Nervous System (Block 6): Goodman Lectures On Cv Pathology

Front 1

what pathology is this showing?

Back 1

circle of willis with atherosclerosis (lipid in the wall of blood vessels)You get narrowing of lumen and eventually may get occlusion. A thrombus may form. Or develop emboli, which break off and clog up blood vessels down the line.

Front 2

what is the major cause of ischemic stroke?

Back 2

Atherosclerosis is Most common cause of stroke. Can be intracranial or extracrainial (in the bifurcation of carotid into int and ext. any branch point in a vessel is where you have turbulent flow and can get atherosclerosis.)

Front 3

what is this? what is its pathogenesis?

Back 3

this is a carotid endarterectomy showing atherosclerosis with complicated plaques. There is gradual encroachment of plaque. For most of its life, it lives beneath endolthelium. On a random day, it breaches the endothelium and then coagulation starts. Once this happens you can have occlusions or emboli. When you get atherosclerosis with breaching of the endothelium, this iscalled a “complicated plaque”

note: Carotid endarterectomy (CEA) is a surgical procedure used to prevent stroke, by correcting stenosis in the carotid artery. Endarterectomy is the removal of material on the inside (end-) of an artery.

Front 4

what pathology is this showing?

Back 4

carotid dissection with accumulation in the adventitia. this squashes blood flow and can eventually lead to stroke

Front 5

what is a "watershed" infarct?

Back 5

area in the junctions of major arterial supply zones that have reduced pressure of perfusion bw the distal portions of arterial supply when there's low BP. classic borderzone is bw anterior and middle cerebral arteries distal territories

- causes weakness of shoulder/hip > leg/upper limb

Front 6

what is shown here?

Back 6

global hypoperfusion = when the ischmic injury is severe enough to cause cortical atrophy of neuron containing structures like BASAL GANGLIA and causes HYDROCEPHALUS EX VACUO

Front 7

what is imaged here?

Back 7

borderzone infarct in the parietal region. bilateral "man in a barrel" with arms. this can follow prolonged cardiac bypass or cardiac arrest.

Front 8

what are the consequences of global ischemia?

Back 8

if brief (minutes) = pt's neurological fxns may be restored with transient confusion

more severe injury may lead to dementia spasticity

if protracted ischemia = pt may go into coma and be in persistent vegetative state

Front 9

what's being shown here?

Back 9

relative watershed; showing that the surface is better perfused than the depths. if a person experiences hypoperfusion, you will see bigger changes in the depths of the sulci (darker than normal tissue).

Front 10

certain cell populations are more vulnerable to ischemic injury with ____>>____>>____. what are the 3 most sensitive populations?

Back 10

neurons>>glia>>endothelium

3 most sensitive:
1. purkinje cells of cerebellum
2. large neurons in Sommer's sector of hippocampus (CA1)
3. middle layers of cerebral cortex - Laminar necrosis

Front 11

name the most sensitive portion of the hippocampus

Back 11

pyrimidal neurons of CA1 - Sommer's sector

Front 12

what pathology is being shown here?

Back 12

global hypoperfusion in the brain leading to ischemia of hippocampus (CA1-Sommer's sector) due to selective vulnerability

Front 13

what pathology is shown here? what clinical sx's will result from such an event?

Back 13

acute middle cerebral artery infarct with discoloration in MCA territory, squashing of the ventricles and cingulate herniation.

clinically, pt will have hemiparesis of contra face/upper limbs, sensory deficit in arms/face, with contra homonymous hemianopsia

Front 14

what pathology is shown here? how would this show up clinically?

Back 14

posterior cerebral artery infarct; could occur from emboli/thrombus

-pt would have difficulty recognizing faces (ventral "what" stream compromised) with hemianopsia

Front 15

what is the pathological evolution of cerebral infarcts?

Back 15

A dead neuron is a red neuron. Cytoplasm becomes eosinophilic and without contents. If you allow 6-8 hrs after hypoperfusion of brain, you’ll start to see this.

By day 2: perfusion will be restored by fibrillogeneis. Macrophages will come in and start cleaning up the mess. There’s not BBB, but still have vascular proliferation. Dead tissue is cleared out by macrophages.

After months: cystic cavity from all the dead tissue being cleared out by macrophages

Front 16

what is the earliest light microscopic change in an infarct in brain tissue?

Back 16

red neurons

Front 17

what pathology is shown here?

Back 17

Remote MCA infarct. After macrophages cleared out tissue. This is the MCA infarct 6 months later. All the dead tissue is cleared out. Theres compensatory enlargement of the ventricles. There used to be neurons here…now theyr/e gone. So their axons are going to degenerate. If you look at cerebral peduncles and other parts of the brain grossly, you’ll see that they’re gone

Front 18

what is this? what is the difference bw left and right side of picture?

Back 18

this is wall of remote infarct cavity.

Foamy macrophages on left.
Glial cells on the right forming glial scar on the wall of infarct.

Front 19

what pathology is shown here?

Back 19

left: atrophy of cerebral peduncle on the left
right: atrophy of medullary pyramid on left of brain stem

BOTH FOLLOWING MCA INFARCT

Front 20

What pathology is shown here? how will this show up clinically?

Back 20

remote pontine infarct in the CST/CBT area. this will lead to contra weakness, contra DC findings

Front 21

what is going on with this brain?!?!

Back 21

multiple hemorrhagic embolic infarcts. when you see multiple hemorrhagic strokes in varying vascular territories, you need to think EMBOLI!! (ie. emboli from the heart)

Front 22

define CNS/systemic vasculitis. what is the one thing you must have in order to classify pathology as such?

Back 22

vessels become inflammed themselves either systemically or witihn the wall of hte brain.

- inflammatory infiltrate MUST involve entire thickness of vessel wall (transmural inflammation)!!

- when you see multifocal stroke, think about emboli or vasculitis!

Front 23

what is this?

Back 23

vasculitis

REMEMBER IT MUST HAVE TRANSMURAL INFLAMMATION!!! aka... the inflammatory infiltrate must involve the entire thickness of the vessel wall

Front 24

what is this?

Back 24

granulomatous vasculitis; showing giant cell

Front 25

what pathology is shown here? how did this happen? what are the Sx's?

Back 25

this is a lacunar infarct that resulted from long standing hypertension which caused small, perforating vessels to become thick-walled...thus leading to ischemia.

Sx's depend on where infarct occurs

Front 26

what is this?

Back 26

Microaneurysm = when there’s a pocket that forms from increased pressure (hypertension) and then it breaks to give a hypertensive intracerebral hemorrhage

Front 27

what is the time frame in which you can give pt TPA for thrombolysis if there's a sudden onstem of thrombotic stroke? what is the other pre-requisite for administering TPA?

Back 27

under 3 hours!
- this Tx can lead to recovery!!

PATIENT CANNOT HAVE HAD A HEMORRHAGIC STROKE IN THE HEAD...so you have to get CT scan to check.

Front 28

besides administering TPA to a pt that just underwent thrombotic stroke, what else do you do (or not do)?

Back 28

- do not allow hypotension
- protect airway if consciousness decreased
- DVT (deep vein thrombosis) with low dose heparin so they won't get a pulmonary embolus down the line
- anti-platelet (baby aspirin)

Front 29

what do you do for a pt with an embolic stroke? (2)

Back 29

- remove source (if possible)
- consider anti-coaguulation (warfarin/heparin)

try to give anti-coagulant to prevent the formation of new emboli...