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Hailey - Neuro > Krafts Diseases and Pearls > Flashcards

Krafts Diseases and Pearls Flashcards

1
Q

cells of CNS

A 
neurons
astrocytes
oligodendrocytes
microglia
ependymal
(last 4: glial)
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2
Q

astrocytes Fx

A

“cell that does the most”
most important glial cells
star shaped, long processes (rosenthal processes)

big responders to injury
provide glucose for brain, ONLY source

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3
Q

oligodendrocytes Fx

A

myelin

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4
Q

microglia Fx

A

macrophages

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5
Q

ependymal cell fx

A

produce CSF

line ventricles

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6
Q

stain used to show astrocytes and their processes

A

silver stain

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7
Q

astrocyte vs oligodendrocyte

A
  1. astrocytes bigger
  2. astrocytes open chromatin pattern
  3. ogd chromatin black dot
  4. ogd in lacunae/space
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8
Q

ependymal cells have

A

cilia (motion)

microvilli (absorption)

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9
Q

when acute CNS injury, think

A

red neurons

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10
Q

associate red neurons with

A

acute injury
loss of blood flow
“red is dead”

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11
Q

inclusion bodies are

A

reactions of neurons to injury
by axonal spheroids
accumulations within nucleus or cytoplasm of neurons

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12
Q

cowdry a

A

herpes

“owl’s eye”

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13
Q

negri

A

rabies

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14
Q

neurofibrillary tangles

A

AD

silver stain, see accumulation of amyloid

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15
Q

lewy bodies

A

PD

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16
Q

gliosis

A

astrocyte proliferation
*important sign of infection
is like scarring in the brain

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17
Q

gemistocytic astrocytes

A

happy, make more proteins

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18
Q

inclusions in astrocytes*

A

rosenthal fibers (processes of astrocytes, thick, tumor, metabolic disease, nonspecific injurious process going on)

corpora amylacea (pearl like, light blue, due to aging)

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19
Q

microglial nodules

A

dead tissue, foreign substance that needs to be chewed up by microglia

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20
Q

genetic metabolic disease shows up when…

A

birth*

missing enzyme that primarily affects CNS –> build up –> lose function

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21
Q

genetic metabolic diseases

A

neuronal storage disease (storage disorders in CNS neurons)

leukodystrophies (affect white matter)

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22
Q

acquired metabolic diseases

A

vitamin deficients
metabolic and toxic disturbances
later in life*

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23
Q

NSDs

A

diagnose by clinical exam, labs, common look of neuron

  1. Neuronal ceroid lipofuscinoses: accumulation of lipofusin –> neuronal dysfxn. blindness, motor probe, seizures
  2. Tay-Sachs Disease: Ashkenazi Jews, deficiency in HEX-A, hexosaminidase A –> breaks down ganglioside (GM2) (a “food” for neurons). baby seems normal at birth, doesn’t meet development milestones (6-8mo), motor impair, paralysis, loss near fxn, death by age 4, cherry red spots
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24
Q

Tay-Sachs Disease

A
  • Ashkenazi Jews
  • deficiency in HEX-A
  • hexosaminidase A –> breaks down ganglioside (GM2 type, a “food” for neurons)
  • baby seems normal at birth, doesn’t meet development milestones (6-8mo)
  • cherry red spots (macula sticks out)*
  • motor impair
  • paralysis
  • loss neurological fxn
  • death by age 4
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25
Q

cherry-red spots

A

whole retina contains neurons stuffed with gangliosides that are white, so entire retina becomes palsied, white —> makes macula more red

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26
Q

Leukodystrophies

A

myelin abnormalitis (ogds, not neurons)

  1. Krabbe Disease
    - galactosylceramidase deficiency
    - accumulation of galactocerebrosie –> TOXIC to OGDs –> loss of myelin –> axons conduct poorly
    - globoid cells: fat macrophages stuffed full of the toxic metabolite, released as OGD dies **does see in other disorders
    - motor
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27
Q

difference between NSDs and LDs?

