6/16- CV Pathology and Pathophysiology Flashcards Preview

Term 5: Neuro > 6/16- CV Pathology and Pathophysiology > Flashcards

Flashcards in 6/16- CV Pathology and Pathophysiology Deck (51):

What are Watershed zones?

Where is the worst?

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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What is the leading cause of ischemic strokes?

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

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What is this?

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Carotid endarterectomy

- Atherosclerosis with complicated plaques


What is a "complicated" plaque?

What does it cause?

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


What is a non-atherosclerotic cause of stroke?

Carotid dissection

- Blood leaves vessel, gets stuck within adventitia, and then compresses vessel lumen

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Where do dissections usually occur?

Areas of trauma to the vessel

- e.g. struck in neck with baseball

- damage to back of throat (near carotid)


What are some symptoms seen in hypotensive ischemic injury?

"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


What is this? 

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

- Infarct = loss of tissue due to ischemia

- Enlarged sulci with shrunken gyri


What is this? 

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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


What is this? 

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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)


Which cells are most vulnerable to ischemia?

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


Secondary mechanism of damage following ischemia?

Major contribution from excitotoxicity secondary to release of aspartate and glutamate


What is this? 

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Shows selective ischemic vulnerability of the neurons in the hippocampus

- Memory problems


What is this? 

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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)


What is this?

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Acute PCA stroke

- Posterior cerebral artery territory infarcts (mesial surface of temporal lobe)

- May result from emboli or thrombosis


Histopathology of Infarction: Temporal Evolution

- Day 1:

- Day 2- weeks:

- Weeks- months:

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!)


- Cystic cavity containing macrophages then CSF

- Wall of reactive astrocytes (reactive gliosis)


What is this?

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Acute infarct with red neurons

- Earliest light microscopic change in CNS infarct

- Red cytoplasm

- No good Nissl substance anymore


What is this?

How long after stroke? 

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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)


What is this?

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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


What does this show?

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Cerebral peduncle and medullary pyramid atrophy following MCA infarct

- Due to loss/degeneration of axons


What is this? 

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Remote pontine infarct (cystic infarct)

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


What is this? 

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Multiple hemorrhagic emoblic infarcts

- Often come from heart valves/dysfunctional wall

- Possible from atherosclerosis in carotids

- Most emboli go ipsilateral


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

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


What is this? 

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Vasculitis (must have transmural inflammation)


What is this?

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Granulomatous vasculitis

- Giant cell


What is this? Symptoms? 

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Lacunar infarct

- Infarct in area of tiny lenticulostriate artery (?)


- Typically asymptomatic

- May have huge effect in internal capsule


What is this?

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

- Kind of curvy

- Compromised/thickened wall


What are the therapeutic principles in ischemic strokes: thrombotic?

- 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


What are the therapeutic principles in ischemic strokes: embolic?

- Remove source if possible

- Consider anti-coagulation (warfarin/heparin)

- Direct thrombin inhibitors


What is this?

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Hypertensive hemorrhage


What is this?

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Catastrophic hypertensive hemorrhage


What is this? 

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Cerebellar hemorrhage

- One of the few hemorrhages that surgery may help (remove hematoma)


What is this? Results?

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Pontine hemorrhage

- Loss of reticular activating system, loss of consciousness...

- Usually lethal


What is the underlying cause of hypertensive hemorrhage?

Microaneurysms of Charcot-Bouchard 

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Is death more common with ischemic stroke or hemorrhagic?



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

Amyloid angiopathy

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What is this? 

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Amyloid angiopathy


What is this? 

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Multiple hemorrhages in metastatic tumors


Therapeutic principles in intracerebral hemorrhage (ICH)?

- 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


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

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

- Up to `15% of pts have multiple

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Different types of aneurysms?

Saccular or berry aneurysms (most)

- 15-20% may be multiple

- Proximal

Mycotic aneurysms

- Also on anterior circulation

- Distal

- Bacterial or fungal (infectious)

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What caused this? Symptoms?

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

- Worst headache of life

- May not have focal deficit

- May lose consciousness


Treatment for aneurysm?

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

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What is this? 

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Cavernous sinus anuerysm

(direct arterial-venous shunting)

- Can take down CN 3, 4, 5, 6

- Bruit over eyeball


Different types of vascular malformations?

Where are these found?

What do they result in?

- 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 

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What are AVMs (arteriovenous malformations) made of?

- 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


Potential of AVMs for significant _____ = ___?

Potential of AVMs for significant hemorrhage = 2-4%


What is this?

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Big AVM in temporal lobe

- Some on surface

- Brownish = hemosiderin staining

On micro see different vascular calibers

- Tissue seen between vessels


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

Microscopic and gross features?


- 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)


What is this? 

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Cavernous malformations in pons and temporal lobe

Grossly: popcorn


Therapeutic principles in aneurysms and vascular malformations?

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