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  • Question 1 - A 36-year-old woman visits her GP complaining of frequent urination. She has been...

    Incorrect

    • A 36-year-old woman visits her GP complaining of frequent urination. She has been waking up several times at night to urinate for the past two weeks and has been feeling more thirsty than usual. Her temperature is 37.3ºC. She has a history of bipolar disorder and is currently on lithium medication.

      What could be the possible cause of her polyuria?

      Your Answer: Central diabetes insipidus

      Correct Answer: Lithium reducing ADH-dependent water reabsorption in the collecting duct

      Explanation:

      The site of action for antidiuretic hormone (ADH) is the collecting ducts. Lithium treatment for bipolar disorder can lead to diabetes insipidus, which is characterized by increased thirst (polydipsia) and increased urination (polyuria). Lithium use can cause nephrogenic diabetes insipidus, where the kidneys are unable to respond adequately to ADH. Normally, ADH induces the expression of aquaporin 2 channels in the collecting duct, which stimulates water reabsorption.

      Central diabetes insipidus occurs when there is damage to the posterior pituitary gland, resulting in insufficient production and release of ADH. However, lithium use causes nephrogenic diabetes insipidus instead of central diabetes insipidus.

      Although insulin resistance and hyperglycemia can also cause polyuria and polydipsia, as seen in diabetic ketoacidosis, the use of lithium suggests that the patient’s symptoms are due to diabetes insipidus rather than diabetes mellitus.

      Lithium inhibits the expression of aquaporin channels in the renal collecting duct, rather than the distal convoluted tubule, which causes diabetes insipidus.

      While a urinary tract infection can also present with polyuria and nocturia, the presence of lithium in the patient’s drug history and the fact that the patient also has polydipsia suggest nephrogenic diabetes insipidus. Diabetes insipidus causes increased thirst due to the excessive volume of urine produced, leading to water loss from the body. In addition, a urinary tract infection would likely cause dysuria (burning or stinging when passing urine) and lower abdominal pain.

      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 2 - A 15-year-old girl comes to the Emergency Department complaining of sudden onset pain...

    Incorrect

    • A 15-year-old girl comes to the Emergency Department complaining of sudden onset pain in the right iliac fossa, along with nausea, vomiting, and fever. She has no significant medical or surgical history. During the examination, you observe rebound tenderness at McBurney's point, guarding, and a positive Rovsing's sign. You suspect appendicitis and decide to take her for surgery.

      What is the most probable physiological response in this situation?

      Your Answer: Reduced cortisol secretion

      Correct Answer: Increased glucagon secretion

      Explanation:

      Glucagon secretion increases in response to physiological stresses such as inflammation of the appendix and surgery. This is because glucagon helps to increase glucose availability in the body through glycogenolysis and gluconeogenesis. During times of stress, the body’s response is to increase glucose and oxygen availability, increased sympathetic activity, and redirect energy towards more crucial functions such as increasing blood pressure and heart rate.

      However, insulin and glucagon have opposite effects on glucose regulation. Therefore, any factor that stimulates glucagon secretion must decrease insulin levels. This is because insulin reduces glucose availability in the body, which weakens the body’s ability to cope with stress.

      The hypothalamic-pituitary-adrenal axis is also activated during times of stress, leading to the production of cortisol. Cortisol plays an important role in releasing glucose from fat storage, which is necessary for the body’s stress response. Therefore, the level of ACTH, which stimulates cortisol production, would increase rather than decrease.

      Cortisol and glucocorticoids also inhibit thyroid hormone secretion. As a result, the level of T4, which is a modulator of metabolic rate, would decrease during times of stress. This is because the body needs to divert energy away from metabolism and towards more acute functions during times of stress.