A

LDs: deterioration of motors skills, spasticity, hypotonia, ataxia (less cognitive issues)

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28
Q

Krabbe Disease hallmarks

A
  1. globoid cells
  2. motor
  3. galactosylceramidase deficiency –> accum galactrocerebroside (TOXIC)
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29
Q

B1 deficiency

A

Thiamine deficiency

  • chronic alcoholism, starvation
  • -> Wernicke/Korsakoff
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30
Q

First stage B1 deficiency (in CNS)

A 
Wernicke encephalopathy
mammillary bodies starved --> hemorrhage, necrosis, eaten up by microglia
EARLY AND REVERSIBLE (give thiamine)
1. confusion
2. ophthalmoplegia
3. ataxia
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31
Q

Second stage B1 deficiency

A 
Korsakoff syndrome
mammillary bodies atrophied
NOT REVERSIBLE
1. Wernicke encephalopathy
2. memory disturbances
3. confabulation
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32
Q

B2 deficiency

A

cobalamin
needed to make DNA
anemia
subacute combined degeneration of spinal cord

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33
Q

Subactue combined degeneration of SC

A

B12 deficiency
motor and sensory tracts loss myelin (ascending and descending)
numbness, ataxia, weakness REVERSIBLE
paraplegia IRREVERSIBLE
*distribution dorsal column, and dosrsolateral columns

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34
Q

Toxins affect CNS

A

carbon monoxide
methanol
ethanol

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35
Q

CO

A

confusion, disoriented –>
delirium –>
coma

goes to CNS first*
particularly: hippocampus, parking cells, cortex
high affinity for Hb (won’t allow proper O2 delivery)
pink discoloration of tissues**

36
Q

Methanol CH3OH

A

30-100ml fatal
4ml cause blindness
prefers to go to ganglionic cells in retina

37
Q

Ethanol CH3CH2OH

A 
prefers to go to cerebellum (middle --> ataxia)
acute effects REVERSIBLE
ataxia, nystagmus
Bergmann gliosis
--> cerebellar atrophy
38
Q

Bergmann gliosis

A

proliferation of astrocytes collect where purine cells should be

39
Q

Peripheral Nerve Diseases

A

neuropathies

  1. Guillian-Barre Syndrome
  2. Hansen’s Disease
  3. VZV
  4. Charcot-Marie-Tooth Disease
  5. Peripheral Neuropathy in Diabetes
  6. Neuropathies associated with malignancy
40
Q

Guillian-Barre Syndrome

A

= Acute Inflammatory Demyelination Polyradiculoneuropathy

  • ascending parasthesia
  • flu-like illness prior
  • immune-mediated (T cells and macrophages cause segmental demyelination*** after having attacked virus)
  • resolves over time
  • plasmaphoresis: remove ab, seem to get better
  • respiratory therapy if paralysis into lungs
41
Q

clinical course of Guillian-Barre

A

symmetric ascending paralysis > rapid-onset weakness > loss deep tendon reflexes > loss of sensation > elevated CSF protein > 2-5% mortality from respiratory paralysis, autonomic instability, cardiac arrest

42
Q

Hansen’s Disease

A 
slowly progressive infection of skin and nerves
Mycobacterium leprae
most of world is naturally immune
endemic in poor tropical countries
disabling deformities
  1. tuberculoid leprosy (less severe, skin disorder, nerve degeneration - anesthesia, ulcers)
  2. lepromatous leprosy (more sever, skin, nerves, eye, mouth, tests, hands, feet - immune system doesn’t respond well to kill pathogen)
43
Q

Tuberculoid leprosy

A

nice T cell response to make enough granulomas, decrease pathogen
Mycobacterium leprae
skin rash*

44
Q

Lepromatous leprosy

A

leonine facies*
autoamputation*
Mycobacterium leprae
immune system doesn’t respond as well

