What is the primary treatment for chronic myeloid leukemia (CML)?A) Imatinib B ) Chemotherapy C) Radiation therapy D) Bone marrow transplant The primary treatment for chronic myeloid leukemia (CML) is: A) Imatinib Explanation: Imatinib is a type of tyrosine kinase inhibitor (TKI) that specifically targets the BCR-ABL protein, which is produced by the Philadelphia chromosome in CML cells. This protein is responsible for the uncontrolled growth of leukemic cells. Imatinib was the first TKI approved for the treatment of CML and has dramatically improved the prognosis of patients with this condition, turning what was once a fatal disease into a manageable chronic condition for many. Other options explained: B) Chemotherapy: Traditional chemotherapy is less effective for CML compared to TKIs and is generally not the first-line treatment. Chemotherapy may be used in certain cases, such as in blast crisis or if TKIs are not effective. C) Radiation therapy: Radiation therapy is not a standard treatment for CML. It may be used in specific situations, such as to shrink an enlarged spleen or to prepare for a bone marrow transplant, but it is not the primary treatment. D) Bone marrow transplant: Bone marrow or stem cell transplant can be a curative treatment for CML, but it is usually reserved for patients who do not respond to TKIs or those in the advanced stages of the disease due to the associated risks and complications. Imatinib remains the cornerstone of treatment for CML in the chronic phase, with other TKIs like dasatinib and nilotinib also available as alternatives or in cases of imatinib resistance.
Which vitamin deficiency is associated with rickets? A) Vitamin A B ) Vitamin B12 C) Vitamin C D) Vitamin D The vitamin deficiency associated with rickets is: D) Vitamin D Explanation: Rickets is a condition that affects bone development in children, leading to soft and weak bones, which can cause bone deformities. The primary cause of rickets is a deficiency in Vitamin D. Vitamin D is essential for maintaining proper levels of calcium and phosphate in the body, which are critical for healthy bone formation. When there is a lack of Vitamin D, the body cannot properly absorb calcium and phosphate, leading to the symptoms seen in rickets, such as bowed legs, thickened wrists and ankles, and in severe cases, skeletal deformities. None of the other vitamins listed (A, B12, C) are directly associated with the development of rickets.
What is the most common type of stroke? A) Ischemic stroke B ) Hemorrhagic stroke C) Lacunar stroke D) Embolic stroke The most common type of stroke is A) Ischemic stroke. Explanation: Ischemic strokes account for approximately 85% of all strokes. This type of stroke occurs when a blood clot or other obstruction blocks blood flow to a part of the brain, depriving brain tissue of necessary oxygen and nutrients. Without the blood supply, brain cells begin to die, leading to neurological deficits depending on the area of the brain affected. Hemorrhagic stroke (B): Occurs when a blood vessel in the brain ruptures, causing bleeding in or around the brain. This type of stroke is less common, accounting for about 15% of all strokes but tends to be more severe and associated with a higher risk of death. Lacunar stroke (C): A subtype of ischemic stroke that occurs when a small artery within the brain becomes blocked. Lacunar strokes represent a smaller portion of ischemic strokes and typically occur in the deeper parts of the brain. Embolic stroke (D): A type of ischemic stroke that occurs when an embolus, usually a blood clot that forms elsewhere in the body, travels to the brain and causes a blockage. It is one of the causes of ischemic stroke but not the most common type overall.
Which of the following is the most common cause of acute pancreatitis? A. Gallstones B. Alcohol C. Hypertriglyceridemia D. Medications The most common cause of acute pancreatitis is A. Gallstones. Gallstones are the most common cause of acute pancreatitis, accounting for approximately 40-70% of cases. Gallstones can obstruct the bile duct, which also shares a passage with the pancreatic duct. When these stones block the flow of bile and pancreatic enzymes, it can cause the enzymes to become activated while still in the pancreas, leading to inflammation and damage to the pancreatic tissue, resulting in acute pancreatitis. Here’s a brief overview of the other options: B. Alcohol: Alcohol is the second most common cause, responsible for about 25-35% of cases. Chronic alcohol consumption can lead to inflammation of the pancreas over time, but acute pancreatitis typically arises after years of heavy drinking. C. Hypertriglyceridemia: This condition can cause acute pancreatitis when triglyceride levels are extremely high (usually above 1000 mg/dL), but it is less common than gallstones and alcohol, accounting for about 1-4% of cases. D. Medications: Certain medications can induce acute pancreatitis, but this is a rare cause, contributing to less than 2% of cases. In summary, gallstones are the leading cause of acute pancreatitis, particularly because they can cause direct physical obstruction of the pancreatic duct.
