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321 - Physiology > Calcium Regulation > Flashcards

Calcium Regulation Flashcards

1
Q

How is growth hormone regulated?

A

GHRH stimulates the release of GH from the adenohypophysis in response to hypoglycemia, lactation, fasting, exercise.

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2
Q

What does GH stimulate the release of?

A

Insulin-like growth factors 1 & 2 (IGF-1 and IGF-2)

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3
Q

What does IGF-1 do?

A

It exerts negative feedback at the hypothalamus.

  • Stimulates the release of GHIH (growth hormone inhibiting hormone)
  • Increased GHIH decreases GH secretion
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4
Q

What is the effect of dopamine on GH?

A

Dopamine reduces GH secretion.

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5
Q

What cells secrete GH?

A

Somatotropes in the adenohypophysis.

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6
Q

What are the effects of IGF-1?

A

IGF-1 promotes proliferation of chondrocytes in the growth plate and ossification of chondrocytes.

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7
Q

What are the effects of growth hormone on bones?

A

Promotes growth of long bones through IGF-1.

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8
Q

What are the effects of GH on milk synthesis?

A
  • Promotes galactopoiesis
  • Maintains alveolar cell numbers and increases milk synthetic activity per cell
  • GH redirects available nutrients towards milk synthesis
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9
Q

Are artificial growth hormones approved in Canada?

A

Hell no girl

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10
Q

What is an example of an artificial growth hormone?

A

Recombinant bovine somatotropin (rbST)

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11
Q

What are the metabolic effects of GH?

A
  • Increases rate of protein synthesis in all body cells
  • Positive energy balance since GH is anabolic (protein and glycogen synthesis)
  • Lipolysis
  • Increases blood glucose concentration
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12
Q

Describe postnatal skeletal muscle growth.

A

Satellite cells can divide under appropriate stimuli (IGF-1) and fuse with the muscle fiber to facilitate muscle hypertrophy. The satellite cell nucleus will be delivered to the muscle fiber so there will be more DNA material in the muscle fiber for its growth and regeneration.

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13
Q

How much of the calcium in blood is bound?

A

50%

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14
Q

How much of the body’s calcium and phosphate reside in the bone?

A

99% of calcium and 85% of phosphate

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15
Q

How much calcium is there in the cytosol?

A

Not much and 99% of it forms insoluble complexes with phosphate

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16
Q

What are the biological functions of calcium?

A
  • Formation of skeletal tissue
  • Transmission of nerve impulses
  • Cell signalling (important second messenger)
  • Modulate activity of many enzymes
  • Blood clotting
  • Component of milk and egg
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17
Q

What hormones increase calcium in the blood?

A
  • Parathyroid hormone
  • Calcitriol
18
Q

What hormones decrease calcium levels in the blood?

A

Calcitonin

19
Q

What cells produce PTH?

A

Chief cells of the parathyroid gland.

20
Q

What induces PTH secretion?

A

Hypocalcemia

21
Q

What effect does persistent hypocalcemia have on the paratyroid gland?

A

Hypertrophy of the parathyroid glands.

(More calcium needed, no negative feedback, increased gland size)

22
Q

How does PTH increase blood calcium levels?

A
  • PTH enhances renal tubular absorption of calcium and excretion of phosphate into urine
  • PTH stimulates intestinal calcium absorption (via Calcitriol)
  • PTH indirectly activates osteoclasts via osteoblasts
23
Q

How does PTH cause bone lysis?

A

Osteolysis (bone breakdown) will be indirectly stimulated in the presence of PTH. There are no receptors of PTH on osteoclasts but there are PTH receptors on osteoblasts. Once PTH activates osteoblasts to secrete various products (to create an acidic environment), osteoclasts will be activated and bone lysis occurs.

24
Q

What organs are involved in calcitriol synthesis?

A

Liver and kidney

25
Q

What is the precursor for calcitriol?

A

Vit D3

26
Q

How is calcitriol produced?

