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4th year passmedicine by topic > Parathyroid/ Calcium > Flashcards

Parathyroid/ Calcium Flashcards

1
Q

What is PTH

A

polypeptide hormone secreted from the parathyroid gland.

It has an important role in calcium homeostasis.

It acts on cell-surface receptors to generate a coordinated response throughout the body and maintain blood calcium within a narrow range.

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2
Q

Calcium enters the body through the

A

intestines

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3
Q

The main reservoir of calcium in the body is the bone, containing

A

1 kg of complexed calcium and phosphate

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4
Q

In the blood, calcium exists in three main forms:

A

free calcium
bound to albumin
complexed with anions

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5
Q

It is free calcium which is physiologically active and can travel into cells to exert a function.

A

true

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6
Q

PTH is secreted from

A

Chief cells of the parathyroid glands, located on the posterior aspect of the thyroid.

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7
Q

Effector organs associated with PTH include the bone and kidney:
At the bone

A

PTH acts to increase the activity of osteoclastic cells, which are responsible for bone resorption. In this way, the bone releases some of its calcium, and phosphate, stores into the bloodstream.

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8
Q

Effector organs associated with PTH include the bone and kidney:
At the kidney

A

PTH as two actions. One is to increase the hydroxylation and activation of vitamin D in the proximal convoluted tubules. Another in to increase calcium reabsorption from the distal convoluted tubules and increase phosphate excretion.

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9
Q

How does active vitamin D work

A

Active vitamin D has a similar action to PTH
One of its unique actions is to increase dietary calcium absorption from the intestine by increasing expression of calcium-binding hormone.

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10
Q

What type of hormone is active vitamin d

A

it is a steroid hormone.

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11
Q

How is PTh regulated?

A

calcium levels in the blood fall, which is detected by the parathyroid gland
chief cells secrete PTH into the blood
calcium is released from bone and reabsorbed from the renal tubules, causing its level to rise
increased calcium levels are detected by the parathyroid gland, which decreases PTH secretion

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12
Q

What is PTHrp

A

polypeptide which has a similar structure to PTH, hence its name ‘related peptide’. It can be secreted from cancer cells, notably squamous cell bronchial carcinoma, to cause hypercalcaemia. PTHrp has all the same effects as PTH, however it cannot activate vitamin D.

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13
Q

Describe the hormone profile in Primary hyperparathyroidism

A

PTH (Elevated)
Ca2+ (Elevated)
Phosphate (Low)

Urine calcium : creatinine clearance ratio > 0.01

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14
Q

Describe the hormone profile in Secondary hyperparathyroidism

A

PTH (Elevated)
Ca2+ (Low or normal)
Phosphate (Elevated)
Vitamin D levels (Low)

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15
Q

Describe the hormone profile in Tertiary hyperparathyroidism

A

Ca2+ (Normal or high)
PTH (Elevated)
Phosphate levels (Decreased or Normal)

Vitamin D (Normal or decreased)
Alkaline phosphatase (Elevated)
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16
Q

Causes of Primary hyperparathyroidism

A

80%: solitary adenoma
15%: hyperplasia
4%: multiple adenoma
1%: carcinoma

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17
Q

Causes of Secondary hyperparathyroidism

A

Parathyroid gland hyperplasia occurs as a result of low calcium, almost always in a setting of chronic renal failure

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18
Q

Causes of Tertiary hyperparathyroidism

A

Occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder, hyperplasia of all 4 glands is usually the cause

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19
Q

How is familial hypocalciuric hypercalcaemia inherited?

A

autosomal dominant genetic disorder

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20
Q

familial hypocalciuric hypercalcaemia diagnosis

A

genetic testing and concordant biochemistry (urine calcium : creatinine clearance ratio <0.01-distinguished from primary hyperparathyroidism).

21
Q

In exams, primary hyperparathyroidism is stereotypically seen in

A

elderly females with an unquenchable thirst and an inappropriately normal or raised parathyroid hormone level.

22
Q

sx primary hyperparathyroidism?

A

Features - ‘bones, stones, abdominal groans and psychic moans’
polydipsia, polyuria
peptic ulceration/constipation/pancreatitis
bone pain/fracture
renal stones
depression
hypertension

23
Q

associations of primary hyperparathyroidism?

A

hypertension

multiple endocrine neoplasia: MEN I and II

24
Q

Ix primary hyperparathyroidism?

