Exam 2 Flashcards
Entire muscle surrounded by
Epimysium
Fascicle surrounded by
Perimysium
Muscle fibers surrounded by
Endomysium
Smallest functional unit of SkM
Sarcomere (made up of myofilaments - actin and myosin)
Calsequestrin
Protein in SR that regulates Ca
Tropomyosin function
Blocks myosin binding site on actin at rest
One Tm runs 7 G-actin (1 F actin)
Lies within actin groove
Troponin function
Regulates tropomyosin
Troponin subunit Tc
Binds Ca
Troponin subunit Ti
Inhibits tropomyosin movement off of myosin binding site
Troponin subunit Tt
Binds troponin to tropomyosin
Proteins that anchor myosin
Titin and M-line proteins
Proteins that anchor actin
Alpha actinin and Dystrophin
“power stroke”
Repetitive crossbridges –> continued force generation
Relaxation of SkM (3 steps)
ATPase pumps pump Ca back into SR
Tc no longer bound to Ca, Tropomyosin slides over myosin binding site
Ti becomes active again
Serial/Vertical orientation of sarcomeres
Facilitate velocity of contraction (greater shortening)
E.g. hamstring
Parallel/ Pennate orientation of sarcomeres
Facilitate force generation (packing of more sarcomeres)
E.g. quads, gastrocnemius
Torque- velocity relationship
Takes eccentric phase into account
Force generation ability: E>I>C
Why do eccentric contractions generate the most force?
- Myosin heads ripping
- CT resists lengthening
Which type of activation do we maintain best with age?
Eccentric
Size of motor unit defined as
Number of fibers innervated by one nerve
Smaller = greater control
Structural changes of muscle with aging
Fast twitch motor units die, fibers are rescued by slow twitch motor units
–> Fewer, slower, larger motor units overall
Increased tensile ability in CT
Fewer muscle fibers
Possibly more precipitous in females
Alpha motor neuron
Efferent neuron to SkM (from muscle spindle reflex)
Gamma motor neuron
Efferent neuron to muscle spindle
Muscle spindle afferent neurons (1a and II endings)
Sense passive elongation of muscle
Golgi Tendon Organs
Lie within tendon, respond to increases in tension.
Muscles with increased tension inhibited
Input is conscious level?
Afferent neurons in golgi tendon reflex sense
Tension in golgi and in extrafusal fibers
Smooth muscle differences from skeletal
3rd filament (intermediate) –> No striation
Dense bodies instead of sarcomeres (actin approximates dense bodies) - analogous to z line approximation
Muscle shortens and widens (nonlinear contractions)
Wider length-tension relationship
Multiunit Smooth Muscle contractions
“Neurogenic” - innervated by ANS
e.g. blood vessels
Single Unit Smooth Muscle contractions
“Myogenic” - activated by stretch
e.g. visceral organs
Atrial muscle
Bilayer - deep fibers specific to one atrium
Ventricular muscle
Coil-like fibers
Hierarchical structure of muscle
Muscle, fascicles, fibers (cell), myofibrils (organelles), myofilaments
Sarcopenia
Age related muscle loss - greatest decline occurs with inactivity
Bone density peaks ____, remains stable for____
After 3rd decade; 20 years
Preclinical disability
Progressive and detectable, but unrecognized decline in physical function (65+ y.o.)
Pt says they can still do everything they want, but objective measures show that their function has declined
–> Increased risk for severe disability. Early intervention important (EXERCISE- both strength and endurance)
Which type of bone is osteoporosis more common in?
Trabecular (vertebrae, epiphysis) - common in hips
Which type of bone is osteoporosis more common in?
