Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro Exam 1 > Neuropathology > Flashcards

Neuropathology Flashcards

1
Q

neuropathology

A

study of pathological mechanisms underlying diseases of CNS/PNS and their clinical manifestations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

selective vulnerability of the CNS

A

-different cells/regions respond differently to injury
-ex: neurons more sensitive than glial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

limited regenerative capacity of CNS

A

*neurons incapable of cell division (injury to a few essential neurons may produce neurologic deficit)
*axonal regeneration varies (myelin debris inhibits regeneration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

why do PNS axons regenerate quickly

A

macrophages clear myelin debris (myelin debris inhibits regeneration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

why do CNS axons regenerate slowly

A

microglia cells cannot phagocytose myelin debris quickly (myelin debris inhibits regeneration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

characteristics of neurons

A

*highly metabolic: continuous supply of O2 and glucose
*postmitotic cells incapable of proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

neuron injury: red neurons

A

*acute injury to neurons
*early ischemic insult (6-12 hours)
*nuclear pyknosis, loss of Nissl
*intense cytoplasmic eosinophilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

neuron injury: neuron degeneration

A

*subacute/chronic injury to neurons
*progressive change (months/years)
*apoptotic death with neuropil vacuolization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

neuron injury: inclusions

A

*degenerative diseases (mis-folded proteins)
examples:
-neurofibrillary tangles (Alzheimer’s)
-Lewy bodies (Parkinson’s)
-abnormal vacuolization of perikaryon (Creutzfeldt-Jakob)
-TDP inclusion (FTD-ALS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

gliosis

A

*astrocytic hypertrophy AND hyperplasia
*“scar” formation in neuropil
*develop numerous stout, ramifying processes
*increased GFAP (glial fibrillary acidic protein)
*basically, the astrocytes proliferate to try to help out the neurons and prevent damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

demyelination of oligodendrocytes

A

*oligodendroglial cell loss
*various causes:
-immune-mediated (MS, SLE)
-infectious (HIV, PML, neurosyphilis)
-toxic/metabolic (B12 deficiency)
-myelin disorders (leukodystrophies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

microglial nodules

A

aggregates around foci of necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

neuronophagia

A

congregate around red neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

cerebral edema

A

*accumulation of fluid in the brain parenchyma
*BBB disruption / permeability leading to increased extracellular fluid (lack of lymphatics impairs resorption of excess extracellular fluid)
*may be localized or generalized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

causes of cerebral edema

A

-inflammation
-ischemic or toxic injury
-space-filling lesions (tumors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

clinical signs/symptoms of cerebral edema

A

*variable: subtle neurologic defects to loss of consciousness
*severe edema causes herniation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

hydrocephalus

A

*accumulation of excessive CSF within ventricular system
*impaired flow and/or resorption of CSF
*expands ventricles and increases ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

communicating hydrocephalus

A

*primarily a failure to REABSORB CSF (it can still flow in the ventricles but cannot get into venous system)
*enlargement of entire ventricular system
*arachnoid fibrosis following meningitis
*CSF overproduction (choroid plexus tumor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

noncommunicating (obstructive) hydrocephalus

A

*focal obstruction
*examples: third ventricle mass; aqueductal stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

normal pressure - ex vacuo hydrocephalus

A

loss of brain parenchyma (atrophy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

clinical signs/symptoms of hydrocephalus

A

*variable with age and chronicity
*infants: rapid increase in head size
*older people: headaches, vomiting, papilledema, mental impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

cerebral herniation

A

*displaced brain tissue
*increased intracranial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

subfalcine (cingulate) cerebral herniation

A

*cerebral hemisphere pushed cingulate gyrus under falx
*compresses anterior cerebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

descending transtentorial (uncinate) cerebral herniation

A

*temporal lobe compressed against tentorium free margin
*compresses third cranial nerve = pupillary dilation / blown pupil
*could also compress PCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

tonsillar cerebellar herniation

A

*cerebellar tonsils push through the foramen magnum
*compresses brain stem = respiratory and cardiac failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

extracranial cerebral herniation

A

*brain tissue external to calvaria through skull bone defect
*post-traumatic or post-surgical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

red staining in red neurons is caused by:

