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Case-based MCQ | #Case_445 | #answer


B

This patient has multiple atherosclerotic risk factors and known coronary artery disease. The key diagnostic clue, in this case, is the worsening of his dull, crampy epigastric pain after eating. His investigations all came back negative, except for mild gastritis, which does not explain his pain

His symptoms and known atherosclerotic disease make chronic mesenteric ischemia (choice B) the most likely diagnosis. This disorder is otherwise known as ‘intestinal angina' because the abdominal pain occurs with increased oxygen demand in the bowel after eating, just like patients with angina pectoris experience chest pain with increased myocardial oxygen demand. The pain may become so intense that patients avoid eating and subsequently lose weight. Chronic mesenteric ischemia usually progresses slowly due to the large amount of collateral vessels supplying the bowel, and patients often do not become symptomatic until there are multiple high-grade stenoses in the visceral vessels.

Non-invasive tools used in the diagnosis of the disease include CT angiogram, MRI/MR angiogram, and duplex ultrasound. Angiography remains the gold diagnostic tool, and subsequent interventional angioplasty and/or stenting can be done in the same setting.

This patient's symptoms are related to ingestion of all foods and not just gluten. Celiac disease (choice A) is also more common in women, and it often presents with diarrhea.

It is recommended that patients with no family history of colorectal cancer (choice C) be screened with a colonoscopy every 10 years after the age of 50. Although this patient's colonoscopy is negative, it is still possible he could have a colorectal neoplasm. However, chronic mesenteric ischemia is more likely given the patient's symptoms and cardiovascular history.

Inflammatory bowel disease (choice D) usually presents with crampy abdominal pain, bloody stools, and weight loss. Colonoscopy will show inflammation, abnormal vascularity and/or pseudopolyps. The patient's symptoms and normal colonoscopy findings support a diagnosis of chronic mesenteric ischemia.

Although the patient has dyspepsia, his endoscopy did not show any gastric or duodenal ulcers found in peptic ulcer disease (choice E).

🔖 Key point:

Chronic mesenteric ischemia typically presents with crampy epigastric pain that worsens with meals and should be considered in patients with atherosclerotic risk factors and/or atherosclerosis. CT angiogram, MR angiogram, and duplex ultrasound are all non-invasive diagnostic tools, which can localize the stenosis or occlusion and identify the best route for subsequent angiography
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Case-based MCQ | #Case_446

A 16-year-old girl brought to your office by her mother because she has not begun menstruating. On further questioning, the patient also complains of decreased sense of smell. There is no significant family history.

Physical examination reveals tall, thin female. There is an absence of breast development and scant pubic and axillary hair. Her vital signs are normal. Pelvic examination reveals no abnormalities including normal uterus. The rest of physical examination is unremarkable.
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Case-based MCQ | #Case_445 | #answer


D

Kallmann syndrome (KS) is isolated gonadotropin-releasing hormone (GnRH) deficiency (IGD), also referred to as idiopathic hypogonadotropic hypogonadism (IHH), with anosmia. It is a congenital genetic disorder where the primary symptom is a failure to start puberty or a failure to fully complete puberty. It occurs in both males and females.
 
Deficient hypothalamic GnRH secretion underlies the markedly abnormal gonadotropin secretion patterns in most patients with KS or idiopathic hypogonadotropic hypogonadism. The result is hypogonadism, infertility, and absent, incomplete, or partial pubertal maturation.
 
Some of the genes involved in the pathogenesis of KS and idiopathic hypogonadotropic hypogonadism have been identified. However, the genes involved remain unidentified in over 50% of patients.
 
The patient most likely has Kallmann syndrome. Patients with this condition have abnormal gonadotropin secretion with subsequent low levels of estrogen production, causing failure to develop secondary sexual characteristics. Growth hormone production is not affected in KS and height is normal. Axillary and pubic terminal hair may be scantly present in these patients because of circulating adrenal androgens. 
 
Pulsatile administration of GnRH by subcutaneous (choice D) or preferably intravenous infusion restores pituitary-gonadal axis function and fertility in the majority of people with KS and idiopathic hypogonadotropic hypogonadism. 
 
Estrogen (choice C), and combined oral contraceptive pills (choice B) will not restore reproductive function in this patient. 

Surgical correction (choice E) and reassurance (choice A) are not appropriate options in this situation.
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Case-based MCQ | #Case_446

A 66-year-old male presents to your office with a 2-day history of a sensation of pressure and hearing loss in his left ear.

A physical examination and neurologic examination are both unremarkable. Placing a vibrating tuning fork in the midline of the forehead reveals sound lateralizing to the right ear. An audiogram reveals a 30-decibel hearing loss at three consecutive frequencies in the left ear, with normal hearing on the right.
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Case-based MCQ | #Case_446 | #answer


E

When a patient presents with sudden hearing loss, it is essential to determine whether it is sensorineural or conductive. This patient's Weber test discloses lateralization to the right, meaning there is sensorineural hearing loss on the left. However, audiometry is vital in establishing the diagnosis. A 30-decibel hearing loss at three consecutive frequencies, with no other cause indicated from the physical examination confirms the diagnosis of sensorineural hearing loss. Sudden sensorineural hearing loss is almost always unilateral. Most cases are idiopathic.

Evaluation for retrocochlear pathology, the most frequently identifiable cause of sudden sensorineural hearing loss, may include auditory brainstem response, MRI, or follow-up audiometry. Treatment with glucocorticoids (choice E) should be initiated within two weeks of symptom onset in all patients with sudden sensorineural hearing loss. Hyperbaric oxygen therapy can be used as adjuvant therapy if available.

