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Gen Path Final > Sweep 1 > Flashcards

Sweep 1 Flashcards

1
Q

c. cytoplasmic eosinophilia (red neurons), observed in

A

hematoxylin and eosin stained sections.

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2
Q
  1. Astrocytes (astroglia)
    b. in response to brain injury, the astrocytes react by producing a dense network of cytoplasmic processes surrounding the area of injury. This is somewhat analogous to a ———- occurring elsewhere in the body, and is known as ———–.
A

fibrous scar

reactive gliosis

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3
Q
  1. Microglia (phagocytes, macrophages)
    a. Microglia derived from ————
    b. serve as
A

circulating monocytes

antigen presenting cells in inflammatory conditions

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4
Q
  1. Types of neuronal injury-share pathology with other cells.
    a. Acute “red neurons” see
A

12-24 h after irreversible hypoxic/ischemic insult.

See shrinkage of the cell body, pyknosis of the nucleus, loss of nucleolus, loss Nissl substance, red cytoplasm, break down in bloodbrain barrier with acute injuries.

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5
Q
  1. Types of neuronal injury-share pathology with other cells.
    a. Astrocytes and injury: Often show
A

astrogliosis (repair and/or scar formation).

Increased bright pink cytoplasm, cytoplasmic swelling, formation Rosenthal fibers (thick eosinophilic protein aggregates seen in chronic gliosis)

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6
Q
  1. Types of neuronal injury-share pathology with other cells.
    a. Ependymal cells: Certain pathogens (e.g. CMV) cause
A

extensive ependymal injury with viral inclusions.

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7
Q
  1. Types of neuronal injury-share pathology with other cells.
    a. Microglia: Fixed macrophages in CNS are ———— positive. Can also note blood borne ————-
A

CD68 and CR3

macrophages with inflammation.

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8
Q
  1. Hydrocephalus

a. Choroid plexus produces CSF. In continuity with ependyma, ————- lined by epithelial cells.

A

intraventricular fibrovascular cores

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9
Q
  1. Hydrocephalus

3 main types

A

Subfalcine
Uncinate
Tonsilar herniation

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10
Q
  1. Hydrocephalus

• Subfalcine (cingulated):

A

Unilateral or asymmetric expansion of the cerebral hemisphere displaces cingulated gyrus under falx cerebri-may compress anterior cerebral artery.

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11
Q
  1. Hydrocephalus

• Uncinate (transtentorial):

A

Medial aspect temporal lobe compressed-CN III compromised-pupils dilate and impairment ocular movements-may also compress posterior cerebral artery-affecting visual cortex-Duret Hemorrhage-midbrain bleeds.

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12
Q
  1. Hydrocephalus

• Tonsillar herniation:

A

Displacement cerebellar tonsils through foramen magnum-life threatening as the brain stem becomes compromised as the breathing and cardiac regulatory centers are located in the medulla oblongata.

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13
Q
  1. Epidural hematomadural arteries most frequently the
A

mid-meningeal artery
• Usually associated with a skull fracture
• Dura separates from blood accumulation. Rupture of a meningeal artery- arterial bleeding
• “Lucid interval”, then progressive loss of consciousness
• Neurosurgical emergency Need PROMPT DRAINAGE as this is a life-threatening condition.

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14
Q

Brain Infarction: evolution

A
  1. Grossly & histologically normal: first 12 hours
  2. 24-36 hours (acute): Red neurons and neutrophil infiltration into the brain parenchyma
  3. 3rd – 5th day (subacute): Involved tissue becomes softer in consistency. Macrophages with foamy cytoplasm begin to infiltrate
  4. 1 month: Soft, irregular, cavitated lesion, loss of brain tissue.
  5. 6 months (chronic): Smooth walled cavity
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15
Q
  1. Hypertensive cerebrovascular disease and intraparenchymal hemorrhage.
    a. ———— is the most common underlying cause of primary parenchymal hemorrhage.
A

Hypertension

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16
Q
  1. Hypertensive cerebrovascular disease and intraparenchymal hemorrhage.
    b. ———— in larger vessels and ————– in smaller vessels weakens the vessel walls.
A

Accelerated atherosclerosis

hyaline arteriolosclerosis

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17
Q
  1. Hypertensive cerebrovascular disease and intraparenchymal hemorrhage.
    c. Subsequently note wall rupture and hemorrhage, which is most common in the regions of the
A

basal ganglia, followed by pons, thalamus and cerebellum.

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18
Q
  1. Hypertensive cerebrovascular disease and intraparenchymal hemorrhage.

Symptoms:

A

e. Severe headache, hemiparesis, hemisensory loss

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19
Q
  1. Subarachnoid hemorrhage

a. Defined as abrupt onset

A

extravasation of blood in space between arachnoid and pia (arterial bifurcations of the circle of Willis) matter due to rupture of vessels in arachnoid space.

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20
Q
  1. Subarachnoid hemorrhage

a. Often are ———, but could also be precipitated by ————-.

