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AE > 2 - Calcium Pathology > Flashcards

2 - Calcium Pathology Flashcards

1
Q

Hyperparathyroidism is a condition of what?

A

Excess PTH secretion

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2
Q

What two types of hyperparathyroidism are there?

A

Primary - within parathyroid gland

Secondary - elsewhere i.e. Chronic renal failure / rickets

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3
Q

What is a common cause of primary hyperthyroidism?

A

Monoclonal parathyroid adenoma (hyperplasia)

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4
Q

What two serum findings result from primary hyperparathyroidism?

A

1) Hypercalcaemia

2) HYPOphosphataemia

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5
Q

What are 2 complications of primary hyperparathyroidism? (bone/kidney)

A

Bone demineralisation - loss of calcium and phosphate.

Renal calculi from hypercalciuria - concentrations get so high it comes out of solution.

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6
Q

What are the most common type of calcium kidney stones?

A

Calcium oxalate

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7
Q

What is a complication of chronic bone demineralisation?

A

Multiple bone cysts

osteitis fibrosa cystica

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8
Q

What are 3 genetic causes of primary HPT?

A

1) Vitamin-D receptor mutation
2) MEN1 mutation
3) Over-expression of cyclin D1

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9
Q

What’s the pathophysiology of a vitamin-D receptor mutation leading to Primary HPT?

A

Vitamin D-R provides negative feedback to parathyroid gland, inhibiting gene expression of PTH.

Mutation = loss of -ve feedback.

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10
Q

What’s the pathophysiology of MEN1 mutation causing primary HPT?

A

MEN1 is a tumour suppressor gene. Mutation results in neoplasia.

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11
Q

What’s the pathophysiology of cyclin D1 over-expression causing primary HPT?

A

Cyclin D1 is a cell-cycle regulator.

Overexpression favours cell division = sporadic parathyroid adenoma.

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12
Q

What other symptoms occurs with hyperparathyroidism?

A

‘Stones, bones, abdominal groans and psychic moans’

Muscle weakness, depression, GI upset, lethargy, aches.

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13
Q

What is tetany?

A

Muscular spasms, caused by a deficiency in calcium (Parathyroid dysfunction)

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14
Q

What is the treatment for primary HPT?

A

Surgery - parathyroidectomy

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15
Q

What is the main complication of a parathyroidectomy?

A

Nephrolithiasis

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16
Q

How do you best avoid nephrolithiasis following a parathyroidectomy?

A

Hydration

Moderate calcium intake

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17
Q

What scan is used to detect parathyroid tumours?

A

Sestamibi

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18
Q

What radioactive isotope is used in the sestamibi scan?

A

Technetium 99

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19
Q

What is the full name of the modern parathyroidectomy?

A

Minimally invasive radio-guided parathyroidectomy (MIRP)

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20
Q

During the MIRP, how does the surgeon confirm excised tissue is a tumour and that they’ve got it all?

A

Radiation-sensitive probe can detect the presence of Technetium 99.

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21
Q

What two pathologies occur in the kidney that can augment secondary hyperparathyroidism?

A

1) Increase phosphate reabsorption (inability to excrete)

2) Decreased 1alpha hydroxylation (less vitamin D)

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22
Q

What 4 factors (2 direct, 2 indirect) therefore, increase the level of PTH secretion?

A

1) High plasma phosphate
1b) Low free calcium
2) Low vitamin D
2b) Decrease calcium GUT absorption

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23
Q

Chronic renal failure results in what area of the kidney being unresponsive to PTH levels?

A

Proximal convoluted tubule

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24
Q

In the non-affected PCT cells, what two proteins are affected by PTH?

A

1) PTH inhibits the NaPi transporter

2) PTH increases activity of 1-alpha-OHase

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25
Q

In chronic renal failure, what three consequences occur in the PCT as a result of a lack of response to PTH?

A

1) Hyperphosphataemia
2) Hypocalcaemia
3) Acidosis

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26
Q

What 3 pharmaceutical agents can be used for secondary hyperthyroidism?

A

1) Vitamin D supplementation
2) Calcimimetics
3) Phosphate binders

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27
Q

How does Vitamin D work in the context of secondary HPT?

A

Increases serum calcium and phosphate levels.

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28
Q

What are the issues with using Vitamin D as a treatment of secondary HPT?

A

Increases phosphate - already high because kidneys can’t get rid of it.

Slow onset.

Does nothing to reverse hyperplasia.

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29
Q

Give an example of a calcimimetic?

A

Cinacalcet

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30
Q

How often is cinacalcet taken?

A

1x daily

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31
Q

How does it work?

A

Positive allosteric modulators - activating the calcium receptor to inhibit PTH secretion.

(chemical parathyroidectomy)

32
Q

Which cohort of patients can receive calcimimetics?

As a result of what risk?

A

Dialysis patients

Risk of hypocalcaemia

33
Q

Which two medications for secondary HPT are usually combined together?

Why?

A

Vit D + Cinacalcet

vitamin D sustains calcium levels that cinacalcet drops

34
Q

Give one example of a phosphate binder?

A

Renagel

35
Q

How do phosphate binders work?

