Pathology Flashcards

1
Q
  • When one cingulate gyrus is pushed underneath the falx

- May result in occlusion of the callosal-marginal branch of the ACA

A

Cingulate (subfalcine) herniation

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2
Q
  • Results when the medial temporal lobe is pushed between the cerebral peduncles and the tentorium cerebelli
  • Stretching of CN 3 produces “fixed dilated pupil” on IPSILATERAL side
  • Crushing of the PCA against the edge of the tentorium results in occlusion (explains the cortical blindness that often follows head injury)
  • **Secondary brainstem hemorrhage (Duret hemorrhage)
A

Uncal (trans-tentorial) herniation

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3
Q
  • Results from herniation of the cerebellar tonsils through the foramen magnum, compressing vital respiratory and cardiovascular centers of the medulla
  • Duret hemorrhages in pons/midbrain, causing “locked-in” state
A

Tonsillar (cerebellar) herniation

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4
Q
  • MC type of cerebral edema
  • (1) Capillaries may be damaged and are leaking protein (infarcts, infection, contusion, lead poisoning)
  • (2) New, leaky capillaries may be forming in an abnormal area (abscess, tumor)
  • Increase in the space between cells
  • White matter will be soft and wet, and more affected than gray
A

Vasogenic (intercellular) edema

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5
Q

Acute mountain sickness is _________ edema.

A

Vasogenic (intercellular)

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6
Q
  • Excessive intracellular water, indicating cells have been damaged (individual cells)
  • Look for this type of edema in early ischemia, acidosis/hypercarbia, Reye’s, and pseudotumor cerebri
  • Gray matter will be more affected
A

Cytotoxic edema

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7
Q
  • Results from obstruction of the flow of CSF (“non-communicating hydrocephalus”)
  • Edema surrounds the ventricles
A

Interstitial edema

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8
Q

-Happens when the plasma is greatly diluted, as in way-out-of-control ketoacidosis

A

Osmotic edema

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9
Q

In edema of any kind, expect to see: (2)

A
  • Flattening of the gyri against the skull

- Narrowing of the sulci

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10
Q

-Results from blockage within the brain
-May be congenital (stenosis or malformation of cerebral aqueduct, Dandy-Walker, Arnold-Chiari, fetal CMV)
May be acquired (tumors, meningitis, compressing a foramen of Munro)

A

Non-communicating hydrocephalus

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11
Q

-Results from over-production of CSF (choroid plexus papilloma), obstruction of subarachnoid space, or problems with the arachnoid villi

A

Communicating hydrocephalus

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12
Q
  • Brain atrophy from cell loss (infarct or injury

- More room for fluid

A

Hydrocephalus ex-vacuo

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13
Q

Radiation injury is _________ edema.

A

Vasogenic (intercellular)

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14
Q
  • Syndrome seen in older folks caused by diminished absorption of CSF by arachnoid villi
  • Gait disturbances
  • Urine incontinence
A

Normal pressure hydrocephalus

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15
Q
  • Increased intracranial pressure first presenting as headache, mental dullness, and N/V
  • Papilledema

Think…

A

Herniation

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16
Q
  • Non-progressive neurologic disability that is attributed to events before or around the time of birth
  • Shows as child develops
  • Related to low birth weight
A

Cerebral palsy

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17
Q

Periventricular leukomalacia (necrosis around the ventricles) is common in:

A

Premature babies

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18
Q

Shrinkage of individual gyri, probably from ischemia:

A

Ulegyria

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19
Q
  • Marbled appearance in the basal ganglia and thalamus

- Result of ischemia, hyperbilirubinemia (infants), other causes

A

Status marmoratus

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20
Q
  • Extreme result of hypoperfusion (newborns)

- Almost all the fiber tracts for the cortex are gone

A

Multicystic leukoencephalopathy

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21
Q

Cerebral laceration and cerebral contusion are similar, but the pia-arachnoid membranes are torn over the site of injury in __________.

