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

6/16- CV Pathology and Pathophysiology Flashcards

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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?

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
A

Vasculitis (must have transmural inflammation)

25
What is this?
Granulomatous vasculitis - Giant cell
26
What is this? Symptoms?
**Lacunar infarct** - Infarct in area of tiny lenticulostriate artery (?) **Symptoms** - Typically asymptomatic - May have huge effect in internal capsule
27
What is this?
**Thickened tortuous** small vessel with **hemosidiren** staining due to long standing HTN - Kind of curvy - Compromised/thickened wall
28
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
29
What are the therapeutic principles in ischemic strokes: **embolic**?
- Remove source if possible - Consider anti-coagulation (warfarin/heparin) - Direct thrombin inhibitors
30
What is this?
Hypertensive hemorrhage
31
What is this?
Catastrophic hypertensive hemorrhage
32
What is this?
**Cerebellar hemorrhage** - One of the few hemorrhages that surgery may help (remove hematoma)
33
What is this? Results?
**Pontine hemorrhage** - Loss of reticular activating system, loss of consciousness... - Usually **lethal**
34
What is the underlying cause of hypertensive hemorrhage?
Microaneurysms of Charcot-Bouchard
35
Is death more common with ischemic stroke or hemorrhagic?
Hemorrhagic
36
What is a major cause of lobar hemorrhage in elderly patients?
Amyloid angiopathy
37
What is this?
Amyloid angiopathy
38
What is this?
Multiple hemorrhages in metastatic tumors
39
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
40
\_\_\_\_\_\_\_\_ 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
41
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)
42
What caused this? Symptoms?
**Rupture aneurysm** ("giant" on top left, smaller mid-right) - Worst headache of life - May not have focal deficit - May lose consciousness
43
Treatment for aneurysm?
**Coiling**- place and pass electrical current to trigger thrombosis; leave coil
44
What is this?
**Cavernous sinus anuerysm** (direct arterial-venous shunting) - Can take down CN 3, 4, 5, 6 - Bruit over eyeball
45
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_
46
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**
47
Potential of AVMs for significant _____ = \_\_\_?
Potential of AVMs for significant **hemorrhage** = **2-4%**
48
What is this?
Big **AVM** in temporal lobe - Some on surface - Brownish = **hemosiderin** staining On micro see different vascular calibers - Tissue seen between vessels
49
**Cavernous angioma** (cavernous hemangioma or cavernoma) made of what? Microscopic and gross features? Genetics?
- 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
What is this?
**Cavernous malformations** in pons and temporal lobe Grossly: popcorn
51
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

Term 5: Neuro (24 decks)

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