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Neurology - step > pathology > Flashcards

pathology Flashcards

1
Q

define dementia please

A

a decrease in cognitive ability, memory of function with intact consciousness

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2
Q

what part of brain is affected in Alzheimer disease

A

frontal, temporal, parietal

occipital usually spared

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3
Q

what part of brain is affected in frontotemporal dementia

A

spares parietal lobe and posterior 2/3 of superior temporal gyrus
frontotemporal atrophy

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4
Q 
name the dementia:
dementia
aphasia
parkinsonism
changes in personality
A

frontotemporal dementia

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5
Q

name the dementia:
dementia
visual hallucinations
parkinsonian features afterwards

A

lewy body dementia

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6
Q

what is most common form of Alzheimer disease

A

late onset

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7
Q

APoE2 has what link to AD?

A

decrease risk

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8
Q

APO E4 has what link to AD?

A

increased risk for familial/early onset form

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9
Q

what genes are associated with familial/early onset AD and their products pelase

A

chromosome 1 - presenlin-1
chromosome 14 - presenlin 2
chromosome 21 - APP

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10
Q

describe gross appearance of brain in Alzheimer disease

A

widespread cortical atrophy with narrowed gyri and widened nuclei

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11
Q

what are the neurotransmitter changes in alzhemier disease

A

decreased ach

also happens with aging

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12
Q

what are two distinguishing histopathos features found in Alzheimer disease

A

senile plaques and neurofibrillary tangles

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13
Q

please describe senile plaques

A

found in gray matter

extracellular beta amyloid core

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14
Q

what is the potentnail consequence of senile plagues

A

deposition ofextracellular beta amyloid may lead to amyloid angiopathy - increase risk for intracranial hemorrhage

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15
Q

how is Abeta/amyloid-beta made?

A

synthesized by cleaving amyloid precursor protein APP

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16
Q

what pathway is involved int eh phosphorylation of both Abeta and tau proteins in AD?

A

no more wnt to inhibit GSK

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17
Q

please describe a neurofibrillary tangle

A

intracellular hyperphosphorylated tau protein - insoluble ytoskeletal elements

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18
Q

what is a marker o the degree of dementia in Alzheimer disease?

A

number of intracellular neurofibrillary tangles form hyper-pid tau protein

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19
Q

where do you see PICK bodies

A

frontotemporal dementia

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20
Q

what is a pick body?

A

silver-staining spherical tau protein aggregate

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21
Q

what is a lewy body?

A

alpha-synculein defect - lewy bodies are primarily cortical

seen in lewy body dementia

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22
Q

time course of creutzdelft jakob disease please

A

rapidly progressive; less than 1 year survival ‘[ weeks to months

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23
Q

what does brain look like in Cj disease please

A

spongiform - bubbles and holes

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24
Q 
name the dementia:
rapid ie weeks to months
dementia
myoclonus
''startle''
A

Creutzfeld Jacob disease

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25
Q

what causes CJ disease

A

prions – PrPc –> PrPsc that form a beta pleated sheet resistant to proteases

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26
Q

risk groups for Cj disease please

A

corneal transplant
contact with human brain - neurosurgeons/pathologists
improper sterilized cortical electrodes
eating beef from cattle with mad cow disease

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27
Q

what is the second most common cause fo dementia in elderly

A

multi infarcts from vascuarl disease

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28
Q

what else can cause dementia

A 
syphilis
HIV
vitamin B1, 3, 12 deficiency
Wilson disease
normal pressure hydrocephalus
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29
Q 
syphilis
HIV
vitamin B1, B3, B12 deficiency
Wilson disease
vascular disease - multi infarct
normal pressure hydrocephalus
A

can all cause dementia

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30
Q

what is subacute sclerosing panencephalitis associated wtih

A

measles/rubeola

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31
Q

describe the pathogenesis fo multiple sclerosis please

A

autoimmune inflammation and demyelination fo the CNS @ brain and sc

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32
Q

how does multiple sclerosis present

A 
remitting and relapsing
optic neuritis - sudden loss of vision resulting in marcus gunn pupils
hemiparesis
hemisensory symptoms
bladder/bowel incontinence
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33
Q

who does ms usually present in

A

white people living further away from equator
females
20-30 years old

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34
Q

what is charcots triad of MS

A

SIIIN

scanning speech
incontinence
intention tremor
intraopthalmoplegia - bilateral
nystagmus
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35
Q

lab findings in MS please

A

oligoconal bands in CSF

increased Ig in CSF

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36
Q

gold standard for ms diagnosis please

A

MRI

shows periventricular plaques caused by areas of oligodendrocyte loss and reactive gliosis with destruction of aonxs