A

Laceration

stab wound

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22
Q
  • Minor type of traumatic brain injury that results from shaking of the brain
  • Temporarily alters brain function
A

Concussion

boxers

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23
Q
  • Traumatic brain injury

- Causes bruising of the brain tissue, resulting in bleeding

A

Contusion

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24
Q

____ contusions result from trauma to the brain directly beneath the site of impact.

A

Coup

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25
Q

__________ contusions occur primarily when the head is in motion (acceleration) but comes to an abrupt stop (deceleration)
-Brain will be flung back and forth, causing a contusion opposite the point of deceleration

A

Contrecoup

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26
Q

TQ:
-traumatic shearing forces
Petechiae in the corpus callosum
-Demonstrated using amyloid-beta precursor protein or silver stains
-can result in persistent vegetative states, coma, or severe mental disability

A

Diffuse axonal injury

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27
Q
  • Results from a second blow to the head sustained by a person who’s recently had a concussion that has not been given enough time to heal properly
  • Causes disastrous cerebral edema
  • Commonly seen in boxers!
A

Second impact syndrome

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28
Q

A skull fracture that lacerates the middle meningeal A leads to:

A

Epidural hematoma

“talk and die”

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29
Q
  • Associated with traumatic brain injury
  • Usually the result of tears in bridging veins that pass through the dura on their way to the dural sinuses
  • May cause an increase in intracranial pressure
A

Subdural hematoma

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30
Q
  • Subdural hematoma
  • Retinal hemorrhage
  • Cerebral edema
  • Fractures of rib, vertebral and long bones may also be observed
  • May present with irritability, alterations in eating habits, seizures, vomiting, bulging or tense fontanelles, altered breathing, and dilated pupils
A
  • *Shaken baby syndrome

- Probably causes diffuse axonal injury

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31
Q

Neurofibrillary tangles are a marker for:

A

Chronic traumatic encephalopathy

boxers: dementia pugilistica

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32
Q
  • Red neurons

- Neuts beginning to infiltrate

A

Early infarct (acute hypoxic/ischemic injury_

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33
Q

An infarct at 10 days would show:

A

Macrophages and gliosis

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34
Q

Histo:

  • Swelling of the dendrites and astrocytes - spongiosis of the neuropil
  • Red/dead neurons
  • Endothelial hyperplasia
  • Microglial reactions
  • Dissolution of parenchyma after several days
A

Ischemia

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35
Q

Seen 12-24 hours after insult:

A

Red neurons

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36
Q

Seen 24 hours to 2 weeks after insult:

A
  • Tissue necrosis
  • Infiltration of macrophages
  • Vascular proliferation
  • Reactive gliosis
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37
Q

Seen 2 weeks after insult:

A

Repair phase:

  • Macrophages remove the necrotic tissue
  • Normal histological organization
  • Gliosis also present
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38
Q

An abrupt course of focal or global neurological signs and symptoms of greater than 24 hours in duration due to a hemorrhagic or ischemic event:

A

Stroke

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39
Q

A stroke in which the symptoms resolve in less than 24 hours:

A

Transient ischemic attack (TIA)

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40
Q

Laminar necrosis (uncontrolled death of cells in a band-like layered pattern) seen in:

A

Strokes

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41
Q

TQ-Another cause of stroke in which the vessels of the circle of Willis become narrowed (fibrosis of the intima) and may also bleed

  • Fairly common in both children and adults
  • May occur in syndromes, including Down’s and sicklers
A

Moyamoya Disease “freidlander fav)

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42
Q
  • Buildup of granular material in the basement membranes between the smooth muscle cells of the arterial walls
  • Dx when pathologist examines skin
  • PAS (+) granules (glycogen) throughout artery walls
  • Gene = Notch-3
  • Progressive loss of cognitive function… little strokes and bleeds
A

CADASIL

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

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43
Q

Microhemorrhages and slit hemorrhages are characteristic of ____________.