45
Q

VZV

A 
common viral inf of PNS
dormant in DRG, cord, or brainstem
neuronal destruction --> pain
"dew drop on a rose petal"
dermatomes
multinucleate giant cells
46
Q

most common hereditary neuropathy

A

Hereditary Motor and Sensory Neuropathy Type 1 = Charcot-Marie-Tooth disease

47
Q

Charcot-Marie-Tooth disease

A

de-myelination then re-myelination*
muscle loss, sensory loss but pain intact**
childhood/early adulthood
autosomal dominant
pes cavus (high arch), foot drop, hammer toes, muscle atrophy
normal life span

48
Q

Peripheral Neuropathy in Diabetes

A

too much sugar in blood > glucose stick to peripheral nerves > irreversible connections with cells
autonomic neuropathy (difficult bladder control) or asymmetric neuropathy (involve one nerve)
*symm M and S neuropathy in distal
decreased pain sensation > ulcers, injury > no heal > amputations
*stocking glove distribution

49
Q

Neuropathies associated with malignancy

A
  1. neoplasms: metastatic, mononeuropathy (push on nerve)
    eg. lung pressing on brachial plexus, obturator palsy from pelvic neoplasms, cranial nerve palsies from brain tumors
  2. paraneoplastic effects: look like hormone effects, polyneuropathy (tumor production of substances/antibodies that start reacting with nerves)
    eg. small cell lung cancer, plasma cell malignancies
50
Q

Skull fractures

A

Linear
Depressed
Diastatic
Basal

51
Q

Linear skull fracture

A

most COMMON
STRAIGHT crack
usually not serious

52
Q

Depressed skull fracture

A

bone displaced INWARD
comminuted (in pieces)
can damage brain

53
Q

Diastatic skull fracture

A

across a SUTURE
suture widens
usually in children

54
Q

Basal skull fracture

A

more force required
distant hematoma (battle sign behind ear, raccoon eyes)
CSF drainage from nose or ear*

55
Q

frontal bone fracture

A

patient unconscious, couldn’t stop self from falling on face

56
Q

Parenchymal injuries

A
  1. Concussion
  2. Second-impact Syndrome
  3. Chronic traumatic encephalopathy
  4. Direct Parenchymal injury
  5. Diffuse axonal injury
  6. Traumatic vascular injury
57
Q

Concussion

A

altered consciousness from head injury due to change in momentum of head (stretching and snapping back of brain)

Sx: amnesia, confusion, HA, visual disturb, N/V, dizzi

58
Q

Second-impact Syndrome

A

rare
CATASTROPHIC: brain swells rapidly
second concussion before first healed

59
Q

Chronic traumatic encephalopathy

A

multiple conconsions
life changing effect on person/personality
progressive degenerative disease
histologically looks like AD: tau protein

Sx: progressive dementia, poor judgement, apathy depression, memory loss, confusion, aggression

60
Q

Direct Parenchymal injury

A

laceration (eg. knife wound)
contusion (bruising)
coup/contrecoup injury

61
Q

Diffuse Axonal injury

A

rotational acceleration, torque side to side > shearing of axons
injury to axons in deep white matter
coma (can exist)
eg. shaken baby syndrome, boxing

62
Q

Direct parencymal vs concussion

A

direct parenchymal: can point to lesion in one localized area

63
Q

Traumatic vascular injury

A

epidural hematoma
subdural hematoma
subarachnoid hemorrhage

64
Q

epidural hematoma

A

above dura
SURGICAL EMERGENCY
rupture middle meningeal artery*
contours are smooth: lens on MRI/CT “tough mother, dura is so tough”

ex: baseball hit to the temple, lucid period*

65
Q

subdural hematoma

A

between dura and arachnoid
shearing of cerebral veins*
contours are not smooth

ex: elderly patient falls, ripped veins as as they run through dura. 1. acute (hours) numbness one side, 2. chronic (months) numb and personality changes

