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Musculoskeletal System > 06. Role of vitamin D and calcitonin in calcium and phosphate metabolism > Flashcards

06. Role of vitamin D and calcitonin in calcium and phosphate metabolism Flashcards

1
Q

what is VITAMIN D IMPORTANT FOR

A

ENHANCES Ca2+ and INORGANIC PHOSPHATE Pi ABSORPTION FROM the GUT/INTENTINE

so ENHANCES BONE MINERALISATION

  • important for normal SKELETAL MUSCLE FUNCTION
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2
Q

VITAMIN D also INCREASES BONE…

A

RESORPTION

so RELEASING Ca2+ and Pi from BONE

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3
Q

what does VITAMIN D METABOLISM START off with (2)

A

provitamin D3 : 7-DHC from SKIN (activated by UVB from SUNLIGHT)
provitamin D2: VIT D from DIET

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4
Q

Where does provitamin D3 : 7-DHC come from for VITAMIN D METABOLISM

A

SKIN
- activated by UVB from SUNLIGHT

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5
Q

where does provitamin D2: VIT D come from for VITAMIN D METABOLISM

A

DIET

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6
Q

VITAMIN D METABOLSIM steps (6)

A
  1. 7-DHC (provitamin D3) from SKIN (activated by UVB from sunlight)
    VITAMIN D (provitamin D2) from DIET
    are ABSORBED and enter CIRCULATION
  2. ENTER LIVER where 25(OH)ASE is ADDED
    - 25(OH)D / CALCIDIOL formed
  3. in KIDNEY 1-ALPHA-(OH)ASE ADDED
    - form ACTIVE FORM 1,25(OH)2D CALCITRIOL
  4. CALCITRIOL 1,25(OH)2D BINDS to VIT D RECEPTORS in various tissues
  5. VIT D RECEPTORS with bound calcitriol BIND to RXR - RETANOIC ACID RECEPTORS to ACTIVATE VITAMIN D RESPONSE ELEMENTS

leading to various GENE consequences

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7
Q

what does VITAMIN D UNDERGO in VITAMIN D METABOLISM to form the active form

A

2 HYDROXYLATION STEPS

– 25(OH) Vitamin D reflects vitamin D status
– 1,25(OH)2 Vitamin D is metabolically active

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8
Q

where do 7-DHC and VIT D ENTER

A

LIVER

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9
Q

what is ADDED to 7-DHC & VIT D in LIVER and what is FORMED

A
  • 25(OH)ASE ADDED

FORM: 25(OH)D
CALCIDRIOL

( 2 OH groups)

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10
Q

what is ADDED to CALCIDRIOL 25(OH)D in KIDNEY and what is FORMED

A
  • 1-ALPHA-(OH)ASE added

FORM: 1,25(OH)2D
CALCITRIOL
- ACTIVE

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11
Q

what does VITAMIN D INHIBIT or increase as NEGATIVE FEEDBACK
(to prevent formation of more active)

A
  • INHIBITS 1-OH-ASE in KIDNEY
  • INHIBITS PTH from PARATHYROID GLANDS

INCREASES 25(OH)ASE - inactive form

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12
Q

VITAMIN D in CIRCULATION is BOUND to..

A

DBP (VITAMIN D BINDING PROTEIN)

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13
Q

what is CaBP and what does it increase

A

Calcium Binding Protein

Increases expression of TRPV6 - CALCIUM CHANNEL

for CALCIUM ABSORPTION

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14
Q

in VITAMIN D METABOLISM what does ACTIVE VITAMIN D (CALCITRIOL) BIND to and what does this lead to (2)

A

binds to VITAMIN D RECEPTORS - VDR

which BIND to RETANOIC ACID RECEPTORS - RXR

ACTIVATION of VITAMIN D RESPONSE ELEMENTS - VDRE

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15
Q

7 CAUSES of VITAMIN D DEFICIENCY

A
  • REDUCED SKIN SYNTHESIS
  • DECREASED BIOAVAILABILITY
  • INCREASED CATABOLISM
  • DECREASED SYNTHESIS of 25(OH)D
  • INCREASED URINARY LOSS OF 25(OH)D
  • DECREASED SYNTHESIS OF 1,23(OH)2D
  • BREAST FEEDING
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16
Q

7 CAUSES of VITAMIN D DEFICIENCY
REDUCED SKIN SYNTHESIS due to:

A
  • SUNSCREEN use: absorption of UVB radiation by sunscreen
  • Skin PIGMENT : absorption of UVB radiation by melanin
  • AGEING : reduced D3 synthesis by ~75% at age 70 y
  • SEASON, latitude and TIME of day: no D3 synthesis between Nov to Feb in UK
  • Skin GRAFTS for burns (skin taken from the person burned, which is used to cover wounds): reduced D3 synthesis
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17
Q

7 CAUSES of VITAMIN D DEFICIENCY
DECREASED BIOAVAILABILITY due to:

A
  • Malabsorption: reduced fat absorption in cystic fibrosis, coeliac disease, etc
  • Obesity: sequestration of Vit D in body fat

(vitamin D is FAT SOLUBLE)

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18
Q

7 CAUSES of VITAMIN D DEFICIENCY
INCREASED CATABOLISM due to:

A

Anticonvulsants, steroids: induce deactivation of 25(OH)D and 1,25(OH)2D

19
Q

7 CAUSES of VITAMIN D DEFICIENCY
DECREASED SYNTHESIS OF 25(OH)D due to:

A

LIVER FAILURE: malabsorption contributes to D deficiency

20
Q

7 CAUSES of VITAMIN D DEFICIENCY
INCREASED URINARY LOSS OF 25(OH)D due to:

A

NEPHROTIC SYNDROME: loss of 25(OH)D bound to Vit D binding protein

21
Q

7 CAUSES of VITAMIN D DEFICIENCY
DECREASED SYNTHESIS OF 1,25(OH)2D due to:

A

CHRONIC KIDNEY DISEASE

22
Q

7 CAUSES of VITAMIN D DEFICIENCY
BREAST FEEDING when..

A

breast milk only source - poor D content in human milk

23
Q

how are VITAMIN D LEVELS ASSESSED

A

by CIRCULATING SERUM CONTENT of 25(OH)D (calcidiol)