A

Hypertension

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44
Q
  • Type of dementia due to white matter atrophy resulting from small vessel disease
  • Dementia pts who have been hypertensive
A

Subcortical leukoencephalopathy (commonly: Binswanger’s disease)

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45
Q

Caused by:

  • Hypertension
  • Cerebral amyloid angiopathy (apple green)
A

Intracerebral hemorrhage

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46
Q

Rupture of little Charcot-Bouchard microaneurysms in the brain parenchyma result in ___________ hemorrhages.

A

Hypertensive

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47
Q

55% of “hypertensive” hemorrhages are seen in the:

A

Putamen

48
Q
  • Usually from a ruptured cerebral aneurysm or head injury

- Rapid onset

A

Subarachnoid hemorrhage

49
Q

Sites favored by berry aneurysms: (4) TQ

A

40% ACoA
34% MCA
20% PCoA
4% Bifurcation of basilar A into PCAs

50
Q

People with ADPKD are prone to:

A

Berry aneurysm

51
Q
  • Masses of blood vessels separated by brain

- May cause neurologic deficits and subarachnoid bleeding

A

AV malformations

52
Q

Pt has fracture in the skull. This can result in a _____________herniation.

A

transcalvarial herniation

53
Q

Pt presents in locked-in state: awake and conscious but selectively de-differenced: having no means of producing speech, limb, or facial movements. Conscious but paralyzed.
SLIT hemorrahges. What type of hemorrhage?

A

Duret hemorrhages

54
Q

Increased intracranial pressure without hydrocephalus can be caused by…. (5)

A
  • Idiopathic
  • Increased central venous pressure
  • Venous thrombi in the brain
  • Vit A toxicity (diet)
  • Tetracycline toxicity
55
Q

Germinal plate bleeds occur in low birth weight babies and is due to the fragility of the _______ ______.

A

Capillary plexus

Can lead to death, cerebral palsy, or mental retardation

56
Q

_________ fractures result from the ability of sutures to move in adults and children.

A

Diastatic fractures

57
Q

Bleeding into the spinal cord (gunshot wound) is called….

A

Hematomyelia

58
Q

Years after spinal cord injury, the old gliotic site of trauma will still be obvious. This is called___________ and is associated with Wallerian degeneration of the tracts (esp post. column and corticospinal tracts)

A

Myelomalacia

59
Q

Glial scars can lead to post-traumatic ______.

A

epilepsy

60
Q

Ischemic damage to brain causes __________, only if ischemia has lasted long enough to cause the glia and neurons to die. Pts in irreversible coma following shock or hypoxia may have brains that look normal.

A

liquefaction

61
Q

Infarction is a result of lack of oxygen to the brain. This can be stained with H&E with Luxol fast blue stain, which stains the..

A

myelin

62
Q

Early_____ (red neurons + neuts infiltrating)–>10 days–>macropahges and gliosis–>separation of nerve fibers and loss of myelin.

A

infarct

63
Q
\_\_\_\_\_\_\_respond to  injury by:
Proliferation (stroke/trauma)
Phagocytosis of debris (stroke/trauma)
Develop elongated nuclei (syphilis)
Form microglial nodules (viruses and rickettsia)
Neuronphagia (viral enceph., polio)
A

Microglia

64
Q

Watershed infarcts between the ACA and MCA are in the _______ border zone.

A

Cortical

65
Q

Watershed infarcts between the LCA and MCA are in the _______ border zone.

A

Internal

66
Q

Watershed infarcts between the MCA and PCA are in the _______ border zone.

A

Cortical

67
Q

______ ______ is due to occlusion of a vessel, usually an artery due to cholesterol embolus.

A

Focal ischemia (stroke)

68
Q

In ______ ______ gyri widen, sulci narrow as the brain swells. Depends on length of time, age, body temp, vascular dz, cardiac output.

A

Global ischemia

69
Q

Infarct overtime….
12-24 hrs: ____ ______
24 hrs-2 wks: tissue necrosis, macrophages, vasc. prolif and gliosis
2 wks +: macrophages remove necrotic tissue causing cavities

A

red neurons

70
Q

Hyperglycemia may cause hyperosmolar coma, causing dehydration. Fluid correction must be slow or _____ _____ ______ may occur.

