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Block 8 Week 4 > Vascular Pathology of Brain- Parks > Flashcards

Vascular Pathology of Brain- Parks Flashcards

1
Q

What are three ways you can get a stroke?

A
  • Thrombotic vessel occlusion
  • Vascular Rupture
  • Embolic vessel occlusion
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2
Q

what does this cause:

Oxyge-rich blood flow to the brain is restricted by a blood clot or other blockage

A

ischemic stroke

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3
Q

Where do you often see an atherosclertoic plaque?

A

carotid bifurcation

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4
Q

When you check for carotid bruits what are you looking for?

A

carotid plaques

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5
Q

If you infarct the internal capsule what do you get?

A

a motor problem

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6
Q

Occlusion at the (blank) causes cortical infarcts with motor and sensory loss and often aphasia.

A

trifurcation

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7
Q

Occlusion of a striate branch transects the internal capsule and causes a (blank)

A

motor deficit

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8
Q

A lipid rich plaque is a (blank) plaque

A

high risk plaque

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9
Q

If you see focal dusky discoloration and swelling where is your infarct?

A

in the middle cerebral artery

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10
Q

YOu can use TPA within (blank) hours

A

4

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11
Q

a lipid rich high risk plaque will causes a (blank) thrombis

A

LOCALIZED

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12
Q

When cells are dying (blank) enters the cell

A

calcium

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13
Q

In ischemia you have a lot of (blank) being released which results in uncontrolled (blank) coming in… this is called (blank)

A

Glutamate
calcium
exocitotoxicity

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14
Q

What is penumbra?

A

area at risk but not dead

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15
Q

In the brain, you can get (blank) necrosis with infarct

A

liquifactive

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16
Q

What can cardiac vegetations cause?

A

stroke via embolization

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17
Q

(blank) follows a cardiac arrest where no blood is bein pumped

A

global ischemia

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18
Q

What does HTN do?

A

gives you blowout hemmorhage and accelerates atherosclerosis

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19
Q

Where are common places to get a blood clot in the head?

Why?

A

in the internal carotid artery and middle cerebral artery

Because there are bifurcations

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20
Q

If you have an atherosclerotic plaque, what are the 2 things that can happen?

A
  • you can get a piece to break off and lodge in there

- aggregation of platelets causing an emboli due to endothelial damage

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21
Q

If you get an occlusion of the striate arteries, what will you be transecting? Resulting in…?

A

the internal capsule

a motor deficit

22
Q

Occlusion at the trifurcation causes (blank) infarcts with motor and sensory loss and often (blank)

A

cortical

aphasia

23
Q

Explain why increased cytosolic calcium in cell injury is bad

A

It will increase activation of cellular enzymes and increase mitochodnrial permeability-> this results in using up all your resources and resulting in a lack of ATP, membrane damage and nuclear damage

24
Q

Increased endonuclease activity due to increase cytosolic calcium will result in (blank)

A

nuclear damage

25
Q

Increased protease and phospholipase activity will result in (blank)

A

membrane damage

26
Q

Increase ATPase and increased Mitochondrial permeability transition will result in (blank)

A

decreased ATP

27
Q

Whats neurotransmitter is unable to be reuptaken (i.e removed) when ischemia is present?
What is the receptor involved in this (i.e overstimulated due to the increased glutamate)? What will this cause the neurons(nerve cell) to do?

A

glutamate
NMDA
swell and explode!

28
Q

If you have a severe excitotoxic insult, what kind of cell death will this result in?

A

Necrosis

29
Q

If you have a mild excitotoxic insult, what kind of cell death will this result in?

A

Apoptosis

30
Q

When you have a severe insult (such as ischemia) and you get a activation of what system that results in superoxide generation followed by formation of ONOO (peroxynitrite)!?!?!?!
What does peroxynitrite do?
What will PARS do?