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37
Q

whats going on to cause problems in ms

A

autoimmune - oligodencrocyte loss and reactive gliosis with destruction of axons leads to periventricular plaques on MRI

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38
Q

how do you slow the progression of ms

A

disease modifying therapies - IFNb and natalizumba

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39
Q

how do you treat acute flares of ms

A

IV steroids

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40
Q

how do you treat neurogenic bladder in ms

A

catheter and muscarinic antagonists

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41
Q

how do you treat spasticity in ms

A

baclofen and GABAb receptor agonists

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42
Q

how do you treat pain in ms

A

opioids

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43
Q 
marcus gunn pupils with suddne loss of vision
intranuclear opthalmoplegia
hemiparesis
hemisensory symptoms
bladder and bowel incontiencne
scanning speech
intention tremor
incontinence
intranuclear opthalmoplegia
nystagmus
A

MULTIPLE SCLEROSIS
young adult female
northern hemispheres

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44
Q

what is the most common cause of acute peripheral neuropathy

A

GUILLIAN BARRE/acute inflammatory demyelinating polyradiculopathy

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45
Q

what is guillian barre?

A

inflammatory infiltrate in the endoneurium
autoimmune condition that destroys schwann cells - inflammation and demyelination of peripheral nerves and motoro fibres after infection with campylobacter jeuni, mycoplasma pneumonia of viral - attach of myelin due to molecular mimcry, inoclautionad and stress

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46
Q

presentation of guillina barre pelase

A

rapid symmetrical ascending motor weakness/paralsysi
facial parpalyss in 50%
may also see autonomic dysregualtion - cardiac irregulatiris, hypo or hypertension
may also see sensory abnormalities

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47
Q

prognosis of gullian barre

A

most survive after complete recovery following weeks to months

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48
Q

lab findings in guillina barre please

A

increased CSF protein with normal cell count

albunimocytlogic dissociation

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49
Q

what can happen due to increased protein in the CSF in guillian barre

A

papilloedema (enlarged blind spot and elevated opti disc with blurred margins on fundoscopy due to optic disc swelling from increased IOP)

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50
Q

how to treat guillian barre

A

respiratory support until recovery
plasmapheresis
IVIg

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51
Q

bugs associated with guillian barre/acute inflammatory demyelinating polyradiculopathy

A

campylobacter jejuni
viruses
mycoplasma pneumoniae

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52
Q

what is acute disseminated/post infectious encephalomyelitis

A

mutifocal periventricuarl infmmation and demyelination after infection or vaccinations

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53
Q

what can cause multifocal periventricular inflammation and demyelingation?

A

infectiosn of MEASLES or VZV

vacinnations of rabies or small pox

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54
Q

what is inheritance pattern of charcot-marie-tooth disease

A

autosomal ominant

55
Q

what is charcot marie tooth disease

A

most common cause of herediatary neuropathy
group fo progressive hereditary nerve disorders related to the defective production of proteisn involved in the structure and function of peripheral nerves or the myelin sheath

56
Q

what is charco marie tooth usually associated with

A

scoliosis

foot deformites

57
Q

scoliosis
foot deformities
peripheral neuropathis

A

charcot marie tooth

58
Q

what is the inheritance pattern of krabbe disease

A

AR

59
Q

what is the inheritance pattern of metachromatic luekodystrophy

A

AR

60
Q

peripheral neuropathy
developmental delay
optic atrophy

A

krabb disease
lysosomal storage disease
definciency in galactocerebrosidase - increased galatocerebroside and psychosine - destroys myelin sheath

61
Q

what enzyme is deficient in krabbe disease

A

galatocerebrosidase - leads to accumulation of galatocerebrosides and psychosine that destroy myelin sheath

