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Medicine > Bone Pathologies > Flashcards

Bone Pathologies Flashcards

1
Q

What are the THREE broad reasons for Rickets/ osteomalacia?

A
  • Vitamin D deficiency
  • Resistance to Vitamin D effects
  • Phosphate pahtologies
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2
Q

What separates the diagnosis of rickets and osteomalacia?

A

Rickets the bone plates have not fused, where as in osteomalacia they have.
i.e rickets effects children and osteomalacia effects adults.

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3
Q

What may be seen on x-rays that looks like fractures but isn’t on patients with Osteomalacia?
Where are these commonly seen?

A

Looser Zones - areas of poor crystallization of the bone, looking like fractures

  • scapula
  • Pelvis
  • Ribs
  • Femur
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4
Q

What are the typical symptoms of Osteomalacia?

A
  • Bone pain
  • Muscle pain - thighs and shoulder usually
  • Weakness - without atrophy
  • Gait changes
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5
Q

What would you expect in blood serums to find for osteomalacia?

A
  • High PTH
  • Low - normal - calcium
  • Low - normal - phosphate
  • Low - normal - Alkaline phosphatase
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6
Q

What is VDDR 1A rickets?

A

Vitamin D Dependent Resistant/ Rickets

  • where 25(OH)D cannot be converted to 1,25 (OH)D

**Mutation in 25 - hyroxyvitamin D - 1 - Alpha hydroxylase

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7
Q

VDDR 1B?

A

Mutation in 25 hyroxylase.

Pre-vitamin 3 never gets converted to 25(OH)D

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8
Q

Why might there be abnormally low levels of phosphate causing Rickets?

A

Mutation in FGF -23 resulting in increased excretion of phosphate

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9
Q

What are the primary blood markers for bone formation?

A
  • Serum Pro-collagen Type 1 - N - Terminal Pro peptide: PINP
  • Total Alkaline Phosphatase levels
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10
Q

What are the primary blood markers for bone resorption?

A

Serum Collagen Type - 1 linked Telopeptide - CTx

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11
Q

What are the stages of Vitamin D synthesis?

A

> 7 - dehydrocholesterol

> Cholecaliferol (Pre-vitamin D)

> 25 dihydroxycholecaliferol

> 1,25 dihydroxycholecaliferol (Calitriol)

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12
Q

In x-linked hypophosphatamia, what is the gene mutated and what is the result?

A

PHREX gene

increased expression of FGF-23

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13
Q

What is oestogensis imperfecta?

A

Due to multiple genetic defects there is abnormal production of type I collagen.

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14
Q

What genes are usually implicated in Osteogensis imperfecta and what mutations are involved?

A

COL1A1
COL1A2

Promoter region mutation - fails to initiate
Stop Condon Mutation - poor mRNA formation
mRNA mutations - mRNA is too fragile and breaks

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15
Q

In mild oestogenesis imperfecta, what is primary problem?

A

Not enough Alpha 1 pre-collagen made - resulting in a LACK of type I collagen

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16
Q

What is the mechanisms behind serve osteogenesis imperfecta?

A

Glyscine is not at every 3rd amino acid base. - helical structure unable to fold.
- extra time in R.E.R

results in over glycosalation of it and other proteins. putting excessive stress on the cell.
- cell may then enter apoptosis.

17
Q

What are the treatments for osteoporosis?

A
  1. Lifestyle changes:
    - increased intake of Calcium
    - increased exercise
    - minimising fall risks
    - reduce smoking
    - reduce alcohol
  2. Anti-absorption drugs
    - bisphosphantes
    - Selective Oestorgen Receptor modulators
  3. Anabolic stimulation of bone growth
    - PTH - Teriparatide
18
Q

What is the experimental drug for achondroplasia? What is its function?

A

Vosoritide

Degrades FGF-3

19
Q

With regard to indirect fracture healing, what are the stages and times associated?

A
  1. Fracture Haematoma and inflammation - 6-8 hours
  2. Fibrocartilage - soft callus. Lasts up to ~ 3 weeks. chondrocytes make fibrocartilage.
    - fibroblasts and progenitor cells invade into the procallus
  3. Hard callus formation. Lasts up to ~ 3-4 months. Osteoblasts lay down woven bone
  4. Osteoclasts remodel the bone into compact or trabecular bone
20
Q

Where in the renal system is calcium re-absorption controlled by PTH?

A

Thick ascending loop of Henle and the distal convoluted tubule

21
Q

Define indirect fracture healing

A

Formation of bone via tissue differentiation until normal skeletal continuity is restored

22
Q

Define direct fracture healing

A

This is a intervention, usually surgical. The bone heals through direct contact without the formation of callus.

23
Q

What are some of the risk factors that can affect fracture healing?

A

Anatomical
- blood supply - surgical neck of humorous

Patient factors:

  • obesity
  • diabetic
  • malnutrition
  • anaemic
  • smoking
  • age

Medication:

  • steroids
  • NSAIDs
  • Bisphosphanates
24
Q

What is VDDR2b

A

Normal expression of 1, 25 D(OH) D. But other molecules are released which inhibit it.

Medicine (33 decks)

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