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Medical Nutrition Therapy II > Chapter 25 Diseases of the Musculoskeletal System) > Flashcards

Chapter 25 Diseases of the Musculoskeletal System) Flashcards

Diseases of the Musculoskeletal System

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USMLE® Step 1 flashcards
1
Q

What are metabolically active cells and tissue that are reserved for calcium and phosphorus?

A
  • cartilage, ligaments, tendons, bones

- which, are in a continual state of change

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2
Q

What are osseous tissue?

A
  • bone (inorganic and organic)
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3
Q

What is inorganic osseous tissue?

A
  • hydroxyapatite (component of bone tissue, crystallite)

- stiffness, weight bearing

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4
Q

What is organic osseous tissue?

A
  • mainly collagen

- flexibility

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5
Q

What are the two calcium reserves that bone provide?

A
  • Hydroxyapatite (99%): massive, but less readily accessible

- 1% readily available pool, which is in our blood

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6
Q

What are the bone abnormalities in serum calcium critical?

A
  • hypocalcemia (excessive excitability of the nervous system, tetany, respiratory arrest, convulsions)
  • hypercalcemia (fatigue, depression, mental confusion, anorexia, nausea, vomiting, constipation, hypercalciuria)
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7
Q

What are the four types of cells found in osseous tissue?

A
  • osteogenic cells
  • osteoblasts
  • osteocytes
  • osteoclasts
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8
Q

What are osteogenic cells?

A
  • stem cells that differentiate into osteoblasts
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9
Q

What are osteoblasts?

A
  • bone building cells

- lay down new bone in high stress areas

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10
Q

What are osteocytes?

A
  • mature osteoblasts, majority of cells in bone
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11
Q

What are osteoclasts?

A
  • bone removing cells that secrete HCL to dissolve mineral component of bone matrix; bone resorption; regulate bone levels
  • remove bone from low stress areas
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12
Q

What is skeletal growth and developement?

A
  • continual state of change; linear and circumferential growth, remodeling
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13
Q

What is cortical bone?

A
  • dense, outer surface of most bones
  • shafts of long bones
  • caps over end of long bones
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14
Q

What is trabecular bone?

A
  • loosely organized with a sponge-like apperance; lattice like pattern
  • found at the “ends” of long bones, primary bone of vertebrae, pelvis, sternum, scapula
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15
Q

What keeps calcium and phosphorous at homeostasis in the hormonal control of bone metabolism?

A
  • cortisol (steroid hormone for break down of bone), growth hormone, thyroid hormones
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16
Q

What are the primary regulators for calcium and phosphorous homeostasis?

A
  • parathyroid hormone (PTH)
  • calcitonin
  • vitamin D
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17
Q

What does the parathyroid hormone (PTH) do in the hormonal control of bone metabolism?

A
  • increases blood calcium when low
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18
Q

How does the parathyroid hormone (PTH) increase the blood calcium when low in the hormonal control of bone metabolism?

A
  • increase in osteoclasts, and bone resorption
  • inhibition of collagen synthesis, and bone deposition
  • calcium resorption by kidneys
  • needs help in final step from vitamin D, enhancing intestinal absorption of calcium
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19
Q

What does calcitonin do in hormonal control of bone metabolism?

A
  • decreases blood calcium when high
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20
Q

How does calcitonin decrease blood calcium when high?

A
  • inhibits activity of osteoclasts
  • stimulates osteoblasts
  • reducing renal reabsorption of calcium and phosphate
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21
Q

What does vitamin D do for the hormonal control of bone metabolism?

A
  • increases blood concentrations of calcium and phosphorous
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22
Q

How does vitamin D increase blood concentration of calcium and phosphorous in hormonal control of bone metabolism?

A
  • promotes their absorption in GI
  • promotes reabsorption by kidneys
  • stimulates osteoclast formation and release of calcium and phosphorous from bone
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23
Q

What are the two types of Vitamin D?

A
  • ergocalciferol (vit. D2) - dietary (fatty fish, milk, fortified foods, cereal, mushrooms)
  • cholecalciferol (vit. D3) - dietary and exposure to sunlight
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24
Q

Both ergocalciferol and cholecalciferol are biologically inactive until?

A
  • modified by liver and kidney to 1-25 dihydroxyvitamin D
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25
Q

What is osteoporosis?

A
  • decreased bone mineral and organic matrix which weakens bones, making them more susceptible to fracture and pain
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26
Q

What does bone strength reflect?

