Braddom Flashcards
Osteoporosis definition
Heterogeneous group of syndromes where bone mass per unit volume is reduced in otherwise healthy bone –> fragile bone that increases fracture risk
Is the mineral/matrix ratio normal in osteoporosis?
Yes; in osteomalacia the mineral content is very reduced
Where does most of the expense of osteoporosis come from?
Hip fractures
Osteoporosis definition by BMD
2.5 SD below peak mean bone mass of young healthy adults (age 35) of same gender
T score vs. Z score
T score: comparing to healthy young person (how we define osteoporosis)
Z score: comparing with people of same demographics (age/sex/race/height/weight)
Normal BMD vs. osteopenia vs. osteoporosis
Normal BMD: T score -1 or higher
Osteopenia: T score between -1 & -2.5
Osteoporosis: T score -2.5 or less
Severe osteoporosis: T score -2.5 or less with a fracture
How much bone is replaced annually by cyclic process of bone remodeling?
20%
Two types of bone cells & functions
Osteoclasts: resorb calcified matrix
Osteoblasts: synthesize new bone matrix
Osteoclast location & origin
Location: on endosteal bone surfaces
Origin: share common precursor with monocytye macrophage; large multi-nucleated cells with 10-20 nuclei
Osteoclast special cell membrane
Has folds that invaginate at interface with bone surface –> ruffled border. At the ruffled border, osteoclasts produce proteolytic enzymes to induce resorption of bone & mineralized bone matrix
Osteoblast origin & function
Origin: derived from mesenchymal cells
Function: mineralization of matrix through budding of vesicles from their cytoplasmic membrane, which are rich in alk phos. Osteoblasts secrete all the growth factors that are trapped in the matrix
Phases of cyclical bone remodeling
Allows maintenance of the bio-mechanical integrity of the skeleton & supports role of bone in the provision of ionic bank for the body & mechanical support:
- Activation: osteoclast activity recruited
- Resorption: osteoclasts erode bone & form a cavity
- Reversal: osteoblasts recruited
- Formation: osteoblasts replace the cavity with new bone
- Quiescence: bone tissue remains dormant until the next cycle starts
What is the process of bone resorption & formation called?
Coupling
Coupling in osteoporosis
Disequilibrium between resorption & formation, favoring resorption –> bone loss
Does trabecular bone or cortical bone have more active remodeling units?
Trabecular bone
Is trabecular bone or cortical bone more metabolically active?
Trabecular bone
Does osteoporosis clinically affect trabecular bone or cortical bone more?
Trabecular bone
Vertebra vs. femoral neck % trabecular bone
Vertebra: 50%
Femoral neck: 30%
Osteoporosis, therefore, occurs in vertebrae before occurring in femoral neck
When is peak adult bone mass achieved?
30-35 years
What is the other name for trabecular bone?
Cancellous bone
Is skeleton comprised mostly of trabecular or cortical bone?
Cortical (80%)
Examples of high-turnover osteoporosis
Hyperparathyroidism, thyrotoxicosis
Why is fracture incidence related to osteoporosis lower in men than women?
Diameter of vertebral bodies & long bones is greater in men at maturity & bone loss is about half that of women throughout life
Most common types of osteoporosis
Post-menopausal or age-related
What is primary osteoporosis?
Rare disorder of idiopathic juvenile osteoporosis, typically occurs before puberty (between 8 & 14). Osteoporosis progresses over 2-4 years with multiple axial or axio-appendicular fractures. Remission occurs spontaneously after 2-4 years. Osteoclast activity is increased while osteoblast activity stays normal. Clinical findings most evident in thoracic & lumbar spine. Radiographic findings may be permanent. Lab values are normal.
Hereditary/congenital causes of osteoporosis
- Osteogenesis imperfecta
- Myotonia congenita
- Werdnig-Hoffmann disease
- Gonadal dysgenesis
Acquired Osteoporosis examples (Generalized)
- Idiopathic (in pre-menopausal women & middle-aged or young men)
- Post-menopausal
- Age-related
- Endocrine disorders: acromegaly, hyperthyroidism, Cushing syndrome (iatrogenic or endogenous), hyper-PTH, T1DM, hypogonadism
- Nutritional issues: malnutrition, anorexia, bulimia, Vit C or D deficiency, Vit OD (A or D), calcium deficiency, high sodium intake, high caffeine intake, high protein intake, high phosphate intake, alcohol abuse
- Sedentary lifestyle, immobility, smoking
- GI disorders: liver disease, malabsorption syndromes, congenital lactase deficiency (alactasia), sub-total gastrectomy, small bowel resection
- Nephropathies
- COPD
- Malignancies: MM, disseminated carcinoma
- Drug use: phenytoin, barbituates, cholestyramine, heparin, excess thyroid hormone replacement, glucocorticoids
Acquired Osteoporosis examples (Localized)
- Inflammatory arthritis
- Fractures & immobilization in cast
- Limb dystrophies
- Muscular paralysis
What hormones can increase rate of bone remodeling?
PTH, thyroxine, GH, Vit D (1, 25)
What hormones can decrease rate of bone remodeling?
Calcitonin, estrogen, glucocorticoids
What is the major hormone for calcium homeostasis?
PTH
PTH physiology
Secreted by parathyroid glands (located behind thyroid glands.
