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Braddom Flashcards

1
Q

Osteoporosis definition

A

Heterogeneous group of syndromes where bone mass per unit volume is reduced in otherwise healthy bone –> fragile bone that increases fracture risk

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2
Q

Is the mineral/matrix ratio normal in osteoporosis?

A

Yes; in osteomalacia the mineral content is very reduced

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3
Q

Where does most of the expense of osteoporosis come from?

A

Hip fractures

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4
Q

Osteoporosis definition by BMD

A

2.5 SD below peak mean bone mass of young healthy adults (age 35) of same gender

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5
Q

T score vs. Z score

A

T score: comparing to healthy young person (how we define osteoporosis)

Z score: comparing with people of same demographics (age/sex/race/height/weight)

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6
Q

Normal BMD vs. osteopenia vs. osteoporosis

A

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

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7
Q

How much bone is replaced annually by cyclic process of bone remodeling?

A

20%

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8
Q

Two types of bone cells & functions

A

Osteoclasts: resorb calcified matrix

Osteoblasts: synthesize new bone matrix

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9
Q

Osteoclast location & origin

A

Location: on endosteal bone surfaces

Origin: share common precursor with monocytye macrophage; large multi-nucleated cells with 10-20 nuclei

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10
Q

Osteoclast special cell membrane

A

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

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11
Q

Osteoblast origin & function

A

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

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12
Q

Phases of cyclical bone remodeling

A

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:

  1. Activation: osteoclast activity recruited
  2. Resorption: osteoclasts erode bone & form a cavity
  3. Reversal: osteoblasts recruited
  4. Formation: osteoblasts replace the cavity with new bone
  5. Quiescence: bone tissue remains dormant until the next cycle starts
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13
Q

What is the process of bone resorption & formation called?

A

Coupling

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14
Q

Coupling in osteoporosis

A

Disequilibrium between resorption & formation, favoring resorption –> bone loss

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15
Q

Does trabecular bone or cortical bone have more active remodeling units?

A

Trabecular bone

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16
Q

Is trabecular bone or cortical bone more metabolically active?

A

Trabecular bone

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17
Q

Does osteoporosis clinically affect trabecular bone or cortical bone more?

A

Trabecular bone

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18
Q

Vertebra vs. femoral neck % trabecular bone

A

Vertebra: 50%
Femoral neck: 30%

Osteoporosis, therefore, occurs in vertebrae before occurring in femoral neck

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19
Q

When is peak adult bone mass achieved?

A

30-35 years

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20
Q

What is the other name for trabecular bone?

A

Cancellous bone

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21
Q

Is skeleton comprised mostly of trabecular or cortical bone?

A

Cortical (80%)

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22
Q

Examples of high-turnover osteoporosis

A

Hyperparathyroidism, thyrotoxicosis

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23
Q

Why is fracture incidence related to osteoporosis lower in men than women?

A

Diameter of vertebral bodies & long bones is greater in men at maturity & bone loss is about half that of women throughout life

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24
Q

Most common types of osteoporosis

A

Post-menopausal or age-related

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25
Q

What is primary osteoporosis?

A

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.

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26
Q

Hereditary/congenital causes of osteoporosis

A
  • Osteogenesis imperfecta
  • Myotonia congenita
  • Werdnig-Hoffmann disease
  • Gonadal dysgenesis
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27
Q

Acquired Osteoporosis examples (Generalized)

A
  • 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
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28
Q

Acquired Osteoporosis examples (Localized)

A
  • Inflammatory arthritis
  • Fractures & immobilization in cast
  • Limb dystrophies
  • Muscular paralysis
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29
Q

What hormones can increase rate of bone remodeling?

A

PTH, thyroxine, GH, Vit D (1, 25)

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30
Q

What hormones can decrease rate of bone remodeling?

A

Calcitonin, estrogen, glucocorticoids

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31
Q

What is the major hormone for calcium homeostasis?

A

PTH

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32
Q

PTH physiology

A

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

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33
Q

PTH in relation to calcium & phosphate

A

Increases serum calcium & decreases serum phosphate (reduces proximal tubular re-absorption of phosphate)

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34
Q

Calcitonin physiology

A

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+

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35
Q

Vit D physiology

A

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

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36
Q

Main endocrine function that occurs at menopause

A

Loss of secretion of estrogen & progesterone from the ovaries

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37
Q

What is the major source of estrogen in post-menopausal women?

A

Estrone (created in fat cells)

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38
Q

Why can bone mass decrease in elderly men?

