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PATHOLOGY > VASCULAR LESIONS > Flashcards

VASCULAR LESIONS Flashcards

1
Q

CLINICAL FORMS OF ANOXIA

A

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);

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2
Q

MECHANISMS OF ANOXIA

A 
Edema
 Lactic acid accumulation, decreased pH
 Increase in free fatty acids
 Increase in extracellular potassium and ammonia
 Abnormalities in calcium flux
 Reperfusion problems
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3
Q

most sensitive to anoxia

A

– 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

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4
Q

Gross pathology of anoxia

A

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

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5
Q

microscopy of anoxia

A

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

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6
Q

Otherwise known as diffuse anoxic

encephalopathy

A

Respirator brain

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7
Q

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

A

Respirator brain

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8
Q

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

A

carbon monxide

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9
Q

pathology of carbon monxide

A

demyelination and cerebral white matter

destruction (Grenker’s myelinopathy)

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10
Q

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

A

Hypoglycemic brain damage

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11
Q

Most common sites of venous thrombosis are ______________

A

superior sagittal sinus, lateral sinuses, and straight sinus

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12
Q

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 ___________

A

edema, congestion, softening

separation of the necrotic
tissue from intact tissue

72 hours

2–3 months to form

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13
Q

microscopic pathology of infarcts

earliest changes:

A

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

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14
Q

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

3–4 days:_______________

7–10 days: __________________ are evident

30 days: ___________

A

macrophage infiltration begins, axonal
swelling

prominent macrophage infiltration

astrocytic proliferation and hypertrophy

intense gliosis

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15
Q

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

A

Lacunar infarct

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16
Q

causes of lacunar infarct

A

Causes: (1) lipohyalinosis; (2) occlusion of small

penetrating vessels; (3) dissection; (4) emboli

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17
Q

aneurysms

Also known as “berry,” congenital or medical
defect

A

saccualr

18
Q

MC SITES of symptomatic aneursyms

A

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

19
Q

“Giant aneurysm” defined as _______

A

> 2.5 cm

20
Q

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-

A

Congenital defects

embryonic vessels

internal elastic membrane

21
Q

associated conditions of aneurysms

A

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
Q

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

A

media

intimal hyperplasia

23
Q

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

A

Infectious (septic) aneurysms

24
Q

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

A

advanced atherosclerosis

Supraclinoid segment
basilar artery

25
Q

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

A

AVM

26
Q

Optic nerve involvement of AVM

A

in Wyburn-Mason

syndrome

27
Q 
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
A

Venous angioma

28
Q

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

A

chromosome 7q

29
Q 
Capillary-sized vessels
 Separated by normal neural parenchyma
 Common in the striate pons
 Often an “incidental” finding at autopsy; prevalence
of about 0.4%
A

Capillary telangiectasia

30
Q

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

A

CAA

31
Q

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

A

Giant cell arteritis

32
Q 
Giant cell arteritis
Associated with polymyalgia rheumatica
– May be a focal process (skip lesions)
– Lymphoplasmacytic inflammation, granulomas,
fibrous scarring with healing
A

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

33
Q

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

A

Takayasu’s arteritis

34
Q

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

A

Primary angiitis of central nervous system

35
Q

________ and ______
walls are the common features of the
vasculitides

A

Segmental inflammation, necrosis of vascular

36
Q

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

A

giant cell arteritis

37
Q

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

A

Binswanger’s disease

myelin loss
reactive astrocytosis

38
Q

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

A

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

39
Q

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)—

A

foam cells, low-density lipoprotein cholesterol

fibrous plaques

40
Q

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

A

right

41
Q

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)

A

chronic HPN

PATHOLOGY (3 decks)

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