Exam 4: Musculoskeletal Pathophysiology

Question 1

Muscle growth occurs by:

Answer 1

Growth of cells, not new muscle fibers; new nuclei added to support additional cell needs

Question 2

How to remember parts of sarcomere:

Answer 2

I band is light
A band is dArk
Z disc is in I band; M line is in A band –> ZIMA

Question 3

How to remember parts of sarcomere:

Answer 3

I band is light
A band is dArk
Z disc is in I band; M line is in A band –> ZIMA

Question 4

Channels involved in NMJ activation:

Answer 4

Pre-synaptic on membrane:
1. Voltage-gated Ca++ (influx stimulates ACh release)

Post-synaptic on membrane:

2. ACh-gated Na+ (influx depolarizes)
3. Voltage-gated Na+ (influx perpetuates depolarization)
4. Voltage-gated Ca++

Intra-cellular:
5. Ca-gated Ca++ on sarcoplasmic reticulum

Question 5

When a muscle motor unit is denervated:

Answer 5

Neighboring nerves will pick up fibers and convert them to their own type (I/II)

Question 6

Role of dystrophin:

Answer 6

Interface between cytoskeleton proteins (actin) and transmembrane proteins (dystroglycans/sarcoglycans)

Question 7

Role of dystroglycans:

Answer 7

Bind the basal lamina to the sarcomeres

Question 8

Basic problem in muscular dystrophy:

Answer 8

Use causes microtearing but no gains in strength from use, only repeated damage
Innervation is intact, just atrophy

Question 9

Changes in CK due to muscular dystrophy:

Answer 9

Early years ↑ CK from muscle damage

Late stages no ∆ because no muscle mass to injure

Question 10

Endomyceum is:

Answer 10

The extra-sarcolemnal fibers that run the length of the muscle and ultimately become the tendon

Question 11

First sign of myasthenia gravis:

Answer 11

Weakness in the eyelids

Question 12

S/s of myasthenia gravis:

Answer 12

Weakness that gets progressively worse with use/throughout the day

Question 13

Basic problem with myasthenia gravis:

Answer 13

Antibodies vs. ACh receptors result in ↓ availability of receptors (down to 20% or so)

Question 14

Reason for daily progressive weakness in myasthenia gravis:

Answer 14

In AM, abundance of ACh means all available receptors used

In PM, ACh levels ↓, so even unbound receptors aren’t all utilized

Question 15

Tx for myasthenia gravis:

Answer 15

Plasmapheresis

Acetylcholinesterase inhibitors

Question 16

Basic problem with myasthenic syndrome:

Answer 16

Antibodies bind to the voltage-gated Ca++ channels and inhibit release of ACh

Question 17

Basic problem with myasthenic syndrome:

Answer 17

Antibodies bind to the voltage-gated Ca++ channels and inhibit release of ACh

Question 18

Basic problem with myasthenic syndrome:

Answer 18

Antibodies bind to the voltage-gated Ca++ channels and inhibit release of ACh

Question 19

S/s of myasthenic syndrome:

Answer 19

Consistent weakness throughout the day

Question 20

Effect of curare at the NMJ:

Answer 20

Blocks the post-synaptic receptors

Question 21

Effect of botulinum toxin on the NMJ:

Answer 21

Prevents fusion of vesicles to membrane and ACh release

Question 22

E1/2t of botulinum toxin:

Answer 22

6 weeks

Question 23

Tx of botulism:

Answer 23

Botulinum toxin antibody

Question 24

Effect of clostridium tetani on NMJ:

Answer 24

Excessive ACh release causes overstimulation of muscle membrane

Question 25

of ACh needed to open ligand-gated Na+ channel:

Answer 25

2

Question 26

DHP receptors are:

Answer 26

Dihydropyridine receptors; voltage-gated Ca++ channel on the sarcolemma

Question 27

Ryanodine receptors are:

Answer 27

Ca-gated Ca++ channels on the sarcoplasmic reticulum

Question 28

3 ways for muscles to stop contracting:

Answer 28

1. Run out of actin for the myosin to grab
2. Ca++ leaves cell, tropomyosin re-covers actin binding sites
3. No more ATP, myosin heads cannot release (rigor mortis)

Question 29

Muscle cell basal lamina is:

Answer 29

Extracellular matrix on the outside of muscle fibers that attaches to the sarcolemma to allow muscles to move bones

Question 30

Osteoclasts are:

Answer 30

Big cell from multiple macrophage; function is to break down bone

Question 31

Osteoblasts are:

Answer 31

Cells that build up bone; left behind, they become osteocytes and live between concentric rings of bone

Question 32

Osteons are also known as:

Answer 32

Haversian systems

Question 33

Kyphosis is:

Answer 33

Anterior flexion of spine/”hunch back”

Question 34

Lordosis is:

Answer 34

Posterior flexion of lumbar spine/”sway back”

Question 35

Scoliosis is:

Answer 35

Lateral curvature of the spine with rotation of vertebral column

Question 36

Scoliosis is:

Answer 36

Lateral curvature of the spine with rotation of vertebral column

Question 37

Post-menopausal women more prone to osteoporosis d/t:

Answer 37

↓ estrogen levels and longer lives to see the effects

Question 38

Bone growth pattern:

Answer 38

Outward; bone resorbed from the inside and added to the outside

Question 39

Pathogenesis of Paget’s disease:

Answer 39

Rapid breakdown and rebuilding of bone

Question 40

Tx for Paget’s disease:

Answer 40

Bisphosphonates (inhibit the enzymes that break down calcium phos)

Question 41

PTH keeps Ca++ normal in three ways:

Answer 41

1. Tells osteocytes to release Ca++ from bone
2. ↓ rate of Ca++ loss from kidney
3. Activation of Vit D in kidney leads to better absorption in the gut

Question 42

Hyperparathyroidism has this effect on the bones:

Answer 42

Chews up bone too quickly, will lead to osteoporosis

Question 43

First stage of osteomyelitis formation:

Answer 43

Blood supply blocked to infection site; subperiosteal abscess forms over site

Question 44

Second stage of osteomyelitis formation:

Answer 44

Sequestrum (dead bone) becomes surrounded with involucrum (new bone formation) leaving a small channel for pus escape

Question 45

Tx of osteomyelitis:

Answer 45

Inject antibiotics into the bone and hope for the best

Question 46

Tx of osteomyelitis:

Answer 46

Inject antibiotics into the bone and hope for the best

Question 47

Bone cancer typically arises from:

Answer 47

Other tumors (metastatic)

Question 48

Osteoarthritis is:

Answer 48

Non-inflammatory joint disease - there will be inflammation but it is an effect, not the cause

Question 49

Causes of osteoarthritis:

Answer 49

Life-long use
Trauma
Dislocation
Sprain
Anything causing mis-tracking of bone

Question 50

Three forms of inflammatory arthritis:

Answer 50

Rhemuatoid
Gouty
Infectious

Question 51

Sites commonly affected by osteoarthritis:

Answer 51

Hips
Knees
Lower lumbar vertebrae
Cervical vertebrae
Interphalangeal joints
Tarsometatarsal joints

Question 52

Rheumatoid arthritis is:

Answer 52

Autoimmune disease that destroys joints by attacking bone

Question 53

S/s of rheumatoid arthritis:

Answer 53

Pain in hands first

Ulnar deviation in fingers

Question 54

Gout is:

Answer 54

Buildup of uric acid in the joints caused by diet rich in purines

Question 55

Pathogenesis of gout:

Answer 55

Macrophages cannot break down uric acid crystals, which are sharp and pierce them; attracts other macrophages, leading to inflammation

Question 56

Formal name for club feet:

Answer 56

Bilateral congential talipes equinovarus

Question 57

Cause of bilateral congential talipes equinovarus:

Answer 57

Being too cramped in utero

Question 58

Tx of bilateral congential talipes equinovarus:

Answer 58

1. Massaging feet back into place
2. Braces/rods
3. Corrective surgery

Question 59

Pathogenesis of osteogenesis imperfecta:

Answer 59

Defect in type I collagen in bone leads to easy breaking

Question 60

Tx for osteogenesis imperfecta:

Answer 60

Place telescoping metal rods in bone to grow with child to add tension strength

Question 61

Cause of rickets:

Answer 61

Lack of mineralization (Ca++ or Vit D) so bones bend easily

Question 62

S/s of Paget disease:

Answer 62

Areas of cortical thickening and osteoporosis