Hyperparathyroidism

Question 1

What are the causes of Hyperparathyroidism?

Answer 1

Primary
Common – Parathyroid Adenoma, Secondary to CKD (Parathyroid hyperplasia due to chronic hypocalcaemia), Primary Parathyroid Hyperplasia

Others - Idiopathic over-secretion, Parathyroid carcinoma, Secondary to vitamin D deficiency or malnutrition (Parathyroid hyperplasia due to chronic hypocalcaemia), Tertiary Hyperparathyroidism (Chronic secondary Hyperparathyroidism causes gland to act autonomously)

Question 2

What will you find on history taking of Hyperparathyroidism?

Answer 2

Symptoms: Caused by hypercalcaemia
Most patients are asymptomatic and picked up incidentally
Stones – Increased Renal Stones (made of calcium phosphate or calcium oxalate) as the kidneys excrete a lot more Ca2+ and so form stones
Bones – Bone pain caused by increased bone breakdown, this also causes osteoporosis
Abdominal Groans – Constipation and abdominal pain, hypercalcaemia causes abnormal gut contraction. Peptic Ulcer (not understood why)
Moans – Lethargy, fatigue, Cramps
Thrones – Polyuria and Polydipsia (Hypercalcaemia causes diabetes insipidus by tubulointerstitial injury caused by calcium deposition)
Psychiatric Overtones – Depression, anxiety, Memory Problems
Pseudogout
Severe Hypercalcaemia - Hypertension, Short QT interval on ECG and cardiac arrhythmias, coma and death.

Risk Factors:
Postmenopausal women – Commonly affected by primary hyperparathyroidism
Family history
Neck Surgery
Diet - Are they vegan?
Underlying bowel disease that may predispose to malabsorption e.g. Crohns/Coeliac

Specific Questions to ask:

Differentials:
Ectopic Parathyroid hormone related peptide secretion by a breast/lung cancer
Drug induced hypercalcaemia – Lithium, Thiazide Diuretics
Myeloma

Question 3

What will you find on examination of Hyperparathyroidism?

Answer 3

Examination is mainly to look for underlying cause - Mostly CKD or parathyroid tumours 
End of the bed:
Itchy – CKD
Reduced mental state/coma
Hands:
Hypertension -  CKD 
Arrhythmias
Neck:
Look for any masses 
Chest:
SOB - Pulmonary oedema - CKD
Palpitations 
Legs:
Swelling of feet and ankles – CKD

Question 4

What investigations will you order in Hyperparathyroidism?

Answer 4

Bedside:
ECG - Hypocalcaemia

Bloods:
Serum Ca2+ (Albumin levels required to work out protein bound calcium) – Raised (In primary or tertiary disease) Low/Normal (In secondary disease). Primary and tertiary disease have the same bloods, differentiate if there is an underlying cause e.g. CKD
Serum PTH - Raised
Serum Phosphate - Low
25-hydroxyvitamin D - Low Vitamin D can cause hypocalcaemia leading to hyperparathyroidism
FBC – To exclude a myeloma
U&E - CKD can cause hypocalcaemia leading to hyperparathyroidism

Imaging:
DEXA scan - to assess bone calcium levels
US kidneys - if symptoms of renal stones

Special Tests:
Parathyroid Biopsy – If parathyroid carcinoma suspected

Question 5

What is the treatment of Secondary Hyperparathyroidism?

Answer 5

Resuscitation:
A-E approach
Get IV Access/Give O2 to maintain sats of 94+ /Attach 12 lead ECG
Assessment with AMPLE history and brief examination
Get help - Cardiology reg on call
Frequent Observations - Constant or 15 minutely
Dilution with IV fluids and furosemide to ensure they do not go into fluid overload
IV Bisphosphonates and Calcitonin (inhibits osteoclasts and Ca2+ resorption in kidney)

Primary Disease:
In mild cases where asymptomatic – Surveillance with yearly DEXA scans and 6 monthly Calcium levels
High Fluid intake to limit renal stones
Once symptomatic – Parathyroidectomy of the affected glands (There are 4 separate parathyroid glands)
Calcium Binder or Bichromates if not for surgical management - reduce the absorption of calcium

Secondary Disease:
Correct underlying cause - Manage CKD, treat Vit D deficiency
Vit D and calcium supplements
 

Question 6

What is hyperparathyroidism?

Answer 6

Hyperparathyroidism is a low level of parathyroid hormone. Parathyroid hormone increases calcium reabsorption in the kidneys, stimulates conversion of vitamin D to its active form and thus promote calcium uptake in the bowel and stimulates osteoclasts to release calcium from bone. Thus, in Hyperparathyroidism, patients get hypercalcaemia and hypophosphatemia