Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Cerebrovascular Disease > Flashcards

Cerebrovascular Disease Flashcards

1
Q

Cerebrovascular Disease

A

Brain disorders involving the blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Stroke

A

All cerebrovascular disease when symptoms begins <24hrs

- Ischemic vs Hemorrhagic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Ischemic stroke

A
  • Embolic or Thrombotic
  • Global or focal hypoxia
  • MRI within hours but CT -ve before 24 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hemorrhagic Stroke

A
  • Vascular rupture
  • Intracranial or subarachnoid
  • MRI & CT immediately after onset
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Global Cerebral Ischemia/ Hypoxia

A

552

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Watershed Border zone

A

Ares of the brain or spinal cord that is most distal to the arterial blood supply
1.
2.
3.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Area of Watershed zone most vulnerable to infarcts

A

Between the ACA & MCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Types of Ischemic strokes

A
  1. Embolic infarctions

2. Thrombotic infarctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Embolic Infarction (source & predisposing factors)

A

Source: Cardiac mural thrombus or carotid atheromatous plaque
- Predisposing factors- A-fib, Valvular disease, Myocardial dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Thrombotic occlusion/infarction

A

Source- thrombus superimposed on atherosclerotic plaque –> Fragment or embolize

  • May lead to lacunar infarcts
  • Anterograde extension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Lacunar infarcts

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Gross morphology of infarcts

A
  • swollen brain w. wide gyri & narrow sulci
  • poor demarcation between white & gray matter
  • tissue liquification & cavity filling w/ fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Microscopic changes of infarcts up to 24 hours (acute)

A

Micro-vacuolation –> Cytoplasmic eosinophilia –> Nuclear pyknosis (red nucleus) & karyorrhexis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Microscopic changes of infarcts 24 hours to 2 weeks (subacute)

A
  • Tissue necrosis
  • Macrophage influx
  • Vascular proliferation
  • Reactive gliosis (astrocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Microscopic changes of infarcts after 2 weeks (repair)

A

Gliosis w/ removal of necrotic tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Types of Intracranial Hemorrhage

A

Intraparenchymal

  • Hypertensive
  • Non-hypertensive

Subarachnoid

17
Q

Intraparenchymal Hemorrhage types

A

Primary intraparenchymal hemorrhage
Hyaline arteriolar Sclerosis
Silt hemorrhages
Lacunar infarcts

18
Q

Hyaline Arteriolar Sclerosis

A
  • Deep penetrating arteries & arterioles of the Basal ganglia, brainstem & hemispheric white matter
  • Weakened walls –> Small microaneurysms –> Rupture.
19
Q

Silt hemorrhage

A

Rupture os small caliber penetrating vessels

20
Q

Lacunar infarcts

A

Small cavitary infarcts secondary to thrombosis of vessel with arteriolosclerosis changes of single penetrating branch

21
Q

Primary Intraparenchymal Hemorrhage

A
  • Rupture of small intraparenchymal vessel

- usually basal ganglia, thalamus, pons & cerebellum

22
Q

Non-hypertensive hemorrhage

A
  1. Amyloid angiopathy - amyloid deposit & weaken walls –> Rupture & hemorrhage
  2. Vascular malformation
  3. Coagulopathy - Vit. k deficiency,
  4. Cortical vein or dural sinus thrombosis
23
Q

Vascular Malformations (AVM)

A
  • 2:1 Male: female; usually presents @ 10-30 years
  • seizures, intracerebral & subarachnoid hemorrhages
  • Newborns = High output CHF due to shunting form arteries to veins
24
Q

Gross changes in vascular malformations

A

tangled network of wormlike vascular channel

25
Q

Microscopic changes in Vascular Malformations

A

Enlarged BV separated by gliotic tissues

- Evidence of previous hemorrhages

26
Q

Berry aneurysms

A
  • Circle of Willis (90% in the anterior circulation- between ACA & Anterior communicating artery)
  • defect in Tunica media
  • RFs- ADPCKD, EDS, smoking & HTN
27
Q

Morphology of Berry aneurysms

A
  • Saccular, thin-walled out-pouchings of arteries.
  • Beyond the neck the muscular wall
  • Sac lined only by thickened hyalinized intima & a covering adventitia
  • Extravasated blood enters the subarachnoid space –> Subarachnoid hemorrhage
28
Q

Clinical features of Subarachnoid hemorrhage

A
  • “Thunderclap headache” or “worst headache”
  • Rapid loss of consciousness
  • Meningismus : Neck stiffness & photophobia

precipitated by increased ICP- straining, orgasm, etc.
NB: the bigger the aneurysm the greater the risk of rupture

29
Q

Investigations for Subarachnoid hemorrhage

A
  • CT scan

- Lumbar puncture - Inc RBCs & Xanthochromia (yellow color due to bilirubin after RBC lysis)

30
Q

Prognosis & complications of Subarachnoid hemorrhage

A

Prognosis is poor w/ high mortality. worsens w/ successive bleeds

  1. Rebleed (common)
  2. Vasospasm (early periods after hemorrhage)
  3. Hydrocephalus (healing & meningeal fibrosis –> Obstruct CSF flow or absorption)

Pathology (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions