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NMSK Exam 3 > Chapter 26 Pt 2 > Flashcards

Chapter 26 Pt 2 Flashcards

1
Q

In what process are myelin ovoids formed?

A

Axonal neuropathies: Wallerian degeneration => Schwann cells will catabolize myelin => unravel and disintegrate into spherical structures.

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2
Q

What do we see on histology in demyelinating neuropathies?

A

Onion bulbs: excess proliferation of Swchwann cells => concentric layers of cytoplasm of Schwann cells and redundant BM wrapped around thinly myelinated axons, like an onion

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3
Q

Type 1 Muscle Fibers

  1. Color
  2. Action
  3. Strength
  4. Physiology
A
  1. Red
  2. Sustained force
  3. Weight-bearing
  4. Slow-twich
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4
Q

Type 2 Muscle Fibers

  1. Color
  2. Action
  3. Strength
  4. Physiology
A
  1. White
  2. Sudden movements
  3. Purposeful motion
  4. Fast-twitch
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5
Q

What causes Type 2 Fiber Atrophy (group atropgy)?

A
  1. Inactivity or disuse (limb fracture, degeneration of pyramidal tract)
  2. Neurodegenerative disease
  3. Corticosteroids => steroid myopathy
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6
Q

What type of reactions do muscle fibers undergo?

A
  1. Segmental necrosis
  2. Vacuolization
  3. Regeneration
  4. Hypertrophy
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7
Q

When a muscle fiber undergoes segmental necrosis, briefly describe the process?

A
  1. Necrosis of segment
  2. Myophagocytosis
  3. Replaced with collagen and fat
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8
Q

Characteristics of muscle fibers that are regenerating

A
  1. Centrally located nuclei
  2. Cytoplasm is red with trichrome stain because alot of RNA
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9
Q

Characteristics of muscle fibers that are undergoing hypertrophy

A

Muscle fiber splitting: cell membrane splits it down middle with adjacent nuclei

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10
Q

What can cause a neurogenic bladder? (6)

A
  1. MS
  2. Parkinsons
  3. DB
  4. Infection of brain/SC
  5. Spina bifida
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11
Q

Course of Bells Palsy

A
  • Occurs 48-72 hours after a URI/DM and resolves spontaneously in pts who are 15 - 60YO
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12
Q

Inflammatory neuropathies: how do we differentiate them?

A
  1. Guillian Barre Neuropathy
  2. Chronic Inflammatory Demyelinating Polyradiculoneuropathy

Differentiate by: time course and whether htey respond to steroids.

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13
Q

MC AQUIRED Inflammatory Peripheral Neuropathy

A

Chronic Inflammatory Demyelinating Peripheral Polyradiculoneuropathy

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14
Q

2/3’s of Guillain-Barre Syndrome cases are preceded by what; which etiologies have been implicated?

A

Acute, influenza-like illness

  1. Campylobacter
  2. CMV,
  3. EBV,
  4. Mycoplasma penumoniae,
  5. Prior vaccination
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15
Q

How is CIDP and AIPD different from one another?

A

CIDP

  1. Chronic: persists more than 2 months and has remissions and relapses
  2. Responds to steroids
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16
Q

Pathophysiology of CIDP?

A

IgM and IgG Ab on myeling sheath

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17
Q

Infectious Polyneuropathies (5)

A
  1. Leprosy (Hansen Disease)
  2. Diptheria
  3. Varicella-Zoster Virus
  4. Lyme Diseae
  5. HIV
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18
Q

MC Viral Infection of the PNS

A
  1. Varicella Zoster
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19
Q

What is Leprosy, Hanson Disese?

A

Mycobacterium Leprea invades Schwann cells and other cells => symmetric polyneuropathy in COOL extrememties

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20
Q

In lepromatous leprosy (Hansen Disease) Schwann cells are invaded by Mycobacterium leprae and what pattern of peripheral nerve damage will be seen?

A
  1. Segmental demyelination and remyelination
  2. Loss of myelinated AND unmyelinated fibers
  3. Endoneurial fibrosis
  4. Multi-layered thickening of perineural sheaths.
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21
Q

What are the clinical symptoms of Leprosy (Hansen Disease)?

A
  1. Symmetric polyneuropathy of pain fibers COOL extremeties => loss of sensation in hands and toes, but nose is often affected first.
  2. Large, traumatic ulcers => pt does not feel it.
22
Q

Leprosy Findings

A
  • AFB (+): multuple uniform-staining acid-fast slender baccili
23
Q

More localized nerve involvement + granulomatous nodules in the dermis is characteristic of what form of leprosy?

A

Tuberculoid leprosy = TH1 (cell-mediated) response

24
Q

Peripheral nerve dysfunction as a result of Diptheria is due to what; what are the early sx’s and later findings?

A

Result of diptheria exotoxin

  1. Early loss of proprioception and vibratory sensation
  2. Bulbar and respiratory muscle dysfunction -> dealth or long-term disability due to suffocation.
25
Q

Lesion seen in peripheral nerves due to Diptheria

A
  1. Selective demyelination that extends to the anterior/posterior roots and into the mixed sensorimotor nerves
26
Q

Diptheria is MC due to what?