A

They bind to phosphate within the GI tract and stop its uptake - decreasing total PTH secretion.

36
Q

What are the two clinical signs of HYPOcalcaemia?

A

Chvostek’s sign

Trousseaus sign

37
Q

What is Chvostek’s sign?

A

Muscular tremor elicited by tapping the facial nerve resulting in mouth spasm.

38
Q

What is Trousseau’s sign?

A

Hand contortion when taking blood pressure

39
Q

What is Vitamin D-dependent Rickets Type 1?

A

An issue in vitamin D synthesis.

40
Q

What is an example of an affected enzyme in the vitamin D pathway in VDDR1?

A

1-alpha hydroxylase

41
Q

Where is 1-alpha-hydroxylase found?

A

Proximal tubule of the nephron

42
Q

What is the pathophysiology of rickets?

A

Growth occuring, but long bone strength is poor - gravity takes its effect by bowing on the femur.

43
Q

What is the definition of osteoporosis?

A

Bone mineral density of >2.5 S.D. below healthy controls.

44
Q

What is the underlying cause of osteoporosis?

A

Imbalance of bone remodelling.

Increase resorption, decrease formation.

45
Q

What is osteopenia?

A

<2.5 S.D. below health controls - en route to osteoporosis.

46
Q

What two changes occur from osteoporosis?

A

1) Reduced bone mass

2) Microarchitectural deterioration

47
Q

Which cohort is the most common to get osteoporosis?

A

Menopausal women

48
Q

Which bones are most commonly fractured in osteoporosis?

A

Hips, pelvis, spine, wrists, shoulder.

49
Q

In women, losing oestrogen has what effect on osteoclasts and osteoblasts?

A

Increase osteoblast apoptosis.

Decrease osteoclast apoptosis.

50
Q

Epidemiology of osteoporosis:
- Prevalence (women / men)

  • Cost to NHS
A

Over 50:
Men: 1/12
Women: 1/3

£2 billion / year

51
Q

What two factors determine adult bone health?

A

1) Peak bone mass (puberty)

2) Rate of bone loss

52
Q

How do estrogens maintain bone mineral density - what do they bind to ?

A

ERalpha (ERbeta?) on osteoblasts

53
Q

K/o studies of ERalpha have what effect on bone?

A

Decreases BMD.

54
Q

Ovarectomy also results in what effect on bone?

A

Decreases BMD

55
Q

What pharmaceutical agents can be used for post-menopausal women who haven’t had a fracture?

A

Bisphosphonates
Strontium ranelate
Raloxifene

56
Q

What hormone, in men, in linked more closely to bone demineralisation?

A

Oestrogen (not testosterone)

57
Q

What pharmaceutical agents can be used for post-menopausal women that have had a fracture?

A

Bisphosphonates
Strontium ranelate
Raloxifene

+ Teriparatide

58
Q

How do bisphosphonates work?

A

Inhibit osteoblast action - slowing bone loss.

59
Q

What needs to be done after taking bisphosphonates?

A

Sit upright for 30 mins - causes heartburn.

60
Q

What class of drug is raloxifene?

A

Selective estrogen-receptor modulator. (SERM)

61
Q

What does teriparatide do? Who’s it given to?

A

Drives bone formation

Post-menopausal women with previous fracture.

62
Q

Loss of function calcium-receptor mutations results in what shift on the calcium-PTH curve?

A

Rightward shift.

i.e. more calcium is required to elicit the same amount of suppression

63
Q

What effect do loss-of-function calcium receptor mutations have on PTH levels?

A

Increased PTH levels (because less suppression)

64
Q

What are two genetic types of calcium-receptor mutations?

A

1) Heterozygous

2) Homozygous

65
Q

A heterozygous calcium-receptor mutation is also called what?

A

Familial hypercalcaemia hypocalciuria

66
Q

What is a homozygous calcium-receptor mutation called?

A

Neonatal severe hyperparathyroidsm

67
Q

Familial hypercalcaemia hypocalciuria presents like what other condition?

What’s the difference?

A

Primary hyperparathyroidism

Hypocalciuria (in Primary HPT, you get hypercalciuria)

68
Q

What is the role of the calcium receptor in the nephron?

A

Reduce calcium reuptake

69
Q

In FHH, what change occurs in the nephron?

A

Becomes less sensitive to calcium, so begins to reabsorb it

70
Q

What two effects does FHH have then?

A

1) Increased PTH secretion because CaR not inhibiting.

2) Increased Ca reabsorption because less sensitive to high concentrations.

71
Q

What finding after a parathyroidectomy would make you think FHH?

A

Persistent hypercalcaemia.

72
Q

what pharmacological agent is used to treat FHH?

A

Calcimimetics (reintroduce calcium sensitivity)

73
Q

What is the treatment for neonatal severe hyperparathyroidism?

A

Early PTX

Lifelong calcium + vitamin D supplementation.

74
Q

What is a gain of function CaR mutation disease called?

A

Autosomal dominant hypocalcaemia

75
Q

Why should you NOT given vitamin D supplements to ADH patients?

A

Increases calcium
Hypercalciuria

= Kidney stones / nephrogenic diabetes insipidus

AE (7 decks)

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