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Pathology exam two > Neuromuscular Diease part 2 > Flashcards

Neuromuscular Diease part 2 Flashcards

1
Q

does a mortons neurom count as a tumor

A

no it is a non-tumor it is just a traumatic neuroma

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2
Q

plexiform neurofibromas are pathognomoic for

A

NF1

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3
Q

Diffuse fibromas often associated with

A

NF1

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4
Q

TQ Pigmented iris hamartomas (lisch nodules

A

Neurofibromatosis, Type 1

Von Recklinghausen Disease

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5
Q

Neurofibromatosis, Type 1

(Von Recklinghausen Disease) three major features

A

– Multiple neural tumors (neurofibromas)
• Can be anywhere on the body
– Numerous pigmented skin lesions, some of which
are café au lait spots
– Pigmented iris hamartomas (lisch nodules)

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6
Q

hallmark lession of NF-1

A

plexiform neurofibromas

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7
Q

NF-1 gene has been maped to chromosome

A

17

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8
Q

cafe au lait spots seen in NF1 or NF2

A

seen in both

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9
Q

lisch nodules seen in

A

only nf1

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10
Q

nf type 2 genetics located on chromosome

A

22 its the merlin gene

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11
Q

what is the most common affected nerve by malignant peripheral nerve sheath tumoir

A

sciatic nerve

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12
Q

Hyperreflexia due to loss of lower motor and
upper motor neurons in the anterior horns of
the spinal cord and in corticospinal tracts is a feature of TQ TQ TQ

A

Amyotrophic Lateral Sclerosis

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13
Q

Amyotrophic Lateral Sclerosis Clincal S and S

A

• Early: asymmetric weakness of hands
• Cramping and spasticity of the arms and legs
• With disease progression, diminished muscle
strength and bulk
• Fasiculations
• Eventually, respiratory muscles involved

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14
Q

Gowers maneuver

A

using the upper extremities to stand up characteristic of ducheene muscular dystrophy

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15
Q

• X-Linked Muscular Dystrophies

A

Duchenne’s Muscular Dystrophy

– Becker’s Muscular Dystrophy

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16
Q

Duchenne’s Muscular Dystrophy Symptoms begin at the

A

pelvic girdle

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17
Q

what is psedohypertrophy and where do you seen in in Duchenne’s Muscular Dystrophy

A

cald muscles, first your muscle will get bigger but then as your myofibers are destroyed they are to be replaced with fat and connective tissue

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18
Q

TQ Dystrophin

A

in DMD there will be no dystrophin , it plays a role in maintaining the integrity of the myocyte membran eduring shape change associated with contraction

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19
Q

function dystrophin

A

Plays a role in maintaining the integrity of the
myocyte membrane during shape change
associated with contraction

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20
Q

TQ DMD: Morphology

A

Degeneration, necrosis, and phagocytosis of
muscle fibers
• Regeneration of muscle fibers
• Proliferation of endomysial connective tissue

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21
Q

becker muscular dystrophy

A

dystropin gene mutation but still have it so the diease is less severe than DMD where you have no dystrophin

22
Q

type 1 autosomal muscular dystrophy

A

AD

23
Q

type 2 autsomal muscular dystrophy

A

AR

24
Q

cardinal neuromuscular symtoms of myotonic dystrophy

A

myotonia, the sustained involuntary contraction of a group of muscle

25
Q

anticipation

A

a diease which tend to increase in severity and appear at a younger age in succeeding generation

26
Q

atrophy of the facial muscle and trouble relaxing the grip after a hand shake seen in

A

myotonic dystropgy

27
Q

floppy baby

A

hypotonia of a the congenital myopathy type

28
Q

central core diease

  1. inheritace
  2. what is affected
A
  1. AD

2. only type 1 fibers are effected

29
Q

Central Core Disease

• Clinical S&S:

A

Early-onset hypotonia and non-progressive
weakness
– Associated with skeletal deformities
– May develop malignant hyperthermia

30
Q

Nemaline Myopathy inheritance:

A

– Both autosomal dominant and recessive

31
Q

Nemaline Myopathy Morphology:

A

– Aggregates of subsarcolemmal spindle-shaped
particles (nemaline rods)
– Occur predominately in type I fibers
– Derived from Z-band material

32
Q

McCardle Syndrome clincal Signs and symptoms

A
  • Painful cramps with strenuous exercise
  • Myoglobinuria in ~50%
  • Muscular exercise fails to raise serum lactate levels
  • Normal longevity
33
Q

lipid myopathies are the result of

A

carnitine deficiency that leads to accumulation of lipid within myocytes

34
Q

TQ mitochondrial myopathies have what inheritance pattern

A

maternal inheritance pattern

35
Q

Ragged red fiber

A

mitochondrial myopathies

36
Q

Cushings syndrome predominately effects what type fibers and proximal or distal muscle

A

proximal muscle weakness of type 2 fibers

37
Q

what occurs in choloroquine myopathy

A

vacuoles within myocytes

38
Q

vacuoles within myocytes seen in

A

chloroquine myopathy

39
Q

what will happen to DTR is hypothyrioism

A

decreased or dimished

40
Q

what will happen to DTR’s in hyperthyriodism

A

increased

41
Q

“Binge” drinking of alcohol can produce an

acute toxic syndrome of ______________

A

RHABDOMYOLYSIS, which leads to renal failure

42
Q

Muscle disease caused by immune-mediated
loss of acetylcholine receptors and having
characteristic temporal and anatomic patterns
as well as drug response

A

Myasthenia Gravis

43
Q

Myasthenia Gravis: Pathogenesis

• Nerve conduction studies:

A

NORMAL

44
Q

MG Electrophysiologic studies:

A

decrease in motor response with repeated stimulation

45
Q

Are autonomic functions effected by MG

A

no

46
Q

in severe cases of MG what type muscle fiber is effected

A

type 2

47
Q

where does weakness typically begin in MG

A

extraocular muscle, thus you can have double vision and ptosis

48
Q

treatment of MG

A

anticholinesterase agents, prednisone, plasmaphheresis, and recesction of thymona

49
Q

Lambert-Eaton Myasthenic

Syndrome electrophysiology if you repeatedly stimulate a motor nerve what will happen

A

muscle response is INCREASED TQ TQ TQ

50
Q

Are autnomic functions effected by Lambert-Eaton Myasthenic syndrome

A

YES dysfunction

51
Q

Lambert-Eaton Myasthenic

Syndrome what has gone wroung

A

fewer vesicle of Ach are released in response to each presynaptic action potential (unlike MG where normal amount released by no receptors for ach are to be found)

52
Q

Fibromyalgia is a diagnosis of TQ

A

exclusion

Pathology exam two (4 decks)

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