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year 2 > parathyroid glands > Flashcards

parathyroid glands Flashcards

1
Q

what are the parathyroid glands composed of

A

chief cells

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2
Q

what do the parathyroid gland chief cells secrete

A

PTH

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3
Q

what does PTH act on

A

CASR (calcium sensing receptor)

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4
Q

what kind of receptor is the CASR

A

GPCR that regulates extracellular calcium homeostasis

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5
Q

what do chief cells look like

A

round cells with moderate cytoplasm and bland round central nuclei

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6
Q

what cells support the chief cells

A

oxyphil cells (slightly larger with acidophilic cytoplasm)

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7
Q

what does PTH do to osteoclast activity

A

increases osteoclast activity releasing Ca and phosphate

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8
Q

what does PTH do to small bowel absorption of calcium and phosphate

A

indirectly increases small bowel absorption of Ca and phosphate by activating vitamin D

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9
Q

what does PTH do to kidney reabsorption of calcium

A

increased calcium reabsorption in distal tubule

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10
Q

what does PTH do to phosphate excretion in kidney

A

decreased phosphate excretion in proximal tubule

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11
Q

what effect does increased serum calcium have on PTH secretion

A

negative feedback

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12
Q

what are the 4 main symptoms of hypercalcaemia

A

BONES
MOANS
STONES
GROANS

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13
Q

BONES

A

pain
fracture
osteoporosis
osteitis fibrosa cystica

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14
Q

what is osteitis fibrosa cystica

A

resorption of bone leading to fibrosis and cystic spaces

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15
Q

what ix should be done in ‘bones’ symptoms of hypercalcaemia

A

DEXA

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16
Q

STONES

A

nephrolithiasis and complications

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17
Q

GROANS

A

GI complications - nausea, constipation, peptic and duodenal ulcers, acute pancreatitis, gall stones, abdominal pain

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18
Q

MOANS

A

depression, lethargy, seizures, weakness and fatigue

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19
Q

what are some other symptoms of hypercalcaemia

A

nephrocalcinosis - calcification of renal tubules - can lead to renal insufficiency and polyuria
calcification of the aortic and mitral valves
hypertension

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20
Q

what are s/s of acute hypercalcaemia

A

thirst
dehydration
confusion
polyuria

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21
Q

what is the treatment of acute hypercalcaemia

A 
fluids (0.9% saline, 4-6L in 2 hours)
loop diuretics (avoid thiazide)
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22
Q

what is the treatment of acute hypocalcaemia

A

IV calcium gluconate (10ml in 50ml saline or dextrose)

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23
Q

what are some s/s of hypocalcaemia

A 
muscle weakness
muscle spasm (tetany)
muscle cramps
fits
fatigue
paraesthesia of fingers, toes and perioral area
bronchospasm or laryngospasm
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24
Q

what is an ECG change of hypocalcaemia

A

QT prolongation

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25
Q

what 2 signs are positive in hypocalcaemia that show muscle spasm/tetany

A

Chovslek’s sign - tapping over facial nerve

Trosseau sign - carpopedal spasm - filling of a BP cuff

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26
Q

how is vitamin D3 formed

A

by the skin on exposure to the sun

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27
Q

where can you get Vitamin D3 and D2

A

from diet

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28
Q

the liver metabolises vitamin D3 to

A

25-OH-vitamin D

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29
Q

the kidney metabolises 25-OH-vitamin D to

A

1,25-hydroxy vitamin D

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30
Q

in what condition will almost always develop a parathyroid adenoma and hypercalcaemia at a young age

A

MEN 1/2

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31
Q

what are some causes of hypocalcaemia

A 
hypoparathyroidism
vit D deficiency
chronic renal failure
pancreatitis
hyperventilation
osteoblastic bone mets
rhabdomyolysis
high turnover - bed ridden, thyrotoxic, Pagets
granulomatous disease e.g. sarcoid/TB
drugs - Vit D, thiazides, lithium
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32
Q 
primary hyperparathyroidism biochemistry:
Ca
PTH
Phosphate
urinary cAMP
ALP
A 
HIGH Ca
HIGH PTH
low phosphate
HIGH urinary cAMP
HIGH ALP
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33
Q

what is primary hyperparathyroidism

A

primary overactivity of the parathyroid galnds

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34
Q

what are the 4 main causes of primary hyperparathyroidism

A

adenoma
hyperplasia
carcinoma
malignancy

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35
Q

what is the most common cause of primary hyperparathyroidism

A

adenoma

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36
Q

how many glands are affected in parathyroid adenoma

A

just one - other glands are atrophic

37
Q

how does an parathyroid adenoma usually present

A

usually asymptomatic hypercalcaemia but may get BSMG

38
Q

what is the treatment of a parathyroid adenoma

A

removal of affected gland

39
Q

although an adenoma may resemble a normal parathyroid gland microscopically, what might you see

A

fibrous connective tissue capsule with adjacent rim of compressed parathyroid tissue

40
Q

what syndromes is parathyroid hyperplasia associated with

A

MEN 1 / MEN2b

41
Q

parathyroid hyperplasia usually involves what glands

A

all glands

42
Q

what is the treatment of parathyroid hyperplasia

A

removal of all affected glands

43
Q

what % of primary hyperparathyroidism is due to hyperplasia

A

5-10%

44
Q

what % of primary hyperparathyroidism is due to carcinoma

A

1%

45
Q

what are some complications of parathyroid excision

A

recurrent laryngeal nerve palsy
hypoparathyroidism
low Ca - hungry bone sydrome

46
Q

what cancer causes a paraneoplastic syndrome there there is release of PTHrp from solid tumours

