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Renal and Endocrine Biology > REB 7. Calcium Homeostasis > Flashcards

REB 7. Calcium Homeostasis Flashcards

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1
Q

What is the source of calcium?

A

It cannot be produced in the body - must be acquired through diet

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2
Q

What is Hydroxylapatite made up of? What is an example of a use of it?

A
  • made up of calcium and phosphorus

- makes up bone and teeth

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3
Q

What is the most abundant mineral in the human body?

A

calcium

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4
Q

If there is a deficit in calcium ions what happens?

A

hyperexcitability of cells

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5
Q

If there is an excess in calcium ions what happens?

A

increases in contractility

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6
Q

What are the main functions of calcium?

A

[1] Muscle Contraction + Nerve Excitability
[2] Neurotransmitter + Hormonal Release
[3] Enzyme Function
[4] Blood Coagulation
[5] Structural Support for Healthy Bone and Teeth
[6] Membrane Integrity + Permeability

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7
Q

The regulation of calcium depends on 3 factors which are?

A

[1] Balance of Intake, Absorption + Excretion

  • dietary calcium
  • vitamin D

[2] Normal Functioning of…

  • Intestine
  • Parathyroid Glands
  • Kidneys

[3] Hormones

  • Parathyroid Hormones (parathyroid gland)
  • Calcitonin (thyroid gland)
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8
Q

What are the 2 separate mechanisms of intestinal calcium absorption? What is the difference between the two and where can it be found?

A

[1] Passive Absorption
- throughout entire small intestine

[2] Active Transport

  • localized in small intestine
  • dependent on vitamin D metabolite
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9
Q

What is the mechanism/steps by which intestinal absorption occurs?

A

main goal: absorb calcium from intestinal lumen into blood stream

Steps:
[1] Ca2+ enters from intestinal lumen across apical brush border mediated by CaT1 channel

[2] Ca2+ is transported across the enterocyte by the calcium binding protein, Calbindin

[3] Ca2+ exits across the basolateral membrane - mediated by the Ca2+-ATPase (PMCA1)

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10
Q

What are the factors affecting calcium metabolism?

A

[1] Dietary Calcium Intake + Urinary Loss

[2] Plasma Hormones + Vitamins

  • parathyroid hormone
  • calcitonin
  • vitamin D (active metabolite)

[3] End-Organ Function

  • intestinal tract
  • kidneys
  • liver
  • parathyroid glands

[4] Plasma Concentration

  • plasma/albumin concentration
  • acid/base changes
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11
Q

What is the function of parathyroid hormone?

A

[1] increases calcium blood level (Ca2+)

[2] acts on bone, kidney and intestine

[3] increases Ca2+ (and Mg2+) reabsorption from kidney

[4] increases Ca2+, HPO4- and Mg2+ uptake from GI tract into blood

[5] increases activity of osteoclasts (bone resorption)

[6] promote formation of active vitamin D (increases activity of 1-alpha-hydroxylase in kidneys)

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12
Q

What inhibits the parathyroid hormone (PTH) in a negative feedback loop?

A

increased plasma free ionised Ca2+

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13
Q

What is PTHrP?

A

Parathyroid Hormone-Related Protein (PRHrP)

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14
Q

Where is PTHrP synthesized?

A
  • it is synthesized by many fetal and adult tissues
  • e.g. cartilage, bone, smooth, cardiac and skeletal muscle, skin, breast, intestines, parathyroid glands, pancreatic islets, pituitary, placenta and central nervous system
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15
Q

What is the difference between PTH and PTHrP?

A
  • they are both structurally related
  • they bind to the same receptor
  • PTHrP binds to several other receptors
  • PTHrP has a broader spectrum of effects than PTH
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16
Q

What are some of the other effects that PTHrP may have that PTH doesn’t?

A
  • mammary gland development and lactation
  • placental transfer of calcium
  • early development (bone mineralization, cartilage differentiation)
  • smooth muscle functioning - thus, acting as a vasodilating hormone
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17
Q

If PTHrP is secreted by a breast tumour or lung cancer what may happen?

