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PHYSL 210 Endocrine > Calcium Balance > Flashcards

Calcium Balance Flashcards

1
Q

Functions of Calcium

A
  • Structure
  • muscle contract
  • vesicle release (neurotransmitter)
  • blood clotting
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2
Q

How is body calclium stored?

A

most stored in bone as hydroxyapatite Ca10(PO4)(OH)2

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3
Q

What cells participate in bone remodelling?

A
  • Osteoblasts → bone depostion via addition of Ca2+ to bone
  • osteoclasts → bone resorption via release of Ca2+ from bone into blood
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4
Q

What three hormones control plasma Ca2+ levels

A
  1. Parathyroid hormone (PTH)
  2. Calcitriol (1,25-dihydroxycholecalciferol)
  3. Calcitonin
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5
Q

What are the target sites for the hormones which control plasma Ca2+?

A
  • Bones → blood Ca added or removed
  • Kidneys → Adds or removes Ca from the blood
  • Digestive tract → stimulates greater absorption of Ca
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6
Q

What stimulates and releases PTH?

A
  • stimulated: by low plasma calcium concentrations
  • site of secretion: released from the chief cells of the parathyroid gland
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7
Q

PTH effects?

A

Overall effect: Increases plasma calcium concentration

Bones (direct)

  • Stimulates bone resorption (promotes the breakdown of bone)

Kidneys (direct)

  • Increases calcium reabsorption (ascending limb & distal tubule)
  • Decreases phosphate reabsorption

GI (indirect)

  • Stimulates synthesis of calcitriol, which leads to increased absorption of calcium in digestive tract (indirect effect in GI)
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8
Q

PTH diseases

A
  • Hyperparathyroidism
  • Hypoparathyroidism
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9
Q

Causes of hyperparathyroidism

A

Excess secretion of PTH

Causes:

  • Tumours or hyperfunction of the parathyroid glands (primary)
    • related to thyroid itself → hyperplasia of chief cells, malignant carcinoma of thyroid gland
  • Vitamin D3 deficiency or chronic kidney disease (secondary)
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10
Q

Causes of hypoparathyroidism

A

Inadequate secretion of PTH resulting in low blood Ca levels

Causes:

  • Trauma to parathyroid glands
  • Autoimmune damage to parathyroid gland
  • Congenital malformation of parathyroid glands
    • * If low blood [Ca2+] but high [PTH]: PTH resistance (inability for receptor to recognize it.
      • pseudohypoparathyroidism
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11
Q

Symptoms of hyperthyroidism

A
  • Non-specific complaints of “not feeling well”
  • Abdominal pain, constipation, indigestion, nausea and vomiting
  • Deposition of calcium-based salts e.g. kidney stones
  • Bones may become painful and subject to fracture
    • osteidis procistica which is bone being prefaced with fibrous tissues and cyst like structure
  • Psychiatric symptoms: lethargy, fatigue, depression, and memory problems
  • Hypertension and heart palpitations
    • may lead to cardiac arrythmias
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12
Q

Symptoms of Hypoparathyroidism

A

Neuromuscular hyperexcitability

  • Neural effects: confusion, memory loss, delirium, depression, and hallucinations and seizures
  • Muscle effects: tingling (often in the lips, tongue, fingers, and feet), muscle aches, spasms of the muscles in the throat (leading to difficulty breathing), stiffening and spasms of muscles (tetany) and abnormal heart rhythms
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13
Q

Why does hypo thyroidism cause hyper excitability?

A

with a steady decline in Ca levels there is an increase membrane permeability to Na and generates more APs in muscles. Ca is required for relaxation so in presence of low Ca it will still be released but not pump it back at the same rate.

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14
Q

Summary process flow of PTH

A
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15
Q

Effects of calcitrol

A

Overall effect: Increases plasma calcium concentration

Digestive Tract (direct)

  • Increases calcium absorption from food we eat

Kidney

  • Increases calcium reabsorption
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16
Q

Synthesis of calcitrol

A
  • Calcitrol is synthesized from vitamin D3 which comes from exposure to sunlight UVB rays and dietary sources.
  • Synthesized in the kidney where D3 is converted to calcitriol
  • calcitriol can then move through circulation to target cells
17
Q

Other names for calcitriol

A
  • 1,25-dihydroxycholecalciferol
  • 1,25-(OH2)D3
18
Q

Getting UVB ray to synthesize vitamin D

A
  • The sunshine vitamin
  • The further from the equator, the less vitamin D
  • Relates to our angle to the sun, our elevation, and the quantity of melanin in our skin
  • In the tropics vitamin D is always available
  • In Canada, we are only table to synthesize significant amounts of vitamin D during the spring and summer
  • lighter skin has less melanin so can absorb more UVB for synthesis.
    • melanin inhibits conversion to vitamin D
19
Q

Vitamin D - Deficiency

A
  • Softening of bones (called rickets in children, osteomalacia in adults)
    • deficient mineralization of the bone matrix
  • Increases risk for the development of cancer: colon, breast, prostate, and ovarian
    • Canadian Cancer Society recommends 1000 IU/day for adults in fall and winter
  • Increases risk for the development of certain autoimmune diseases
    • can lead to too much Ca in blood causing nausa, dizziness, frequent urination
20
Q

What secretes calcitonin?

A

Secreted from C cells (parafollicular cells) of the thyroid gland

21
Q

What type of hormone is calciitonin?

A

peptide hormone → hydrophilic therefore binds to target cell receptor on the membrane

22
Q

What triggers calcitonin?

A

release is triggered by high plasma Ca

23
Q

Effects of calcitonin

A

Overall effect: Decreases plasma calcium concentration

  • Reduces activity of osteoclasts (inhibits bone resorption)
    • by attaching to receptors
  • stimulates osteoblasts to lay down bone
  • Inhibits calcium reabsorption by kidneys
    • increases excretion
  • Protect the skeleton from Ca2+ loss during pregnancy and lactation
    • a time when milk production increases demand for Ca
24
Q

Overall regulation of plasma calcium

A
25
Q

Osteoporosis

A

Osteoporosis = porous bone

  • Decreased bone mass leading to bone fragility and increased fracture risk
  • most common metabolic bone disorder
26
Q

Bone density exam

A

special x-ray to measure how many grams of Ca and other minerals are packed into segments of bone and fairly good indicator of diseases.

27
Q

Risk factors of osteoporosis

A
  • Aging
  • Menopause
  • Lack of exercise (especially weight bearing)
  • Poor diet
  • Current cigarette smoking
  • Excessive alcohol consumption
  • Genetics
28
Q

What happens to bone with aging?

A

Bone formation exceeds bone resorption until about our 30s when we reach our max density, decreases by about 0.7% per year after that and some more so than others including the vertebrae, pelvis, femur

29
Q

How does menopause contribute to osteoporosis?

A

Decrease in estrogen stimulates isle 6 production from osteoblasts which is an interludin in which can act in a paracrine manner on osteoclasts to stimulate resorption

30
Q

Prevention of osteoporosis

A
  • Balanced diet (rich in calcium and vitamin D)
  • Exercise regularly (muscle strengthening)
  • Don’t smoke
  • Avoid excessive alcohol consumption
31
Q

Treatment options for osteoporosis

A
  • Calcium and vitamin D supplementation
  • Bisphosphonates: inhibit osteoclast activity
  • Estrogen/hormone therapy
  • Selective estrogen receptor modulators
  • Calcitonin
  • Parathyroid hormone (severe cases)
  • Denosumab: inhibits a downstream effector of PTH
    • FDA/Health Canada approved in 2010

PHYSL 210 Endocrine (8 decks)

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