A

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

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39
Q

Hyperprolactinemia causing osteoporosis

A

Failure of the gonadal axis –> substantial loss in bone

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40
Q

Other sex hormone factors causing osteoporosis

A
  • 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
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41
Q

What heavily influences bone growth & remodeling?

A

Rate of change in strain

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42
Q

What happens to bone in the normal aging process?

A

Deficit between resorption & formation because osteoblastic activity lags compared to osteoclastic –> bone loss during each cycle of remodeling

Activation is decreased –> low turnover osteoporosis

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43
Q

What happens to Vit D levels as people age?

A

Decreases by about 50% in both men & women

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44
Q

Growth hormone production during aging process

A

Decreases

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45
Q

Growth hormone & osteoporosis

A

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

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46
Q

Vit K therapy in elderly a/w decrease in rate of bone resorption as demonstrated by this urine marker

A

Hydroxyproline

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47
Q

Are plasma calcitonin levels higher in men or women?

A

Men (levels do not change with age)

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48
Q

Do thyroid levels change with age?

A

No, but if they do, it is a slight decrease

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49
Q

Does PTH change with age?

A

Increases, probably because of mild hypocalcemia & decreased active Vit D

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50
Q

Why does active Vit D decrease with age?

A

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

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51
Q

Recommended dose of calcium & Vit D in estrogen-deficient women

A

Calcium: 1,500 mg/day
Vit D: 800 IU/day

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52
Q

Can osteoporotic vertebral fractures go unnoticed?

A

Yes, often found incidentally on CXR

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53
Q

Most common areas for osteoporotic fractures

A

Mid-thoracic (T7/8) & upper lumbar spine (L1/2), proximal femur (hip), distal forearm (Colles)

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54
Q

Highest incidence for osteoporotic fractures

A

White women

Female: male-
Vertebral fx- 7:1
Hip fx- 2:1
Colles- 5:1

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55
Q

Which fracture site is of greatest concern clinically?

A

Hip fx –> risk of death is 15-20%

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56
Q

Management of osteoporotic spine fracture

A

Immobilization of the involved vertebral bodies & analgesia (these fractures heal by becoming more condensed)

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57
Q

What should you look for if there is non-union in appendicular fractures?

A

Osteomalacia or hyperparathyroidism

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58
Q

How to typically manage proximal humerus (surgical neck) fracture in osteoporosis

A

Conservative, typically

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59
Q

How long can a compression fracture appear normal on XR?

A

Up to 4 weeks. You need to lose 25-30% of BMD for it to be picked up on XR

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60
Q

How can vertebral fractures from osteoporosis cause chronic pain?

A

Spinal deformity –> kyphotic postural change

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61
Q

Management of acute pain in patients with osteoporosis

A

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

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62
Q

What can increase the possibility of compressing vertebrae in the fragile osteoporotic spine?

A

Disproportionate weakness in back extensor musculature relative to body weight or spinal flexion strength

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63
Q

Why is development of kyphotic posture bad?

A

Can lead to postural back pain & predispose to falls

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64
Q

What can spinal pain related to osteoporosis be from?

A

Caused by deformity from vertebral wedging & compression, as well as by secondary ligamentous strain

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65
Q

What happens to inter-vertebral disks as we age?

A

Increase in number & diameter of collagen fibrils in the disk –> progressive decrease in disk resilience –> loss of distinction between nucleus pulposus & annulus fibrosis

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66
Q

Therapy for chronic back pain 2/2 osteoporosis

A

Back extensor resistance training –> studies show less amount of vertebral fractures long-term compared to controls with osteoporosis

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67
Q

What else can chronic pain in back from osteoporosis be from?

A

Micro-fractures, only visible on bone scan

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68
Q

What position is recommended for back strengthening exercise in osteoporosis?

A

Prone –> improves horizontal trabecular connections; needs to be progressive, resistive, & non-loading to avoid vertebral compression fracture

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69
Q

Vertebroplasty & kyphoplasty

A

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

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70
Q

Why does kyphotic posture lead to instability?

A

Places center of gravity closer to limit of stability

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71
Q

What are two general types of hip fracture?

A

Intra-capsular (femoral neck) or extra-capsular (trochanteric)

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72
Q

Which hip fracture has a high surgical failure rate?

A

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)

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73
Q

Operative treatment choice for trochanteric fracture

A

Internal fixation

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74
Q

When do patients get a NWB status after hip fracture?

A

Severely comminuted or fractures where the operative result was non-satisfactory

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75
Q

Hip pads for fracture ppx

A

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

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76
Q

Sacral insufficiency fractures

A

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

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77
Q

Who should be getting a BMD evaluation?