Trabecular (vertebrae, epiphysis) - common in hips
Pain is severe and localized
Osteoporosis Treatment
Try to stop progression of disease:
Promote weight bearing
Meds, supplemental Ca
Paget’s disease
High bone turnover, but new bone is weakened (fibrous tissue)
Osteoclasts gone wild
Paget’s disease Sxs
Bowing of legs, bone pain, fx, OA
*slow progression, often not caught early
Paget’s disease Tx goal:
Normalize bone activity
Note: Avoid high impact exercise
Osteomyelitis
Inflammation of bone due to infection - usually Staph
Becoming more common due to bacterial resistance and prosthetic implants
Acute vs. chronic osteomyelitis
Acute: Children, spreads through bloodstream from other infection site
Chronic: Adults, esp. immunosupressed
Osteomyelitis sxs
Fever, pain, erythema (children)
Vague sxs, back pain (adults)
Pain with weight bearing
Sausage toe
Dx of Osteomyletis
- Systemic signs (fever, WBC increase)
- Only 50-80% have positive bacterial culture
- MRI, bone scans (X-rays only effective after 10 days)
Osteomyelitis treatment
IV Antibiotics for 3-4 weeks
Acute: good prognosis. Chronic: Poor
Infectious (Septic) Arthritis
Infection in joint
Happens at any age
Either due to direct infection (bacterial, viral, fungal) or reactive from infection elsewhere in body.
Infectious (Septic) Arthritis Treatment
Medical emergency - IV antibiotics
Muscular dystrophy
X-linked recessive error in dystrophin
Spinal Muscular Atrophy
Autosomal recessive reduced number of anterior horn cells
Marked hypotonia and weakness
Spinal Muscular Atrophy diagnosis
EMG studies to check nerve conduction
Plagiocephaly
Mishapen head, can be side effect of torticollis
Callous formation stage of bone healing
Cartilage replaced with bone
Strongest predictor of mortality in older adults with surgery to repair hip fx
Inability to stand up, sit down, walk after 2 weeks
Most common intervertebral discs for DDD
L4-L5
Greatest risk factor for DDD
Family history
age, overweight, underweight also risk factors
3 stages of age-related disc degeneration
- Dysfunction (tear in annulus, hypermobility of facter jts)
- Instability (degeneration of facet jts, subluxation)
- Stabilization (spinal stenosis)
DDD symptoms
LBP - but many cases asymptomatic
Slow progression of pain
Worse with activity and prolonged static position, better with rest
Disc herniation common
DDD diagnosis and treatment
Xray and MRI findings poorly coordinate with symptoms
Conservative vs. surgery: = outcomes
NSAIDs, PT, weight loss
Signs of disc herniation
Ankle dorsiflexion, great toe extensor weakness
Impaired ankle reflexes, loss of sensation in foot
Osgood- Schlatter
Mechanical problem related to extensor mechanism of knee - fibers of patellar tendon pull immature bone from tibia
Occurs before complete fusion of epiphysis
Osgood-schlatter treatment
Rest from painful activities until sxs abate - no immobilization
NSAIDs and ice
Address inefficient extensor mechanism, stretch and strengthen
-90% respond well to above treatment
Arthrogryposis Multiplex Congenita
Non-progressive disease characterized by severe muscle contractures, weakness, fibrosis at birth. (Sometimes have muscles missing).
Osteogenesis Imperfecta
Non progressive, diffuse osteoporosis (both types of bone)
Autosomal dominant
Bowing of long bones, extremities appear small compared to trunk
Osteogenesis Imperfecta pathology
Defect in collagen synthesis (dysplasia) –> Bone, ligament, muscle weakness
Differentiating child abuse from osteogenesis imperfecta
Epiphyseal fractures common in abuse, rare in OI
Developmental Hip Dysplasia
Congenital abnormal growth, dislocation, or sublaxation of hip (shallow acetabulum)
To develop normally, hip needs:
Muscle balance
Bony congruence
Weight bearing forces through joint
^ Wolfe’s Law
Developmental Hip Dysplasia clinical presentations
Decreased hip ROM, especially ABD
Asymmetrical gait, posture, muscle bulk
Developmental Hip dysplasia, diagnosis needed before
18-36 months
Legg-Calve-Perthes Disease
Avascular necrosis of femoral head (medial femoral circumflex artery)
Predictable, self limiting course
4 Stages of Perthes disease
Takes 1-3 years
Incidence of Perthes disease
4-8 year old thin, active boy
Caucasian
20% bilateral
Often associated with learning disability
Clinical presentation of Perthes disease
Limp, Trendelenburg gait Limited ABD and ER Pain: Groin, knee, anterior medial thigh Buttock and thigh atrophy No history of obvious injury
Steps to take if you find a case of Perthes
Refer to a surgeon (not and emergency)
Slipped Capital Femoral Epiphysis Incidence
African american males around puberty
75% obese
25-33% bilateral
Slipped Capital Femoral Epiphysis clinical presentation
Antalgic limp
Held in ER
Decreased ABD, flex, and IR
Pain: Groin, knee, anteromedial thigh
What to do if you suspect a SCFE
Medical emergency - send to surgeon
SCFE vs. Perthes
SCFE: Overweight, puberty, african american, held in ER, limited ABD, flex, IR
Perthes: Thin, active, 4-8 y.o., cuacasian, limited ABD and ER
Both have increased risk of degenerative arthritis as adults
Club foot clinical presentation
Forefoot adduction
Hindfoot varus, small calcaneus
Hypoplastic muscles
Ankle equinus - unable to DF
Club foot treatment
Medical emergency
Serial casting immediately
Surgery, PT, taping, manipulation
Kyphosis –>
SC compression
Scoliosis –>
Spinal nerve compression
Fetal age when terratogens –> Limb deficiencies
3-8 weeks
Complications of Myelography
HA, meningitis, allergic reaction to dye
What is myelography?