      Glucagon: The Hormonal Antagonist to Insulin

      Glucagon is a hormone that is released from the alpha cells of the Islets of Langerhans in the pancreas. It has the opposite metabolic effects to insulin, resulting in increased plasma glucose levels. Glucagon functions by promoting glycogenolysis, gluconeogenesis, and lipolysis. It is regulated by various factors such as hypoglycemia, stresses like infections, burns, surgery, increased catecholamines, and sympathetic nervous system stimulation, as well as increased plasma amino acids. On the other hand, glucagon secretion decreases with hyperglycemia, insulin, somatostatin, and increased free fatty acids and keto acids.

      Glucagon is used to rapidly reverse the effects of hypoglycemia in diabetics. It is an essential hormone that plays a crucial role in maintaining glucose homeostasis in the body. Its antagonistic relationship with insulin helps to regulate blood glucose levels and prevent hyperglycemia. Understanding the regulation and function of glucagon is crucial in the management of diabetes and other metabolic disorders.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 3 - An 8-year-old girl has been brought to the GP by her mother who...

    Incorrect

    • An 8-year-old girl has been brought to the GP by her mother who is worried that her daughter may be starting puberty too early. The mother reports an enlargement in nipple size, some breast development, and the appearance of light hairs on the edge of the labia majora.

      At what Tanner stage is the girl currently?

      Your Answer: III

      Correct Answer: II

      Explanation:

      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 4 - A 25-year-old male patient presents to the endocrine clinic with delayed-onset puberty. His...

    Incorrect

    • A 25-year-old male patient presents to the endocrine clinic with delayed-onset puberty. His history revealed a cleft palate as a child which had been repaired successfully. On direct questioning, he revealed he had anosmia but was told this was due to a minor head injury aged 5. On examination, he was 1.80 metres tall, had sparse pubic hair and small volume testes (Tanner staging grade 1).

      Blood results revealed:

      FSH 2 IU/L (1-7)
      LH 2 IU/L (1-8)
      Testosterone 240 ng/dL (280-1100)

      What is the most likely cause of this patient's condition?

      Your Answer:

      Correct Answer: Kallmann syndrome

      Explanation:

      The minor head injury is unlikely to be the cause of the patient’s anosmia. However, the combination of anosmia and cleft palate, along with the blood test results indicating hypogonadotropic hypogonadism, suggests that the patient may have Kallmann’s syndrome, which is an X-linked inherited disorder. Constitutional developmental delay is less likely due to the patient’s age and abnormal blood test results.

      Empty sella syndrome is a condition where the sella turcica, the area of the brain where the pituitary gland is located, is empty and filled with cerebrospinal fluid. Although this condition can be asymptomatic, it can also present with symptoms of hypopituitarism. However, since the patient also has anosmia and cleft palate, empty sella syndrome is less likely.

      Klinefelter’s syndrome is characterized by tall stature, gynecomastia, and small penis/testes. Blood tests would reveal elevated gonadotropins and low testosterone levels. However, since the patient’s FSH and LH levels are low, Klinefelter’s syndrome can be ruled out.

      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 5 - 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:

      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 6 - 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:

      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 7 - A 14-year-old arrives at the Emergency Department complaining of abdominal pains, nausea, and...

    Incorrect

    • A 14-year-old arrives at the Emergency Department complaining of abdominal pains, nausea, and vomiting. Upon conducting blood tests, the following results are obtained:

      - Glucose: 24 mmol/L (4.0-11.0)
      - Ketones: 4.6 mmol/L (<0.6)
      - Na+: 138 mmol/L (135 - 145)
      - K+: 4.7 mmol/L (3.5 - 5.0)

      Based on these findings, the patient is started on a fixed insulin regimen and given intravenous fluids. After repeating the blood tests, it is observed that the K+ level has dropped to 3.3 mmol/L (3.5 - 5.0). What mechanism is responsible for this effect caused by insulin?

      Your Answer:

      Correct Answer: Stimulation of the Na+/K+ ATPase pump

      Explanation:

      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 8 - What is the half life of insulin in the circulation of a typical...

