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Neuro DRx > 04b: Path > Flashcards

04b: Path Flashcards

1
Q

Main 3 causes of brain (parenchymal) hemorrhage:

A
  1. HT
  2. Trauma
  3. Cerebral amyloid angiopathy
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2
Q

(X) hemorrhage results from rupture of parenchymal arterioles that have become less
compliant/weakened due to
replacement of (Y) tissue by (Z) tissue.

A 
X = HT brain (parenchymal) hemorrhage
Y = smooth muscle
Z = fibrocollagenous

(Arteriosclerosis due to chronic HT)

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3
Q

List some main causes of weakened vessels, leading to spontaneous SAH.

A
  1. Berry (saccular) aneurysm***
  2. Infective aneurysms
  3. AV malformations
  4. Cerebral amyloid angiopathy
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4
Q

(X) hemorrhage usually results from trauma (rapid acceleration/deceleration). Why does this motion cause injury?

A

X = Subdural (acute)

Causes traction/tearing of the bridging veins between brain and dura

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5
Q

(X) hemorrhage is due to cycles of organization and re-bleeding, due to the formation of densely vascular granulation
tissue around the original hematoma.

A

X = Subdural (chronic)

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6
Q

(X) hemorrhage: momentary loss of consciousness, followed by asymptomatic
period (1-48 hrs), followed by the (Y) symptom. If not treated with surgery, patient will die.

A 
X = epidural
Y = high ICP
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7
Q

(X) hemorrhage often results
from a skull fracture that
produces tearing of the
(Y) artery.

A 
X = epidural
Y = middle meningeal
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8
Q

Epidural hemorrhage: Most common in the (X) fossa in adults and in (Y) fossa in children

A 
X = temporal
Y = posterior
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9
Q

(CD4/CD8) lymphocytes predominate in active MS lesions. And (CD4/CD8) in less active lesions.

A

CD4; CD8

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10
Q

T/F: Macrophages present in MS plaque.

A

True

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11
Q

T/F: Axonal bodies are damaged in MS.

A

False - preserved

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12
Q

Presence of reactive (X) is seen in MS plaque.

A

X = astrocytes

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13
Q

(X) Myopathy: Subsarcolemmal and/or intermyofibrillary aggregates that appear reddish (Y) stain.

A 
X = mitochondrial
Y = Gomori Trichrome
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14
Q

Soleus has Type (I/II) muscle fibers.

A

I (one slow fat red ox)

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15
Q

(X) myopathies characterized by “ragged red fibers”.

A

X = mitochondrial

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16
Q

Muscular dystrophy: marked by (acquired/inherited) abnormality, (acute/chronic) weakness and elevated serum (X).

A

Inherited (genetic);
Chronic/progressive;
X = CK

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17
Q

Duchenne muscular dystrophy: (X) inheritance pattern with which mutated protein?

A

X = X-linked

Cytoskeletal protein dystrophin

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18
Q

(X) myopathy characterized by perifascicular atrophy of muscle fibers and lymphocytic infiltrates

A

X = DERMATOMYOSITIS (an inflammatory myopathy)

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19
Q

Group atrophy of muscles is indicative of (nerve/muscle) pathology.

A

Nerve (denervation)

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20
Q

Neuronopathy: is a category of (myelin/axon) neuropathy where the primary abnormality is in the (X), with synchronous injury to the (Y). Is regeneration possible?

A

Axon;
X = cell body
Y = axon

No

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21
Q

Repeated episodes of (X) results in “schwannian onion-bulb proliferation”.

A

X = segmental demyelination and remyelination

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22
Q

MCI (mild cognitive impairment) definition

A

Subjective and objective decline in cognitive abilities that is not severe enough to cause obvious functional impairment

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23
Q

T/F: MCI can revert to normal

cognition.

A

True

24
Q

Most dementia syndromes are either due to (X) or (Y) or some combination of these two.

A

X = neurodegenerative disorders
Y = vascular brain
injury

25
Q

AD: neurofibrillary tangles consist of (X), a(n) (Y) protein that is critical for axonal transport.

A 
X = hyperphosphorylated tau
Y = MT-associated
26
Q

AD: the severity of dementia (Braak stages) is quantified based on…

A

How many tangles (density) and where in the cortex they are found (distribution)

27
Q

AD: Initiating event is (X) pathology.

