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  • Question 1 - A 30-year-old male visits his GP complaining of chronic thirst, polyuria, and nocturia...

    Incorrect

    • A 30-year-old male visits his GP complaining of chronic thirst, polyuria, and nocturia that have persisted for 4 months. He has a medical history of OCD, which was diagnosed 2 years ago. After a series of tests, the patient is diagnosed with primary polydipsia.

      What would be the probable outcome of this patient's water deprivation test?

      Your Answer: Low urine osmolality after fluid deprivation, but medium (500-700 mOsmoles/kg) after desmopressin

      Correct Answer: High urine osmolality after both fluid deprivation and desmopressin

      Explanation:

      The water deprivation test is a diagnostic tool used to assess patients with polydipsia, or excessive thirst. During the test, the patient is instructed to refrain from drinking water, and their bladder is emptied. Hourly measurements of urine and plasma osmolalities are taken to monitor changes in the body’s fluid balance. The results of the test can help identify the underlying cause of the patient’s polydipsia. Normal results show a high urine osmolality after the administration of DDAVP, while psychogenic polydipsia is characterized by a low urine osmolality. Cranial DI and nephrogenic DI are both associated with high plasma osmolalities and low urine osmolalities.

    • This question is part of the following fields:

      • Endocrine System
      43.5
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  • Question 2 - A 54-year-old man with type 2 diabetes mellitus visits the Endocrinology clinic for...

    Incorrect

    • A 54-year-old man with type 2 diabetes mellitus visits the Endocrinology clinic for evaluation. He is currently on maximum doses of metformin and glibenclamide, but his HbA1c levels have increased from 58 mmol/mol to 67 mmol/mol over the past six months. The consultant recommends adding sitagliptin as a third antidiabetic medication. What is the mechanism of action of this new medication?

      Your Answer: Trigger the closure of ATP-sensitive K+ channels, stimulating insulin exocytosis

      Correct Answer: Inhibit the peripheral breakdown of incretins, enhancing their ability to stimulate insulin release

      Explanation:

      Diabetes mellitus is a condition that has seen the development of several drugs in recent years. One hormone that has been the focus of much research is glucagon-like peptide-1 (GLP-1), which is released by the small intestine in response to an oral glucose load. In type 2 diabetes mellitus (T2DM), insulin resistance and insufficient B-cell compensation occur, and the incretin effect, which is largely mediated by GLP-1, is decreased. GLP-1 mimetics, such as exenatide and liraglutide, increase insulin secretion and inhibit glucagon secretion, resulting in weight loss, unlike other medications. They are sometimes used in combination with insulin in T2DM to minimize weight gain. Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as vildagliptin and sitagliptin, increase levels of incretins by decreasing their peripheral breakdown, are taken orally, and do not cause weight gain. Nausea and vomiting are the major adverse effects of GLP-1 mimetics, and the Medicines and Healthcare products Regulatory Agency has issued specific warnings on the use of exenatide, reporting that it has been linked to severe pancreatitis in some patients. NICE guidelines suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems, a thiazolidinedione is contraindicated, or the person has had a poor response to a thiazolidinedione.

    • This question is part of the following fields:

      • Endocrine System
      36.9
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  • Question 3 - A 23-year-old male comes to his doctor with a 5-month history of headaches,...

    Correct

    • A 23-year-old male comes to his doctor with a 5-month history of headaches, palpitations, and excessive sweating. He also mentions unintentional weight loss. Upon examination, the patient is found to be tachycardic and sweating profusely. The doctor suspects that the man may have a tumor affecting the tissue responsible for producing adrenaline.

      What is the probable location of the tumor?

      Your Answer: Adrenal medulla

      Explanation:

      The secretion of adrenaline is primarily carried out by the adrenal medulla. A patient with a phaeochromocytoma, a type of cancer that affects the adrenal medulla, may experience symptoms such as tachycardia, headaches, and sweating due to excess adrenaline production.

      The adrenal cortex, which surrounds the adrenal medulla, is not involved in adrenaline synthesis. It is responsible for producing mineralocorticoids, glucocorticoids, and androgens.

      The medulla oblongata, located in the brainstem, regulates essential bodily functions but is not responsible for adrenaline secretion.

      The parathyroid gland, which produces parathyroid hormone to regulate calcium metabolism, is not related to adrenaline secretion.

      The Function of Adrenal Medulla

      The adrenal medulla is responsible for producing almost all of the adrenaline in the body, along with small amounts of noradrenaline. Essentially, it is a specialized and enlarged sympathetic ganglion. This gland plays a crucial role in the body’s response to stress and danger, as adrenaline is a hormone that prepares the body for the fight or flight response. When the body perceives a threat, the adrenal medulla releases adrenaline into the bloodstream, which increases heart rate, blood pressure, and respiration, while also dilating the pupils and increasing blood flow to the muscles. This response helps the body to react quickly and effectively to danger. Overall, the adrenal medulla is an important component of the body’s stress response system.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 4 - A 65-year-old male, who is a known type 2 diabetic, visits his GP...

    Correct

    • 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: 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 5 - A 10-year-old boy visits his paediatrician with his mother. He is worried that...

    Incorrect

    • A 10-year-old boy visits his paediatrician with his mother. He is worried that he hasn't started puberty yet while some of his classmates have. The paediatrician explains to the young boy and his mother that the onset of puberty can vary and that it is considered delayed if there are no signs of puberty by the age of 13 years. The paediatrician reassures the boy that there is no need to worry and that he should be patient. What is the first sign of puberty the boy should expect?

      Your Answer: Height growth spurt

      Correct Answer: Testicular enlargement

      Explanation:

      The initial indication of male puberty is the growth of the testicles. This typically happens between the ages of 9.5 and 13.5 years and is the first sign of male puberty. Testicular enlargement is the only pubertal change present in Tanner stage 1.

      During Tanner stage 2, which usually occurs between the ages of 10.5 and 14.5 years, penis growth begins.

      Pubic hair development also starts during Tanner stage 2, between the ages of 9.9 and 14.0 years.

      The height growth spurt occurs at age 14 and reaches a maximum of 10cm/year in Tanner.

      The voice changes during Tanner stage 3, which typically happens around 13.5 years old.

      Puberty: Normal Changes in Males and Females

      Puberty is a natural process that marks the transition from childhood to adolescence. In males, the first sign of puberty is testicular growth, which typically occurs around the age of 12. Testicular volume greater than 4 ml indicates the onset of puberty. The maximum height spurt for boys occurs at the age of 14. On the other hand, in females, the first sign of puberty is breast development, which usually occurs around the age of 11.5. The height spurt for girls reaches its maximum early in puberty, at the age of 12, before menarche. Menarche, or the first menstrual period, typically occurs at the age of 13, with a range of 11-15 years. Following menarche, there is only a slight increase of about 4% in height.

      During puberty, it is normal for boys to experience gynaecomastia, or the development of breast tissue. Girls may also experience asymmetrical breast growth. Additionally, diffuse enlargement of the thyroid gland may be seen in both males and females. These changes are all part of the normal process of puberty and should not be a cause for concern.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 6 - A young male with a history of diabetes mellitus type 1 is admitted...

