🧩 Medical Mnemonics

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#rheumatology
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©Medical Mnemonics

⏳ Case-based MCQ | #Case_427 | #answer
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✅ D

The location and circumstances are classic for Morton's neuroma, a benign neuroma of the third plantar interdigital nerve. Gout happens to obese, elderly males, and redness and signs of inflammation in the affected joint are evident. Hallux rigidus is osteoarthritis of the first metatarsophalangeal joint. There is deformity and limitation of motion. The joint is tender on physical examination. Metatarsophalangeal articulation pain is likewise associated with misalignment of joint surfaces. There is pain when examining the joint, and there is no history of numbness, burning, or tingling. Plantar fasciitis produces sharp pain on physical examination when pressing the plantar surface of the heel

⏳ Case-based MCQ | #Case_428
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Parents of a 6-year-old girl bring her for pre-school physical examination. The girl reports that sometimes she gets short of breath when “she plays too much” but otherwise she is fine. The child’s past medical history is unremarkable. Her immunizations are up to date. Vital signs reveal variation in blood pressure between the left and right arms. The femoral pulses are decreased.

⏳ Case-based MCQ | #Case_428 | #answer
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✅ C

This child presents with no significant past medical history, immunizations are uptodate, but the shortness of breath she reports should be explored even though it is attributed to physical activity. The difference in the BP measurements in the arms and the decreased femoral pulses are common findings in coarctation of aorta (choice C). It is a relatively common defect that accounts for 5-8% of all congenital heart defects. The diagnosis of this condition is often delayed until complications such as congestive heart failure develop.

Coarctation of the aorta is defined as a constricted aortic segment that comprises localized medial thickening, with some infolding of the medial and superimposed neointimal tissue. The classic coarctation of the aorta is located in the thoracic aorta distal to the origin of the left subclavian artery at about the level of the ductal structure. This imposes significant afterload on the left ventricle, which results in increased wall stress and compensatory ventricular hypertrophy. The anatomy results in hypertension proximal to the lesion, with diminished blood pressure distal to the obstruction.

⚠ Patent ductus arteriosus (choice A) may be a comorbidity found in patients who have coarctation of aorta but it is not the cause of the difference in BP in the patient’s arms or decreased femoral pulse.

⚠ Aortic stenosis (choice B) would not be the cause of the differing BP measurements in the arms or the decreased femoral pulse.

⚠ Ventricular septal defect (choice D) is associated with a holosystolic murmur along the lower left sternal border. While it may be present in some patients with coarctation of aorta, itself it wouldn’t be the cause of differences in BP in the arms or delayed femoral pulse.

⚠ Renal artery fibromuscular dysplasia (choice E) causes secondary hypertension, may cause abdominal or femoral artery fruits, but it is not associated with varying BP measurements in the arms or decreased femoral pulse.

🔖 Key point:

The clinical presentation of shortness of breath, BP measurements differences in the arms, and decreased femoral pulse is highly suggestive of coarctation of aorta. The classic coarctation of the aorta is located in the thoracic aorta distal to the origin of the left subclavian artery

⏳ Case-based MCQ | #Case_428
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A 68-year-old woman presents to your department with worsening dyspnea. Past medical history includes COPD, coronary artery disease, and Stage III chronic kidney disease. Her brain natriuretic peptide is 1200 pg/mL (normal < 100 pg/mL).

⏳ Case-based MCQ | #Case_429 | #answer
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✅ D

This patient presents with dyspnea and has elevated brain natriuretic peptide (BNP). The BNP is secreted by the brain and heart ventricles and is elevated in traumatic brain injury, left ventricular dysfunction, and congestive heart failure (CHF). In the patient with dyspnea, overlapping or even conflicting historical, physical, and radiographic findings often hinder the differentiation between cardiac and noncardiac etiology. Initial misdiagnosis occurs in approximately 15-20% of patients presenting to the emergency department with dyspnea secondary to an acute exacerbation of CHF. This misdiagnosis may incur clinically significant morbidity and mortality. The primary value of BNP testing in the ED is its diagnostic value in the differential diagnosis of acute dyspnea and possible CHF. BNP levels > 400 pg/mL are suggestive of CHF.

Since this patient has no history of traumatic brain injury and is presenting with elevated BNP, the most likely cause is decompensated CHF. Initial approach to treatment of ADHF includes supplemental oxygen and ventilatory support (noninvasive ventilation [NIV] or intubation) as indicated, diuretic therapy, and vasodilator therapy (choice D).


