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Block 3 > Path 2 > Flashcards

Path 2 Flashcards

1
Q

ischemic stroke vs TIA vs hemorrhagic stroke

A

occluded blood vessel –> acute infarct vs transient neuro dysfxn d/t focal brain, spinal cord, retinal ischemia w/o acute infarct; short –> pre/syncope, long –> permanent neuro injury vs ruptured blood vessel –> acute infarct

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2
Q

causes of focal vs global ischemic stroke

A

cerebral embolism (types), atherosclerosis (sites), sm vessel dz in sm penetrating aa in A/MCA (lacunar infarcts), vasculitis/hypercoag, cryptogenic vs circ failure (Selective neuronal nec, infarcts)

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3
Q

unmodifiable vs modifiable risk factors of stroke

A

o >55yo
o men > women
o African American > Caucasian
o Fhx of stroke in first degree relatives
o hereditary dyslipidemia, protein C & S or antithrombin deficiency
vs
o Arterial HTN, TIA, cardiac dz, hyperchol, DM, smoking/alc, OCP, obese/inactive

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4
Q

hypoxic-ischemic encephalopathy. sel neuronal vulnerability?

A

circ/resp failure –> O2 deprivation in brain –> brain injury –> shrunken eos neurons. Hippo/CA1 of pyramidal cell layer/Sommer sector > cortex layers 3-5, cerebellum/Purkinje > thal > BG > brainstem > hypothal > spinal cord

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5
Q

borderzone/watershed infarcts. ant vs post vs internal/subcortical vs external

A

b/w 2 main nonanastomosing arterial territories from proximal stenosis of cerebral a + severe systemic hypoTN. frontal cortex b/w ACA/MCA vs occipital cortex b/w PCA/MCA vs cigar shaped deep to A/M/PCA territories w/ recurrent a of Heubner, lenticulostriate, ant choroid a territories vs wedge shaped

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6
Q

pathogenesis of hypoxic-ischemic encephalopathy?

A

gluE synapses on dendritic spines –> pckg gln into vesicles –> exocytosis –> gluE bind to postsynaptic receptor –> influx depolarize neuron, transporters in astrocytes remove gluE from synaptic space

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7
Q

gluE excitotox d/t dysfxn of?

A

transporters in astrocytes: cardiac arrest –> cerebral blood perfusion dec –> hypoxia –> impaired intake of gluE by astrocytes –> neuronal death when [gluE] = 10umol/L. malfxn of gluE NMDA receptors: influx of Na+ & Ca2+ into cell, efflux of K+ from cell; Ca2+ for synaptic plasticity & mem; too much intracellular Ca2+ –> apop

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8
Q

hemorrhagic stroke/intracerebral hemorrhage: deep/ganglionic vs lobar vs cerebellum vs brainstem

A

BG, internal capsule, periventriular white matter, thal vs sub/cortical areas crossing 1+ lobes of brain vs cerebellum vs brainstem

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9
Q

cause of deep intracerebral hemorrhage?

A

HTN –> sometimes into ventricular system –> subfalcine/transtentorial/tonsillar hern –> myelin sheath breaks down –> hemosiderin from RBC lysis –> phag –> cystic activity => encephalomalacia
* Spont rupture of sm penetrating a from A/M/PCA
* Hyaline arteriolosclerosis, Lipohyalinosis, Fibrinoid necrosis
* Charcot-Bouchard aneurysm esp in lenticulostriate

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10
Q

cause 1 of lobar intracerebral hemorrhage: cerebral amyloid angiography

A

inc age –> amyloid protein deposit in cortical & leptomeningeal tunic media & adventitia of arterioles in occ > front > temp > par.
* Rigid nonbranching apple-green birefringent fibrils w/ Congo red
* APP gene –> amyloid precursor glycoprotein –> amyloid-B pep
* APOE 2/4 > 3 inc risk (also seen in Alzheimer’s)

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11
Q

cause 2 of lobar intracerebral hemorrhage: vascular malformations in young ppl

A
  • Arteriovenous malformations: abnl vessels b/w feeding a & draining v –> direct communication w/o capillaries; mostly MCA
  • Cavernous hemangioma: abnl dil vessels w/ back-to-back arrangement & no intervening neural parenchyma in endothel lining of fibrous adventitia of subcortical front-par
  • Venous angioma
  • Capillary telangiectasia
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12
Q

causes of subarach hemorrhage. sites?