62
Q

central demyelination
peripheral demyelination
dementia
ataxia

A

metachromatic luekodystrophy
lysosomal storage disease
arylsultafase A deficienty - sulfatides build up and imapri production and destroy myelin sheat

63
Q

what is enzyme deficiency in metachromatic leukodystrophy

A

arylsulfatase A definciency - ulfatides build up that inhibit production and destroy myelin sheath

64
Q

what is progressive multifocal leukoencephaopathy

A

demyelination of CNS due to destruction of oligodendrocytes

65
Q

what demyelinating disease is JC virus associated with

A

progressive multifocal leukoencephaoloatphy (destruction of oligodendrocytes)

66
Q

what increases risk of PML

A

natulizimab and rituximab use

HIV > 50 CD4/mm^3 due to reactivation of JC virus

67
Q

what is clinical course of PML

A

rapidly progressive and usually fatal

68
Q

what is a seizure

A

high frequency coordinated neuronal firing

69
Q

inheritance pattery of arenoleukodystrophy

A

xlinked recessive

70
Q

what is the pathophys of adrenoleukodystrophy

A

enzyme deficiency ro beta oxidation fo very/long chain fatty acids in perioxisomes - instead build up

71
Q

where do VLCFA build up in adrenoluekodystrophy

A

adrenal cortex
testes
nervous system
generalized loss of meylin

72
Q

what are consequences fo adrenoleukodstryophy

A

can lead to long term coma/death and adrenal gland insufficiency

73
Q

describe a partial seizure

A

affects single area of brain; often preceeded with an aura; can be followed by a gernalzied

74
Q

which typically has an aura, generalized or partial zeisure

A

partial

75
Q

where is origin most often in partial seizures

A

medial temporal lobe

76
Q

what is a simple partial seizure

A

consciousness intact

motor, sensory, autominc, psychic symptoms

77
Q

what is a complex partial seizure

A

no consciousness intact

78
Q

what is epilepsy

A

disorder of recurrent seizures

79
Q

are febrile seizures epilepsy

A

noppers

80
Q

what is status epilepticus

A

continuous or recurring seizures that mayr esult in brain injury
>10-30 mins but variable

81
Q

what can cause seizures in children

A

genetics, infection, trauma, congenital and metabolic

82
Q

what can cause seizures in adults

A

tumor, trauma, stroke infection

83
Q

what can aause stroke in elderly

A

stroke, tumor trauma, etabolic or infection

84
Q

what can cause seizures in children, adults and elderly

A

infection, trauma

85
Q

what can cause seizures in children and adults

A

metabolic, trauma

86
Q

what can cause seizures in adults and elderly

A

trauma, infection, stroke

87
Q

what causesa headaches

A

pain due to irritation fo structures such as dura, cranial nerves or exgtracrinal structires

88
Q

what type of headaches are unilateral

A

cluster and migraine

89
Q

what type of headache are bilateral

A

tension

90
Q

how long is a cluster headache

A

15 mins to 3 hours and repetititve

91
Q

how long is a tension headache

A

> 30 mins (typically 4-6 hours) constant

92
Q

how long is a migraine headache

A

4-72 hours

93
Q

headache with excricuating perioribtal pain

A

cluster

94
Q

headache with lacrimation and rhinorrhea

A

cluster

95
Q

headache more common in males

A

cluster

96
Q

headache with possibly horner syndrome

A

cluster

97
Q

treatment of cluster headache

A

100% O2

sumitriptan

98
Q

bilateral headache with no photophobia or phonophobia or aura

A

tension headache

99
Q

how to treat tension hedache

A

analgecis
NSAIDs
acetaminophem
amitriptyline for chronic

100
Q

pulsating pain, which head ache?

A

migraine

101
Q

photophbia, nausea or phonophobia headache?

A

migraine

102
Q

what causes pain in a migraine?

