Case-based MCQ

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⏳ Case-based MCQ | #Case_400 | #answer 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 ✅ A The clinical picture is consistent with superior vena cava (SVC) syndrome. SVC syndrome results from any condition that leads to obstruction of blood flow through the SVC. Obstruction can be caused by external compression of the SVC by adjacent pathologic processes involving the right lung, lymph nodes, and other mediastinal structures, or by thrombosis within the SVC. In some cases, both external compression and thrombosis coexist. Conditions that can lead to SVC syndrome can be malignant or non-malignant: ▫Malignant causes - malignant mediastinal tumors are the most common cause (>80%). Of malignant tumors bronchogenic carcinoma accounts for 75-80% of cases, with most of these being small cell carcinomas. Non-Hodgkin lymphoma is responsible for 10-15% of mediastinal malignancies resulting in SVC syndrome. Rare malignant causes include Hodgkin lymphoma, metastatic cancers, primary leiomyosarcoma of the mediastinal vessels and plasmocytomas. ▫Non-malignant causes - some of these causes are: Mediastinal fibrosis Vascular diseases, such as aortic aneurysm, vasculitis, and arteriorvenous fistulas Infections, such as histoplasmosis, tuberculosis, syphilis, and actinomycosis. Benign mediastinal tumors such as teratoma, cystic hygroma, thymoma, and dermoid cyst. Cardiac causes, such as pericarditis and atrial myxoma. Thrombosis related to the presence of central vein catheters. Early in the clinical course of SVC syndrome, partial obstruction of SVC may be asymptomatic, or the symptoms are so minor that are overlooked, but as it advances toward complete SVC obstruction, the classic symptoms and signs become more obvious: ✔ Dyspnea - the most common symptom (63% of patients) ✔ Facial swelling ✔ Head fullness ✔ Cough ✔ Arm swelling ✔ Chest pain ✔ Dysphagia ✔ Orthopnea ✔ Distorted vision ✔ Hoarseness ✔ Stridor ✔ Headache ✔ Nasal stuffiness ✔ Nausea ✔ Pleural effusion ✔ Lightheadedness The characteristic physical findings include venous distention of the neck and chest wall, facial edema, upper extremity edema, mental status changes, plethora, cyanosis, papilledema, stupor and even coma. Bending forward or lying down can aggravate the signs and symptoms. Since most cases of SVC are due to mediastinal malignancies, a chest X-ray is always the most appropriate initial investigation. Chest X-ray may reveal a widened mediastinum or a mass in the right side of the chest. One study showed that only 16% of patients with SVC syndrome had a normal chest X-ray. CT scan, MRI, and angiography (option E) can be use for more detailed evaluation, but not as initial assessment. ⚠ RAST (option D) stands for radioallergosorbent test and is a blood test for finding the allergen a patient is allergic to, and has no role in diagnosis of SVC syndrome. ⚠ ECG (option C) and echocardiography (option B) are not diagnostic for SVC

⏳ Case-based MCQ | #Case_400 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 A 67-year-old man presents to the emergency department with facial puffiness and swelling of the right arm and upper chest. He is moderately short of breath. On examination, his face, arm and upper chest are slightly cyanosed and puffy. The rest of the exam is inconclusive.

