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  • Question 1 - A 32-year-old man visits the clinic complaining of weakness and frequent muscle cramps...

    Incorrect

    • A 32-year-old man visits the clinic complaining of weakness and frequent muscle cramps that have been ongoing for the past two weeks. Upon examination, you observe widespread hyporeflexia. A blood test reveals hypokalaemia, but the cause has not yet been determined. Which of the following conditions is linked to hypokalaemia?

      Your Answer: Rhabdomyolysis

      Correct Answer: Conn's syndrome

      Explanation:

      Primary hyperaldosteronism, also known as Conn’s syndrome, can lead to hypertension, hypernatraemia, and hypokalemia. This condition is caused by an excess of aldosterone, which is responsible for maintaining potassium balance by activating Na+/K+ pumps. However, in excess, aldosterone can cause the movement of potassium into cells, resulting in hypokalaemia. The kidneys play a crucial role in maintaining potassium balance, along with other factors such as insulin, catecholamines, and aldosterone. On the other hand, congenital adrenal hypoplasia, Addison’s disease, rhabdomyolysis, and metabolic acidosis are all causes of hyperkalaemia, which is an excess of potassium in the blood. Addison’s disease and adrenal hypoplasia result in mineralocorticoid deficiency, which can lead to hyperkalaemia. Acidosis can also cause hyperkalaemia by causing positively charged hydrogen ions to enter cells while positively charged potassium ions leave cells and enter the bloodstream.

      Primary hyperaldosteronism is a condition characterized by hypertension, hypokalaemia, and alkalosis. It was previously believed that adrenal adenoma, also known as Conn’s syndrome, was the most common cause of this condition. However, recent studies have shown that bilateral idiopathic adrenal hyperplasia is responsible for up to 70% of cases. It is important to differentiate between the two causes as it determines the appropriate treatment. Adrenal carcinoma is an extremely rare cause of primary hyperaldosteronism.

      To diagnose primary hyperaldosteronism, the 2016 Endocrine Society recommends a plasma aldosterone/renin ratio as the first-line investigation. This test should show high aldosterone levels alongside low renin levels due to negative feedback from sodium retention caused by aldosterone. If the results are positive, a high-resolution CT abdomen and adrenal vein sampling are used to differentiate between unilateral and bilateral sources of aldosterone excess. If the CT is normal, adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia.

      The management of primary hyperaldosteronism depends on the underlying cause. Adrenal adenoma is treated with surgery, while bilateral adrenocortical hyperplasia is managed with an aldosterone antagonist such as spironolactone. It is important to accurately diagnose and manage primary hyperaldosteronism to prevent complications such as cardiovascular disease and stroke.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 2 - A 34-year-old male presents with tingling in his thumb, index, and middle finger,...

    Incorrect

    • A 34-year-old male presents with tingling in his thumb, index, and middle finger, along with complaints of excessive fatigue and snoring. Upon examination, he displays a prominent brow ridge and significant facial changes over time. Following blood tests and an MRI scan, the patient is prescribed octreotide. What is the mechanism of action of this medication?

      Your Answer: Growth hormone receptor antagonist

      Correct Answer: Somatostatin analogue

      Explanation:

      Acromegaly is a condition that results from excessive growth hormone production. The release of growth hormone is directly inhibited by somatostatin, which is why somatostatin analogues are used to treat acromegaly.

      To answer the question, one must first recognize the symptoms of acromegaly, such as carpal tunnel syndrome, sleep apnea, and changes in facial features over time. The second part of the question involves identifying octreotide as a somatostatin analogue commonly used to treat acromegaly.

      While dopamine agonists were previously used to treat acromegaly, they are no longer preferred due to the availability of more effective treatments. Dopamine antagonists have never been used to treat acromegaly. Pegvisomant is an example of a growth hormone antagonist, but antagonists for insulin growth factor-1 release have not yet been developed.

      Acromegaly is a condition that can be managed through various treatment options. The first-line treatment for the majority of patients is trans-sphenoidal surgery. However, if the pituitary tumour is inoperable or surgery is unsuccessful, medication may be indicated. One such medication is a somatostatin analogue, which directly inhibits the release of growth hormone. Octreotide is an example of this medication and is effective in 50-70% of patients. Another medication is pegvisomant, which is a GH receptor antagonist that prevents dimerization of the GH receptor. It is administered once daily subcutaneously and is very effective, decreasing IGF-1 levels in 90% of patients to normal. However, it does not reduce tumour volume, so surgery is still needed if there is a mass effect. Dopamine agonists, such as bromocriptine, were the first effective medical treatment for acromegaly but are now superseded by somatostatin analogues and are only effective in a minority of patients. External irradiation may be used for older patients or following failed surgical/medical treatment.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 3 - A 25-year-old woman has a total thyroidectomy to treat papillary carcinoma of the...