Routinely prescribing antiviral agents (choice A), thrombolytics, vasodilators (choice D), vasoactive substances, or antioxidants is not recommended.

Routine laboratory tests (choice B) are not recommended unless there is clinical suspicion for a particular etiology of the hearing loss.

The guidelines recommend against CT (choice C) of the head as part of the initial evaluation.

🔖 Key point:

Sudden sensorineural hearing loss is almost always unilateral, and most cases are idiopathic. It is diagnosed by audiometry. Treatment with glucocorticoids should be initiated within two weeks of symptom onset.
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Case-based MCQ | #Case_447

A 63-year-old Asian man with a long history of cigarette smoking presents with weakness, lethargy, and mental confusion. A physical examination is normal, without signs of dehydration, edema, or pigmentary changes.

Laboratory findings:
Serum sodium 122 mmol/L
Serum potassium 4.1 mmol/L
Plasma osmolality 260 mOsm/kg H2O
BUN 1.4 mmol/L
Urine osmolality 280 mOsm/kg H2O
Urine sodium 25 mmol/L 
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Case-based MCQ | #Case_447 | #answer


B

The syndrome of inappropriate secretion of antidiuretic hormone (choice B) should be suspected in any patient who has hyponatremia and excretes urine that is hypertonic relative to plasma. A urine sodium concentration >20 mmol/L combined with a low BUN level provides further support for the diagnosis. Additional findings may include weakness, lethargy, mental confusion, and weight gain.

Sodium depletion (choice A) usually causes clinical features of dehydration, an elevated BUN level, and a urine sodium concentration <20 mmol/L.

Primary polydipsia (choice C) almost invariably results in dilute urine with low osmolality when compared to serum. Renal failure is unlikely with a BUN level of 1.4 mmol/L.

Adrenal insufficiency (choice D) is also unlikely, as most patients will have skin pigmentation, weight loss, and hypotension. A normal serum potassium level is also inconsistent with the diagnosis of adrenal insufficiency.

 Diabetes insipidus (choice E) is characterized by hypovolemia, increased serum sodium concentration, increased urine output, and decreased urine sodium concentration.

🔖 Key point:

The syndrome of inappropriate secretion of antidiuretic hormone should be suspected in any patient who has hyponatremia and excretes urine that is hypertonic relative to plasma. A urine sodium concentration >20 mmol/L combined with a low BUN level provides further support for the diagnosis
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Case-based MCQ | #Case_448

A 35-year-old female presented complaining of a rash on her upper trunk and upper arms. She denied any fever, pruritus, and drainage. She has returned from a recent trip to Peru. The rash started when she was camping at Machu Picchu. Her past medical history was unremarkable.

You suspected Tinea versicolor. The patient returns one month later for a follow-up. She has finished two weeks of topical selenium sulphide to no avail. She then tried topical ketoconazole 2% cream also to no avail. Her hyperpigmented lesions have expanded.
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Case-based MCQ | #Case_448 | #answer


C

Tinea versicolor is a common skin infection. It is caused by Malassezia yeast, which is part of normal skin flora. It most commonly occurs in tropical climates with exposure to hot and humid weather, hyperhidrosis, and the use of topical skin products. It is more common in adolescents, young adults, and immunosuppressed patients but can occur in anyone.

Topical antifungals, such as ketoconazole, are effective and well-tolerated first-line therapy for Tinea versicolor. Topical selenium sulphide and topical zinc pyrithione are also considered first-line therapy. Treatment involves a topical application for two weeks.

With resistant Tinea versicolor that is refractory to topical treatment, oral antifungals are used. Both oral fluconazole (choice C) and itraconazole can be used. However, it is very important to remember that persistent skin colour changes are not an indication of treatment failure. Pigmentary changes will take months to resolve.

There is no need to further extend topical treatment as it has failed (choice A).

There is no role for laser therapy in the treatment of Tinea versicolor (choice B).

Oral terbinafine (choice D) and oral griseofulvin are two antifungals which should not be used to treat Tinea versicolor as they are ineffective.

Triple therapy with topical agents (choice E) is incorrect, as explained above. Oral antifungals should be employed at this point.

🔖 Key point:

With resistant Tinea versicolor that is refractory to topical treatment, oral antifungals are used. Both oral fluconazole and itraconazole can be used.
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Case-based MCQ | #Case_449

A 50-year-old man arrives into your ED complaining of severe chest pain that radiates to his jaw and left arm. He rates his pain as 10/10 and says it began suddenly one hour ago and has been constant in intensity. He is sweating profusely and feels nauseous.

Vitals: HR 130 bpm, BP 150/90 mmHg (right arm) 120/85 mmHg (left arm), RR 19 bpm, T 37°C
EKG: within normal limits (WNL)
Troponins: negative
CBC: WNL
Serum chemistries: WNL
BUN, Cr: WNL
Amylase: WNL
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Case-based MCQ | #Case_449 | #answer


C

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.
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Case-based MCQ | #Case_450

A 45-year-old white female presents to your department with a palpable mass in her neck. She also complains of palpitations, sweating, and weight loss despite her ravenous appetite, for a month.

Her vital signs are within normal limits. Physical examination shows a painless movable mass in the left thyroid gland that does not compress adjacent organs. No cervical lymphadenopathy is noted. The colour Doppler ultrasound image shows a “red light,” single well circumscribed 2cm mass in diameter in the left thyroid. It is confined within its boundaries and has a different growth pattern from surrounding thyroid parenchyma. Laboratory test results show that her TSH is lower than normal and her free T4 levels are elevated.
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D

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
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