    Incorrect

    • A young male with a history of diabetes mellitus type 1 is admitted to the emergency department. He was previously found to be confused by his roommates in his room. As well as this, he complains of nausea and abdominal pain.

      An ECG is performed and shows tall tented T waves.

      A simple blood test reveals marked hyperglycemia. A urinalysis shows the presence of ketones ++.

      His bloods show the following:

      Hb 136 g/L Male: (135-180)
      Platelets 210 * 109/L (150 - 400)
      WBC 9.5 * 109/L (4.0 - 11.0)

      Na+ 137 mmol/L (135 - 145)
      K+ 7.1 mmol/L (3.5 - 5.0)
      Bicarbonate 31 mmol/L (22 - 29)
      Urea 8.0 mmol/L (2.0 - 7.0)
      Creatinine 155 µmol/L (55 - 120)

      He is given insulin, calcium gluconate and IV saline.

      What is the main mechanism as to why the patient's potassium level will decrease?

      Your Answer: Insulin signals increase of voltage-gated potassium channels

      Correct Answer: Insulin increases sodium potassium pump

      Explanation:

      Insulin stimulates the Na+/K+ ATPase pump, leading to a decrease in serum potassium levels. This is primarily achieved through increased activity of the sodium-potassium pump, which is triggered by phosphorylation of the transmembrane subunits in response to insulin. While calcium gluconate is used to protect the heart during hyperkalaemia-induced arrhythmias, it does not affect potassium levels. Although IV fluids can improve renal function and potassium clearance, they are not the primary method for reducing potassium levels. Calcium-activated potassium channels are present throughout the body and are activated by an increase in intracellular calcium levels during action potentials.

      Insulin is a hormone produced by the pancreas that plays a crucial role in regulating the metabolism of carbohydrates and fats in the body. It works by causing cells in the liver, muscles, and fat tissue to absorb glucose from the bloodstream, which is then stored as glycogen in the liver and muscles or as triglycerides in fat cells. The human insulin protein is made up of 51 amino acids and is a dimer of an A-chain and a B-chain linked together by disulfide bonds. Pro-insulin is first formed in the rough endoplasmic reticulum of pancreatic beta cells and then cleaved to form insulin and C-peptide. Insulin is stored in secretory granules and released in response to high levels of glucose in the blood. In addition to its role in glucose metabolism, insulin also inhibits lipolysis, reduces muscle protein loss, and increases cellular uptake of potassium through stimulation of the Na+/K+ ATPase pump.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 7 - A 45-year-old male is recovering from trans-sphenoidal surgery for a non-functioning pituitary adenoma....

    Incorrect

    • A 45-year-old male is recovering from trans-sphenoidal surgery for a non-functioning pituitary adenoma. He reports excessive thirst and increased water intake to the doctors during the ward round, four days after the surgery. The patient's fluid chart shows a urine output of 7 litres in the past 24 hours, and his blood glucose level is 5.2mmol/L. To confirm the diagnosis, the doctors plan to conduct a water-deprivation test and a vasopressin test.

      What are the expected results of the urine osmolality investigations, given the likely diagnosis?

      Your Answer: After fluid deprivation, high; after desmopressin, high

      Correct Answer: After fluid deprivation, low; after desmopressin, high

      Explanation:

      The patient has developed cranial diabetes insipidus after pituitary surgery. Water deprivation testing showed low urine osmolality after fluid deprivation and high urine osmolality after desmopressin administration. This condition can also be caused by head trauma or occur idiopathically. Water deprivation testing can also be useful for investigating psychogenic polydipsia. Nephrogenic diabetes insipidus is the other main cause, where the kidneys cannot properly respond to vasopressin.

      The water deprivation test is a diagnostic tool used to assess patients with polydipsia, or excessive thirst. During the test, the patient is instructed to refrain from drinking water, and their bladder is emptied. Hourly measurements of urine and plasma osmolalities are taken to monitor changes in the body’s fluid balance. The results of the test can help identify the underlying cause of the patient’s polydipsia. Normal results show a high urine osmolality after the administration of DDAVP, while psychogenic polydipsia is characterized by a low urine osmolality. Cranial DI and nephrogenic DI are both associated with high plasma osmolalities and low urine osmolalities.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 8 - A 28-year-old female with a three year history of type 1 diabetes complains...

    Incorrect

    • A 28-year-old female with a three year history of type 1 diabetes complains of sudden confusion and excessive sweating. Upon examination, her pulse is 105 bpm, respiratory rate is 16/min, and she appears disoriented. What would be the most suitable initial test to perform for this patient?

      Your Answer: Arterial blood gases

      Correct Answer: Plasma glucose concentration

      Explanation:

      Differentiating Hypoglycaemia from Diabetic Ketoacidosis in Critically Ill Patients

      When assessing a critically ill patient, it is important not to forget the E in the ABCDE algorithm. In the case of a woman presenting acutely, with a normal respiratory rate, it is more likely that she is hypoglycaemic rather than experiencing diabetic ketoacidosis (DKA). To confirm this, it is essential to check her glucose or blood sugar levels and then administer glucose as necessary.

      It is crucial to differentiate between hypoglycaemia and DKA as the treatment for each condition is vastly different. While hypoglycaemia requires immediate administration of glucose, DKA requires insulin therapy and fluid replacement. Therefore, a correct diagnosis is essential to ensure the patient receives the appropriate treatment promptly.

      In conclusion, when assessing a critically ill patient, it is vital to consider all aspects of the ABCDE algorithm, including the often-overlooked E for exposure. In cases where a patient presents acutely, with a normal respiratory rate, it is essential to differentiate between hypoglycaemia and DKA by checking glucose levels and administering glucose or insulin therapy accordingly.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 9 - A 28-year-old female patient presents to her GP with concerns about the appearance...

    Correct

    • A 28-year-old female patient presents to her GP with concerns about the appearance of lumps in her lower abdomen. She has been diagnosed with type 1 diabetes and has been using insulin for more than a decade. The lumps have developed in the areas where she administers her insulin injections.

      What is the probable cause of the lumps?

      Your Answer: Lipodystrophy

      Explanation:

      Small subcutaneous lumps at injection sites, known as lipodystrophy, can be caused by insulin.

      The type and location of the lump suggest that lipodystrophy is the most probable cause.

      Deposits of insulin and glucose are not responsible for the formation of these lumps.

      While a lipoma could also cause similar lumps, it is less likely than lipodystrophy, which is a known complication of insulin injections, especially at the injection site. These lumps can occur in multiple locations.

      Insulin therapy can have side-effects that patients should be aware of. One of the most common side-effects is hypoglycaemia, which can cause sweating, anxiety, blurred vision, confusion, and aggression. Patients should be taught to recognize these symptoms and take 10-20g of a short-acting carbohydrate, such as a glass of Lucozade or non-diet drink, three or more glucose tablets, or glucose gel. It is also important for every person treated with insulin to have a glucagon kit for emergencies where the patient is not able to orally ingest a short-acting carbohydrate. Patients who have frequent hypoglycaemic episodes may develop reduced awareness, and beta-blockers can further reduce hypoglycaemic awareness.