A

ruptured saccular/berry > fusiform > mycotic aneurysms mostly from ant circ/Circle of Willis; By head trauma –> bleed into subarach space –> ICP.
ACA/ACOM > ICA > MCA > BA > PCOM > PCA

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13
Q

risk factors of subarach hemorrhage: familial vs acquired

A
  • Fhx of intracranial aneurysms
  • Acquired: smoking, HTN –> shift tensile forces on arterial wall @ bifurcation –> breakdown of internal inelastic lamina –> degrade ECM –> disorganize sm muscle cells –> disrupt endothelial cells
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14
Q

how to dx subarach hemorrhage? complications?

A

head CT at basal cisterns; LP for inc opening pressure, inc RBC; xanthochromia d/t bilirubin in CSF; cerebral angiography. rebleeding, delayed cerebral ischemia, intraventricular hemorrhage

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15
Q

Intraventricular hemorrhage –> obstructive hydrocephalus: infants vs adults?

A

germinal matrix hemorrhage in premies:
 Immature germinal matrix vessels, no cerebral autoreg
 Dx: cranial US
vs
arteriovenous malformations, cavernous malformations, choroid plexus tumors:
 Sudden HA, loss consc, N/V + photophobia + stiff neck, sz
 Dx: noncontrast CT

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16
Q

vasc dementia: mild cog impairment vs Binswanger dz vs Cerebral sm vessel dz

A

elderly w/ mem problems but have nml living skills vs ischemic brain dmg in periventricular white matter w/ hyaline arteriolosclerosis from leptomeningeal border zone vs hyaline arteriosclerosis (from age); lipohyalinosis, microaneurysm (from HTN), amyloid-B deposit (from cerebral amyloid angiopathy)

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17
Q

clin pres of ischemic stroke vs TIA vs hemorrhagic stroke vs subarach hemorrhage

A

neuro sxs that may slowly improved for mo vs inc risk of cerebral infarct vs sudden HA, loss consc, N/V, delirium, sz, hemiparesis if big enough vs asx; chronic HA, dizzy, facial or eye pain, visual loss, CN palsies

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18
Q

know main diff b/w lysosomal storage dz vs leukodystrophies. but describe leukodystrophies more

A
  • Auto dom, auto rec, X linked
  • Dec brain wt b/c dec white matter vol, ventriculomegaly; spares subcortical arcuate U fibers; diffuse pallor, soft, cystic, spongy white matter; diffuse dec/absent myelin staining –> axon degen, loss of oligodendrocytes
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19
Q

Krabbe dz. clin pres: infant vs juvenile/adult. dx?

A

GALC mutation encoding galactosylceramidase catab galactosylceramide in myelin –> buildup of psychosine, GalCer undergoes acetylation by acid ceramidase –> demyelin & apop oligodendrocytes –> fibrillary astrocytic gliosis –> PAS-pos globoid cell/macs w/ tubular or filamentous inclusions infiltrate. hyperirritability, hyperactive reflexes, spastic, blind/deaf, facial paralysis, sz
vs weak, blind/deaf, intellect disability. GalCer in leuks

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20
Q

metachromatic leukodystrophy. clin pres. dx?

A

Auto rec ARSA mutation encoding arylsulfatase A breaking cerebroside 3-sulfate in myelin to cerebroside & sulfate –> buildup of cerebroside 3-sulfate in lysosomes of oligodendrocytes & Schwann cells –> disrupt lysosomal system –> dmg & loss myelin in white matter & corticospinal tracts –> PAS macs infiltrate. abnl Gait, motor, speech, intellect. ARSA activity in leuks

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21
Q

adrenoleukodystrophy. clin pres. dx?