Secreted based on level of plasma Ca2+
Regulates plasma [Ca2+] in 3 ways:
1. Stimulates bone resorption & release of Ca2+ & phosphate (in presence of active Vit D)
2. Produces calcitriol in the kidneys to increase intestinal absorption of Ca2+ & phosphate
3. Increases active re-absorpion of C12+ ions in renal distal tubule
PTH in relation to calcium & phosphate
Increases serum calcium & decreases serum phosphate (reduces proximal tubular re-absorption of phosphate)
Calcitonin physiology
Secreted by parafollicular cells of thyroid gland
Major stimulus of its production is serum Ca2+ level
Directly prohibits calcium & phosphate resorption through inhibition of osteoclastic activity, lowering serum Ca2+
Vit D physiology
Main regulators of synthesis: serum levels of Vit D, Ca2+, phosphate, & PTH
Can be synthesized through exposure to sun & conversion in liver
PTH is the major driver of production of Vit D in the kidney (via 1-alpha-hydroxylase to turn inactive Vit D to active Vit D)
Active Vit D increases intestinal absorption of Ca2+ & phosphate
Vit D is required for appropriate bone mineralization
Active Vit D stimulates osteoblast activity
Main endocrine function that occurs at menopause
Loss of secretion of estrogen & progesterone from the ovaries
What is the major source of estrogen in post-menopausal women?
Estrone (created in fat cells)
Why can bone mass decrease in elderly men?
In some men, bone mass decreases along with a decline in gonadal function (testosterone decreases with age due to decreased # of Leydig cells in the testes)
Male hypogonadism is typically a/w bone loss
Hyperprolactinemia causing osteoporosis
Failure of the gonadal axis –> substantial loss in bone
Other sex hormone factors causing osteoporosis
- Amenorrheic athletes who exercise excessively with lower than normal body weight –> have lower circulating estradiol, progesterone, and prolactin levels (a/w hypothalamic hypogonadism) –> excessive bone loss that can mostly be reversed
What heavily influences bone growth & remodeling?
Rate of change in strain
What happens to bone in the normal aging process?
Deficit between resorption & formation because osteoblastic activity lags compared to osteoclastic –> bone loss during each cycle of remodeling
Activation is decreased –> low turnover osteoporosis
What happens to Vit D levels as people age?
Decreases by about 50% in both men & women
Growth hormone production during aging process
Decreases
Growth hormone & osteoporosis
GH stimulates renal production of active Vit D
Secretion of GH is decreased in patients with osteoporosis
GH & IGF-1 have positive effects on calcium homeostasis –> osteoblast proliferation, osteoclast differentiation, & bone resorption
Vit K therapy in elderly a/w decrease in rate of bone resorption as demonstrated by this urine marker
Hydroxyproline
Are plasma calcitonin levels higher in men or women?
Men (levels do not change with age)
Do thyroid levels change with age?
No, but if they do, it is a slight decrease
Does PTH change with age?
Increases, probably because of mild hypocalcemia & decreased active Vit D
Why does active Vit D decrease with age?
Decreased consumption of dietary Vit D, decreased exposure to sunlight, decreased skin capacity for Vit D conversion, reduced intestinal absorption, & reduced 1-alpha-hydroxylase activity
Recommended dose of calcium & Vit D in estrogen-deficient women
Calcium: 1,500 mg/day
Vit D: 800 IU/day
Can osteoporotic vertebral fractures go unnoticed?
Yes, often found incidentally on CXR
Most common areas for osteoporotic fractures
Mid-thoracic (T7/8) & upper lumbar spine (L1/2), proximal femur (hip), distal forearm (Colles)
Highest incidence for osteoporotic fractures
White women
Female: male-
Vertebral fx- 7:1
Hip fx- 2:1
Colles- 5:1
Which fracture site is of greatest concern clinically?
Hip fx –> risk of death is 15-20%
Management of osteoporotic spine fracture
Immobilization of the involved vertebral bodies & analgesia (these fractures heal by becoming more condensed)
What should you look for if there is non-union in appendicular fractures?
Osteomalacia or hyperparathyroidism
How to typically manage proximal humerus (surgical neck) fracture in osteoporosis
Conservative, typically
How long can a compression fracture appear normal on XR?
Up to 4 weeks. You need to lose 25-30% of BMD for it to be picked up on XR
How can vertebral fractures from osteoporosis cause chronic pain?
Spinal deformity –> kyphotic postural change
Management of acute pain in patients with osteoporosis
Bed rest (2 days), analgesics (avoid constipating meds), avoidance of constipation, PT (initially cold packs then mild heat & massage), avoidance of exertion, avoidance of excessive spinal strain, back support if needed to decrease pain & expedite ambulation, gait aids as needed
What can increase the possibility of compressing vertebrae in the fragile osteoporotic spine?
Disproportionate weakness in back extensor musculature relative to body weight or spinal flexion strength
Why is development of kyphotic posture bad?
Can lead to postural back pain & predispose to falls
What can spinal pain related to osteoporosis be from?
Caused by deformity from vertebral wedging & compression, as well as by secondary ligamentous strain
What happens to inter-vertebral disks as we age?
Increase in number & diameter of collagen fibrils in the disk –> progressive decrease in disk resilience –> loss of distinction between nucleus pulposus & annulus fibrosis
Therapy for chronic back pain 2/2 osteoporosis
Back extensor resistance training –> studies show less amount of vertebral fractures long-term compared to controls with osteoporosis
What else can chronic pain in back from osteoporosis be from?
Micro-fractures, only visible on bone scan
What position is recommended for back strengthening exercise in osteoporosis?
Prone –> improves horizontal trabecular connections; needs to be progressive, resistive, & non-loading to avoid vertebral compression fracture
Vertebroplasty & kyphoplasty
Vertebroplasty: Injection of acrylic cement (such as polymethylmethacrylate) into a partially collapsed vertebral body
Kyphoplasty: balloon dilation catheter to restore vertebral height
Unclear if either actually helps based on studies
Why does kyphotic posture lead to instability?
Places center of gravity closer to limit of stability
What are two general types of hip fracture?
Intra-capsular (femoral neck) or extra-capsular (trochanteric)
Which hip fracture has a high surgical failure rate?
Femoral neck fractures repaired by internal fixation
Most surgeons prefer arthroplasty for this reason (hemi-arthroplasty of femoral head & neck for older, frailer patients with a prognosis of limited mobility)
Operative treatment choice for trochanteric fracture
Internal fixation
When do patients get a NWB status after hip fracture?