A

raised calcium, low phosphate
PTH may be raised or (inappropriately, given the raised calcium) normal
technetium-MIBI subtraction scan

25
Q

What is a classic x ray finding for primary hyperparathyroidism

A

pepperpot skull is a characteristic X-ray finding of hyperparathyroidism

26
Q

Mx primary hyperparathyroidism

A

the definitive management is total parathyroidectomy
conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage
calcimimetic agents such as cinacalcet are sometimes used in patients who are unsuitable for surgery

27
Q

Basic problems in chronic kidney disease

A

low vitamin D (1-alpha hydroxylation normally occurs in the kidneys)
high phosphate
low calcium: due to lack of vitamin D, high phosphate
secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D

28
Q

Primary hyperparathyroidism

Indications for surgery

A

Elevated serum Calcium > 1mg/dL above normal
Hypercalciuria > 400mg/day
Creatinine clearance < 30% compared with normal
Episode of life threatening hypercalcaemia
Nephrolithiasis
Age < 50 years
Neuromuscular symptoms
Reduction in bone mineral density of the femoral neck, lumbar spine, or distal radius of more than 2.5 standard deviations below peak bone mass (T score lower than -2.5)

29
Q

How is Secondary hyperparathyroidism usually managed?

A

medical therapy.

30
Q

Indications for surgery in secondary (renal) hyperparathyroidism:

A

Bone pain
Persistent pruritus
Soft tissue calcifications

31
Q

Tertiary hyperparathyroidism mx

A

Allow 12 months to elapse following transplant as many cases will resolve
The presence of an autonomously functioning parathyroid gland may require surgery. If the culprit gland can be identified then it should be excised. Otherwise total parathyroidectomy and re-implantation of part of the gland may be required.

32
Q

The main symptoms of hypoparathyroidism are secondary to

A

hypocalcaemia

33
Q

Sx HYPOparathyroidism?

A 
tetany: muscle twitching, cramping and spasm
perioral paraesthesia
Trousseau's sign
Chvostek's sign
if chronic: depression, cataracts
34
Q

What is Trousseau’s sign?

A

carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systoli

35
Q

What is Chvostek’s sign?

A

tapping over parotid causes facial muscles to twitch

36
Q

What ECg changes would you see in hypocalcaemia?

A

prolonged QT interval

37
Q

Hormone profile hypoparathyroidism?

A

decrease PTH secretion

low calcium, high phosphate

38
Q

Mx hypoparathyroidism

A

treated with alfacalcidol

39
Q

What is Pseudohypoparathyroidism?

A

target cells being insensitive to PTH

due to abnormality in a G protein

40
Q

Pseudohypoparathyroidism associations

A

low IQ, short stature, shortened 4th and 5th metacarpals

41
Q

Pseudohypoparathyroidism hormone profile

A

low calcium, high phosphate, high PTH

42
Q

Pseudohypoparathyroidism diagnosis

A

diagnosis is made by measuring urinary cAMP and phosphate levels following an infusion of PTH. In hypoparathyroidism this will cause an increase in both cAMP and phosphate levels.

43
Q

Pseudohypoparathyroidism I vs II

A

pseudohypoparathyroidism type I neither cAMP nor phosphate levels are increased whilst in pseudohypoparathyroidism type II only cAMP rises.

44
Q

What is Pseudopseudohypoparathyroidism?

A

similar phenotype to pseudohypoparathyroidism but normal biochemistry

45
Q

Hypocalcaemia: causes?

A

vitamin D deficiency (osteomalacia)
chronic kidney disease
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
pseudohypoparathyroidism (target cells insensitive to PTH)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis

46
Q

Contamination of blood samples with EDTA may also give falsely low calcium levels.

A

True

47
Q

Management hypocalcaemia?

A

acute management of severe hypocalcaemia is with intravenous replacement. The preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
intravenous calcium chloride is more likely to cause local irritation
ECG monitoring is recommended
further management depends on the underlying cause

48
Q

Two conditions account for 90% of cases of hypercalcaemia:

A
  1. Primary hyperparathyroidism: commonest cause in non-hospitalised patients
  2. Malignancy: the commonest cause in hospitalised patients. This may be due to number of processes, including; bone metastases, myeloma, PTHrP from squamous cell lung cancer
49
Q

Other causes of hypercalcaemia include

A 
sarcoidosis
vitamin D intoxication
acromegaly
thyrotoxicosis
Milk-alkali syndrome
drugs: thiazides, calcium containing antacids
dehydration
Addison's disease
Paget's disease of the bone

4th year passmedicine by topic (96 decks)

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