia of large pyramidal neurons?

Back 5

pseudolaminar necrosis of the cerebral cortex

Front 6

Which section of the hippocampus is particularly senstive?

Back 6

Sommer section

Front 7

What cells of the cerebellum are senstive to ischemia?

Back 7

purkinje

Front 8

Besides neurons which CNS cells have a hard time with ischemia?

Back 8

glial cells

Front 9

What causes a "flat" EEG?

Back 9

severe global cerebral ischemia

Front 10

Where are Border zone infarcts?

Back 10

lay at the most distal fields of arterial irrigation

Front 11

Where is the area at greatest risk for border zone infarcts?

Back 11

the area between the anterior and middle cerebral arteries

Front 12

When is a brain at risk for border zone infarcts?

Back 12

usually after a hypotensive episode

Front 13

What is the physical morphology of a border zone infarct?

Back 13

wedge shaped

Front 14

When do red neurons occur?

Back 14

12-24 hrs

Front 15

When do necrosis, influx of macros, and reactive gliosis occur?

Back 15

24 hrs - 2 weeks

Front 16

What happens 2 weeks post global cerebral ischemia?

Back 16

removal of necrotic tissue, loss of normal CNS structure, and gliosis

Front 17

Which structures have no collateral circulation?

Back 17

thalamus, basal ganglia, deep white matter

Front 18

Where does an embolism most ususally lodge?

Back 18

a branch point or stenotic area

Front 19

With what is a non-hemorrhagic infarct most often associated?

Back 19

thrombosis

Front 20

Which cerebral artery is most oftern victim of embolism?

Back 20

middle cerebral artery

Front 21

In focal infacrt, when does the boundary of infarct become more distinct?

Back 21

2-10 days

Front 22

What happens at 10days - 3 weeks, post non-Hemorrhagic infarct?

Back 22

liquification, fluid filled cavity

Front 23

Why, during the first 48 hrs post non-H infarct, does the corticomedullary jxn become indistinct?

Back 23

cerebral edema

Front 24

In a focal ischemic event, when do red neurons appear?

Back 24

12 hours

Front 25

In a focal ischemia event when do neutros and microglia appear?

Back 25

48 hrs

Front 26

When does gliosis begin after a focal ischemia event?

Back 26

2-3 weeks

Front 27

After a focal ischemic event when does astrocyte enlargemnt recede?

Back 27

months

Front 28

What is the most common cause of a hemorrhagic infarction?

Back 28

embolism

Front 29

What is the morphology of a hemorrhagic infarction?

Back 29

same as for ischemic infarct, but with blood extravasation and resotption?

Front 30

Venous infarcts are often...

Back 30

hemorrhagic

Front 31

What can predispose to venous thrombosis?

Back 31

carcinoma or localized infection

Front 32

Spinal cord infarction is rarely caused by occlusion of ....

Back 32

ASPA by thrombosis or embolism

Front 33

Hypertensive lacunar infarcts often affect deep penetrating arteries and arteioles of the...

Back 33

Basal Ganglia

Hemispheric white matter

Brain stem

Front 34

What are the results of hypertensive lacunar infarcts?

Back 34

Tissue loss

scattered fat laden macros

gliosis

Front 35

Hypertensive lacunar infarcts often occur in the ......

(LTIDwCP)

Back 35

lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus, pons

Front 36

How severe are hypertensive lacunar infarcts?

Back 36

silent to severe

Front 37

What ususally causes small hemorrhages that resorb, causing a slit like cavity surrounded by a brownish discoloration

Back 37

hypertension

Front 38

What is Binswanger disease?

Back 38

multifocal vascular disease, involving multiple infarcts, predominately in the white matter.

Front 39

What can be caused by multiple infarcts resulting from hypertensive encephaolopathy?

Back 39

Dementia

gait abnormalities

pseudobulbar signs

and often super imposed neurological deficits

Front 40

Trauma usually causes hemmorrhage into the ......?

Back 40

epidural or subdural space

Front 41

Why would hemorrhage occur in the parenchyma and subarcachnoid space?

Back 41

underlying cerebrovascular disease

Front 42

What causes more than 50% of intraparenchymal hemorrhages?

Back 42

HTN

Front 43

What does htn cause in large vessels?

Back 43

accelerated atherosclerosis

Front 44

What does htn cause in smaller vessels?

Back 44

hyaline arteriosclerosis

Front 45

What 2 changes are often caused in the cerebral vasculature due to sever htn?

Back 45

proliferative changes and necrosis of the arterioloes

Front 46

Where are Charcot-Bouchard microaneurysms most often found?

Back 46

basal ganglia

Front 47

What are the main locations of intraparenchymal hemorrhage when due to htn?

Back 47

putamen(most), thalamus, pons, cerebellar hemispheres (rarely)

Front 48

What are the main causes of cerebral lobar hemorrhages?

Back 48

hemorrhagic diathesis, neoplasm, drug abuse, infection, non-infectious vasculitis, amyloid (congophilic) angiopathy of Alzheimers disease.

Front 49

With regard to intraparenchymal bleed, clinical improvement is often seen with....

Back 49

resolution of the hematoma

Front 50

What is THE most common cause of subarachnoid hemorrhage?

Back 50

rupture of a saccular aneurysm

Front 51

-Rupture of Berry aneurysm
-extension of traumatic hematoma
-Ruprue of a hypertensive intracerebral hemorrhage into the ventricular system
-vascular malformation
-hematologic disturbance
-tumor

Back 51

All causes of subarachnoid hemorrhage

Front 52

-Basilar atherosclerotic rupture
-mycotic
-traumatic
-dissecting

Back 52

All aneurysms NOT bleeding into the subA space

Front 53

Where do 90% of berry aneurysms occur?

Back 53

ANTERIOR circulation at major branch points

Front 54

-AD KPD
-Ehlers-Danlos IV
-Neurofibromatosis I
-Marfan
-fibromuscular dysplasia of extra cranial arteries
-coarctation of the aorta
-smoking
Htn

Back 54

All factors that predispose people to subaracnoid hemorrhage and berry aneurysm

Front 55

Is propensity toward subA aneurysm noticeablle at birth?

Back 55

NO

Front 56

Where does a saccular aneurysm usually rupture?

Back 56

APEX of the sac.

Front 57

Who has more Sub A ruptures?

Back 57

women at or after 50 years

Front 58

What are 2 main sequelae of Sub A hemorrhages?

Back 58

Meningeal fibrosis and scarring

obstruction to CSF flow and reabsorption

Front 59

Which gender is predisposed to AV malformations?

Back 59

Males 2x

Front 60

Where is the most common site for AV malformations?

Back 60

Middle Cerebral Artery, especialliay posterior branches

Front 61

For what is a newborn at risk if they have an AV malformation that occurs in the internal cerebral (galen) vein?

Back 61

CHF due to shunt

Front 62

What does the AV malform look like?

Back 62

tangled web, pulsatile, Sub A or intra cerebral

Front 63

Greatly distended, loosely organized vascular chanels, with thin collagenized walls which are devoid of intervening nervous tissue?

Back 63

Cavernous Hemangioma

Front 64

Where are the most common locations for a cavernous hemangioma?

Back 64

Cerebellum
Pons
Subcortical Regions

Front 65

How are cavernous hemangioma and capillary telangiectasia differentiated from eachother?

Back 65

capillary telangiectasia has neuronal tissue, where as cavernous hemangioma does not

Front 66

What is the most common locagtion for capillary telangiaectasia?

Back 66

pons

Front 67

Aggregates of ectatitic venous channels

Back 67

Venous Angiomas (varices)