A

irritation of CN V, meningnes or blood vessels - dubtance P, calcitonin gene related petide and vaosciative petides are reelase

103
Q

which headache may have aura

A

migraines

104
Q

treatment of migraines

A

abortive therapies like triptan and NSAIDs

prophylaxis - propranolol, topiramate, CCB, amitriptyline

105
Q

POUNDS for migrans please

A 
Pulsatile
One day duration
Unilateral
Nausea
disabling
106
Q

what else can cause headaches

A

subarachnoid hemorrhage, meningitis, hydrocephalus, neoplasia, arteritis

107
Q

describe pain with trigeminal neuralgia

A

repetitive shooting pain in the CN V distribution that typically lasts for < 1 minute

108
Q

define vertigo

A

sensation of spinning while actuallys tationaty

109
Q

what type of vertigo is most common

A

peripheral

110
Q

what causes peripheral vertigo

A

inner ear stuffs - semicircular canal debris, vetibular nerve infection, Meniere disease

111
Q

what will show up in positional testing with peripheral vertigo

A

delayed horizontal nystagums

112
Q

what causes cenral vertigo

A

brain stem or cerebellar lesion: stroke affectin estibular nuclie or posterior fossa tumor

113
Q 
directional change of nystagmus
skew deviation
diplopia
dysmetria
focal neurological findings
A

central vertigo

114
Q

cxpx of central vertigo please

A 
directional change of nystagmus
skew deviation
diplopia
dysmetria
focal neurological findings
115
Q

what happens in positional testing for central vertigo

A

immediate nystagmus seen in any direction that mae change firections and focal nerological findings

116
Q

genetics of struge weber syndrome

A

somatic mosaicism

GNAQ gene activating mutation that causes developmental anomaly of neural crest deriviatves in mesoderma nd ectoderm

117
Q

pathophys of sturg weber syndrome please

A

GNAQ gene activiating mutation that causes developmental anomalies of neural crest cell derivatives in mesoderm and ectoderm
affects small blood vessels

118
Q

cxpx of sturg weber pelase

A

port wine stain/ nevus flammeus @ CN V1 and V2 unilateral
leptomeningeal angiomas - seizure and epilepsy
intellectual disability
episcleral hemangiomas - increased IOP - early onset glaucoma

119
Q

intellectual disability
port winde staine
seizures and epilepsy
early onset glaucoma

A

surg weber syndrome

120
Q

what si a nevus falmmeus

A

non neoplastic ‘‘birthmark;; in CN V1 and V2

121
Q

inheritance pattern of tuberous sclerosis please

A

autosomal dominant

122
Q

describe cxpx of tuberous sclerosis please

A 
angiofibromas in skin
ash leef/sheegreen hypopigmented patches
rhabdomyoma at heart
mitral regurgitation
angiomyolipoma at kidney
mental retardation
increased risk of subependymomal astrocytoma and ungal fibromas
123
Q

main characteristic of tuberous sclerosis

A

hamartomas in the CNS and skin

124
Q 
angiofibromas at skin
rhabdomyomas at heart
hitral regurgitation
angiomyolipoma t kidney
mental retardation
ash leaf
shagreen
A

tuberous sclerosis

125
Q

inheritance pattern of tuberous sclerosis

A

autosomal dominant

126
Q

genetics of neurofibromatosis I pelase

A

chromome 17, NF1 gene, tumor supporessor of RAS, neurofibrominin

127
Q

pathophys of nf-1

A

skin tumors are derivatives of abberant neural crest cells

128
Q

cxpx of neurofibromatosis I

A

neurofibromas in skin
optic gliomas
lisch nodules - pigmented nodules in iris
pheochromocytoma
increased risk of wilms tumor, pheochromoctyoma and CML
café au lait spots

129
Q

what are of increased risk with NF1

A

CML
wilms tumor
pheochromocytomas

130
Q

what are of increased risk in tuberous sclerosis

A

subependymal astrocytomas

uncal fibromas

131
Q

describe genetics of von hippel lindau

A

chromosome 3 HVL - tumor supporessor of HIF-1

132
Q

describe pathos of von hippel lindaue

A

hemangioblastmas - high vascularity with hyperchromatic nuclei

133
Q

cxpx of von hippel lindau

A

hemangioblastomas in retina, cerebellum, spinal cord and brain stem
angiomatosis in skin, mucosa, organs
bilateral renal cell carcinoma
pheocrhrmocytoma

134
Q

hemangiobalstoma in retina, cerebellum, spc, brain stem
angiomatosis in skin, m;ucos, organs
bilateral renal cell carcinoma
pheochromocytomas

A

von hippel lindau

Neurology - step (10 decks)

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