A
  • bone density (measured by dexascan)

- bone quality (harder to measure; by fractures)

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27
Q

True or False? Hip fractures increases mortality and morbidity among persons 65 yrs. of age or older.

A
  • True
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28
Q

When does bone mineral density (BMD) rapidly increase?

A
  • during the growth spurt (ages 11 - 14)
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29
Q

When does bone mineral density reach its max?

A
  • in late 20’s and 30’s

- has to maintain from here

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30
Q

Who loses bone mineral density faster, men or women?

A
  • women

- rate of loss increases during menopause

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31
Q

What are the primary etiology of osteoporosis?

A
  • disease of elderly
  • cumulative impact of bone mineral loss
  • deterioration of bone with age
  • “age related”, “postmenopausal”
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32
Q

What are the secondary etiology of osteoporosis?

A
  • due to other diseases

- associated with drugs (2/3 cases of men)

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33
Q

What is kyphosis?

A
  • unnatural curvature of back

- loss of height due to compression fractures of spine

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34
Q

What are the most common sites of fractures due to osteoporosis?

A
  • hip, spine, wrist

- hip fractures have severe impact on morbidity and mortality (20% die within first year; 20% end up in nursing homes

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35
Q

What are the nutritional risk factors for osteoporosis?

A
  • calcium
  • vitamin D
  • phosphorous, protein, sodium, caffeine, fluoride, and trace minerals
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36
Q

What maintains serum calcium levels to combat bone resorption?

A
  • calcium
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37
Q

What helps achieve peak bone mass and minimize bone mineral loss?

A
  • calcium
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38
Q

Lower intakes of animal protein, sodium, and caffeine helps prevent?

A
  • osteoporosis
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39
Q

Increased consumption of what helps prevent osteoporosis?

A
  • fruits, vegetables, legumes, and whole grains
  • more physical activity
  • 10-15 mins./day sun exposure
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40
Q

How would you increase your calcium levels?

A
  • consume calcium rich foods (dairy, bread, cereal, salmon w/ bone, OJ)
  • calcium fortified foods
  • calcium supplements (calcium carbonate, calcium citrate, calcium with vit. D)
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41
Q

How much calcium can the body absorb at once?

A
  • 500mg
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42
Q

Overt deficiency of vitamin D causes what?

A
  • rickets in children

- osteomalacia in adults (insufficiency found in dark skin, older, in northern latitudes

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43
Q

What is essential for bone formation, but Americans get too much of?

A
  • phosphorus
  • found in a lot of animal meats
  • found in soft drinks, which can contribute to bone loss
44
Q

What interferes with Ca+ absorption and cause bone loss?

A
  • caffeine and phytates (food components found in spinach, beans, and wheat bran)
  • more than 3 cups/day (24oz) of coffee
45
Q

Calcium can’t be absorbed well from foods high in what?

A
  • oxalates (found in spinach, rhubarb, beet greens, and some beans
46
Q

What increases urinary calcium losses?

A
  • high protein or sodium
47
Q

What foods/minerals are associated with higher bone mineral density?

A
  • potassium, magnesium, fruits, and vegetables
48
Q

Cigarette smoking is causally related to what when talking about osteoporosis?

A
  • lower bone density
  • increased bone mineral loss
  • increased risk of fracture in males and females
49
Q

What is toxic to osteoblasts?

A
  • nicotine and cadmium
50
Q

Nicotine reduces and lowers what, when talking about osteoporosis?

A
  • reduces intestinal calcium absorption

- lowers intake of vitamin D, and lower serum vitamin D

51
Q

What kind of physical activity improves osteoporosis?

A
  • weight bearing

- impact type

52
Q

Osteoporosis is commonly found in who?

A
  • chronic alcoholism
53
Q

Moderate alcohol consumption may increase what and reduce what only in women?

A
  • increase BMD

- reduce bone mineral loss

54
Q

What adversely impacts vitamin D and overall nutritional status?

A
  • alcohol
55
Q

What increases calcium and magnesium losses?

A
  • alcohol
56
Q

What are the pathophysiology of osteoporosis?

A
  • failure to build bone and reach peak bone mass as a young adult. (late 20’s N 30’s)
  • bone loss later in life (modifiable N unmodifiable risk factors)
57
Q

What accounts for up to 80% of the variance in peak bone mass?

A
  • genetics

- RANK/RANKL/OPG signaling pathway is essential for development of osteoclasts.

58
Q

How would you conclude osteoporosis as the medical diagnosis?

A
  • measure bone density (w/ DXA scan)
  • occurrence of adulthood hip or vertebral fracture in absence of trauma
  • quantitative ultrasound of the heel (in conjunction w/ risk assessment
  • PQCT
59
Q

How is bone mineral density (BMD) measured?

A
  • DXA (dual-energy x-ray absorptiometry
  • “T-score” (comparing patients BMD to healthy young reference population
  • at hip and lumbar spine
  • see WHO criteria
60
Q

What is osteopenia?

A
  • low bone mineral density, but, not low enough to be classified as osteoporosis, although fracture risk is increased
61
Q

What is the treatment for osteoporosis?

A
  • adequate intake of calcium and vitamin D
  • physical activity and fall prevention (weight bearing exercise)
  • smoking cessation
  • avoidance of excessive alcohol intake
  • depends on disease or problem to asses and treat
62
Q

What are the medical management of osteoporosis?

A
  • risk factor modification
  • dietary treatment
  • drug therapy (to prevent further loss)
63
Q

What is the normal value of serum calcium?

A
  • 9-10.5 mg/dL (does not reflect dietary intake)
64
Q

What is the formula to “correct” calcium levels if low albumin?

A
  • (normal alb. - observed alb.) x 0.8 + serum calcium =

- use 4.0 for normal albumin

65
Q

what are the pharmacologic prevention and treatment for osteoporosis?

A
  • estrogens/hormone therapy (can cause breast cancer)
  • selective estrogen receptor modulators (SERMs)
  • bisphosphonates (tells osteoclasts to stop)
  • teriparatide (synthetic PTH)
  • drug-nutrient interactions
66
Q

What is the nutritional diagnosis for osteoporosis?

A
  • inadequate vit. D and/or calcium intake
  • physical inactivity
  • food and nutrition related knowledge deficit
  • altered GI functions (ex. celiac)
  • predicted food-medication interaction
  • malnutrition
  • excessive alcohol intake
67
Q

what is the nutrition intervention for osteoporosis?

A
  • depends on etiology of nutrition diagnosis
  • includes educational component
  • may include referral to smoking/alcohol cessation program
  • calcium supplements
68
Q

how would you monitor and evaluate the nutrition intervention of osteoporosis?

A
  • reassessment of calcium and vitamin D intakes
  • tolerance or consistency to supplements
  • 25 (OH) vitamin D3 labs
  • amount and type of exercise
69
Q

What is Paget disease?

A
  • localized, progressive, crippling disorder of bone remodeling d/t overactive osteoclasts and bone resorption followed by rapid formation of new bone which is structurally inferior
70
Q

What is Paget disease caused by?

A
  • genetics and viral factors
71
Q

what results from the Paget disease?

A
  • bowing, deformity, fracture, poor healing
72
Q

where in the body is the Paget disease most affecting?

A
  • upper femur, pelvis vertebral bodies, skull, tibia
73
Q

which nutrients are most important to take in if you have Paget disease?

A
  • vitamin D and calcium
74
Q

What is rickets?

A
  • kinda like osteoporosis in children

- inadequate maturation and mineralization of bone d/t vitamin D deficiency

75
Q

when is rickets first seen in a child?

A
  • about 36 months or when the child starts to walk
76
Q

what are the symptoms of rickets?

A
  • lethargy
  • weakness
  • growth stunting
  • enlargement of ends of long bones and ribs
  • abnormally shaped thorax
  • bowing of legs
77
Q

what are the risk factors for rickets?

A
  • maternal vit D deficiency
  • prolonged breastfeeding without vit D supplementation
  • living in a temperate climate
  • lack of sunshine
  • dark skin pigmentation
  • calcium deficiency
  • intake of phytates from diets high in unrefined grains
78
Q

How can you prevent rickets?

A
  • exclusively breast fed infants should receive supplement of 400 IU vit D
  • fortified infant formulas (if fed <500ml/day, take multivitamin)
  • after one year switch to vit D fortified cows milk
79
Q

what is the treatment for rickets?

A
  • balanced age-appropriate diet
  • adequate vit D, calcium, phosphorus
  • posture
80
Q

what is Osteomalacia?

A
  • adult form of rickets

- organic matrix of bones inadequately mineralized in adults

81
Q

what results from Osteomalacia?

A
  • muscular weakness
  • bone pain
  • deformities of ribs, pelvis, legs
82
Q

what is the etiology of Osteomalacia?

A
  • due to vit D deficiency
  • impaired D action
  • calcium deficiency
  • hypophosphatemia
83
Q

what is the treatment for Osteomalacia and rickets?

A
  • address underlying cause
  • multivitamin supplementation
  • calcium supplementation
  • pharmacological doses of vit D
84
Q

where in the body does arthritic conditions affect?

A
  • affect joints
  • tissues surrounding joints
  • connective tissues
85
Q

name some common arthritic conditions?

A
  • Osteoarthritis
  • Rheumatoid arthritis
  • Gout (affects all ages)
86
Q

Who are affected with arthritic conditions?

A
  • one in five Americans

- one in four reports activity limitations

87
Q

what are the modifiable and non-modifiable risk factors for arthritic conditions?

A

modifiable: overweight (most common), joint injuries, infections
non-modifiable: family history, female sex, age

88
Q

what is Osteoarthritis?

A
  • disease process involving all structures of the joint
  • loss of load-bearing articular cartilage
  • inflammation
  • joint pain, stiffness, limited movement
  • wasting of periarticular muscles
  • joint instability and deformity
89
Q

what are the major risk factors of osteoarthritis?

A
  • age
  • female sex
  • family history
  • major trauma to joint or soft tissue
  • repetitive joint stress related to occupation
  • obesity
90
Q

what are the treatments for osteoarthritis?

A
  • reduce joint inflammation, pain, maintain mobility, minimize disability
  • improve body posture
  • proper footwear
  • weight reduction
  • periodic rest of affected joint
  • heat and cold compresses
  • physical activity/therapeutic exercise
  • drug therapy - pain relief (NSAIDs, Glucosamine, Chondroitin)
91
Q

What is Rheumatoid arthritis?

A
  • chronic inflammatory disease
92
Q

what gets inflamed when dealing with rheumatoid arthritis?

A
  • synovial membrane
93
Q

what results from the synovial membrane inflammation in rheumatoid arthritis?

A
  • swelling, stiffness, pain, limited range of motion, joint deformity, disability
  • periods of exacerbation and remission
  • autoimmune response
94
Q

which part of the body is rheumatoid arthritis most affects?

A
  • joints of hands, wrists, knees, feet
95
Q

When inflammation results in thickening of the synovial membrane, it is called?

A
  • Pannus
96
Q

why is pannus, thickening of synovial membrane, bad?

A
  • enzymes from pannus digest adjacent bone and cartilage
97
Q

what is the treatment for rheumatoid arthritis?

A
  • reduce pain and inflammation
  • protect joint
  • maintain function
  • control systemic infections
  • pharmacological agents: NSAIDs, glucocorticoids, immunosuppressives, DMARDs
98
Q

what is the nutritional intervention for rheumatoid arthritis?

A
  • increase consumption of fruits and vegetables/antioxidants
  • include sources of EPA and DHA (fish oils) (omega-3)
  • fish oil supplementation
  • exclusion of red meats, dairy, cereals, wheat gluten
  • evaluate and test for food allergy
99
Q

What is Gout, arthritic condition?

A
  • inflammatory disease resulting in swelling, redness, heat, pain, and stiffness in affected joint
100
Q

what is the most painful arthritic condition?

A
  • Gout

- most common in men

101
Q

what is the etiology of Gout?

A
  • elevated serum concentrations of uric acid, formation of uric acid crystals
102
Q

what is hyperuricemia?

A
  • high levels of serum uric acid
103
Q

what causes elevation of serum uric acid, hyperuricemia?

A
  • results from overproduction of uric acid
  • inadequate elimination of uric acid by the kidneys
  • or combination of both
104
Q

what is the clinical manifestation of Gout?

A
  • symptoms usually develop rapidly, resulting is sudden, severe joint pain and swelling along with shiny, red skin and extreme tenderness around joint
  • typically resolves in 5-10 days, may reoccur
105
Q

what would acute attacks of Gout be from?

A
  • excessive exercise
  • certain medications; aspirin, diuretics, nicotinic acid, cyclosporine, levodopa
  • purine rich foods (anchovies, sardines, fish roe, organ meats, nutritional yeast)
  • excessive alcohol consumption
  • crash dieting
106
Q

what is the treatment of Gout?

A
  • NSAIDs, glucocorticoids, colchicine (anti-inflammatory)
  • treat uricemia
  • lifestyle modifications

Medical Nutrition Therapy II (2 decks)

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