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ENDO > Week 7 > Flashcards

Week 7 Flashcards

1
Q

What are the different forms of Calcium.

A
  • Ionised Calcium (difffusible through the capillary membrane, biologically active)
  • Bound form (protein bound calcium, non diffusible through the capillary membrane)
  • Complex form (calcium complex with anions; combined to anionic substances of the plasma and interstitial fluids (ctirates and phosphates))
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2
Q

Briefly explain the three tissues, three hormones, and three cell types involved in Calcium regulation.

A

Calcium regulation involves:

Three tissues - bone, intestine, kidney
Three hormones - PTH, calcitonin, vitamin D
Three cells - osteoblasts, osteocytes, osteoclasts

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3
Q

What are some of the functions of calcium

A
  • structural integrity of metabolism and bone
  • synaptic transmission
  • coenzyme function
  • control of excitability of nerve and muscle cells
  • excitation-contraction coupling
  • stimulus- secretion coupling
  • regulation of trans membrane ion transport
  • second messenger in signal transduction pathways
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4
Q

Tell me something about the parathyroid gland.

A
  • Four small glands
  • located behind the thyroid gland: one behind each of the upper and each of the lower poles of the thyroid; 6 millimeters long, 3 millimeters wide, and 2 millimeters thick
  • has a macroscopic appearance of dark brown fat
  • the chief cells are believed to secrete most of the PTH
  • Oxyphil cells function not known
  • Gland is essential for life
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5
Q

What type of hormone is the Parathyroid hormone (PTH), what’s its half life, briefly what does it do, and how does it bind to its receptor?

A
  • 84 amino acid polypeptide, with a molecular weight of 9500
  • serum level ranges from 10-60 pg/ml
  • The circulating half-life is 2 - 4 minutes
  • Maintains the plasma ionised calcium level
  • PTH binds to plasma membrane G-protein coupled receptors on target cells in bones and kidneys
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6
Q

How does PTH get secreted?

A

The calcium sensing receptor on the parathyroid cell surface. The receptor detects the serum calcium concentration. It determine the set point for the serum PTH concentration.

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7
Q

What are the actions of PTH on Bone

A
  • Liberates calcium from bone (bone resportive effective)

- Transports calcium from bone to ECF

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8
Q

Removal of calcium and phosphate from bone due to PTH have two phases. Explain plz.

A

Rapid phase (begins in minutes and increases progressively for several hours). PTH activates the ALREADY EXISTING bone cells (mainly osteocytes) to promote calcium and phosphate removal (calcium and phosphate moves from bone to ECF)

Slower phase (several days or weeks to become fully developed). Proliferation of osteoclasts, followed by greatly increase osteolastic resporption of bone. In bone, osteoblast is the important target cell.

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9
Q

Explain briefly PTH Receptors. Which one is more abundant?

A

PTH 1R receptor and PTH 2 receptor. Kidney and bone have the greatest abundance of PTH 1R receptors.

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10
Q

What are PTH actions on GIT.

A
  • uptake of calcium (calcium absorption)
  • increased absorption of phosphate
  • Indirect action of PTH for Ca absorption - through Vitamin D (which increases intestinal calcium absorption by inducing calcium-binding protein in the duodenal and jejunal mucosa)
  • Acts synergistically with Vit D to absorb calcium and phsophate
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11
Q

Explain PTH actions on Kidney.

A
  • Increased reabsorption of calcium
  • Increased urinary excretion of phosphate
  • Stimulates the renal hydroxylation of 25-hydroxy vitamin D3 to 1,25-dihydroxyvitamin D3
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12
Q

Talk me through the process of Calcium absorption.

A

Ca2+ enters the cell across the apical membrane through a channel.

  • Inside the cell, the Ca2+ is buffered by binding proteins, such as calbindin, and is also taken up into intracellular organelles (such as the ER)
  • The intestinal cell then extrudes Ca2+ across the basolateral membrane through a Ca2+ pump and an Na-Ca exchanger
  • 1,25 dihydroxyvitamin D stimulates all three steps of transcellular Ca2+ absorption
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13
Q

What is Bone remodeling? How does it work? How is PTH associated with it?

A

Bone remodelling involves the continuous removal of bone (bone resorption) followed by synthesis of new bone matrix and subsequent mineralisation (bone formation).

Osteoblasts express abundant surface receptors for PTH - osteoclasts do not. PTH acts on osteoblasts to induce the production of several cytokines that increase both the number and activity of bone-resorbing osteoclasts.

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14
Q

What is Bone remodeling? How does it work? How is PTH associated with it?

A

Bone remodelling involves the continuous removal of bone (bone resorption) followed by synthesis of new bone matrix and subsequent mineralisation (bone formation).

Osteoblasts express abundant surface receptors for PTH - osteoclasts do not. PTH acts on osteoblasts to induce the production of several cytokines that increase both the number and activity of bone-resorbing osteoclasts.