    Incorrect

    • What is the half life of insulin in the circulation of a typical healthy adult?

      Your Answer:

      Correct Answer: Less than 30 minutes

      Explanation:

      Enzymes in the bloodstream break down insulin, resulting in a half-life of under 30 minutes. In type 2 diabetes, there may be irregularities in the insulin clearance process.

      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 9 - A 32-year-old female patient visits your clinic complaining of fatigue and unexplained weight...

    Incorrect

    • A 32-year-old female patient visits your clinic complaining of fatigue and unexplained weight gain. She mentions feeling extremely sensitive to cold temperatures. You suspect hypothyroidism and decide to conduct a test on her serum levels of thyroid stimulating hormone (TSH) and free thyroxine (T4). Which of the following hormones is not secreted from the anterior pituitary gland, where TSH is released?

      Your Answer:

      Correct Answer: antidiuretic hormone

      Explanation:

      The hormone ADH (also known as vasopressin) is secreted by the posterior pituitary gland and acts in the collecting ducts of the kidneys to increase water reabsorption. Unlike ADH, all of the other hormone options presented are released from the anterior pituitary. ACTH is a component of the hypothalamic-pituitary-axis and increases the production and release of cortisol from the adrenal gland. GH (also called somatotropin) is an anabolic hormone that stimulates growth in childhood and has metabolic effects on protein, glucose, and lipids. FSH is a gonadotropin that promotes the maturation of germ cells.

      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 10 - A 28-year-old woman complains of amenorrhoea and galactorrhoea for the past six months....

    Incorrect

    • A 28-year-old woman complains of amenorrhoea and galactorrhoea for the past six months. She has not been taking any medication and has been in good health otherwise. A pregnancy test has come back negative. What would be the most suitable investigation for this patient?

      Your Answer:

      Correct Answer: Prolactin concentration

      Explanation:

      Galactorrhoea and Prolactinomas

      Galactorrhoea is a condition where breast milk is secreted, commonly seen during pregnancy and the early postpartum period. However, if a pregnancy test is negative, it may indicate the presence of a prolactinoma. Prolactinomas are tumors that develop in the pituitary gland, which can be either small or large. These tumors cause symptoms such as menstrual disturbance, infertility, and galactorrhoea due to the secretion of prolactin. Macroprolactinomas can also cause visual field defects, headache, and hypopituitarism due to their mass effect on the pituitary gland. Women with prolactinomas tend to present early due to menstrual cycle and fertility issues, while men may present later.

      The diagnosis of prolactinomas is made by measuring serum prolactin levels and performing MRI imaging of the pituitary gland. Serum prolactin levels are typically several thousand, with a reference range of less than 690 U/L. Elevated prolactin levels can also be caused by pregnancy and lactation, hypothyroidism, and certain medications such as antipsychotics, anti-depressants, and anti-convulsants.

      The treatment for prolactinomas involves drugs such as bromocriptine or cabergoline, which work by inhibiting prolactin release through the dopamine system. These drugs can cause significant tumor shrinkage over several weeks and months of treatment. Patients are typically monitored with serum prolactin levels and MRI scans for several years while continuing the medication. Some patients may be able to stop the medication without any further issues, while others may experience a relapse and need to resume treatment.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 11 - A 27-year-old mother is concerned about her infant's skin tone. The baby was...

    Incorrect

    • A 27-year-old mother is concerned about her infant's skin tone. The baby was delivered naturally 18 days ago and is now showing signs of jaundice. Despite having normal vital signs, what could be the possible reason for the baby's prolonged jaundice?

      Your Answer:

      Correct Answer: Congenital hypothyroidism

      Explanation:

      The age of the baby is an important factor in determining the possible causes of neonatal jaundice. Congenital hypothyroidism may be responsible for prolonged jaundice in newborns. The following is a summary of the potential causes of jaundice based on the age at which it appears:

      Jaundice within 24 hours of birth may be caused by haemolytic disease of the newborn, infections, or G6PD deficiency.