      Another potential side-effect of insulin therapy is lipodystrophy, which typically presents as atrophy or lumps of subcutaneous fat. This can be prevented by rotating the injection site, as using the same site repeatedly can cause erratic insulin absorption. It is important for patients to be aware of these potential side-effects and to discuss any concerns with their healthcare provider. By monitoring their blood sugar levels and following their treatment plan, patients can manage the risks associated with insulin therapy and maintain good health.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 10 - Sarah is a 15-year-old female who presented to the clinic with concerns about...

    Correct

    • Sarah is a 15-year-old female who presented to the clinic with concerns about her development. She has not grown as expected and remains shorter than most of the girls in her class. She also notes that she has not started her period yet, which is affecting her confidence.

      On examination, she is 150cm tall and has no breast development. Pubic hair is sparse and axillary hair is absent. The uterus and ovaries are not palpable. A cleft palate is noted on examination of the mouth. When cranial nerve I was examined, she was unable to detect the smell of the odours sampled.

      Blood tests show low levels of estrogen, follicular stimulating hormone (FSH) and luteinizing hormone (LH). Liver function tests were normal. Blood glucose reading was 5.6mmol/L. Iron studies were unremarkable.

      What is the likely cause for her symptoms?

      Your Answer: Kallmann syndrome

      Explanation:

      The patient’s symptoms of delayed puberty and underdeveloped secondary sexual characteristics, along with a cleft palate and anosmia, suggest Kallmann syndrome. This condition is characterized by hypogonadotropic hypogonadism, as evidenced by low-normal levels of LH and FSH, as well as low testosterone levels. Kallmann syndrome is an X-linked inherited disorder caused by the failure of gonadotrophin-releasing hormone-producing neurons to migrate properly during fetal development.

      While Klinefelter syndrome can also cause delayed puberty and small testes, it is associated with hypergonadotropic hypogonadism, which is characterized by elevated levels of FSH and LH but low testosterone levels. Anosmia is not typically a symptom of Klinefelter syndrome.

      Hemochromatosis, a condition in which iron accumulates in the body, can also cause hypogonadotropic hypogonadism by affecting the hypothalamus. However, this is unlikely in this case as the patient’s iron studies were normal and anosmia is not a common symptom of hemochromatosis.

      Kallmann’s syndrome is a condition that can cause delayed puberty due to hypogonadotropic hypogonadism. It is often inherited as an X-linked recessive trait and is believed to be caused by a failure of GnRH-secreting neurons to migrate to the hypothalamus. One of the key indicators of Kallmann’s syndrome is anosmia, or a lack of smell, in boys with delayed puberty. Other features may include hypogonadism, cryptorchidism, low sex hormone levels, and normal or above-average height. Some patients may also have cleft lip/palate and visual/hearing defects.

      Management of Kallmann’s syndrome typically involves testosterone supplementation. Gonadotrophin supplementation may also be used to stimulate sperm production if fertility is desired later in life. It is important for individuals with Kallmann’s syndrome to receive appropriate medical care and monitoring to manage their symptoms and ensure optimal health outcomes.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 11 - A 15-year-old male arrives at the emergency department with complaints of abdominal pain,...

    Correct

    • A 15-year-old male arrives at the emergency department with complaints of abdominal pain, nausea, and shortness of breath. He has a history of insulin-dependent diabetes and is diagnosed with diabetic ketoacidosis after undergoing tests. During treatment, which electrolyte should you be particularly cautious of, as it may become depleted in the body despite appearing normal in plasma concentrations?

      Your Answer: Potassium

      Explanation:

      Insulin normally helps to move potassium into cells, but in a state of ketoacidosis, there is a lack of insulin to perform this function. As a result, potassium leaks out of cells. Additionally, high levels of glucose in the blood lead to glycosuria in the urine, causing potassium loss through the kidneys.

      Even though patients in a ketoacidotic state may have normal levels of potassium in their blood, their overall potassium levels in the body are often depleted. When insulin is administered to these patients, it can cause a dangerous drop in potassium levels as the minimal amount of potassium left in the body is driven into cells.

      Diabetic ketoacidosis (DKA) is a serious complication of type 1 diabetes mellitus, accounting for around 6% of cases. It can also occur in rare cases of extreme stress in patients with type 2 diabetes mellitus. DKA is caused by uncontrolled lipolysis, resulting in an excess of free fatty acids that are converted to ketone bodies. The most common precipitating factors of DKA are infection, missed insulin doses, and myocardial infarction. Symptoms include abdominal pain, polyuria, polydipsia, dehydration, Kussmaul respiration, and breath that smells like acetone. Diagnostic criteria include glucose levels above 11 mmol/l or known diabetes mellitus, pH below 7.3, bicarbonate below 15 mmol/l, and ketones above 3 mmol/l or urine ketones ++ on dipstick.

      Management of DKA involves fluid replacement, insulin, and correction of electrolyte disturbance. Fluid replacement is necessary as most patients with DKA are deplete around 5-8 litres. Isotonic saline is used initially, even if the patient is severely acidotic. Insulin is administered through an intravenous infusion, and correction of electrolyte disturbance is necessary. Long-acting insulin should be continued, while short-acting insulin should be stopped. Complications may occur from DKA itself or the treatment, such as gastric stasis, thromboembolism, arrhythmias, acute respiratory distress syndrome, acute kidney injury, and cerebral edema. Children and young adults are particularly vulnerable to cerebral edema following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology, etc.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 12 - A 64-year-old man comes in for a follow-up of his type 2 diabetes....

    Incorrect

    • A 64-year-old man comes in for a follow-up of his type 2 diabetes. Despite being on metformin therapy, his HbA1c levels are at 62mmol/mol. To address this, you plan to initiate sitagliptin for dual hypoglycemic therapy.

      What is the mechanism of action of sitagliptin?

      Your Answer: Decreases levels of GIP incretins

      Correct Answer: Decreases GLP-1 breakdown

      Explanation:

      Sitagliptin, a DPP-4 inhibitor, reduces the breakdown of GLP-1 and GIP incretins, leading to increased levels of these hormones and potentiation of the incretin effect, which is typically reduced in diabetes.

      Diabetes mellitus is a condition that has seen the development of several drugs in recent years. One hormone that has been the focus of much research is glucagon-like peptide-1 (GLP-1), which is released by the small intestine in response to an oral glucose load. In type 2 diabetes mellitus (T2DM), insulin resistance and insufficient B-cell compensation occur, and the incretin effect, which is largely mediated by GLP-1, is decreased. GLP-1 mimetics, such as exenatide and liraglutide, increase insulin secretion and inhibit glucagon secretion, resulting in weight loss, unlike other medications. They are sometimes used in combination with insulin in T2DM to minimize weight gain. Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as vildagliptin and sitagliptin, increase levels of incretins by decreasing their peripheral breakdown, are taken orally, and do not cause weight gain. Nausea and vomiting are the major adverse effects of GLP-1 mimetics, and the Medicines and Healthcare products Regulatory Agency has issued specific warnings on the use of exenatide, reporting that it has been linked to severe pancreatitis in some patients. NICE guidelines suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems, a thiazolidinedione is contraindicated, or the person has had a poor response to a thiazolidinedione.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 13 - A 65-year-old man with type 2 diabetes mellitus has been taking metformin 1g...