    Incorrect

    • A 25-year-old woman has a total thyroidectomy to treat papillary carcinoma of the thyroid. During examination of histological sections of the thyroid gland, the pathologist discovers the presence of psammoma bodies. What is the primary composition of these bodies?

      Your Answer: Aggregations of macrophages

      Correct Answer: Clusters of calcification

      Explanation:

      Clusters of microcalcification, known as psammoma bodies, are frequently observed in papillary carcinomas.

      Thyroid cancer rarely causes hyperthyroidism or hypothyroidism as it does not usually secrete thyroid hormones. The most common type of thyroid cancer is papillary carcinoma, which is often found in young females and has an excellent prognosis. Follicular carcinoma is less common, while medullary carcinoma is a cancer of the parafollicular cells that secrete calcitonin and is associated with multiple endocrine neoplasia type 2. Anaplastic carcinoma is rare and not responsive to treatment, causing pressure symptoms. Lymphoma is also rare and associated with Hashimoto’s thyroiditis.

      Management of papillary and follicular cancer involves a total thyroidectomy followed by radioiodine to kill residual cells. Yearly thyroglobulin levels are monitored to detect early recurrent disease. Papillary carcinoma usually contains a mixture of papillary and colloidal filled follicles, while follicular adenoma presents as a solitary thyroid nodule and malignancy can only be excluded on formal histological assessment. Follicular carcinoma may appear macroscopically encapsulated, but microscopically capsular invasion is seen. Medullary carcinoma is associated with raised serum calcitonin levels and familial genetic disease in up to 20% of cases. Anaplastic carcinoma is most common in elderly females and is treated by resection where possible, with palliation achieved through isthmusectomy and radiotherapy. Chemotherapy is ineffective.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 4 - A 55-year-old man with a smoking history of over 30 years presented to...

    Incorrect

    • A 55-year-old man with a smoking history of over 30 years presented to the emergency department with acute confusion and disorientation. He was unable to recognize his family members and relatives. He had been experiencing unexplained weight loss, loss of appetite, and occasional episodes of haemoptysis for the past few months. Urgent blood tests were performed, revealing abnormal levels of electrolytes and renal function.

      Based on the likely diagnosis, what is the mechanism of action of the hormone that is being secreted excessively in this case?

      Your Answer: Decreased urine osmolarity

      Correct Answer: Insertion of aquaporin-2 channels

      Explanation:

      Antidiuretic hormone (ADH) plays a crucial role in promoting water reabsorption by inserting aquaporin-2 channels in principal cells. In small-cell lung cancer patients, decreased serum sodium levels are commonly caused by the paraneoplastic syndrome of inadequate ADH secretion (SIADH) or ADH released during the initial lysis of tumour cells after chemotherapy. It is important to note that arteriolar vasodilation, promoting water excretion, decreased urine osmolarity, and increased portal blood flow are not functions of ADH.

      Understanding Antidiuretic Hormone (ADH)

      Antidiuretic hormone (ADH) is a hormone that is produced in the supraoptic nuclei of the hypothalamus and released by the posterior pituitary gland. Its primary function is to conserve body water by promoting water reabsorption in the collecting ducts of the kidneys through the insertion of aquaporin-2 channels.

      ADH secretion is regulated by various factors. An increase in extracellular fluid osmolality, a decrease in volume or pressure, and the presence of angiotensin II can all increase ADH secretion. Conversely, a decrease in extracellular fluid osmolality, an increase in volume, a decrease in temperature, or the absence of ADH can decrease its secretion.

      Diabetes insipidus (DI) is a condition that occurs when there is either a deficiency of ADH (cranial DI) or an insensitivity to ADH (nephrogenic DI). Cranial DI can be treated with desmopressin, which is an analog of ADH.

      Overall, understanding the role of ADH in regulating water balance in the body is crucial for maintaining proper hydration and preventing conditions like DI.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 5 - A 45-year-old male has been diagnosed with Cushing's disease due to a pituitary...