A

ABCD1 encoding ABC transporter in peroxisomal membrane for transporting VLCFA to peroxisomal matrix for B[O] –> buildup of VLCFA in plasma, white matter, spinal cord –> ROS toxic to myelin & adrenal cortex –> inc malondialdehyde & 4-hydroxynonenal –> demyelinate splenium CC, pyramidal tracts, centrum ovale. adrenal insufficiency. high VLCFA C22/26 in plasma

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22
Q

mito encephalopathy

A

point mutations in mDNA or nDNA for mito components via mito inheritance from females –> oxidative phosphorylation defic –> resp chain fails to make ATP –> affects tissue w/ high energy needs

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23
Q

MELAS vs MERRF vs Leigh syndrome/subacute necrotizing encephalomyopathy w/ clin pres

A

MT-TL1 point mutation for leu RNA transporter –> multisystemic w/ COX-pos red ragged fiber myopathy, encephalopathy w/ sz/dementia, lactic acidosis, stroke-like episodes; cortical laminar nec, sub/cortical infarct-like lesions. Prodromal sxs: migraines, mental changes; dec consc (lethargy to coma), sz, focal neuro deficit vs MTTK point mutation for lys RNA transporter –> multisystemic red ragged fiber myoclonus, epilepsy, ataxia. Optic n atrophy, sensorineural hearing loss, exer intol, dementia, dil cardiomyopathy, Wolff-Parkinson-White syndrome, short stature vs Auto rec/X linked/mito mutations in 50+ m/nDNA encoding subunits of PDH or resp complexes I/II –> inc blood lac –> nec lesions in grey matter brainstem, BG, cerebellum, spinal cord bil. Loss motor milestones, hypotonia, movement d/o, emesis

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24
Q

acquired metab encephalopathies: thiamine/B1 vs B12 defic

A

psychotic sxs, ophthalmoplegia
o Wernicke encephalopathy: hemorrhage & nec in mamillary bodies in 3/4th ventricle; w/ Korsakoff syndrome => Wernicke-Korsakoff syndrome
o Cerebellar dysfxn –> ataxia, abnl gait, nystagmus; atrophic sup vermis, wide spaces b/w folia
vs
megaloblastic anemia, subacute combined degen of spinal cord, pernicious anemia (autoimmune dmging parietal cells secreting intrinsic factor)
o Numb/tingly extremities, ataxia, spastic LE, complete paraplegia

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25
Q

hypo vs hyperglycemia

A

low glu –> similar sxs in hypoxia b/c brain really sensitive to glu vs assoc w/ ketoacidosis, hyperosmolar coma in unctrled DM pts –> dehydration, confusion, stupor, coma

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26
Q

intox: CO vs methanol vs ethanol

A

bil GP nec; injury to cortical layers 3/5, hippo, cerebellar Purkinje vs blind d/t degen retinal ganglion cells & formate vs cerebellar dysfxn –> ataxia, abnl gait, nystagmus; atrophy & loss of granule cell layer in ant cerebellar vermis; Bergmann gliosis (loss of Purkinje & prolif of astrocytes b/w granular & molecular layers)

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27
Q

what are lysosomes? what is ELS? what are lysosomal enzymes?

A

catab organelles break down & recycle complex substrates; can be acid hydrolases, nonenzymatic proteins; pH4.5-5; part of endosomal-lysosomal system. early/recycling/late endosomes & lysosomes that interconvert. made in ER & transported to Golgi to add M6P residues on lumen –> endosome matures –> released from M6P & go to lysosomes

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28
Q

what are lysosomal storage dzs?