⚠ Inhaled ipratropium bromide (choice A) would be used in an acute exacerbation of COPD. The elevated BNP helps us determine the cause of dyspnea in this patient, it is cardiogenic in nature and CHF is the most likely diagnosis.

⚠ Peritoneal dialysis (choice B) would be done if the patient had end-stage renal disease or acute renal failure. No findings suggest this diagnosis in this patient.

⚠ Mannitol (choice C) is incorrect. Circulatory overload due to expansion of extracellular fluid is a serious adverse effect of mannitol. As a consequence, pulmonary edema can be precipitated in a patient with diminished cardiac reserve.

⚠ Diltiazem (choice E) is a calcium channel blocker and is contraindicated in patients with CHF and abnormal LV ejection fraction. While measurements of LV ejection fraction of this patient are not mentioned, studies have shown that there is a negative linear correlation between BNP and LV ejection fraction, and high BNP levels can predict decreased LV ejection fraction levels. Use of diltiazem has been shown to have negative outcomes in CHF.

🔖 Key point:

BNP can be used to differentiate cardiogenic dyspnea from non-cardiogenic dyspnea. BNP levels > 400 pg/mL are suggestive of CHF. Initial therapy includes the initiation of treatments aimed at rapidly correcting hemodynamic and intravascular volume abnormalities, such as diuretics and intravenous vasodilator therapy.

⏳ Case-based MCQ | #Case_429
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An elderly alcoholic male is brought to the hospital by his grandson, who found him in poor condition. The grandson reports that his family has not seen the patient in months.

The patient denies complaints, but is obviously malnourished, poorly washed, and mildly intoxicated. You admit the patient to the hospital and begin providing supportive care, including intravenous fluids with dextrose, a regular diet, and physical therapy evaluation. On the evening of the second day he becomes weak and more confused. His blood pressure is 88/56 mm Hg, and he has a seizure. Your evaluation includes the following laboratory findings:

Glucose: 3.3 mmol/L
BUN: 3.2 mmol/L
Creatinine: 230 µmol/L
Creatine kinase: 480 U/L
Troponin I: < 0.1 µg/L
Albumin: 27 g/L
Calcium: 0.97 mmol/L
Phosphate: 0.27 mmol/L
ALT (SGPT): 68 U/L
AST (SGOT): 88 U/L

⏳ Case-based MCQ | #Case_429 | #answer
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✅ E

Severe hypophosphatemia (choice E) is a medical emergency. In poorly nourished patients, refeeding syndrome can occur. Symptoms usually occur by the second or third day of improved nutrition, and are often multisystemic. Findings may include weakness, confusion, dysrhythmias, respiratory failure, congestive heart failure, hypotension, ileus, metabolic acidosis, seizures, coma, and sudden death. This constellation of problems results from decreased insulin secretion as stores of intracellular phosphate become depleted. Providing carbohydrates through intravenous fluids or refeeding increases insulin secretion, which stimulates cells to take up phosphate, causing severe hypophosphatemia. In this setting cells are unable to produce enough 2,3 diphosphoglycerate and adenosine triphosphate to meet metabolic demands

⚠ While hypoglycemia (choice A) is another medical emergency, this patient’s glucose level is not low enough to cause these symptoms.

⚠ Similarly, renal failure (choice B) of some type is present, as is an elevated creatine kinase (choice C) suggesting rhabdomyolysis; however, neither of these problems would be expected to cause this patient’s symptoms.

⚠ Hypocalcemia (choice D) can cause multisystemic problems, including weakness and seizures, but this level is not critically low and is not associated with hypotension.

⏳ Case-based MCQ | #Case_430
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A 37-year-old female presents to your department because complaining of nausea and vomiting for the last 3 days. She has also been having headaches. Physical examination is only remarkable for abdominal distension and BP 165/100 mmHg. Her BP has been high the last 3 months despite treatment with amlodipine that was started at 5 mg once a day and was later increased to 10 mg once a day. Comprehensive metabolic panel reveals:

BUN: 7 mmol/L
Creatinine: 80 micromol/L
Calcium: 2.40 mmol/L
Chloride: 96 mmol/L
Bicarbonate: 31 mmol/L  
Glucose test: 5 mmol/L
Potassium test: 2.7 mmol/L
Sodium: 148 mmol/L
Albumin: 42 g/L