DEXA t scores and z scores
T-score: Compared to healthy young adults (peak BMD)
Z-score: Compared to age-matched controls
Complications of Arthrocentesis
Infection, hemorrage
Contraindications of arthrography
Active arthritis, joint infection
Complications of arthroscopy
Infection, hemarthrosis, swelling, synovial rupture
Contraindications for EMG
Anticoagulant meds, skin infection
Inner layer of periosteum
Cambrium - precursor cels to osteoblasts
Osteocytes
Mature osteoblasts surrounded by the collagen matrix they secrete
Increase in bone thickness
Osteoblast activity - add new bone to cambrium
Increase in bone length
Chondrocyte activity -
Chondrocytes near epiphysis multiply
Chondrocytes on epiphyseal side of line multiply
Older chondrocytes near diaphysis hypertrophy and are ossified
Growth hormone
Promotes growth in both length and thickness of bone
Bones most susceptible to effects of DID
Weight bearing bones of lower extremity, pelvis, lumbar spine
-Demineralization occurs in trabecular bone - not externally apparent
What type of cartilage forms growth plate?
Hyaline
Proteoglycans
Protein + GAG, syrupy substance that hold cartilage cells together.
e.g. hyaluronic acid, chondroitin and keratan sulphate
Superficial layer of cartilage
Fibers horizontal, easily compressed, resist friction
Middle layer of cartilage
Increases tensile strength and compression resistance
Fibers oblique to superficial layer
Deep layer of cartilage
Greatest resistance
More proteoglycans, less water
Calcified layer of cartilage
Anchors cartilage to bone
2 classes of ligaments
Capsular and non capsular (non capsular can be internal and external)
Most common IV General anesthetic
Propofol
Most common inhaled general anesthetic
Nitrous oxide
Types of neuromuscular junction blockers
Non depolarizing (iums) - block ACh receptors Depolarizing (succinyl-choline) - Prevent re-polarization
General anesthetics mechanism of action
- Stimulate GABA receptors - hyperpolarize cell
2. Inhibit ACh receptors
Local anesthetic mechanism of action
Bind Na chanels in membrane of afferent neuron –> blocks depolarization, no pain sensation sent to brain
Typical level of epidural or spinal block
L3-4 or 4-5, to avoid spinal chord
Order of anesthesia
Small, unmyelinated nerves first, then larger, myelinated ones.
Pain, temp, pressure, proprio, motor
Drugs that treat spasm
Polysynaptic inhibitors
Receptor specific drugs
Polysnaptic inhibitors
Decrease excitatory input at alpha motor neuron to block pain - spasm - pain cycle
(Smooth muscle affected too - constipation)
Tolerance and dependence possible.
Meprobomate - antianxiety
Drugs to treat spasticity
Diazepam (valium) Baclofen Tizanidine/ Clonidine Gabapentin (neuronin) Dantrolene Na
Ascending mechanism of opioids
Block release of pain neurotransmitters; hyperpolarize post-synaptic terminal
Descending mechanism of opioids
Bind opioid receptors in brain, activating pain inhibitory pathways
Proteins responsible for pain, fever, inflammation, etc.
Prostoglandins (produced via cyclooxygenase pathway)
*COX 2 is the pathway with the negative products
S/s of ASA overdose:
Hearing loss, tinnitus, confusion, HA