    Correct

    • A 45-year-old male has been diagnosed with Cushing's disease due to a pituitary adenoma, resulting in elevated plasma cortisol levels. Which part of the adrenal gland is responsible for producing cortisol hormone?

      Your Answer: Zona fasciculata

      Explanation:

      The adrenal gland comprises two primary parts: the cortex and medulla.

      The adrenal medulla is accountable for the production of adrenaline and noradrenaline, which are catecholamines.

      The adrenal cortex is divided into three layers: glomerulosa, fasciculata, and reticularis. The glomerulosa primarily produces mineralocorticoids, while the reticularis mainly produces sex steroids. As a result, the Zona fasciculata is the primary source of glucocorticosteroids.

      Cortisol: Functions and Regulation

      Cortisol is a hormone produced in the zona fasciculata of the adrenal cortex. It plays a crucial role in various bodily functions and is essential for life. Cortisol increases blood pressure by up-regulating alpha-1 receptors on arterioles, allowing for a normal response to angiotensin II and catecholamines. However, it inhibits bone formation by decreasing osteoblasts, type 1 collagen, and absorption of calcium from the gut, while increasing osteoclastic activity. Cortisol also increases insulin resistance and metabolism by increasing gluconeogenesis, lipolysis, and proteolysis. It inhibits inflammatory and immune responses, but maintains the function of skeletal and cardiac muscle.

      The regulation of cortisol secretion is controlled by the hypothalamic-pituitary-adrenal (HPA) axis. The pituitary gland secretes adrenocorticotropic hormone (ACTH), which stimulates the adrenal cortex to produce cortisol. The hypothalamus releases corticotrophin-releasing hormone (CRH), which stimulates the pituitary gland to release ACTH. Stress can also increase cortisol secretion.

      Excess cortisol in the body can lead to Cushing’s syndrome, which can cause a range of symptoms such as weight gain, muscle weakness, and high blood pressure. Understanding the functions and regulation of cortisol is important for maintaining overall health and preventing hormonal imbalances.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 6 - A 38-year-old woman presents with symptoms of irritability and changes in bowel habits....

    Correct

    • A 38-year-old woman presents with symptoms of irritability and changes in bowel habits. During examination, a smooth enlargement of the thyroid gland is noted. Thyroid function tests are ordered and the results are as follows:
      TSH 0.1 mug/l
      Free T4 35 pmol/l
      What is the most likely underlying diagnosis?

      Your Answer: Graves disease

      Explanation:

      When TSH receptor antibodies are present, they stimulate the thyroid to produce T4. This results in a decrease in TSH levels due to negative feedback on the pituitary. However, in cases where hyperthyroidism is caused by pregnancy, the TSH levels are usually elevated.

      Understanding Thyroid Disease and its Management

      Thyroid disease can present with various manifestations, which can be classified based on the presence or absence of clinical signs of thyroid dysfunction and the presence of a mass. To assess thyroid disease, a thorough history and examination, including ultrasound, are necessary. If a nodule is identified, it should be sampled through an image-guided fine needle aspiration. Radionucleotide scanning is not very useful.

      Thyroid tumors can be papillary, follicular, anaplastic, medullary, or lymphoma. Multinodular goitre is a common reason for presentation, and if the patient is asymptomatic and euthyroid, they can be reassured. However, if they have compressive symptoms, surgery is required, and total thyroidectomy is the best option. Patients with endocrine dysfunction are initially managed by physicians, and surgery may be offered alongside radioiodine for those with Graves disease that fails with medical management or in patients who prefer not to be irradiated. Patients with hypothyroidism do not generally get offered a thyroidectomy.

      Complications following surgery include anatomical damage to the recurrent laryngeal nerve, bleeding, and damage to the parathyroid glands resulting in hypocalcaemia. For further information, the Association of Clinical Biochemistry guidelines for thyroid function tests and the British Association of Endocrine Surgeons website can be consulted.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 7 - A 49-year-old man visits the clinic with complaints of muscle cramps and constipation...

    Incorrect

    • A 49-year-old man visits the clinic with complaints of muscle cramps and constipation that have been present for a week. He appears to be in good health otherwise. Upon conducting a serum potassium test, you discover that his levels are below the normal range. Your next step is to determine the underlying cause of his hypokalaemia. Which of the following medical conditions is commonly linked to low potassium levels?

