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Physiology- The Muscleoskeletal System And The Skin > 2- Bone And Metabolism > Flashcards

2- Bone And Metabolism Flashcards

1
Q

What is the endocrine regulation of bone?

A

Parathyroid hormone:
- role in Ca metabolism

Thyroid hormone:
- role in bone development
- controls the rate of chondrocyte differentiation

Growth hormone:
- regulates osteoblast differentiation

Insulin growth factor (IGF):
- chondrocyte differentiation

Oestrogen:
- inhibits bone remodelling

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2
Q

What are the 3 organs involved in calcium metabolism?

A
  • Gastrointestinal tract (GI tract): Ca absorbed from diet
  • Kidney: Ca is excreted
  • Bone: Ca is stored
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3
Q

How can we influence the amount of calcium entering and exiting the circulation?

A

GI tract:
- calcium intake approx. 1g/day
- 30% Ca is absorbed

Kidney:
- calcium is excreted in urine
- moderated by reabsorption

Bone:
- major store of calcium
- reservoir to maintain homeostasis

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4
Q

What is the role of the parathyroid gland?

A
  • release parathyroid hormone (PTH)
  • PTH acts to increase Ca2+ levels
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5
Q

What are the functions of PTH?

A
  • it acts to increase circulating calcium levels
  • increase bone resorption
  • increased Ca reabsorption by the kidney
  • stimulates active Vitamin D3 production
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6
Q

Describe how low calcium stimulates PTH release

A

1) Low circulating levels of Ca (below optimal homeostatic range)
2) Parathyroid glands detect low Ca, which stimulates the parathyroid glands to secrete PTH
3) PTH acts on bone cells – causes an increase in bone resorption
4) Some of bone is broken down to release Ca and phosphate that is stored in the bone into the circulatory system

This is done by the RANKL/OPG pathway

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7
Q

Describe how PTH stimulates resorption via RANKL/OPG

A

PTH has a direct effect on osteoblasts and an indirect effect on osteoclasts via the PTH1 receptor
This stimulates osteoblast release of RANKL and inhibits OPG production
The ratio is altered so differentiation in osteoclast is increased therefore resorption increases

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8
Q

PTH also stimulates osteoblast differentiation, what are the effects of PTH treatments?

A

Intermittent PTH treatment is anabolic:
- increase in bone mass
- increase in formation
- increase in osteoblast differentiation

Continuous PTH treatment is catabolic:
- decrease in bone mass
- increase in osteoclasts resorption
- increase in RANL production
- increase inhibition of OPG

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9
Q

Describe the actions of PTH on the kidney

A
  • Low circulating levels of Ca is detected by the parathyroid glands
  • PTH is secreted by the parathyroid gland
  • PTH acts on the kidney to increase calcium reabsorption and reduces calcium excretion
  • PTH decreases phosphate reabsorption by increasing phosphate excretion. More phosphate filtered and excreted by the kidneys
  • Increases the production of active vitamin D3 (1,25-dihydroxy vitamin D) - Hormone produced by kidneys
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10
Q

Describe the production of active vitamin D3

A

1) Large majority of prohormone form of Vitamin D3 produced in skin when exposed to UV radiation from sunlight

2) Prohormone VD3 converted to 25-hydroxy vitamin D3 in the liver

3) 25-hydroxy vitamin D3 converted to (active) 1,25-dihydroxy vitamin D3 in the kidneys
- Active vitamin D3 acts on GI tract à increase Ca absorption from diets. Very little Ca can be absorbed in the absence of active D3
- Acts on parathyroid gland à inhibition of PTH from parathyroid gland
- PTH acts on kidney to increase active vitamin D3 production

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11
Q

What are the uses of active vitamin D?

A
  • increase calcium absorption in the GI tract
  • act on the parathyroid gland to decrease PTH secretion
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12
Q

What factors inhibit PTH production in the parathyroid gland?

A
  • high levels of Ca in the circulation (increased reabsorption)
  • high levels of active vitamin D3 in circulation
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13
Q

What 3 organs are involved in phosphate metabolism?

A
  • GI tract absorption
  • kidney: excretion
  • bones: stored
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14
Q

Describe how osteocytes are classed as endocrine cells?

A
  • osteocytes communicate with systematic circulation as well as bone cells
  • high serum phosphate stimulates FGF23 synthesis in osteocytes
  • high serum phosphate detected by osteocytes
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15
Q

What is FGF23?

A
  • Fibroblast Growth Factor 23
  • activating mutations in FGF23 were identified in patients with autosomal dominant hypophosphatemia (low phosphate levels) rickets
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16
Q

What is the action of FGF23 and how does it work?

