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Endocrine ­ FRCEM Success 6/9/2017 Endocrine ­ FRCEM Success Dashboard Subscription expires in: 1 Days Extend You have scored 24% You answered 34 correct out of 144 questions. Your answers are shown below: Effects of thyroid hormones include all but which one of the following: a) Increased heart rate b) Increased stroke volume c) Increased lipolysis d) Decreased gluconeogenesis e) Increased glycolysis Something wrong? The release of thyroid hormones is regulated by the anterior pituitary gland which secretes thyroid-stimulating hormone (TSH) and the hypothalamus which secretes thyrotropin-releasing hormone (TRH). The thyroid follicles secrete two hormones; thyroxine (T4) – a prohormone that acts as a plasma reservoir and tri- iodothyronine (T3) – the active hormone. T3 and T4 synthesis involves the processing of tyrosine and iodine. About 90% of thyroid hormones are secreted in the form of T4, with the remainder as T3. About 80% of the T4 is converted to the more active T3 (under stimulation of TSH) in the liver and kidney. Secretion of the thyroid hormones is stimulated by long-term exposure to cold temperatures acting on the anterior pituitary, oestrogens acting on the anterior pituitary and adrenaline acting directly on the thyroid gland. Increased serum levels of T3 inhibit secretion of TSH. Most of the thyroid hormones in the blood are bound to plasma proteins (of these, 70% are bound to thyroid-binding globulin (TBG) and 30% are bound to albumin), which allows them to circulate without being broken down by enzymes. http://frcemsuccess.com/rev/sc­26/ 1/110 6/9/2017 Endocrine ­ FRCEM Success Only a fraction of the circulating thyroid hormones (about 0.1% of T4 and 1% of T3) are unbound and thus biologically active. The thyroid hormones act to increase the basal metabolic rate and are important for growth and normal foetal development. Effects of thyroid hormones include: increased heart rate and stroke volume, and increased lipolysis, glycolysis and gluconeogenesis. Which of the following is NOT an endocrine cause of hypercalcaemia: a) Pseudohypoparathyroidism b) Hyperthyroidism c) Pheochromocytoma d) Addison’s disease e) Acromegaly Something wrong? Causes of hypercalcaemia include: primary hyperparathyroidism (most commonly due to a benign parathyroid adenoma) familial hypocalciuric hypercalcaemia sudden acidosis (resulting in release of bound calcium) malignancy sarcoidosis chronic renal failure thyrotoxicosis pheochromocytoma Addison’s disease acromegaly ingestion of excess calcium (milk-alkali syndrome) or vitamin D drugs e.g. lithium, thiazide diuretics, theophylline toxicity prolonged immobilisation bone destruction usually by secondary deposits from malignancy or myeloma hypermagnesaemia Pseudohypoparathyroidism (PHP) is a heterogeneous group of disorders characterised by hypocalcemia, hyperphosphatemia, increased serum concentration of parathyroid hormone (PTH), and insensitivity to the biologic activity of PTH. The commonest causes of hypercalcaemia are primary hyperparathyroidism (most common) and hypercalcaemia of malignancy. Features of hypercalcaemia include: STONES (renal calculi) BONES (bone pain, fragile bones) GROANS (lethargy, fatigue, generalised muscle weakness) http://frcemsuccess.com/rev/sc­26/ 2/110 6/9/2017 Endocrine ­ FRCEM Success GROANS (lethargy, fatigue, generalised muscle weakness) MOANS (constipation, abdominal pain, nausea/vomiting, pancreatitis, peptic ulcer) THRONES (polyuria, polydipsia, dehydration, renal failure) PSYCHIATRIC OVERTONES (confusion, depression, anxiety, hallucinations, insomnia) Parathyroid hormone (PTH) release is primarily simulated by which of the following: a) High serum Ca2+ b) Low serum Ca2+ 3- c) High serum PO4 3- d) Low serum PO4 e) Activated vitamin D Something wrong? Parathyroid hormone (PTH) is synthesised by the chief cells in the parathyroid gland. PTH is released in response to falling plasma ionised calcium levels and increasing blood phosphate levels (indirectly by its binding to ionised calcium and thereby effective reduction of blood calcium levels). PTH release is inhibited by normal blood calcium levels and hypomagnesaemia. PTH acts to: increase calcium and phosphate resorption from bone (via indirect upregulation of osteoclast activity) increase calcium reabsorption in the distal tubule of the nephron (by activating Ca2+ entry channels in the apical membrane and the Ca2+ ATPase pump on the basolateral membrane) increase phosphate excretion by inhibiting reabsorption in the proximal tubule of the nephron inhibit renal bicarbonate reabsorption stimulating a metabolism acidosis which favours dissociation of calcium from plasma proteins stimulate 1-alpha-hydroxylase in the kidneys to produce activated vitamin D indirectly increase calcium and phosphate