Endocrinology

Thyroid cancer: papillary (70%): most common, local spread follicular (10%): more likely to spread to lung and bone medullary (5-8%) arise from parafollicular calcitonin-producing C cells lymphomas (4-10%): usually non-Hodgkin's Hürthle cell carcinoma (3-10%) Anaplastic: most aggressive, origin from follicular cells but doesn't retain original cell functions

Presentation: painless thyroid mass (hard and fixed) enlarging rapidly over a period of a few weeks. Palpable cervical lymphadenopathy. Insidious or persistent pain lasting for several weeks. Vocal cord paralysis (hoarseness) implies involvement of the recurrent laryngeal nerve Diagnosis: TFT serum calcitonin (medullary cancer) Ultrasound Fine-needle aspiration cytology CT and MRI radionuclide imaging

Pituitary adenomas:Classification by function:- Non-functioning adenomas Prolactinomas Growth hormone (GH)-secreting Adrenocorticotrophic hormone (ACTH)-secreting Thyroid-stimulating hormone (TSH)-secreting Leutinising hormone/follicle-stimulating hormone (LH/FSH)-secreting tumours Classification by size:- microadenomas : macroadenomas : >1cm

Local Effects: Headaches: are classically retro-orbital or bitemporal. They tend to be worse on waking. Sudden catastrophic headaches may result from pituitary apoplexy.  Very large pituitary tumours may cause obstruction of CSF, resulting in hydrocephalus and expansion of the lateral ventricles. Visual field defects: compression of optical nerve/chiasm. Bitemporal hemianopia is the classic abnormality Ocular nerve palsies cause a squint. Extensive extension into the hypothalamus may result in disorders of appetite, thirst, temperature regulation and consciousness. Clinical consequences: Panhypopituitarism or varying degrees of loss of any of the six hormones may occur. Hypopituitarism tends to occur in the following order of LH, GH, TSH, and lastly ACTH and FSH. Symptoms: infertility, oligo/amenorrhoea, decreased libido and erectile dysfunction. Deficiency of LH and GH may result in decreased muscle bulk, decreased body hair, central obesity and small, soft testes. In children, hypopituitarism commonly presents with delayed puberty or impairment of growth. Diabetes insipidus is rarely a presenting feature but may occur following surgery for a pituitary adenoma. Hypersecretion of the involved pituitary hormone -acromegaly,hyperprolactinaemia, Cushing's disease, thyrotoxicosis.

Addison's Disease:  adrenal insufficiency (reduced glucocorticoids and mineralocorticoids) progressive destruction of the adrenal glands - most likely the result of cytotoxic T lymphocytes, although 50% of patients have circulating adrenal antibodies. Symptoms: Fatigue and weakness. Anorexia. Nausea. Vomiting. Weight loss. Abdominal pain. Diarrhoea. Constipation. Syncope. Dizziness. Confusion. Personality change. Irritability. Amenorrhoea. Signs: Cutaneous and mucosal pigmentation - look at mucosa and in new scars. Hypotension. Postural hypotension.

Symptoms: Truncal obesity, supraclavicular fat pads, buffalo hump, weight gain. Facial fullness, moon facies, facial plethora. (Lemon on stick) Proximal muscle wasting and weakness. Diabetes or impaired glucose tolerance. Gonadal dysfunction, reduced libido. Hypertension. Nephrolithiasis. Skin: skin atrophy, purple striae, easy bruising, hirsutism, acne; pigmentation occurs with ACTH-dependent causes. Psychological problems: depression, cognitive dysfunction and emotional lability. Osteopenia or osteoporosis. Oedema. Women may complain of irregular menses. Thirst, polydipsia, polyuria. Impaired immune function: increased infections, difficulty with wound healing. Child: growth restriction. Patients with an ACTH-producing pituitary tumour may develop headaches, visual problems, and galactorrhoea. Destruction of the anterior pituitary may cause hypothyroidism and amenorrhoea.

Cushing's syndrome: prolonged exposure to elevated levels of either endogenous or exogenous glucocorticoids.Causes of Cushing's syndrome can be divided into two groups: Adrenocorticotropic hormone (ACTH)-dependent disease: excessive ACTH from the pituitary (Cushing's disease), ectopic ACTH-producing tumours or excess ACTH administration. Non-ACTH-dependent: adrenal adenomas, adrenal carcinomas, excess glucocorticoid administration.

Normal calcium control:regulated by the actions of 1,25-Dihydroxycholecalciferol (the biologically active form of Vitamin D), parathyroid hormone (PTH), calcitonin and direct exchange with the bone matrix. PTH: increases calcium levels by: increase kidney excretion of phosphate and triggering release of calcium from bones (resorption), active reabsorption of calcium in kidneys, and increasing the production of activated vitamin D (increase absorption in intestines). Vitamin D: active form (Calcitriol) increases blood calcium levels ([Ca2+]) by promoting absorption of dietary calcium from the gastrointestinal tract, increasing renal tubular reabsorption of calcium, and  stimulates release of calcium from bone  Calcitonin: released by parafollicular cells in thyroid to reduce serum calcium by opposing action of PTH

Causes:Primary hyperparathyroidism Malignancy - the most common cause of non-PTH-mediated hypercalcaemia. Granulomatous conditions - eg, sarcoidosis and tuberculosis. Endocrine conditions - eg, thyrotoxicosis, phaeochromocytoma and primary adrenal insufficiency. Drugs - eg, thiazide diuretics, vitamin D and vitamin A supplements.[7]  Familial - eg, familial hypocalciuric hypercalcaemia.[5]  Other - eg, prolonged immobilisation, calcium-alkali syndrome, AIDS.

Causes of hypocalcaemiaPrimary Hypoparathyroidism (low PTH): Parathyroid agenesis  Parathyroid destruction - due to surgery, radiotherapy, infiltration by metastases or systemic disease (eg amyloidosis, sarcoidosis). Autoimmune disorder. Reduced parathyroid secretion - due to gene defects, hypomagnesaemia, neonatal hypocalcaemia (may be due to maternal hypercalcaemia), hungry bone disease (after parathyroidectomy), mutation in calcium-sensitive receptor (CaSR). Secondary hypoparathyroidism: Vitamin D deficiency - due to nutritional lack, malabsorption, liver disease, receptor defects. Vitamin D resistance (rickets) - renal tubular dysfunction (Fanconi's syndrome) or receptor defect. PTH resistance - pseudohypoparathyroidism, hypomagnesaemia. Other causes: Acute pancreatitis. Malignancy - tumour lysis (following chemotherapy) or osteoblastic metastases (most common in prostate and breast cancers). Acute rhabdomyolysis - usually in relation to crush injuries. Drugs - calcium chelators (citrate in blood transfusion); bone resorption inhibitors (bisphosphonates, calcitonin); drugs affecting vitamin D (phenytoin,ketoconazole), foscarnet.

Thyroid cancer

Pituitary adenoma

adrenal disease

hypercalcaemia

hypocalcaemia