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Neuro B1 - WLB > Week 1 - Kraft > Flashcards

Week 1 - Kraft Flashcards

0
Q

What are glial cells?

A

Refers to every neuronal cell besides neurons

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1
Q

What are the main patterns of neuronal injury?

A
  • Acute injury –> red neurons
  • Subacute/chronic injury –> degeneration, neuron loss/disappearance (Alzheimer’s disease)
  • Axonal reaction –> cut close to neuron cell body
  • Axonal spheroids –> ?
  • Inculsions –> viral or degenerative
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2
Q

What is the structure & function of Oligodendrocytes?

A

Function: Produce myelin.

Structure: Contain darker chromatin than astrocytes and are smaller than astrocytes.

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3
Q

What is the structure & function of Ependymal cells?

A

Function: Make CSF

Structure: Line the ventricles (choroid plexus), have cilia for fluid movement and microvilli for absorption

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4
Q

When do Red Neurons occur?

A
  • Acute injuries (infarction)
  • Loss of blood flow
  • Dying neurons
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5
Q

When do Cowdry Bodies occur?

A

Herpesvirus

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6
Q

When do Negri Bodies occur?

A

Rabies virus

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7
Q

When do Neurofibrillary Tangles occur?

A

Degenerative disease (Alzheimer’s disease)

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8
Q

When do Lewy Bodies occur?

A

Parkinson’s disease

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9
Q

What is the normal structure of astrocytes?

A
  • Long star-like processes
  • Open chromatin pattern
  • Larger than oligodendrocytes
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10
Q

What is the function of astrocytes?

A
  • React to injury
  • Establish/maintain the blood brain barrier
  • Provide structure for CNS
  • Provide food (glycogen and lactate) for cells in CNS
  • Can proliferate
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11
Q

Define Gliosis.

A

Proliferation of astrocytes.

(Equivalent to scar formation in the brain)

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12
Q

What is a Gemistocytic astrocyte?

A

Increased size and increased number of astrocytes as a result of injury.

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13
Q

What are the two types of inclusion bodies discussed in class?

A

Rosenthal fibers & Corpora amylacea

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14
Q

What are Rosenthal fibers?

A

Injurious processes that contain proteins, seen in many diseases (not very specific)

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15
Q

What is Corpora amylacea?

A
  • Pearl like, lamellated, collections of glycosaminoglycans
  • Part of the normal aging process, not pathological
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16
Q

What is the normal structure of microglia?

A
  • Twisting cells that look squished or bent
  • elongated long nuclei
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17
Q

What is the function of microglia?

A
  • MACROPHAGES OF THE BRAIN!
  • Proliferate
  • Phagocytose intruders
  • Form nodules around dead cells, bacteria, or foreign substances
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19
Q

When do ependymal cells acquire inclusions?

A

Cytomegalovirus (CMV)

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20
Q

What are neuronal storage disease?

A

Autosomal recessive enzyme deficiencies that result in accumulation of enzyme substrate (sphingolipids, mucopolysaccharides, or mucolipids) within neuronal lysosomes.

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21
Q

What do neuronal storage diseases lead to?

A
  • Loss of cognitive function
  • Possibly seizures
  • Ballooned neurons
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22
Q

What enzymes are deficient in Neuronal Ceroid Lipofuscinoses?

A

Enzymes involved in protein modification/degratdation

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23
Q

What is the result of enzyme deficiency in Neuronal Ceroid Lipofuscinoses?

A

Lipofuscin accumulates within neurons —> leads to neuronal dysfunction

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24
Q

What are some symptoms of Neuronal Ceroid Lipofuscinoses?

A
  • Blindness
  • Mental and motor deterioration
  • Seizures
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25
Q

When is the onset of Neuronal Ceroid Lipofuscinoses?

A

Ranges from Childhood to Adulthood

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26
Q

What enzyme is deficient in Tay-Sachs?

A

Hexosaminidase A

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27
Q

What is the result of enzyme deficiency in Tay-Sachs?

A

Accumulation of ganglioside in all tissues

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28
Q

What are the symptoms of Tay-Sachs?

A

Nervous system shows the most symptoms.

  • Developmental delay
  • “Cherry-red” spot in retina
  • Paralysis
  • Loss of neurologic function
  • Death within several years
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29
Q

When is the onset of Tay-Sachs?

A

Usually begins in early Infancy

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30
Q

What are Leukodystrophies?

A

Mostly autosomal recessive diseases that affect white matter.

Characterized by myelin abnormalities/affecting oligodendrocytes that involve lysosomal or peroxismal enzymes.

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31
Q

What do Leukodystrophies lead to?

A

Deterioration of motor skills, spastiity, hypotonia, ataxia

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32
Q

What enzyme is deficient in Krabbe disease?