A

Central pontine myelinolysis (osmotic demyelination syndrome)

71
Q

HVLA of the neck puts a pt at risk for _______ artery rupture

A

Vertebral

72
Q
  • Most abundant in the gray matter (Protoplasmic type)
  • Play a role in regulation of electrolyte balance, NT metabolism, GABA, serotonin, glutamate
  • Phagocytic, role in repair of brain
  • cytoplasmic processes are GFAP (+)
A

Astrocytes

73
Q
  • Reactive astrocytes
  • Hypertrophic, eosinophilic cytoplasm
  • Increase in # during gliosis
  • Strongly GFAP (+)
A

Gemistocytes

swollen astrocytes

74
Q

Cytoplasmic inclusions that are:

  • Eosinophilic twisted rod or sausage shape
  • Found in astrocytic processes
  • GFAP (+), alpha-beta crystallin (+), ubiquitin (+)
  • Ultrastructure
A

Rosenthal fibers

75
Q

Specialized ependymal cells that have processes extending to the pial surface:

A

Tanycytes

-3rd ventricle region

76
Q

Cells that are found around dying neurons (seen in viral infections):

A

Microglia

77
Q

Hypertrophy and proliferation of astrocytes at sites of injury, the counterpart of “scarring” elsewhere in the body:

A

Gliosis

78
Q

Red neurons are indicative of:

A

Acute necrosis due to ischmia

79
Q
  • Non-specific response to axonal injury
  • Axonal transection
  • Metabolic conditions
  • Pellagra
  • When the axons are cut, the neurons respond by clumping cytoplasmic material due to increased protein synthesis
A

Central chromatolysis axonal reaction

80
Q

When microglia proliferate, a process of microgliosis, they may form _______, which are often associated with _____ ____________.

A
  • Nodules

- Viral encephalitis

81
Q

Gitter cells (the result of microglia phagocytosing infectious material or cellular debris) are present in: (2)

A
  • Destructive lesions

- Demyelination

82
Q

Macrophages that form microglial (“typhus”) nodules. Think…

A

Viral infection

-In USA, think “West Nile”

83
Q
  • Meninges (dura, arachnoid) herniate through skull or vertebral column
  • A form of spinal bifida
A

Meningocele

84
Q
  • Herniation of both the leptomeninges (neural tissue) and spinal cord through a vertebral defect
  • Assoc with hydrocephalus, Chiari type 2, other spinal cord anomalies
  • A form of spinal bifida
A

Meningomyelocele

“myelocele”

85
Q

A neural tube defect characterized by sac-like protrusions of the brain and the membranes that cover it through openings in the skull:

A

Encephalocele

“cranium bifidum”

86
Q

Congenital fissure of the skull and spine:

A

Craniorachischisis

87
Q
  • Absence of convolutions (gyri and sulci), except for the hemispheric and sylvian fissures
  • Widening of the cortical thickness
A

Agyria

“Lissencephaly type 1”

88
Q

The formation of abnormal tissue or of normal tissue in an abnormal location:

A

Heteroplasias / Heterotopia

89
Q

Between what ages do neuroepithelial (colloid) cysts develop?

A

20-50 years of age

90
Q
  • Hypoplasia or aplasia of cerebellar vermis
  • Cystic dilatation of 4th ventricle (fills enlarged posterior fossa)
  • Assoc with hydrocephalus and spina bifida
  • 20-50% have mental retardation
A

Dandy-Walker syndrome

91
Q
  • Seen in adults
  • Downward herniation of cerebellar tonsils
  • Usually asymptomatic in childhood
  • Assoc with syringomyelia (50% of cases
A

Arnold-Chiari, Type I

92
Q
  • Seen in infants
  • Malformed baso-cranial bones
  • Significant herniation of cerebellar tonsils and vermis through foramen magnum with aqueductal stenosis and hydrocephalus
  • Often presents with lumbosacral myelomeningocele and paralysis below defect
A

