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Neuropathology > Pathology of CV Disease > Flashcards

Pathology of CV Disease Flashcards

1
Q

Causes of CV disease

Atherosclerosis

A

Atherosclerosis (AS) is the major predisposing factor for cerebrovascular disease. Severity of AS involvement may differ between intracranial and extracranial vessels. It is important to note that intracranial damage can result from disease in the extracranial (neck) vessels (ICA, vertebral artery) in the absence of disease in intracranial vessels.

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2
Q

Causes of CV disease

Important vascular diseases

A
  • arteriosclerosis and arteriolosclerosis due to chronic hypertension and diabetes mellitus
  • aneurysms (saccular, atherosclerotic, mycotic, etc.) * cerebral amyloid angiopathy
  • others (e.g., vasculitis, vascular malformations, CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarctions and leukoencephalopathy) * clotting disorders (coagulopathies, RBC diseases, etc.)
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3
Q 
Brain is supplied by which vessels
internal carotid arteries (anterior circulation) give rise to:
vertebral arteries (posterior circulation) give rise to:
A

internal carotid arteries (anterior circulation) give rise to

  • middle cerebral arteries (MCA),
  • anterior cerebral arteries (ACA)

vertebral arteries (posterior circulation) give rise to

  • basilar artery and branches
  • posterior cerebral arteries (PCA) are terminal branches of basilar artery
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4
Q

Major cerebral arteries

path

A

Most major cerebral arteries ramify in the leptomeninges over the brain surface and then penetrate the brain as superficial or deep perforators. Important perforators include the lenticulostriate arteries arising from MCA, supplying the basal ganglia, and thalamic perforators arising from the PCA, supplying the thalamus.

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5
Q

General considerations of CNS vasculature

A
  • collateral circulation is poorly developed:
  • perforating arteries are end arteries: collaterals exist only at capillary level and are usually inadequate.
  • border zones (“watershed zones”) between arterial
    territories are susceptible to decreased blood flow or
    oxygen delivery.
  • occlusion of vessel can lead to a well defined infarction limited to that vessel’s territory.
  • because of limited collateralization of major intracranial vessels, occlusion of proximal portions of these vessels in the neck may cause major intracranial damage.
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6
Q

Stroke

def

A

Many cerebrovascular diseases present as stroke, defined as: “an acute neurologic dysfunction, global or focal, usually developing over minutes or hours and continuing for more than 24 h, occurring as a result of parenchymal damage due to a vascular process.”

NOTE: a vascular process whose symptoms resolve in less than 24 h is called transient ischemic attack (TIA)

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7
Q

Strokes are caused by…

A
  1. cerebral infarctions (“ischemic stroke”)

2. non-traumatic intracranial hemorrhages (“hemorrhagic stroke”)

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8
Q

Other forms of vascular disease in stroke

A
  1. diffuse hypoxic-ischemic injury, usually reflecting a global brain insult such as systemic hypotension or hypoxia
  2. acute or chronic hypertensive encephalopathy
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9
Q

Trauma can mimic or result in some forms of CV disease

A
  1. traumatic hemorrhages
  2. diffuse brain damage
  3. cerebrovascular consequences of trauma
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10
Q

Cerebral infarctions

Def/arise from…

A

focal ischemic necrosis of brain tissue due to occlusive vascular disease or other forms of vascular insufficiency

Most cerebral infarctions arise from occlusion of an artery due to atherosclerosis and/or thromboembolus.

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11
Q

Ischemic stroke

Clinical presentation

A

rapid onset of neurologic deficit
maximal deficit develops rapidly
secondary effects may occur
recovery is variable

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12
Q

Lacunes

def

A

lacunes are small infarcts (<1 cm) arising from occlusion of small vessels, generally in the setting of chronic hypertension.

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13
Q

Physiology of brain vascular damage

Injury may result from…

A

a. ischemia (reduced blood flow)
* focal cerebral ischemia: reduced flow in one vessel
* global cerebral ischemia: failure of systemic circulation

b. hypoxia (usually systemic)
c. hypoglycemia (usually systemic)

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14
Q

Physiology of brain vascular damage

mechanism

A

a. O2 deprivation: functional hypoxia
b. metabolic disruption: Ca++, lactate, free radicals
c. injury by released excitotoxins: glutamate, aspartate

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15
Q

Physiology of brain vascular damage

Factors affecting patterns and extent of injury

Selective vulnerability

A

cell type: neurons > oligodendrocytes > astrocytes

sensitive populations of neurons

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16
Q

Physiology of brain vascular damage

Factors affecting patterns and extent of injury

Duration of ischemic injury

A

~ 8-10 seconds: cessation of function

~ 4-8 minutes: irreversible damage begins

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17
Q

Physiology of brain vascular damage

Factors affecting patterns and extent of injury

BP/temp

A

maintenance of blood flow (blood pressure) can reduce injury, possibly by removing toxic metabolites

temperature: hypothermia (under 30°C) permits longer period of ischemic cell survival

