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2 - MEH > Calcium Metabolism + Exercise > Flashcards

Calcium Metabolism + Exercise Flashcards

1
Q

What is normal serum calcium level

A

2.2-2.6 mmol/L

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2
Q

What are some roles of calcium in the body

A

Hormone secretion, muscle contraction, nerve conduction, exocytosis, activation/inactivation of enzymes

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3
Q

What are some roles of phosphate in the body

A

ATP production, membrane formation, genetic information (RNA/DNA)

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4
Q

What hormones regulate serum calcium

A

Parathyroid hormone
Vitamin D (calcitriol)
Calcitonin

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5
Q

What are the actions of parathyroid hormone

A
  • Elevates calcium concentration and lowers serum phosphate
    • Stimulates bone reabsorption and calcium release into circulation
    • Stimulates calcium reabsorption in kidney and excretion of phosphate
      • Stimulates activation of vitamin D (calcitriol)
  • Shorter term regulation
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6
Q

Where are parathyroid hormones produced

A
  • Produced in chief cells in parathyroid gland
    • Preprohormone cleaved to form PTH
    • Water soluble
    • Short half life (4.5 min)
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7
Q

What are the actions of vitamin D

A
  • Elevate serum calcium and serum phosphate
    • Increase intestinal absorption and renal reabsorption of calcium and phosphate
    • Increase bone reabsorption
  • Longer term regulation
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8
Q

How is vitamin D obtained and activated

A
  • Obtained from sun exposure, food and supplements
  • Active form known as calcitriol - produced in liver and kidney
    • D3 - cholecalciferol requires sunlight - formed in skin and from diet
    • D2 - ergocalciferol from yeast and fungi added to margarines
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9
Q

What are the actions of calcitonin

A
  • Lowers serum calcium and serum phosphate

- Counteracts PTH effects

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10
Q

Where is calcitonin produced

A

Produced in C cells (parafollicular cells) in thyroid

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11
Q

What cells are in the parathyroid hormone

A
  • Parathyroid gland discrete glandular structures at the back of the thyroid gland
  • Chief cells - pink, not much cytoplasm
    • Produce parathyroid hormones
  • Oxyphil cells - paler pink, lots of cytoplasm
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12
Q

What is the role of bone for calcium control

A
  • Structural support and maintenance of serum calcium concentration
    • Control release and uptake of calcium phosphate
  • Calcium phosphate crystals found within collagen fibrils (hydroxyapatite crystals)
  • Bone deposition - osteoblasts produce collagen matrix which is mineralised hydroxyapatite
  • Bone reabsorption - osteoclasts dissolve hydroxyapatite crystals
    • PTH increase osteoclasts
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13
Q

What is the role of kidney in calcium control

A
  • PTH and calcitriol affect reuptake of calcium in distal convoluted tubule and ascending limb
    • Increase reabsorption to blood
  • PTH increase phosphate loss in kidney - inhibit reabsorption
    - Prevents calcium stone formation
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14
Q

What is the role of gut in calcium control

A
  • Normally, only 30% of dietary calcium is absorbed

- PTH stimulates conversion of vitamin D to calcitriol in gut to increase calcium absorption

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15
Q

Explain the regulation of parathyroid hormone and vitamin D

A
  • High serum calcium binds to calcium G protein receptor
    • Slow down release and production (transcription) of PTH
    • PTH continually synthesised but Chief cells degrade hormone when in excess
    • Released PTH cleaved in liver
  • PTH stimulates activation of vitamin D to calcitriol
  • Both regulated through negative feedback
    • High serum calcium causes release of calcitriol which lowers calcium concentration
      • Leads to release of PTH to increase calcium concentration back to normal
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16
Q

How is calcium used in EDTA

A
  • Calcium is factor IV in the clotting cascade
  • EDTA is a calcium chelator - binds to calcium to prevent blood clotting in blood samples and transfusions
  • IV calcium given after patient gives blood calcium is chelated
17
Q

How can cancer cause hypercalcaemia

A
  • Malignant osteolytic bone metastases - breaking up bone into circulation
  • Multiple myeloma - cancer spreading through bone
  • Common cancers that metastasise to bone causing lytic lesion and hypercalcaemia - breast, lung, renal, thyroid
  • Prostate gland common cause of bone metastases - doesn’t break down bone - osteoblastic
  • Common sites for metastases are the vertebrae, pelvis, femur, ribs, proximal part of humerus, skull
    • Sites are active, produce many red blood cells, good blood supply
  • Osteoblastic does not increase calcium concentration
18
Q

What are the effects of Parathyroid hormone related peptide (PTHrP)

A
  • Peptide produced by cancer cells leading to humeral hypercalcaemia of malignancy (HNM)
    • Produced in squamous cell tumours on head, neck and lung
  • Produced commonly in patients with breast or prostate cancer, occasionally in myeloma
  • PTHrP shares many actions with PTH leading to increased calcium release from bone, reduced renal calcium excretion and reduced renal phosphate reabsorption
  • Does not increase activation of vitamin D to calcitriol
19
Q