A

a combination of protein denaturation and loss of RNA within the cytoplasm of the affected neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

acute infarct appearance

A

*swollen appearance from edema
*accumulation of fluid within the necrotic cells and within the interstitium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

remote (old) infarct appearance

A

cavitary defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

organizing infarcts appearance

A

*presence of lipid-laden macrophages (characterized by foamy cytoplasm)
*organization of the infarct begins within the first week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

cerebrovascular disorders

A

*brain injury as a consequence of altered blood flow
*compromised blood supply to brain leads to tissue infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

major mechanisms of cerebrovascular disorder

A
  1. ischemia/hypoxia
  2. hemorrhage (CNS vessel rupture)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

stroke

A

neurologic signs and symptoms explained by vascular mechanism
*acute onset and persist > 24 hours
*if symptoms disappear < 24 hours = TIA

34
Q

ischemia & cerebrovascular disorders

A

*impairment of blood supply/oxygenation of CNS
*clinical manifestations: determined by anatomic distribution of damaged area, rather than underlying cause
*develop rapidly ~ minutes

35
Q

focal cerebral ischemia

A

*partial/complete arterial obstruction to localized area
*extend of injury is influenced by duration of ischemia and adequacy of collateral flow
*causes: thrombotic occlusion, embolism, and/or hypertension

36
Q

focal cerebral ischemia - morphology

A

*pale, nonhemorrhagic at onset
*evolve into red hemorrhagic lesions (if damage to collateral small blood vessels in affected area)

37
Q

acute focal cerebral ischemia

A

*immediate edematous gelatinous, friable tissue
*red neurons = cytoplasmic eosinophilia

38
Q

organizing focal cerebral ischemia

A

*liquefaction
*infiltration of neutrophils and then monocytes

39
Q

remote focal cerebral ischemia

A

*cystic cavity
*surrounding astrocytes are activated (reactive gliosis)

40
Q

global cerebral ischemia/hypoxia

A

*generalized reduction of cerebral perfusion
*diffuse hypoxic/ischemic encephalopathy

41
Q

causes of global cerebral ischemia/hypoxia

A

*decreased perfusion (cardiac arrest, shock, severe hypertension)
*decreased O2 carrying capacity of blood

42
Q

mild global cerebral ischemia/hypoxia - clinical manifestations

A

*transient confusional state
*complete recovery

43
Q

moderate global cerebral ischemia/hypoxia - clinical manifestations

A

*border zone / “watershed” infarcts
*between anterior and middle cerebral arteries
*bilateral cortical hemorrhagic infarcts

44
Q

severe global cerebral ischemia/hypoxia - clinical manifestations

A

*widespread neuronal death
*survival = persistent vegetative state
*brain may gradually undergo widespread liquefaction (so-called “respiratory brain)

45
Q

acute epidural hematoma

A

*occurs after rupture of meningeal artery (usually middle meningeal)
*almost always the result of skull fractures

46
Q

danger of epidural hematomas

A

*arterial in origin, epidural hematomas tend to enlarge very rapidly
*cause increased ICP and decreased brain perfusion

47
Q

subdural hematomas

A

*develop between the arachnoid mater and the inner surface of the dure whenever tears occur in the VEINS

48
Q

pathogenesis of subdural hematomas

A

*head trauma (milder head trauma in elderly patients)
*preexisting cerebral atrophy increased the risk of subdural hemorrhage

49
Q

chronic subdural hematomas

A

*hematoma may organize over time to form encapsulated massed between the arachnoid and inner surface of the dura mater
*often bilateral

50
Q

intracranial hemorrhage

A

*tearing of blood vessels leading to focal collection of blood

51
Q

epidural and subdural hematomas

A

*secondary to trauma that does not extend into the brain
*epidural = arterial
*subdural = venous

52
Q

subarachnoid hemorrhage

A

*ruptured saccular (berry) aneurysms

53
Q

parenchymal hemorrhages

A

*arteriosclerosis of small arteries
*typically affects basal ganglia, thalamus, pons, and cerebellum
*hypertension is the most common cause
*other causes = trauma, tumors, ischemic infarcts, angiopathy

54
Q

parenchymal brain injury

A

injury associated with transmission of kinetic energy to brain

55
Q

contusion

A

blunt trauma tissue ecchymosis

56
Q

coup injury

A

*contusion at site of impact

57
Q

contrecoup injury

A

*contusion opposite impact site
*brain strikes opposite surface of skull after sudden deceleration