A

auto rec/X linked d/o from accumulation of undigested substrates. enzyme activity in dried blood spots, dec lysosomal hydrolase in fibroblasts or leuks; pathogenic mutations in leuks for nonenzymatic lysosomal proteins

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29
Q

ceramide vs cerebroside vs sulfatide vs globoside vs ganglioside

A

sphingosine + LCFA vs ceramide + 1 sugar vs cerebroside + sulfate vs ceramide + polysacch vs globoside + N-acetylneuraminiciacid

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30
Q

describe GM2 gangliosidosis

A

loss of fxn auto rec HEXA –> α subunit of β-hexosaminidase –> Tay Sachs; HEXB –> β subunit of β-hexosaminidase –> Sandhoff; GM2A –> GM2 activator protein –> AB variant

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31
Q

histo of Tay Sachs. how to dx?

A

o Lg, pale neurons; lysosomes w/ gangliosides; cytoplasmic inclusions, whorls
o Destroyed neurons, prolif microglia, accumulation of complex lipids in phags
o Fat stains/oil red O pos
little to no β-hexosaminidase activity, genetic tests

32
Q

Tay Sachs clin pres: classic infantile vs juvenile vs adult. clin pres of Sandhoff & AB variant?

A

6-10mo: can’t overturn, sit, crawl; loss vision, stiff/spastic vs Abnl gait, bal, falls, speech vs Progressive, psychosis. indistinguishable from TS

33
Q

Niemann-Pick dz

A

SMPD1 mutation –> defic acid sphingomyelinase –> sphingomyelin builds up in reticuloendothelial system

34
Q

Niemann-Pick dz clin pres: A vs B vs C

A

hepatosplenomegaly –> lg lymph nodes & spleen w/ Niemann-Pick cells (sphingomyelin laden macs); fail to thrive, recurrent infxns, irritability, progressive loss motor & intellect; die w/in 2-3yo vs hepatosplenomegaly –> lg lymph nodes & spleen w/ Niemann-Pick cells; thrombocytopenia; cough/dyspnea/recurrent infxns, short, delayed puberty vs Hepatosplenomegaly; fail to thrive, hypotonia/spastic, loss developmental milestones, vertical supranuclear gaze, sz

35
Q

describe Niemann-Pick C dz. how to dx?

A

auto rec NPC1/2 mutation –> impaired transport LDL from lysosomes to cyto –> unesterified chol builds up in lysosomes. genetic test for NPC1/2

36
Q

Gaucher dz. dx?

A

auto rec GBA1 mutation encoding glucocerebrosidase hydrolyzing glucosylceramide into ceramide + glu –> build up of glucosylceramide in lysosomes of reticuloendothelial system. dec glucocerebrosidase activity in peripheral blood leuks or cxed fibroblasts; genetic tests

37
Q

histo of Gaucher dz. where else can you find it?

A

Excess glucosylceramide in macs –> lg vacuolated blue ovoid histiocytes in wrinkled paper => Gaucher cells –> expanded red bone marrow
 Spleen has lots of Gaucher cells
 Liver shows lg foamy Kupffer cells & Gaucher cells in portal tracts
 Lung bxs show intraalveolar Gaucher cells
 Brain shows perivascular lipid-laden macs, astrogliosis, microglia

38
Q

Gaucher dz 1 vs 2 vs 3 clin pres

A

Hepatosplenomegaly –> thrombocytopenia, bone marrow dz –> anemia, skel dz –> bone crises w/ fever & leukocytosis –> osteonec, no primary CNS involved vs Hepatosplenomegaly –> thrombocytopenia; no glucocerebrosidase activity –> neck/trunk rigidity, bulbar signs, oculomotor paralysis vs Hepatosplenomegaly, skel dz; supranuclear gaze, strabismus, myoclonic epi, ataxia

39
Q

mucopolysaccharidosis

A

involve glycosaminoglycans; types 1-4, 6-7, 9 involving 11 genes

40
Q

MPS I/Hurler’s syndrome vs MPS II/Hunter’s syndrome genetics

A

auto rec IDUA encoding α-L-iduronidase –> buildup of dermatan & heparan sulfate vs X linked IDUA

41
Q

MPS I clin pres

A

Coarse facial features, skel dysplasia, short, stiff joints, thoracolumbar kyphosis, genu valgum, thick mitral & aortic valves/mitral & aortic regurg, hepatosplenomegaly, corneal clouding, vision/hearing, intellect