A
  • it acts to increase phosphate excretion in the kidney to reduce serum phosphate levels
  • inhibits PTH production
  • inhibits active vitamin D3 production

KIDNEY:
- Acts via its’ receptor FGF1 in the kidney
- Inhibits reabsorption of phosphate – kidneys excrete more phosphate as a result
- Inhibits production of active D3 in the kidneys
-(D3 acts on GI tract to increase absorption of calcium and phosphate)
- Results in indirect inhibition of phosphate intake from the diet (as it’s absorbed by the GI tract)

PARATHYRIOD GLAND:
- Inhibits PTH secretion
- Prevents further PTH-induced release of phosphates from bone and into the serum by inhibiting PTH synthesis in the parathyroid gland
- Inhibits PTH action on the kidney

17
Q

What is a metabolic bone disease?

A

A group of diseases that cause reduced bone mass and reduced bone strength

Due to imbalance of various chemicals in the body (vitamins, hormones, minerals, etc)

Cause altered bone cell activity, rate of mineralisation, or changes in bone structure
- Osteoporosis is a metabolic bone disease

18
Q

What is osteomalacia?

A

Malacia = soft
Defective mineralisation of normally synthesized bone matrix

  • Osteoid is laid down by osteoblasts but cannot be mineralised into mature bone – remains as organic portion of bone in adults
  • Rickets in children
  • Called osteomalacia in adults but rickets in children as both disease present differently (due to onset at different stages of development)
19
Q

What are the two types of osteomalacia?

A

Deficiency of vitamin D3 (causing hypocalcemia)
- Means calcium cannot be absorbed from the GI tract
- Hypocalcaemia – not enough Ca will be available to produce material for bones

Deficiency of Phosphate
- No phosphate incorporated in calcium hydroxyapatite à no mineralisation of bones

20
Q

What is oncogenic osteomalacia?

A

Mesenchymal tumours producing excess FGF23
- Results in excess excretion of phosphate from the kidney
- Leads to hypophosphatemia rickets

21
Q

What are the outcomes of osteomalacia?

A

1) Bone pain/tenderness

2) Fracture
- Loosers Zones fractures – fracture through one side of bone at 90˚ to cortical bone (in adults)

3) Proximal weakness
- Muscles close to torso (muscles of upper arms and legs are weak)
- ^results in difficulty in completing some activities such as climbing stairs or getting out of a chair (typical presentation in both legs within children)

4) Bone deformity
- Bone is too soft to maintain weight in the correct form/morphology
- Bones change shape in order to support weight – results in wide, abnormally shaped growth plates
- These are long-term deformities that are common in adults (i.e. come with long-term development)

22
Q

What is hyperparathyroidism?

A
  • characterised by excess PTH
  • causes hypercalcemia
  • causes hyperphosphatemia
23
Q

How can hyperparathyroidism cause hypercalcemia?

A

Hypercalcemia
- PTH production not inhibited by high serum calcium
- Consistent production of PTH à continuous release of Ca from bone
- Results in high Ca levels in serum

24
Q

How can hyperparathyroidism cause hypophosphatemia?

A

Hypophosphatemia
- PTH inhibits reabsorption of phosphates from the kidneys
- More PTH = more phosphate excretion from kidney
- Results in low serum phosphate

25
Q

How is hyperparathyroidism characterised?

A

Primary :
Generally due to malignancy
- Parathyroid adenoma (85-90%)
- Uncontrolled release of PTH
- Chief cell hyperplasia

Secondary:
An effect of another condition
- Chronic renal deficiency Affects production of D3 in kidneys
- Prevents both absorption of Ca and inhibitory affects of D3 on PCH production
- Vit D deficiency
- Can directly cause hyperparathyroidism

26
Q

What is osteitis fibrosa cystica?

A

Osteitis fibrosa cystica – inflammatory cyst due to some parts of bone being converted into fibrous tissue
An effect of continuous PTH release causing continuous bone remodelling

  • Osteitis – bone inflammation
  • Fibrosa – fibrous
  • Cystica – cysts
  • Cysts seen as dark spots on X-ray – little-to-no bone is present in this areas
27
Q

What happens during hyperparathyroidism?

A

Stones (Kidney stones)
- Due to hypercalcaemia

Bones (Pain from osteitis fibrosa cystica and excess bone resorption)

Abdominal Moans (acute pancreatitis)

Psychic Groans (psychosis & depression)
- Due to imbalance in calcium

Physiology- The Muscleoskeletal System And The Skin (6 decks)

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