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year 2 - endocrinology > Calcium & Phosphate Regulation > Flashcards

Calcium & Phosphate Regulation Flashcards

1
Q

Main parts of the body involved in the reabsorption of Ca2+?

A

Bone

Kidney

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2
Q

Calcidiol & Calcitriol?

A

Calcidiol - made in LIVER (first hydroxylation step)

Calcitriol - made in the KIDNEYS (second hydroxylation step)

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3
Q

Effects of VitD, PTH and calcitriol on Ca2+ homeostatis?

A

VitD - goes on to make calcidiol/calcitriol

PTH
o causes bone to release Ca2+
o causes kidney to INCREASE calcitriol synthesis
o causes kidney to DECREASE Ca2+ excretion

Calcitriol
o causes Ca2+ RELEASE in BONE
o causes Ca2+ reabsorption in GUT

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4
Q

The 2 ways that PO4 is regulated?

A
  1. Kidneys
    o Na+/PO4(3-) co-transporter increases PO4 reabsorption from the urine to the PCT and to the blood
  2. PTH
    o INHIBITS the co-transporter so MORE PO4 loss in urine
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5
Q

Another factor that regulated phosphate?

A

FGF23

-ve feedback on the co-transporter

IT ALSO -ve feedback on CALCITRIOL so:
o LESS PO4 reabsorption in the GUT

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6
Q

How is PTH regulated?

A

via. Parathyroid cells

HIGH [Ca2+]:
o Ca2+ binds to receptors
o receptor activation leads to INHIBITION of PTH secretion

LOW [Ca2+]:
 o Ca2+ NOT binds to receptor
 o NO INHIBITION
 o PTH is secreted
 o PTH action in body leads to INCREASED [Ca2+]
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7
Q

2 ways to get VitD in the body?

A
  1. DIET

2. SUNSHINE (UVB light)

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8
Q

Precursor of VitD, VitD3 and VitD2?

A

Precursor - 7-dehydrocholesterol

VitD3 - Cholecalciferol

VitD2 - Ergocalciferol

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9
Q

What causes the inactive VitD to become activated?

A

RENAL 1alpha-hydroxylase

o Stimulated by PTH
o Changes calciferol TO calcitriol

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10
Q

5 principal causes of VitD deficiency?

A
  1. Block in UVB light catalysation
  2. Malabsorption OR Diet insufficiency
    o e.g. Chron’s OR coeliac disease OR inflam BD
  3. Liver disease
    o NO 1st hydroxylation
  4. Renal disease
    o NO 2nd hydroxylation
  5. Receptor defects
    o autosomal recessive - RARE!!
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11
Q

HIGH EC Ca2+?

A

HYPERcalcaemia

Ca2+ BLOCKS Na+ influx
SO
LESS membrane excitability

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12
Q

LOW EC Ca2+?

A

HYPOcalcaemia

Allows for GREATER Na+ influx
SO
MORE membrane excitability

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13
Q

Normal serum range of Ca2+?

A

2.2 - 2.6 mmol/L

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14
Q

Symptoms of HYPOcalcaemia?

A

TOO MUCH excitability
o muscle cramps/tetany
o tingling

PCAT

P - parasthesia (hands, mouth, feet, lips)
C - convulsions
A - arrhythmias (Ca2+ has effect on heart)
T - tetany

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15
Q

Signs of HYPOcalcaemia?

A
  1. Chvostek’s Sign
    - indicates neuromuscular irritability due to hypocalcaemia

o Tap FACIAL NERVE just BELOW zygomatic arch
o Positive response = twitching of facial muscles

  1. Trousseau’s Sign
    - carpopendal spasm, neuromuscular irritability due to hypocalcaemia

o Inflate BP cuff for several minutes
o Positive response = carpopedal spasm

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16
Q

Causes of HYPOcalcaemia?

A
  1. VitD deficiency
    - LOW calcitriol
  2. LOW PTH levels - HYPOparathyroidism
    - due to surgical (neck surgery), auto-immune, Mg2+ deficiency
  3. PTH resistance
    - pseudohypoparathyroidism
  4. Renal failure
    - Impaired 1alpha-hydroxylation SO decreased production of calcitriol
17
Q

Symptoms of HYPERcalcaemia?

