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Flashcards in VASCULAR LESIONS Deck (41):
1

CLINICAL FORMS OF ANOXIA

Anoxic—insufficient oxygen reaches blood (e.g.,
drowning)
Anemic—insufficient oxygen content in blood
(e.g., carbon monoxide [CO] poisoning)
Histotoxic—poisons interfere with oxygen utilization
(e.g., cyanide, sulfide)
Stagnant—mostcommon,decreased cerebral perfusion,
(e.g., cardiac arrest);

2

MECHANISMS OF ANOXIA

Edema
Lactic acid accumulation, decreased pH
Increase in free fatty acids
Increase in extracellular potassium and ammonia
Abnormalities in calcium flux
Reperfusion problems

3

most sensitive to anoxia

– Hippocampal, Sommer’s sector (CA1) is most
sensitive
– Cerebral cortex, layers III, V, and VI (which
contain larger neurons)
– Cerebellar Purkinje cells (if patient survives for
a period of time, may see Bergmann gliosis)
– Caudate and putamen

4

Gross pathology of anoxia

Swollen, soft
Gray matter is dusky
Areas of cavitation in a laminar pattern may be
observed
– Pseudolaminar is used to describe involvement
of more than one cortical layer

5

microscopy of anoxia

Dendrite and astrocyte swelling, i.e., sponginess of
the neuropil
Ischemic (homogenized) neurons, i.e., “red and
dead”
Endothelial hyperplasia
Microglial reaction
Dissolution of neurons after several days

6

Otherwise known as diffuse anoxic
encephalopathy

Respirator brain

7

Grossly—dusky brown discoloration of cortex,
blurring of gray-white junction, general friability
of tissue (brain often does not fix well in formalin)

Microscopically—ischemic neurons everywhere,
frequently with infarcts

Respirator brain

8

directly binds to iron-rich areas of brain
(globus pallidus and pars reticulata of substantia
nigra)
Pathologically marked by necrosis of globus
pallidus and substantia nigra

carbon monxide

9

pathology of carbon monxide

demyelination and cerebral white matter
destruction (Grenker’s myelinopathy)

10

Causes selective neuronal necrosis-like ischemia
Different mechanism of injury than ischemia
– Decreased lactate and pyruvate
– Tissue alkalosis
Neuronal necrosis in cerebral cortex superficial
layers, hippocampus (CA1 and dentate) and
caudate; no Purkinje cell necrosis

Hypoglycemic brain damage

11

Most common sites of venous thrombosis are ______________

superior sagittal sinus, lateral sinuses, and straight sinus

12

gross pathology of infracts

Unequivocal alterations require up to 24 hours; early
changes include ________________

48 hours: “cracking”_______________


_________: infarcted area is usually clearly delineated;
cortex is friable and soft


A 1-cm cavity takes ___________



edema, congestion, softening


separation of the necrotic
tissue from intact tissue

72 hours


2–3 months to form

13

microscopic pathology of infarcts

earliest changes:

(1) astrocytic swelling;
(2) interstitial edema;
(3) pyknosis;
(4) hypereosinophilia
of neurons;
(5) microvacuolization of
neurons (swollen mitochondria)

14

24 hours: __________________, may see neutrophilic infiltration (ceases by day 5)

3–4 days:_______________

7–10 days: __________________ are evident

30 days: ___________

macrophage infiltration begins, axonal
swelling

prominent macrophage infiltration

astrocytic proliferation and hypertrophy

intense gliosis

15

Infarcts range in size from 3–4mm up to 1.5 cm

Lacunar infarct

16

causes of lacunar infarct

Causes: (1) lipohyalinosis; (2) occlusion of small
penetrating vessels; (3) dissection; (4) emboli

17

aneurysms

Also known as “berry,” congenital or medical
defect

saccualr

18

MC SITES of symptomatic aneursyms

--Middle cerebral artery trifurcation
– Anterior communicating artery-anterior cerebral
artery junction
– Internal carotid artery—posterior communicating
artery junction

19

“Giant aneurysm” defined as _______

> 2.5 cm

20

Theories behind anuerysms

---_____________of part or all of the media at
the arterial bifurcation, does not explain why
most arise in adulthood

– Remnants of _______________

– Focal destruction of the ___________ resulting from hemodynamic alterations,about 3–9% of patients with arteriovenousmalformations (AVMs) have aneurysms

– Abnormalities in specific collagen subsets-


Congenital defects



embryonic vessels


internal elastic membrane

21

associated conditions of aneurysms

Polycystic kidney disease, autosomal dominant
• Ehlers-Danlos syndrome (types IV and VI)
• Neurofibromatosis type I
• Coarctation of the aorta
• Fibromuscular dysplasia
• Marfan syndrome
• Pseudoxanthoma elasticum

