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Anatomic Pathology > Cerebrovascular Disease > Flashcards

Cerebrovascular Disease Flashcards

1
Q

Two forms of cerebrovacular disease ?

A

1) Hypoxia, Ischemia, infarction; impairment of blood supply and oxygenation of CNS tissue
2) Hemorrhagic; rupture of CNS vessels

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2
Q

Common etiology of CNS infarction?

A

Embolism, can be global or focal

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3
Q

Common etiologies of hemorrhagic accident in the CNS

A
  • Hyoertension
  • Vascularanomalies (aneurysms and malformations )
  • trauma
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4
Q

Stroke is defined as ?

A

Sudden onset of neurological deficit resulting from hemorrhage or or focal ischemia

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5
Q

Epidemiology of cerebrovadcular disease?

A
  • their most common cause of death: (after heart disease and cancer)
  • most common cause of neurological morbidity and mortality
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6
Q

Biological process that takes place in ischemia?

A

Ischemia leads to
- ATP Depletion
- loss of membrane potential needed for neuronal electrical activity
- elevation of cytoplasmic calcium levels
- inappropriate release of excitatory amino acid neurotransmitters that cause cell damage via calcium influx
- Glutamate release through N methyl D aspartate type glutamate receptors (NMDA)

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7
Q

Zones of ischemic injury

A

1) umbra - necrotic tissue
2) penumbra - At risk tissue

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8
Q

Clinicalpathologic form of CVD includes?

A
  • Global cerebral ischemia (diffuse ischemic encephalopathy)
  • Transient ischemic attack ( TIA)
  • Stroke ( hemorrhagic or ischemic )
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9
Q

Causes of diffuse ischemic encephalopathy

A
  • fall in blood flow to the brain (shock, cardiac arrest, hypotension)
  • Infarcts in watershed areas (between anterior and middle cerebral arteries)
  • Damage to vulnerable regions (purkinje neurons, hippocampus pyramidal cell layer -CA1 (sommer sector), pyramidal neurons of the cortex )
  • cortical laminar necrosis *(diffuse ischemic necrosis of the neocortex, may lead to brain death)
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10
Q

Morphological features of DIE

A
  • Gross; ischemic areas are edmatous with widened gyri and narrowed sulci
  • Loss of hey and white matter differentiation
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11
Q

Pseudo-laminar necrosis pattern is formed from?

A

Uneven cortical neuronal loss and gliosis alternating with preserved zones

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12
Q

TIA symptoms last for about how many hours?

A
  • less than 24hrs
  • Due to small platelet thrombi or artheroemboli
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13
Q

Infarction (85%) in stroke can be due to ?

A

1) thrombotic occlusion
- atherosclerosis of the cerebral arteries
- leads to anemic /white infarcts
2) embolic occlusion
- leads to hemorrhagic infarcts
- throboemboli from cardiac chambers
3) small-vessel disease
- related to hypertension
- hyaline atherosclerosis
- leads to lacunae infarcts/lacunae

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14
Q

Inflammatory process that leads to infarction include?

A
  • Infectious vasculitis
  • Polyarteritis nodosa
  • Primary angitis of the CNS
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15
Q

Microscopic changes associated with cerebral infarction

A

Microscopy**:
- Red neurons (12-24hrs after injury)
- neutrophilic infiltration (24-48hrs)
- histiocytic infiltration and disappearance of neurons (2-10days)
- liquefactive necrosis, histiocytes filled with products of myelin breakdown (2-3weeks)
- fluid filled cavity, reactive astrocytes, lipid-layden macrophages (glitter cells) (3 wks- 1 month )
- Reactive gliosis (astrogliosis) - (years after)

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16
Q

Gross changes associated with infarction

A
  • Little to no change in cerebrum (0 - 24hrs)
  • Indistinct gray-white mater junction (24-48hrs)
  • friable tissue with marked edema (2-10days)
  • tissue liquefies (2-3weeks)
  • fluid filled cavity demarcated by gliotic scar (3weeks to months)
  • old cyst surrounded by gliotic scar (years)
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17
Q

What causes white infarcts and red infarcts?

A

Thrombosis - white infarcts (anemic infarcts)
Embolism - red infarcts ( hemorrhagic infarcts)

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18
Q

Lacunae Infarcts Commonly affect?

A
  • The putamen and caudate
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19
Q

Intra-cerebral hemorrhage / Intraparenchymal hemorrhage most commonly caused by?

A

Hypertension:
- Basal ganglia (putamen in 50% - 60% of cases)
- Thalamus, pons, centrum semiovale and cerebellum rarely

20
Q

Other causes of intracerebral hemorrhage?

A
  • Vascular malformations (AVMs)
  • Cerebral amyloid angiopathy
  • Neoplasms
  • Vasculitides
  • Abnormal hemostasis
  • Hematological malignancies
  • Infection
21
Q

Symtoms of hemorrhagic strike?