A

nitric oxide synthatse (NOS)

  • results in oxidation of protein, lipid and DNA (which results in cell death) and ACTIVATES PARS
  • ATP and NAD depletion
31
Q

Activation of (blank) will cause mitochondrial swelling, and rupture of outer membrane, resulting in impaired ATP generation (thus reduction in ATP).

A

PTP

32
Q

If you have a mild excitotoxic insult, what wil happen?

A

you will get activation of NOS system resulting in superoxides which will initiate caspases to induce apoptosis

33
Q

What is a penumbra?

A

tissue at risk of necrosis, that is still alive and if reprofused fast enough will survive

34
Q

A very new infarct will show what kind of histopathology?

A

edema, hypereosinophilic neurons and perivascular polymorphonuclear leukocytes and Pyknotic nuclei of dying neurons

35
Q

Why do you get edema in cerebral infarcts?

A

due to naturemia

36
Q

Between (blank) of stroke patients develop enough edema to cause obtundation or brain herniation. Edema peaks on the (blank) day but can cause a mass effect for 10 days.
Stroke can cause brain herniation due to increased (blank)

A

5 and 10%
2 or 3rd
edema

37
Q

If you have too much edema, what surgical procedure can you do?

A

hemicraniotomy (take a piece of brain out to allow for expansion)

38
Q

What is different about liquifactive necrosis in the brain versus different organs in the body?

A

in the brain, it happens WITHOUT even having an infection, can happen just with ischemia

39
Q

What is a cystic infarct?

A

it when you get a lesion in the brain due to liquifactive necrosis

40
Q

If you open up a heart and see (blank), this is a huge risk factor for embolization

A

Vegetations (bacterial growth)

41
Q

(blank) follows a cardiac arrest where no blood is being pumped. This follows severe hypotension in shock, such as hypovolemic shock from severe blood loss.

A

Global ischemia

42
Q

Ischemic/hypoxic encephalopathy will result in (blank)

A

global ischemia

43
Q

What is a watershed infarct?

A

Ischemia that is localized to the border zones between two major arteries in the brain (ie. between middle cerebral and anterior cerebral)

44
Q

What is laminar necrosis?

A

the uncontrolled death of cells in the cerebral cortex of the brain in a band-like pattern, with a relative preservation of cell immediately adjacent to the meninges

45
Q

How do you get a hemorrhagic stroke and what does it cause to happen?

A

weakened/disease blood vessels rupture and blood leaks into brain tisue

46
Q

Are watershed and laminar necrosis caused by ischemic or hemorrhagic stroke?

A

ischemic stroke

47
Q

What does hypertension accelerate? WHat does it cause?

A

atherosclerosis

lacunar stroke

48
Q

Lacunar strokes are caused by (ischemic/hemorrhagic) stroke

A

hemorrhagic

49
Q

What is this:
A small aneurysm that looks like a berry and classically occurs at the point at which a cerebral artery departs from the circular artery (the circle of Willis) at the base of the brain.

Where do you most often get these in the circle of willis?

A

A berry/sacular aneurysm

between anterior communicatiing and anterior cerebral artery

50
Q

What are all the places you can get a berry aneurysm in the circle of willis?

A
  • between anterior communication and anterior cerebral artery
  • b/w posterior communicating artery and middle cerebral artery
  • b/w middle cerebral artery and its first branch
  • between basilar artery and posterior cerebral artery
51
Q

Berry aneurysms can rupture and caused (Blank) hemorrhage. What disease is this associated with?

A

subarachnoid

-polycystic kidney disease

52
Q 
In an (blank), arteries connect directly to veins without a capillary bed in between.This creates a problem called a high-pressure shunt or fistula. Veins are not able to handle the pressure of the blood coming directly from the arteries. The veins stretch and enlarge as they try to accept the extra blood. The weakened blood vessels can rupture and bleed and are also more likely to develop aneurysms.
What will be the first symptom if it ruptures?
A

AV malformation

- a headache

Block 8 Week 4 (8 decks)

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