    Incorrect

    • A 65-year-old man with type 2 diabetes mellitus has been taking metformin 1g twice daily for the past 6 months. Despite this, his HbA1c has remained above target at 64 mmol/mol (8.0%).

      He has a history of left ventricular failure following a myocardial infarction 2 years ago. He has been trying to lose weight since but still has a body mass index of 33 kg/m². He is also prone to recurrent urinary tract infections.

      You intend to intensify treatment by adding a second medication.

      What is the mechanism of action of the most appropriate anti-diabetic drug for him?

      Your Answer: Binding to KATP channels on pancreatic beta cells to stimulate insulin release

      Correct Answer: Inhibition of dipeptidyl peptidase-4 (DPP-4) to increase incretin levels

      Explanation:

      Diabetes mellitus is a condition that has seen the development of several drugs in recent years. One hormone that has been the focus of much research is glucagon-like peptide-1 (GLP-1), which is released by the small intestine in response to an oral glucose load. In type 2 diabetes mellitus (T2DM), insulin resistance and insufficient B-cell compensation occur, and the incretin effect, which is largely mediated by GLP-1, is decreased. GLP-1 mimetics, such as exenatide and liraglutide, increase insulin secretion and inhibit glucagon secretion, resulting in weight loss, unlike other medications. They are sometimes used in combination with insulin in T2DM to minimize weight gain. Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as vildagliptin and sitagliptin, increase levels of incretins by decreasing their peripheral breakdown, are taken orally, and do not cause weight gain. Nausea and vomiting are the major adverse effects of GLP-1 mimetics, and the Medicines and Healthcare products Regulatory Agency has issued specific warnings on the use of exenatide, reporting that it has been linked to severe pancreatitis in some patients. NICE guidelines suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems, a thiazolidinedione is contraindicated, or the person has had a poor response to a thiazolidinedione.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 14 - A 40-year-old woman comes to her doctor complaining of sudden palpitations and occasional...

    Correct

    • A 40-year-old woman comes to her doctor complaining of sudden palpitations and occasional headaches without any apparent cause. She has no significant medical history and denies any stress in her personal or professional life. During the examination, she appears to be sweating and has a pale conjunctiva. Her heart rate is 120 beats per minute, regularly regular, and her blood pressure is 150/100 mmHg. The doctor suspects a phaeochromocytoma, a tumor of the adrenal medulla.

      Which test is the most likely to provide a definitive diagnosis?

      Your Answer: Urinary free adrenaline

      Explanation:

      Extra-adrenal tumors are often located near the aortic bifurcation and can be identified through a urinary free adrenaline test, which measures the levels of adrenaline and noradrenaline produced by the adrenal medulla. Meanwhile, a 24-hour urinary free cortisol test is used to diagnose Cushing’s Disease, which is caused by excessive cortisol production from the zona fasciculata of the adrenal cortex. The aldosterone-renin ratio test is used to diagnose Conn’s Disease, which is caused by excessive aldosterone production from the zona glomerulosa of the adrenal cortex. Androgens are produced by the zona reticularis of the adrenal cortex. Addison’s Disease, a deficiency of cortisol, can be diagnosed through a short synacthen test.

      Adrenal Physiology: Medulla and Cortex

      The adrenal gland is composed of two main parts: the medulla and the cortex. The medulla is responsible for secreting the catecholamines noradrenaline and adrenaline, which are released in response to sympathetic nervous system stimulation. The chromaffin cells of the medulla are innervated by the splanchnic nerves, and the release of these hormones is triggered by the secretion of acetylcholine from preganglionic sympathetic fibers. Phaeochromocytomas, which are tumors derived from chromaffin cells, can cause excessive secretion of both adrenaline and noradrenaline.

      The adrenal cortex is divided into three distinct zones: the zona glomerulosa, zona fasciculata, and zona reticularis. Each zone is responsible for secreting different hormones. The outer zone, zona glomerulosa, secretes aldosterone, which regulates electrolyte balance and blood pressure. The middle zone, zona fasciculata, secretes glucocorticoids, which are involved in the regulation of metabolism, immune function, and stress response. The inner zone, zona reticularis, secretes androgens, which are involved in the development and maintenance of male sex characteristics.

      Most of the hormones secreted by the adrenal cortex, including glucocorticoids and aldosterone, are bound to plasma proteins in the circulation. Glucocorticoids are inactivated and excreted by the liver. Understanding the physiology of the adrenal gland is important for the diagnosis and treatment of various endocrine disorders.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 15 - A 20-year-old man was admitted to hospital with a 5 day history of...

    Correct

    • A 20-year-old man was admitted to hospital with a 5 day history of vomiting, fever and chills. He developed a purpuric rash on his lower limbs and abdomen. During examination, the patient was found to have a pulse rate of 100 beats per minute and a systolic blood pressure of 70mmHg. A spinal tap was performed for CSF microscopy and a CT scan revealed adrenal haemorrhage. Based on the CT scan, the doctor suspected Waterhouse-Friderichsen syndrome. What is the most common bacterial cause of this syndrome?

      Your Answer: Neisseria meningitidis

      Explanation:

      The most frequent cause of Waterhouse-Friderichsen syndrome is Neisseria meningitidis. This syndrome is characterized by adrenal gland failure caused by bleeding into the adrenal gland. Although any organism that can induce disseminated intravascular coagulation can lead to adrenal haemorrhage, neisseria meningitidis is the most common cause and therefore the answer.

      Understanding Waterhouse-Friderichsen Syndrome

      Waterhouse-Friderichsen syndrome is a condition that occurs when the adrenal glands fail due to a previous adrenal haemorrhage caused by a severe bacterial infection. The most common cause of this condition is Neisseria meningitidis, but it can also be caused by other bacteria such as Haemophilus influenzae, Pseudomonas aeruginosa, Escherichia coli, and Streptococcus pneumoniae.

      The symptoms of Waterhouse-Friderichsen syndrome are similar to those of hypoadrenalism, including lethargy, weakness, anorexia, nausea and vomiting, and weight loss. Other symptoms may include hyperpigmentation, especially in the palmar creases, vitiligo, and loss of pubic hair in women. In severe cases, a crisis may occur, which can lead to collapse, shock, and pyrexia.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 16 - A 29-year-old male attends a pre-operative assessment clinic for thyroidectomy due to failed...

    Correct

    • A 29-year-old male attends a pre-operative assessment clinic for thyroidectomy due to failed treatment with carbimazole and radio-iodine for Grave's disease. What is the potential complication that he is at a high risk of developing during this procedure?