Severely comminuted or fractures where the operative result was non-satisfactory
Hip pads for fracture ppx
Questionable benefit but may work for some who are compliant
Landing on buttocks is less traumatic to hips than landing on greater troch –> teaching this may be more beneficial than hip pads
Sacral insufficiency fractures
Pelvic fractures are common in osteoporosis
Fractures of pubic rami/sacrum can occur with minimal strain (most patients cannot recall a traumatic event
Treated conservatively typically
Wheeled walker recommended initially –> crutches/cane
WB is as tolerated
Who should be getting a BMD evaluation?
Estrogen-deficient women with risk factors, women 65 or older, women in post-menopausal stage who have at least 1 risk factor for osteoporosis, people who have a vertebral abnormality indicative of bone loss, taking medication like Prednisone, T1DM, liver/kidney disease, thyroid disease, family history of menopause, & women who underwent early menopause.
May also want to include alcohol abusers/smokers
When should follow-up BMD testing be done?
After 2 years or longer, depending on baseline T-score & patient risk factors
Bone markers
Bone formation: calcium, phosphorus, PTH, bone-specific alk phos, serum osteocalcin, pro-collagen type I, C, & N pro-peptides
Resorption: 24-hour urine hydroxyproline/calcium excretion (corrected by creatinine excretion)/pyridinium cross-links
These markers are clouded in patients with osteoporosis because many variations among people exist. Indices of bone turnover have seasonal & circadian variations
Evaluation studies for osteoporosis
- H&P (FH of osteoporosis, general dietary calcium intake), level of physical activity, height/weight
- CXR, Spine XR (r/o lymphomas, rib fractures, compression fractures, etc)
- BMD eval (at menopause & every 2 years for high-risk patients, 5 years for low-risk patients)
- CBC (r/o anemias a/w malignancy)
- Chemistries (alk phos which may be increased in osteomalacia, Paget disease, bony mets/fracture, intestinal malabsorption, Vit D deficiency, chronic liver disease, alcohol abuse, Phenytoin use, hypercalcemia of hyperparathyroidism, hypophosphatemia of hyperparathyroidism & osteomalacia, malabsorption, or malnutrition)
- ESR & SPEP (MM or other gammopathies)
- Total thyroxine (increase may be a cause of osteoporosis because of increased bone turnover)
- Immunoreactive PTH (hyperparathyroidism with hypercalcium)
- Vit D (inactive & active) (GI disease, osteomalacia)
- UA & 24-hour urine (check for proteinuria caused by nephrotic syndrome & for low pH from RTA; 24-hour urine can r/o hypercalciuria)
- Optional: bone scan, iliac crest biopsy
Radiographic findings of osteoporosis
Increased lucency of vertebral bodies with loss of horizontal trabeculae, increased prominence of the cortical end plates, vertically oriented trabeculae, reduction in cortex thickness, & anterior wedging of vertebral bodies
What is the degree of wedging that indicates a true fracture?
15-25% reduction in anterior height relative to posterior height of the same vertebra
Other morphological change in osteoporosis
Bioconcavity of vertebral bodies
Definition of complete compression fracture
Reduction in both anterior & posterior heights by at least 25% c/w adjacent normal vertebrae
Available methods to evaluate bone mass
- Photon absorptiometry (single or dual)
- Finger XR spectrometry
- U/s densitometry
- Qualitative CT
- DEXA (dual-energy XR absorptiometry) –> most common due to high precision. Usually measure BMD of spine & hips (femoral neck), but spine measurements may be erroneous due to OA of the spine. Amount of radiation used is < 3 mrad
Specialties who should be on board with osteoporosis
Endocrinology, PM&R, pharmacology, psychology, nutrition
SPEED program for osteoporosis
SPEED: spinal proprioceptive extension exercise dynamic
Provides decreased step width, improved steadiness of gait, decreased risk for falls at obstacles, increased velocity/cadence/stride length
Suggested Rehab for osteopenia
Back strengthening exercises, limit load-lifting (10-20 lbs max), aerobic exercises (walk 40 minutes/day), weight-training 3x/week, postural exercises (WKO with pelvic tilt & back extension), Frenkel exercises, Tai chi
Suggested rehab for osteoporosis
Pharmacologic intervention, pain management, ROM/strengthening/coordination, mid-day rest, heat/cold/massage, back extensor strengthening, walking 40 mins/day as tolerated, Frenkel exercises, aquatic exercises once or twice weekly, fall prevention program, postural exercises (WKO with pelvic tilt & back extension), prevention of vertebral compression fractures (orthoses as needed), prevention of spinal strain (do not lift over 10 lbs), eval of balance & use gait aid if needed, grab bars, counter adjustments, OT consult, start strengthening program with 1-2 lb & increase as tolerated to 5 lb in each hand, SPEED program if needed, hip protective measures
High-impact bone-loading sports that have high rates/magnitudes of bone strain leading to site-specific increases in BMD
Gymnastics, badminton, tennis, volleyball, basketball. Gymnasts have higher BMD than volleyball players except in the pelvis
Swimming can improve muscle strength but not bone mass
Minimum effective strain stimulus theory
Minimum threshold of mechanical loading must be achieved to evoke an increased level of BMD. The greatest osteogenic effect from mechanical loading occurs with high strain, repeated daily, short duration, & applied to specific bone site
High-impact exercises for people with normal BMD
Aerobics, jogging, skiing
Non-straining exercises for people with osteoporosis
Walking for 45 mins 3x/week or 30 mins/daily
Aquatic exercises are recommended for patients who are unable to perform antigravity exercises because of pain or weakness. The non-strenuous low-resistance exercises can be advanced to anti-gravity & strengthening exercises if MSK condition allows
What type of exercise program can improve bone mass in inactive individuals?
Supervised, non-strenuous, progressive, & resistive
Most effective back-strengthening exercise
Progressive, resisted back extension
What exercise should be added to complement a posture training exercise program?
