6/16- CV Pathology and Pathophysiology Flashcards

1
Q

What are Watershed zones?

Where is the worst?

A

Areas supplied by multiple arteries (but the very end of these arteries)

  • Infarcts may result from hypotension

Worst = high posterior parietal cortex (“triple border zone area”)

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2
Q

What is the leading cause of ischemic strokes?

A

Atherosclerosis spawning emboli or thrombus formation (may be intracranial or extracranial)

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3
Q

What is this?

A

Carotid endarterectomy

  • Atherosclerosis with complicated plaques
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4
Q

What is a “complicated” plaque?

What does it cause?

A

When an atherosclerotic plaque erodes through the endothelium

  • Causes thrombogenesis
  • May lead to emboli or breaking off or local thrombosis with occlusion of the vessel
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5
Q

What is a non-atherosclerotic cause of stroke?

A

Carotid dissection

  • Blood leaves vessel, gets stuck within adventitia, and then compresses vessel lumen
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6
Q

Where do dissections usually occur?

A

Areas of trauma to the vessel

  • e.g. struck in neck with baseball
  • damage to back of throat (near carotid)
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7
Q

What are some symptoms seen in hypotensive ischemic injury?

A

“Watershed” or arterial border zone infarcts

  • Dorsolateral aspects of the cerebral hemispheres
  • “Man in a barrel” weakness
  • Rims of the cerebellar hemispheres

If sufficiently severe, global damage with atrophy of neuron containing structures:

  • Laminar necrosis
  • Basal ganglia shrinkage
  • Hydrocephalus ex vacuo
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8
Q

What is this?

A

Watershed infarct of high posterior parietal cortex (although can involve motor strip)

  • Infarct = loss of tissue due to ischemia
  • Enlarged sulci with shrunken gyri
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9
Q

What is this?

A

Result of global hypoperfusion

  • Not much cortex left (innermost layers go first- laminar necrosis)
  • No thalamus, caudate….
  • Hydrocephalus ex vacuo
  • Person would be unconscious; persistent vegetative state
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10
Q

What is this?

A

Sulcal depth discoloration seen in relative watershed

  • Depth of sulcus is relatively less well perfused than surface
  • Opposite of contusions (affect surface of gyri more)
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11
Q

Which cells are most vulnerable to ischemia?

A

Neurons >> Glia > Endothelium

  • Purkinje cells of cerebellum
  • Pyramidal neurons of CA1 (Sommer’s sector of the hippocampus)
  • Middle layers of the cerebral cortex- laminar necrosis
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12
Q

Secondary mechanism of damage following ischemia?

A

Major contribution from excitotoxicity secondary to release of aspartate and glutamate

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13
Q

What is this?

A

Shows selective ischemic vulnerability of the neurons in the hippocampus

  • Memory problems
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14
Q

What is this?

A

Acute Middle Cerebral Artery Infarct

  • Discoloration in MCA territory
  • Ventricular effacement
  • Cingulate herniation
  • Probably pretty proximal block, because so much area affected
  • Pt’s life is endanger from brain swelling (may need hemi-craniectomy)
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15
Q

What is this?

A

Acute PCA stroke

  • Posterior cerebral artery territory infarcts (mesial surface of temporal lobe)
  • May result from emboli or thrombosis
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16
Q

Histopathology of Infarction: Temporal Evolution

  • Day 1:
  • Day 2- weeks:
  • Weeks- months:
A

Day 1:

  • Red neuron and rarefaction of neuropil (first sign/change that can be seen of infarction; light microscopy)

Day 2-weeks:

  • Neuronal drop out
  • Rarefaction of neuropil
  • Influx of macrophages and fewer lymphocytes and poly’s
  • Astrogliosis
  • Vascular proliferation (beware of contrast ehancement!)

Weeks-months:

  • Cystic cavity containing macrophages then CSF
  • Wall of reactive astrocytes (reactive gliosis)
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17
Q

What is this?

A

Acute infarct with red neurons

  • Earliest light microscopic change in CNS infarct
  • Red cytoplasm
  • No good Nissl substance anymore
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18
Q

What is this?

How long after stroke?

A

Remote middle cerebral artery infarct

Several months later

  • Neurons/tissue cleared out by macrophages
  • Large ventricle compensating for volume loss
  • If this hits motor strip, person will probably be hemiparetic (face and arm worse than leg b/c ACA still okay)
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19
Q

What is this?

A

Wall of remote infarct cavity

  • Macrophages (foamy cytoplasm)
  • Rarefied tissue- not many cells
  • Reactive astrocytes (big, bottom right) in wall; much cytoplasm- doing their best to wall off the cyst
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20
Q

What does this show?

A

Cerebral peduncle and medullary pyramid atrophy following MCA infarct

  • Due to loss/degeneration of axons
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21
Q

What is this?

A

Remote pontine infarct (cystic infarct)

  • Near midline, so mesial/medial perforating infarct of the pons from arteries from the basilar coming straight in
22
Q

What is this?

A

Multiple hemorrhagic emoblic infarcts

  • Often come from heart valves/dysfunctional wall
  • Possible from atherosclerosis in carotids
  • Most emboli go ipsilateral
23
Q

In addition to atherosclerosis and carotid dissection, what else can cause a stroke?

A

Vasculitis- inflammation of the wall of the blood vessel (entire thickness)

  • May be part of systemic vasculitis or may be confined to CNS
  • Inflammatory infiltrate MUST involve the entire thickness of the vessel wall; transmural inflammation
  • May cause multifocal strokes
24
Q

What is this?