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18
Q

Physiology of brain vascular damage

Factors affecting patterns and extent of injury

Glucose stores

A

hyperglycemia: may promote damage
hypoglycemia: when mild, may prevent damage

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19
Q

Physiology of brain vascular damage

penumbra

A

following an injury, tissue at the transition between already necrotic and viable tissue (the “penumbra” of the infarct) may be at risk for damage by apoptosis but still salvageable by appropriate timely intervention

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20
Q

Physiology of brain vascular damage

reperfusion

A

reperfusion of a previously ischemic area may save marginally injured cells but may promote free radical production with further injury or even conversion to hemorrhagic infarct

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21
Q

Encephalomalacia

def

A

brain infarction is known as encephalomalacia (brain softening)

22
Q

Pathology of infarcts

Acute infarcts

A

acute infarction: histologic signs of irreversible cell injury— cell necrosis (“red neurons”) appear by around 12-24h post injury

23
Q

Pathology of infarcts

Evolution of necrotic area

A
  • early changes (15-24 h) : acute inflammation: early blood vessel response, PMN’s & fluid enter
  • subacute changes (1-5 d): influx of macrophages, beginning of liquefaction, inflammatory edema peaks * later changes (>1 w): proliferation of astrocytes around infarct, progressive liquefaction and removal of necrotic debris
  • later changes (weeks to months): cavitation and gliosis
24
Q

Conversion of bland to hemorrhagic infarct

Most common in…

A

conversion of bland to hemorrhagic infarct is most common in embolic infarct, where embolus breaks up and flow is re- established to damaged tissue

25
Q

Secondary changes in brain following infarct

A

a. Wallerian degeneration of affected fiber pathways b. atrophy of involved or adjacent structures
c. compensatory ventricular enlargement (“hydrocephalus ex vacuo”)

26
Q

Diffuse hypoxic/ischemic injury

Results from…

A

results from transient or prolonged global cerebral ischemia, usually following profound systemic hypotension (cardiac arrest, shock, etc.) or other systemic conditions (systemic hypoxemia. Severe hypoglycemia, CO poisoning, etc. also cause patterns of diffuse brain damage.

27
Q

Diffuse hypoxic/ischemic injury

Pattern of damage

A

Although brain damage is often symmetrical, reflecting the systemic nature of the insult, existing vascular disease causing stenosis or occlusion may result in earlier or more severe damage in the territory supplied by the affected vessel.

28
Q

Diffuse hypoxic/ischemic injury

Most vulnerable neuronal cell populations

A
  • hippocampus: especially Sommer’s sector (area CA1)
  • cerebral cortex: laminar necrosis with maximal damage involving middle cortical layers (often 3-4)
  • watershed zones between vascular territories
  • cerebellar Purkinje cells
29
Q

Diffuse encephalopathy

forms

A
  1. transient post-ischemic confusional state: reflecting mild injury
  2. hypoxic-ischemic encephalopathy with permanent deficits, e.g., learning/memory difficulty due to hippocampal damage
  3. persistent vegetative state reflecting severe irreversible brain damage with sparing of some autonomic and brainstem functions
  4. brain death: irreversible cessation of brain function, including brainstem function, usually cessation of electrical activity, and cessation of cerebral blood flow
  5. “respirator brain”: autolytic change resulting from failure of perfusion following diffuse brain swelling
30
Q

Intracranial hemorrhage

Divisions/due to…

A

Divided into non-traumatic and traumatic hemorrhages.

Non-traumatic hemorrhages due to spontaneous rupture of blood vessel often present clinically as “hemorrhagic stroke.”

31
Q

Intracranial hemorrhages

Classified by…

A

Hemorrhages are classified by anatomic compartment: intraparenchymal, subarachnoid, subdural, epidural. Most non-traumatic hemorrhages are subarachnoid hemorrhages (SAH) or intraparenchymal hemorrhages (IPH). Trauma can produce hemorrhage in any compartment. Most subdural hemorrhages (SDH) or epidural hemorrhages (EDH) are due to head trauma.

32
Q

Intraparenchymal hemorrhages

Divisions

list

A

Ganglionic (“deep”, “hypertensive”) hemorrhages

Lobar hemorrhages

Subarachnoid hemorrhages

33
Q

Ganglionic hemorrhages

Where do they typically arise/cause

A

typically arise in putamen, thalamus, pons, or deep cerebellar hemisphere, and are usually due to chronic hypertensive vascular disease. This causes arteriosclerosis of small arteries, especially prominent in the perforating arteries of the basal ganglia and thalamus, and can lead to formation of microaneurysms known as Charcot-Bouchard aneurysms. Rupture of the blood vessels or microaneurysm leads to hemorrhage, often massive.