      Your Answer: Recurrent laryngeal nerve palsy

      Explanation:

      The risk of complications during thyroidectomy is relatively low, but there are still potential risks to be aware of. One of the most common complications is damage to the recurrent laryngeal nerve, which can result in vocal cord paralysis and hoarseness. However, the vagal nerve and phrenic nerve are rarely damaged during the procedure as they are not in close proximity to the operating site. Trauma to the esophagus is also uncommon. If the parathyroid glands are inadvertently removed during the procedure, it can result in hypoparathyroidism rather than hyperparathyroidism.

      Thyroid disorders are commonly encountered in clinical practice, with hypothyroidism and thyrotoxicosis being the most prevalent. Women are ten times more likely to develop these conditions than men. The thyroid gland is a bi-lobed structure located in the anterior neck and is part of a hypothalamus-pituitary-end organ system that regulates the production of thyroxine and triiodothyronine hormones. These hormones help regulate energy sources, protein synthesis, and the body’s sensitivity to other hormones. Hypothyroidism can be primary or secondary, while thyrotoxicosis is mostly primary. Autoimmunity is the leading cause of thyroid problems in the developed world.

      Thyroid disorders can present in various ways, with symptoms often being the opposite depending on whether the thyroid gland is under or overactive. For example, hypothyroidism may result in weight gain, while thyrotoxicosis leads to weight loss. Thyroid function tests are the primary investigation for diagnosing thyroid disorders. These tests primarily look at serum TSH and T4 levels, with T3 being measured in specific cases. TSH levels are more sensitive than T4 levels for monitoring patients with existing thyroid problems.

      Treatment for thyroid disorders depends on the cause. Patients with hypothyroidism are given levothyroxine to replace the underlying deficiency. Patients with thyrotoxicosis may be treated with propranolol to control symptoms such as tremors, carbimazole to reduce thyroid hormone production, or radioiodine treatment.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 17 - A patient with a recent diagnosis of schizophrenia at the age of 40...

    Correct

    • A patient with a recent diagnosis of schizophrenia at the age of 40 is prescribed risperidone. During their consultation with the doctor, they are informed that some of the potential side effects are caused by elevated levels of prolactin.

      What is the mechanism behind this occurrence?

      Your Answer: Inhibition of dopamine activity

      Explanation:

      Dopamine plays a crucial role in inhibiting the release of prolactin. As atypical antipsychotics like risperidone block dopamine activity, they can lead to increased levels of prolactin. While these drugs may also inhibit histamine and serotonin to varying degrees, it is the inhibition of dopamine that is directly linked to prolactin release. Stimulation of dopamine or serotonin activity would not interfere with prolactin release in the same way that dopamine inhibition does.

      Understanding Prolactin and Its Functions

      Prolactin is a hormone that is produced by the anterior pituitary gland. Its primary function is to stimulate breast development and milk production in females. During pregnancy, prolactin levels increase to support the growth and development of the mammary glands. It also plays a role in reducing the pulsatility of gonadotropin-releasing hormone (GnRH) at the hypothalamic level, which can block the action of luteinizing hormone (LH) on the ovaries or testes.

      The secretion of prolactin is regulated by dopamine, which constantly inhibits its release. However, certain factors can increase or decrease prolactin secretion. For example, prolactin levels increase during pregnancy, in response to estrogen, and during breastfeeding. Additionally, stress, sleep, and certain drugs like metoclopramide and antipsychotics can also increase prolactin secretion. On the other hand, dopamine and dopaminergic agonists can decrease prolactin secretion.

      Overall, understanding the functions and regulation of prolactin is important for reproductive health and lactation.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 18 - A 38-year-old male visits his primary care physician complaining of polyuria, nocturia, and...

    Incorrect

    • A 38-year-old male visits his primary care physician complaining of polyuria, nocturia, and chronic dry mouth that have persisted for 4 months. He has a medical history of systemic lupus erythematosus (SLE) with associated renal involvement. His recent eGFR result was:

      eGFR 23ml/min/1.73m²

      The physician orders a water deprivation test along with other investigations.

      What is the probable diagnosis for this patient, and what can be expected from his water deprivation test?

      Your Answer: High urine osmolality after both fluid deprivation and desmopressin

      Correct Answer: Low urine osmolality after both fluid deprivation and desmopressin

      Explanation:

      The correct answer is low urine osmolality after both fluid deprivation and desmopressin in the water deprivation test for a patient with nephrogenic diabetes insipidus (DI). This condition is characterized by renal insensitivity to antidiuretic hormone (ADH), resulting in an inability to concentrate urine. As a result, urine osmolality will be low even during water deprivation and will not respond to desmopressin (synthetic ADH). This is in contrast to primary polydipsia, where high urine osmolality would be seen after both fluid deprivation and desmopressin, and cranial DI, where low urine osmolality would be seen during water deprivation but high urine osmolality would be seen after desmopressin.

      The water deprivation test is a diagnostic tool used to assess patients with polydipsia, or excessive thirst. During the test, the patient is instructed to refrain from drinking water, and their bladder is emptied. Hourly measurements of urine and plasma osmolalities are taken to monitor changes in the body’s fluid balance. The results of the test can help identify the underlying cause of the patient’s polydipsia. Normal results show a high urine osmolality after the administration of DDAVP, while psychogenic polydipsia is characterized by a low urine osmolality. Cranial DI and nephrogenic DI are both associated with high plasma osmolalities and low urine osmolalities.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 19 - A 65-year-old woman with type 2 diabetes mellitus is being evaluated by her...

    Correct

    • A 65-year-old woman with type 2 diabetes mellitus is being evaluated by her diabetic nurse. Despite taking metformin for the past 6 months, her glycaemic control remains poor. To improve management, the decision is made to add sitagliptin (a dipeptidyl-peptidase 4 (DPP-4) inhibitor) to her current metformin regimen.

      What is the mechanism of action of the newly prescribed medication?

      Your Answer: Increased levels of glucagon-like peptide 1 (GLP-1)

      Explanation:

      DPP-4 inhibitors, like sitagliptin, work by inhibiting the breakdown of incretins such as GLP-1 and GIP. This leads to higher levels of insulin being released, as incretins increase insulin release. These inhibitors are often weight-neutral, but can occasionally cause weight loss.

      The answer Increases cell sensitivity to insulin is incorrect, as this is the mechanism of action of metformin, not DPP-4 inhibitors. Metformin increases cell sensitivity to insulin, but the exact mechanism is not fully understood.

      Similarly, Inhibition of sodium-glucose co-transporter (SGLT2) is incorrect, as this is the mechanism of action of SGLT2 inhibitors, not DPP-4 inhibitors. SGLT2 inhibitors prevent glucose absorption in the kidneys, leading to higher levels of glucose in the urine and an increased risk of urinary tract infections.

      Lastly, Increases adipogenesis is incorrect, as this is the mechanism of action of thiazolidinediones, not DPP-4 inhibitors. Thiazolidinediones stimulate adipogenesis, causing cells to become more dependent on glucose for energy.