Isometric abdominal muscle-strengthening
What exercises are used to reduce kyphotic posture?
Pectoral & shoulder extensor stretching
Exercises good for CV fitness that are not harmful in osteoporosis (although don’t improve BMD)
Swimming or short periods of stationary biking
Postural issues in osteoporosis
Reduced paraspinal muscle strength & forward tendency of head & trunk related to the effect of gravity –> iliocostal friction syndrome & flank pain –> this pain does not respond to conventional orthoses, but postural training programs to decrease kyphosis CAN reduce iliocostal friction syndrome
What intervention can provide re-education of the paraspinal muscles for improvement in kyphotic posturing & reduce risk of falls?
Posture training programs, such as the application of a weighted kypho-orthosis 2-3x/day in cases of severe kyphosis or less frequently in milder cases while contracting back extensors
What does a weight kypo-orthosis (WKO) do?
Provides counter-forces to enable wearers to contract their erector spinae muscles better & decrease kyphotic posturing (in some severe cases back extension is not possible without a WKO)
Pharmacotherapy for improving bone mass
Efficacious in prevention of skeletal deformities but must also be in conjunction with rehabilitation
Best osteoporosis prevention
Improving back strength & peak bone mass before 30 years old & reducing bone loss thereafter
Most common osteoporosis pharmacologic treatments
Calcium, Vit D, & bisphosphonates
Anti-resorptive agents in osteoporosis
Estrogens, androgens, calcitonin, & bisphosphonates
Osteoblast-stimulator agents in osteoporosis
Fluoride & PTH (fluoride is not approved by US FDA because of increased risk of appendicular fractures)
PTH (1-34) analogs for treatment of osteoporosis
Teriparatide (Forteo) is a subq med used for post-menopausal women at high risk of fracture & cannot use other osteoporosis meds
Decrease risk of vertebral fractures & increase vertebral, femoral, & total body BMD
Contraindicated in patients with h/o CA
ADR’s: nausea, dizziness, leg cramps, HA, hypercalcemia
Side effect of bisphosphonates
Osteonecrosis of jaw
Lifestyle modification for osteoporosis
Cessation of tobacco & alcohol abuse
Recommendations for women with estrogen deficiency
1,500 mg of Ca daily in divided doses & 800-1000 IU of Vit D daily (Vit D dose varies based on diet & sun exposure)
When treating women with an intact uterus, what medication should you also provide?
Progesterone (to prevent endometrial hyperplasia & possibly endometrial carcinoma
Contraindication to estrogen replacement therapy
Liver or GB disease, recent h/o throboembolism or thrombophlebitis, & suspected breast or endometrial carcinoma
Adverse effects of progestin administration
Fatigue, depression, breast tenderness, bloating, menstrual cramps, HA, weight gain, increased serum TG, increased serum BG, & abdnormal vaginal bleeding
Is estrogen replacement therapy indicated to prevent osteoporosis?
No
Why is calcitonin (works as anti-resorptive agent by inhibiting osteoclasts) limited in use in osteoporosis?
Most effective in patients whose rate of bone turnover is high & is approved for treatment of established osteoporosis
Long-term fracture-reducing efficacy is not well-established
Subcutaneous IM injection of salmon calcitonin every other day is usually used. Adverse effects of parenteral use: flushing, nausea, development of antibodies
Nasal spray exists but can lead to nasal irritation, crusting, & ulcerations
Where do bisphosphonates work?
Trabecular bone, especially lumbar spine –> can see BMD increases of 5-10% during first 2 years of treatment
Taking bisphosphonates for osteoporosis
Alendronate sodium –> aminobisphosphonate –> can normalize rate of bone turnover & increase bone mass
Alendronate can be qD or qWeekly & must be taken with full glass of water on awakening. Patient should not eat or recline for 30-45 mins after taking due to risk of esophageal irritation
Risedronate is another option & can significantly decrease incidence of vertebral & non-vertebral fractures in post-menopausal osteoporosis
What is a potential adverse effect of oral bisphosphonates?
Esophageal irritation, especially in patients with GERD or other esophageal dysfunction
Thiazide diuretics & osteoporosis
Inhibit urinary calcium excretion of calcium & can slow bone loss & reduce rate of fractures in patients with osteoporosis
Sodium fluoride in treatment of osteoporosis
Stimulates osteoblastic activity
Can increase BMD up to 8% in the lumbar spine & 4% in the proximal femur, but decreases cortical bone density in the radius by about 2% per year
Reports of increased rate of non-vertebral fractures
Used in some European countries but not used in USA
Estrogen receptor mixed agonist-antagonists (Tamoxifen & Raloxifene) in treatment of osteoporosis (AKA SERMs- selective estrogen receptor modulators)
Anti-estrogen effect on breast tissue
Tamoxifen ADR: uterine hyperplasia (not a concern with Raloxifene)
Raloxifene: decreases serum total cholesterol & LDL. Currently only used in post-menopausal stage of osteoporosis. ADRs: leg cramps, hot flashes, DVT
Treatment of osteoporosis in men
Usual supplementation with calcium & Vit D, limitation of alcohol use, cessation of smoking
For hypogonadism, must refer to Endo & they may use Testosterone replacement
Bisphosphonates can also be useful
Management of steroid-induced osteoporosis
Calcium & Vit D supplementation, use of oral anti-resorptive agents such as alendronate sodium or risendronate & implementation of a proper weight-bearing & weight-training exercise program
Brand names of common osteoporosis medications
Alendronate: Fosamax, Binosto
Risendronate: Actonel, Atelvia
Calcitonin: Miacalcin (used also for Paget disease of bone)
Appropriate medical equipment for a marathon
Devices for rapid electrolyte blood testing, cardiac monitoring capabilities, AED’s (automatic electronic defibrillators), rectal thermometers, rapid warming & cooling protocols & equipment, & personnel/equipment for starting IV’s
Body’s adaption to physical training
Metabolically & neuromuscularly specific to the exercise performed
Sport specificity
Importance of training in the same sport that the athlete will be competing in
Example: Although cycling & cross-country skiing are great for aerobic exercise, an athlete who is training to run a marathon needs to focus on running as the major component of training to ultimately maximize running performance
Individuals do respond differently to the same training stimulus
Periodization
A structured training approach developed by a Russian physiologist in the 1960’s
Training is divided into defined periods to allow buildup of training stresses, time for rest & adaptation to training, & continual progression of fitness
How long are periods in periodization?