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15
Q

Explain the regulation of PTH secretion

A
  • The primary signal that stimulates PTH secretion is low circulating Ca++
  • Powerful feedback system: the extracellular calcium is sensed by the parathyroid chief cell through a Ca++ sensing receptor (CaSR)
  • In the parathyroid gland, increasing amounts of extracellular Ca++ bind to the CaSR and activate signalling pathways that repress PTH secretion
  • Decreased plasma calcium - increased PTH
  • Persistent decrease - hypertrophy of parathyroid glands (Glands are enlarged in pregnancy and lactation)
  • Increased plasma calcium - decreased PTH secretion
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16
Q

What is Calcitonin?

A
  • Has opposite effect to PTH
  • Straight chain polypeptide
  • From parafollicular cells, or C cells of thyroid gland
  • Major stimulus is increased plasma calcium cocnentration
17
Q

What are the main actions of Calcitonin?

A
  • Decrease the absorptive activities of the osteoclasts in the bone (inhibits osteoclastic bone resorption; without bone, the osteoclast (which lacks PTH receptors, appear to be principal target of calcitonin)
  • Increased deposition of calcium in bone
  • Decreased formation of new osteoclasts (prolonged effect)
  • In kidneys - opposite to PTH (minor effect)
18
Q

Tell me about Vitamin D. Does it share similar characteristics/origin with anything? Where is it formed? Where does it become biologically active?

A
  • Vitamin D shares striking similarities in orgin with steroid hormones
  • Is formed in the skin as a result of irradiation of 7-dehydrocholesterol, by ultraviolet rays
  • Cholealciferol is converted to 25- hydroxycholecalciferol in liver
  • 25-hydroxycholecalciferol is converted to 1,25-dihydroxycholecalciferol in the proximal tubule (which is active form of Vit D, conversion requires PTH)
19
Q

What are the actions of Vitamin D3?

A
  • Increases intestinal calcium absorption
    - Rapid phase (1-6hrs) increased calcium absorption via increased Na++/Ca++ exchange activity
    - Slow phase (48-96 hrs) increased calcium absorption via increased synthesis of calcium binding proteins (calbindins)
  • Increases calcium binding protein in the intestine
  • In brush border (intestines) increases calcium absorption
  • Increases phosphate absorption
  • Increases calcium and phosphate re absorption in the kidneys
  • Increases calcium transporters through cellular membranes in the bone
20
Q

What does Vitamin deficiency lead to in children and in adults?

A

Rickets in kids. Osteomalacia in adults.

21
Q

What is hypoparathyroidism?

A

No sufficient PTH from the parathyroid glands. Effects of hyperparathyroidism include:

  • decreased bone resorption; decreased osteocytic and osteoclastic activities
  • Decreased calcium in ECF which leads to hypoglycemia; increased nervous system excitability, increased neuronal membrane permeability to sodium ions, easy initiation of AP; spontaneous nervous impulses from peripheral nerves to skeletal muscles; tetanus muscle contractions; seizures (increasing excitability in brain)
22
Q

What are some of the effects of hypocalemia?

A
  • increased neuromuscular excitability (tetany)
  • laryngeal stridor
  • cardiac effects: re polarisation is delayed, with prolongation of the QT interval
  • Dermatologic effects: the skin is often dry and flaky and the nails are brittle
23
Q

What is a Trousseaus sign of latent tetany?

A

When blood concentration of clcium falls from its normal level of 10mgl/dL to 6mg/dL.
Causes is tetany - spastic contraction of skeletal muscle without elaxation
Essentially it is a carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure for 3 minutes

24
Q

What is the Chvostek’s sign?

A

Twitching of facial muscles in response to tapping over the area of the facial nerve.

25
Q

What is pseudo-hypoparathyroidism?

A
  • Target-organs (bone, kidneys and guts are resistant to PTH)
  • Congenital defect in the G-protein associated with the PTHR
  • Plasma Ca2+ is low
  • Plasma phosphate is high
  • Defect in growth and development of skeleton
26
Q

What is primary hyperparathyroidism?

A
  • Tumour of parathyroid gland, parathyroid adenomas or hyperplasia
  • excess PTH secretion
  • Increased calcium in the ECF
  • Extensive decalcification of bone
  • Large cystic areas in bone (bone disease in hyperparathyroidism - osteitis fibrosca cystica)
27
Q

What is secondary hyperparathyroidism?

A
  • Compensation for hypocalcaemia
  • Increased parathyroid hormone
  • Secondary hyperparathyroidism is a complication that occur in chronic renal failure
  • Damaged kidneys - unable to produce sufficience 1,25 DHCC
  • Reduction in plasma 1,25 DHCC and moderate decreases in ionised Ca2+ –> greater synthesis and secretion o PTH

ENDO (10 decks)

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