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Disease and Therapeutics 1 > Bones > Flashcards

Bones Flashcards

1
Q

Which cells have the RANK receptor?

A

Osteoclasts and Osteoclast Precursors

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2
Q

What happens when RANKL binds the RANK receptor on Osteoclasts?

A

Binding stimulates survival and generation of Osteoclasts and increases NFKB (not for keeping bone)

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3
Q

What is Osteoprotegrin?

A

Osteoprotegrin is produced by Stromal Cells or Osteoblasts and inhibites RANKL-RANK receptor interaction

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4
Q

What is M-CSF?

A

M-CSF is a cytokine produced by osteoblasts or stromal cells that results in the generation and survival of osteoclasts –> increased bone resorption and increased plasma Ca levels

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5
Q

What is the function of the WNT/Beta-Catenin Pathway?

A

WNT is produced from stromal cells and binds Osteoblasts (through LRP5 and LRP6) to increase secretion of Osteoprotegrin, blocking RANK-RANKL interaction**Note that a LOF mutation in LRP5/6 –> Osteoporosis and a GOF mutation in LRP5/6 –> Drastic increase in bone mass

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6
Q

What is the main component of the bone’s organic matrix?

A

Type 1 Collagen

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7
Q

What is Woven Bone?

A

Random Collagen deposition, pathologic, seen in rapid bone growth (ex-healing a fracture)

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8
Q

What are the subtyes of Lamellar Bone? Describe its characteristics

A
  1. Compact Bone2. Spongy Bone-Stronger bone with ordered collagen deposition; replaces woven bone
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9
Q

What will be increased with increased Osteoblast activity?

A

Osteopontin (osteocalcin) and Alkaline Phosphatase

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10
Q

RANK Ligand is located on which cells?

A

Osteoblasts and Marrow Stroma Cells

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11
Q

The end of a bone (distal to the growth plate) is the

A

Epiphysis

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12
Q

The area beneath the growth plate is call the

A

metaphysis

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13
Q

The central region of a long bone is the

A

Diaphysis

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14
Q

What is dystosis?

A

LOCAL problems in migration of mesenchyme and its condensationEx- bradydactyly because of HOXD13 defect

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15
Q

What is dysplasia?

A

GLOBAL defect in regulation of skeletal organogenesisEx- achondroplasia

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16
Q

What is the defect causing Cleidocranial Dysplasia and describe the symptoms

A

RUNX2 transcription factor defect-Short stature, abnormal clavicles, wormian bones, too many teeth

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17
Q

What is the cause of Achondroplasia?

A

FGFR3 mutation –> GOF that inhibits cartilage growth because of decreased chondrocyte proliferation in growth plates

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18
Q

Continuation of appositional and intramembranous bone formation in Achondroplasia results in what?

A

Thick cortical bone

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19
Q

What are the physical characteristics of Achondroplasia?

A

Short proximal limbs, normal trunk length, big forehead and head, depressed root of noseNormal life span, intelligence and reproductive status

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20
Q

What is the cause of Thanatophoric Dwarfism and describe the symptoms

A

FGFR3 GOF mutation (same as Achondroplasia)-See short, bowed limbs, frontal bossing with macrocephaly, bell shaped chest (so respiratory failure) and CLOVERLEAF Skull

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21
Q

What is Osteoporosis Pseudoglioma Syndrome?

A

Disease caused by LOF mutation of LRP5 that causes skeletal fragility and loss of vision

22
Q

What is the cause of Osteopetrosis (Marble Bone Disease)?

A

Disease of decreased osteoclast bone resorption caused by a defect in RANKL, LRP5 GOF mutation, or Carbonic Anhydrase II (CAII) deficiency (so cannot acidify pit)AD- benign, AR- malignant

23
Q

What are the clinical findings of Osteopetrosis?

A
  1. Extramedullary hematopoiesis –> hepatosplenomegaly2. Bulbous long bones (erlenmeyer flask deformity)3. Narrow neural foramina (mild cranial nerve defects)4. Brittle Bones, multiple fractures5. Mild anemia **TREAT- with Bone Marrow Transplant
24
Q

What is the cause of Osteogenisis Imperfecta?

A

Mutation in the alpha 1 or alpha 2 chains of TYPE 1 COLLAGEN

25
Q

What are the clinical characteristics of Osteogenisis Imperfecta?

A
  1. Brittle bones and multiple fractures (may decrease after puberty)2. Blue Sclerae3. Hearing Loss4. Loose joints
26
Q

What are mucopolysaccharidoses?

A

Defects in enzymes degrading dermatan sulfate, heparan sulfate and keratan sulfate –> abnormal hyaline cartilage –> malformed bones

27
Q

What are some potential causes of Osteoporosis?

A
  1. Nutritional (lack of Ca)2. Menopause (increased RANK/RANKL expression –> increased osteoclast activity)3. Physical Activity (space flight)4. Aging (decreased replication of progenitor cells and synthetic activity of osteoblasts)5. Vitamin D Receptor Polymorphism6. Drugs, diabetes, malignancy, liver/ GI disease
28
Q

What is osteoporosis?