A

spontaneous

traumatic injury

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21
Q
  1. Subarachnoid hemorrhage

a. Chief complaint of patient

A

“Worst headache of my life”.

22
Q
  1. Subarachnoid hemorrhage

a. ————- is the most common cause of non-traumatic hemorrhage.

A

Ruptured berry (saccular) aneurysm (of major brain arteries)

23
Q
  1. Subarachnoid hemorrhage

a. Most aneurysms arise from branches of the

A

middle cerebral, internal carotid and the junction between the anterior cerebral and anterior communicating arteries.

24
Q
  1. Subarachnoid hemorrhage

a. Probably represents an acquired, degenerative process, aggravated by

A

hypertension.

25
Q
  1. Subarachnoid hemorrhage

a. Subarachnoid hemorrhage i.e. blood in CSF may be seen together with

A

intraparenchymal hemorrhage.

26
Q
  1. Vascular malformations.

a. Etiology: most commonly from ——— in developing brain.

A

abnormal angiogenesis

27
Q
  1. Vascular malformations.

b. Types are

A

arteriovenous malformation (AVM), cavernous angioma, capillary telangiectasias and venous angioma.

28
Q
  1. Vascular malformations.

c. AVMs

A

(Collection of abnormal blood vessels of variable caliber) are most common and most likely to result in intraparenchymal and/or subarachnoid bleeds.

29
Q
  1. Acute bacterial meningitis

a. Infections resulting in inflammation of the

A

leptomeninges and subarachnoid space.

30
Q
  1. Acute bacterial meningitis

Brain is swollen. Purulent exudate under

A

subarachnoid space, over the cerebral hemispheres. Purulence within the ventricles

31
Q
  1. Acute bacterial meningitis

c. Chronic leptomeningitis is caused by both

A

bacterial e.g Mycobacterial tuberculosis and fungal e.g. Cryptococcus neoformans organisms.

32
Q

Acute bacterial meningitis

e. Symptoms include

A

neck stiffness, neurologic impairment, headache, photophobia.

33
Q
  1. Tuberculous Meningitis (chronic meningitis)

a. > 2-3 weeks of

A

headache, lethargy, nausea & vomiting

34
Q
  1. Tuberculous Meningitis (chronic meningitis)

Path:

A

b. Cranial nerve palsies, epilepsy

c. Gelatinous exudate, may appear nodular.

35
Q
  1. Tuberculous Meningitis (chronic meningitis)

d. Histology:

A

Lymphocytes, macrophages, and multinucleated giant cells form granulomas.

36
Q
  1. Tuberculous Meningitis (chronic meningitis)

Mycobacteria may be demonstrable by

A

acid fast stain

37
Q
  1. Cryptococcal Meningitis (chronic meningitis)

a. —————, found in ————-

A

Spherical budding yeast

soil and bird excrement

38
Q
  1. Cryptococcal Meningitis (chronic meningitis)

symptoms

A

b. Low grade fever, debility, headache

39
Q
  1. Cryptococcal Meningitis (chronic meningitis)

Path

A

c. Slimy exudate, capsular material

40
Q
  1. Encephalitis.

a. Diffuse inflammation of the ———- caused by a number of

A

brain parenchyma

viral agents e.g. HSV most common, HIV, cytomegalovirus and also many arthropod-borne encephalitis viruses.

41
Q
  1. Encephalitis.

b. Clinical symptoms:

A

headache, neck stiffness, pyrexia (fever) and focal seizures.

42
Q
  1. Encephalitis.

c. Without treatment,

A

usually fatal.

43
Q
  1. Encephalitis.

d. Microscopically can note

A

perivascular lymphocytosis, microglial nodules and neuronophagia.

44
Q

Encephalitis

May also note

A

viral inclusions e.g. Cowdry A and Negri bodies.

45
Q

Huntington’s Disease

e. Microscopically note severe ——- in the

A

neuronal loss

basal ganglia, accompanied by fibrillary gliosis.

46
Q
  1. Gliomas

a. ———- (infiltrating) comprise 80% of adult tumors.

A

Astrocytomas

47
Q
  1. Gliomas

Symptoms include

A

seizures, headaches and focal neurologic deficits.

48
Q
  1. Gliomas

b. In adults, mostly affects the

A

cerebral hemisphere

49
Q
  1. Gliomas

c. Pilocytic astrocytoma (Grade I) →

A

Astrocytoma (Grade II) → Anaplastic astrocytoma (Highly cellular with mitotic figures, Grade III) → Glioblastoma (Necrosis and microvascular proliferation, Grade IV). Glioblastoma → note endothelial cell proliferation.

50
Q
  1. Gliomas

d. Clinical features-may remain “silent” until

A

increase in growth.

51
Q

Gilomas

Treatment consists of

A

surgical resection, then radiation and chemotherapy. ~ 15 month survival.

52
Q

Gilomas

e. Pilocytic astrocytoma:

A

Less aggressive, often in pediatric patients, usually located in the cerebellum.

Gen Path Final (18 decks)

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