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MHD > Bone 1 > Flashcards

Bone 1 Flashcards

1
Q

Stages of Callus formation

A 
Hematoma Stage- hours to days
Inflammatory Stage-within 48hrs
Granulation Tissue-2-12 days
Soft Callus- one week-several months
Hard callus-one week-several months
Remodeling-several months
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2
Q

What are common osteoporotic fracture sites?

A

proximal humerus
spinal compression fractures
hip fractures
distal radius

reduction in trabecular bone mass despite normal bone mineralization

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3
Q

Primary osteoporosis type 1 vs 2

A

Primary osteoporosis
Type 1
-postmenopausal, increase of bone resorption due to estrogen decrease
Type 2
-senile osteoporosis: affects men and women 70 y/o (age related calcium deficiency)

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4
Q

How does menopause lead to osteoporosis?

A
  1. decreased serum estrogen
  2. increased IL1,IL6, and TNF levels
  3. Increased expression of RANK, RANKL
  4. Increased osteoclast activity
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5
Q

How does aging lead to osteoporosis?

A
  1. decreased replicative activity of osteoprogenitor cells
  2. decreased synthetic activity of osteoblasts
  3. decreased biologic activity of matrix-bound growth factors
  4. Reduced physical activity
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6
Q

Secondary Osteoporosis Causes

A 
1. Endocrine 
Hyperthyroidism
-accelerated turnover of bone and increased osteoclastic activity
Hypogonadism
-woman-estrogen
men-anabolic androgens 
Hyperparathyroidism
-osteoclast recruitment and increased osteoclastic activity
  1. Drugs
    Corticosteroids
    -Inhibit osteoblastic activity (suppression expression)
    Alcohol
    -direct inhibitor of osteoblast, may inhibit calcium absorption
  2. Gastrointestinal
    Malnutrition
    Malabsorption
    -impaired absorption of calcium, phosphate and vitamin D
  3. Neoplasia
    Multiple Myeloma
    -Secretion of osteoclast activating factor
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7
Q

What are the symptoms of osteoporosis? What does it look like on xray/labs?

A

Fractures
Vertebral Fractures
Pain
Additional complication: pulmonary embolism, pneumonia

NOT detectable on x ray until 30-40% bone mass lost
Blood Calcium, Phosphorous, alkaline phosphatase levels NOT diagnostic

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8
Q

Bone densitometry-dual energy xray absorptiometry (DEXA) scans measure what

A

bone thickness/density at different parts of the body

-two x ray beans of different energy levels

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9
Q

WHat is the bone mineral content of of a normal, osteopenia, osteoporosis patient?

A

Normal: Bone mineral content not more than 1 SD below the young adult mean (T score above -1)

Osteopenia: Bone mineral content between 1SD and 2.5SD below the young adult mean (T score between-1 to-2.5)

Osteoporosis: Bone mineral density 2.5 or more below the young adult mean (T-score at or below -2.5)

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10
Q

What are the indications for bone density test?

A
  1. woman 65 regardless additional risk factors
  2. Estrogen deficient women at risk for low bone density
  3. Patient treated with glucocorticoids
  4. patients with asymptomatic primary or secondary hyperparathyroidism
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11
Q

What are treatments/prevention for osteoporosis?

A
  1. exercise
  2. calcium and vitamin D
  3. bisphosphonates
  4. estrogen replacing agents
  5. recombinant PTH
  6. RANK ligand inhibitor (denosumab)
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12
Q

Rickets/Osteomalacia

A

Etiology=vitamin D deficiency
Bone mineralization defect
Accumulation of osteoid (unmineralized bone, soft bone)

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13
Q

Osteomalacia-Adults

A 
Loss of skeletal muscle mass(density)-osteopenia
Fractures and microfractures
-vertebral bodies and femoral neck
Bone pain 
lots of osteoid
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14
Q

Rickets-children
Pathology
Symptoms
Treatment

A

Excess unmineralized bone-growing bones

  • growth plate not adequately mineralized
  • osteoclasts do not resorb growth plate cartilage
  • growth plate irregular, thickened, lobulated
  • loss of structural rigidity of bones

Symptoms :

  1. Bowing of legs
  2. Rachitic Rosary-osteoid deposition at the costochondral junction
  3. Pigeon Breast Deformity-inward bending of ribs with anterior protrusion of the sternum
  4. Occipital bones flattened
  5. Parietal bones buckled
  6. Frontal bossing (enlarged forehead)/squared appearance of head

How common:
very common!

Treatment:
vitamin D

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15
Q

Hyperparathyroidism are causes of primary and secondary hyperparathyroidism?

