Endocrine surgery Flashcards
Causes of Primary hyperparathyroidism
Single or double adenomas (80-85%)
Multi-gland hyperplasia (15%)
Carcinoma (<1%)
Localisation studies for primary hyperparathyoidism
Technetium 99 Sestamibi - SPECT or SPECT-CT
85% successful
Co-localising US to increase specificity yada sensitive - 95% if concordant
Medical management of hypercalcaemia
Rehydration, furosemide diuresis, steroids.
Cinacalcet- given and continued on discharge til surgery
Bisphosphonates can also be used but take 48-72hrs
Surgical approach
Bilateral neck exploration or focused
IF cannot find need to check high in the neck, low in the thymus or thyrothymic ligament, carotid sheath and enclosed within thyroid
Hemithyroidectomy or mediastinal exploration should only be considered at a second operation
Secondary hyperparathyroidism
Excessive secretion secondary to low calcium causing hyperplasia of glands and raised PTH
Commonly caused by CKD, low Vitamin D or high dose phosphate
Pathophysiology of secondary hyperparathyroidism
initially FGF 23 from bones keeps phosphate levels down by increased excretion and decreasing 1 alpha hydroxylation.
AS disease progresses Kidneys become resistant to FGF-23 and decrease 1-alpha hydroxylation of Vitamin D - decreased phosphate excretion
Deficiency in Vit D cause reduced calcium reabsorption for urine, Gut and failing kidneys result in low calcium and high phosphate which triggers PTH secretion and growth of gland
Management of 2nd Hyperparathyroidism
Medical Tx - depends on aetiology
If Vit D deficient - replace - Cholecalciferol for 8 weeks
In CKD - managed bone disease and ectopic calcification
Use dietary phosphate restriction and phosphate binders and Vitamin D supplimentation and calcimimetic (cinacalcet - binds to calcium sensing receptor - decrases PTH)
Indications for surgery in 2nd
Prolonged severe hyperparathyroidism
Calciphylaxis
Refractory hyperpohsphataemia
Hypercalcaemia
Evidence of bone disease
Extraskeletal calcification
Surgery improves overall mortality of dialysis patients
Total (4 gland or subtotal (3 and a half glands)
Multinodular Goitre
Enlarged thyroid gland consisting of multiple nodules (toxic or non-toxic.
Most develop as a result of TSH stimulation secondary to low thyroid hormone levels
Nodules are extremely common - up to 60% of population have them
Symptoms and signs of goitre
Compressive symptoms
Dysphagia
Pembertons sign - distension of veins when arms raised - retrosternal extension
Red Flag - Rapid onset and progression, pain referring to ear, family Hx, Genetic condition (PTEN,MEN2,FAP), severe dysphagia, stridor and previous radiation exposure
Risk of recurrent laryngeal nerve injury and EBSLN
RLN -Approx 1% with benign goitre - thought to be relatively low risk
EBSLN - can be as high as 40%
Causes of hyperthyroidism
Graves disease
Antibody mediated activation of TRH receports
Toxic nodule with autonomous secretion
Thyroditis
Medications
Pituitary adenoma, struma ovarii
thyroid cancer
Management of hyperthyroidism
Betablockers for tachycardia and anxiety
Block and replace using Carbimazole (40-60mg OD) - more likely to induce remission
Remain of media for 12-18months
50% relapse rate
Definitive Tx is surgery or radioidodine
Investigation of adrenal mass
Check if functional (<10%)
Serum and urine metanephrines and normetanephrines - pheo
Serum K and renin to aldosterone ration - Conns
Sport cortisol and ACTH - Cushing
Testosterone and oestrogen - possible cancer
CT adrenal protocol - cancer has poor washout, >4cm (25% malignancy), high hounsfield units, poorly defines, irregular heterogenous or areas of necrosis
Well differentiated Thyroid cancer
Histological subtype of cancer from thyroid follicular cells
Papillary
Mixed Papillary follicular
follicular and Hurtle cell
Papillary subtype more common than follicular except in iodine deficient areas