A

squamous cell lung cancer

breast/renal cell carcinomas

47
Q

how is hyperparathyroidism caused by malignancy diagnosed

A 
raised Ca and ALP
xray
CT
MRI
isotope bone scan
48
Q

what is PTH like in hyperparathyroidism caused by malignancy

A

PTH low - PTHrp causes high Ca which negatively feeds back to PTH

49
Q

what is familial isolated hyperparathyroidism

A

inherited form of hyperparathyroidism

get an adenoma

50
Q

what are the indications for a parathyroidectomy

A

end organ damage (bone disease, gastric ulcers, renal stones)
Ca > 2.85
< 50
eGFR < 60

51
Q

what is secondary hyperparathyroidism

A

chronic hypocalcaemia causes compensatory over activity of the parathyroid glands

52
Q 
secondary hyperparathyroidism biochemistry
Ca
PTH
phosphate
ALP
A

LOW calcium
HIGH PTH
HIGH phosphate
raised ALP

53
Q

what is the most common cause of secondary hyperparathyroidism

A

chronic renal failure

54
Q

how does chronic renal failure lead to secondary hyperparathyroidism

A

renal insufficiency leads to decreased phosphate excretion
increased serum phosphate binds to free Ca
decreased free Ca stimulates all 4 parathyroid glands
increased PTH —> bone resorption

55
Q

what is the parathyroid tissue like in secondary hyperparathyroidism

A

hyperplastic

56
Q

what is the treatment for secondary hyperparathyroidism

A

phosphate binders

vit D

57
Q

what else might be raised in secondary hyperparathyroidism

A

25-OH vit D

metabolised by the kidneys so accumulation

58
Q

what is tertiary hyperparathyroidism

A

parathyroid gland becomes autonomous due to many years over over activity e.g. in renal failure

59
Q

tertiary hyperparathyroidism biochemistry
Ca
PTH
Phosphate

A

HIGH Ca
HIGH PTH
raised phosphate

60
Q

what is cinacalcet

A

calcium mimetic

61
Q

when is cinacalcet used

A

tertiary hyperparathyroidism
carcinoma
primary if not fit for surgery

62
Q

how does cinacalcet decrease PTH

A

increases sensitivity of parathyroid cells to Ca so decreases PTH secretion

63
Q

familial hypocalciuric hypercalcaemia biochemistry
Ca
urine Ca
PTH

A

mild hypercalcaemia
decreased urine calcium excretion
marginally elevated PTH
usually benign/asymptomatic

64
Q

what is the inheritance of FHH

A

autosomal dominant

65
Q

what is the genetic cause of FHH

A

deactivating mutation in CASR

66
Q

what does vit D deficiency lead to with regard to calcium levels

A

low calcium

67
Q 
Low calcium
muscle wasting - proximal myopathy
dental defects (Caries, enamel)
tender bones/fractures/rib deformitity/limb deformity
waddling gait 
loosers zones
A

osteomalacia

rickets in children

68
Q

what is Vitamin D resistant rickets

A

X linked hypophosphataemia

69
Q

what is the gene mutation in X linked hypophosphataemia

A

PHEX or FGF23

70
Q

what does the FGF23 gene usually do

A

regulates phosphate levels in plasma

71
Q

what are the levels of phosphate and vitamin D like in vitamin D resistant rickets

A

high vitamin D

low phosphate

72
Q

what is the treatment for vitamin D resistant rickets

A

phosphate and vitamin D supplements

73
Q

what are some long term consequences of vitamin D deficiency

A

bone disease
malignancy (esp colon)
heart disease
diabetes

74
Q

what is the treatment for vitamin D deficiency

A

Vit D3 tablets
calcitrol
alfacalcidol
combined calcium + vit D e.g. adcal D3

75
Q

what is the PTH and Ca level in hypoparathyroidism

A

low PTH

low Ca

76
Q

what is the treatment of hypoparathyroidism

A

calcium supplements and vitamin D tablets
calcitrol
synthetic PTH

77
Q

is hypo or hyper parathyroidism more common

A

hyper

hypo is very rare

78
Q

what are some causes of hypoparathyroidism

A 
usually post op - surgery/radiotherapy
malignancy
congenital absence - Di George Syndrome (22q11.2)
familial 
hypomagnesaemia
79
Q

how does hypomagnesaemia cause hypoparathyroidism

A

calcium release from cells + PTH secretion both rely on magnesium

80
Q

what is the treatment of hypomagnesaemia

A

calcium and magnesium replacement

81
Q

what can cause hypomagnesaemia

A

alcohol, drugs (thiazide, PPI), GI illness, pancreatitis, malabsorption

82
Q

what is pseudohypoparathyroidism

A

failure of target cell response to PTH

83
Q

what is the genetic defect in pseudohypoparathyroidism

A

dysfunction of G protein (Gs alpha subunit)

GNAS-1 gene

84
Q

what is the biochemistry of pseudohypoparathyroidism
Ca
phosphate
PTH

A

Low Ca
High phosphate
High PTH

85
Q

what are some s/s of pseudohypoparathyroidism

A 
obesity/round face
subcutaneous calcification
learning disability
calcified basal ganglia
AD form assoc. short stature and brachydactylyl of 4th and 5th metacarpals
bone abnormalities
86
Q

what is the treatment of pseudohypoparathyroidism

A

calcium and vit D supplements

87
Q

what is pseudopseudohypoparathyroidism

A

normal biochemistry but morphological features of pseudohypoparathyroidism

88
Q

what is another name for pseudopseudohypoparathyroidism

A

albright’s hereditary osteodystrophy

89
Q

what is a sign of mccune albright syndrome in bones

A

areas of abnormal fibrous scarring in bones

year 2 (19 decks)

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