A

Vasculitis (must have transmural inflammation)

25
Q

What is this?

A

Granulomatous vasculitis

  • Giant cell
26
Q

What is this? Symptoms?

A

Lacunar infarct

  • Infarct in area of tiny lenticulostriate artery (?)

Symptoms

  • Typically asymptomatic
  • May have huge effect in internal capsule
27
Q

What is this?

A

Thickened tortuous small vessel with hemosidiren staining due to long standing HTN

  • Kind of curvy
  • Compromised/thickened wall
28
Q

What are the therapeutic principles in ischemic strokes: thrombotic?

A

- Thrombolysis (TPA) if under 4.5 hrs of Sx onset and no hemorrhagic component (activates endogenous system to break down clots)*

  • Vigorous supportive care (do not allow hypotension; protect airway if level of consciousness decreased; DVT prophylaxis)
  • Anti-platelet treatment (baby aspirin, 86 mg)

*Not eligible if person woke up with a stroke and doesn’t know timeline

29
Q

What are the therapeutic principles in ischemic strokes: embolic?

A
  • Remove source if possible
  • Consider anti-coagulation (warfarin/heparin)
  • Direct thrombin inhibitors
30
Q

What is this?

A

Hypertensive hemorrhage

31
Q

What is this?

A

Catastrophic hypertensive hemorrhage

32
Q

What is this?

A

Cerebellar hemorrhage

  • One of the few hemorrhages that surgery may help (remove hematoma)
33
Q

What is this? Results?

A

Pontine hemorrhage

  • Loss of reticular activating system, loss of consciousness…
  • Usually lethal
34
Q

What is the underlying cause of hypertensive hemorrhage?

A

Microaneurysms of Charcot-Bouchard

35
Q

Is death more common with ischemic stroke or hemorrhagic?

A

Hemorrhagic

36
Q

What is a major cause of lobar hemorrhage in elderly patients?

A

Amyloid angiopathy

37
Q

What is this?

A

Amyloid angiopathy

38
Q

What is this?

A

Multiple hemorrhages in metastatic tumors

39
Q

Therapeutic principles in intracerebral hemorrhage (ICH)?

A
  • Vigorous supportive care; NO ASA
  • Surgical evacuation of cerebellar hemorrhage; data does not support evacuation of ICH at other sites
  • Ventricular drainage if the hemorrhage extends into ventricles

- Activated Factor VII being evaluated to see if ICH expansion can be slowed or stopped by increasing coagulation and that this impacts impact– mixed results

40
Q

________ are the major cause of non-traumatic subarachnoid hemorrhage (SAH)?

A

Berry aneurysms are the major cause of non-traumatic subarachnoid hemorrhage (SAH)

  • Up to `15% of pts have multiple
41
Q

Different types of aneurysms?

A

Saccular or berry aneurysms (most)

  • 15-20% may be multiple
  • Proximal

Mycotic aneurysms

  • Also on anterior circulation
  • Distal
  • Bacterial or fungal (infectious)
42
Q

What caused this? Symptoms?

A

Rupture aneurysm (“giant” on top left, smaller mid-right)

  • Worst headache of life
  • May not have focal deficit
  • May lose consciousness
43
Q

Treatment for aneurysm?

A

Coiling- place and pass electrical current to trigger thrombosis; leave coil

44
Q

What is this?

A

Cavernous sinus anuerysm

(direct arterial-venous shunting)

  • Can take down CN 3, 4, 5, 6
  • Bruit over eyeball
45
Q

Different types of vascular malformations?

Where are these found?

What do they result in?

A

- Ateriovenous malformation (AVM)**

- Cavernous angioma**

- Venous angioma

- Capillary telangectasia

These are in the brain parenchyma, but are so close to the surface, they can cause subarachnoid bleeds (?)

**Clinically significant

46
Q

What are AVMs (arteriovenous malformations) made of?

A
  • Composed of anastomosed abnormal arteries and veins (no intervening capillary bed)
  • Arterial component contains internal elastic lamina (elastic stain)
  • Intervening neuropil is gliotic (sometimes with Rosenthal fibers)- reactive, abnormal tissue between vessels
  • Hemosiderin deposition and granular bodies
47
Q

Potential of AVMs for significant _____ = ___?

A

Potential of AVMs for significant hemorrhage = 2-4%

48
Q

What is this?

A

Big AVM in temporal lobe

  • Some on surface
  • Brownish = hemosiderin staining

On micro see different vascular calibers

  • Tissue seen between vessels
49
Q

Cavernous angioma (cavernous hemangioma or cavernoma) made of what?

Microscopic and gross features?

Genetics?

A
  • Cluster of vascular channels with hyalinized walls
  • Varying caliber
  • May contain fibrin thrombi
  • No intervening neuropil
  • No arterial component
  • Popcorn” appearance on MR with hemosiderin deposition

- CCM1: krit mutation (AD)

50
Q

What is this?

A

Cavernous malformations in pons and temporal lobe

Grossly: popcorn

51
Q

Therapeutic principles in aneurysms and vascular malformations?

A

Prevent additional hemorrhage (neurosurgical or endovascular therapy)

  • Clip or coil aneurysm
  • Remove or glue vascular malformation
  • Not all vascular malformations require treatment

Subarachnoid blood causes vasospasm that may lead to ischemia

  • Vasospasm maximal 2-14 days after SAH
  • Intervene early if possible, otherwise will have to wait
  • Treat/prevent vasospasm