Case-based MCQ

⏳ Case-based MCQ | #Case_453 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 You are reviewing laboratory findings in a 64-year-old male hospitalized with acute renal failure. The patient is not on any long-term medications. His renal function has previously been normal, but currently, his serum creatinine level is 270 μmol/L, BUN 28.4 mmol/L, and fractional excretion of sodium (FENa) 0.75%. His urine specific gravity is 1.025, and the urine sediment shows only hyaline casts.

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⏳ Case-based MCQ | #Case_452 | #answer 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 ✅ E Nephrotic syndrome is caused either by primary kidney diseases like minimal change disease and membranous glomerulonephritis or by systemic diseases affecting the kidney like diabetes, hypertension, and systemic lupus erythematosus. The basic pathogenesis is increased permeability of glomeruli to plasma proteins, specifically albumin. This would cause a reduction in plasma colloid osmotic pressure and shifts the Starling forces in favour of fluid flux from the blood vessels to the interstitial space resulting in edema. Prognosis of nephrotic syndrome depends on the underlying cause and the age of the patient. Focal segmental glomerulosclerosis (FSGS), membranous glomerulonephritis (MGN) and minimal change disease (MCD) are the causes of nephrotic syndrome in up to 70% of cases in adults. These three diseases require different treatments and have different prognoses, and hence correct diagnosis must be made. This can be done only by renal biopsy (choice E). ⚠ Steroid therapy (choice A) is part of the treatment of FSGS, MGN, MCD and some other causes of nephrotic syndrome. However, this treatment should not be started before the diagnosis is confirmed by renal biopsy. ⚠ Immunosuppressive therapy (choice B) is used in the treatment of MGN, but it should not be started before the diagnosis is confirmed by renal biopsy. ⚠ In nephrotic syndrome, IV albumin (choice C) is given only when contraction of blood volume is very severe, as indicated by anuria and severe hypotension. ⚠ CT scan (choice D) of the abdomen has little if any role in finding the causes of nephrotic syndrome. 🔖 Key point: Focal segmental glomerulosclerosis (FSGS), membranous glomerulonephritis (MGN) and minimal change disease (MCD) are the causes of nephrotic syndrome. These three diseases require different treatments and have different prognoses, and hence correct diagnosis must be made by renal biopsy

⏳ Case-based MCQ | #Case_452 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 A 43-year-old man presented to his family physician with breathlessness, swelling of his feet and frothy urine. The diagnosis of nephrotic syndrome was established on the basis of nephrotic range proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Chest X-ray showed bilateral pleural effusion, and abdominal ultrasound revealed ascites. Tests for HIV, hepatitis B and C were negative. Anti-glomerular basement membrane (GBM), antiphospholipid, ASO, anti-DNAase, anti-neutrophil cytoplasmic (ANCA), and antinuclear (ANA) antibodies were negative.

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⏳ Case-based MCQ | #Case_451 | #answer 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 ✅ E Travellers to developing countries with high incidence of infectious diarrhea may develop diarrhea (traveller’s diarrhea) during their stay in those countries or after arrival in their home country. Traveller’s diarrhea may be caused by bacteria, viruses or parasites especially protozoa. The diarrhea may be either inflammatory or non-inflammatory or may be watery or in the form of dysentery depending on the causative organism. The likely cause of traveller’s diarrhea can inferred from knowledge of the usual causes of diarrhea in the region visited, temporal relationship between development of diarrhea and visit as well as the clinical features of the disease. Giardia lambilia (choice E) should top the list of potential causes of diarrhea in this patient. Giardia lambilia has an incubation period of 1-2 weeks or longer and thus, our patient who returned from Latin America two weeks ago could have contracted the infection any time during his stay there. Furthermore, the clinical picture is also suggestive of Giardia infection, which starts with watery diarrhea, abdominal pain, loss of appetite and flatulence due to malabsorption of sugars, which frequently accompanies Giardia infection. ⚠ Aeromonas enteritis (choice A) is a rather unlikely cause of diarrhea in this patient. Although, this organism may present with watery diarrhea and abdominal cramps, fever usually accompanies diarrhea caused by this organism. In addition, the incubation period of this microorganism is between 24 to 48 hours and thus, infection by this microorganism is unlikely to explain traveller’s diarrhea in this patient, who returned from Latin America 2 weeks ago. ⚠ Cryptosporidium (choice B) may present with a clinical picture similar to that of Giardia lambilia and like Giardia it has an incubation period of 1 to 2 weeks. However, Cryptosporidium is a less common cause of traveller’s diarrhea than Giardia lambilia. ⚠ Despite being the most common cause of traveller’s diarrhea, Enterotoxigenic E. coli (choice C) is an unlikely cause of traveller’s diarrhea in this patient. The incubation period of this organism ranges between 1 to 3 days and so, it cannot be the cause of traveller’s diarrhea in our patient who returned from his trip 2 weeks ago. ⚠ Enterohemorrhagic E coli (choice D) is a rather unlikely cause of traveller’s diarrhea in this patient. This microorganism causes inflammatory diarrhea with bloody stool and fever. Also, the median incubation period for microorganism is about 4 days; diarrhea caused by this organism is expected to develop during his stay in Latin America or shortly after arrival to home country. 🔖 Key point: Diarrhea caused by microorganisms with short incubation periods is more likely to develop during stay or shortly after return to home country. When diarrhea develops weeks after travel, it is either traveller’s diarrhea caused by organisms with long incubation periods like Giardia lambilia or Entamoeba histolytica or non-traveller’s diarrhea due to locally acquired infectious agents or non-infectious disease.