A

Galactosylceramidase enzyme

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33
Q

What is the result of enzyme deficiency in Krabbe disease?

A
  • Accumulation of glactocerebroside that is converted to galactosylsphingosine –> which is TOXIC to oligodendrocytes.
  • Loss of myelin and oligodendrocytes in the CNS and PNS.
34
Q

What type of cells is characteristic of Krabbe disease?

A

“Globoid cells” = fat macrophages in the brain

(eat dead material and toxic oligodendrocytes)

35
Q

What are the symptoms of Krabbe disease?

A

Rapidly progressive muscle weakness and stiffness

36
Q

When is onset of Krabbe disease?

A

3-6 months

37
Q

What are the clinical features of Thiamine Deficiency (Vit B1)?

A
  • Chronic alcoholism
  • Classic Triad: Confusion, Ophthalmoplefia, and Ataxia in Wernicke Encephalopathy
  • Memory disturbances and confabulation in Korsakoff Syndrome
38
Q

What are the histologic findings seen in Thiamine Deficiency (Vit B1)?

A
  • Wernicke Encephalopathy: Hemorrhage and necrosis in mammillary bodies and walls of 3rd/4th ventricles
  • Korsakoff Syndrome: Cystic spaces, hemosiderin-laden macrophages in mammillary bodies and ventricle walls with thalamic lesions
39
Q

What are the two conditions associated with Thiamine Deficiency (Vit B1)?

A
  • Wernicke Encephalopathy (acute & reversible)
  • Korsakoff Syndrome (prolonged & mostly irreversible)
40
Q

What are the clinical features of Cobalamin Deficiency (Vit B12)?

A
  • Anemia
  • Lower extremity numbness, ataxia, weakness
  • Paraplegia
41
Q

What are the histological features of Cobalamin Deficiency (Vit B12)?

A
  • Myelin gets damaged –> Swells up!
  • Swelling of myelin layers, vacuolization
  • Subacute combined degeneration of spinal cord due to deficient myelin (ascending & descending tracts involved)
42
Q

What are the clinical features of Carbon Monoxide Poisoning?

A
  • Confusion
  • Disorientation
  • Delirium
  • Pink discoloration of skin/tissues (usually on autopsy)
43
Q

What are the histological features of Carbon Monoxide Poisoning?

A
  • Demyelination of white matter tracts
  • Particularly affects cortex (layers III/V), hippocampus, Purkinje cells
44
Q

How does Carbon Monoxide cause injury?

A

Injury due to hypoxia!

-Higher affinity CO displaces O2 on hemoglobin

45
Q

What are the clinical features of Methanol Toxicity?

A
  • Blindness
  • Suicide attempt
46
Q

What are the histological features of Methanol Toxicity?

A
  • Preferentially affects retina
  • Degeneration of ganglion cells
47
Q

How much Methanol can cause blindness?

A

10 mL

48
Q

How much Methanol could potentially cause death?

A

30 mL - 100 mL

49
Q

What are the clinical features of Ethanol Toxicity?

A
  • Truncal ataxia
  • Unsteady gait
  • Nystagmus (uncoordinated eye movements)
  • Trouble maintaining balance
50
Q

What are the histological features of Ethanol Toxicity?

A
  • Preferentially affects cerebellum
  • Cerebellar atrophy -Loss of granule cells
  • Loss of Purkinje cells
  • Bergmann gliosis (proliferation of astrocytes (“scarring”) where purkinje cells should be)
51
Q

What is the cause of Guillian-Barre Syndrome?

A
  • Inflammatory Neuropathy
  • acute inflammatory (immune-mediated) demyelinating polyradiculoneuropathy
52
Q

What is the clinical course of Guillian-Barre Syndrome?

A
  • 2/3rds of cases start with acute flu-like illness
  • then rapid onset weakness, symmetric, with loss of deep tendon reflexes and some sensation
  • progresses to acute ascending paralysis with immune-mediated demylination that resolves over time with remyelination
  • Elevated CSF protein without lymphocytes -2-5% mortality due to respiratory paralysis, autonomic instability, cardiac arrest, complications of treatment
53
Q

What are the histologic findings of Guillian-Barre Syndrome?

A
  • Inflammation around venules/nerves
  • Lymphocytes, macrophages, and plasma cells widely distributed thorughout the PNS
  • Macrophages are right next to the myelin sheath –> unwrapping
  • Most intense demyelination in spinal and cranial nerve motor roots and adjacent nerves
54
Q

What is the cause of Leprosy (Hansen Disease)?

A
  • Mycobacterium leprae that causes Infectious Polyneuropathy (slowly progressive infection of skin and nerves)
  • Transmitted through respiratory droplet
  • 95% of world’s pop’n is immune, but it is endemic in poor tropical countries
55
Q

What is the clinical course of Leprosy (Hansen Disease)?