⏳ Case-based MCQ | #Case_430 | #answer
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✅ C

This patient is presenting with a history of hypertension that is not responding to calcium channel blockers and has non-specific symptoms like nausea and vomiting. The major clue to the cause of this patient’s condition is the laboratory tests results that show hypokalemia and mild hypernatremia. These electrolyte abnormalities are associated with hyperaldosteronism and given the history of resistant hypertension, the patient’s most likely diagnosis is Conn’s syndrome (choice C).
Other aspects of clinical presentation that may be noted are weakness, abdominal distention, Ileus from hypokalemia (which can cause nausea and vomiting), findings related to complications of hypertension such as cardiac failure, hemiparesis due to stroke, carotid bruits, abdominal bruits, proteinuria, renal insufficiency, and hypertensive encephalopathy.

⚠ Liver cirrhosis (choice A) may cause abdominal distension and vomiting with portal hypertension and ascites and even hypokalemia. Hypokalemia in liver cirrhosis is usually multifactorial and may be associated with diuretics use, magnesium depletion in alcoholics, vomiting, and secondary hyperaldosteronism. However, this patient’s scenario doesn’t present risk factors of liver cirrhosis and primary aldosteronism is far more common than secondary aldosteronism.

⚠ Cushing's syndrome (choice B) can also cause hypertension and even hypokalemia with extremely high levels of cortisol. However, it would also cause findings often remarkable on physical examination such as facial plethora, hirsutism, buffalo hump, etc.

⚠ Pheochromocytoma (choice D) presents with episodes of severe hypertension due catecholamine secretion. Other classic 3 symptoms are diaphoresis, palpitations, and headaches. It may be associated with multiple endocrine neoplasia type II. Hypernatremia and hypokalemia are more likely to be seen with elevated aldosterone secretion than with increased catecholamine secretions.

⚠ Addison’s disease (choice E) is adrenal insufficiency and would cause the inverse of what is noted in this patient, with hypotension, hyponatremia, and hyperkalemia being the major findings.

🔖 Key point:

Hyperaldosteronism such as seen in Conn's syndrome is associated with hypertension, hypernatremia, and hypokalemia

🧩 Medical Mnemonics

Learn Fish-vertebra sign in Osteoporosis by #visual_mnemonics.

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🖥 IMAGING Explanation

The “fish-vertebra” sign is a smooth deformity of the vertebral bodies, with a characteristic biconcave body occurring due to a squared-off depression of the vertebral end-plates and compression by adjacent intervertebral discs. This radiologic sign can be seen in osteoporosis, osteomalacia, hyperparathyroidism, Paget disease, sickle cell disease, multiple myeloma and systemic lupus erythematosus.

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#radiology
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©Medical Mnemonics

⏳ Case-based MCQ | #Case_431
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A 13-year-old white female reports a 6 month history of intermittent abdominal cramping, with each episode becoming progressively worse. Based on her history, there is no obvious relationship to eating, voiding, or defecating. She report that she has not yet begun menstruating and is not sexually active. Her weight has been stable. She appears to be in mild emotional distress about being the “last girl in her class to have a period”. She is in no physical discomfort and her vital signs are normal. Secondary sexual characteristics appear to be developing normally. She is in the 57th percentile for height and the 65th percentile for weight. A complete physical examination confirms your presumptive diagnosis.

⏳ Case-based MCQ | #Case_431 | #answer
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✅ C

The key to making a diagnosis of imperforate hymen, aside from the obvious finding on physical examination, lies in the systematic drawing of inferences. One can speculate that this patient’s recurrent crescendo abdominal cramping represents six menstrual sheddings, with no egress from the body. Her delay in menarche, despite normal growth parameters, offers another clue that the structural amenorrhea is present. Amounts of retained blood vary among patients; up to 3000 mL have been reported. A large volume can accumulate without causing any permanent damage, and subsequent fertility is usually normal. Hymenotomy will relieve the pressure, and normal menses should ensue.

⏳ Case-based MCQ | #Case_432
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A 58-year-old male presents with nausea and vomiting for two days. He had noticed that he lost 7 kg over the last two months but he did not think too much about it, as he was overweight. Past medical history is significant for smoking 20 packs of cigarettes a year.

Physical examination reveals an enlarged, hard, painless left-sided supraclavicular lymph node.