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Path II > Muscle/Nerve > Flashcards

Muscle/Nerve Flashcards

1
Q

What are the three groups of peripheral nerve pathology?

A

Wallerian Degeneration

Distal Axonopathy

Segmental demyelination/remyelination

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2
Q

What can skeletal muscle disease fall into?

A

Neurogenic: Primary problem is the motor neuron/axon

Myopathic: Primary problem is with the muscle

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3
Q

What are major types of myopathic disease?

A

Muscular dystrophy

Inflammatory myopahties

Metabolic myopathies

Congenital myopathies

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4
Q

How are muscle fibers distributed in a normal individual?

A

THe different motor units are intermixed with each other

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5
Q

How many muscle fibers are innervated by a single axon?

A

10-2000

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6
Q

What is the muscle findings in an individual who has demyelination and remyelination?

A

The motor units are multipled from a single motor unit

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7
Q

What are types of axonal degeneration

A

Peripheral neuropathy

  • Classic Wallerian Degeneration: Injury of vascular disease
  • Distal axonopathy: Systemic meta disease, toxins, some genetic disease

Starts distal because of how metabolic toxics hit the periphery first

Demyelination/Remyelination
-Inflammation, toxins, some genetic diseases

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8
Q

What are some Ischemic neuropathies?

A

Cause axonal degeneration

Vasculitis (PAN)
Collagen Vascular diseases
Paraneoplastic Microvasculitis
Diabetic symmetrical sensorimotor neuropathy

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9
Q

What are the steps of axonal degeneration in a crush injury?

A

Schwann cells distal to injury dye and demylinate

Macrophages come and clean up the debris

Proliferation of schwann cells back in to myelinate the axon

Regenerated axon

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10
Q

What is seen in vasculitis?

A

Fibrinoid necrosis of the vessel wall

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11
Q

In vasculitic neuropathy what occurs to the axons?

A

They are preferentially hit, due to the blood supply some of the neurons may be spared

-Fascile to Fascicle variation in degree of axon loss

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12
Q

What is diabetic neuropathy?

A

A axonal degeneration due to acquired metabolic/toxic neuropathy

Predominated by axonal degen with some regen

Often has ischemic componenet
Endoneural microvascular thickening: ischemia

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13
Q

How can you tell a loss of axon density?

A

The axonal loss is seen as less dark areas in an LFB stain

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14
Q

What is a demyelinating neuropathy?

A

Pattern is segmental demyelination

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15
Q

What is the etiology of demyelinating neuropathy?

A

Inflammatory (immune-mediated)
- Guillain-Barre Syndrome or Acute inflammatory demyelinating polyradiculoneuropathy

Toxins

Some genetic diseases, CHARCOT TOOTH DISEASE

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16
Q

What is the clinical presentation of GBS?

A

Ascending paralysis

Involve resp muscles sometimes

Slowed conduction velocity

Elevated CSF protein

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17
Q

What type of inflammation is seen in GBS?

A

Endoneurial and perineurial
Lymphs, Macros»»> plasmas

Segmental demyelination

Some dmg to axons, in severe disease

Remyelination is seen: THINNER SHEATH

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18
Q

How do you see segmental demyelination?

A

Teased fiber preparation

Variation in myelin sheath thickness and internodal length

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19
Q

What is seen around a naked neuron?

A

Myelin Debris surrounding a naked axon

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20
Q

What is Charcot-Marie-Tooth Disease

A

Most common hereditary periphearl neuropathy

Progressive muscular atrophy of CALVES; weak

Genetically heterogeneous

Demyelinating neuropathy: Repetitive demyelination and remyelination

Pathy:
Thin myelinated axons
Hypertrophic ONION BULB neuropathy

21
Q

What causes onion bulb neuropathy?

A

Chronic demyelination and remyelination

Concentric rings of Schwann cell processes

22
Q

What is seen in normal muscle biopsy?

A

Frozen section shows peripheral nuclei

23
Q

What is seen in normal muscle biopsy?

A

Frozen section shows peripheral nuclei

24
Q

What is the content of a type 1 muscle fiber?

A

Sustained force, SLOW TWITCH

Color: Red

Lipids: Abundant

Glycogen: Scant

Enzyme content: NADH Dark, ATPase light (ph 9.4)

25
Q

What is the content of a type 2 muscle fiber?