24
Q

SUFFICIENT VIT D LEVELS:
OPTIMAL FIT D LEVELS:

A

sufficient: 50-74 mmol/L
optimal: 75-100 mmol/L

> 370 nmol/L = Intoxication

25
Q

VIT D INSUFICIENCY/DEFICIENCY is ASSOCIATED with INCREASED RISK FOR:

A

Rickets/osteomalacia, osteoporosis & fractures, muscle WEAKNESS& falls, osteoarthritis

Reduced IMMUNITY (increased susceptibility for TB)

CANCER: colon, prostate, breast; lymphoma

AUTOIMMUNE diseases: Multiple Sclerosis, Diabetes Mellitus, Rheumatoid Arthiritis,

Hypertension and CARDIOVASCULAR disease

Depression and schizophrenia

26
Q

EFFECTS of VITAMIN D/ SERUM 25(OH)D DEFICIENCY

A
  • DECREASED Ca2+ and Pi ABSORPTION from INTENSTINES
    so SERUM CALCIUM FALLS
  • INCREASED PTH from PARATHYROID
    so INCREASED BONE RESORPTION
  • DECREASED Ca2+ and Pi ABSORPTION from KIDNEY
    so INCREASED PHOSPHATE WASTING
27
Q

major CLINICAL CONSEQUENCE of VIT D DEFICIENCY in CHILDREN:

A

RICKETS

28
Q

major CLINICAL CONSEQUENCE of VIT D DEFICIENCY in ADULTS:

A

OSTEOMALACIA

29
Q

what is RICKETS

A

Bone disease associated with DECREASED SERUM CALCIUM AND/OR PHOSPHATE
leading primarily to WIDENING and DELAY of MINERALISATION of GROWTH PLATES in bones.

  • Rickets is also associated with osteomalacia
    (softening of bone)
30
Q

what happens in a HEALTHY human GROWTH PLATE (PHYSIS) (3)

A
  • MATURATION of CHONDROCYTES
  • HYPERTROPHIC CHONDROCYTES undergo APOPTOSIS
  • CARTILAGE MATRIX CALCIFIES and is REPLACED with MINERALISED BONE
31
Q

what happens in a RACHITIC (ABNORMAL) GROWTH PLATE (in RICKETS) (5)

A
  • INCREASED WIDTH
  • PERSISTENCE of HYPERTROPHIC CHONDROCYTES (NO APOPTOSIS)
  • normal CHONDROCYTE COLUMNS are LOST
  • IMPAIRED CHONDROCYTE APOPTOSIS
  • IMPAIRED CARTILAGE MATRIX MINERALISATION
32
Q

CLINICAL MANIFESTATIONS of RICKETS (8)

A
  • Progressive BOWING deformities
  • Other SKELETAL DEFORMITIES (wrist-widening, knock-knees, bow legs)
  • WADDLING GAIT / DELAY in WALKING
  • Bone PAIN, FATIGUE
  • FRACTURES
  • SHORT stature
  • TETANY (involuntary muscle contractions and overly stimulated peripheral nerves) & SEIZURES
  • CARDIOMYOPATHY (disease of the heart muscle that makes it harder for the heart to pump blood to the rest of the body)
33
Q

what is OSTEOMALACIA

A

SOFTENING of the bone
due to DEFECTIVE MINERALISATION of NEWLY-FORMED BONE in a MATURE (adult) SKELETON

34
Q

CLINICAL PRESENTATIONS of OSTEOMALACIA

A
  • bone PAIN
  • Bone TENDERNESS (particularly in sternum, anterior tibia)
  • FRACTURES (spontaneous & pseudo-)
  • Muscular WEAKNESS
  • MALAISE (general feeling of discomfort, illness, or lack of well-being)
  • TETANY
  • LOW bone MINERAL DENSITY
35
Q

which STAIN shows WIDENED OSTEOID

A

TOLUIDINE BLUE

36
Q

which STAIN shows Increased UNMINERALISED OSTEOID, DECREASED MINERALISED (calcified) OSTEOID

A

VAN KOSSA

37
Q

VDR (vit D receptor) is expressed in ..

A

SKELETAL MUSCLE CELLS

38
Q

VIT D DEFICIENCEY causes MUSCLE…

A

WEAKNESS

& FALLS

39
Q

What is the ROLE of CALCITONIN (from THYROID)

A

LOWER SERUM CALCIUM (and Pi)

40
Q

how does CALCITONIN LOWER serum CALCIUM and Pi (2)

A
  • REDUCED BONE RESORPTION
  • REDUCED Ca2+ and Pi REABSORPTION from KIDNEY
    so INCREASED Ca2+ and Pi WASTING
41
Q

Medullary Thyroid Carcinoma causes

A

INCREASED CALCITONIN production

42
Q

CALCITONIN can be used for

A

SHORT-TERM TREATMENT of HYPERCALCAEMIA

43
Q

HORMONES that regulate CALCIUM HOMEOSTASIS

A

PARATHYROID HORMONE
1,25(OH)2 VITAMIN D

44
Q

is 1,25(OH)2 VITAMIN D a HORMONE

A

YES

Musculoskeletal System (18 decks)

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