Which of the following is a hallmark sign of pericarditis? A. Pulsus paradoxus B. Kussmaul's sign C. Pericardial friction rub D. Water bottle heart The hallmark sign of pericarditis is C. Pericardial friction rub. Explanation: Pericardial friction rub is the most characteristic physical finding in pericarditis. It is caused by the rubbing of the inflamed pericardial layers against each other and is best heard with the patient sitting up and leaning forward, using the diaphragm of the stethoscope at the left lower sternal border. The rub is often described as a scratching, grating, or squeaking sound and may have up to three components corresponding to atrial systole, ventricular systole, and ventricular diastole. Other options: A. Pulsus paradoxus: This is a drop in systolic blood pressure of more than 10 mm Hg during inspiration. It is more commonly associated with cardiac tamponade, although it can sometimes be seen in severe cases of pericarditis. B. Kussmaul's sign: This is an increase in jugular venous pressure on inspiration and is more typical of constrictive pericarditis or right heart failure. D. Water bottle heart: This refers to the appearance of an enlarged, rounded heart shadow on a chest X-ray, typically due to a large pericardial effusion rather than pericarditis itself.
Which of the following is the most common cause of end-stage renal disease (ESRD)? A. Hypertension B. Diabetes mellitus C. Glomerulonephritis D. Polycystic kidney disease The most common cause of end-stage renal disease (ESRD) is B. Diabetes mellitus. Explanation: Diabetes mellitus is the leading cause of ESRD worldwide. High blood sugar levels over time can damage the blood vessels in the kidneys, leading to diabetic nephropathy. This condition progressively impairs kidney function and can eventually lead to ESRD, where the kidneys can no longer effectively filter waste and excess fluids from the blood. Other options: A. Hypertension: Hypertension is the second most common cause of ESRD. It damages the kidneys' blood vessels, reducing their ability to function properly. C. Glomerulonephritis: This condition is a less common cause of ESRD and involves inflammation of the kidney's filtering units (glomeruli). D. Polycystic kidney disease: While it is a significant cause of ESRD, it is less common than diabetes mellitus and hypertension. This genetic disorder leads to the development of cysts in the kidneys, progressively impairing their function.
Which imaging modality is the gold standard for diagnosing pulmonary embolism? A. Chest X-ray B. Ventilation-perfusion (V/Q) scan C. CT pulmonary angiography D. MRI The gold standard imaging modality for diagnosing pulmonary embolism is C. CT pulmonary angiography. Explanation: CT pulmonary angiography (CTPA) is the preferred and most accurate imaging technique for diagnosing pulmonary embolism (PE). It provides detailed images of the pulmonary arteries and can directly visualize the clot within the vessels. CTPA is highly sensitive and specific, making it the gold standard for PE diagnosis. Other options: A. Chest X-ray: A chest X-ray is often performed as an initial imaging study to rule out other conditions, but it is not specific for diagnosing PE. Chest X-rays are generally normal in patients with PE or may show non-specific findings. B. Ventilation-perfusion (V/Q) scan: A V/Q scan can be used to assess for PE, particularly in patients who cannot undergo CTPA due to contrast allergies or renal insufficiency. However, it is less specific than CTPA and is not the gold standard. D. MRI: MRI is not commonly used for diagnosing PE due to lower availability, higher cost, and longer scan times compared to CTPA. It is also less sensitive for detecting PE.