A

X = amyloid (abnormal generation/clearance)

28
Q

AD: The amyloid cascade involved inappropriate cleavage of (X), a transmembrane protein normally encoded on chromosome (Y).

A 
X = APP (amyloid precursor protein)
Y = 21
29
Q

AD: Cleavage of APP by a (X), followed by a (Y) leads to the formation of Aβ amyloid fragments.

A 
X = beta secretase
Y = gamma secretase
30
Q

An important clearance pathway Aβ fragments are poorly understood but an
important pathway is the (X) system, most active during (Y) sleep.

A 
X = perivascular glymphatic 
Y = slow wave
31
Q

T/F: In evaluating dementia, it’s most important to focus on current cognitive abilities/tests.

A

False - HISTORY; focus on changes in cognitive abilities,

usual activities and interests and behaviors in the past 1-5 years

32
Q

T/F: In evaluating dementia patient, important to talk with all available caregivers/child/spouse, preferably as a group.

A

False - preferably alone (Different family

members may differ in their perceptions of whether something is abnormal and if so what)

33
Q

The general neurological exam will usually be affected in (early/late) dementia.

A

Late

34
Q

Diagnosis of “definite” AD requires:

A

BOTH pathological confirmation as well as

documentation of the clinical picture

35
Q

T/F: Diagnosis of “probable” AD can be made in most cases based on the clinical
presentation

A

True

36
Q

(MRI/CT) is preferred for dementia/AD patients. Why are some reasons the other imaging is used?

A

MRI;

CT may be used because:
faster, easier to obtain, lower cost, pacemakers ok

37
Q

AD: CSF has (increased/decreased) tau and P-tau levels, (increased/decreased) beta-amyloid.

A

Increased; decreased

more Aβ is deposited in brain, less reaches CSF

38
Q

AD: med Rx regimen starts with…

A

discontinuing medications that could be causing confusion or poor cognition (ex: anticholinergics, sedatives)

39
Q

AD: to enhance cognition, patients with (mild/severe) AD should be started on (X) drug type and be continued until..

A

Mild/early;
X = cholinesterase inhibitors

Indefinitely or until the disease is so severe that there seems to be little function left

40
Q

List main cholinesterase inhibitor used in AD.

A

Donepezil

41
Q

Combination of a (X) and (Y) is typically used in moderate AD

A 
X = cholinesterase inhibitor
Y = Memantine
42
Q

Memantine, used for (X) disease, MOA:

A

X = AD (in combo with cholinesterase)

  1. Uncompetitive antagonist at the NMDA glutamate R
  2. Dopamine agonist
43
Q

Lewy Body dementia: where do the lewy bodies accumulate?

A

Substantia nigra

44
Q

Lewy Body dementia Sx:

A
  1. Atypical Parkinsonism
  2. Episodic confusion
  3. Early prominent/vivid visual hallucinations of animals/people
  4. REM-sleep behavior disorder (don’t lose muscle tone during REM; attack/violent in sleep)
45
Q

Lewy Body dementia patients: brain shows (amyloid plaques/hyperphosphorylated tau).

A

Amyloid plaques; no tau/tangles

46
Q

T/F: Lewy Body dementia responds as to levodopa as PD.

A

False - may have modest response, but LB patients more likely to experience side effects or increased hallucinations and worsening confusion

47
Q

Pick bodies are a type of (X) seen in (Y) disorder.

A 
X = inclusion bodies (that stain for either tau or ubiquitin)
Y = FTD (fronto-temporal dementia)
48
Q

T/F: Like AD, cholinesterase is helpful in patients with FTD.

A

False

49
Q

Mixed Dementia consists of:

A

Vascular + Alzheimer’s

50
Q

Which dementia accounts for most clinical cases?

A

Mixed

51
Q

Some AD Genes not expressed in neurons, only in (X) cells, indicating they’re important in pathology of AD.

A

X = microglia

52
Q

Which NT abnormalities seen in AD?

A

Decrease ACh

Increased Glu

53
Q

Lewy Body dementia has (tau/amyloid) and (X) pathology

A

Amyloid;

X = Synuclein

54
Q

Fronto-temporal dementia has (tau/amyloid) and (X) pathology

A

Tau

X = ubiquitin

55
Q

Prominent and severe language impairment is a key clinical sign of (X) dementia.

A

X = fronto-temporal

Neuro DRx (10 decks)

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