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year 2 - endocrine > bone and parathyroid disease > Flashcards

bone and parathyroid disease Flashcards

1
Q

what are osteoblasts

A

bone forming cells

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2
Q

what are osteoclasts

A

bone resorbing cells

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3
Q

what is the biologically active form of vitamin D

A

calcitriol

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4
Q

what is calcitonin produced by

A

parafollicular cells in the thyroid gland

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5
Q

what is osteoporosis

A

progressive systemic skeletal disease characterised by low bone mass and micro-architecture deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility of fracture

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6
Q

osteoporosis cause

A

increase in bone turnover due to imbalance in bone turnover, leading to a shift towards increased resorption which induced bone mass and causes the micro-architectural changes

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7
Q

osteoporosis risk factors

A
  • age
  • family history
  • anorexia
  • myeloma
  • rheumatoid arthritis
  • liver/renal failure
  • drugs (prolonged steroids)
  • smoking, alcohol, immobility, low BMI
  • hyperthyroidism, hyperparathyroidism, diabetes, hypogonadism, early menopause
  • chronic liver disease, IBD, pancreatitis, malabsorptive conditions (coeliac)
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8
Q

osteoporosis presentation

A
  • asymptomatic until minimal trauma fracture occurs
  • common fractures are colles, hip and vertebral wedge
  • domino effect of one fracture leading to increased change of anther
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9
Q

DEXA score > 1 =

A

good bone mineral density

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10
Q

DEXA score 1 to -1 =

A

normal bone mineral density

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11
Q

DEXA score -1 to -2.5 =

A

osteopenia

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12
Q

DEXA score < -2.5 =

A

osteoporosis

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13
Q

osteoporosis lifestyle management

A

smoking cessation, alcohol reduction, resistance training, calcium supplements, education about fall prevention (given to patients with osteoporosis and osteopenia)

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14
Q

osteoporosis pharmacological management

A
  • bisphosphonates (prevent bone resoprtion by killing off osteoclasts)
  • strontium ranelate (reduces bone resorption)
  • teriparatide
  • denosumab (monoclonal antibody against RANKL)
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15
Q

Paget’s disease pathophysiology

A
  • metabolic disease of bone
  • characterised by increased bone turnover associated with increased number of both osteoblasts and osteoclasts
  • result is bone remodelling with resultant bone being deposited in a disorganised manner
  • consequences of bone remodelling include bone enlargement and deformity due to disorganised bone being weaker
  • primarily affects the tibia, femur, vertebrae, skull and pelvis
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16
Q

Paget’s presentation

A
  • most are asymptomatic
  • deep, boring bone pain that is worse at night and with weight bearing
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17
Q

Paget’s investigations

A
  • bloods: high ALP, normal calcium, normal phosphate

x-ray
- early disease: lytic lesions
- late disease: cortical thickening, deformity
- skull disease: cotton wool appearance

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18
Q

what is Ricket’s

A

abnormal bone mineralisation during periods of active bone growth ad before fusion of epiphyseal plates

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19
Q

what is osteomalacia

A

abnormal bone mineralisation in the time after the fusion of the epiphyseal plates

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20
Q

osteomalacia/Rickets pathophysiology

A

abnormal bone mineralisation (normal amount of bone, but mineral content of this bone is low)

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21
Q

osteomalacia/Rickets causes

A
  • vitamin D deficiency
  • renal bone disease
  • liver disease (cirrhosis)
  • drugs (anti-convulsant)
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22
Q

Rickets presentation

A
  • growth retardation
  • bow legged or knock kneed
  • hypotonia
  • apathy
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23
Q

osteomalacia presentation

A
  • bone pain
  • fractures, especially femoral neck
  • proximal myopathy
  • waddling gait
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24
Q

osteomalacia/Rickets diagnosis

A

bloods: hypocalcaemia
- vitamin D deficiency: low calcium, PO4 and vitamin D, high ALP and PTH
- renal bone disease: low calcium, high PO4, PTH and ALP

x-ray
- looser zones, rugged metaphyseal plates, reduced cortical bone
- looser zones are characteristic (they are pseudo-fractures and are sclerotic lines that lie perpendicular to cortical bone)
- rugged metaphyseal plates are seen in rickets

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25
Q

osteomalacia/Rickets caused by vitamin D deficiency management

A

calcium/vitamin D supplements

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26
Q

osteomalacia/Rickets caused by renal disease management

A

diet restriction, phosphate binders, alfacalcidol (vitamin D)

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27
Q

primary hyperparathyroidism causes

A
  • result of either solitary parathyroid gland adenoma or hyperplasia of all four parathyroid glands
  • may present as part of MEN
28
Q

primary hyperparathyroidism presentation

A
  • hypertension
  • bone resorption: bone pain, fractures, osteoporosis
  • hypercalcaemia: fatigue, weakness, thirst, renal stone, abdominal pain, pancreatitis, depression
29
Q

primary hyperparathyroidism diagnosis

A
  • 24 hour urinary calcium
  • blood: increased PTH, calcium, low PO4
  • imaging: sesatimbi scan to visualise glands
30
Q

primary hyperparathyroidism diagnostic criteria

A
  • hypercalcaemia, high PTH
  • normal UE
  • high urine calcium
  • not on lithium or thiazide
31
Q

primary hyperparathyroidism management

A
  • watchful waiting
  • surgical removal of adenoma or all four parathyroid glands (total parathyroidectomy)
32
Q

what is secondary hyperparathyroidism

A

physiological response to low serum calcium, with the increase seen being appropriate to the deficit

