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5200: Structural Integrity > MSK Histology/Path > Flashcards

MSK Histology/Path Flashcards

1
Q

what is this a cross-section of? (in Green)

A

area of myofibrils (each green dot is a cross section of one myofibril)

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2
Q

True/false:

A myofibril is composed of many mucle cells

A

FALSE!

Muscle cells (myocyte) are made up of multiple myofibrils

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3
Q

what level of skeletal muscle organization is shown in green

A

Muscle bundle (aka fascicle)

a fascicle is a bundle of myocytes/muscle cells and their associated endomysium

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4
Q

Each skeletal muscle cell is
surrounded by reticular connective
tissue called _______, contains type ___
collagen fibers)

A

endomysium

type III collagen

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5
Q

what connective tissue ensheaths each fascicle

A

perimysium

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6
Q

what connective tissue ensheaths the whole muscle

A

epimysium

(e.g. the biceps is covered by an epimysium)

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7
Q

Each cell contains myofibrils; each myofibril is
made up of __________

A

myofilaments (thin actin
filaments and thick myosin filaments)

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8
Q

what are myofibers

A

another name for myocytes and muscle cell

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9
Q

what delineates a sarcomere?

A

Z line to Z line of a myofibril and is the basic contractile unit of a muscle cell

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10
Q

sarcolemma vs sarcoplasmic reticulum

A
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11
Q

True/False

skeletal muscle cells are held together by cell junctions

A

FALSE

instead, their membranse are fused into a multinucleated
syncytium

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12
Q

muscle cells have limited regenerative capacity, but ___________ cells can act as a stem cell and differenciate into a muscle cell

A

satellite –> myoblast –> myofiber

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13
Q

T/F: mitochondria and nuclei are located just beneath the cell membrane

A

True

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14
Q

where in a muscle cell does the sarcolemma invaginate into a T tubule

A

on either side of the A bands (strip of myosin)

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15
Q

what are type 1 muscle fibers

A

Type I muscle fibers= slow oxidative fibers à slow-twitch

  1. specialized for aerobic activity.
  2. contain a high amount of myoglobin (carries oxygen), capillaries, and mitochondria
  3. low glycolysis activity à less ATPase à don’t stain brown
    1. àlow lactic acid production
  4. more NADH à stain blue
  5. appear red in fresh tissue.
  6. Low power but fatigue-resistant motor units.

e.g. Muscles of the deep back responsible for maintaining posture are mostly made up of Type I slow oxidative fibers.

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16
Q

T/F: all muscles of the same type are group together in normal physiological muscle

A

FALSE

No single muscle fiber is entirely surrounded by muscle
fibers of its own type. When groups occur and are welldeveloped, the question of denervation-reinnervation
must be raised.

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17
Q

compare the muscle fiber types

A
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18
Q

myasthenia gravis vs lambert eaton myasthenic syndrome

A
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19
Q

an action potential starts in the dorsal or ventral horn of the spinal cord

A

ventral (ie anterior)

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20
Q

How is acetylcholine made?

A

Acetyl CoA comes from mitochondria (end product of glycolysis) and choline comes from re-uptake from synaptic cleft. (also diet?)

–> choline acetyltransferase converts these^ to acetylcholine

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21
Q

what is the FIRST thing to happen when acetylcholine (2molecules per receptor) binds to nicotinic receptors on post-synaptic neurons

A

Na+ influx causes a small change in membrane potential = miniature end-plate potential (mEPP) in the myofiber membrane (<1mV/vesible)

IS NOT the same as the action potential

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22
Q

how is an AP generated in a muscle cell

A

the endplate potential (EPP) must be above threshold. if it is, then voltage gated sodium channels open succession, causing AP run along sarcolemma. Once it hits the T tubules of sarcolemma, causes Ca2+ release from SR –> muscle contraction

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23
Q

Where does all the calcium come from during a musclar excitation?

A

NO calcium comes from extracellular space (it’s only involved in pre-synaptic mechanism of Ach release). Instead, it comes from the sarcoplasmic reticulum, which stores TONS of calcium. It is gated by a Ryanodine Receptor (RyR).

