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Putthoff Lectures/CIS > Part 3 > Flashcards

Part 3 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 brainAlso 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 associationsDiastatic, general fracture, basilar skull fracture

A

general–artherosclerotic change–epidural hematomabasilar skull fracture–ocular n entrapment, hemotympariumdiastatic–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 LOBECMV=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 inclusionsCMV=PROMINENT intranuclear inclusionsRabies=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 eyelidchildrentourets 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 bothalpha synuclein–AD; lipid binding protein associated with synapses, point mutations and amplificationsLRRK2–also AD; leucine rich repeat kinase 2Mitochondrial 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 NEURONSMSA 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 AD10-26 normal, 27-41 premutation, 36-121=diseaselasts 15-20 years; writhing movements progresses to cognitive decline dementia and death

58
Q

3 categories of spinocerebellar degenerations

A

all AD1) molecularly/genetically similar to HD2)non-coding region repeats similar to mytonic dystrophy3) point mutations

59
Q

Friedreich Ataxia–genes, also associated with what disease

A

ARfrataxin genedie of cardiomyopathy; also associated with diabetes

60
Q

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

A

ARATM protein mutatedassociated with recurrent sinopulmonary infections (mucor is noteworthy of infections of sinus)

61
Q

Primary lateral sclerosis vsProgressive muscular atrophy vsProgressive bulbar atrophy vsPseudobulbar palsy

A

PLS: UMN onlyPMA: LMN onlyPBA: LMN bulbar region onlyPBP: 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 ADSOD1, C9orf72d, TDP43, FUSFamilial 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

Putthoff Lectures/CIS (4 decks)

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