A
  • Severe headache
  • Frequent projectile vomiting and nausea
  • Steady progression of symtoms over 15-20mins
  • Coma
22
Q

Intracerebral hemorrhage account for how many percentage of death in chronic hypertensive patients ?

A
  • 15% of death in chronic hypertensive patients
23
Q

How does hyoertension lead to hemorrhagic stroke ?

A

1) hypertension leads to weakening of the vessel through hyaline arteriosclerosis
2) Focal vessel necrosis
3) formation of micro-aneurysms (Charcot Bouchard aneurysms)

24
Q

The second most common etiology of Intraparenchymal hemorrhage is ??

A

Cerebral amyloid angiopathy (CAA)

  • Amyloidogenic oeotide deposit in vessel walls leading to weakening of vessels.
    Similar to that in Alzheimer’s disease
25
Q

stiff Amyloid deposition characteristically involves the?

A

leptomeningeal and cerebral cortical vessels

26
Q

A rare form of.stroke caused by NOTCH3 receptor mutation is ?

A

CADASIL - cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy
- abnormal folding of extra cellular membrane
- concentric medial and adventitial thickening
- Basophilic granular osmophilic deposits and smooth muscle dropout

27
Q

Most common cause of SAH?

A

Ruptured berry aneurysms

  • extension of intracerebral/subdural hematoma
  • vascular malformations
  • trauma
  • hypertensive intracerebral hemorrhage
  • abnormal hemostasis
    tumors
28
Q

Symptoms of SAH?

A
  • Thunderclap headache
  • Nuchal rigidity
  • Neurological deficiency on one side
  • Stupor
29
Q

Berry aneurysms are ?

A
  • Thin walled saccular out-pouching, consisting of intima and adventitia only
  • congenital focal weakness of an artery, not identifiable at birth
  • occur in 2% of the population
  • 20-30% of patients have multiple aneurysms
  • most cases are sporadic
30
Q

Most common site of berry aneurysms is?

A

The anterior circle of willis at branching points
- Anterior cerebral artery branching

31
Q

Disorders associated with berry aneurysms ?

A
  • Marfan syndrome
  • Ehler Danlos syndrome type 4
  • Neurofibromatosis type 1
  • Fibromuscular dysplasia
  • Adult polycystic kidney disease
32
Q

Risk factors for berry aneurysms?

A
  • Cigarette smoking
  • Hypertension
33
Q

Epidemiology and prognosis go berry aneurysms

A
  • Rupture is precipitated by sudden increase in blood pressure
  • slightly more common in women in 5th decade of life
  • prognosis; 1/3 Die, 1/3 recover, 1/3 rebleed
34
Q

List the vessels involved in the different type of Cerebral hemorrhages?

A
  • Epidural hematoma - middle meningeal artery
  • subdural hematoma - Bridging veins
  • subarachnoid hemorrhage - Berry aneurysm rupture
  • Intraparenchymal hemorrhage- chronic hypertension
35
Q

The most important effects of hypertension on the brain include ?

A
  • Lacunar infarcts
  • slit hemorrhages
  • hypertensive encephalopathy
  • massive hypertensive intracerebral hemorrhage
36
Q

What are lacunar infarcts?

A

Small (<15mm) cystic infarcts resulting from cerebral arteriolar sclerosis and occlusion

Tissue loss is accompanied by Lipid laden macrophages and surrounding gliosis

37
Q

Most commonly affected spots in lacunar infarcts?

A
  • Lenticular nucleus
  • Thalamus
  • Internal capsule
  • Deep white matter
  • Caudate nucleus
  • Pons
38
Q

Slit hemorrhages occur when?

A

Occurs when hypertension causes small vessels rupture

They resorb but leave residual hemosiderin laden macrophages and associated gliosis

39
Q

AHE (Acute hypertensive encephalopathy) is defied as?

A
  • Clinicooathological syndrome caused by Increased ICP
  • Manifest as Diffuse cerebral dysfunction
  • headcahe, confusion, projectile vomiting, convulsions, coma
  • post mortem examination; edematous brain, occasionally with herniation, Petechiae and anterior fibrinoid necrosis
40
Q

Vascular (Multi-infarct) dementia so

A

Caused by Recurrent small infarcts
Characterized by
- dementia
- gait abnormalities
- Pseudobulbar signs

41
Q

Causes of vascular dementia?

A
  • Cerebral atherosclerosis
  • Vessel thrombosis or embolization
  • Cerebral arteriolar sclerosis
42
Q

Binswanger disease - Chroninc hypertensive injury

A
  • recurrent ischemic injury involved a subcortical white matter
  • myelin and axonal loss
43
Q

Primary Intraparenchymal hemorrhage are common in what regions of the brain?

A
  • White matter
  • Deep gray matter
  • Posterior fossa contents
44
Q

What are boundary zones of the brain?

A

Regions of the cerebrum with the least robust vascular supply

45
Q

Dissolution of an embolism and the repercussion can result into?

A

Hemorrhagic transformation of ischemic infarct

Anatomic Pathology (12 decks)

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