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24
Q

what opens the Ryanodine Receptor on the sarcoplasmic reticulum?

A

Dihydrophyridineb Receptor*. It’s technically a voltage gated channel that causes shape change. Mechanically connected to RyR. AP causes DHP to change it’s shape a bit pulling open the RyR receptors and releasing calcium. (Presence of calcium prompts RyR to stay open a bit longer because the calcium binds to it). Calcium pumps eventually puts calcium back in storage stopping the muscle contraction.

*Not a true receptor in the case of skeletal muscle because it was named for its response to dihydrophyridine which is not present. but we keep the name

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25
Q

what are the anti-cholinesterase agents? (3)

A
  1. physostigmine,
  2. neostigmine
  3. pyridostigmine
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26
Q

what is edrophonium

A

a medication that temprarily relieves the sx of Myasthenia gravis –> used for diagnosis

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27
Q

T/F: there is usually only one NMJ /motor end plate per muscle fiber

A

TRUE

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28
Q

approx how many vessicles are leased into the synaptic cleft of NMJ per action potential running down the pre-synaptic neuron

A

~125 vessicles

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29
Q

what is the specific function of the postjuncrtional folds in a NMJ

A

increase surface area for endplate potentials

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30
Q

how long does ACh remain in the synaptic space

A

a few milliseconds

31
Q

T/F: ALL the ACh in the synaptic cleft is destroyed by Acetylcholinesterase

A

FALSE : some diffuses out of the space and is no longer available

32
Q

a-actin versus F-actin

A
33
Q

what comprises a complete thin filament

A
34
Q

sarcomere histo

A
35
Q

T/F:

during muscle contraction, the A band gets shorter

A

FALSE, the A band is the myosin which doesn’t change size.. the other bands change size as the actin slides along the unmoving myosin

36
Q

latent phase of muscle contraction

A

calcium has bound to troponin, exposing the active site and ATP has been hydrolyzed into ADP and Pi on the myosin head, triggering the myosin to cock back and bind to the actin–> crossbridge formation –> ready for contraction but hasn’t contracted yet

37
Q

what chemical shifts allows the relaxation phase to occur after muscle contraction

A

K+ ions leaving the cell

Ca2+ being taken back up by the sarcoplasmic reticulum

38
Q

DHP versus ryanodine receptors

A
39
Q

What is Gower’s Sign

A

a classic physical exam finding in people with MD… patient has to push on knees to get up due to prosimal hip/leg muscle weakness

40
Q

diff between becker and duchenne on a molecular genetic level - in terms of the different mutations

A
41
Q

where is dystrophin located specifically

A
42
Q

a patient with the following physical exam findings presents to your office with a history of symmetrical muscle weakness and tenderness that has been slowly progressing over the past 3-6 months. lab values show elevated serum creatine kinase. what is the most likely dx?

A

dermatomyositis

follow up studies are likely to reveal:

abnormal EMG/NCS and abnormal muscle biopsy

43
Q

pathophysiology of dermatomyositis

A
  1. autoimmune
  2. characterized by perimysial inflammation and atrophy due to vasculitis of associated vessels d/t complement deposition on the vessels
    1. perimysium is closer to the skin and therefore has cutaneous manifestations – “dermato”
  3. Inflammatory cells are mostly CD 4+ T-cells, B cells + complement proteins
  4. muscle damage from: inflammation –> ischemia –> necrosis
44
Q

pathophysiology of polymyositis

A
  1. think of it as dermatomyositis but without the rash
  2. differences:

immune cells= Cytotoxic (CD8) T cells

inflammation of endomysium (not perimesium)

myophagocytosis instead of necrosis

45
Q

inclusion body myositis

A
  1. insideous onset, of uncertain etiology (inflammation vs degenerative) that is comonest myopathy of older (>65 yo) populations.
  2. characterized by ASYMMETRIC distal weakness and slow progression + can include dysphagia
  3. inflammation is similar to polymyositis with cytotoxic CD8 lymphocytes destroying myofibers, but the affected myofibers have cytoplasmic rimmed vacuoles with basophilic granules
  4. namesake inclusion bodies (not the same thing as the vacuoles)
46
Q

what are the possible causes of Rhabdomyolysis

A

Influenza infections, strenuous
exercise, heat stroke, halothane, Alcohol

47
Q

why would you be concerned about acute renal failure in a patient with rhabdomyolysis?