      Diabetes mellitus is a condition that has seen the development of several drugs in recent years. One hormone that has been the focus of much research is glucagon-like peptide-1 (GLP-1), which is released by the small intestine in response to an oral glucose load. In type 2 diabetes mellitus (T2DM), insulin resistance and insufficient B-cell compensation occur, and the incretin effect, which is largely mediated by GLP-1, is decreased. GLP-1 mimetics, such as exenatide and liraglutide, increase insulin secretion and inhibit glucagon secretion, resulting in weight loss, unlike other medications. They are sometimes used in combination with insulin in T2DM to minimize weight gain. Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as vildagliptin and sitagliptin, increase levels of incretins by decreasing their peripheral breakdown, are taken orally, and do not cause weight gain. Nausea and vomiting are the major adverse effects of GLP-1 mimetics, and the Medicines and Healthcare products Regulatory Agency has issued specific warnings on the use of exenatide, reporting that it has been linked to severe pancreatitis in some patients. NICE guidelines suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems, a thiazolidinedione is contraindicated, or the person has had a poor response to a thiazolidinedione.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 20 - A 15-year-old male arrives at the emergency department with intense abdominal pain and...

    Incorrect

    • A 15-year-old male arrives at the emergency department with intense abdominal pain and a decreased Glasgow coma score (GCS). Over the past few weeks, he has been experiencing excessive urination, abnormal thirst, and weight loss. Laboratory results reveal:

      Ketones 4.2 mmol/L (<0.6 mmol/L)
      Glucose 20 mmol/L
      pH 7.25

      What is the probable cause of the acidosis and hyperketonemia in this case?

      Your Answer: Uncontrolled ketolysis

      Correct Answer: Uncontrolled lipolysis

      Explanation:

      The likely cause of the patient’s condition is diabetic ketoacidosis, which is a result of uncontrolled lipolysis. This process leads to an excess of free fatty acids that are eventually converted into ketone bodies. It is important to note that proteolysis, the breakdown of proteins into smaller polypeptides, does not yield ketone bodies and is not the cause of this condition. While glycogenolysis and gluconeogenesis are increased due to the lack of insulin and rise of glucagon, they do not result in acidosis or elevated levels of ketone bodies. It is ketogenesis, not ketolysis, that leads to the increased levels of ketone bodies.

      Diabetic ketoacidosis (DKA) is a serious complication of type 1 diabetes mellitus, accounting for around 6% of cases. It can also occur in rare cases of extreme stress in patients with type 2 diabetes mellitus. DKA is caused by uncontrolled lipolysis, resulting in an excess of free fatty acids that are converted to ketone bodies. The most common precipitating factors of DKA are infection, missed insulin doses, and myocardial infarction. Symptoms include abdominal pain, polyuria, polydipsia, dehydration, Kussmaul respiration, and breath that smells like acetone. Diagnostic criteria include glucose levels above 11 mmol/l or known diabetes mellitus, pH below 7.3, bicarbonate below 15 mmol/l, and ketones above 3 mmol/l or urine ketones ++ on dipstick.

      Management of DKA involves fluid replacement, insulin, and correction of electrolyte disturbance. Fluid replacement is necessary as most patients with DKA are deplete around 5-8 litres. Isotonic saline is used initially, even if the patient is severely acidotic. Insulin is administered through an intravenous infusion, and correction of electrolyte disturbance is necessary. Long-acting insulin should be continued, while short-acting insulin should be stopped. Complications may occur from DKA itself or the treatment, such as gastric stasis, thromboembolism, arrhythmias, acute respiratory distress syndrome, acute kidney injury, and cerebral edema. Children and young adults are particularly vulnerable to cerebral edema following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology, etc.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 21 - A 54-year-old man with a history of type II diabetes mellitus presents for...

    Correct

    • A 54-year-old man with a history of type II diabetes mellitus presents for a routine check-up. He reports no symptoms of increased urination or thirst. Laboratory results reveal an HbA1c level of 67 mmol/mol and a random plasma glucose level of 15.6 mg/l. The patient is currently taking metformin, and his physician decides to add gliclazide to his medication regimen. What is the mechanism of action of gliclazide?

      Your Answer: Stimulates sulphonylurea-1 receptors

      Explanation:

      The primary mode of action of gliclazide, which belongs to the sulphonylurea class, is to activate the sulphonylurea-1 receptors present on pancreatic cells, thereby promoting insulin secretion. The remaining choices pertain to alternative medications for diabetes.

      Common Medications for Type 2 Diabetes

      Type 2 diabetes is a chronic condition that affects millions of people worldwide. Fortunately, there are several medications available to help manage the disease. Some of the most commonly prescribed drugs include sulphonylureas, metformin, alpha-glucosidase inhibitors (such as acarbose), glitazones, and insulin.

      Sulphonylureas are a type of medication that stimulates the pancreas to produce more insulin. This helps to lower blood sugar levels and improve glucose control. Metformin, on the other hand, works by reducing the amount of glucose produced by the liver and improving insulin sensitivity. Alpha-glucosidase inhibitors, like acarbose, slow down the digestion of carbohydrates in the small intestine, which helps to prevent spikes in blood sugar levels after meals.

      Glitazones, also known as thiazolidinediones, improve insulin sensitivity and reduce insulin resistance. They work by activating a specific receptor in the body that helps to regulate glucose metabolism. Finally, insulin is a hormone that is naturally produced by the pancreas and helps to regulate blood sugar levels. In some cases, people with type 2 diabetes may need to take insulin injections to help manage their condition.

      Overall, these medications can be very effective in helping people with type 2 diabetes to manage their blood sugar levels and prevent complications. However, it’s important to work closely with a healthcare provider to determine the best treatment plan for each individual.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 22 - A 56-year-old patient visits his primary care physician for a follow-up on his...

    Incorrect

    • A 56-year-old patient visits his primary care physician for a follow-up on his diabetes treatment. He is currently taking metformin and expresses concern about adding more medications that may lead to hypoglycemia. The patient has a medical history of bladder cancer, which was treated through surgery. On examination, the only notable finding is an elevated body mass index of 32 kg/m².

      Based on recent blood test results, with an HbA1c level of 61 mmol/L (<48), the GP wants to prescribe a medication that does not cause weight gain or hypoglycemia. What is the probable mechanism of action of this drug?

      Your Answer: Binding of ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells

      Correct Answer: Reduction of the peripheral breakdown of incretins such as glucagon-like peptide (GLP-1)

      Explanation:

      Diabetes mellitus is a condition that has seen the development of several drugs in recent years. One hormone that has been the focus of much research is glucagon-like peptide-1 (GLP-1), which is released by the small intestine in response to an oral glucose load. In type 2 diabetes mellitus (T2DM), insulin resistance and insufficient B-cell compensation occur, and the incretin effect, which is largely mediated by GLP-1, is decreased. GLP-1 mimetics, such as exenatide and liraglutide, increase insulin secretion and inhibit glucagon secretion, resulting in weight loss, unlike other medications. They are sometimes used in combination with insulin in T2DM to minimize weight gain. Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as vildagliptin and sitagliptin, increase levels of incretins by decreasing their peripheral breakdown, are taken orally, and do not cause weight gain. Nausea and vomiting are the major adverse effects of GLP-1 mimetics, and the Medicines and Healthcare products Regulatory Agency has issued specific warnings on the use of exenatide, reporting that it has been linked to severe pancreatitis in some patients. NICE guidelines suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems, a thiazolidinedione is contraindicated, or the person has had a poor response to a thiazolidinedione.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 23 - A 62-year-old male with type 2 diabetes is urgently referred by his GP...