42
Q

MPS I dx

A

 Excess glycosaminoglycan in urine
 Neu/lymphocytes/monocytes in blood smears showing purple red granules in cyto stained w/ Toluine blue; metachromasia
 Dec enzyme activity in leuks or cxed fibroblasts
 Pathogenic mutations

43
Q

peripheral nerve tumors w/ clin pres

A

elong spindle-shaped cells w/ uniform nuclei around nerve fibers & nerve trunks –> soft tissue grey mass, pain, sensory/motor changes, electrodiag studies

44
Q

schwannoma. mutation?

A

benign tumor from Schwann cells; most common solitary & sporadic peripheral nerve tumor –> affects spinal roots; cervical, sympathetic, vagus, peroneal, ulnar nerves (Tinel’s sign). Inactivating NF2 mutation –> no merlin –> neurofibromatosis 2 –> bil schwannomas of cranial nerves mostly CN8

45
Q

histo of schwannomas: Antoni A vs B. both are what?

A

compact hypercellular, Palisaded nuclei = Verocay bodies vs myxoid hypocellular, Hyalinized stroma containing collagen fibers. S100-immunoreactive –> derived from neural crests

46
Q

neurofibroma w/ clin pres

A

elong spindle-shaped Schwann cells w/ wavy hyperchromatic nuclei + wirelike strands of collagen like shredded carrots. skin dermis; painless superficial tumors from cutaneous nerves

47
Q

mutation of neurofibroma

A

NF1 mutation –> no neurofibromin –> inc Ras-GTPase activation –> overexpressed tyr kinases/MAPK –> mixed non-neoplastic peripheral nerve components, not well encapsulated

48
Q

plexiform vs diffuse neurofibroma

A

Mult nodular growths of fascicles along long seg of major nerve trunk –> extend to minor nerve branches –> look like rosary beads, bag of worms vs Head & neck –> spreads laterally along tissue planes –> plaque-like thickening of skin –> yellow-gray mass on subq tissues

49
Q

malig peripheral nerve tumors w/ clin pres

A

fusiform white opaque surface from Schwann cells or pluripotent cells of neural crest –> major nerve trunks like sciatic nerve, brachial/sacral plexus –> hem & nec. lg palpable mass w/ neuro deficits like radicular pain, paresthesia, motor weakness

50
Q

mutations of malig periph n tumor

A

NF1 –> no neurofibromin –> Ras-GTPase –> tyr kinase/MAPK
CDKN2A –> no p16 –> overexpressed CDK4&6 –> no retinoblastoma protein
no p14 –> no p53 as tumor suppressor
SUZ12 & EED –> Ras –> MAPK
TP53 –> no p53 as tumor suppressor

51
Q

histo of malig periph n tumor

A

resembles fibrosarcoma: hypercellular spindles w/ hyperchromatic nuclei, eos cyto, brisk mitosis activity –> invade surrounding tissue or vasc. 1+ histo differentiation => divergent differentiation –> exhibit rhabdomyosarcoma (malig triton tumor), osteo/chondro/angiosarcoma, adenocarcinoma

52
Q

neurofibromatosis type 1 mutation. what does neurofibromin nmlly do?

A
  • Auto dom NF1 mutation –> no neurofibromin –> Ras –> MAPK
    o neurofibromin pos reg cAMP –> astrocytic growth & differentiation in brain
    o Follows 2-hit hypothesis: heterozygous NF1 mutation –> neurofibromas
53
Q

neurofibromatosis type 1 clin pres/dx

A

o (6+) Café au lait macules d/t inc epidermal melanin in melanocytes & keratinocytes
o Axillary & inguinal freckles
o (2+) Lisch nodules: hamartomas of iris; don’t affect vision
o (2+ any type or 1 plexiform) Soft cutaneous neurofibromas
o Segmental neurofibromatosis: by somatic mosaicism d/t postzygotic mutation NF1 –> neurofibromas +/- café au lait unilateral w/o crossing midline
o Optic pathway gliomas (low grade pilocytic astrocytomas) w/ proptosis, strabismus, nystagmus; chiasmal gliomas w/ vision loss
o Sphenoid wing dysplasia: no greater wing –> temp lobe hern into orbital cavity –> exophthalmos & facial deformity
o Cog deficits & learning disabilities