Differentiate between primary and secondary hyperparathyroidism

A
  • Primary - one of parathyroid glands develops adenoma and secretes excessive parathyroid hormones
    • Increases serum calcium and decreases serum phosphate
  • Secondary -all 4 parathyroid glands become hyperplastic
    • Vitamin D deficiency - not enough sunlight, diet insufficiency, chronic renal failure
    • Low calcium absorption resulting in low serum calcium levels, causing PTH levels to rise (parathyroid hyperplasia)
    • Raised PTH activates osteoclasts to mobilise calcium from bone
    • Symptoms - bone pain due to osteomalacia in vitamin D deficiency
      • Renal osteodystrophy in renal failure
20
Q

How can you differentiate between primary and secondary hyperparathyroidism and malignant hypercalcaemia through blood components

A

Primary - high serum calcium, medium/low serum phosphate, normal alkaline phosphatase, high serum PTH
Secondary - low serum calcium, high serum phosphate,, high serum alkaline phosphatase, high serum PTH
Malignant hypercalcaemia - high serum calcium, normal serum phosphate, high serum alkaline phosphatase, lower serum PTH

21
Q

What is alkaline phosphatase

A
  • Alkaline phosphatase high in secondary hyperparathyroidism
    • Enzyme present on osteoblasts and in plasma
    • Marker of bone turnover - increase bone formation
22
Q

What are symptoms of primary hyperparathyroidism

A
  • Moans - tired, exhausted, depressed
  • Groans - constipation, pancreatitis
  • Stones - kidney stones, polyuria
  • Bones - bone and muscle aches
23
Q

How does calcium affect neuronal activity

A
  • Hypercalcaemia suppresses neuronal activity - raises threshold of depolarisation
    • Coma, confusion, lethargy
  • Hypocalcaemia leads to excitable nerves - tingling, muscle tetany, epilepsy
24
Q

What are symptoms of severe hypercalcaemia

A
  • Symptoms of severe hypercalcaemia > 3.0 mmol/L
    • Polyuria can lead to dehydration which further increases hypercalcaemia
      • Lethargy, weakness, confusion, coma, renal failure
    • Rehydration main treatment
25
Q

What are signs of hypocalcaemia

A
  • < 2.1 mmol/L
  • Seen mostly in patients after removal of thyroid gland (inadvertent removal of parathyroid gland)
  • Tingling around mouth and in fingers, tetany of muscles
  • Carpopedal spasms - flexor strongest at elbow, wrist, fingers
  • Can result in death due to laryngeal muscle spasm
26
Q

Differentiate between osteoporosis and osteomalacia

A
  • Osteoporosis - decreased bone density with normal mineral
    • Degeneration of already constructed bone leads to brittle bones prone to fracture
  • Osteomalacia - not enough mineral content
    • Affect bone building in children (rickets) or bone mineralisation in adults
    • Leads to soft bones prone to bending
27
Q

Describe the metabolic responses to starvation and explain how they are controlled

A
  • Reduction in blood glucose stimulates release of cortisol from adrenal cortex and glucagon from pancreas
  • Stimulate gluconeogenesis and breakdown of protein and fat
  • Reduction in insulin and anti-insulin effects of cortisol, prevent most cells from using glucose and fatty acids are preferentially metabolised
  • Glycerol from fat provides important substrate for gluconeogenesis, reducing the need for breakdown of proteins
  • Liver starts to produce ketone bodies and brain starts to utilise these sparing glucose requirement from protein
  • Kidneys begin to contribute to gluconeogenesis
  • Once fat stores depleted, system must revert to use protein as fuel
  • Death related to loss of muscle mass
28
Q

Describe the metabolic and hormonal responses to various types of exercise

A
  • ATP stores in muscle are limited to ~2 seconds during a sprint
    • Needs to be rapidly resynthesised to meet metabolic demand
  • Muscle creatine phosphate stores can rapidly replenish ATP for ~5 seconds during a sprint
  • Further ATP supplied by glycolysis (ineffective) and oxidative phosphorylation (needs oxygen)
  • In intensive exercise (anaerobic) - muscle glycogen can sustain for ~2 minutes
  • In low intensity exercise, if enough oxygen can be supplied for oxidation of glucose and glycogen stores, could last for ~60 minutes
    • In aerobic conditions, triacylglycerol stores in adipose tissues can slowly be released
    • Capacity limited by carnitine shuttle
29
Q

Explain the benefits of exercise

A
  • Body composition changes - decrease adipose, increase muscle
  • Glucose tolerance improves - increase muscle glycogenesis
  • Insulin sensitivity of tissue increases
  • Blood triglycerides decrease - decrease in VLDL and LDL, increase HDL
  • Blood pressure falls
  • Psychological effects - feeling of well-being

2 - MEH (16 decks)

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