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NS2 Test 2 > Puthoff CIS/ Lectures Part 2 > Flashcards

Puthoff CIS/ Lectures Part 2 Flashcards

1
Q

Clinical features produced by infarction are determined by?

A

ANATOMIC distribution of the damage rather than the underlying cause

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2
Q

Lacunar inracts lodge where?

A

distal smaller vessels–lenticulostriate vessels

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3
Q

Brain morphology of respirator brain

Also seen in what kind of disorders of babies?

A

liquefactive necrosis; seen in encephalomalacia and leukoencephalopathy in babies

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4
Q

cerebral amloid angiopathy is a feature of what?

A

seen in aging; primary inflammation

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5
Q

Are isolated subarachnoid hemorrhages associated with trauma??

A

NO!

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6
Q

Types of fractures and associations

Diastatic, general fracture, basilar skull fracture

A

general–artherosclerotic change–epidural hematoma
basilar skull fracture–ocular n entrapment, hemotymparium
diastatic–separates bones at sutures–linear fractures

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7
Q

Last suture to fuse is?

A

Lamboid suture–doesnt fuse till 60 years!

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8
Q

What is craniosynostosis?

A

premature fusion of cranial sutures

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9
Q

What kind of lesion do you get months after aneurysms rupture? Cause?

A

cavitary lesions–caused by microglial cells pahocytizing ; seen in CT/ MRI

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10
Q

Disorders related to hypertension in brain

A

slit hemorrhage, lacunar infarcts, hypertensive encephalopathy, Binswanger disease

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11
Q

Binswanger disease affects what part of brain?

A

white matter infective encephalopathy

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12
Q

CADASIL is what and associated with what?

A

Leukoencephalopathy–soft brain (white); associated with subcortical infarcts; scandanivia

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13
Q

Virchow Robins space

A

subarachnoid space (affected by meningitis) around blood vessels

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14
Q

Most CNS infections spread ____

A

hematogenously

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15
Q

Viruses that affect peripheral nerves

A

Rabies and HSV

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16
Q

Chemical meningitis

A

from chemotheraphy

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17
Q

What do you see in chronic meningitis (syphillis, TB, cryptococcus, neuroborrelia)

A

FIBROSIS resulting in communicating hydrocephalus

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18
Q

Eye finding in meningitis or meningoencephalitis

A

papilledema (need to check fundus before lumbar tap)

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19
Q

Once an infection gets out of the virchow robins space into the brain, its called?

A

Encephalitis syndrome

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20
Q

Children meningtis order of organisms

A

GBS, Listeria, E Coli

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21
Q

Older adults meningtitis

A

S. pneumonia, E Coli (if immunocompromised), Listeria

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22
Q

Meningitis extending into vessels or brain parenchyma can lead to?

A

Phlebitis or hemorrhagic infarction

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23
Q

What is chronic adehesive arachnoiditis?

A

thickening fibrosis that occurs with meningitis in the leptomeninges

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24
Q

Pleomorphic cells are seen in what kind of meningitis?

A

Aseptic

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25
Q

Difference between Herpes and CMV in terms of location affected in the brain

A

Herpes=TEMPORAL LOBE

CMV=PERIVENTRICULAR LOCATIONS

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26
Q

Rubella infection–how get it?

A

intrauterine viral infection

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27
Q

Post-encephalitic parkinsonism appears when?

A

After being infected by influenza virus

28
Q

Viral encephalitis morphology

A

lymphocytic meningoencephalitis, inflammatory cells accumulate around vessels, multifocal necrosis throughout brain, neuronophagia, microglial nodules (HIV), viral inclusions, when severe–necrotizing vasculitis w/focal hemorrhage

29
Q

Inclusions of Herpes, CMV, Rabies

A

Herpes=Intranuclear inclusions
CMV=PROMINENT intranuclear inclusions
Rabies=negri bodies=CYTOPLASMIC INCLUSIONS

30
Q

Acute focal suppurative infections=

A

Brain abcess, subdural empyema, extradural abscess (NOCARDIA!! fUNGUS LIKE BACTERIA)–extradural abcscess associated with antecedent trauma?

31
Q

SSPE associated with?

A

Antecedent MEASLES infection

32
Q

Degenerative diseases affecting neocortex

A

AD, FTLD, ALS

33
Q

Diseases affecting brainstem

A

Parkinsons, Dementia with lewy bodies, Atypical parkinson syndrome (progressive supranuclear palsy, coticobasilar degeneration), MSA, Huntingtons, spinocerebellar degenerations (spinocerebellar ataxia, Friedreich ataxia, ataxia telangiectasia

34
Q

In AD what reflects inflammatory changes?

A

Betal amyloid=chronic inflammation

35
Q

AD laterality and region of brain

A

Diffuse bilateral cortical atrophy–susceptible to subdural hematomas

36
Q

Hirano bodies are associated with?

A

AD–Granulovacuolar degeneration

37
Q

CAA–morphology

A

chronic inflammation, reactive gliosis

38
Q

Is Tau in AD associated with plaques or tangles?