54
Q

neurofibramotosis type 2 mutation

A
  • Auto dom NF2 mutation –> no merlin –> nervous system tumors
    o Follows 2-hit hypothesis: heterozygous NF2 mutation –> tumor
    o Mosaicism
55
Q

neurofibramotosis type 2 clin pres

A

o Bil vestibular schwannomas: intracranial, extra-axial, vestibular part of CN8 –> brainstem compression, hydrocephalus if untxed
 Press against cochlear nerve –> hearing loss, tinnitus; vestibular nerve –> dizziness
o Meningioma: cranial & spinal, blind
o Ependymoma: cervical > thoracic > lumbar cord
o Café au lait, astrocytomas of spinal cord

56
Q

axonal neuropathies. can they regen? electrophys?

A

dmg to axon –> distal part of axon degen => Wallerian degen –> myelin degen –> phag by macs to remove debris. if 2 cut sections = close to e/o; if not –> painful nodular traumatic neuroma. dec amp b/c low axons but preserved conduction velocity

57
Q

demyelinating neuropathies

A

breakdown & loss myelin over few seg => segmental demyelination –> phag by macs –> Schwann cells prolif & remyelinate –> onion bulbs if rpted –> hypertrophic neuropathy. loss saltatory conduction –> dec conduction vel but preserved axons

58
Q

neuronopathy vs mononeuropathy vs polyneuropathy vs mononeuritis multiplex

A

destroyed motor neurons or DRG –> secondary degen axon & dendrites –> motor, sensory, autonomic neuropathy –> sensory deficits, ataxia vs affects single nerve d/t trauma, entrapment, infxn vs affects mult sensory & motor nerves in length dependent fashion –> deficits in feet & ascend vs dmgs several nerves in haphazard

59
Q

plexopathy vs radiculopathy

A

affects brachial/lumbar/sacral plexus d/t trauma, compression, penetrating wounds, ca –> pain, weak, sensory deficit, loss DTRs at lvl of plexus & distal in ipsi extremity vs affects spinal nerve roots d/t chronic pressure, herniated disc –> pain, loss sensation in dermatome, muscle weakness innervated by that nerve root

60
Q

vasculitis neuropathy examples vs toxic neuropathy examples

A

polyarteritis nodosa, granulomatosis w/ polyangiitis, eos granulomatosis w/ polyangiitis, mononeuritis multiplex –> axon degen vs platinum drugs, taxanes, vinca alkaloids, myeloma tx from chemotherapy-induced peripheral neuropathy

61
Q

neuropathies from physical force: amputation vs compression/entrap neuropathy; electrodiag studies?

A

hyperplastic rxn to peripheral nerve dmg 1-12mo post amputation –> disorganized bundles of interlacing regen axons in fibrous stroma vs peripheral nerve chronically subjected to inc pressure; carpal tunnel –> paresthesia, ischemic dmg –> de/remyelin; slow motor nerve conduction velocity, prolonged distal motor latencies

62
Q

neuropathies w/ tumor: brachial plexopathy vs Horner vs obturator neuropathy

A

lung ca invading brachial plexus –> pain in shoulder, axilla vs lung, br ca invading lower cervical/upper thoracic spinal cord –> ipsi ptosis, miotic but reactive pupil, facial anhidrosis vs pelvic neoplasms, urothelial ca of bladder –> obturator n compression –> paresthesia, sensory loss, pain in medial thigh

63
Q

paraneoplastic neuropathies = caused by ca but not via direct invasion: paraneoplastic sensory vs sensorimotor vs autonomic neuropathy