A

Body receives Vit D3 (cholecalciferol) through diet. In addition, it can be produced in the skin of mammals due to the action of UV light on a milk-derived sterol molecule. Vit D3 will be converted to calcidiol (25-hydroxy cholecalciferol) in the liver. Subsequently, calcidiol will be converted to calcitriol (1,25- dihydroxycholecalciferol) by the kidney.

27
Q

What are the effects of calcitriol?

A
  • Differentiation of stem cells into osteoclasts
  • Directly stimulates osteoclast activity
  • Increased absorption of calcium from the small intestine
  • Increases reabsorption of calcium in the kidney tubules
28
Q

What cells produce calcitonin and what stimulates its release?

A

Produced by C cells (parafollicular cells) in the thyroid in response to hypercalcemia

29
Q

What are the effects of calcitonin?

A
  • Calcitonin decreases blood calcium by inhibiting
    osteoclast activity (blocking effects of PTH and calcitriol)
  • Increase urinary excretion of calcium
30
Q

What is hypocalcemia?

A

Hypocalcemia is a condition that can be caused by low calcium intake or excessive drainage of calcium due to production needs. This condition is commonly observed in postpartum females.

31
Q

What are common clinical signs of hypocalcemia?

A

Restlessness, seizures, incoordination, tetany and muscle tremor.

32
Q

What are the mechanisms that cause neuromuscular signs of hypocalcemia?

A

Under hypocalcemic conditions, nerves become more permeable to sodium as the normal inhibition by Ca2+ of sodium movement through voltage-gated sodium channels is lost. This can lead to spontaneous generation of action potentials (random firing of neurons). However, muscle paresis is the predominant sign in cows as hypocalcemia affect acetylcholine release and calcium is required for muscle contraction.

33
Q

When does hypercalcemia become life threatening?

A

Blood calcium concentration > 18 mg/dl is associated with life threatening signs

34
Q

What are the clinical signs of hypercalcemia?

A
  • PU/PD: Inhibition of ADH and direct stimulation of the thirst center
  • Inappetence, vomiting and constipation: due to decreased excitability of GI smooth muscle
  • Weakness, shivering, stiff gait: due to decreased neuromuscular excitability (high calcium prevents sodium entry)
35
Q

What is hypoparathyroidism and what causes it?

A

Impaired PTH secretion caused by:

  • Auto-immune diseases and destruction of the parathyroid glands
  • Thyroidectomy
36
Q

What are the results of hypoparathyroidism?

A
  • Hypoparathyroidism leads to hypocalcemia (immediate effect)
  • Long-term effect: Lack of stimulus for bone resorption leads to increase in cortical bone thickness and mineral content (osteopetrosis)
37
Q

Primary hyperparathyroidism

A

Primary hyperparathyroidism is due to functional adenoma of the parathyroid gland (fibrous osteodystrophy)

  • Dogs are most commonly affected
  • High blood calcium concentration
  • Loose teeth, radioluscent areas within the bones
38
Q

Pseudohyperparathyroidism

A

Secretion of PTH-like peptide

  • Lymphosarcoma
  • Tumors of the apocrine glands of anal sac (anal sac adenocarcinoma)
39
Q

Secondary hyperparathyroidism

A

Normal parathyroid glands but they are forced to secrete excess PTH

40
Q

What are the causes of secondary hyperparathyroidism?

A
  • Nutritional (Deficiency of calcium, vit D3, excess phosphorus)
  • Chronic renal failure (Decreased synthesis of calcitriol leads to decreased absorption of calcium from kidney and intestine = hypocalcemia and retention of phosphate)
41
Q

What is big head disease?

A

Secondary hyperparathyroidism in horses characterized by fibrous osteodystrophy of skull
and jaw bones

42
Q

Hyperphosphatemia

A

Due to bone resorption and decreased excretion of phosphate through urine due to kidney failure.

  • Precipitation of calcium by formation of calcium phosphate
  • Blocks 1alpha hydroxylase, the enzyme involved in the conversion of Calcidiol to Calcitriol

321 - Physiology (52 decks)

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