A

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

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78
Q

When should follow-up BMD testing be done?

A

After 2 years or longer, depending on baseline T-score & patient risk factors

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79
Q

Bone markers

A

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

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80
Q

Evaluation studies for osteoporosis

A
  • 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
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81
Q

Radiographic findings of osteoporosis

A

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

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82
Q

What is the degree of wedging that indicates a true fracture?

A

15-25% reduction in anterior height relative to posterior height of the same vertebra

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83
Q

Other morphological change in osteoporosis

A

Bioconcavity of vertebral bodies

84
Q

Definition of complete compression fracture

A

Reduction in both anterior & posterior heights by at least 25% c/w adjacent normal vertebrae

85
Q

Available methods to evaluate bone mass

A
  • 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
86
Q

Specialties who should be on board with osteoporosis

A

Endocrinology, PM&R, pharmacology, psychology, nutrition

87
Q

SPEED program for osteoporosis

A

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

88
Q

Suggested Rehab for osteopenia

A

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

89
Q

Suggested rehab for osteoporosis

A

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

90
Q

High-impact bone-loading sports that have high rates/magnitudes of bone strain leading to site-specific increases in BMD

A

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

91
Q

Minimum effective strain stimulus theory

A

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

92
Q

High-impact exercises for people with normal BMD

A

Aerobics, jogging, skiing

93
Q

Non-straining exercises for people with osteoporosis

A

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

94
Q

What type of exercise program can improve bone mass in inactive individuals?

A

Supervised, non-strenuous, progressive, & resistive

95
Q

Most effective back-strengthening exercise

A

Progressive, resisted back extension

96
Q

What exercise should be added to complement a posture training exercise program?

A

Isometric abdominal muscle-strengthening

97
Q

What exercises are used to reduce kyphotic posture?

A

Pectoral & shoulder extensor stretching

98
Q

Exercises good for CV fitness that are not harmful in osteoporosis (although don’t improve BMD)

A

Swimming or short periods of stationary biking

99
Q

Postural issues in osteoporosis

A

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

100
Q

What intervention can provide re-education of the paraspinal muscles for improvement in kyphotic posturing & reduce risk of falls?

A

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

101
Q

What does a weight kypo-orthosis (WKO) do?

A

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)

102
Q

Pharmacotherapy for improving bone mass

A

Efficacious in prevention of skeletal deformities but must also be in conjunction with rehabilitation

103
Q

Best osteoporosis prevention

A

Improving back strength & peak bone mass before 30 years old & reducing bone loss thereafter

104
Q

Most common osteoporosis pharmacologic treatments

A

Calcium, Vit D, & bisphosphonates

105
Q

Anti-resorptive agents in osteoporosis

A

Estrogens, androgens, calcitonin, & bisphosphonates

106
Q

Osteoblast-stimulator agents in osteoporosis

A

Fluoride & PTH (fluoride is not approved by US FDA because of increased risk of appendicular fractures)

107
Q

PTH (1-34) analogs for treatment of osteoporosis

A

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

108
Q

Side effect of bisphosphonates

A

Osteonecrosis of jaw

109
Q

Lifestyle modification for osteoporosis

A

Cessation of tobacco & alcohol abuse

110
Q

Recommendations for women with estrogen deficiency

A

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)

111
Q

When treating women with an intact uterus, what medication should you also provide?

A

Progesterone (to prevent endometrial hyperplasia & possibly endometrial carcinoma

112
Q

Contraindication to estrogen replacement therapy

A

Liver or GB disease, recent h/o throboembolism or thrombophlebitis, & suspected breast or endometrial carcinoma

113
Q

Adverse effects of progestin administration

A

Fatigue, depression, breast tenderness, bloating, menstrual cramps, HA, weight gain, increased serum TG, increased serum BG, & abdnormal vaginal bleeding

114
Q

Is estrogen replacement therapy indicated to prevent osteoporosis?

A

No

115
Q

Why is calcitonin (works as anti-resorptive agent by inhibiting osteoclasts) limited in use in osteoporosis?

A

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

116
Q

Where do bisphosphonates work?

A

Trabecular bone, especially lumbar spine –> can see BMD increases of 5-10% during first 2 years of treatment

117
Q

Taking bisphosphonates for osteoporosis

A

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

118
Q

What is a potential adverse effect of oral bisphosphonates?