      Jaundice appearing between 24-72 hours may be due to physiological factors, sepsis, or polycythaemia.

      Jaundice appearing after 72 hours may be caused by extrahepatic biliary atresia, sepsis, or other factors.

      Understanding Congenital Hypothyroidism

      Congenital hypothyroidism is a condition that affects approximately 1 in 4000 newborns. If left undiagnosed and untreated within the first four weeks of life, it can lead to irreversible cognitive impairment. Some of the common features of this condition include prolonged neonatal jaundice, delayed mental and physical milestones, short stature, a puffy face, macroglossia, and hypotonia.

      To ensure early detection and treatment, children are screened for congenital hypothyroidism at 5-7 days of age using the heel prick test. This test involves taking a small sample of blood from the baby’s heel and analyzing it for thyroid hormone levels. If the results indicate low levels of thyroid hormone, the baby will be referred for further testing and treatment.

      It is important for parents and healthcare providers to be aware of the signs and symptoms of congenital hypothyroidism and to ensure that newborns receive timely screening and treatment to prevent long-term complications. With early detection and appropriate management, children with congenital hypothyroidism can lead healthy and fulfilling lives.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 12 - A 20-year-old woman arrives at the emergency department complaining of abdominal pain, nausea,...

    Incorrect

    • A 20-year-old woman arrives at the emergency department complaining of abdominal pain, nausea, and vomiting. She reports having a cough and fever for the past few days. Upon examination, she has dry mucous membranes and her breath has a fruity odor. Her vital signs are as follows: blood pressure 95/55 mmHg, heart rate 120/min, respiratory rate 29/min, temperature 37.8ºC (100ºF), and oxygen saturation 98% on room air. Laboratory results show:

      - Sodium (Na+): 124 mmol/L (135 - 145)
      - Potassium (K+): 5.5 mmol/L (3.5 - 5.0)
      - Bicarbonate: 13 mmol/L (22 - 29)
      - Serum glucose: 30 mmol/L (4 - 7.8)
      - pH: 7.15 (7.35 - 7.45)
      - Serum ketones: 3.5 mmol/L (0 - 0.6)

      What is the most likely cause of the increased ketones in this patient?

      Your Answer:

      Correct Answer: Lipolysis

      Explanation:

      DKA is a condition that arises due to uncontrolled lipolysis, leading to an excess of free fatty acids that are converted to ketone bodies. This life-threatening complication of diabetes is characterized by elevated levels of blood glucose, ketones, and acidosis, with symptoms such as nausea, vomiting, abdominal pain, dehydration, and fruity breath odor. DKA is commonly observed in type 1 diabetes mellitus and can be triggered by non-compliance with treatment or an infection. Insulin deficiency and increased levels of counterregulatory hormones cause lipolysis in adipose tissue, leading to the release of free fatty acids that undergo hepatic oxidation to form ketone bodies. In DKA, increased gluconeogenesis and glycogenolysis occur due to insulin deficiency and counterregulatory hormones, leading to the synthesis of glucose from non-carbohydrate precursors and breakdown of glycogen, respectively. Glycolysis is not involved in DKA as it does not lead to the breakdown of fatty acids.

      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 13 - A 43-year-old woman with a history of severe ulcerative colitis (UC) presents to...

    Incorrect

    • A 43-year-old woman with a history of severe ulcerative colitis (UC) presents to the emergency department with her fourth acute flare in the past 6 months. She has a past medical history of recreational drug use and depression. The patient is given IV hydrocortisone and appears to be responding well. She is discharged after a day of observation with a 7-day course of prednisolone, but the consultant is considering long-term steroid therapy due to the severity of her condition. Which of the following is associated with long-term steroid use?