A
  • Tuberculoid Leprosy: dry, localized, scaly, skin lesions with nerve degeneration (less severe anaesthesia, ulcers, contractures)
  • Lepromatous Leprosy: more severe widespread lesions in the skin, nerves, eyes, mouth, hands, feet, and testes that can turn in to nodules and fluid-filled vesicles
56
Q

What is the bodies response in Leprosy (Hansen Disease)?

A
  • Tuberculoid Leprosy: nice T-CELL RESPONSE to the bug with granuloma formation by macrophages
  • Lepromatous Leprasy: body makes FOAMY HISTIOCYTES that are formed by macrophages (no granuloma formation)
57
Q

What are the histological findings in Leprosy (Hansen Disease)?

A
  • Obligate intracellular bacterium that is Acid-fast
  • Does not gram stain
  • Cell wall is waxy, which enables immune evasion
58
Q

What is the cause of Varicella-Zoster Virus Infection?

A
  • Common viral infection of the PNS caused by Herpes Virus 3 alpha
  • Remains dormant in the sensory ganglia of the spinal cord and brainstem
  • Eventually reactivates causing a painful, vesicular, dermatomal rash called shingles
59
Q

What are the histological findings in Varicella-Zoster Virus Infections?

A

-Neuronal destruction with MULTINUCLEATED GIANT CELLS

60
Q

What is the cause of Charcot-Marie-Tooth Disease, demyelinating type?

A

-Hereditary neuropathy caused by repetitive demyelination and remyelination

61
Q

What are the histological findings in Charcot-Marie-Tooth Disease, demyelinating type?

A

Onion bulb formation around peripheral nerves

62
Q

What is the clinical course in Charcot-Marie-Tooth Disease, demyelinating type?

A
  • Loss of sensation and motor function of skin/muscles that surround the feet and lower leg
  • Pain sensation remains intact
  • High arches, hammer toes, muscle atrophy
  • Can appear in childhood or early adulthood
  • Normal life span
63
Q

What are the three main patterns of peripheral nerve disease in adult-onset diabetes mellitus?

A
  1. Symmetric sensory and motor neuropathy involving distal nerves
  2. Autonomic neuropathy (bladder incontinence)
  3. Aysmmetric neuropathy (one-sided sensory and motor neuropathy)
64
Q

What are the common MONOneuropathies associated with malignancies?

A
  1. Brachial plexopathy from lung neoplasms
  2. Obturator palsy from pelvic neoplasms
  3. Cranial nerve palsies from brain tumors
65
Q

What are the common POLYneuropathies associated with malignancies?

A
  1. Small cell lung cancer
  2. Plasma cell malignancies (Polyneuropathy can occur as a PARANEOPLASTIC effect and produce antibodies that attack nerves)
66
Q

What type of skull fracture is most common?

A

Linear (straight crack)

67
Q

When do frontal hits often occur?

A

Patient was unconscious prior to falling.

68
Q

When do occipital hits often occur?

A

When patient remains conscious during fall.

69
Q

What is a depressed skull fracture?

A
  • bone displaced inward
  • comminuted (in pieces)
  • can damage brain
70
Q

What is a diastatic skull fracture?

A
  • fracture that spans or crosses a suture
  • causes suture to widen
71
Q

What age patient usually obtains a diastatic skull fracture?

A

Usually children

72
Q

What is a basal skull fracture?

A
  • fracture to base of the skull
  • very forceful
73
Q

What often occurs in basal skull fractures?

A
  • Distant hematomas
  • CSF drainage
  • Battle sign (bruising behind ear)
74
Q

What is the definition of a concussion?

A

Altered consciousness from head injury due to change in momentum of head (e.g. head hits rigid surface).

-unkown mechanism

75
Q

What are common symptoms of concussion?

A
  • Amnesia
  • Confusion
  • Headache
  • Visual disturbances
  • Nausea & Vomitting
  • Dizziness
76
Q

How are concussions graded?

A

Grade 1: no LOC, lasts <15 min

Grade 2: no LOC, lasts >15 min

Grade 3: LOC

77
Q

What is the typical clinical setting for an epidural hematoma?

A

Hit in temple with baseball.

  • may have luccid period, then LOC
  • neurosurgical emergency
78
Q

What is the typical clinical setting for an subdural hematoma?

A

Elderly patient falls, seems okay after.

Acute: develop progressive numbness hours after.

Chronic: develop symptoms months after.

79
Q

What is the typical clinical setting for a subarachnoid hematoma?

A

Patient states “Worst headache I have ever had,” after sustaining head contusion.

-neurosurgical emergency (ruptured berry aneurysms)

80
Q

What is the typical clinical setting for a diffuse axonal injury?

A

Angular acceleration/deceleration

  • “Shaken Baby” syndrome
  • Boxing

Neuro B1 - WLB (8 decks)

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