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MSK sem3 > disorders of calcium balance > Flashcards

disorders of calcium balance Flashcards

1
Q

what glands are the main control of calcium release and storage in the bone?

A

parathyroid glands

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2
Q

outline the development of the superior and inferior parathyroid glands as well as the thymus

A
  • thymus and inferior parathyroid gland are formed from the third pharyngeal pouch/ arch
  • the arch forms they thymus as it gets dragged down
  • superior parathyroid comes from the fourth pharyngeal arch
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3
Q

what pulls the inferior parathyroids into its position

A

the descending of the thymus pulls them into their position

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4
Q

what cells secrete parathyroid hormone

A

chief cells

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5
Q

outline the sequence by which the skin and body use sunlight to produce active vitamin D

A
  • 7-dehydrocholesterol in the skin under the influence of sunlike is converted into cholecalciferol
  • cholecalciferol is transported to the liver and it converted into the inactive 25 OH Vit D
  • 25 OH Vit d is turned into its active form 1,25 di OH Vit D in the kidney via hydroxylation
  • using the enzyme 1-alpha hydroxylase
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6
Q

outline the 3 main action of PTH (parathyroid hormone)

A
  • inc Vit D, which acts on the gut inc Ca absorption
  • act on the bone, stimulating osteoblasts to express RANK ligand to cause osteoclasts to resorb bone and inc plasma Ca
  • inc Ca resorption and inc phosphate excretion, causing more free calcium in the plasma
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7
Q

What are the biological processes that occur when calcium levels are too high?

A
  • 1-alpha hydroxylation of vitamin D in the kidney is inhibited
  • inhibition of PTH production to compensate for high Ca
  • calcitonin is produced from the c-cells of the thyroid gland
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8
Q

What is the action of calcitonin on bone?

A
  • inhibit action of PTH, stopping the activation of osteoblasts with RANK ligand and stopping osteoclast resorption of bone
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9
Q

outline causes of hypercalcaemia

- divide causes by PTH level

A

high PTH causes

  • hyperparathyroidism (most common)
  • rare = cancers

low PTH causes
- excessive Vit D levels bc of- exogenous release, granulomatous disease, William’s syndrome

inc bone turnover
- such as in acromegaly or thyrotoxicosis

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10
Q

what is the rhyme for the symptoms and then outline them regarding :

  • neuro
  • cardio
  • GI
  • renal
  • bones
A
  • bones, stones and psychic moans
  • neuro: confusion, fatigue
  • cardio: shortening of QT interval, dec. refractory period
  • GI: release of gastrin, inc acid output, peptic ulcer disease
    renal: kidney stones, distal renal acidosis
    bones: muscle weakness, osteoporosis
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11
Q

outline primary hyperparathyroidism

A
  • serum calcium is high
  • there is a tumour on the parathyroid gland which produces too much PTH
  • so PTH levels are high
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12
Q

outline secondary hyperparathyroidism

A
  • serum calcium is low
  • PTH levels are high but this is a normal physiological response to low calcium
  • can be resistance to PTH
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13
Q

what conditions and why would result in secondary hyperparathyroidism?

A
  • renal disease because there is no activation of Vit D
  • liver disease
  • calcium malabsorption
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14
Q

outline tertiary hyperparathyroidism

A
  • PTH is high
  • Ca levels start to rise too high
  • this is because the gland has become autonomous and can’t turn itself off, even though it isn’t required because Ca levels have normalised
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15
Q

what is required for tertiary hyperparathyroidism is occur

A
  • secondary hyperparathyroidism
  • where the patient must have a past reason for having low calcium levels such as renal disease and have now had a kidney transplant or where Vit D deficient but are now taking supplements
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16
Q

outline some epidemiology facts regarding primary hyperthyroidism

A
  • most common cause of elevation PTH and calcium levels
  • patients usually older than 40
  • much more common in females
  • high PTH levels may be related to multiple endocrine neoplasia (MEN)
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17
Q

what cancers can produce PTH?

A

small cell lung cancers

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18
Q

what cancers produce PTH-RP?

A

lung cancers, myeloma, lymphoma

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19
Q

what solid tumours go to bone and cause hypercalcaemia and how do they cause this?

A
  • lung, kidney, breast

- go to the bone, destroying it (osteolytic), releasing calcium

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20
Q

why do multiple myeloma cells not show up on bone scans? what scanning technique must therefore be used?

A
  • as myeloma cells produce osteoclast-activating factor
  • these only stimulate osteoclasts who’s activity cannot be picked up by bone scans
  • so X-rays of every bone of the body must be taken instead
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21
Q

what can be used to measure osteoblast activity?

what do osteosclerotic conditions do?

A
  • bone scans

- make bones more solid

22
Q

what does bone resorption signalling rely on?

what do cancer cells do then they invade bone?

A
  • inflammatory cytokines from the osteoblast to activate the osteoclast
  • they set up an inflammatory response which produces cutlines and immune mediators
  • these activate osteoclasts to resorb bone and calcium is released
23
Q

what are granulomatous disease?

A
  • characterised by immune response
  • granulomas are to deal with big parasites that macrophages cannot be consumed by macrophages
  • so granulomas surround the invader and wall it off
  • granulomas contain macrophages and the enzyme 1-alpha hydroxylase which activates Vit D
24
Q

name 3 examples of granulomatous disease

A
  • sarcodiosis
  • tuberculosis
  • berylliosis (heavy metal poisoning)
25
Q

outline 5 other miscellaneous reasons for hypercalcaemia

A
  • immobilisation of bone
  • recovery from renal transplant (tertiary hyperparathyroidism)
  • familial hypocaciuric hypercalcemia
  • milk-alkali syndrome (large intake of milk to soothe acid and osteoporotic problems)
  • thiazide diuretics (inc resorption of calcium)
26
Q

why does bone immobilisation cause hypercalcaemia?