      Your Answer:

      Correct Answer: Increased risk of mania

      Explanation:

      Long-term use of steroids can lead to a higher risk of psychiatric disorders such as depression, mania, psychosis, and insomnia. This risk is even greater if the patient has a history of recreational drug use or mental disorders. While proximal myopathy is a known adverse effect of long-term steroid use, distal myopathy is not commonly observed. However, some studies have reported it as a rare and uncommon adverse effect. Steroids are also known to increase appetite, leading to weight gain, making the last two options incorrect.

      Corticosteroids are commonly prescribed medications that can be taken orally or intravenously, or applied topically. They mimic the effects of natural steroids in the body and can be used to replace or supplement them. However, the use of corticosteroids is limited by their numerous side effects, which are more common with prolonged and systemic use. These side effects can affect various systems in the body, including the endocrine, musculoskeletal, gastrointestinal, ophthalmic, and psychiatric systems. Some of the most common side effects include impaired glucose regulation, weight gain, osteoporosis, and increased susceptibility to infections. Patients on long-term corticosteroids should have their doses adjusted during intercurrent illness, and the medication should not be abruptly withdrawn to avoid an Addisonian crisis. Gradual withdrawal is recommended for patients who have received high doses or prolonged treatment.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 14 - Which hormonal agent will enhance the secretion of water and electrolytes in pancreatic...

    Incorrect

    • Which hormonal agent will enhance the secretion of water and electrolytes in pancreatic juice?

      Your Answer:

      Correct Answer: Secretin

      Explanation:

      The secretion of water and electrolytes is stimulated by secretin, while cholecystokinin stimulates the secretion of enzymes. Secretin generally leads to an increase in the volume of electrolytes and water in secretions, whereas cholecystokinin increases the enzyme content. Secretion volume is reduced by somatostatin, while aldosterone tends to preserve electrolytes.

      Pancreatic Secretions and their Regulation

      Pancreatic secretions are composed of enzymes and aqueous substances, with a pH of 8 and a volume of 1000-1500ml per day. The acinar cells secrete enzymes such as trypsinogen, procarboxylase, amylase, and elastase, while the ductal and centroacinar cells secrete sodium, bicarbonate, water, potassium, and chloride. The regulation of pancreatic secretions is mainly stimulated by CCK and ACh, which are released in response to digested material in the small bowel. Secretin, released by the S cells of the duodenum, also stimulates ductal cells and increases bicarbonate secretion.

      Trypsinogen is converted to active trypsin in the duodenum via enterokinase, and trypsin then activates the other inactive enzymes. The cephalic and gastric phases have less of an impact on regulating pancreatic secretions. Understanding the composition and regulation of pancreatic secretions is important in the diagnosis and treatment of pancreatic disorders.

    • This question is part of the following fields:

      • Endocrine System
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  • Question 15 - Which one of the following does not trigger insulin secretion? ...

    Incorrect

    • Which one of the following does not trigger insulin secretion?

      Your Answer:

      Correct Answer: Atenolol

      Explanation:

      The release of insulin is prevented by beta blockers.

      Factors that trigger insulin release include glucose, amino acids, vagal cholinergic stimulation, secretin/gastrin/CCK, fatty acids, and beta adrenergic drugs.

      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.

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  • Question 16 - A young man presents with polyuria, polydipsia and weight loss. He is subsequently...

    Incorrect

    • A young man presents with polyuria, polydipsia and weight loss. He is subsequently diagnosed with type 1 diabetes mellitus. What is he at an increased risk of developing?

      Your Answer:

      Correct Answer: Addison's disease, Grave's disease, coeliac disease

      Explanation:

      Type 1 diabetes is linked to other autoimmune disorders like Addison’s disease, Grave’s disease, and coeliac disease, due to its own autoimmune nature. The other choices are incorrect as they contain a non-autoimmune disorder.