A
  1. Incomplete immunization
  2. Waning adult immunty
27
Q

MC viral infection of PNS

A

Varicella-Zoster Virus

28
Q

What damage to nerves occurs in Varicella-Zoster?

A
  1. Loss of affected ganglia and neurons: mononuclear infilrate, regional necrosis and hemorrohage
  2. Death of sensory neurons => causes death of axons of peripheral nerves
  3. Focal destruction of large motor neurons in anterior horns or CN motor nuclei at affected level
29
Q

Lyme Disease

  1. Causes what damage to peripheral nerves?
  2. Clinical symptoms
A
  1. Polyradiculopathy
  2. Unilateral/bilateral facial N palsy
30
Q

HIV

  1. Causes what damage to peripheral nerves?
  2. Clinical symptoms
A
  1. Mononeuritis multiplex
  2. Late stages => demyelinating disorder that resembles GB or CIDP
    1. Distal sensory neuropathy
31
Q

MCC of peripheral neuropathy

A

DB

32
Q

MCC of symmetrical neuropathy that involves dista*l sensory + motor* nerves

A

DB

33
Q

What is the most common pattern of peripheral neuropathy seen with Diabetes?

A

Ascending distal symmetric sensorimotor polyneuropathy

34
Q

Prevalence of peripheral neuropathy associated with diabetes is dependent on what?

A

Duration of the disease; 80% of ppl with DM for over 15 years

35
Q

Clinical symptoms of Diabetees

A
  1. Ascending distal symmetric sensorimotor polyneuropathy =>
    1. Numbing
    2. Loss of pain
    3. Paresthesias and dysthesias => pain
    4. Balance
  2. ANS sx:
    1. Postural hypotension
    2. Incomplete bladder emptying => IC risk of infections
36
Q

Lesion in DB

A
  1. Segmental demyelination => thin myelinated fibers
  2. Loss of small myelinated and unmyelinated fibers
  3. Endoneurorial arterioles => thick, hyalinzed and PAS +
37
Q
  • Uremic neuropathy seen in setting of renal failure is a causes what type of neuropathy?
  • Symptoms?
A
  1. Distal symmetric neuropathy
  2. Asymptomatic in some; or
    1. Muscle cramps
    2. Distal dysthesias
    3. DEC DTR
38
Q

Lesion is Renal failure (uremic syndrome)

A
  1. Axonal degeneration, then regeneration after recovery after dialysis
39
Q

Thyroid dysfunction can cause what type of neuropathy?

A
  1. HypOthyroidism => carpal tunnel compression neuropathy
  2. HypERthyroidism => GB
40
Q

Other toxic neuroapthies

A

Pb (lead)

Chemo

41
Q

Which type of neuropathy is the most common paraneoplastic syndrome and which malignancy is it most commonly associated with?

A

Small cell lung cancer => Sensorimotor neuronopathy

42
Q

What is a a distinctive presentation of neuropathy associated with monoclonal gammopathies (B-cell neoplasms)?

A
  • Paraprotein deposts in between non-compacted myelin lamalle
  • POEMS: Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal gammopathy, and Skin changes
43
Q

“Saturday night palsy” is due to compression of which nerve?

A

Radial nerve in the upper arm

44
Q

Which nerve is affected in Morton neuroma and what histologic finding is seen?

A

- Interdigital nerve at intermetatarsal sites –> metatsalgia =>

  • => ball of foot is painful/inflamed and feels like “walking on a marble”
  • Histologically = perineural fibrosis
45
Q

What is the MC inherited peripheral neuropathy, which should ALWAYS be in a DDX of someone with a peripheral neuoropathy?

A

Charcot -Marie Tooth (CMT)

46
Q

What is CMT?

A

Hereditary demyelination of MOTOR + SENSORY nerves that is slowly progressive, presenting in early 20s.

47
Q

What is the most common subtype of hereditary motor and sensory neuropathy (CMT) disease, what is the inheritance pattern, when and how does it present?

A

CMT1 = AD mutation of PMP22 (peripheral myelin protein 22) on Chr 17.

  • -Presents in 20s: w/ slowly progressive distal demyelinating motor and sensory neuropathy
48
Q

Which structures are injured in the CMT2 variant of CMT disease and when does it present?

A

AD mutation of MDN2 gene mitochondrial fusion

Axonal injury; typically severe w/ early childhood onset

49
Q

Clinical Sx of Charcot Marie Tooth

A
  1. Presents in 20s
  2. Peroneal neuropathy => clumsy child that has problems walking/runniing: lower leg atrophy => deformed LE (looks like inverted bottle)
  3. Foot deformities: pes cavus and hammer toe
  4. DEC or no DTR
  5. Foot drop
  6. EMG = slowing of motor nerve conduction velocity
50
Q

What is Familal Amyloid Polyneuropathy?

A

Amyloid deposition in the peripheran nerve

51
Q

How do traumatic neuromas aka pseudotumors grow?

A

Despite misalignment, axons contineu to grow into small swirls that are randomly oriented, but surrouned by ORGANIZED layers of Schwaanc cells, fibroblasts and perineural cells

NMSK Exam 3 (17 decks)

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