A

Esophageal irritation, especially in patients with GERD or other esophageal dysfunction

119
Q

Thiazide diuretics & osteoporosis

A

Inhibit urinary calcium excretion of calcium & can slow bone loss & reduce rate of fractures in patients with osteoporosis

120
Q

Sodium fluoride in treatment of osteoporosis

A

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

121
Q

Estrogen receptor mixed agonist-antagonists (Tamoxifen & Raloxifene) in treatment of osteoporosis (AKA SERMs- selective estrogen receptor modulators)

A

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

122
Q

Treatment of osteoporosis in men

A

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

123
Q

Management of steroid-induced osteoporosis

A

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

124
Q

Brand names of common osteoporosis medications

A

Alendronate: Fosamax, Binosto

Risendronate: Actonel, Atelvia

Calcitonin: Miacalcin (used also for Paget disease of bone)

125
Q

Appropriate medical equipment for a marathon

A

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

126
Q

Body’s adaption to physical training

A

Metabolically & neuromuscularly specific to the exercise performed

127
Q

Sport specificity

A

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

128
Q

Periodization

A

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

129
Q

How long are periods in periodization?

A

Macrocycles (usually about a year) divided into shorter mesocycles (1 month) & then sub-divided into microcycles (1 week)

129
Q

Typical year-long training program with periodization

A

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

130
Q

Most efficient strategy to maximize performance gains

A

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

131
Q

Overtraining syndrome

A

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

132
Q

Treatment for overtraining syndrome

A

Rest for weeks-months with gradual resumption of training. Prevention is the best treatment & recommended to follow a formal periodized training program

133
Q

Altitude tents

A

Simulate living at high altitude for athletes attempting to train in these environments (like mountainous regions).

134
Q

Proposed mechanism for primary physiologic effects responsible for effect of altitude training on sea-level performance

A

Accelerated erythropoiesis, improved muscle efficiency at the mitochondrial level, glucose transport alterations, enhanced muscle-buffering capacity via pH regulation

135
Q

Most effective form of altitude/hypoxic training

A

Live-high train-low method –> training low means training at higher intensity with improved O2 influx to induce beneficial metabolic & neuromuscular training adaptations

136
Q

Optimal dose of altitude training

A

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

137
Q

Kinetic chain model

A

Each complex, athletic movement is the summation of its constituent parts

138
Q

“Catch-up” in kinetic chain model

A

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

139
Q

Tissue diagnosis: Biomechanical diagnosis

A

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

140
Q

How many injury phases are there?

A

4

141
Q

First phase of injury

A

Initial injury + inflammation, edema, & pain. This phase is usually short (days)

142
Q

Reparative phase of injured tissue

A

Might last 6-8 weeks –> cell proliferation, granulation tissue formation, neovascularization

143
Q

Last phase of injured tissue

A

Remodeling –> occurs as tissue matures & realigns. Can experience excessive scar tissue formation that leads to chronic/recurrent injury

144
Q

Return to Play phases (3)

A

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

145
Q

When can an athlete advance to final stage of return to play (functional)?

A

Once pain-free ROM is achieved & strength is 75-80% or greater when compared to non-injured side

146
Q

Kinetic chain when throwing ball

A

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

147
Q

Where does velocity from a pitch come from?

A

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

148
Q

Six phases of throwing a pitch

A
  1. Wind-up (start to hands apart)
  2. Early cocking (hands apart to lead foot down)
  3. Late cocking (foot down to maximum external rotation)
  4. Acceleration (maximum external rotation to ball release)
  5. Deceleration (early ball release)
  6. Follow-through (late ball release)
149
Q

Other name for early cocking

A

Stride phase

150
Q

Early cocking (stride phase)

A

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

151
Q

Late cocking

A

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

152
Q

When do most injuries occur when throwing a ball?

A

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

153
Q

Common injuries in late cocking phase of pitching

A
  • Anterior instability
  • Internal (posterior-superior) impingement
  • Type II SLAP lesion
  • Articular surface RTC tears
  • Bicipital tendinopathy
  • Medial tension injuries at elbow (UCL injury)
154
Q

Motion of shoulder during acceleration phase

A

Shoulder is powerfully internally rotated from 175 degrees of ER to 90-100 degrees ER at ball release

155
Q

What determines what position the arm is relative to vertical plane when throwing a ball in acceleration phase?

A

Trunk lateral flexion

156
Q

Trunk lateral flexion in “over the top” vs “sidearm” throwers

A

Over the top: greater contralateral trunk flexion

Sidearm: less contralateral trunk flexion

157
Q

What is “dropped elbow” when throwing?

A

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

158
Q

What is another injury that can occur during acceleration phase of throwing?