33
Q

what is tertiary hyperparathyroidism

A

hyperplastic changes in the parathyroid glands in response to prolonged hypocalcaemia

34
Q

secondary and teriarty hyperparathyroidism causes

A
  • vitamin D deficiency
  • chronic kidney disease
35
Q

secondary and tertiary hyperparathyroidism pathophysiology

A

elevated PTH in response to hypocalcaemia

36
Q

secondary hyperparathyroidism diagnosis

A
  • low calcium
  • high PTH
  • high PO4
37
Q

tertiary hyperparathyroidism diagnosis

A
  • high calcium
  • very high PTH
  • low PO4
38
Q

secondary and tertiary hyperparathyroidism management

A
  • treat underlying cause
  • renal disease: diet restriction, phosphate binders
39
Q

what is malignant hyperparathyroidism

A
  • parathyroid related protein released by following cancers: small cell lung, renal and breast
  • protein mimics PTH and acts to increase serum calcium
40
Q

malignant hyperparathyroidism diagnosis

A
  • high calcium
  • low PTH
41
Q

what is hypoparathyroidism

A

low PTH due to gland failure

42
Q

hypoparathyroidism causes

A
  • decrease Mg2+
  • autoimmune
  • DiGeorge syndrome
  • haemochromatosis/Wilson’s
  • iatrogenic: thyroid surgery or radio-ablation
43
Q

hypoparathyroidism presentation

A
  • hypocalcaemia
  • numbness
  • muscle cramps
  • spasms
  • wheeze
  • anxiety
44
Q

hypoparathyroidism diagnosis

A
  • low calcium
  • low PTH
  • high PO4
45
Q

hypoparathyroidism management

A
  • treatment of underlying cause
  • calcium and vitamin D supplements
46
Q

what is pseudohypoparathyroidism

A

genetic condition associated with peripheral resistance to PTH

47
Q

pseudohypoparathyroidism presentation

A
  • low IQ
  • obesity
  • short stature
  • bradydactylyl of 4th metacarpal
48
Q

pseudohypoparathyroidism diagnosis

A
  • low calcium
  • high PTH
  • high PO4
49
Q

pseudohypoparathyroidism

A

calcium and vitamin D supplements

50
Q

what is psuedo pseudohypoparathyroidism

A

genetic condition (may be associated with some of the morphological features of pseudo-hypoparathyroidism but with normal biochemistry)

51
Q

pseudo pseudohypoparathyroidism diagnosis

A
  • normal calcium
  • high PTH
  • normal PO4
52
Q

hypercalcaemia causes

A
  • dehydration
  • parathyroid disease
  • familial hypocalciuric hypercalcaemia (autosomal dominant condition associated with reduction in calcium sensing abilities of parathyroid glands. produces mild but symptomatic hypercalcaemia. may be associated with recurrent episodes of pancreatitis)
  • bone pathology: malignancy, myeloma, vitamin D excess
  • drugs: thiazides
53
Q

hypercalcaemia presentation

A
  • bones, stones, groans and psychiatric moans
  • fatigue, weight loss, thirst
  • polyuria, dehydration
  • abdominal pain, vomiting, constipation
  • osteoporosis, weakness
  • kidney stones, renal failure
  • confusion, depression
54
Q

hypercalcaemia general diagnosis

A
  • bloods (always check PTH)
  • urine: 24 hours urinary calcium
  • ECG: short QT interval
55
Q

hypercalcaemia caused by dehydration diagnosis

A

raised albumin and urea

56
Q

hypercalcaemia caused by familial hypoalciuric hypercalcaemia diagnosis

A
  • normal or low albumin
  • normal or high PTH
  • high urinary calcium
57
Q

hypercalcaemia caused by bone metastasis diagnosis

A
  • normal or low albumin
  • high PO4
  • low PTH
  • high ALP
58
Q

hypercalcaemia caused by myeloma or vitamin D excess diagnosis

A
  • normal or low albumin
  • high PO4
  • low PTH
  • normal ALP
59
Q

hypercalcaemia management

A
  • acute hypercalcaemia: rehydration and bisphosphonates (IV pamidronate)
  • treat underlying cause
  • increase fluid intake
  • working out the cause
60
Q

hypocalcaemia with associated increased PO4 causes

A
  • hypoparathyroidism
  • pseudo-hypoparathyroidism
  • vitamin D deficiency
  • chronic kidney disease
  • low magnesium
61
Q

hypocalcaemia with normal or decreased PO4 causes

A
  • osteomalacia
  • acute pancreatitis
  • over hydration
  • respiratory alkalosis
62
Q

hypocalcaemia presentation

A
  • dry skin
  • peri-oral paraesthesia, seizures
  • muscle weakness, spasms of hands of feet
  • increased smooth muscle tone: wheeze, dysphagia, colic
  • anxiety, irritability, irrational behaviour, confusion, disorientation
63
Q

hypocalcaemia diagnosis

A
  • ECG: long QT interval
  • Choystek’s sign:
  • trousseau’s sign
64
Q

what is Choystek’s sign

A

twitching of corner of mouth on tapping the facial nerve over the parotid

65
Q

what is trousseau’s sign

A

inflation of blood pressure cuff above systolic causes spasms of the hand

66
Q

hypocalcaemia acute/severe management

A

calcium gluconate

67
Q

hypocalcaemia chronic/mild management

A

calcium and vitamin D supplements

year 2 - endocrine (6 decks)

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