‍ ‍ ⏳ Case-based MCQ | #Case_399 | #answer 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 ✅ E With gasterectomy in history, dumping syndrome is the most likely underlying cause to this presentation. Dumping syndrome is the effect of altered gastric reservoir function, abnormal gastric motor function, and/or pyloric emptying mechanism. In term of temporal relation to eating, dumping syndrome can have early or late manifestations: ▫ Early dumping: Symptoms of early dumping syndrome occur 30-60 minutes after a meal and are believed to result from accelerated gastric emptying of hyperosmolar contents into the small bowel. This leads to fluid shift from the intravascular compartment into the bowel lumen, resulting in rapid small bowel distention and increase in the frequency of bowel contractions. Even in healthy persons without gastric surgery, rapid instillation of liquid meals into the small bowel has shown to induce dumping syndrome. Rapid shift of fluid into the intestinal lumen results in decreased circulating volume, triggering a vasomotor response presenting with tachycardia and lightheadedness. ▫Late dumping: Late dumping occurs 1-3 hours after a meal. The pathogenesis is thought to be related to the early development of hyperinsulinemic (reactive) hypoglycemia. Rapid delivery of a meal to the small intestine results in an initial high concentration of carbohydrates in the proximal small bowel and rapid absorption of glucose. This is replied by a hyperinsulinemic response. The high insulin levels stay for longer period and are responsible for the subsequent hypoglycemia. The diagram summarises the mechanism through which the dumping syndrome develops. The clinical presentation of dumping syndrome can be categorized as abdominal versus vasomotor symptoms, and based on the time of onset as early versus late. 🔺Early dumping systemic symptoms: Desire to lie down, Palpitations, Fatigue, Faintness, Syncope, Diaphoresis, Headache, Flushing 🔺 Early dumping abdominal symptoms: Epigastric fullness, Diarrhea, Nausea, Abdominal cramps, Borborygmi These symptoms can be collectively referred to as dyspepsia. 🔻Late dumping symptoms: Perspiration, Shakiness, Difficulty to concentrate, Decreased consciousness, Hunger For patients with dumping syndrome, dietary modification is the firstline management option. The following pieces of advice are appropriate: ✔ Daily energy intake is divided into 6 meals. ✔ Fluid intake during and with meals be restricted and liquids be avoided for at least half an hour after a meal. ✔ Avoiding simple sugars. ✔ Milk and milk products are generally not tolerated and should be avoided. ✔ Because carbohydrate intake is restricted, protein and fat intake should be increased to fulfill energy needs. ➕ Additional points to consider: Supplementation with dietary fiber has proven effective in the treatment of hypoglycemic episodes. Many medical therapies have been tested, including pectin, guar gum, and glucomannan. These dietary fibers form gels with carbohydrates, resulting in delayed glucose absorption and prolongation of bowel transit time. Dietary change to a low-carbohydrate, high protein diet, as well as the use of alpha-glucosidase inhibitors, may be useful to control the symptoms of dumping. This is preferential to subtotal or total pancreatectomy in those persons with severe symptoms. Most patients have relatively mild symptoms and respond well to dietary changes. In some patients with postprandial hypotension, lying supine for 30 minutes after meals may delay gastric emptying and also increase venous return, thereby minimizing the chances of syncope

‍ ⏳ Case-based MCQ | #Case_398 | #answer 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 ✅ E With gasterectomy in history, dumping syndrome is the most likely underlying cause to this presentation. Dumping syndrome is the effect of altered gastric reservoir function, abnormal gastric motor function, and/or pyloric emptying mechanism. In term of temporal relation to eating, dumping syndrome can have early or late manifestations: ▫ Early dumping: Symptoms of early dumping syndrome occur 30-60 minutes after a meal and are believed to result from accelerated gastric emptying of hyperosmolar contents into the small bowel. This leads to fluid shift from the intravascular compartment into the bowel lumen, resulting in rapid small bowel distention and increase in the frequency of bowel contractions. Even in healthy persons without gastric surgery, rapid instillation of liquid meals into the small bowel has shown to induce dumping syndrome. Rapid shift of fluid into the intestinal lumen results in decreased circulating volume, triggering a vasomotor response presenting with tachycardia and lightheadedness. ▫Late dumping: Late dumping occurs 1-3 hours after a meal. The pathogenesis is thought to be related to the early development of hyperinsulinemic (reactive) hypoglycemia. Rapid delivery of a meal to the small intestine results in an initial high concentration of carbohydrates in the proximal small bowel and rapid absorption of glucose. This is replied by a hyperinsulinemic response. The high insulin levels stay for longer period and are responsible for the subsequent hypoglycemia. The diagram summarises the mechanism through which the dumping syndrome develops. The clinical presentation of dumping syndrome can be categorized as abdominal versus vasomotor symptoms, and based on the time of onset as early versus late. 🔺Early dumping systemic symptoms: Desire to lie down, Palpitations, Fatigue, Faintness, Syncope, Diaphoresis, Headache, Flushing 🔺 Early dumping abdominal symptoms: Epigastric fullness, Diarrhea, Nausea, Abdominal cramps, Borborygmi These symptoms can be collectively referred to as dyspepsia. 🔻Late dumping symptoms: Perspiration, Shakiness, Difficulty to concentrate, Decreased consciousness, Hunger For patients with dumping syndrome, dietary modification is the firstline management option. The following pieces of advice are appropriate: ✔ Daily energy intake is divided into 6 meals. ✔ Fluid intake during and with meals be restricted and liquids be avoided for at least half an hour after a meal. ✔ Avoiding simple sugars. ✔ Milk and milk products are generally not tolerated and should be avoided. ✔ Because carbohydrate intake is restricted, protein and fat intake should be increased to fulfill energy needs. ➕ Additional points to consider: Supplementation with dietary fiber has proven effective in the treatment of hypoglycemic episodes. Many medical therapies have been tested, including pectin, guar gum, and glucomannan. These dietary fibers form gels with carbohydrates, resulting in delayed glucose absorption and prolongation of bowel transit time. Dietary change to a low-carbohydrate, high protein diet, as well as the use of alpha-glucosidase inhibitors, may be useful to control the symptoms of dumping. This is preferential to subtotal or total pancreatectomy in those persons with severe symptoms. Most patients have relatively mild symptoms and respond well to dietary changes. In some patients with postprandial hypotension, lying supine for 30 minutes after meals may delay gastric emptying and also increase venous return, thereby minimizing the chances of syncope