A
  • uncontrolled secretion leads to hypercalcemia
  • stimulates calcium resorption from bone
  • suppresses calcium loss in urine
  • unlike PTH, PTHrP does NOT stimulate vitamin D
  • unlike PTH, PTHrP does NOT incrrease intestinal calcium absorption
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18
Q

What are the 2 types of PTH receptors? (just name them)

A

[1] Type I PTH Receptor

  • binds to PTH + PTHrP
  • GPCR (hormone binds activating 2nd messenger - adenylate cyclase)
  • 7-transmembrane segments

[2] Type 2 PTH Receptor

  • binds to PTH + low affinity for PTHrP
  • mRNA expressed in only a few tissues
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19
Q

Where is the Type I PTH Receptor abundant in (where is it most abundant in)?

A
  • bone (chondrocytes at growth plates)
  • kidney
  • other tissues at lower levels
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20
Q

What is the main function of Calcitonin?

A

opposes the effects of PTH

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21
Q

What stimulates the secretion of Calcitonin?

A
  • secreted from the thyroid (parafollicular cells)

- stimulated by raised plasma ionized Ca2+

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22
Q

What is the mechanism of action of Calcitonin?

A
  • binds to calcitonin receptor (GPCR) on osteoclasts inhibiting their activity
  • stimulates osteoblasts
  • lower plasma calcium concentration by inhibiting Ca2+ resorption from bone
23
Q

What are the 2 types of cells/locations that code the calcitonin gene? How do they differ?

A

[1] C-Cells of Thyroid Gland (Parafollicular Cells)

  • codes for preprocalcitonin (calcitonin precursor)
  • inhibits bone resorption
  • N-terminal peptide
  • C-terminal peptide
  • mRNA contains 4/6 exons!!

[2] CNS

  • codes for calcitonin-gene related peptide (CGRP)
  • potent vasodilator
  • N-terminal peptide
  • C-terminal peptide (CTP-2)
  • mRNA contains 5/6 exons!!1
24
Q

What is the function of C-cells of the thyroid gland?

A

codes for preprocalcitonin which inhibits bone resorption

25
Q

What is the function of CNS of the thyroid gland?

A

codes for calcionin-gene related peptide which is a potent vasodilator

26
Q

What is a source of Ergocalcigerol (D2)?

A

vegetables

27
Q

What is a source of Cholecalciferol (D3)?

A

meat

28
Q

What is the endogenous form of vitamin D (that is created on skin)?

A

7-dehydrocholesterol synthesis

29
Q

What is the name for the active form of vitamin D?

A

1,25 Dihydroxycholecalciferol (1,25-diOH-D3)

aka Calcitrol

30
Q

What is the process of changing 7-dehydrocholesterol into 1,25 Dihydroxycholecalciferol (1,25-diOH-D3)?

A

[1] presence of UV light
[2] hydroxylation in the liver
[3] hydroxylation in the kidney
[4] active form is now made!

31
Q

What hormone helps convert 25-OH D3 to 1,25-OH D3?

A

Parathyroid Hormone

32
Q

What stimulates the release of PTH to convert 25-OH D3 to 1,25-OH D3?

A

[1] low plasma PO4 3-

[2] low plasma Ca2+

33
Q

What inhibits the release of PTH to convert 25-OH D3 to 1,25-OH D3?

A

excess 1,25-diOH-D3

34
Q

What are the functions of calcitrol/active vitamin D?

A

To maintain adequate serum levels of Ca2+ by:

  • increasing Ca2+ uptake in intestine
  • minimizing Ca2+ loss by kidney by increasing resorption in kidney tubule
  • stimulating resorption (demineralization) of bone when blood Ca2+ is low
  • resorption is enhanced by PTH
35
Q

How is calcium excreted?

A
  • excreted via urine and faeces
    • normal daily urinary excretion in adults
    • < 250 mg for women
    • < 300 mg for men
  • dermal loss < 50mg/d unless excessive perspiration
36
Q

What is the normal daily urinary excretion in adults (males and women)?

A

Males – < 300 mg for men

Females – < 250 mg for women

37
Q

What are some factors that increase calcium excretion?

A 
[1] Increased Plasma Ca2+
[2] Deprivation of Phosphate 
[3] Excess of Vitamin D
[4] Increased Urinary Excretion of Sodium
[5] Immobilization 
[6] Corticosteroid Administration 
[7] Increased Dietary Ca2+
[8] Metabolic Acidosis
[9] Hyperthyroidism
38
Q

What are some factors that decrease calcium excretion?