      Your Answer: Addison's disease

      Correct Answer: Cushing's syndrome

      Explanation:

      Cushing’s syndrome is the correct answer as it causes excess cortisol which can exhibit mineralocorticoid activity and lead to hypokalaemia. The kidneys play a major role in maintaining potassium balance, but other factors such as insulin, catecholamines, and aldosterone also influence potassium levels. The other options listed (congenital adrenal hypoplasia, Addison’s, rhabdomyolysis, metabolic acidosis) all cause hyperkalaemia. Addison’s disease and adrenal hypoplasia result in mineralocorticoid deficiency, leading to hyperkalaemia. Acidosis and rhabdomyolysis also cause hyperkalaemia. Symptoms of hypokalaemia include fatigue, muscle weakness, myalgia, muscle cramps, constipation, hyporeflexia, and rarely paralysis.

      Causes of Cushing’s Syndrome

      Cushing’s syndrome is a condition that can be caused by both endogenous and exogenous factors. However, it is important to note that exogenous causes, such as the use of glucocorticoid therapy, are more common than endogenous ones. The condition can be classified into two categories: ACTH dependent and ACTH independent causes.

      ACTH dependent causes of Cushing’s syndrome include Cushing’s disease, which is caused by a pituitary tumor secreting ACTH and producing adrenal hyperplasia. Ectopic ACTH production, which is caused by small cell lung cancer, is another ACTH dependent cause. On the other hand, ACTH independent causes include iatrogenic factors such as steroid use, adrenal adenoma, adrenal carcinoma, Carney complex, and micronodular adrenal dysplasia.

      In some cases, a condition called Pseudo-Cushing’s can mimic Cushing’s syndrome. This is often caused by alcohol excess or severe depression and can cause false positive results in dexamethasone suppression tests or 24-hour urinary free cortisol tests. To differentiate between Cushing’s syndrome and Pseudo-Cushing’s, an insulin stress test may be used.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 8 - A 65-year-old male, who is a known type 2 diabetic, visits his GP...

    Incorrect

    • A 65-year-old male, who is a known type 2 diabetic, visits his GP for a diabetes check-up. He is currently taking metformin and his GP has prescribed a sulphonylurea to improve his blood sugar management. What is the mode of action of this medication?

      Your Answer: Opens potassium-ATP channels on the beta cells

      Correct Answer: Closes potassium-ATP channels on the beta cells

      Explanation:

      Sulfonylureas bind to potassium-ATP channels on the cell membrane of pancreatic beta cells, mimicking the role of ATP from the outside. This results in the blocking of these channels, causing membrane depolarisation and the opening of voltage-gated calcium channels. As a result, insulin release is stimulated.

      While acute use of sulfonylureas increases insulin secretion and decreases insulin clearance in the liver, it can also cause hypoglycaemia, which is the main side effect. This can lead to the serious complication of neuroglycopenia, resulting in a lack of glucose supply to the brain, causing confusion and possible coma. Treatment for this should involve oral glucose, intramuscular glucagon, or intravenous glucose.

      Chronic exposure to sulfonylureas does not result in an acute increase in insulin release, but a decrease in plasma glucose concentration does remain. Additionally, chronic exposure to sulfonylureas leads to down-regulation of their receptors.

      Sulfonylureas are a type of medication used to treat type 2 diabetes mellitus. They work by increasing the amount of insulin produced by the pancreas, but only if the beta cells in the pancreas are functioning properly. Sulfonylureas bind to a specific channel on the cell membrane of pancreatic beta cells, known as the ATP-dependent K+ channel (KATP).

      While sulfonylureas can be effective in managing diabetes, they can also cause some adverse effects. The most common side effect is hypoglycemia, which is more likely to occur with long-acting preparations like chlorpropamide. Another common side effect is weight gain. However, there are also rarer side effects that can occur, such as hyponatremia (low sodium levels) due to inappropriate ADH secretion, bone marrow suppression, hepatotoxicity (liver damage), and peripheral neuropathy.

      It is important to note that sulfonylureas should not be used during pregnancy or while breastfeeding.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 9 - A 42-year-old woman visits her GP complaining of chest pain. She has a...

    Correct

    • A 42-year-old woman visits her GP complaining of chest pain. She has a history of hypertension and is currently taking metformin for diabetes. The GP observes that her BMI is 45. What is a possible complication of the metabolic syndrome in this case?

      Your Answer: Ischemic stroke

      Explanation:

      Metabolic syndrome is a group of risk factors for cardiovascular disease that are caused by insulin resistance and central obesity.