Which of the following is the most common presenting symptom of Hodgkin lymphoma? A. Night sweats B. Weight loss C. Painless lymphadenopathy D. Fever The most common presenting symptom of Hodgkin lymphoma is C. Painless lymphadenopathy. Explanation: Painless lymphadenopathy, particularly in the cervical, supraclavicular, or mediastinal regions, is the hallmark and most common initial symptom of Hodgkin lymphoma. Patients typically notice swollen, non-tender lymph nodes that gradually enlarge. Other symptoms, known as "B symptoms," include: A. Night sweats: These can occur in Hodgkin lymphoma but are not as common as the initial symptom. B. Weight loss: Unexplained weight loss is another B symptom and can be seen, but again, it is less common as a presenting symptom. D. Fever: Intermittent fever, often referred to as "Pel-Ebstein fever," is a classic symptom but is not the most common initial symptom. The presence of these B symptoms (night sweats, weight loss, and fever) can indicate more advanced disease and may have prognostic implications. However, painless lymphadenopathy remains the most common and usually the first symptom noticed in Hodgkin lymphoma.
Which of the following is a risk factor for developing hepatocellular carcinoma? A. Chronic hepatitis B B. Chronic hepatitis C C. Cirrhosis D. All of the above The correct answer is D. All of the above. Explanation: Hepatocellular carcinoma (HCC) is a primary malignancy of the liver, and several risk factors are strongly associated with its development: Chronic hepatitis B (HBV): Chronic infection with hepatitis B virus is a significant risk factor for HCC. The virus can integrate into the host's genome, leading to genetic mutations that promote cancer development. HBV-related HCC can occur even in the absence of cirrhosis. Chronic hepatitis C (HCV): Chronic infection with hepatitis C virus also increases the risk of developing HCC, particularly in individuals who progress to cirrhosis. The virus causes chronic inflammation, leading to liver damage and eventual carcinogenesis. Cirrhosis: Cirrhosis, regardless of its underlying cause, is one of the most important risk factors for HCC. Cirrhosis leads to continuous liver cell injury and regeneration, which increases the likelihood of genetic mutations and malignant transformation of hepatocytes. Given that all the listed factors (chronic hepatitis B, chronic hepatitis C, and cirrhosis) are well-established risk factors for hepatocellular carcinoma, the correct answer is D. All of the above.
Which test is most specific for diagnosing rheumatoid arthritis? A. Rheumatoid factor (RF) B. Anti-citrullinated protein antibody (ACPA) C. Erythrocyte sedimentation rate (ESR) D. C-reactive protein (CRP) The most specific test for diagnosing rheumatoid arthritis (RA) is: B. Anti-citrullinated protein antibody (ACPA) Explanation: Anti-citrullinated protein antibody (ACPA) is highly specific for rheumatoid arthritis, with specificity often reported above 90%. ACPAs are autoantibodies that target proteins in the body that have undergone a process called citrullination, which is associated with the pathogenesis of RA. The presence of ACPA is strongly associated with RA and is considered a key marker in the diagnosis of this disease, especially in early stages. Rheumatoid factor (RF) is another common marker used in diagnosing RA, but it is less specific than ACPA. RF can be positive in a variety of other conditions, such as other autoimmune diseases, chronic infections, and even in a small percentage of healthy individuals. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are nonspecific markers of inflammation. While they may be elevated in RA, they are not specific to the disease and can be elevated in a wide range of inflammatory conditions. Therefore, ACPA is the most specific test for diagnosing rheumatoid arthritis.
Which of the following is a common side effect of corticosteroid therapy? A. Hypoglycemia B. Osteoporosis C. Hyperkalemia D. Bradycardia The correct answer is B. Osteoporosis. Explanation: Corticosteroids are a class of drugs commonly used to reduce inflammation in conditions such as asthma, rheumatoid arthritis, and autoimmune diseases. While they are effective, they come with a range of potential side effects, especially when used long-term. A. Hypoglycemia: Corticosteroids actually tend to raise blood sugar levels, leading to hyperglycemia, not hypoglycemia. Therefore, hypoglycemia is not a common side effect. B. Osteoporosis: This is a well-known side effect of long-term corticosteroid therapy. Corticosteroids can decrease bone formation, increase bone resorption, and reduce calcium absorption, all of which can lead to weakened bones and an increased risk of fractures. C. Hyperkalemia: Corticosteroids generally cause hypokalemia (low potassium levels), not hyperkalemia, by promoting potassium excretion in the kidneys. D. Bradycardia: Corticosteroids do not typically cause bradycardia. In fact, they may cause tachycardia (increased heart rate) due to fluid retention and hypertension. Therefore, osteoporosis is the most common and concerning side effect associated with long-term corticosteroid therapy.
What is the most common cause of secondary hypertension? A. Renal artery stenosis B. Cushing's syndrome C. Pheochromocytoma D. Hyperaldosteronism D. hyperaldosteronism (often referred to as Conn's syndrome) is the most common cause of secondary hypertension. Hyperaldosteronism: Primary hyperaldosteronism occurs when the adrenal glands produce too much aldosterone, a hormone that increases sodium retention and potassium excretion. This sodium retention leads to an increase in blood volume and, consequently, blood pressure. It is often caused by an adrenal adenoma (a benign tumor of the adrenal gland) or adrenal hyperplasia. Patients typically present with resistant hypertension, hypokalemia (low potassium levels), and metabolic alkalosis. Why Not the Other Options? Renal artery stenosis (A) can cause secondary hypertension due to reduced blood flow to the kidneys, prompting the kidneys to release more renin and thereby increase blood pressure. However, it's less common than hyperaldosteronism. Cushing's syndrome (B) results from excess cortisol production, which can also lead to secondary hypertension, but it is less frequent. Pheochromocytoma (C) is a rare tumor of the adrenal medulla that secretes catecholamines (adrenaline and noradrenaline), leading to episodic hypertension. It is a rare cause of secondary hypertension. Summary: Hyperaldosteronism is the most frequent cause of secondary hypertension due to its direct effect on sodium retention and blood pressure elevation, making it the most common among the listed options.
Which of the following is used to reverse the effects of warfarin? A. Vitamin K B. Protamine sulfate C. Fresh frozen plasma D. Activated charcoal The correct answer is: A. Vitamin K Explanation: Warfarin is an anticoagulant that works by inhibiting the synthesis of vitamin K-dependent clotting factors (II, VII, IX, and X) in the liver. When the anticoagulant effects of warfarin need to be reversed, especially in the case of bleeding or an upcoming surgical procedure, vitamin K is the primary treatment option. Vitamin K: Vitamin K acts by promoting the synthesis of these clotting factors, effectively reversing the anticoagulant effect of warfarin. Administering vitamin K can restore normal clotting, although it may take several hours for the full reversal effect, depending on the dose and the route of administration (oral or intravenous). Why Not the Other Options? Protamine sulfate (B) is used to reverse the effects of heparin, not warfarin. It works by binding to heparin and neutralizing its anticoagulant activity. Fresh frozen plasma (C) contains all the clotting factors, including the vitamin K-dependent ones, and can be used to reverse warfarin’s effects in cases of major bleeding. However, it's typically used in more severe cases or when rapid reversal is needed because it works faster than vitamin K alone. Activated charcoal (D) is used to absorb certain toxins in cases of overdose if administered soon after ingestion, but it is not effective in reversing the effects of warfarin. Summary: Vitamin K is the standard treatment for reversing the anticoagulant effects of warfarin, as it directly counteracts the mechanism by which warfarin inhibits clotting factor production. Fresh frozen plasma can also be used in more urgent situations, but vitamin K remains the primary reversal agent.
Which of the following is the primary cause of Addison's disease? A. Pituitary adenoma B. Adrenal hemorrhage C. Autoimmune destruction of adrenal cortex D. Tuberculosis The correct answer is: C. Autoimmune destruction of adrenal cortex Explanation: Addison's disease, also known as primary adrenal insufficiency, occurs when the adrenal glands do not produce enough of certain hormones, specifically cortisol and aldosterone. The primary cause of Addison's disease is the autoimmune destruction of the adrenal cortex. Autoimmune Destruction of Adrenal Cortex: Autoimmune destruction accounts for about 70-90% of all cases of Addison's disease in developed countries. In this condition, the body's immune system mistakenly attacks and destroys the adrenal cortex, which is the outer layer of the adrenal glands responsible for producing cortisol, aldosterone, and androgens. The destruction leads to a deficiency in the production of these hormones, which are critical for various body functions, including metabolism, immune response, blood pressure regulation, and electrolyte balance. Why Not the Other Options? Pituitary adenoma (A) is associated with secondary adrenal insufficiency, not Addison's disease. In secondary adrenal insufficiency, the issue is with the pituitary gland failing to produce enough adrenocorticotropic hormone (ACTH), which stimulates the adrenal glands. It does not cause Addison's disease directly because the problem in Addison's disease is at the level of the adrenal glands themselves. Adrenal hemorrhage (B) can cause Addison's disease if there is significant bleeding into the adrenal glands, leading to destruction. However, it is a less common cause than autoimmune destruction. It is often associated with conditions such as Waterhouse-Friderichsen syndrome (seen in severe bacterial infections) but is not the primary cause. Tuberculosis (D) was historically a common cause of Addison's disease and still is in developing countries. Tuberculosis can infect the adrenal glands and lead to their gradual destruction. However, in developed countries, the autoimmune cause is now more common. Summary: The primary cause of Addison's disease is the autoimmune destruction of the adrenal cortex, leading to a lack of essential hormones produced by the adrenal glands. Other causes like adrenal hemorrhage or tuberculosis are less common in developed countries today.
Which of the following bacteria is most commonly associated with peptic ulcers? A. Helicobacter pylori B. Escherichia coli C. Streptococcus pyogenes D. Staphylococcus aureus Answer: A. Helicobacter pylori Explanation: Helicobacter pylori (H. pylori) is the bacterium most commonly associated with peptic ulcers. This bacterium is a spiral-shaped, gram-negative microorganism that can survive in the acidic environment of the stomach. It is known to colonize the gastric mucosa and is a major cause of both gastric and duodenal ulcers. How H. pylori causes peptic ulcers: Colonization and Mucosal Damage: H. pylori can adhere to the epithelial lining of the stomach and the upper part of the small intestine (duodenum). Production of Urease: The bacterium produces an enzyme called urease, which breaks down urea in the stomach into ammonia, creating a more alkaline environment around the bacteria and protecting it from stomach acid. Induction of Inflammation: H. pylori induces an inflammatory response, which damages the gastric or duodenal mucosa. The inflammation and damage can lead to the formation of ulcers. Disruption of Protective Mucus Layer: The bacteria also contribute to the breakdown of the stomach's mucus layer, which normally protects the lining from the acidic gastric juices. When this protective barrier is compromised, acid can further damage the stomach lining, leading to ulcer formation. Other Options: B. Escherichia coli (E. coli): Commonly found in the intestines, E. coli is primarily associated with foodborne illnesses and urinary tract infections, not peptic ulcers. C. Streptococcus pyogenes: This bacterium is known for causing strep throat, skin infections, and invasive diseases like necrotizing fasciitis but is not associated with peptic ulcers. D. Staphylococcus aureus: Typically associated with skin infections, respiratory infections, and sometimes food poisoning, Staphylococcus aureus is not known to cause peptic ulcers. Thus, Helicobacter pylori (A) is the correct answer as it is the most common bacterial cause of peptic ulcers.
Which of the following is the most common cause of bacterial meningitis in adults? A. Streptococcus pneumoniae B. Neisseria meningitidis C. Haemophilus influenzae D. Listeria monocytogenes A. Streptococcus pneumoniae Explanation: Streptococcus pneumoniae is the most common cause of bacterial meningitis in adults. This bacterium, also known as the pneumococcus, is a gram-positive, encapsulated organism that is a leading cause of bacterial meningitis in adults, particularly in developed countries. It can cause severe illness and is associated with a high mortality rate, especially in older adults, individuals with chronic health conditions, and those with compromised immune systems. Why Streptococcus pneumoniae is the most common cause: Frequency and Carriage: S. pneumoniae is a common inhabitant of the upper respiratory tract and can colonize the nasopharynx asymptomatically. It becomes pathogenic when it spreads to other parts of the body, such as the meninges. Predisposing Factors: The risk of pneumococcal meningitis increases in people with certain risk factors, including alcoholism, splenectomy, diabetes, and chronic respiratory or heart disease. Pathogenic Mechanisms: S. pneumoniae can cross the blood-brain barrier, leading to inflammation and infection of the meninges. Its capsule, a major virulence factor, protects it from phagocytosis by the host's immune cells. Other Options: B. Neisseria meningitidis: While N. meningitidis (meningococcus) is a significant cause of bacterial meningitis, it is more commonly associated with outbreaks among young adults, particularly in settings like college dormitories or military barracks. It is the second most common cause of bacterial meningitis in adults. C. Haemophilus influenzae: H. influenzae type b (Hib) used to be a common cause of bacterial meningitis in children before the introduction of the Hib vaccine. With widespread vaccination, the incidence of H. influenzae meningitis has significantly declined, making it a less common cause in adults. D. Listeria monocytogenes: L. monocytogenes can cause meningitis, particularly in neonates, pregnant women, elderly individuals, and immunocompromised patients. However, it is not the most common cause in the general adult population. In summary, Streptococcus pneumoniae is the most common cause of bacterial meningitis in adults due to its prevalence in the nasopharynx and its ability to invade the meninges, particularly in individuals with underlying risk factors.
Which of the following is the most common cause of Cushing's syndrome? A. Adrenal adenoma B. Pituitary adenoma C. Exogenous corticosteroids D. Ectopic ACTH production The primary cause of Cushing's syndrome is: C. Exogenous corticosteroids Explanation: Cushing's syndrome is a condition characterized by prolonged exposure to high levels of cortisol. It can be caused by several factors: Exogenous corticosteroids (Option C): This is the most common cause of Cushing's syndrome. It occurs when patients take corticosteroid medications (such as prednisone) in high doses for extended periods. These medications can mimic the effects of cortisol, leading to symptoms of Cushing's syndrome. Pituitary adenoma (Option B): Also known as Cushing's disease, this is the most common endogenous cause of Cushing's syndrome. A pituitary adenoma is a benign tumor of the pituitary gland that secretes excess adrenocorticotropic hormone (ACTH), which in turn stimulates the adrenal glands to produce more cortisol. Adrenal adenoma (Option A): This is a less common cause of Cushing's syndrome. It involves a benign tumor of the adrenal gland that directly produces excess cortisol without being stimulated by ACTH. Ectopic ACTH production (Option D): This occurs when non-pituitary tumors (often small cell lung cancer or carcinoid tumors) produce ACTH, leading to increased cortisol production by the adrenal glands. It is a less common cause of Cushing's syndrome compared to exogenous corticosteroids and pituitary adenomas. In summary, while there are several causes of Cushing's syndrome, exogenous corticosteroids (Option C) are the primary and most common cause.
Which of the following is the most common cause of jaundice in newborns? A. Breast milk jaundice B. Physiological jaundice C. Hemolytic disease of the newborn D. Biliary atresia The most common cause of jaundice in newborns is: B. Physiological jaundice Explanation: Physiological jaundice is the most common cause of jaundice in newborns. It is a normal condition that occurs in most newborns due to the immaturity of the liver and its ability to process bilirubin. Here's a breakdown of why this is the case and how it compares to the other options: Physiological Jaundice (Option B): Occurs in the majority of newborns, typically appearing between 2 to 4 days after birth and peaking around the 4th or 5th day. It is caused by the breakdown of fetal red blood cells and the immature liver's inability to process the resulting bilirubin efficiently. This type of jaundice is usually harmless and resolves on its own as the baby's liver matures, typically within 1 to 2 weeks. Breast Milk Jaundice (Option A): This type of jaundice can occur in some breastfed infants, usually after the first week of life and can last for several weeks. It is thought to be related to substances in the breast milk that inhibit the metabolism of bilirubin. While relatively common, breast milk jaundice is not as common as physiological jaundice and is generally mild. Hemolytic Disease of the Newborn (Option C): This condition is caused by blood group incompatibility between the mother and baby (such as Rh incompatibility or ABO incompatibility), leading to the destruction of the newborn's red blood cells. It can cause severe jaundice soon after birth but is less common than physiological jaundice. Biliary Atresia (Option D): A rare condition in which the bile ducts inside or outside the liver are blocked or absent, leading to a buildup of bilirubin. This is a serious condition requiring surgical intervention and is not a common cause of jaundice compared to physiological jaundice. In summary, physiological jaundice (Option B) is the most common cause of jaundice in newborns due to the natural immaturity of the liver and increased red blood cell turnover after birth.
What is the primary treatment for acute gout attack? A. Allopurinol B. Colchicine C. Probenecid D. Febuxostat The primary treatment for an acute gout attack is: B. Colchicine Explanation: An acute gout attack is characterized by sudden onset of intense pain, swelling, and redness in a joint, most commonly the big toe. The goal of treatment during an acute gout attack is to reduce inflammation and relieve pain. Here is why colchicine is the correct choice among the options listed: Colchicine (Option B): Colchicine is an anti-inflammatory medication specifically used to treat acute gout attacks. It works by reducing the inflammation caused by uric acid crystals in the joint. It is particularly effective if taken early, ideally within the first 12 to 24 hours of the onset of symptoms. It is often used when NSAIDs (non-steroidal anti-inflammatory drugs) are contraindicated or not tolerated. Allopurinol (Option A): Allopurinol is not used for treating acute gout attacks; it is a urate-lowering therapy used to prevent future attacks. It works by reducing the production of uric acid in the body. Starting or adjusting the dose of allopurinol during an acute attack can actually worsen the attack. Probenecid (Option C): Probenecid is another urate-lowering therapy used for the prevention of gout attacks by increasing the excretion of uric acid in the urine. It is not used to treat an acute attack. Like allopurinol, it is used for long-term management to prevent future episodes, not for acute management. Febuxostat (Option D): Febuxostat is similar to allopurinol as it is a xanthine oxidase inhibitor that lowers uric acid levels in the body, used to prevent gout attacks. It is also not effective for treating an acute attack and should not be started or altered during an acute flare. Conclusion: During an acute gout attack, the primary treatment is to reduce inflammation and pain. Colchicine (Option B) is one of the primary treatments, along with NSAIDs or corticosteroids, and is specifically used to manage the symptoms of an acute attack. Other medications like allopurinol, probenecid, and febuxostat are used for the long-term management of gout to prevent future attacks, not for acute treatment.
Which of the following is the primary cause of acromegaly? A. Adrenal adenoma B. Pituitary adenoma C. Thyroid adenoma D. Pancreatic adenoma The primary cause of acromegaly is: B. Pituitary adenoma Explanation: Acromegaly is a hormonal disorder that results from the excess production of growth hormone (GH) in adults. This condition is most commonly caused by a benign tumor (adenoma) of the pituitary gland. Pituitary adenoma (Option B): The pituitary gland, located at the base of the brain, produces several hormones, including growth hormone (GH). In acromegaly, a pituitary adenoma (a noncancerous tumor of the pituitary gland) secretes excess growth hormone. This excess GH leads to increased levels of insulin-like growth factor 1 (IGF-1), which causes the characteristic symptoms of acromegaly, such as enlarged hands, feet, and facial features. Pituitary adenomas are the most common cause of acromegaly, accounting for over 95% of cases. The condition typically develops gradually over several years, making early diagnosis challenging. Adrenal adenoma (Option A): An adrenal adenoma is a benign tumor of the adrenal glands that may produce hormones like cortisol, aldosterone, or androgens. While adrenal adenomas can cause conditions like Cushing's syndrome or primary hyperaldosteronism, they are not associated with the overproduction of growth hormone or acromegaly. Thyroid adenoma (Option C): A thyroid adenoma is a benign tumor of the thyroid gland that can cause hyperthyroidism. However, it does not produce growth hormone and is not related to the development of acromegaly. Pancreatic adenoma (Option D): A pancreatic adenoma is a benign tumor of the pancreas, which might involve the islet cells that produce insulin, glucagon, or other hormones. It does not affect growth hormone production or lead to acromegaly. Conclusion: The primary cause of acromegaly is a pituitary adenoma (Option B), which secretes excess growth hormone, leading to the symptoms associated with this condition. The other options involve tumors in different glands that do not produce growth hormone and are not related to acromegaly.