    Incorrect

    • A 62-year-old male with type 2 diabetes is urgently referred by his GP due to poor glycaemic control for the past three days, with home blood glucose readings around 25 mmol/L. He is currently being treated with metformin and lisinopril. Yesterday, his GP checked his U+E and found that his serum sodium was 138 mmol/L (137-144), serum potassium was 5.8 mmol/L (3.5-4.9), serum urea was 20 mmol/L (2.5-7.5), and serum creatinine was 350 µmol/L (60-110). On examination, he has a temperature of 39°C, a pulse of 108 bpm, a blood pressure of 96/60 mmHg, a respiratory rate of 32/min, and oxygen saturations of 99% on air. His cardiovascular, respiratory, and abdominal examination are otherwise normal. Further investigations reveal a plasma glucose level of 17 mmol/L (3.0-6.0) and urine analysis showing blood ++ and protein ++, but ketones are negative. What is the likely diagnosis?

      Your Answer: Hyperosmolar non-ketotic state

      Correct Answer: Sepsis

      Explanation:

      The causes of septic shock are important to understand in order to provide appropriate treatment and improve patient outcomes. Septic shock can cause fever, hypotension, and renal failure, as well as tachypnea due to metabolic acidosis. However, it is crucial to rule out other conditions such as hyperosmolar hyperglycemic state or diabetic ketoacidosis, which have different symptoms and diagnostic criteria.

      While metformin can contribute to acidosis, it is unlikely to be the primary cause in this case. Diabetic patients may be prone to renal tubular acidosis, but this is not likely to be the cause of an acute presentation. Instead, a type IV renal tubular acidosis, characterized by hyporeninaemic hypoaldosteronism, may be a more likely association.

      Overall, it is crucial to carefully evaluate patients with septic shock and consider all possible causes of their symptoms. By ruling out other conditions and identifying the underlying cause of the acidosis, healthcare providers can provide targeted treatment and improve patient outcomes. Further research and education on septic shock and its causes can also help to improve diagnosis and treatment in the future.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 24 - A 38-year-old woman is diagnosed with hyperthyroidism and started on carbimazole. What is...

    Incorrect

    • A 38-year-old woman is diagnosed with hyperthyroidism and started on carbimazole. What is the mechanism of action of this medication?

      Your Answer: Prevents thyroxine (T4) conversion to triiodothyronine (T3)

      Correct Answer: Prevents iodination of the tyrosine residue on thyroglobulin

      Explanation:

      Carbimazole is a medication used to treat thyrotoxicosis, a condition where the thyroid gland produces too much thyroid hormone. It is usually given in high doses for six weeks until the patient’s thyroid hormone levels become normal, after which the dosage is reduced. The drug works by blocking thyroid peroxidase, an enzyme that is responsible for coupling and iodinating the tyrosine residues on thyroglobulin, which ultimately leads to a reduction in thyroid hormone production. In contrast, propylthiouracil has a dual mechanism of action, inhibiting both thyroid peroxidase and 5′-deiodinase, which reduces the peripheral conversion of T4 to T3.

      However, carbimazole is not without its adverse effects. One of the most serious side effects is agranulocytosis, a condition where the body’s white blood cell count drops significantly, making the patient more susceptible to infections. Additionally, carbimazole can cross the placenta and affect the developing fetus, although it may be used in low doses during pregnancy under close medical supervision. Overall, carbimazole is an effective medication for managing thyrotoxicosis, but its potential side effects should be carefully monitored.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 25 - A 65-year-old male with a diagnosis of lung cancer presents with fatigue and...

    Incorrect

    • A 65-year-old male with a diagnosis of lung cancer presents with fatigue and lightheadedness. Upon examination, the following results are obtained:

      Plasma sodium concentration 115 mmol/L (137-144)
      Potassium 3.5 mmol/L (3.5-4.9)
      Urea 3.2 mmol/L (2.5-7.5)
      Creatinine 67 µmol/L (60-110)

      What is the probable reason for his symptoms based on these findings?

      Your Answer: Hypoadrenalism due to adrenal metastases

      Correct Answer: Syndrome of inappropriate ADH secretion

      Explanation:

      Syndrome of Inappropriate ADH Secretion

      Syndrome of inappropriate ADH secretion (SIADH) is a condition characterized by low levels of sodium in the blood. This is caused by the overproduction of antidiuretic hormone (ADH) by the posterior pituitary gland. Tumors such as bronchial carcinoma can cause the ectopic elaboration of ADH, leading to dilutional hyponatremia. The diagnosis of SIADH is one of exclusion, but it can be supported by a high urine sodium concentration with high urine osmolality.

      Hypoadrenalism is less likely to cause hyponatremia, as it is usually associated with hyperkalemia and mild hyperuricemia. On the other hand, diabetes insipidus is a condition where the kidneys are unable to reabsorb water, leading to excessive thirst and urination.

      It is important to diagnose and treat SIADH promptly to prevent complications such as seizures, coma, and even death. Treatment options include fluid restriction, medications to block the effects of ADH, and addressing the underlying cause of the condition.

      In conclusion, SIADH is a condition that can cause low levels of sodium in the blood due to the overproduction of ADH. It is important to differentiate it from other conditions that can cause hyponatremia and to treat it promptly to prevent complications.

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      • Endocrine System
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  • Question 26 - What is the association between brown tumours of bone and a specific condition...

    Incorrect

    • What is the association between brown tumours of bone and a specific condition or disease?

      Your Answer: Hypoparathyroidism

      Correct Answer: Hyperparathyroidism

      Explanation:

      Brown tumors are bone tumors that develop due to excessive osteoclast activity, typically in cases of hyperparathyroidism. These tumors are composed of fibrous tissue, woven bone, and supporting blood vessels, but lack any matrix. They do not appear on x-rays due to their radiolucent nature. Osteoclasts consume the trabecular bone that osteoblasts produce, leading to a cycle of reparative bone deposition and resorption that can cause bone pain and involve the periosteum, resulting in an expansion beyond the typical shape of the bone. The tumors are called brown due to the deposition of haemosiderin at the site.

      Primary Hyperparathyroidism: Causes, Symptoms, and Treatment

      Primary hyperparathyroidism is a condition that is commonly seen in elderly females and is characterized by an unquenchable thirst and an inappropriately normal or raised parathyroid hormone level. It is usually caused by a solitary adenoma, hyperplasia, multiple adenoma, or carcinoma. While around 80% of patients are asymptomatic, the symptomatic features of primary hyperparathyroidism may include polydipsia, polyuria, depression, anorexia, nausea, constipation, peptic ulceration, pancreatitis, bone pain/fracture, renal stones, and hypertension.

      Primary hyperparathyroidism is associated with hypertension and multiple endocrine neoplasia, such as MEN I and II. To diagnose this condition, doctors may perform a technetium-MIBI subtraction scan or look for a characteristic X-ray finding of hyperparathyroidism called the pepperpot skull.

