Exam 4: Musculoskeletal Pathophysiology Flashcards
Muscle growth occurs by:
Growth of cells, not new muscle fibers; new nuclei added to support additional cell needs
How to remember parts of sarcomere:
I band is light
A band is dArk
Z disc is in I band; M line is in A band –> ZIMA
How to remember parts of sarcomere:
I band is light
A band is dArk
Z disc is in I band; M line is in A band –> ZIMA
Channels involved in NMJ activation:
Pre-synaptic on membrane:
1. Voltage-gated Ca++ (influx stimulates ACh release)
Post-synaptic on membrane:
- ACh-gated Na+ (influx depolarizes)
- Voltage-gated Na+ (influx perpetuates depolarization)
- Voltage-gated Ca++
Intra-cellular:
5. Ca-gated Ca++ on sarcoplasmic reticulum
When a muscle motor unit is denervated:
Neighboring nerves will pick up fibers and convert them to their own type (I/II)
Role of dystrophin:
Interface between cytoskeleton proteins (actin) and transmembrane proteins (dystroglycans/sarcoglycans)
Role of dystroglycans:
Bind the basal lamina to the sarcomeres
Basic problem in muscular dystrophy:
Use causes microtearing but no gains in strength from use, only repeated damage
Innervation is intact, just atrophy
Changes in CK due to muscular dystrophy:
Early years ↑ CK from muscle damage
Late stages no ∆ because no muscle mass to injure
Endomyceum is:
The extra-sarcolemnal fibers that run the length of the muscle and ultimately become the tendon
First sign of myasthenia gravis:
Weakness in the eyelids
S/s of myasthenia gravis:
Weakness that gets progressively worse with use/throughout the day
Basic problem with myasthenia gravis:
Antibodies vs. ACh receptors result in ↓ availability of receptors (down to 20% or so)
Reason for daily progressive weakness in myasthenia gravis:
In AM, abundance of ACh means all available receptors used
In PM, ACh levels ↓, so even unbound receptors aren’t all utilized
Tx for myasthenia gravis:
Plasmapheresis
Acetylcholinesterase inhibitors
Basic problem with myasthenic syndrome:
Antibodies bind to the voltage-gated Ca++ channels and inhibit release of ACh
Basic problem with myasthenic syndrome:
Antibodies bind to the voltage-gated Ca++ channels and inhibit release of ACh
Basic problem with myasthenic syndrome:
Antibodies bind to the voltage-gated Ca++ channels and inhibit release of ACh
S/s of myasthenic syndrome:
Consistent weakness throughout the day
Effect of curare at the NMJ:
Blocks the post-synaptic receptors
Effect of botulinum toxin on the NMJ:
Prevents fusion of vesicles to membrane and ACh release
E1/2t of botulinum toxin:
6 weeks
Tx of botulism:
Botulinum toxin antibody
Effect of clostridium tetani on NMJ:
Excessive ACh release causes overstimulation of muscle membrane
of ACh needed to open ligand-gated Na+ channel:
2
DHP receptors are:
Dihydropyridine receptors; voltage-gated Ca++ channel on the sarcolemma
Ryanodine receptors are:
Ca-gated Ca++ channels on the sarcoplasmic reticulum
3 ways for muscles to stop contracting:
- Run out of actin for the myosin to grab
- Ca++ leaves cell, tropomyosin re-covers actin binding sites
- No more ATP, myosin heads cannot release (rigor mortis)
Muscle cell basal lamina is:
Extracellular matrix on the outside of muscle fibers that attaches to the sarcolemma to allow muscles to move bones
Osteoclasts are:
Big cell from multiple macrophage; function is to break down bone
Osteoblasts are:
Cells that build up bone; left behind, they become osteocytes and live between concentric rings of bone
Osteons are also known as:
Haversian systems
Kyphosis is:
Anterior flexion of spine/”hunch back”
Lordosis is:
Posterior flexion of lumbar spine/”sway back”
Scoliosis is:
Lateral curvature of the spine with rotation of vertebral column
Scoliosis is:
Lateral curvature of the spine with rotation of vertebral column
Post-menopausal women more prone to osteoporosis d/t:
↓ estrogen levels and longer lives to see the effects
Bone growth pattern:
Outward; bone resorbed from the inside and added to the outside
Pathogenesis of Paget’s disease:
Rapid breakdown and rebuilding of bone
Tx for Paget’s disease:
Bisphosphonates (inhibit the enzymes that break down calcium phos)
PTH keeps Ca++ normal in three ways:
- Tells osteocytes to release Ca++ from bone
- ↓ rate of Ca++ loss from kidney
- Activation of Vit D in kidney leads to better absorption in the gut
Hyperparathyroidism has this effect on the bones:
Chews up bone too quickly, will lead to osteoporosis
First stage of osteomyelitis formation:
Blood supply blocked to infection site; subperiosteal abscess forms over site
Second stage of osteomyelitis formation:
Sequestrum (dead bone) becomes surrounded with involucrum (new bone formation) leaving a small channel for pus escape
Tx of osteomyelitis:
Inject antibiotics into the bone and hope for the best
Tx of osteomyelitis:
Inject antibiotics into the bone and hope for the best
Bone cancer typically arises from:
Other tumors (metastatic)
Osteoarthritis is:
Non-inflammatory joint disease - there will be inflammation but it is an effect, not the cause
Causes of osteoarthritis:
Life-long use Trauma Dislocation Sprain Anything causing mis-tracking of bone
Three forms of inflammatory arthritis:
Rhemuatoid
Gouty
Infectious
Sites commonly affected by osteoarthritis:
Hips Knees Lower lumbar vertebrae Cervical vertebrae Interphalangeal joints Tarsometatarsal joints
Rheumatoid arthritis is:
Autoimmune disease that destroys joints by attacking bone
S/s of rheumatoid arthritis:
Pain in hands first
Ulnar deviation in fingers
Gout is:
Buildup of uric acid in the joints caused by diet rich in purines
Pathogenesis of gout:
Macrophages cannot break down uric acid crystals, which are sharp and pierce them; attracts other macrophages, leading to inflammation
Formal name for club feet:
Bilateral congential talipes equinovarus
Cause of bilateral congential talipes equinovarus:
Being too cramped in utero
Tx of bilateral congential talipes equinovarus:
- Massaging feet back into place
- Braces/rods
- Corrective surgery
Pathogenesis of osteogenesis imperfecta:
Defect in type I collagen in bone leads to easy breaking
Tx for osteogenesis imperfecta:
Place telescoping metal rods in bone to grow with child to add tension strength
Cause of rickets:
Lack of mineralization (Ca++ or Vit D) so bones bend easily
S/s of Paget disease:
Areas of cortical thickening and osteoporosis