A

Action: sudden movement, purposeful

Enzymes: NADH (light), ATPase (Dark) different stain than type 1, how to distinguish

Lipids: Scant

Glycogen: Abundant

Physiology: Fast-twitch

Color: White

26
Q

What color are type two muscle fibers in ATPase stain (9.4)

A

Dark

27
Q

What color are type 1 muscle fibers in ATPase stain (9.4)

A

Light

28
Q

What are neurogic muscle diseases?

A

Motor neuron disease:

  • ALS
  • Spinal muscular atrophy

Peripheral neuropathy

NMJ
-Myasthenia gravis

29
Q

What are myopathic muscle diseases?

A

Dystrophy
-Duchennes

Inflammatory
-Polymyositis

Metabolic
-Storage diseases

Congenital
-Centronuclear myopathy

30
Q

What are clinical features of a neurogenic muscle disease?

A

Site: DISTAL

Pain/tender: NONE

Fasciculations: Present

Serum Enzymes: Normal

EMG: Fibrillations potential

Nerve conduction: Variable

31
Q

What are clinical features of myogenic muscle disease?

A

Site: Proximal

Pain/tender: Variable

Fasciculations: Absent

Serum Enzymes: Elevated (CK)

EMG: Polyphasic potential

Nerve conduction: NOrmal

32
Q

What are the histological differences between neuropathy and myopathy?

A

Atrophy

  • Neuropathy: Angular fibers, Grouped
  • Myopathy: Rounded fibers, scattered

Neuropathy: Target fibers

Myopathy: Fiber necrosis, inflammation, internal nuclei, endomysial fibrosis

33
Q

Where are angulated fibers seen in neuopathy?

A

Grouped

34
Q

What happens after regeneration in neuropathy?

A

The muscle fibers are in large groups

35
Q

What causes duchennes muscular dystrophy?

A

A mutation in the dystrophin gene

Cytoplasmic protein that anchors to the extracellular action

36
Q

What is seen in early muscular dystrophy?

A

Myocyte necrosis

Atrophy and hypertrophy of next muscle fiber

37
Q

What happens in late muscular dystrophy?

A

There is endomysial fiboris and fatty replacement

Atrophy and hypertrophy still seen

38
Q

What is seen in myotonic dystrophy?

A

Autosomal Dominatn disease

Trinucleotide repeat disease

Path: Myopathic features with INTERNAL NUCLEI, occasional ring fibers

NEED GENETIC TESTING

39
Q

What are some inflammatory myopathies?

A

Primary

  • Polymyositis
  • Inclusion body myositis
  • Dermatomyositis

Secondary
-Other CT diseases,, immune processes, or infections

40
Q

What are some inflammatory myopathies?

A

Primary

  • Polymyositis
  • Inclusion body myositis
  • Dermatomyositis

Secondary
-Other CT diseases,, immune processes, or infections

41
Q

What is seen in early polymyositis?

A

Inflammation (endomysial) and muscle fiber necrosis

42
Q

What is seen in late polymyositis?

A

Regnerating muscle

Scarring fibrosis

Inflammation

43
Q

What is seen in inclusion body myositis?

A

Gradual onset/progression

Male predominance

Proximal and distal weakness

Dysphagia in some

Lymphocytic inflammation, angular annd round atrophy

Autophagic “rimmed” vacuoles

44
Q

What is the main histo feature to look for inclusion bodymyositis?

A

Rimmed Vacuoles

Abnormal filaments

45
Q

What are some metabolic myopathies?

A

Glycogen storage diseases
- Type II (pompe disease): Def a1,4-glucosidase (acid maltase)

-Type V (McArdle disease): Def myophosphorylase (not lysosomal)

Lipid storage myopathy: (carnitine def)

MIto myopathy: Ragged Red fibers

46
Q

What is seen on PAS of Pompe disease?

A

Lots of glycogen seen in vacuoles

47
Q

What are some characteristics of mitochondrial DNA?

A

Maternally inherited

Circular

Heteroplasmy

48
Q

What is mitochondrial heteroplasmy?

A

Each cell has hundreds of mitos

Each mitochondrion has 2-10 copies of mtDNA

Each cell has thousands of mtDNA

MItosis, mitos are randomly distributed

If abnormal mtDNA it will be different in each cell

49
Q

What is the hallmark of mito myopathy?

A

Ragged red fibers

Paracrystalline inclusions

Path II (11 decks)

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