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AY Endocrine > Parathyroid physiology > Flashcards

Parathyroid physiology Flashcards

1
Q

What stimulates the parathyroid gland to release PTH?

A

Decreased calcium

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2
Q

Where is vitamin D3 produced?

A

Skin

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3
Q

How is calcidiol produced?

A

Converted from Vit D3 in the liver

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4
Q

What enzyme converts calcidiol to calcitriol?

A

a-hydroxylase

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5
Q

What does PTH stimulate?

A

Kidney (a-hydroxylase to convert calcidiol to calcitriol)
Bone (release calcium & phosphate)
DCT (increase calcium reabsorption)

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6
Q

What exhibits a negative feedback mechanism on PTH?

A

Calcitriol

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7
Q

Whatdoes calcitriol stimulate?

A

Bone (release calcium & phosphate)
GI tract (absorb calcium & phosphate)
PCT (reabsorb calcium)

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8
Q

What stimulates release of calcitonin from the thyroid gland?

A

Decreased calium

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9
Q

What is the parathyroid gland composed of?

A

Chief cells

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10
Q

Symptoms/signs of hyperparathyroidism

A

Bone disease (pain, fracture, osteoporosis)
Renal stones
GI (constipation, nausea, peptic ulcer, gallstones, pancreatitis)
CNS (depression, lethargy, seizures)
Muscular weakness & fatgue
CVS (Calcification of aortic + mitral valves)

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11
Q

Causes of hperparathyroidism

A

Adenoma

Hyperplasia

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12
Q

Management of hyperparathyroidism

A

Surgery

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13
Q

Indications for parathyroid surgery

A

End organ damage

Very high calcium (>2.85)

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14
Q

What is primary hyperparathyroidism?

A

Primary overactivity of parathyroid (e.g.adenoma)

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15
Q

What are the biochemical findings of primary hyperparathyroidism?

A

High PTH
High Calcium
Normal Alk Phos
Low phosphate

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16
Q

What is secondary hyperparathyroidism?

A

Physiological response to low calcium due to chronic hypocalcaemia
(parathyroid is hyperplastic)

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17
Q

Causes of secondary hyperparathyroidism

A

Renal failure
Low calcium intake
Vit D deficiency

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18
Q

Biochemical findings of secondary hyperparathyroidism

A

Low calcium

High PTH

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19
Q

What is tertiary hyperparathyroidism?

A

Parathyroid becomes autonomous after many years of secondary

20
Q

Biochemical findings of tertiary hyperparathyroidism

A

High calcium

High PTH

21
Q

What can be a congenital cause of absent parathyroid glands?

A

Di George syndrome

22
Q

Causes of hypoparathyroidism

A

Congenital abscence
Destruction (surgery, malignancy, radiotherapy)
Autoimmune
Hypomagnaesmia

23
Q

Treatment of hypoparathyroidism

A

Calcium & Vitamin D supplements

24
Q

What is a mild type of osteogenesis imperfecta?

A

Type I

25
Q

What are the severe types of osteogenesis imperfecta?

A

Types III & IV

26
Q

Which type of osteogenesis imperfecta causes nneonatsl death?

A

Type II

27
Q

What is osteogenesis imperfecta associated with?

A

Blue sclerae

Dentinogenesis

28
Q

Management of osteogenesis imperfecta

A

No cure

Bisphosphonates

29
Q

Causes of vitamin D deficiency

A

Dietary deficiency
Malabsorption
Chronic renal failure
Drugs (anti-convulsants)

30
Q

Features of osteomalacia

A

Low calcium
Proximla muscle wasting
Dental defects
Bone tenderness

31
Q

What mutation causes vitamin D resistant rickets?

A

PHEX gene mutation

32
Q

Treatment of vitamin D resistant rickets

A

Phosphate + Vit D3

33
Q

Why does hypomagnasaemia affect calcium levels?

A

Calcium release from cells is dependent on magnesium
Means increased intracellular calcium
PTH release is inhibited
Skeletal + muscles receptors less sensitive to PTH

34
Q

Cuases of hypomagnasaemia

A

Alcohol (+/- PPI)
Drugs (thiazide, PPI)
GI illness (malabsorption)
Pancreatitis

35
Q

What is pseudohyperparathyroidism a genetic defect of?

A

GNAS 1

36
Q

Biochemical findings of pseudohyperparathyroidism

A

Low calcium

High PTH

37
Q

Features of pseudohyperparathyroidism

A 
Bone abnormalities (McCune Labright) 
Obesity 
Subcutaneous calcification 
Learning diability 
Brachdactyly (4th metacarpal)
38
Q

Difference between pseudohyperparathyroidism & pseudo-pseudohyperparathyroidism

A

Pseudo-pseudo has normal calcium

patients can change from pseudo to pseudo-pseudo

39
Q

What is Paget’s disease?

A

Abnormal osteoclastic activity followed by increased osteoblastic activity = abnormal bone structure

40
Q

Which bones are typically affected by Paget’s?

A

Long bones
Pelvis
Lumbar spine
Skull

41
Q

How does Paget’s present?

A

Incidenc increases with age
Bone pain
Deformity
Deafness

42
Q

What is a rare complication of Paget’s?

A

Osteosarcoma

43
Q

Treatment of Paget’s

A

Treat with bisphosphates if pain not responding to analgesia

44
Q

Biochemical findings of FHH

A

High calcium
Normal PTH
Normal Alk Phos
Normal phosphate

45
Q

Biochemical findings of hypoparathyroidism

A

Low calcium
Low PTH
Normal Alk Phos
Normal phosphate

46
Q

Biochemical findings of osteomalacia

A

Low calcium
High PTH
High Alk Phos
Low phosphate

47
Q

Biochemical findings of Paget’s

A

Normal calcium
Normal PTH
High Alk Phos
Normal phosphate

AY Endocrine (18 decks)

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