Macrocycles (usually about a year) divided into shorter mesocycles (1 month) & then sub-divided into microcycles (1 week)
Typical year-long training program with periodization
3 macrocycles: pre-season AKA buildup phase, competitive season AKA maintenance & fine-tuning phase, & post-season AKA recovery phase
Pre-season macrocycle is typically longest & is designed to develop fitness in anticipation of the more intense training to follow –> higher volume & lower intensity exercise
Competitive season macrocycle develops & maintains peak fitness –> high-intensity training & sport-specific technique drills with significantly reduced volume
Post-season macrocycle has an early portion for active rest. Important to adequately recover from injuries, prevent over-training, & take a mental break from competitive season
Most efficient strategy to maximize performance gains
2-week taper just before competition during which training volume is exponentially reduced by 41-60%
The ideal taper for endurance athletes keeps training intensity & frequency stable, but volume is progressively reduced
Overtraining syndrome
Unexplained performance deficit, generalized fatigue, mood disturbance, poor sleep, increased rates of injury/illness. Symptoms persist despite >2 weeks of rest
Can lead to chronic maladaptations
Treatment for overtraining syndrome
Rest for weeks-months with gradual resumption of training. Prevention is the best treatment & recommended to follow a formal periodized training program
Altitude tents
Simulate living at high altitude for athletes attempting to train in these environments (like mountainous regions).
Proposed mechanism for primary physiologic effects responsible for effect of altitude training on sea-level performance
Accelerated erythropoiesis, improved muscle efficiency at the mitochondrial level, glucose transport alterations, enhanced muscle-buffering capacity via pH regulation
Most effective form of altitude/hypoxic training
Live-high train-low method –> training low means training at higher intensity with improved O2 influx to induce beneficial metabolic & neuromuscular training adaptations
Optimal dose of altitude training
Living at elevation of 2,000-2,500 meters for 22 hr/day for 4 weeks
If using simulated environments, 12-16 hours of hypoxic exposure at 2500-3000m
Kinetic chain model
Each complex, athletic movement is the summation of its constituent parts
“Catch-up” in kinetic chain model
When an athlete tries to compensate with one segment for a deficiency in a separate segment –> higher stress on tissues of the distal segment & predisposes it to injury
Tissue diagnosis: Biomechanical diagnosis
Lateral/medial epiconylitis: Posterior deltoid weakness
Hamstring strain: Overly tight hamstring, weak gluteal musculature
Metatarsal stress fracture: Supinated foot
Athletic pubalgia: Weak core musculature, tight hip girdle
PFPS- patellar cartilage irritation or chondromalacia: Quad & glut weakness or inhibition, over-pronation
Repetitive ankle sprains: Weak peroneals, proprioceptive dysfunction
How many injury phases are there?
4
First phase of injury
Initial injury + inflammation, edema, & pain. This phase is usually short (days)
Reparative phase of injured tissue
Might last 6-8 weeks –> cell proliferation, granulation tissue formation, neovascularization
Last phase of injured tissue
Remodeling –> occurs as tissue matures & realigns. Can experience excessive scar tissue formation that leads to chronic/recurrent injury
Return to Play phases (3)
Acute: allow injured tissue to heal; decrease sx, maintain ROM
Recovery: increasing demands on athlete; flexibility, strength, proprioception, endurance training; kinetic chain corrections; maintain CV fitness through cross-training
Functional: advance toward full return to play, advance CV fitness
When can an athlete advance to final stage of return to play (functional)?
Once pain-free ROM is achieved & strength is 75-80% or greater when compared to non-injured side
Kinetic chain when throwing ball
When an initial segment of the body (like the trunk) accelerates, the next segment (like the arm) within the kinetic chain is left behind. When the trunk decelerates, momentum is transferred to the arm with an increased velocity of the arm that is accentuated by the forces acting on the shoulder/arm –> forces & motion are transferred to ball
Where does velocity from a pitch come from?
50% from step & body rotation (from potential energy stored in large leg & trunk musculature) & 50% from smaller muscles of shoulder, elbow, wrist, & hand
Peak velocity in water polo is 50% that of baseball because of the lack of a GRF
Six phases of throwing a pitch
- Wind-up (start to hands apart)
- Early cocking (hands apart to lead foot down)
- Late cocking (foot down to maximum external rotation)
- Acceleration (maximum external rotation to ball release)
- Deceleration (early ball release)
- Follow-through (late ball release)
Other name for early cocking
Stride phase
Early cocking (stride phase)
Less risk of injury because most forces are from trunk & lower limbs; trapezius & serratus anterior show moderate-high activity to protract & upwardly rotate scapula. Middle deltoid generates the abduction force
Late cocking
Hallmark of this phase is when maximal shoulder ER is obtained. Shoulder begins phase in 50 degrees ER & ends in about 175 at max. Amount of ER obtained correlates with speed of pitch
When do most injuries occur when throwing a ball?