⏳ Case-based MCQ | #Case_399 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 A 48-year-old man presents to your practice several months after gastrectomy with complaint of dyspepsia. This problem occurs mostly 30 minutes after meals. Dyspepsia is worse when he takes toast and cereal for his breakfast.

⏳ Case-based MCQ | #Case_398 | #answer 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 ✅ E The scenario is a typical description of a pseudoaneurysm as a complication of femoral artery catheterization. A pseudo aneurysm is a hematoma that forms as the result of a leaking hole in an artery. The hematoma forms outside the arterial wall and is contained by the surrounding fibromuscular tissue. The hematoma must continue to communicate with the artery to be considered a pseudoaneurysm. Pseudoaneurysm occurs in up to 7.5% of femoral artery catheterizations and can cause distal embolization, extrinsic compression on the neurovascular structures, rupture, and hemorrhage. A pseudoaneurysm presents with a painful pulsatile groin mass. A bruit over the mass may or may not be heard. Duplex Doppler ultrasound may provide evidence of extra-arterial flow or there may be classic ‘toand-fro’ Doppler waveform in the neck of the pseudoaneurysm. Ultrasound-guided thrombin injection for the pseudoaneurysms of the iliac, femoral and peroneal arteries is safe, effective, and associated with few complications. It has emerged as the preferred treatment modality for pseudoaneurysms occurring as a result of percutaneous femoral arterial interventions (success rate: 97%). The procedure should be performed by a physician and an ultrasonographer to enable continuous visualization of the pseudoaneurysm. Thrombin is injected into the sac of the pseudoaneurysm away from the neck under direct ultrasound guidance. ⚠ (Option A) The ultrasound-guided compression is successful in 90% of case and was the treatment of choice previously; however, this approach is not favorable anymore because it needs prolonged compression time (up to 120 minutes), makes the patient uncomfortable, is associated with early recurrence and has limited success in treating large pseudoaneurysms. ⚠ (Option B) Urgent surgical exploration is indicated for a threatened limb and when a percutaneous approach is not feasible. This method was the treatment of choice before 1985. ⚠ (Option C) Vitamin K is not a treatment option. Any options suggesting cessation of clopidogrel is incorrect as this is associated with high mortality rate in a patient who has just undergone angioplasty. Moreover, it does not treat the aneurysm. ⚠ (Option D) Angiographic intervention via a retrograde approach from the contralateral common femoral artery is only indicated if acute vessel occlusion due to distal emboli occurs. The event presents with the patient complaining of pain, pallor, parenthesis or decreased movement in the respective limb. Clinical examination may reveal a cold ischemic limb with absent pulses, an ankle-brachial index (ABI) <0.5, or absent color flow and Doppler waveform on duplex ultrasound in the index artery

⏳ Case-based MCQ | #Case_398 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 A 65-year-old female patient undergoes percutaneous coronary intervention and stent placement through femoral artery, and is started on aspirin andclopidogrel. After 24 hours, she develops a pulsatile painful mass in the groin though which the catheter was sent in.

⏳ Case-based MCQ | #Case_397 | #answer 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 ✅ E Significant findings on this X-ray of the shoudler are a humeral head out of the glenoid fossa and displaced inferiorly. These findings are typical for anterior dislocation of the glenohumeral joint. Shoulder dislocations often result in injury of the axillary nerve. Axillary nerve runs inferiorly to the humeral head and wraps around the surgical neck of the humerus. Axillary nerve innervates the deltoid and terese minor muscles and the skin of the lateral shoulder (shoulder badge region). Axillary nerve dysfunction manifests as loss of sensation in a 'shoulder badge' distribution and deltoid muscle weakness. It is impractical to ask the patient to move the affected arm due to pain; however, in the presence of axillary nerve injury, the patient is often unable to isometrically contracts the deltoid muscle. No other muscle mentioned in the options are innervated by the axillary nerve; hence, unaffected by axially nerve injury.

⏳ Case-based MCQ | #Case_397 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 25. A young man presents to the emergency department after injuring his shoulder in a fall. His X-ray is shown in the following photograph.