A

’ Stones, abdominal moans and psychic groans’
i.e. everything SLOWS DOWN (atonal muscles)

Stones = RENAL effects
 o Polyuria & thirst
 o Nephrocalcinosis (deposits of Ca2+ accumulate), renal colic, chronic renal failure
Abdominal moans = GI effects
 o Anorexia
 o Nausea
 o Dyspepsia
 o Constipation
 o Pancreatitis 
Psychic groans = CNS effects
 o Fatigue
 o Depression
 o Impaired concentration
 o Altered mentation
 o Coma
18
Q

Causes of HYPERcalcaemia?

A
  1. PRIMARY hyperparathyroidism
    o benign adenoma of parathyroid
    o HIGH PTH = HIGH Ca2+ (NO -ve feedback as autonomous)
  2. Malignancy
    o tumours/metastases
    o often secrete a PTH-like peptide
  3. Condition with a HIGH BONE TURNOVER
    o e.g. hyperthyroidism, Paget’s disease of bone
  4. VitD Toxicosis
    o RARE!!
19
Q

Diagnostic approach to HYPERcalcaemia when 1o HYPERPARATHYROIDISM?

A

1o HYPERPARATHYROIDISM

HIGH Ca2+ & HIGH PTH

o RAISED Ca2+
o LOW PO4
o RAISED (unsuppressed) PTH

20
Q

Diagnostic approach to HYPERcalcaemia when MALIGNANCY?

A

HIGH Ca2+
BUT
LOW PTH

-ve feedback still works!!! (compared to 1o hyperparathyroisim)

21
Q

Principal effects of VitD on intestine & kidney?

A

Intestinal:
o ABSORPTION of Ca2+, Mg2+ & PO4

Kidneys:
o REABSORPTION of Ca2+
o DECREASED PO4 reabsorption (via. FGF23)

22
Q

Definition of VitD deficiency?

A

Lack of MINERALISATION in bone

23
Q

What does VitD deficiency lead to?

A

‘Softening’ of bone
Bone deformities
Bone pain
Severe proximal myopathy

Children = RICKETS
Adults = OSTEOMALACIA (NOT osteoporosis!!!)
24
Q

Treatment of 1o hyperparathyroidism?

A

Parathyroidectomy

25
Q

2o hyperparathyroidism?

A

NO Calcitriol (VitD deficiency!)

SO LOWER Ca2+ (can be normal if PTH normalises it!)
BUT
HIGH PTH to try to normalise serum Ca2+

26
Q

Biochemical findings in VitD deficiency?

A
  1. Plasma calciferol is usually LOW
    (do NOT measure calcitriol to assess body VitD dtores normally!)
  2. Plasma Ca2+ is LOW
    (may be normal if 2o hyperparathyroidism develops)
  3. Plasma PO4 is LOW
    (reduced gut absorption)
  4. PTH is high
    (2o hyperparathyroidism)
27
Q

Radiological findings of VitD deficiency?

A

Widened osteoid seams i.e. ‘Brown Tumours’

bone lesions showing excessive osteoclastic bone resorption

28
Q

What does treatment of VitD deficiency depend on?

A

Renal function

29
Q

Treatment of VitD deficiency in patients with NORMAL renal function?

A

Give synthetic Calciferol
- hydroxylases further via. kidney

Ergocalciferol - VitD2
Cholecalciferol - VitD3

30
Q

Treatment of VitD deficiency in patients with IMPAIRED renal function?

A

Inadequate 1alpha-hydroxylase SO give ready-hydroxylated VitD

Alfacalcidol - 1alpha-hydroxycholecalciferol

31
Q

What can VitD toxicosis lead to?

A

HYPERcalcaemia & HYPERcalciuria!

as INCREASED intestinal absorption of Ca2+!

32
Q

VitD toxicosis can occur as a result of?

A
  1. Excessive treatment w. active metabolites of VitD
    e. g. alfacalcidol
  2. Granulomatous diseases
    e.g. sarcoidosis, leprosy and TB
    o macrophages in the granuloma produce 1alpha-hydoxylase, which overproduced VitD

year 2 - endocrinology (19 decks)

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