A

since myoglobin is released form muscles, you get Myoglobinuria: acute renal failure
You also get dark urine d/t myoglobinuria

48
Q

pathology of rhabdomyolysis

A

notice:

  1. foci of necrosis
  2. clusters of macrophages
  3. degeneration of muscle fibers
49
Q

Gottron’s papules pathognomonic of ___________

A

dermatomyositis

50
Q

young versus old muscle pathological features

A

notice: shrinkage, (size and loss of fibers), groupingand loss of type II fibers (black)

51
Q

how to interpret this kind of stain

A

fibers have distinct myosin isoforms. Type 1 fibers are rich in oxidative enzymes, mitochondria, myoglobin (an oxygen carrier), and lipid –> darker stain.

Type 2 fibers are rich in glycogen and glycolytic enzymes. They are capable of fast, powerful, tonic contraction. By varying the pH of the ATPase preincubation, type 2 fibers can be further subdivided into 2a and 2b

52
Q

how do type 1 versus Type 2 muscle fibers change with age

A

Types IIA and IIB muscle fibers decrease with age in the area percentage, fiber number percentage, and mean fiber area, whereas Type I fibers increase in area and number but not in size. Morphologically, Type II fibers appeared smaller and flatter.

53
Q

what is the characteristic radiologic finding in benign bone tumors?

A
54
Q

what bone pathology is shown

A

osteochondroma

(at metaphysis and appears to be a lateral bony projection of growth plate)

55
Q

typical radiographic features of osteosarcome (malignant)

A
56
Q

pathology of osteosarcoma

A
57
Q

is most metastatic spread FROM bone tumors lymphatic or hematogneous spread?

A

hemotogenous –> lung most common site

58
Q

what is titin

A
59
Q

what causes rigor mortis

A

upon death, the clacium leaks our of SR and myosin heads bind to active site on actin. but ATP is degraded, so it is not available to detach the mysoin head again –> muscles stay contracted

60
Q

isotonic versus isometric muscle contraction

A
61
Q

Which of the following histopathological features is consistent with a diagnosis of dermatomyositis?

  1. endomysial inflamation
  2. necrotic fibers
  3. rimmed vacuoles
  4. perifascicular atrophy
A

4: perifascicular atrophy

hallmark feature of dermatomyositis

62
Q

rimmed vacuoles on microscopic appearance is characteristic of what muscle disease?

A

along with inclusion bodies, these vaculose are found in inclusion body myositis

63
Q

characteristic histology for the dystrophinopathies

A
64
Q

characteristic findings of McArdle Disease

A

mn: just get over the Mc”Hurdle”

65
Q

is there a greater risk of malignancy in dermatomyositis or polymyositis?

A

dermatomyositis

66
Q

dermatoyositis presents with weakness of which 2 classice areas

A

shoulder girdle (difficulty raising arms above head) and difficulty rising from a chair

67
Q

what is enchondromatosis

A

formation of bone tumors at the ends of long bones near growth plates

complication is advancement of the cancer to a chondrosarcoma

68
Q

what are the digit disorders

A
69
Q

in Becker muscular dystrophy, patients can typically ambulate until ___ years

A

35-40

70
Q

A patient with frontal baldness struggles to release when shaking your hand. Of the following, which is the most likely diagnosis?

A

myotonic dystrophy type 1

71
Q

which myopathy is characterized by early contractures (joint deformities)

A

Emery-Dreifuss Muscular Dystrophy

72
Q

Which of the following is characteristically occasionally complicated by malignant hyperthermia (from anesthesias)?

Emery-Dreifuss Muscular Dystrophy

Pompe Disease (Acid Maltase Deficiency)

Familial Periodic Paralysis

Central Core Myopathy

A

Central Core Myopathy

mn: central core in nuclear reactor gets really hot

73
Q
A

5200: Structural Integrity (19 decks)

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