      Understanding Diabetes Mellitus: A Basic Overview

      Diabetes mellitus is a chronic condition characterized by abnormally raised levels of blood glucose. It is one of the most common conditions encountered in clinical practice and represents a significant burden on the health systems of the developed world. The management of diabetes mellitus is crucial as untreated type 1 diabetes would usually result in death. Poorly treated type 1 diabetes mellitus can still result in significant morbidity and mortality. The main focus of diabetes management now is reducing the incidence of macrovascular and microvascular complications.

      There are different types of diabetes mellitus, including type 1 diabetes mellitus, type 2 diabetes mellitus, prediabetes, gestational diabetes, maturity onset diabetes of the young, latent autoimmune diabetes of adults, and other types. The presentation of diabetes mellitus depends on the type, with type 1 diabetes mellitus often presenting with weight loss, polydipsia, polyuria, and diabetic ketoacidosis. On the other hand, type 2 diabetes mellitus is often picked up incidentally on routine blood tests and presents with polydipsia and polyuria.

      There are four main ways to check blood glucose, including a finger-prick bedside glucose monitor, a one-off blood glucose, a HbA1c, and a glucose tolerance test. The diagnostic criteria are determined by WHO, with a fasting glucose greater than or equal to 7.0 mmol/l and random glucose greater than or equal to 11.1 mmol/l being diagnostic of diabetes mellitus. Management of diabetes mellitus involves drug therapy to normalize blood glucose levels, monitoring for and treating any complications related to diabetes, and modifying any other risk factors for other conditions such as cardiovascular disease. The first-line drug for the vast majority of patients with type 2 diabetes mellitus is metformin, with second-line drugs including sulfonylureas, gliptins, and pioglitazone. Insulin is used if oral medication is not controlling the blood glucose to a sufficient degree.

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  • Question 17 - 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:

      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.

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  • Question 18 - A man in his early 50s comes to the hospital with a fever...

    Incorrect

    • A man in his early 50s comes to the hospital with a fever and cough. An X-ray shows pneumonia in his left lower lobe. Upon arrival at the emergency department, his blood pressure is 83/60mmHg and his heart rate is 112/min. The doctor prescribes antibiotics and IV fluids.

      What is the primary way the body reacts to a drop in blood pressure?

      Your Answer:

      Correct Answer: Insertion of AQP-2 channels in collecting ducts

      Explanation:

      When blood pressure drops, the body initiates several physiological responses, one of which is the activation of the renin-angiotensin aldosterone system (RAAS). This system breaks down bradykinin, a potent vasodilator, through the action of angiotensin-converting enzyme (ACE).

      RAAS activation results in increased aldosterone levels, which in turn increases the number of epithelial sodium channels (ENAC) to enhance sodium reabsorption.

      Another response to low blood pressure is the release of antidiuretic hormone, which promotes the insertion of aquaporin-2 channels in the collecting duct. This mechanism increases water reabsorption to help maintain fluid balance in the body.

      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.

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  • Question 19 - As a medical student observing a metabolic medicine clinic, a 40-year-old woman comes...

    Incorrect

    • As a medical student observing a metabolic medicine clinic, a 40-year-old woman comes in seeking answers about her obesity. With a BMI of 46 kg/m² and a family history of obesity, she is referred for further investigation. After genetic sequencing, it is discovered that she has a mutation in a hormone-regulating gene that is secreted by adipose tissue.

      Which hormone is likely impacted by this genetic mutation?

      Your Answer:

      Correct Answer: Leptin

      Explanation:

      Leptin is produced by adipose tissue and is responsible for regulating feelings of fullness and satiety. Mutations in the leptin gene can lead to severe obesity in infants due to increased appetite and reduced feelings of satiety. Ghrelin, on the other hand, is a hormone released by the stomach that stimulates hunger. Melatonin, produced by the pineal gland, regulates the sleep-wake cycle and circadian rhythms but is not known to play a significant role in obesity. Obestatin, released by stomach epithelial cells, has a controversial role in obesity.

      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.

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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:

      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.

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      • Endocrine System
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