34
Q

Lobar hemorrhages

Location/result from…

A

Lobar hemorrhages are located more superficially in cerebral hemispheres (lobes) and result from a variety of small vessel disease (hypertensive vasculopathy with arteriosclerosis and arteriolarsclerosis, cerebral amyloid angiopathy (often seen in older individuals and patients with Alzheimer disease), DIC, other forms of coagulopathy, infectious or autoimmune vasculitis, etc.)

35
Q

Lobar hemorrhages

pathology

A

a. acute mass of hemorrhage (hematoma) disrupts brain parenchyma and causes acute mass effect
b. in survivors, organization and resorption of hematoma occurs from periphery and is accompanied by edema (peaks in 2-3 d)
c. resorbed hematoma can eventually evolve into a cavity with wall of gliotic hemosiderin-stained brain

36
Q

SAH

Arise from

A

These usually arise from larger arteries and may be massive.

Most important causes are rupture of a saccular (“berry”) aneurysm or of a congenital arteriovenous malformation (AVM)

37
Q

Saccular aneurysm’s

Originate from…

A

originate from a congenital defect in the arterial wall at arterial branch points at base of brain; they occur with increased frequency in patients with autosomal dominant polycystic kidney disease and several other genetic conditions

38
Q

Saccular aneurysms

Most common sites

A

most common sites are at junction of ACA-Acomm, MCA- Pcomm, or MCA-lenticulostriate branches

39
Q

Saccular aneurysm

Exacerbated by…

A

aneurysm itself is not present at birth but develops and enlarges over time; enlargement is exacerbated by hypertension, smoking, and other factors; risk of rupture is 1-2%/year and is maximal at 10mm diameter. Large aneurysms may thrombose.

40
Q

Saccular aneurysms

Rupture produces…

A

rupture usually produces acute massive SAH at base of brain.

41
Q

IPH and SAH

Clinical presentation

A

Typical clinical presentation includes acute onset of severe headache, due to stretching of blood vessels, accompanied by rapid deterioration of neurologic function, due to increasing intracranial pressure and direct brain damage.

42
Q

IPH and SAH

Complications of hemorrhage

Acute/chronic

A

acute: arterial vasospasm, leading to ischemia/ infarction in structures supplied by spastic vessels
chronic: breakdown of hematoma and subsequent scarring may interfere with CSF circulation and cause hydrocephalus

43
Q

Epidural and subdural hemorrhages

Usually result from…

A

Head trauma

44
Q

Epidural hematoma

chars

A

Epidural hematoma: accumulation of arterial blood between the dura and the inner table of skull, usually results from fracture- induced laceration of meningeal vessels, especially middle meningeal artery.

Note: Following trauma, the patient may appear well for a short time before developing symptoms of increasing ICP. This is known as the “silent interval” and usually lasts between 6 and12 hrs.

45
Q

SDH

Results from

A

Accumulation of blood between the dura and arachnoid usually results from shearing of bridging veins along superior sagittal sinus

may occur after relatively mild trauma in elderly individuals with brain atrophy resulting in stretching of bridging veins.

46
Q

SDH

chronology

A
  • acute: clotted blood
  • subacute: clotted and liquefying blood
  • chronic: liquid blood
  • subdural hygroma: CSF-like fluid accumulation replacing hematoma
47
Q

SDH

Chronic forms

A

chronic forms: may develop weeks or months after injury; associated with formation of subdural membrane of organization tissue encapsulating hematoma.

48
Q

Hypertensive CV disease

Effects of chronic HTN

pathology

A

i. Lacunar infarcts (see above): most commonly occur in basal ganglia and deep cerebral white matter.
ii. Charcot-Bouchard aneurysms (see below)
iii. Etat criblé: loss of tissue density without infarction around small arteries in basal ganglia or white matter
iv. Slit hemorrhages: small linear hemorrhages around blood vessels

49
Q

Hypertensive CV disease

Effects of chronic HTN

clinical

A

Clinical: chronic hypertensive encephalopathy: progressive syndrome (“multi-infarct or vascular dementia”) of dementia, abnormalities in gait, loss of inhibition of reflexes (“pseudobulbar signs”), and focal deficits

50
Q

Hypertensive CV disease

Effects of acute severe HTN

A

Effects of acute severe hypertension: acute hypertensive encephalopathy (“malignant hypertension”), characterized clinically by ↑ ICP, confusion, headache, and pathologically by brain edema, petechial hemorrhages, and fibrinoid necrosis of arterioles.

Neuropathology (29 decks)

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