⏳ Case-based MCQ | #Case_451 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 A 6-year-old girl is brought to family physician with mild watery diarrhea, flatulence, loss of appetite, and mild abdominal discomfort of three days' duration. The family returned form a two-week visit to Latin America two weeks ago. Past medical history and family history are unremarkable. Vital signs are stable and the rest of physical examination is normal. You suspect traveller’s diarrhea and you decide to treat your patient empirically.

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This patient presents with a thyroid nodule and symptoms that suggest hyperthyroidism. Thyroid nodules are usually found incidentally. On palpation, their prevalence is estimated to be between 4% and 7% of the population. However, more people have undiagnosed thyroid nodules, as demonstrated by studies that showed 50% of the population to have thyroid nodules on ultrasonography. Based on the statistics of the most prevalent thyroid nodules, the fact that this patient's nodule does not compress adjacent tissues, absence of lymphadenopathy and ultrasound showing a single well-circumscribed mass of 2 cm in diameter, it is most likely a benign nodule, and the most likely diagnosis is follicular adenoma. Only 5% of thyroid nodules are malignant, while 95% are benign. Follicular adenoma is the most common neoplasm of the thyroid (benign and malignant combined). For a hyperfunctioning follicular adenoma of this size, in a woman who is neither pregnant nor breastfeeding, radioiodine non-surgical ablative therapy (choice D) is the most appropriate treatment option. The aim of radioiodine treatment is the ablation of the autonomously functioning areas to achieve euthyroidism. Radioiodine therapy normalizes thyroid function in 85% to 100% hyperfunctioning single thyroid nodules or toxic multiple nodular goitres (Plummer's disease). Beta-blockers, especially propranolol, are indicated as initial treatment for symptomatic relief. Propranolol decreases serum triiodothyronine by 30% through the inhibition of the 5'-monodeiodinase that converts thyroxine (T4) to T3. ⚠ Sequential sonograms (choice A) for size increase would be advised in a hot nodule that does not cause symptomatic hyperthyroidism. This option would be insufficient for the appropriate management of a hyperfunctioning follicular adenoma. ⚠ Propranolol and left lobe thyroidectomy (choice B) is indicated when a benign nodule causes dysphagia, choking sensation, shortness of breath, dyspnea on exertion, hoarseness, or pain. Surgery also should be considered if the nodule is growing fast or there's a change in ultrasonogram features despite benign FNA results. ⚠ Levothyroxine therapy for thyroid suppression (choice C) has been used as an initial treatment for benign nodules for a period of 6 to 12 months to determine if the nodule decreases in size. A clinically significant (50%) decrease has been observed in follicular adenomas with colloid features. However, no consensus exists regarding the use of levothyroxine because it requires long-term commitment as nodule regrowth occurs after cessation of therapy. This should be avoided in this patient who is getting close to menopause as long-term levothyroxine is associated with osteoporosis; moreover, there is a three-fold increase of atrial fibrillation in patients treated with levothyroxine. Many specialists do not recommend levothyroxine suppression therapy. ⚠ Percutaneous radiofrequency ablation (choice E) is currently not recommended for routine management of benign thyroid nodules. 🔖 Key point: For a hyperfunctioning follicular adenoma, in a woman who is neither pregnant nor breastfeeding, radioiodine non-surgical ablative therapy is the most appropriate treatment option

⏳ Case-based MCQ | #Case_449 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 A 40-year-old female is found to have a thyroid nodule during her annual physical examination. Her TSH level is normal. Ultrasonography of her thyroid gland shows a solitary solid nodule measuring 1.2 cm. The patient becomes anxious and says, "my mother had a thyroid cancer surgery last year."

⏳ Case-based MCQ | #Case_449 | #answer 〰〰〰〰〰〰〰〰〰〰〰〰〰〰 ✅ B This patient’s severe and unyielding chest pain with radiation is suggestive of myocardial infarction (MI), aortic dissection or acute pancreatitis from the available choices. The lack of dyspnea is less suggestive of pneumothorax. The normal CBC, serum chemistries, amylase, EKG and the negative cardiac enzymes do not necessarily rule out pancreatitis or MI; however, when you further consider the difference in blood pressures between arms (30 mmHg), and the widened mediastinum on x-ray, you should be leaning more towards aortic dissection (choice C) in your differential. A definitive diagnosis would be made via CT or MRI. Treatment includes the reduction of systolic blood pressure to 110 mmHg with beta-blockade then maintenance with nitroprusside. Surgical options will depend on the type of dissection, Stanford type A or B (a topic that will not be covered here). ⚠ Acute pancreatitis (choice A) would typically produce elevated levels of amylase and lipase, leukocytosis, electrolyte imbalances, and an elevated CRP. It would not demonstrate a widened mediastinum on x-ray; rather, a sentinel loop (or an isolated distended loop of bowel seen near the site of the injured viscus-usually in left hypochondrium) would more likely be seen on abdominal x-ray. ⚠ Myocardial Infarction (choice B) would typically yield elevated cardiac enzymes and EKG changes (e.g. ST elevation). Further investigation would include echo or angiography. MI alone would not demonstrate a widened mediastinum on x-ray. ⚠ A patient with a pneumothorax (choice D) or tension pneumothorax (choice E) would present with dyspnea along with their chest pain (a history of trauma would also be likely for tension pneumothorax). Generally, on x-ray, one hemithorax may seem darker (more radiolucent) than the other as the area beyond the collapsed lung will have no pulmonary vessel markings. The pleural edge of the collapsed lung will be seen. Occasionally, there will be a shift in the mediastinal structures. 🔖 Key point: Severe, sudden chest pain, blood pressure differences between arms and a widened mediastinum on x-ray should make you suspect aortic dissection.