absorption in the small intestine (via activated vitamin D) Overall PTH acts to increase plasma calcium levels and decrease plasma phosphate levels. Regarding the position of the pituitary gland, which of the following statements is CORRECT: a) The pituitary gland lies in a bony hollow of the ethmoid bone. b) The pituitary gland is covered by the brous diaphragma sellae of the dura mater. c) The optic chiasm lies directly posterior to the anterior pituitary. d) The anterior pituitary is connected to the median eminence of the hypothalamus by the pituitary stalk. e) The sphenoid sinuses lie lateral to the pituitary gland. Something wrong? http://frcemsuccess.com/rev/sc­26/ 3/110 6/9/2017 Endocrine ­ FRCEM Success The pituitary gland lies in a bony hollow of the sphenoid bone (the sella turcica), and it is covered by the brous diaphragma sellae of the dura mater. The optic chiasm lies directly superior to the anterior pituitary. The posterior pituitary is connected to the median eminence of the hypothalamus by the pituitary stalk (also known as the infundibulum). The cavernous sinuses (including cranial nerves III – VI) lie lateral to the pituitary gland. Insulin secretion is stimulated by all but which one of the following: a) Fatty acids and ketones b) Glucagon c) Secretin d) Somatostatin e) Growth hormone Something wrong? Insulin is a polypeptide hormone consisting of two short chains (A and B) linked by disulphide bonds. Insulin is formed from the cleaving of proinsulin (derived from preproinsulin synthesised in the rough endoplasmic reticulum) into insulin and C-peptide in the Golgi body of β cells in the islets of Langerhans. Since insulin and C-peptide are produced in equimolar amounts, C-peptide acts as a useful marker of β cell activity in diabetics who receive insulin treatment. Insulin secretion is stimulated directly by high blood glucose levels, but also by metabolites such as amino acids, fatty acids and ketones, by glucagon, some gastrointestinal tract peptides (e.g. secretin), GH, ACTH and TSH. Insulin secretion is inhibited by low blood glucose levels, adrenaline, somatostatin, hypocalcaemia and sympathetic innervation. (N.B. insulin secretion never ceases completely, there is always a basal level of insulin in the blood) Which of the following is NOT an expected nding in hyperprolactinaemia: a) Amenorrhoea b) Failure of postpartum lactation c) Infertility d) Loss of libido e) Erectile dysfunction Something wrong? Prolactin acts on the mammary glands and reproductive organs to promote growth of these organs and initiate lactation. http://frcemsuccess.com/rev/sc­26/ 4/110 6/9/2017 Endocrine ­ FRCEM Success lactation. Prolactin secretion is stimulated by prolactin-releasing factor (PRF) and thyrotropin-releasing hormone (TRH) from the hypothalamus. Prolactin secretion is inhibited by dopamine secreted by the hypothalamus. Prolactin levels rise physiologically in pregnancy, puerperium, and breast stimulation. Excess levels of prolactin may be caused by: a prolactinoma (prolactin-secreting pituitary adenoma) compression of the pituitary stalk by a pituitary or hypothalamic tumour preventing normal dopaminergic inhibition of prolactin release head injury neurosurgery hypothyroidism (due to increased synthesis of TRH) Cushing’s syndrome severe liver disease polycystic ovary syndrome (PCOS) drugs e.g. dopamine antagonists, antidepressants. Hyperprolactinaemia causes symptoms such as oligomenorrhoea/amenorrhoea, galactorrhoea, loss of libido, erectile dysfunction and infertility (via inhibition of the release of GnRH from the hypothalamus). Prolactin deciency results in failure of postpartum lactation. Which of the following is NOT a well known cause of hypoglycaemia: a) Addison’s disease b) Propranolol c) Hypothermia d) Cushing’s syndrome e) Alcohol Something wrong? Hypoglycaemia is dened as a level of glucose < 3 mmol/L, although generally patients are not symptomatic unless plasma glucose reaches < 2.2 mmol/L. It can occur due to: oral hypoglycaemic drugs excess exogenous insulin alcohol hepatic failure renal impairment http://frcemsuccess.com/rev/sc­26/ 5/110 6/9/2017 Endocrine ­ FRCEM Success overwhelming sepsis hypothermia Addison’s disease insulinoma malignancy certain medications e.g. beta blockers or salicylates inadequate levels of exercise or carbohydrate intake in patients with diabetes mellitus Symptoms of hypoglycaemia result from a catecholamine surge and include: feelings of hunger, tremor, nausea, sweating, anxiety/irritability, pallor, tachycardia or palpitations, headaches, tingling in the extremities or lips. Symptoms of cognitive impairment reect neuroglycopenia and include confusion, poor concentration, seizures and ultimately coma. Patients should be given oral glucose if possible (e.g. Lucozade
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