CVD Flashcards
What is the brain’s energy source
How much CO goes to the brain
How much 02 is consumed
AEROBIC metabolism
20% of cardiac output
15% of O2 consumption
After cerebral ischemia, how much time can elapse to…
maintain normal brain function?
before irreversible damage occurs?
Two main causes of cesseation of blood flow:
For normal brain function: 8-10 seconds
Irreversible damage after 6-8 minutes
NO 02 reserve in the brain, a constant supply of 02 is needed
*hypotension (reduction in the perfusion pressure)
*occlusion (small or large vessel)
Which cells are most sensitive to ischemia?
Which neurons are more susceptible to ischemia?
Neurons > oligodendrocytes > endothelial cells > astrocytes
Variable neuronal susceptibility to ischemia:
Pyramidal neurons in CA1 region of hippocampus, purkinje cells of cerebellum and certain layers in the cortex
What are the major etiologies of global cerebral ischemia? (4)
- Low perfusion (atherosclerosis, near or compete occlusion)
- Acute decrease in blood flow (cardiogenic shock)
- Chronic Hypoxia (although the brain is less sensitive to hypoxia vs ischemia)
- Repeated episodes of hypoglycemia
What type of damage can occur in a global cerebral ischemia:
Mild global ischemia –?
Severe –?
Mododerate –
Mild – usually no permanent damage
Severe – DIFFUSE damage, vegetative state
Moderate – increased vulnerability in watershed areas (anterior and middle cerebral arteries) and selecively vulnerable regions
Global Cerebral ischemia
When can damage be seen histologically?
What is the underlying pathology and associated changes to the cell (3):
Histological changes appear 6-12 hours after insult
Pathology: RED DEAD nucleus
cytoplasmic eosinophilia, loss of Nissl substance, shrunken/dark pyknotic nuclei
Global Ischemia:
Where are areas of neuronal vulnerability in adults (3) and in infants (4)?
Adults: “big neurons”, cortical layers 3&5, CA1 of hippocampus, Purkinje cells of cerebellum
Infants: Subiculum, Thalamus, pontine nuceli, white matter (cerebellum)
What type of histology can be observed with laminar cortical necrosis?
which areas are highly vulnerable?
Brown discoloration, pitting of cortex, band-like fashion, and microscopically will show loss and vaculation
Less vulnerable superficial cortex is preserved
Selective vulnerability: CA1 area of hippocampus (Sommer’s sector), watershed or border zone infarcts
What are the three types of ischemic strokes and what are their major affected arteries (3)?
- Thrombic- in situ thrombosis, atherosclerotic plaque (75%) esp at bifurcation of internal cartoid and MCA
- Embolic (10%) - cardioembolic (Afib, MI –>MCA), atheroembolic (carotid, vertebra from damaged endothelium)
- Small vessel disease (HTN, DM, vasculitis) - lacunar stroke (lenticulostriate vessels, cystic infarct <1.5 cm), internal capsule - motor or thalamus - sensory
What type of vasular insult is pictured?
What is the major artery affected?
What are the major associated sx:
Ischemic hemispheric infarct
MCA territory
SX: midline shift, contralateral hemiparesis affecting the lower face and upper extremity more than the leg, similar distribution contralateral hemisensory loss, contralateral visual field deficits,
Dominant hemisphere infarct highly associated with expressive aphasia, whereas non-dominant infarct is associated with neglect sydrome
What are major differences between acute, subacute and chronic ischemic infarcts?
Acute - indistinct borders, bluring of the cortex, white matter
Subacute - boarders more distinct, tissue liquefaction; early PMNs and late macrophages, vascular proliferation
Chronic - cystic spaces, +/- hemosiderin, gliosis
Typical characteristics of embolic infarcts (4):
Smaller, centered at gray-white junction
can be single or multiple
may invovle more than one vascular territory
MCA is the most common artery invovled
Lacunar infarcts:
usually occurs secondary to ______, complication of long standing ______.
most commonly involved ______ artery which leads to small _____ areas of infraction, aka _____.
Common locations (4)
involvement of the internal capsule –> pure _____ stroke
involvement of the thalamus —> pure _____ stroke
Lacunar infarcts:
usually occurs secondary to hyaline atherosclerosis, complication of long standing HTN
most commonly involved lenticulostriate vessels which leads to small, cystic areas of infraction (up to 1.5 cm in size) = small-lake infractions
Common locations: putamen, thalamus, pons, cerebellum
involvement of the internal capsule –> pure MOTOR stroke
involvement of the thalamus —> pure SENSORY stroke
What are the different intracranial hemorrhages that can occur above the arachnoid and below the arachnoid?
Above the arachnoid:
mostly traumatic in nature
–> epidural and subdural hematomas
Below the arachnoid:
underlying cerebrovascular disease
–> aneurysms => subarachnoid hemorrhages (SAH)
–> HTN => parenchymal hemorrhages
Intraparenchyma hemorrhages:
Common locations (4)-
microscopic changes (3)-
Intraparenchymal hemorrhages are secondary to rupture of _______ also called ______
(highly seen at _____ arteries)
Similar distribution to _____ infarcts
Common vessels (4)
Common locations: putamen, thalamus, pons, cerebllum
Microscopic: recent hemorrhage surrounded by central edema, minimal tissue necrosis, resolution leaves behind cystic space with macrophages containing hemosiderin
Intraparenchymal hemorrhages are secondary to rupture of pseudoaneurysms also called charcot-bouchard (highly seen at the lenticulostriate arteries, with rupture after hyline arterosclerosis)
Similar distribution to LACUNAR infarcts
Common vessels (4): lenticulostriate arteries, paramedial pontine vessels, short circumferential vessels of the cerebellum and in teh central white matter (end arteries)
Subarachnoid Hemorrhage
Etiologies (3):
CSF will show _________, yellow hue due to bilirubin
Pathology:
bleeding into the subarachnoid space
Causes:
1. Berry aneurysm: common cause of non-traumatic spontaneous subarachnoid hemorrhage
2. AVM (arterious-venous malformations)
3. Anticoagulated state
CSF shows XANTHOCHROMIA
Pathology of subarachnoid hemorrhage:
gross: thin-walled no_____ outpouching from arterial branching points
site of rupture is at the _____
associated vascular spasms produced _________
gross: thin-walled no MEDIA outpouching from arterial branching points
site of rupture is at the DOME
associated vascular spasms produced GLOBAL CEREBRAL ISCHEMIA