A
  • there is no electrical signal to tell osteoblasts to work
  • so osteoclast work more than osteoblasts
  • so more bone resorption
  • so inc in calcium
27
Q

outline familial hypocalcuiric hypercalcaemia

A
  • PTH and calcium high
  • little calcium in the urine which is a normal renal response to inc calcium
  • this is as theres is defect in the calcium- sensing gene (CaSR gene) which encodes the a calcium sensing receptor - is present in the bone
  • so even though calcium in the blood is raised it doesn’t affect their physiology
  • condition is asymptomatic despite them having hypercalcaemia and hypocalciuria
28
Q

what are the investigations carried out for suspected hypercalcaemia?

A

look at levels of:

  • calcium
  • phosphate
  • vit D
  • PTH
  • urinary calcium excretion
29
Q

what investigations would be carried out to look at the causes of hypercalcaemia?

A
  • chest xray
  • measure ACE levels
  • myeloma screen
30
Q

what investigations would be carries out in hypercalcaemia with high PTH levels

A
  • assume this is someone with primary hypercalcaemia
  • localise the tumour in order to remove it
  • look at kidneys to look for stones
  • DEXA scan to measure calcium in bone (as high PTH can cause osteoporosis
31
Q

what are the issues with scanning the parathyroids? how is this overcome?

A
  • when scanning the parathyroids the markers go to both the parathyroids and they thyroid
  • making them indistinguashable
  • so use SetsaMIBI scanning where marker will go to both but will be retained in the parathyroids longer
32
Q

outline the treatment for hypercalcaemia

A
  • rehydrate the patient with saline, which allows the Na/Ca exchanger to work
  • furosemide (loop diuretic) to flush calcium out of the body
  • steroid (prednisolone) to suppress the immune response/ activity
  • calcitonin
  • biphospates to inhibit osteoclast activity to maintain existing bone mineralisation if patient has gotten osteoporosis
  • calcimimetics that active the calcium sensing receptors, so induce the processes to reduce calcium levels
33
Q

what happens when there is low calcium in regards to Vit D?

A

when calcium is low:

  • PTH release is stimulated
  • inc activation of 1-alpha hydroxylase to activate Vit D
34
Q

what are the causes of hypocalcaemia when PTH is low?

A

hypoparathyroidism

35
Q

what are the causes of hypocalcaemia when PTH is high?

A
  • psudohypoparathyroidism
  • Vit D deficiency (renal/ liver disease)
  • poor dietary calcium
  • malabsorption of calcium
  • chelation
36
Q

outline primary hypoparathyroidism

A
  • can be congenital eg. Digeorges syndrome

- autoimmune conditions where antibiodies attack the parathyroid and stop them working

37
Q

outline secondary hypoparathyroidism

A

usually to do with things in the neck:

  • after surgery/ trauma damaging the parathyroidism
  • radioiodine
38
Q

what is the cause of neonatal hypoparathyroidism?

A
  • if child is born too early
  • parathyroids have not adequately developed
  • PTH-RP stops being produced after birth
  • so PTH deficiency
39
Q

what condition to do with magnesium can cause hypoparathyroidism and why?

A
  • hypomagnesemia or hypermagnesmia

- as magnesium is an important co-factor in PTH production

40
Q

how is calcium chelation used?

A
  • Stop blood clotting by placing citrate which takes out calcium
  • this stops the clotting cascade
  • this is put into blood that will be used for transfusion to stop it clotting
  • When put into person it will work again because citrate will not be present in recipients blood
  • when high levels of blood are transfused it can cause calcium level drops
41
Q

signs and symptoms of hypocalcaemia

A
  • pins and needs (paresthesias)
  • chvostek’s sign
  • trousseau’s sign
  • prolonged QT interval on ECG
42
Q

what is chvostek’s sign?

A

when tap on the facial nerve and there is a facial spasm in patients with hypocalcaemia

43
Q

what is trousseau’s sign?

A
  • when BP cuff is put on the arm and inflated to a level above systolic BP
  • held for 3 mins
  • patients hand will go into titanic spasm
44
Q

investigations for hypocalcaemia

A
  • ECG

- same as hypercalcaemia

45
Q

treatment of hypocalcaemia

A
  • give calcium and and Vit D supplementation
  • if patient is fitting or unconscious give an IV
  • if person has kidney disease you cant give Vit D bc kidney wont be able to activate it so calcidol is given
  • calcidol is artificial 1-alpha hydroxylase
46
Q

what will you see in the biochemistry of a patient with pseudoparathyroidism?

A
  • high PTH
  • low calcium
  • high phosphate
  • low active Vit D
47
Q

what are the classic physical features of a person with pseudoparathyroidism?

A
  • short stature
  • obese
  • moon/ round face
  • ectopic calcification (calcium deposits in the wrong places)
  • reduced intelligence
  • short 4th and 5th fingers
48
Q

outline testing for psuedoparathyroidism

A
  • infuse patient with PTH and look at the action of the PTh receptor
  • in the kidney measure cAMP in the urine
49
Q

outline type 2 psuedoparathyroidism

A

characterized by:

  • resistance to parathyroid hormone (PTH) which manifests with hypocalcemia, hyperphosphatemia
  • elevated PTH levels
50
Q

outline type 1a psuedoparathyroidism

A
  • body unable to respond to PTH

- group of symptoms called Albert’s hereditary osteodystrophy which include short stature, round face and obesity

MSK sem3 (1 decks)

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