      Obesity is associated with higher rates of illness and death, as well as decreased productivity and functioning, increased healthcare expenses, and social and economic discrimination.

      The consequences of obesity include strokes, type 2 diabetes, heart disease, certain cancers (such as breast, colon, and endometrial), polycystic ovarian syndrome, obstructive sleep apnea, fatty liver, gallstones, and mental health issues.

      The Physiology of Obesity: Leptin and Ghrelin

      Leptin is a hormone produced by adipose tissue that plays a crucial role in regulating body weight. It acts on the hypothalamus, specifically on the satiety centers, to decrease appetite and induce feelings of fullness. In cases of obesity, where there is an excess of adipose tissue, leptin levels are high. Leptin also stimulates the release of melanocyte-stimulating hormone (MSH) and corticotrophin-releasing hormone (CRH), which further contribute to the regulation of appetite. On the other hand, low levels of leptin stimulate the release of neuropeptide Y (NPY), which increases appetite.

      Ghrelin, on the other hand, is a hormone that stimulates hunger. It is mainly produced by the P/D1 cells lining the fundus of the stomach and epsilon cells of the pancreas. Ghrelin levels increase before meals, signaling the body to prepare for food intake, and decrease after meals, indicating that the body has received enough nutrients.

      In summary, the balance between leptin and ghrelin plays a crucial role in regulating appetite and body weight. In cases of obesity, there is an imbalance in this system, with high levels of leptin and potentially disrupted ghrelin signaling, leading to increased appetite and weight gain.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 10 - A 38-year-old woman presents to the Emergency Department with a 2-day history of...

    Correct

    • A 38-year-old woman presents to the Emergency Department with a 2-day history of left flank pain. She has been recently diagnosed with osteoporosis after a low-energy, femoral neck fracture.

      Her blood results show the following:

      Na+ 140 mmol/L (135 - 145)
      K+ 3.6 mmol/L (3.5 - 5.0)
      Calcium 2.9 mmol/L (2.1-2.6)
      Phosphate 0.6 mmol/L (0.8-1.4)

      Her urine dip is positive for erythrocytes making a diagnosis of renal calculi likely.

      What is the pathophysiological reason for the low serum phosphate level, given the likely underlying pathology?

      Your Answer: Decreased renal phosphate reabsorption

      Explanation:

      The decrease in renal phosphate reabsorption is caused by PTH.

      The symptoms presented are indicative of a kidney stone, which can be a sign of hyperparathyroidism. Primary hyperparathyroidism, caused by a functioning parathyroid adenoma, can result in low phosphate and high calcium levels. PTH reduces renal phosphate reabsorption, leading to increased phosphate loss in urine. Pituitary adenomas are associated with osteoporosis due to excessive PTH causing bone resorption.

      PTH activates vitamin D, which increases phosphate absorption in the gastrointestinal tract. However, the renal loss of phosphate is greater than the increase in absorption, resulting in a net loss of phosphate when PTH levels are high.

      PTH also increases renal vitamin D activation, leading to increased intestinal absorption of calcium and phosphate, as well as increased osteoclast activity. This results in elevated levels of serum calcium and phosphate.

      Hypothyroidism does not significantly affect phosphate regulation, so it would not cause low serum phosphate levels.

      Increased osteoclast activity caused by PTH leads to bone resorption and the release of calcium and phosphate into the blood. However, the renal loss of phosphate is greater than the increase in serum phosphate due to osteoclast activity, resulting in an overall decrease in serum phosphate levels.

      Understanding Parathyroid Hormone and Its Effects

      Parathyroid hormone is a hormone produced by the chief cells of the parathyroid glands. Its main function is to increase the concentration of calcium in the blood by stimulating the PTH receptors in the kidney and bone. This hormone has a short half-life of only 4 minutes.

      The effects of parathyroid hormone are mainly seen in the bone, kidney, and intestine. In the bone, PTH binds to osteoblasts, which then signal to osteoclasts to resorb bone and release calcium. In the kidney, PTH promotes the active reabsorption of calcium and magnesium from the distal convoluted tubule, while decreasing the reabsorption of phosphate. In the intestine, PTH indirectly increases calcium absorption by increasing the activation of vitamin D, which in turn increases calcium absorption.

      Overall, understanding the role of parathyroid hormone is important in maintaining proper calcium levels in the body. Any imbalances in PTH secretion can lead to various disorders such as hyperparathyroidism or hypoparathyroidism.

    • This question is part of the following fields:

      • Endocrine System
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