A

Increased parathyroid hormone level
Primary: Adenoma, Hyperplasia, Carcinoma
Secondary: Prolonged hypocalcemia stimulates PTH hypersecretion

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16
Q

Hyperparathyroidism results in increased PTH what does this do?
What are the symptoms

A
  1. sensed by osteoblast receptors
  2. release mediators of osteoclastogenesis
  3. increased osteoclast activity
  4. bone resorption
  5. decreased bone mass
  6. pain
  7. fractures-stress fractures
17
Q

How does this hyperparathyroidism appear histologically?

A

dissecting osteitis

railroad tracks

18
Q

What type of tumor can hyperparathyroidism lead to?

A

brown tumor

19
Q

What is osteitis fibrosa cystica?

A

hyperparathyroidism

-bone replaced with fibrous tissue and cystic change

20
Q

Paget’s disease
Etiology
Histology

A

Disease caused by osteoclast dysfunction

  • characterized by excessive breakdown of bone tissue followed by abnormal bone formation
  • affecting MEN 2:1
  • mid adulthood
  • axial skeleton, proximal femur involved up to 80% of patients

Etiology:

  1. slow virus infection
    - Paramyxovirus (remains hypothesis)
    - Induces IL6 secretion, increased RANK expression
    - stimulates osteoclast activity
  2. Genetic
    - gene mutation leading RNK mediated osteoclast stimulation
    - Mutations in RANKL and RANK/OPG

Histology:
1. mosaic pattern of bone -prominent cement lines

21
Q

What are the three stages of Paget Disease?

A
  1. Osteolytic (osteoclasts)
  2. Osteolytic-osteoblastic (mixed osteoclasts + osteoblasts)
  3. osteosclerotic (osteoblasts)
22
Q

what are the symptoms of paget’s disease? HOw do you diagnosis it?

A

Symptoms:

  1. Pain in affected bones
    - microfractures
    - bone overgrowth compressing nerves, spinal roots
  2. Platybasia-flattening of the skull base impinging on foramen magnum
  3. Leontiasis ossea
  4. secondary arthritis
  5. thickening of skull
  6. bowing of tibia
23
Q

What can paget’s disease lead to?

A
  1. High output cardiac failure
    - hypervascularity of Pagetic bones-polyostotic-increased blood flow
    - elevated resting cardiac index beyond normal range 2.5-4 L/min per m2
  2. Sarcoma
    - 5-10%
    - osteosarcoma, fibrosarcoma
24
Q

HOw do you diagnosis it?WHat are the labs in paget’s disease f

A

Diagnosis:
radiographs-bone scan-increased osteoblast activity

Labs:
elevated serum alkaline phosphatase
-serum calcium , phosphorus unaffected

25
Q

What is the treatment of paget disease?

A

Acetaminophen Nsaids
Bisphosphonates- (induce apoptosis of osteoclasts)
Calcitonin-(inhibits osteoclast function)

26
Q

Osteogenesis Imperfecta
Defect
Symptoms
Goals of treatmetn

A

brittle bone disease
Defect in extracellular structural protein
-type 1 collagen (mutation for the alpha 1 and alpha 2 chains of the collagen molecule)

Symptoms:

  1. Too little bone
  2. Hearing loss
  3. Dental imperfection (blue yellow-teeth)
  4. blue sclera

Treatment

  1. maximize mobility/function
  2. minimize fracture risk
  3. pain control
  4. psychosocial
27
Q

What are the types of osteogenesis imperfecta?

A 
Type 1-mildest form
-autosomal dominant
Type 2-lethal, perinatal disease
-autosomal recessive
Type 3- progressive, most severely deforming type
-usually autosomal dominant
Type 4-similar to type 1 (normal sclerae) 
-autosomal dominant
28
Q

Achondroplasia

A
  • Most common disease of growth plate
  • –Dwarfism
  • Autosomal dominant
  • 80% new mutations
  • failure of longitudinal bone growth (endochondral ossification)-short limbs
  • membranous ossification not affected-large head

Defect in signal transduction system-Mutation in FGF receptor 3

  1. Activating mutation of FGFR3
    - FGFR3 normally inhibits cartilage proliferation
  2. constant activation
  3. Inhibits chondrocyte differentiation and proliferation
  4. Retards growth plate development
29
Q

Osteonecrosis (avascular necrosis)

A

bone death (infarction)
-bone and bone marrow
Gross: subchondral wedge shaped pale yellow area
Histology:dead bone-empty lacunae
Pathogenesis: Ischemia-Mechanical, corticosteroids, thrombosis/embolism, vessel injury(vasculitis, radiation), vascular compression
Etiology: trauma, corticosteroids, infection dysbarism, radiation therapy, connective tissue disorders, sickle cell anemia, tumors, pregnancy, gaucher disease, idiopathic

30
Q

What causes osteonecrosis of the Jaw?

A

high dose IV disphosphonates
Predisposing factors: dental disease, dental surgery, periodontitis, poor dental hygiene, treatment with chemo or corticosteroids

MHD (81 decks)

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