22

Pathology of aneurysms
____ is usually defective


_____________ and sometimes a gap in
the internal elastic membrane can be seen

– Aneurysm wall usually contains fibrous tissue
– Atherosclerotic changes occasionally seen
– Phagocytosis and hemosiderin deposition may
be present


media


intimal hyperplasia

23

Arterial wall is weakened by pyogenic
bacteria, which usually reach the wall by an
infected embolus
– May be multiple
– Located on distal branches of the middle cerebral
artery

Infectious (septic) aneurysms

24

Fusiform aneurysms

Seen commonly with _____________

Related to dolichoectasia (elongation, widening,
and tortuosity of a cerebral artery)


________ of internal carotid artery
and ________ are most common sites

Fusiform aneurysm refers to dilated segment of
artery



advanced atherosclerosis




Supraclinoid segment
basilar artery

25

Accounts for 1.5–4% of all brain masses; most
supratentorial
Admixture of arteries, veins, and intermediatesized
vessels
Vessels are separated by gliotic neural
parenchyma
Foci of mineralization and hemosiderin deposition
are common

AVM

26

Optic nerve involvement of AVM

in Wyburn-Mason
syndrome

27

Veins of varying sizes
Vessels separated by mostly “normal”
parenchyma
Less compact than AVM or cavernous malformation
May have a large central draining vein
Varix is a single dilated/large vein

Venous angioma

28

Cavernous malformation (angioma)

Some familial cases related to CCM1 gene mutation
on_________
Large, sinusoidal-type vessels in apposition to
each other
Little or no intervening parenchyma
Compact malformations
Mineralization and ossification are common;
occasionally massive

chromosome 7q

29


Capillary-sized vessels
Separated by normal neural parenchyma
Common in the striate pons
Often an “incidental” finding at autopsy; prevalence
of about 0.4%

Capillary telangiectasia

30

Highlighted on Congo red (apple green
birefringence with polarized light due to
-pleated-sheet configuration of the protein),

CAA

31

The most common of the granulomatous
vasculitides
– Older patients >50 years; incidence 15–25/
100,000 persons
– Females > males
– Primary target is extracranial arteries of head,
but may involve cerebral vessels

Giant cell arteritis

32

Giant cell arteritis
Associated with polymyalgia rheumatica
– May be a focal process (skip lesions)
– Lymphoplasmacytic inflammation, granulomas,
fibrous scarring with healing

Associated with polymyalgia rheumatica
– May be a focal process (skip lesions)
– Lymphoplasmacytic inflammation, granulomas,
fibrous scarring with healing

33

Aortic arch and branches and descending aorta
– Younger patients (15–40 years), Asian
females at higher risk
– Lymphoplasmacytic inflammation of the
media with fibrosis, granulomas/giant cells

Takayasu’s arteritis

34

Headaches, multifocal deficits, diffuse
encephalopathy
– Adults (age 30–50 years)
– Males > females
– Sedimentation rate normal or mildly elevated
– Biopsy of nondominant temporal tip including
leptomeninges (highest yield area), cortex and
white matter recommended

Primary angiitis of central nervous system

35

________ and ______
walls are the common features of the
vasculitides

Segmental inflammation, necrosis of vascular

36

_______,___________, and _________involve vessels in the subarachnoid
space, peripheral nervous system, or the extracranial
vessels

giant cell arteritis

37

Also called subcortical arteriosclerotic
encephalopathy

Moderate intermittent hypertension and
progressive, often profound dementia are
features

Widespread vascular alterations and white
matter changes are seen and readily demonstrated
with neuroimaging

Focal and diffuse ________ with associated
____________ in the deep hemispheric
white matter

Binswanger’s disease









myelin loss
reactive astrocytosis

38

Mutation of notch 3 gene on chromosome
19
Strokes and vascular dementia; slowly progressive
with death in 15–25 years

Cerebral autosomal dominant arteriopathy with
subcortical infarcts and leukoencephalopathy
(CADASIL)

39

Initial atherosclerotic lesion is fatty streak
marked by __________ filled with __________

Fatty streaks may develop into _________
(especially at outer aspects of arterial bifurcation
where laminar flow is disturbed)—

foam cells, low-density lipoprotein cholesterol

fibrous plaques

40

Hypertensive angiopathy shifts the autoregulation
(maintains cerebral blood flow at a
constant level between mean arterial pressures
of 50–150 mmHg) curve to the __________, raising
the lower limit of regulation at which adequate
cerebral flow can be maintained

right

41

Causes small vessel disease with disruption
of blood-brain barrier resulting in basal
lamina thickening and reduplication, smooth
muscle degeneration, fibrinoid change
(necrosis), and increased collagen deposition
(lipohyalinosis—collagenous fibrosis)

chronic HPN