      The definitive management for primary hyperparathyroidism is total parathyroidectomy. However, conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal, the patient is over 50 years old, and there is no evidence of end-organ damage. Patients who are not suitable for surgery may be treated with cinacalcet, a calcimimetic that mimics the action of calcium on tissues by allosteric activation of the calcium-sensing receptor.

      In summary, primary hyperparathyroidism is a condition that can cause various symptoms and is commonly seen in elderly females. It can be diagnosed through various tests and managed through surgery or medication.

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      • Endocrine System
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  • Question 27 - A 47-year-old female has been diagnosed with Grave's disease, experiencing weight loss, heat...

    Incorrect

    • A 47-year-old female has been diagnosed with Grave's disease, experiencing weight loss, heat intolerance, and a tremor that is affecting her job as a waitress. Despite being prescribed carbimazole, she is unhappy with the results after 3 days. What other medication options are available for symptom management?

      Your Answer: Propylthiouracil

      Correct Answer: Beta blockers

      Explanation:

      To alleviate symptoms, beta blockers like propranolol can be used to block the sympathetic effects on the heart. Guanethidine can also be administered to reduce catecholamine release. Statins and calcium channel blockers are not effective in treating the patient’s symptoms. Although benzodiazepines have anxiolytic and sedative properties, they may not be the most suitable option in this case.

      Graves’ Disease: Common Features and Unique Signs

      Graves’ disease is the most frequent cause of thyrotoxicosis, which is commonly observed in women aged 30-50 years. The condition presents typical features of thyrotoxicosis, such as weight loss, palpitations, and heat intolerance. However, Graves’ disease also displays specific signs that are not present in other causes of thyrotoxicosis. These include eye signs, such as exophthalmos and ophthalmoplegia, as well as pretibial myxoedema and thyroid acropachy. The latter is a triad of digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation.

      Graves’ disease is characterized by the presence of autoantibodies, including TSH receptor stimulating antibodies in 90% of patients and anti-thyroid peroxidase antibodies in 75% of patients. Thyroid scintigraphy reveals a diffuse, homogenous, and increased uptake of radioactive iodine. These features help distinguish Graves’ disease from other causes of thyrotoxicosis and aid in its diagnosis.

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      • Endocrine System
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  • Question 28 - A teenage girl and her mother come to the doctor's office with concerns...

    Incorrect

    • A teenage girl and her mother come to the doctor's office with concerns about ambiguous genitalia. Upon conducting a thorough medical history and various tests, the doctor diagnoses the girl with congenital adrenal hyperplasia. What is the reason for adrenal hyperplasia being a characteristic of this condition?

      Your Answer: Increased testosterone synthesis

      Correct Answer: Inefficient cortisol synthesis

      Explanation:

      Low cortisol production and compensatory adrenal hyperplasia are caused by 21-hydroxylase deficiency, leading to increased androgen production and ambiguous genitalia. The enzymes 11-beta hydroxylase and 17-hydroxylase are also involved. Testosterone and estrogen synthesis is not affected as they are produced in the testes and ovaries, respectively. Congenital adrenal hyperplasia is not caused by aldosterone synthesis, despite it occurring in the adrenal cortex.

      Congenital adrenal hyperplasia is a genetic condition that affects the adrenal glands and can result in various symptoms depending on the specific enzyme deficiency. One common form is 21-hydroxylase deficiency, which can cause virilization of female genitalia, precocious puberty in males, and a salt-losing crisis in 60-70% of patients during the first few weeks of life. Another form is 11-beta hydroxylase deficiency, which can also cause virilization and precocious puberty, as well as hypertension and hypokalemia. A third form is 17-hydroxylase deficiency, which typically does not cause virilization in females but can result in intersex characteristics in boys and hypertension.

      Overall, congenital adrenal hyperplasia can have significant impacts on a person’s physical development and health, and early diagnosis and treatment are important for managing symptoms and preventing complications.

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      • Endocrine System
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  • Question 29 - A 70-year-old man with chronic back pain and renal failure presents with the...

    Correct

    • A 70-year-old man with chronic back pain and renal failure presents with the following blood test results:

      Reference range
      Ca2+ 2.10 2.15-2.55 mmol/l
      Parathyroid hormone 9.8 1-6.5 pmol/l
      Phosphate 0.75 0.6-1.25 mmol/l

      What is the probable diagnosis?

      Your Answer: Secondary hyperparathyroidism

      Explanation:

      Secondary hyperparathyroidism is characterized by elevated levels of PTH, while calcium levels are either normal or low. This condition occurs due to the parathyroid glands’ hyperplasia in response to chronic hypocalcemia or hyperphosphatemia, which is a natural physiological reaction. The body releases calcium from the kidneys, gastrointestinal system, and bones.

      Parathyroid Glands and Disorders of Calcium Metabolism

      The parathyroid glands play a crucial role in regulating calcium levels in the body. Hyperparathyroidism is a disorder that occurs when these glands produce too much parathyroid hormone (PTH), leading to abnormal calcium metabolism. Primary hyperparathyroidism is the most common form and is usually caused by a solitary adenoma. Secondary hyperparathyroidism occurs as a result of low calcium levels, often in the setting of chronic renal failure. Tertiary hyperparathyroidism is a rare condition that occurs when hyperplasia of the parathyroid glands persists after correction of underlying renal disorder.

      Diagnosis of hyperparathyroidism is based on hormone profiles and clinical features. Treatment options vary depending on the type and severity of the disorder. Surgery is usually indicated for primary hyperparathyroidism if certain criteria are met, such as elevated serum calcium levels, hypercalciuria, and nephrolithiasis. Secondary hyperparathyroidism is typically managed with medical therapy, while surgery may be necessary for persistent symptoms such as bone pain and soft tissue calcifications. Tertiary hyperparathyroidism may resolve on its own within a year after transplant, but surgery may be required if an autonomously functioning parathyroid gland is present. It is important to consider differential diagnoses, such as benign familial hypocalciuric hypercalcaemia, which is a rare but relatively benign condition.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 30 - A 9-year-old girl is being treated by a paediatrician for bedwetting at night....

    Correct

    • A 9-year-old girl is being treated by a paediatrician for bedwetting at night. Non-invasive methods have not yielded any results and her family is interested in trying medication. The paediatrician has approved a trial of desmopressin.

      What is the site of action of this drug?

      Your Answer: The collecting ducts of the kidney

      Explanation:

      Desmopressin is a synthetic version of antidiuretic hormone (ADH) that acts on the collecting ducts in the kidneys. ADH is released by the posterior pituitary gland in response to increased blood osmolality. By increasing the reabsorption of solute-free water in the collecting ducts, ADH reduces blood osmolality and produces small volumes of concentrated urine. This mechanism is effective in reducing the volume of urine produced overnight in cases of nocturnal enuresis (bed-wetting). The distal tubule, glomerulus, and proximal tubule are not sites of ADH action. Although the posterior pituitary gland produces ADH, it exerts its effects on the kidneys.

      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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