66
Q

subarachnoid hemorrhage

A 
in arachnoid space
NEUROSURGICAL EMERGENCY
actual bleed cerebral arteries*
contusions, ruptured berry aneurysms*
(40% ACA, 20% internal carotid, 34% MCA branches, 4% PCA)

ex: “worst headache I have ever had”

67
Q

ICP increased in

A 
brain swelling/inflammation
hematoma
rumors
hydrocephalus
increased CSF
68
Q

cerebral edema

A
  1. vasogenic
    cause: leaky vessels/inc vascular permeability
    space between cells
    localized or generalized
  2. cytotoxic
    cause: cell membrane injury (hypoxia or metabolic damage > messes channels in/out of cells)
    space within cells: cells r swole

often occur together whenever cerebral edema

69
Q

local vasogenic cerebral edema tx

A
  1. steroid: dexamethasone (reduce water permeability of tight junctions)
  2. mannitol: osmotic diuretic, will draw water out of CSF into blood
70
Q

cytotoxic tx

A

no known treatment

71
Q

hydropcephalus

A

accumulation of excessive CSF within ventricular system

infancy > head enlarges (sutures aren’t closed)
adulthood > ventricles expand, increased ICP

72
Q

Five kinds hydrocephalus

A
  1. communicating
  2. non-communicating
  3. ex vacuo
  4. increased CSF production
  5. normal pressure
73
Q

Non-communicating

A

blockage in one way circulation

eg. congenital malformation, mass, collection of blood/hematoma

74
Q

Communicating

A

block exit of CSF into sinus

eg. resolving meningitis

75
Q

Craniopharygioma

A

blocks CSF, pituitary oma, rare

76
Q

Ex vacuo

A

no block in ventricular system
degenerative
BRAIN ATROPHY > RESULTING HYDROCEPHALUS
dilated ventricular system

77
Q

Choroid Plexus Papilloma

A

increased CSF production?, rare

78
Q

Normal pressure

A 
Triad: wet, wobbly, wacky
1. urinary incontinence
2. magnetic gait
3. dementia
REVERSIBLE
no cortical atrophy, ventricles enlarge
can be confused with AD
*something blocked CSF by some arachnoid blockage, CSF couldn't get out, then somehow, pressure normalizes*
79
Q

How differentiate normal pressure hydrocephalus from AD?

A

Dementia is different. NP H the gait is unusual, patient doesn’t really care about incontinence issues (frontal lobe changes, apathy)

80
Q

Tx hydrocephalus

A

goal: reduce fluid volume and pressure
1. surgery, shunt to drain CSF
2. decrase CSF production with acetazolamide (CA inhibitor) or furosemide (NKCC inhibitor)

81
Q

critical enzyme: carbonic anhydrase

A

converst CO2 and water to H ion and bicarbonate
block CA > reduce HCO3 > less transport of Cl and Na > less production of CSF

SE: reduced stomach acid production, more sodium release, increased urine output, many

82
Q

increased ICP

A

mass effect (edema, tumor, hematoma)
compromised blood flow to brain > pain, papilledema, decreased consciousness
feared outcome: herniation

83
Q

common herniations

A
  1. subfalcine hernation
  2. transtentorial hernation
  3. tonsilar hernation
84
Q

herniation Sx

A

focal neurological symptoms
brainstem symptoms: respiratory and cardiac arrest, coma
often fatal

85
Q

subfalcine herniation

A

cingulate gyrus pushed under falx cerebri

compresses ACA

86
Q

transtentorial uncinate hernation

A

uncus through tentorium

compresses:
- CN III (fixed, dilated pupil, ophthalmoplegia)
- brainstem (rip blood vessels, duret hemorrhages) FATAL
- PCA (ischemia in 1* visual cortex)
- contralateral cerebral peduncle (hemiparesis)

87
Q

tonsilar hernation

A

cerebellar tonsils through foramen magnum
compresses medulla (compromises vital resp and cardiac centers)
LIFE THREATENING

Hailey - Neuro (10 decks)

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