⏳ Case-based MCQ | #Case_396 | #answer 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 ✅ A If not contraindicated, antithrombotic therapy should be started for all patients with ischemic stroke. In patients with AF, warfarin is the antithrombotic of choice to start. The need for anticoagulation is assessed based on CHA2DS2-VASC system. ⚠ (Options B and C) Aspirin or dipyridamole alone does not appear to provide adequate anticiagulation in patients with AF. ⚠ (Option D) Thrombolyitc therapy is indicated within the first 4.5 hours of symptoms onset. In this patient, 48 hours has past since the start of symptom; therefore, thrombolytic therapy with rTPA is not beneficial for her. ⚠ (Option E) Combination of aspirin and clopidogrel is not recommended for secondary prevention of cerebrovascular disease in patients who do not have acute coronary disease or a recent coronary stent placement. This is due to significantly increased risk of bleeding that outweighs the additional benefit of combinations therapy if no other indication than prevention of ischemic stroke is desired

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⏳ Case-based MCQ | #Case_396 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 A 72-year-old woman, who is a known case of diabetes and hypertension and on multiple medications, is brought to the emergency department with complaint of left-sided weakness for the past 48 hours. On examination, she has a blood pressure of 150/100 mmHg and an irregular pulse of 98 bpm. Her blood sugar is 8 mmol/L. Three years ago, she had an episode of sudden-onset right vision loss for few hours before she completely recovers. She, however, did not seek any medical attention at that time.

⏳ Case-based MCQ | #Case_395 | #answer 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 ✅ A The history of prolonged constipation as well as the exam findings of a tympanic distended abdomen colicky abdominal pain and an empty rectum is more consistent with sigmoid volvulus as the most likely diagnosis (A is correct) A colonic volvulus occurs when a part of the colon twists on as mesentery, causing colonic obstruction. Such obstruction can be acute, subacute or chronic. Although volvulus can occur in any portion of the large bowel the sigmoid colon is the most frequently affected part followed by volvulus of the right colon and terminal ileum namely cecal or cecocolic volvulus. In very rare cases volvulus may develop in the transverse colon or the splenic flexure Patients with colonic volvulus are commonly elderly debilitated and bedridden. A history of dementia or neuropsychtalrtc impairment is often present. The symptoms are acute in more than 60-70% of patients wbie the rest present with subacute or chronic symptoms. A history of chronic constipation is common. The patient may describe previous episodes of abdominal pain distention and obstipation which suggest repeated subctinical episodes of volvulus. Regardless of its anatomic site colonic volvulus presents the same way with cramping abdominal pain distention constipation and/or obstipation. Abdominal distention often increases progressively. The distention ts characteristically tympanic over the gas-filled thin wall colon loop. Tenderness or rebound tenderness indicates that peritonitis has occurred or is just imminent. With progressive obstruction nausea and vomiting occur. The development of constant abdominal pain is an ominous sign indicating the development of a closed-loop obstruction with significant intraluminal pressure. This, m turn portends the development of ischemic gangrene and bowel wall perforation Plain abdominal films are the initial imaging choice. Massive dilation of the sigmoid colon loop arising from the pelvis and extending to the diaphragm is a typical finding of sigmoid volvulus The wais of the loop are evident as three bright lines converging m the pelvis to create a beaklike appearance ⚠ (Option B) A sigmoid tumor can also he the underlying cause of this clinical picture Left sided colon cancer can present with bloody stool, changes m bowel habits and abdominal pain specialty if the tumor has caused partial or complete obstruction However a sigmoid tumor large enough to cause complete obstruction of the colon to result in obstipation is expected to have more pronounced exam findings ⚠ (Option C) Obstruction caused by the entrapment of a loop of the small bowel in an adhesion band formed from previous surgery can cause small bowel obstruction In fact adhesions from previous abdominal surgeries ts the most common cause of small bowel obstruction In this patient however, the clinical picture more favors large bowel rather than small bowel obstruction because in small bowel obstruction nausea and vomiting is a prominent feature that occurs earlier In the course of the process. This patient has not vomited after 24 hours of symptoms onset. ⚠ (Option D) An obstructed hernia is expected to cause constant abdominal pain and tenderness. However in early stages and before the strangulation occuis these findings might be absent. This patient has no clinical findings suggestive of a hernia as the likely cause of this presentation. Furthermore, with obstructed hernias presentation will favor that of the small bowel obstruction with early onset nausea and vomiting the course of the disease ⚠ (Option E) As the name implies this kind of obstruction is caused by impaction of fecal matter often in the rectum An empty rectum excludes this diagnosis