Late cocking & deceleration
Late cocking: due to forces needed to stabilize shoulder in this extreme ROM- dynamic stabilizers of anterior shoulder (long head of biceps, subscapularis, pec major) are very active in this phase; static stabilizers (GH ligaments, capsule, labrum) are active as well
Common injuries in late cocking phase of pitching
- Anterior instability
- Internal (posterior-superior) impingement
- Type II SLAP lesion
- Articular surface RTC tears
- Bicipital tendinopathy
- Medial tension injuries at elbow (UCL injury)
Motion of shoulder during acceleration phase
Shoulder is powerfully internally rotated from 175 degrees of ER to 90-100 degrees ER at ball release
What determines what position the arm is relative to vertical plane when throwing a ball in acceleration phase?
Trunk lateral flexion
Trunk lateral flexion in “over the top” vs “sidearm” throwers
Over the top: greater contralateral trunk flexion
Sidearm: less contralateral trunk flexion
What is “dropped elbow” when throwing?
Less than 90 degrees of shoulder abduction during acceleration phase due to fatigue, weakness, or poor form –> decreased pitch velocity & increased risk of injury to RTC & mUCL
What is another injury that can occur during acceleration phase of throwing?
Sub-acromial impingement as arm internally rotates & adducts the abducted arm
Deceleration phase of throwing
Large eccentric muscular forces of posterior shoulder girdle to decelerate the rapid internal rotation of acceleration phase (why lots of injuries can occur here)
This phase ends when IR is 0 degrees
Posterior shoulder girdle is active in this phase (scapular muscles, RTC external rotators- specifically teres minor, & posterior deltoid)
Follow-through phase of throwing
Passive phase- low grade eccentric loading of shoulder musculature & therefore little risk of injury
What is the max amount of time young pitchers should be competing in baseball in a calendar year?
9 months
In other 3 months, should not participate in overhead sports
Age-based pitch counts
9-10: 50 pitches per game, 75 per week, 1000 per season, 2000 per year
11-12: 75 pitches per game, 100 per week, 1000 per season, 3000 per year
13-14: 75 pitches per game, 125 per week, 3000 per year
Differences in walking vs running gait cycle
- There is a third phase in running called “float phase” –> neither foot is in contact with the ground & occurs at beginning of initial swing & end of terminal swing
- Walking gait has a period of double limb support (occurs in first & last 10% of stance phase) that is not present in running
- Stance phase is decreased from 60% while walking to 30% while running & 20% while sprinting. As speed increases, velocity & ROM in LE increases –> minimizes vertical displacement & improves efficiency. Body lowers its CoG by increasing HF, KF, & AD –> major kinematic difference between walking & running occurs in sagittal plane of motion
- In slower running & walking, contact is heel-to-toe. As speed increases, foot strike occurs with forefoot & heel simultaneously, or forefoot strikes initially followed by heel lowering to ground. In sprinting, athlete maintains WB on forefoot from loading response to toe-off
- Angle of gait is different (angle between longitudinal bisection of foot & line of progression). Walking: 10 degrees, Running: approaches 0 degrees as foot strike is on the line of progression to allow more efficient locomotion by limiting deviation of CoG
First phase of swim stroke (common to freestyle, backstroke, & butterfly)
Entry/catch –> hand entry into water until beginning of its backward movement
Propulsive phase of swimming
Divided into pull & push sub-phases
Pull: ends as the hand arrives in the vertical plane of the shoulder
Push: hand is positioned below the shoulder & pushes through water until its exit from water (usually at level of greater troch)
During this phase, arm is moved through adduction & IR starting from stretched position of abduction & ER. Pec major & lat dorsi are major contributors with assistance from serratus anterior & subscapularis/teres major
Final phase of swimming
Recovery phase –> aerial return of hand
Scapular retraction is provided by rhomboids & middle trap; shoulder ER provided by posterior deltoid, teres minor, & infraspinatus
In preparation for hand entry during mid-recovery, the serratus anterior & upper trap upwardly rotate the scapula for shoulder stabilization
Kick patterns in swimming
Flutter kick in freestyle: knee flexes only to 30-40 degrees & minimal HF
Breaststroke kick: whip-kick that creates significant valgus moment at knee (see more medial knee injuries in breastroke swimmers- related to MCL or medial plica/synovitis)
Why does shoulder pain happen to swimmers?
Impingement/RTC tendinopathy due to dynamic muscle imbalances, weakness, & biomechanical faults
Major tenet of shoulder rehab for the swimmer
Scapular stabilization with focus on endurance training of serratus anterior (active throughout swim cycle) & lower trapezius, stretching internal rotatiors & posterior capsule, cervical/thoracic mobilization
Jumping/landing injury in sport
ACL (injury occurs more frequently with knee in less flexion) –> greater knee extensor loads with greater forces creating anterior tibial translation
More common injuries in females, who land more erect with less knee & hip flexion, less hip ER & abduction. Females also generally have imbalance of increased quad:hamstring activation, creating greater knee extension & lesser knee flexion forces
Tylenol in sport
Can be linked to decreased muscle building after exercise (similar to Ibuprofen)
Prostaglandins are normally released after eccentric resistance exercise, which may be blunted after consumption of max doses of Ibuprofen/Acetaminophen
Corticosteroids prohibited by WADA
Oral, rectal, IV, or IM
Allowed: topicals for skin, eye, ear, nose, or buccal cavity; also allowed for iontophoresis (transdermal drug delivery by use of a voltage gradient on the skin)
Therapeutic use exemption (TUE) can be given for epidural or IA steroid injections (or inhaled steroids)
Diuretics & sport
Decrease plasma volume, CO, & PVR. Banned for elite athletes due to theoretical ability to increase urine output & mask use of other banned agents (although this rarely works)
BB in sport
Can reduce exercise tolerance by increasing perceived effort. Can also inhibit glycolysis & glycogenolysis with resulting hypoglycemia after exercise. Can decrease HR after exercise via chronotropic effect. Banned in certain sports because of anxiolytic effects
Diabetes meds in sport
May need to adjust insulin doses when starting new sport; 20-40% reduction is typical because of increased insulin sensitivity with exercise
High-intensity exercise (VO2max >80%) can cause a temporary increase in BG 2/2 increased sympathoadrenal activation (if occurs, should use smaller amount of insulin than would be given for hyperglycemia at rest)
Avoid IM insulin –> muscle contraction can accelerate insulin absorption
Heat can increase absorption rates of insulin & cold can decrease absorption rates (IDDM should avoid hot or cold whirlpools); extreme ambient temp can also reduce insulin action in athletes
Asthma drugs in sport
Exercise-induced bronchospasm can be treated with a short-acting B-agonist (albuterol) within 15 minutes before exercise. If not sufficient, can use a mast cell stabilizer (like cromolyn) in addition.