58
Q

laceration

A

object penetration with tissue tearing

59
Q

routes of CNS infection

A

1) hematogenous spread
2) direct implantation
3) local extension
4) peripheral nervous system

60
Q

CNS infection - meningitis

A

*inflammation of leptomeninges and CSF
*most common agents: bacterial or viral

61
Q

acute septic meningitis

A

bacterial

62
Q

acute aseptic meningitis

A

viral

63
Q

clinical presentation of meningitis

A

triad: headache, nuchal rigidity, fever
other: photophobia, vomiting, altered mental status

64
Q

most common causes of bacterial meningitis in infants

A

*group B strep
*E. coli
*listeria monocytogenes
*haemophilus influenza

65
Q

most common causes of bacterial meningitis in children/young adults

A

*neisseria meningitidis
*coxsackievirus

66
Q

most common causes of bacterial meningitis in adults/elderly

A

strep pneumo

67
Q

most common causes of bacterial meningitis in immunocompromised

A

*fungi
*mycoplasma tuberculosis

68
Q

CNS infection: encephalitis (acute bacterial abscess)

A

*acute focal suppurative infections (STREP AND STAPH MOST COMMON)
*discrete lesions
*CSF with high neutrophil count
*risk = acute bacterial endocarditis, congenital heart disease, and systemic disease with immunosuppression

69
Q

chronic bacterial encephalitis

A

1) tuberculosis (granulomas with caseous necrosis and giant cells)
2) neurosyphilis (obliterative arteritis with plasma cells)

70
Q

viral encephalitis

A

*neural/glial tropism (specific cell types or specific areas)
*perivascular lymphocytes
*microglial nodules

71
Q

causes of viral encephalitis

A

1) HSV - predilection for medial temporal lobes
2) polio
3) rabies
4) HIV
5) JC
6) arboviruses

72
Q

fungal encephalitis

A

*cryptococcus, candida, mucor, aspergillus
*present as meningitis/vasculitis
*parenchymal invasion as granulomas or abscesses
*usually presents in immunocompromised pts

73
Q

toxoplasmosis encephalitis

A

*adults = opportunistic infection (HIV)
-abscesses with central necrosis
*congenital = transplacental (chorioretinitis, hydrocephalus, and intracranial calcifications)
*usually presents in immunocompromised pts

74
Q

amebiasis encephalitis

A

*rapidly fatal necrotizing encephalitis
*history of freshwater exposure
*organisms identified in CSF
*caused by naelgeria fowleri

75
Q

demyelinating diseases

A

*characterized by preferential damage to myelin with relative preservation of axons
*limited capacity of CNS to regenerate normal myelin
*clinical defects due to effect of myelin loss on axon impulse transmission

76
Q

groups of demyelinating diseases

A
  1. immune-mediated myelin destruction (MS)
  2. infections (PML from JC virus; subacute sclerosing panencephalitis from measles)
  3. metabolic (leukodystrophies or inherited diseases)
77
Q

multiple sclerosis

A

*autoimmune destruction of myelin
*most common demyelinating disorder
*episodic disease activity, separated in time, from white matter lesions separated in space

78
Q

pathogenesis of multiple sclerosis

A

*CD4+ Th1 and Th17 T-cells recognize myelin and active myelin-destroy macrophages
*antibodies against myelin or oligodendrocytes contribute to the demyelination

79
Q

risk factors of multiple sclerosis

A

HLA-DRB11501
*latitude dependence and decreased vitamin D in winter
*smoking
*EBV ?

80
Q

clinical features of multiple sclerosis

A

*typically young adult onset with vision loss, paresthesias or weakness of extremities, or abnormal gait and balance
*relapse-remitting and progression

81
Q

CSF presentation in multiple sclerosis

A

*elevated protein from IgG antibodies (oligoclonal bands)
-moderate lymphocytosis
-presence of myelin basic protein

82
Q

morphology of multiple sclerosis

A

*plaques = area of myelin loss
*active lesion = inflammatory macrophages with myelin debris
*inactive lesion = areas of demyelination and gliosis but preservation of axons!

Neuro Exam 1 (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions