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Pathophysiology > Disorders of the Skeletal System > Flashcards

Disorders of the Skeletal System Flashcards

1
Q

What cells are the cells of origin for osteoclasts?

A

macrophages fuse together to form osteoclasts.

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2
Q

Which cells express RANKL and OPG? Which express RANK?

A
  • RANKL on osteochondroprogenitor cells (can turn into osteoblasts)
  • Osteoclast precursor cells
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3
Q

Discuss how the bone multicellular unit (BMU) is regulated by RANK, RANKL, and OPG levels

A

If RANKL and RANK bind, osteoclasts will increase bone break. OPG can block RANKL from binding to RANK. OPG produced by osteoblasts and osteochondroprogenitor cells.

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4
Q

How do hormones like estrogen, testosterone, glucocorticoids (e.g., cortisol), and PTH influence the production of OPG and the expression of RANKL?

A
  • Estrogen: Increase OPG production and decreased RANKL expression
  • Testosterone: Increase OPG production and decreased RANKL expression
  • Glucocorticoids: decreased OPG and increased expression of RANKL
  • PTH: decreased OPG and increased expression RANKL
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5
Q

What is the difference between osteopenia and osteoporosis?

A
  • Osteopenia: less common and precursor for osteoporosis (BMD: 1-2.5 standard deviations below adult)
  • Osteoporosis: loss of both bone mineral and bone matrix material (BMD: greater than 2.5 standard deviations below adults)
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6
Q

Is there a decrease in the organic bone matrix, in the mineral content of bone, or in both with osteoporosis?

A

Both

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7
Q

What is a T-score? What T-score values suggest osteoporosis and osteopenia?

A

T-score is the number of standard deviations that a value falls relative to the normal curve for a 30 year old.
Osteopenia: -1
Osteoporosis: -2.5

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8
Q

How do age, genetics, race, body size, and hormone factors play a role in the risk for the development of osteoporosis

A

Age: decrease osteoblast activity
Genetics:
Race: white and Asian people increase risk`
Body size: weight bearing exercises increases osteoblast activity.
Hormones: lower sex hormones, menopause decreases hormones=increase osteoclasts

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9
Q

Secondary osteoporosis

A

Endocrine disorders: Cushing’s disease, hyperthyroidism, hyperparathyroidism
Malabsorption: calcium/vitamin D deficiency, high-protein diets (cannot absorb calcium)
Alcoholism: increase reuptake inhibits osteoblasts and calcium absorption
Multiple Myeloma:
Medications: Antacids containing aluminum, anticonvulsants

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10
Q

Describe the female athlete triad and how it can increase the risk for premature osteoporosis.

A
  1. Patterns of disordered eating and extreme exercise
  2. Nutritional deficits that lead to menstrual dysfunction
  3. Lowered sex hormones that lead to decreased bone density
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11
Q

Tx for Osteoporosis

A

Denosumab: RANKL inhibitor
Teriparatide: Recombinant PTH-> activates osteoblasts
Calcitonin: increase osteoblast activity
Raloxifene: selective estrogen receptor modifiers
Alendronate: bisphosphonate which kills osteoclasts when they eat it

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12
Q

How can Thiazide diuretics sometimes be used to increase blood calcium

A

Blocks Na+/Cl- symporters on DCT. This lowers Na+ intracellularly, therefore increasing the want therefore increasing activity for Na+/Ca++ pump, therefore pumping out calcium into the blood while pumping sodium into the cell.

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13
Q

Why might a Thiazide be used to reduce the risk of calcium-containing kidney stone formation?

A

Because they help with the reabsorption of calcium.

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14
Q

Where are the most common location for fractures associated with osteoporosis? What is a Dowager hump?

A
  • humerus, distal radius and the neck of the femur
  • abnormal curvature of the spine caused by compression of the anterior vertebral bodies causing it to collapse and protrude posteriorly
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15
Q

What two methods are used to diagnose osteoporosis?

A
  • BMD assessment using energy x-ray absorptiometry (DEXA)

- checking of the patient’s height to see if it has changed

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16
Q

Difference between Osteomalacia and Rickets

A
  • Osteomalacia: inadequate mineralization of the bone. More collagen than hydroxyapatite / calcium phosphate
  • Rickets: bone softening in the growing bones of children
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17
Q

Describe what vitamin D is and how it is synthesized

A

7-dehydrocholesterol is produced and altered by UVB radiation from the sun. C-C bond is broken creating Vitamin D3 (cholecalciferol). This travels to the liver where it becomes 25-hydroxyvitamin D. This travels to the kidney where it becomes 1,25 dihydroxyvitamin D. This is the active form of vitamin D

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18
Q

What does Vitamin D do in the body?

A
  • absorbs calcium
  • stimulates absorption of phosphate and magnesium
  • facilitates production of bone matrix and mineralization
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19
Q

What are some causes of Vitamin D deficiency?

A
  1. Intestinal malabsorption can decrease the dietary form of Vitamin D3.
  2. Lack of sunlight to the epidermis can decrease the synthesis of Vitamin D3.
  3. Medications like anticonvulsants are known to inhibit the liver from hydroxylating cholecalciferol.
  4. Liver or Renal failure can diminish the activation steps on cholecalciferol.
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20
Q

Paget Disease and what its caused by

A
  • dysregulation of bone formation
  • genetic susceptibility can trigger disease if environmental conditions arise (viral infections)
  • mutations in genes that encode for proteins involved in the RANK signaling pathway
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21
Q

How does Paget Disease start?

A

disease begins with furious osteoclast activity followed by osteoblast laying down new bone in a chaotic manner that results in weakened bones that increase the risk for bowing and fractures.

22
Q

Why does Pagetic bone become highly vascularized?

A

To support the excessive osteoblast activity. Also, the marrow becomes filled with dense fibrous connective tissue

23
Q

In more severe Paget’s disease, why can patients develop heart failure?

A
  • Because of neovascularization(new blood vessels), the heart has a difficult time maintaining blood flow.
  • Increased risk of developing osteosarcoma
24
Q

What is OA? Describe the joint changes that are associated with OA and the manifestations that these lead to.

A
  • Most common type and most disabling

- degeneration of articular cartilage (at the ends of bone)

25
Q

What are some risk factors for the development of OA, and what influences the time of onset for OA? Does it more often affect men or women?

A
  • Immobility, bony misalignment, repetitive motion, older age, obesity and joint trauma
  • It affects more women
26
Q

What is the primary cause of OA?

A

The primary cause is mechanical stress and dysregulation of cartilage nutrition and repair.

27
Q

How does the blood absent cartilage normally receive nutrition?

A

Waste is removed from the hyaline cartilage during compression and then once compression is released, more nutrients come in.

28
Q

What stimulates the production of proteases that are destructive to the joint surfaces?

A

When a joint is unstable during force, the chondrocytes get damaged and release cytokines and stimulate proteases to work on the matrix. This is what causes destruction

29
Q

What are joint mice, osteophytes and eburnation?

A
  • Fibrillations: “joint mice” cartilage fragments
  • eburnation: when the cartilage runs out and the bones rub together to become smooth
  • osteophytes: irregular structures of bone deposition that can have sharp edges (bc of osteoblasts)
30
Q

How does OA progress to cause cartilage destruction and osteophyte formation?

A

Because of eburnation the bone is being destroyed. This causes osteoblasts to increase their work and cause weird formations called osteocytes.

31
Q

What does it mean to say we see a decreased narrowed joint space?

A

It is a sign that someone has arthritis

32
Q

Describe the cardinal symptoms of OA

A

Pain and stiffness.

33
Q

Describe Heberden’s and Bouchard’s nodes

A
  • Heberden’s: enlargement on the distal interphalangeal joints
  • Bouchard’s: enlargement on the proximal interphalangeal joint
34
Q

How is OA treated?

A
  • Lifestyle changes: weight loss,
  • analgesics, anti-inflammatory
  • ointments with NSAIDS
  • shot of glucocorticoids
  • joint replacement surgery
35
Q

What is RA? What joints are affected most by RA?

A

chronic autoimmune disease that tends to affect small joints first (hands, feet, and neck)

36
Q

What other body tissues can RA affect besides joints?

A
  • nodules on bony prominences
  • the lungs
  • the eyes
37
Q

What is Sjogrens syndrome?

A

dry mouth secondary to autoimmune destruction of salivary glands

38
Q

What is Felty syndrome?

A

triad that includes RA, enlargement of the spleen and neutropenia

39
Q

What MHC antigen is most commonly associated with an increased risk of RA?

A

HLA-DR4

40
Q

What are ACPAs and RF?

A
  • ACPAs: anticitrullinated protein antibodies-> bind specific proteins that have undergone a citrullination process (created by PAD)
  • RF: rheumatoid factor-> autoantibody-> binds Fc portion of IgG-> unnecessary inflammation and break down of healthy tissue
41
Q

What is a citrullinated protein? How is it involved with the pathogenesis of RA?

A

RA presents with antibodies against citrullinated proteins (found in healthy tissues)

42
Q

What are the three phases of RA progression?

A
  1. Initiation: non specific tissue damage
  2. Amplification: T and B cell activation against citrullinated proteins and IgG antibodies
  3. Chronic inflammation: flare ups where area get hot, red, and sore
43
Q

Pannus

A
  • hyper stimulated synovial cells that results in a thickening and expansion of the fibrous synovium (joint)
  • pannus over hyaline cartilage-> pannus destroys cartilage-> pannus tissue fills joint-> joint ankyloses (fusing of joints)
44
Q

What is Gout and how does it occur?

A
  • recurrent attacks of severe articular and periarticular inflammation.
  • caused by elevated uric acid levels in the serum
45
Q

What are purines?

A

Example: adenine and guanine (from DNA and RNA)

-These are then converted into uric acid which crystalizes and causes gout

46
Q

Give at least three causes for elevated uric acid levels in the blood (hyperuricemia)?

A
  1. enzyme defects (i.e. overactive xanthine oxidase)
  2. diet (foods high in purines)
  3. chronic kidney disease (have trouble excreting uric acid)
47
Q

Give 2 reasons why uric acid is more likely to precipitate in the joints

A
  1. synovial fluids are as good a solvent as blood

2. synovial fluids temperature is lower than blood

48
Q

What does uric acid do in the body?

A
  • chemotactic to WBC
  • attract neutrophils which try to phagocytose the uric acid and get destroyed while trying, releasing lysozymes and H+ ions.
49
Q

What is the name of the hard nodules that can form in the joints and tissues?

A

Tophi

-acute gout attacks are severely painful and can last days or weeks

50
Q

What are some purine rich foods that gout patients should avoid?

A

meats, seafood, alcohol

51
Q

Tx for Gout

A
  • Nonsteroidal anti-inflammatories (ibuprofen)
  • colchicine
  • Allopurinol: hypouricemic-> inhibits enzyme xanthine oxidase
52
Q

Probenecid (uric acid Tx)

A
  • Uricosuric agent
  • lowers uric acid by blocking reabsorption of uric acid in the PCT
  • increased risk of kidney stones

Pathophysiology (10 decks)

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