A

Sub-acromial impingement as arm internally rotates & adducts the abducted arm

159
Q

Deceleration phase of throwing

A

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)

160
Q

Follow-through phase of throwing

A

Passive phase- low grade eccentric loading of shoulder musculature & therefore little risk of injury

161
Q

What is the max amount of time young pitchers should be competing in baseball in a calendar year?

A

9 months

In other 3 months, should not participate in overhead sports

162
Q

Age-based pitch counts

A

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

163
Q

Differences in walking vs running gait cycle

A
  • 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
164
Q

First phase of swim stroke (common to freestyle, backstroke, & butterfly)

A

Entry/catch –> hand entry into water until beginning of its backward movement

165
Q

Propulsive phase of swimming

A

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

166
Q

Final phase of swimming

A

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

167
Q

Kick patterns in swimming

A

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)

168
Q

Why does shoulder pain happen to swimmers?

A

Impingement/RTC tendinopathy due to dynamic muscle imbalances, weakness, & biomechanical faults

169
Q

Major tenet of shoulder rehab for the swimmer

A

Scapular stabilization with focus on endurance training of serratus anterior (active throughout swim cycle) & lower trapezius, stretching internal rotatiors & posterior capsule, cervical/thoracic mobilization

170
Q

Jumping/landing injury in sport

A

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

171
Q

Tylenol in sport

A

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

172
Q

Corticosteroids prohibited by WADA

A

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)

173
Q

Diuretics & sport

A

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)

174
Q

BB in sport

A

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

175
Q

Diabetes meds in sport

A

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

176
Q

Asthma drugs in sport

A

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)

177
Q

Anabolic steroids general effects

A
  1. By binding androgen receptors, they stimulate mRNA synthesis, increasing structural & contractile protein synthesis & produce an anabolic state
  2. Anti-catabolic via competitive inhibition of the glucocorticoid receptor, inhibiting the catabolic effects of cortisol, preserving muscle mass
  3. Emotional effects, pushing athletes to train more intensely & more often
178
Q

Negative effects of anabolic steroids

A

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

179
Q

Anabolic Steroid Control Act of 1990

A

Prohibited use of steroids for any use other than disease treatment –> Schedule III drugs within the Controlled Substances Act

180
Q

EPO & Blood Doping

A

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

181
Q

Pseudoephedrine (Sudafed)

A

Commonly used stimulant. Mixed results in studies if it gives advantage in sport

182
Q

Herbals: ephedra, ma huang

A

similar structural properties & physiologic effects to Sudafed. Ephedra containing products were taken off market in 2004. Banned by NCAA, IOC

183
Q

Caffeine

A

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

184
Q

What is a supplement?

A

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

185
Q

Creatine

A

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

186
Q

Illegal drugs

A

Testosterone (unless prescribed for diseased state), androstenedione, HGH (unless prescribed for disease state)

187
Q

PPE goals

A

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

188
Q

Look up standard (present day) for PPE exam

A

Cardiovascular (EKG?, TTE?)
Hearing, vision?
Etc

189
Q

Can a physician performing PPE be found liable?

A

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

190
Q

Emergency action plan (EAP)

A

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

191
Q

Leading cause of death in young athletes

A

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

192
Q

Helmets in football

A

Decreased incidence of ICH but increased C-spine injury

193
Q

Most common cause of collapse in marathon runner

A

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

194
Q

Ddx of exercise-associated collapse

A
  • Benign exercise-associated collapse
  • Cardiac arrest
  • Heat-related illness (heat exhaustion, heat stroke)
  • Hypoglycemia
  • Hyponatremia
  • Hypothermia
  • Muscle cramps
  • Other medical/neurologic conditions
195
Q

Exercise-associated hyponatremia

A

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

196
Q

Heat-related illness as cause of exercise-associated collapse

A

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

197
Q

Stinger (burner)

A

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.

198
Q

Exercise-induced bronchospasm

A

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)

199
Q

Anemia in athlete

A

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

200
Q

Women with athletic amenorrhea

A

P/w reduction in LH pulse frequencies, which depend on EA

201
Q

When is peak bone mass achieved?

A

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

202
Q

Estrogen

A

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

203
Q

When do children lose the most flexibility?

A

Puberty, due to muscle-tendon imbalances that occur with rapid growth

204
Q

Pediatric growth plate

A

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

205
Q

Salter Harris classifications

A

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

206
Q

Management based on Salter Harris

A

I & II: closed reduction, casting, or splinting

III & IV: ORIF

V: emergent ortho; germinal matrix may be involved which can lead to growth arrest

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