For chronic persistent asthma (FEV1 <80% of predicted & symptoms >2x/week), inhaled corticosteroids are standard treatment (do not appear to have ergogenic or anabolic effects)
Anabolic steroids general effects
- By binding androgen receptors, they stimulate mRNA synthesis, increasing structural & contractile protein synthesis & produce an anabolic state
- Anti-catabolic via competitive inhibition of the glucocorticoid receptor, inhibiting the catabolic effects of cortisol, preserving muscle mass
- Emotional effects, pushing athletes to train more intensely & more often
Negative effects of anabolic steroids
CV: increases total LDL, decreases HDL, HTN, myocardial ischemia/infarction, CVA
Hepatic: transaminitis, peliosis hepatis (benign intrahepatic vascular disorder), HCC
Male GU: oligospermia, azoospermia, gynecomastia, decreased testicular size
Female GU: decreased LH, FSH, progesterone. Menstrual irregularities, male pattern alopecia, hirsutism (irreversible), clitoromegaly (irreversible), deepening voice (irreversible)
Skeletal: premature closure of the epiphyses
Skin: acne (increased # of sebaceous glands), striae
Psych: decreased libido, mood swings, hypermania/hypomania, aggressive behavior, withdrawal, depression, addiction
Most common reasons for death: suicide, MI
Anabolic Steroid Control Act of 1990
Prohibited use of steroids for any use other than disease treatment –> Schedule III drugs within the Controlled Substances Act
EPO & Blood Doping
Endurance athletes are sensitive to O2-carrying capacity in their blood; the advantage of training at altitude can be reproduced by blood doping, blood transfusion, or administration of the drug recombinant human EPO (rhEPO)
EPO: glycoprotein hormone produced in kidney in response to tissue hypoxia. EPO is part of a negative feedback cycle that controls tissue O2 delivery by controlling the # of erythrocytes in the blood
Both rhEPO & transfusions have been shown to increase VO2max
Risks of artificially elevated Hgb/HCT: CVA, MI, PE
Pseudoephedrine (Sudafed)
Commonly used stimulant. Mixed results in studies if it gives advantage in sport
Herbals: ephedra, ma huang
similar structural properties & physiologic effects to Sudafed. Ephedra containing products were taken off market in 2004. Banned by NCAA, IOC
Caffeine
Adenosine receptor antagonist with stimulant properties.
Ergogenic in most exercise situations. Acts by binding to adenosine receptors in most tissues, including brain, heart, smooth muscle, fat, & skeletal muscle
Stimulates secretion of epinephrine & CNS & enhances neuromuscular transmission & muscle contractility
Has not shown to be risk for dehydration in athletes. Not prohibited by WADA
What is a supplement?
A substance taken to augment the diet
B-hydroxy-B-methylbutyrate (HMB) & creatine: both have sufficient evidence to conclude they significantly augment lean body mass & strength with resistance training
Creatine
Naturally occurring compound made from AA glycine, arginine, & methionine –> most popular nutritional supplement on the market
Benefits short-duration, high-intensity, repetitive exercise by enhancing ATP regeneration
Common side effects: GI distress, muscle cramping; some cases of renal failure (reversible with removal of creatine)
Many NFL players use it. NCAA does not allow teams to provide creatine to players
Illegal drugs
Testosterone (unless prescribed for diseased state), androstenedione, HGH (unless prescribed for disease state)
PPE goals
Identify life-threatening conditions, identify conditions that can limit competition, identify factors that predispose athlete to injury, meet legal requirements of institution & state
Can also discuss preventive health, high-risk behaviors, establish rapport with athlete, evaluate general health of potentially underserved population
Not intended to replace comprehensive eval by PCP
Look up standard (present day) for PPE exam
Cardiovascular (EKG?, TTE?)
Hearing, vision?
Etc
Can a physician performing PPE be found liable?