A 
[1] Decreased Plasma Ca2+
[2] Decreased Glomerular Filtration Rate
[3] Parathyroid Hormone
[4] Decreased Dietary Ca2+
[5] Increased Dietary Phosphate
[6] Increased Ca2+ Utilization (growth, pregnancy, lactation)
39
Q

What form of calcium is biologically active?

A

free-ionized calcium

40
Q

What are the 3 different types of cells that regulate bone turnover?

A

[1] Osteoclasts

  • “bone-resorbing cells”
  • destruction of old worn out bone
  • necessary for repair and remodelling

[2] Osteoblasts

  • “bone forming cells”
  • secrete osteoid (unmineralised collagen)
  • influence activity of osteoclasts

[3] Osteocytes

  • “embedded osteoclasts”
  • involved in sensing internal bone environment
41
Q

What is hyperparathyroidism?

A
  • increased bone resorption
42
Q

What is osteomalacia/rickets? What is the difference between them?

A

both are a disorder of vitamin D deficiency leading to net bone demineralization

Osteomalacia: (adults)

  • demineralization of pre-existing bones
  • increased susceptibility to fractures

Rickets: (children)
- continued formation of collagen bone matrix, but incomplete mineralization leads to SOFT, PLIABLE BONES

43
Q

What is the diagnosis of osteomalacia/rickets?

A
  • Xrays of affected bones
  • serum calcium
  • serum alkaline phosphatase
  • serum phosphorus
44
Q

What is the treatment of osteomalacia/rickets?

A

Cholecalciferol - Vitamin D

45
Q

What is Osteoporosis a disease of?

A

disorder of reduced bone matrix

  • not a primary disorder of Ca2+ metabolism
  • resembles osteomalacia, but plasma Ca2+ and phosphate are normal
46
Q

What is the diagnosis of osteoporosis?

A
  • fractures with little trauma

- bone mineral density testing (DEXA scan)

47
Q

What is the treatment of osteoporosis?

A
  • Calcitrol (active form of Vitamin D)
  • Bisphosphonates (e.g. Fosamax or Boniva)
  • Calcitonin
  • Hormone Replacement Therapy (HRT)
48
Q

What is Paget’s Disease?

A

it is a progressive bone disorder with unclear aetiology

  • genetic or viral exposure
  • characterized by mixed lytic + sclerotic bone changes
  • areas of bone resorption (increased osteoclastic activity)
  • abnormal new growth leading to pain (deformity and fracture)
  • can progress to bone cancer
49
Q

What is the diagnosis of Paget’s Disease?

A
  • X-rays + other imaging tests (MRI + CT scans)

- elevated serum alkaline phosphotase

50
Q

What is the management of Paget’s Disease?

A

goal: relieve bone pain and prevent the progression of the disease
- calcitonin + bisphosphonates
(long term use of bisphosphonates can lead to osteomalacia due to impairment of new bone formation - thus given cyclically)

51
Q

What are the clinical features of hypercalcaemia on CNS, renal, bones, abdominal and cardiac?

A

CNS:

  • malaise, weakness and vomiting….
  • psychiatric disturbances, confusion…

Renal:

  • polyuria, polydipsia
  • renal stones and nephrocalcinosis

Bones:
- bone pain

Abdominal:

  • constipation
  • duodenal ulceration

Cardiac:
- dysarrhythmias

52
Q

What are the clinical features of hypocalcaemia on CNS, bones and neuromuscular?

A

Neuromuscular:

  • numbness and tingling of extremities
  • muscle cramps/spasms (positive Chvostek and Trousseau’s sign)
  • proximal myopathy (waddling gait)

Bone:

  • bone pain
  • bone fractures

CNS:

  • psychiatric disturbances
  • memory loss/confusion
  • convulsions (newborn and infancy)
  • cataracts
53
Q

What is Trousseau’s sign?

A

Induction of carpopedal spasm by inflation of a sphygmomanometer above SBP for 3 minutes

response: carpopedal spasm characterized by…
- adduction of thumb
- flexion of MCP joints
- extension of IP joints
- flexion of wrist

54
Q

What is Chvostek’s sign?

A

Contraction of the facial muscles by tapping on facial nerve just anterior to ear

response: twitching of lip to spasm of all facial muscles

Renal and Endocrine Biology (25 decks)

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