A

Neurofibrillary tangles

39
Q

Major component of plaques in AD

A

Beta amyloid

40
Q

NF tangles morphology

A

black, thick, condensed

41
Q

common MECHANISM of death in AD

A

pneumonia, sepsis, DVT but cause of death is AD

42
Q

FTLD vs AD

A

FTLD are NOT diffuse cortical disease like AD; it is LOBAR related to atrophic changes in frontal and temporal regions primarily
-FTLD is one of the more common causes of early onset dementia

43
Q

3 types of FTLD and associated depositions

A
  • FTLD tau: tau neuronal depositions, not Beta amyloid
  • FTLD-TDP: similar distribution of atrophy as FTLD tau but has TDP43 (RNA binding protein) –progranulin mutation resulting in deficiency causes it
  • FTLD-FUS: fusion designation of sarcoma protein
  • most are diagnosed at AUTOPSY–no good biomarkers
44
Q

FTLDS S/S vs AD

A

FTLD: personality changes, behavior changes, and aphasia (speech problems), in contrast to declining cognitive abilities seen in AD; dementia occurs OVER time; Also, FTLDs are present EARLIER than AD!

45
Q

Paraneoplastic syndromes can have secondery movement disorders:

  • blepharospasm is what?
  • spasmodic toritcollis seen in?
  • Ballismus seen in ?
A

fasciculations of eyelid
children
tourets syndrome

46
Q

The dopaminergic nogrostriatal pathway in basal ganglia modulate feedback from ____ to ____

A

thalamus to motor cortex

47
Q

Clinical features of PD

A

decreased facial expression (mask like facies), cogwheel rigidity, bradykinesia, pill rolling tremor, festinating gait (short steps, leaning forward)

48
Q

Are genetic forms of PD AD or AR? List the proteins associated with genetic PD

A

Can be both
alpha synuclein–AD; lipid binding protein associated with synapses, point mutations and amplifications
LRRK2–also AD; leucine rich repeat kinase 2
Mitochondrial dysfunction Parkinsons–AR associated with mutation in genes encoding proteins like DJ1, PINK1 and parkin

49
Q

Drug associated Parkins results from what drugs?

A

Dopamine antagonists and toxins

50
Q

Characteristic inclusions seen in PD and other morphology

A

Lewy bodies; pallor of substantia nigra and locus cereleus

51
Q

Progressive PD clinical features

A

Autonomic involvement (bowel, bladder), decreased cognitive ability, dementia, seborrhea (eczema of scalp and face)

52
Q

Difference bw PD and Dementia with Lewy Bodies

A

Dementia with Lewy Bodies may have EARLY dementia and is NOT responsive to L-DOPA

53
Q

Difference bw PD and PSNP (progressive supranuclear palsy)

A

-atypical Parkinson syndrome; has TAU inclusions instead of alpha synuclein!!

54
Q

What is corticobasilar degeneration?

What is post traumatic parkinsonism

A
  • CBD: progressive TAUPATHY

- PTP: more likely to be CTE but affects basal ganglia have PD symptoms

55
Q

Difference bw MSA and PD?

A

Both have alpha synuclein and both affect basal ganglia but MSA has CYTOPLASMIC INCLUSIONS of alpha synuclein in OLIGODENDROCYTES while PD has alpha synuclein in NEURONS
MSA also has autonomic degeneration–>ORTHOSTASIS

56
Q

HD affects what part of basal ganglia?

A

caudate nucleus

57
Q

HD cause

A

AD; huntingtin gene mutated; gOF ; CAG repeats; NO sporadic form–all AD
10-26 normal, 27-41 premutation, 36-121=disease
lasts 15-20 years; writhing movements progresses to cognitive decline dementia and death

58
Q

3 categories of spinocerebellar degenerations

A

all AD

1) molecularly/genetically similar to HD
2) non-coding region repeats similar to mytonic dystrophy
3) point mutations

59
Q

Friedreich Ataxia–genes, also associated with what disease

A

AR
frataxin gene
die of cardiomyopathy; also associated with diabetes

60
Q

Ataxia telangiectasias; AD or AR? protein mutated? Associated with?

A

AR
ATM protein mutated
associated with recurrent sinopulmonary infections (mucor is noteworthy of infections of sinus)

61
Q

Primary lateral sclerosis vs
Progressive muscular atrophy vs
Progressive bulbar atrophy vs
Pseudobulbar palsy

A

PLS: UMN only
PMA: LMN only
PBA: LMN bulbar region only
PBP: UMN bulbar region only

62
Q

ALS affects what parts of the brain?

A

Axons in Internal capsule, brainstem and CST; LMN in CNS, Anterior horn SC; UMN in motor cortex

63
Q

ALS clinical features (incidence, age, sporadic vs familial)

A

increased incidence in males; presents in 40s; sporradic more common than familial; cognitive function spared but sometimes see

64
Q

Familial forms of ALS–AD or AR? Associated genes?

A

Almost all are AD
SOD1, C9orf72d, TDP43, FUS
Familial occurs earlier than sporadic

65
Q

How are ALS and FTLD similar?

A

Both can have FUS involved and look similar

66
Q

Characteristic feature of Spinal Bulbar Atrophy (Kennedy Disease)

A

Rosenthal fibers —astrocytic hyaline deposits usually seen in pilocytic astrocytoma

NS2 Test 2 (16 decks)

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