A

A disease of decreased bone mass and increased porosity –> increased risk of fractures**May be described as osteopenia (decreased bone mass) to the point of risk for fracture

29
Q

What determines most hereditary osteoporosis?

A

Vit D receptor, Collagen 1A1 and the Estrogen Receptor

30
Q

How does decreased estrogen result in Osteoporosis in post-menopausal women?

A

Decreased Estrogen –> increased inflammatory cytokines that increase RANKL and decrease OPG**Estrogen replacement is effective treatment, but increases risk of breast cancer

31
Q

What are common causes of secondary osteoporosis?

A
  1. Hyperparathyroidism (most commonly caused by parathyroid adenoma)2. Neoplasia3. Multiple Myeloma4. Vit. D Defficiency (ricketts and osteomylasia)5. Anticoagulants6. Corticosteroids7. Immobilization
32
Q

What is Dual-energy absorptiometry used for?

A

Detection of Osteoporosis

33
Q

Describe the clinical features of Hyperparathyroidism

A
  1. Increased osteoclast fxn –> subperiosteal resorption that thins the cortices2. Loss of lamina dura around teeth3. Bone loss on radial aspect of middle phalanges of index and middle finger4. General Osteopenia5. Brown Tumor- bone that is replaced by fibrovascular tissue (fractures will result in hemorrhage and you see granulation tissue and hemosiderin)
34
Q

What is renal osteodystrophy?

A

-Altered OC/OB activity –> osteomalacia (delayed mineralization), osteosclerosis and osteoporosis-Hyperparathyroidism-Decreased activation of Vit D-Metabolic Acidosis

35
Q

What are the stages of Paget’s Disease?

A
  1. Osteolytic Stage- loss of bone mass due to osteoclasts (see very thick cortex with “V shaped blade of grass” lesion2. Mixed Stage- Prominent Osteoblasts and Osteoclasts3. Osteosclerotic Stage- mosaic pattern of lamellar bone- jigsaw puzzle like cement lines
36
Q

What is the important histological finding of Paget’s Disease?

A

Bone mosaic with disorganized lamellae (look like swirls)

37
Q

What are the clinical findings of Paget’s Disease?

A
  1. Pain from microfractures2. Increased Alkaline Phosphatase3. Normal Ca and PO44. Bone Overgrowth causing -Cranial Nerve Palsy -Heavy skull that is hard to hold up -Severe secondary osteoarthritis -Chalk stick-type fracture
38
Q

Paget’s Disease can cause what clinical problems?

A
  1. High-output cardiac failure2. Tumors (benign and malignant)
39
Q

What is used to treat Paget’s Disease?

A

Calcitonin and Biphosphonates

40
Q

Describe the order of healing after a fracture

A

Soft Tissue Callus (procallus) –> Boney CallusProcallus- hematoma/fibrin framework that activates osteoprogenitor cells; is not rigid and can be easily disruptedBoney Callus- made of woven bone +/- cartilage for enchondral ossification

41
Q

What is avascular necrosis (osteonecrosis) and what are the common causes?

A

-Infarction of bone and marrow due to vessel injury; the dead bone/fat is replaced by Calcium Soaps-Causes: *Corticosteroids, infection, dysbarsim, pregnancy, sickle cell disease

42
Q

What is a medullary infarct?

A

Subtype of avascular necrosis; can be small or large; large are painful (ex- dysbarism, sickle cell)

43
Q

What is a Subchondral Infarct?

A

Subtype of avascular necrosis that results in a WEDGE SHAPED subchondral bone crack; secondary collapse may –> osteoarthritis

44
Q

How would osteomyelitis appear on an X-Ray?

A

As a lytic bone lesion with surrounding sclerosis

45
Q

What are the bacterial causes of osteomyelitis?

A
  1. S aureus2. E coli, Pseudomonas, Klebsiella (infections of IV drug users)3. H flue and Group B Strep (infants)4. Salmonella (Sickle Cell Patients)
46
Q

Describe the common locations for osteomyelitis for different age groups

A
  1. Neonate- Metaphysis or Epiphysis2. Children- Metaphysis Adult- Epiphyses and subchondral bone
47
Q

What is a Brodie Abscess?

A

A small intraosseous abscess often in the cortex walled off by reactive bone

48
Q

What is Sclerosing Osteomyelitis of Garre

A

Osteomyelitis in the jaw with extensive new bone formation

49
Q

A draining sinus of pyogenic osteomyelitis can develop into what?

A

Squamous Cell Carcinoma

50
Q

What is the clinical characteristics of TB Osteomyelitis?

A
  1. Occurs in immunosuppressed2. Pott’s Disease: Lumbar and Thoracic Spine –> breaks through discs to other vertebrae –> scoliosis and kyphosis
51
Q

What are the features of syphilis of the bone?

A

Saddle Nose and Saber Shin (tibia)

Disease and Therapeutics 1 (7 decks)

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