Arnold-Chiari, Type II

93
Q

Classic triad:

  • Adenoma sebaceum
  • Seizures*
  • Mental retardation
A

Tuberous sclerosis

-Seen grossly as tuber or potato-like growth on the brain that may calcify with age (become sclerotic)

94
Q
  • Cortical scarring in the deep regions of the sulcus that leads to distortion of the gyri
  • Due to hypoxic ischemic injury in the perinatal period
A

Ulegyria

95
Q
  • Cysts, usually found in the temporal lob region

- EMA (+) by IHC

A

Arachnoid cysts

96
Q

The dreaded “brain damage” of preemies:

A

Periventricular leukomalacia

97
Q

Negri bodies. Think…

A

Rabies

98
Q

Abnormal carbohydrate metabolism accumulation of polyglucosan:

A

Lafora body disease

99
Q

What would you seen in neuronophagia?

A

Microglial aggregates around dying neurons

-Viral infections

100
Q
  • Round inclusions with a dense, eosinophilic core and peripheral halo
  • Ubiquitin(+), a-synuclein(+), Tau protein(–), Actin(–)
  • Seen in normal aging, as well as in Parkinson’s dz
  • Common location of Substantia nigra
A

Lewy bodies

101
Q

Abnormally broad gyri, usually occurring in areas of lissencephaly or polymicrogyria

A

Pachygyria

102
Q
  • A smooth brain without cortical gyri

- May be partial or complete

A

Lissencephaly

103
Q

Numerous narrow convolutions in a complex pattern:

A

Polymicrogyria

104
Q

Well-demarcated, round, slightly basophilic inclusions

  • Silver(+), Ubiquitin, tubulin, Tau-protein, Neurofilament protein, and chromogranin (+)
  • Common locations: Dentate granule cells, amygdala, cerebral cortical laminae II & III
A

Pick bodies

105
Q
  • Monstrously enlarged astrocytes with huge, dark nuclei

- Seen in Subacute Sclerosing Panencephalitis (SSPE) and Progressive Multifocal Leukoencephalopathy (PML)*

A

Alzheimer I astrocyte

Alzheimer Glia, Type 1

106
Q
  • Astrocytes with edematous-looking, swollen nuclei

- Seen in liver failure and other states with high blood ammonia

A

Alzheimer II astrocyte

Alzheimer glia, Type 2

107
Q
  • Small vacuoles containing small, dense round granules
  • Most often found in CA1 region of hippocampus
  • Seen in normal aging, Alzheimer’s dz, and Picks dz
  • Ubiquitin(+), Tau-protein(+)
A

Granulovacuolar degeneration

108
Q
  • Rod-shaped, eosinophilic cytoplasmic inclusions

- Assoc w/ neurodegenerative disorders - Alzheimer’s and Creutzfeldt-Jakob dz

A

Hirano bodies

109
Q

Kuru plaques in _____ dz.

A

Prion

-Spongiform change

110
Q

Plaques adjacent to superolateral angle of the lateral ventricles suggests:

A

Multiple sclerosis (MS)

111
Q
  • Round, basophilic, PAS(+) inclusions that resemble corpora amylacea
  • Composed of polyglucosans
  • Common locations: CNS, sweat glands, liver, sk muscle
A

Lafora bodies

112
Q
  • Absence of major portion of brain, skull, and scalp
  • “Frog-like appearance”
  • Malformation of rostral end of the neural tube, usually btw days 23-26 of conception
A

Anencephaly

113
Q
  • Failure of L and R hemispheres to separate
  • Usually occurs during weeks 5-6
  • Mutations in sonic hedgehog signaling pathway
  • Moderate form = cleft lip/palate
  • Severe form = cyclopia
A

Holoprosencephaly

114
Q

Berry aneurysm is an example of what type of hemorrhage?

A

Subarachnoid hemorrhage

115
Q

Too few gyri in _________ syndrome.

A

-Zellweger

116
Q

JC papovavirus inclusions in oligodendroglia in:

A

PML