A

autoimmune against tumor ag similar to DRG; SCLC w/ antiHu vs mimics chronic inflamm demyelinating polyneuropathy; SCLC w/ antiHu & antiCV2, lymphoma, br/ov ca vs SCLC w/ antiHu, pancreas, thyroid, rectum, Hodgkin lymphoma

64
Q

diabetic neuropathy affects peripheral & autonomic nervous systems: Distal symmetric polyneuropathy vs Diabetic autonomic neuropathy vs Diabetic mononeuropathy vs Diabetic polyradiculoneuropathy

A

loss sensory & motor neurons –> stock & glove deficits vs cardiovasc, gastric, intestinal, urinary, genital, cutaneous sxs vs median n > ulnar n > radial n > common peroneal n (fib head) vs lumbosacral roots, peripheral nerves –> unilateral pain, muscle weakness, proximal leg atrophy

65
Q

Charcot-Marie-Tooth type 1 v type 2

A

Duplication PMP22 –> overexpress PMP22 –> intracellular degrad of membrane –> high arched feet, atrophy of calf => stork leg/inverted champagne bottle vs MFN2 mutation –> abnl mito fusion –> distal muscle weakness & atrophy; electrophys studies show dec cmpd muscular AP but nml conduction vel

66
Q

hereditary sensory & autonomic neuropathies type 1

A

auto dom SPTLC1 encoding serine palmitoytransferase in sphingolipid biosynthesis –> amyloid deposits in auto & peripheral nervous system –> no pain/temp, distal to prox muscle weakness, impaired sweating

67
Q

familial amyloid polyneuropathy

A

Auto dom TTR mutation encoding transthyretin transporting T4 & retinol in serum –> amyloid deposits in auto & peripheral nervous system –> carpal tunnel, sensorimotor polyneuropathy (stock & glove), autonomic neuropathy (orthostatic hypoTN), incont/retention, ED

68
Q

MS

A

multifactorial autoimmune dz w/ relapsing-remitting d/o affecting white matter in CNS that’s separated by space & time d/t DRB1*1501

69
Q

MS: active vs Inactive vs Shadow plaques

A

myelin breakdown w/ foamy macs vs hypocellular densely gliotic lesions, no macs or oligodendrocytes vs remyelin lesions by surviving oligodendrocytes, no macs

70
Q

path vs clin pres of MS

A

little blue stain vs optic neuritis, CN sxs, spinal cord sxs

71
Q

img vs CSF of MS

A

T2 showing Dawson fingers vs clear/colorless, inc igG & oligoclonal bands

72
Q

central pontine myelinolysis = caused by Osmotic demyelination syndrome

A

osmotic myelinolysis of white matter tracts dmging oligodendrocytes –> cerebral edema –> hyponatremia –> brain loses K+ –> water leaves brain to dec swelling –> hypotonic brain cells –> hyponatremia sxs

73
Q

Neuromyleitis optica/Devic dz

A

infectious viral prodrome –> ab-mediated synchronous or sequential optic neuritis & spinal cord inflamm –> targets astrocytes –> vision loss, para/quadriplegia, sensory loss, incont

74
Q

labs vs CSF of Neuromyleitis optica/Devic dz

A

AQP4 autoab in serum vs lymphocytic pleiocytosis / inc protein & nml glu; no oligoclonal bands

75
Q

Acute disseminated encephalomyelitis

A

infxn or viral vax –> acute multifocal demyelin d/t myelin autoag –> buildup of lipid-laden macs, axonal dmg in white matter of subcortical regions, cerebellum, brainstem, spinal cord –> encephalopathy, sleepy/lethargy/coma

76
Q

img vs CSF of Acute disseminated encephalomyelitis

A

T2W shows hyperintensity in white matter vs inc protein, WBC, ig; rare oligoclonal bands

77
Q

acute hemorrhagic leukoencephalitis

A

necrotizing vasculitis of sm vessels w/ fibroid nec, perivascular microhemorrhages /in cerebral white matter, perivascular demyelin w/ inflamm cellular infiltrates in children –> more severe sxs of ADEM

Block 3 (23 decks)

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