Yes, even as volunteer, if athlete is cleared to play despite presence of a medically contraindicated condition
Liability waivers are not acceptable in presence of medically contraindicated conditions
Emergency action plan (EAP)
Must be reviewed & practiced annually with all members of the SM team
Must have early access to defibrillation within 3 minutes from collapse to first shock
Leading cause of death in young athletes
Sudden cardiac death, typically a result of structural cardiac abnormality (most common is HCM, then commotio cordis, then coronary artery abnormalities)
Coronary artery abnormalities are most common cause of SCA in young female athletes
Higher incidence in males
Vigorous exercise is trigger for lethal arrhythmias (90% of SCA occurs during training or competition)
Most are found to be in asystole or PEA > VF/VT
Survival rates are very poor
Helmets in football
Decreased incidence of ICH but increased C-spine injury
Most common cause of collapse in marathon runner
Benign exercise-associated collapse –> considered a form of postural hypotension (venous pooling of blood in legs when runner stops & blood stops being pumped through circulation via muscle contraction). Exacerbated in warm environments because blood flow is shunted from the core to skin to facilitate skin cooling –> important to keep walking after marathon. Oral rehydration & lying athlete down with legs & pelvis elevated above heart is usually sufficient
Ddx of exercise-associated collapse
- Benign exercise-associated collapse
- Cardiac arrest
- Heat-related illness (heat exhaustion, heat stroke)
- Hypoglycemia
- Hyponatremia
- Hypothermia
- Muscle cramps
- Other medical/neurologic conditions
Exercise-associated hyponatremia
Hypervolemic hyponatremia –> fluid shifts from low osmotic pressure in the blood causing cerebral edema & then neurogenic pulmonary edema
Risk factors: weight gain during the race, marathon time >4 hours, BMI extremes, runners who ingest too many fluids on race course (gain weight). Slower runners have more of an opportunity to drink excessively, & smaller runners generally need less fluid to dilute their serum Na levels. General guidelines is 400-800 mL (14-27 oz) per hour of racing; drink when you are thirsty
Treatment:
- Minimal sx: close observation & fluid restriction while natural diuresis occurs
- Progressive encephalopathic symptoms: high flow O2, bolus of 3% NaCl, quick transport to ER
Only if athlete is a very salty sweater or if competition lasts >6 hrs should Na or electrolyte replacement be necessary. Course should space out water stations every 1.5 miles to limit excessive drinking
Heat-related illness as cause of exercise-associated collapse
Heat exhaustion: inability to continue exercise in heat but NOT related to body temp. This is a failure of CV response to workload, high environmental temps, and dehydration
Heat stroke: medical emergency due to multi-organ system failure 2/2 hyperthermia. Rectal core temp >39C. Treatment is immediate body cooling –> ice bath/cold water immersion, taco method, ice to head/neck/axilla/groin. Mortality rate & organ damage is proportional to length of time between core temp elevation & treatment. Can occur in cool environments & may be a genetic predisposition to excessive endogenous heat production
Stinger (burner)
Nerve injury that occurs within the peripheral neural axis at a specific but variable point from the nerve root to brachial plexus. Can result from tensile or compressive injury to cervical nerve root or plexus (brachial plexus tensile overload is most common way).
Tensile injury –> younger, weaker neck & shoulder girdle musculature, vulnerable to contralateral neck sidebending with ipsi shoulder & arm depression
Cervical root compression –> older, stronger, more experienced athlete during forceful cervical extension and rotation, narrowing the neuroforamen.
Presentation: sudden-onset lancinating, burning pain in one upper limb after a traumatic event. Sx typically follows a single dermatomal distribution, most commonly C5, 6, or 7. Pain lasts seconds to mins & sensory issues resolve quickly; weakness can persist. First one typically gets better quickly; each one after, more neuro sequelae may exist including persistent motor weakness. C5 motor (deltoid, biceps) issue is most common if exists. History of cervical disk disease or neuroforaminal narrowing increases overall risk.
Treatment: pain control, strengthening, and rehab of postural faults & muscle imbalances. Can also do fluoro ESI for persistent symptoms. Research is lacking in equipment modifications.
Exercise-induced bronchospasm
Can be present with chronic asthma but generally a separate entity. Symptoms: breathlessness w/wo coughing/wheezing or even just decreased performance during vigorous endurance training or competition. Winter sport athletes most commonly have this (cold, dry air).
Thought to be from water loss & cooling in the airway that occurs with hyperventilation –> bronchoconstriction
Treatment: adequate warm-up, short-acting beta-agonist 15 mins before exercise (if this doesn’t work, add cromylyn (mast cell stabilizer)). Inhaled corticosteroids can be added before exercise if refractory to aforementioned. Can then add chronic asthma therapy (inhaled corticosteroids –> long-acting B-agonists –> leukotriene-receptor antagonists)
Anemia in athlete
3 most common causes: IDA, physiologic (psuedoanemia), foot-strike hemolysis
IDA: blood loss or poor iron intake (microcytic); serum ferritin <30; iron given with vit c because iron is best absorbed in acidic environment
Pseudoanemia: seen commonly in endurance athletes- lower Hgb concentration because of expansion of plasma volume; adaptation & does not inhibit performance
Foot-strike hemolysis: RBC destruction in feet from running impact; intravascular hemolysis can also be seen in cyclists & swimmers –> mild, don’t need tx
Women with athletic amenorrhea
P/w reduction in LH pulse frequencies, which depend on EA
When is peak bone mass achieved?
During first 3 decades of life, with Tanner stages 2 & 3 (early to mid puberty) as the maturational stage in which physical activity has the greatest impact on bone
Estrogen
Cardio-protective effects (increases HDL, decreases LDL); stimulates production of NO (potent vasodilator & inhibitor of platelet aggregation, leukocyte adhesion, and vascular smooth muscle proliferation & migration).
Flow-mediated vasodilation (FMD) results from NO release in response to shear stress & increased blood flow. Athletic amenorrhea is a/w decreased endothelium-dependent dilation of the brachial artery (a measure of FMD) & unfavorable lipid profile. Tx with OCP has been shown to improve FMD
When do children lose the most flexibility?
Puberty, due to muscle-tendon imbalances that occur with rapid growth
Pediatric growth plate
AKA physis (situated between the epiphysis & metaphysis)
2 types of epiphyses: traction & pressure.
Traction (apophysis)- point of attachment of tendon to bone. Injuries here are not a/w growth disturbance (Osgood-Schlatter’s, Sever’s disease, medial epicondylopathy)
Pressure- found at end of long bones such as distal femur & proximal tibia. Injuries here can lead to limb-length discrepancies or angular deformities. Most common cause of acute injury is a fall. Injuries are designated by Salter-Harris classification. Chronic injuries result from ongoing stress to physis, such as distal radial injuries in young gymnasts
Salter Harris classifications
Type I: S- straight across (the physis) with or without displacement
Type II: A- above (oblique fracture from physis going up to metaphysis)
Type III: L- lower (going down to epiphysis instead of up like in II)
Type IV: TE- through everything (horizontal physeal fracture + vertical epiphyseal & oblique metaphyseal fracture)
Type V: R: cRush- compression fracture of physis
Management based on Salter Harris
I & II: closed reduction, casting, or splinting
III & IV: ORIF
V: emergent ortho; germinal matrix may be involved which can lead to growth arrest
