A middle-aged woman is diagnosed with hypertension and counseled about starting an antihypertensive medication. The patient agrees to start hydrochlorothiazide, but wants to know about potential side effects that she might experience.
Which of the following is a potential adverse effect of this medication?
Hypercholesterolemia. Thiazide diuretics (e.g., hydrochlorothiazide, chlorthalidone) are common agents used for hypertension and work by blocking the sodium–chloride cotransporter in the distal convoluted tubule. The adverse effects of these agents, as well as other classes of diuretics are extremely high yield for the shelf examination. It is important to know that excessive diuresis can produce hypotension as well as electrolyte and metabolic abnormalities. Hypercholesterolemia is one of the important adverse effects of thiazide diuretics. (A, C, D) Thiazide diuretics may also cause hypokalemia, hyperglycemia, and hypercalcemia, so these answer choices are opposites. Other important effects include hyponatremia, hypomagnesemia, hyperuricemia (consider this in patients with gout), metabolic alkalosis, and a cross-sensitivity in patients with a sulfa allergy (causing a skin rash, AIN, etc.). Loop diuretics (e.g., furosemide, bumetanide, ethacrynic acid) work by blocking the sodium–potassium–chloride (Na+ /K+ /2Cl− ) cotransporter in the loop of Henle. Important adverse effects include the same electrolyte changes as in thiazides (except hypocalcemia instead of hypercalcemia), hyperuricemia, metabolic alkalosis, hypersensitivity reactions, and ototoxicity. Potassium-sparing diuretics work on principal cells of the nephron to block either aldosterone receptors (e.g., spironolactone, eplerenone) or aldosterone-sensitive sodium channels (e.g., amiloride, triamterene). High yield adverse effects of these agents include hyperkalemia and metabolic acidosis. Spironolactone can cause agranulocytosis and also acts as an antiandrogen and can produce effects such as gynecomastia. Eplerenone is more selective for the mineralocorticoid receptor and therefore does not cause gynecomastia.
A 28-year-old woman presents to her physician complaining of abdominal pain. A urinalysis shows 8 RBCs with no WBCs or protein, and no dysmorphic cells or casts. She is eventually diagnosed with gastroenteritis and is sent home. A urine culture comes back negative several days later.
What should be done next in the workup of this patient with hematuria?
Repeat urinalysis in a few days. This patient has microscopic hematuria that has no obvious relationship to the given diagnosis of gastroenteritis. There are many causes of hematuria, but hematuria is usually transient and benign in younger patients. Fever and exercise are examples of common causes of benign transient hematuria; however, the cause is often not determined. In addition, the menstrual history of this woman is not given, and this could also be the cause. Before any invasive procedures are performed, it would be wise to repeat a urinalysis to see if this patient has either transient or persistent hematuria. (B, C) Cystoscopy and a CT scan may be helpful in the workup of persistent hematuria; however, it should be confirmed as persistent first. (E) Given that malignancy is a potential cause of persistent microscopic hematuria, reassurance should only be offered after the urinalysis is repeated.
A 62-year-old woman presents to the Emergency Department because of new onset swelling and tea-colored urine. She has a history of GERD, but reports being healthy otherwise. She had a fever and sore throat 2 weeks ago but did not see a physician at that time. Currently she is afebrile with a blood pressure of 158/96 mmHg and a heart rate of 89 beats per minute. She has generalized edema with a normal cardiac examination. Her creatinine is 1.6 mg/dL (baseline 0.9 mg/dL), and urine dipstick shows 3+ blood and 2+ protein with WBCs and dysmorphic RBCs.
What would you expect the rest of her laboratory results to be? (Note: ANA is antinuclear antibody, ANCA is antinuclear cytoplasmic antibody, and ASO is antistreptolysin O antibody.)
Negative ANA, Negative ANCA, Positive ASO, Low C3, Normal C4. A patient presenting with nephritic syndrome (gross hematuria with proteinuria and dysmorphic RBCs), acute kidney injury, and a recent sore throat suggests poststreptococcal glomerulonephritis. Although the diagnosis might not have been particularly challenging, the reader must know the expected laboratory findings in this condition. In most patients, ASO antibodies will be positive indicating a recent strep infection, and C3 will be low with a normal or mildly low C4. The mechanism of this disease most likely involves in situ immune complex formation within the glomeruli in response to deposited streptococcal antigens, which will activate the alternative complement pathway. (C) In contrast, SLE will cause the activation of the classical complement pathway, causing low C3 and C4. (D) The history of a recent sore throat makes poststreptococcal glomerulonephritis more likely than ANCA-positive glomerulonephritides such as granulomatosis with polyangiitis, microscopic polyangiitis, and eosinophilic granulomatosis with polyangiitis (Churg–Strauss syndrome).
For patients with possible glomerulonephritis, it is first useful to rule out conditions that may mimic glomerulonephritis (Figure below). Criteria or evidence for nephrotic or nephritic syndrome should then be assessed, and if the cause is not readily apparent then a renal biopsy may be indicated for the diagnosis.
A 38-year-old woman with SLE presents with shortness of breath. The symptoms began acutely 2 hours ago and occurred while at rest. On examination, she has a blood pressure of 102/70 mmHg, heart rate of 112 beats per minute, and respiratory rate of 24 breaths per minute. She appears weak and is diffusely edematous. A CT angiogram confirms pulmonary embolism, and further workup reveals renal vein thrombosis. Her laboratory values and workup are shown below.
Which of the following is the most likely condition that increased this patient’s risk for pulmonary embolism?
Membranous nephropathy. This patient has nephrotic syndrome, as evidenced by her proteinuria, hypoalbuminemia, edema, and lipiduria (waxy casts). Patients with nephrotic syndrome are in a hypercoagulable state and can form clots in the arterial and venous circulations. This is partly due to urinary losses of antithrombin and plasminogen. Renal vein thrombosis is a potential complication of nephrotic syndrome and can be chronic, potentially manifesting with pulmonary embolism. The most common type of nephrotic syndrome associated with thrombotic complications is membranous nephropathy, typically with very high levels of proteinuria (>10 g/d). About 10% to 20% of lupus patients develop membranous nephropathy, and having lupus in addition to membranous nephropathy further increases the risk of renal vein thrombosis. (A, B, C) These conditions are causes of nephrotic syndrome but are less associated with thrombotic complications than membranous nephropathy. Membranoproliferative glomerulonephritis can also cause nephritic syndrome. (IgA nephropathy, Alport syndrome, Granulomatosis with polyangiitis) are causes of nephritic syndrome (although Alport syndrome can also present with nephrotic syndrome). Chronic pyelonephritis (e.g., xanthogranulomatous pyelonephritis) will not present with nephrotic range proteinuria but will present with urine studies suggestive of an infection (e.g., WBCs, leukocyte esterase, etc.).
The police brought a 32-year-old man to the Emergency Department. He is extremely disheveled and appears inebriated, making it difficult to obtain a history. On examination, there is horizontal gaze nystagmus but no afferent pupillary defect. He also has tenderness along the right flank. His laboratory values are shown below.
The patient is found to have a high serum osmolal gap. The patient’s airway is secured, and he is placed on mechanical ventilation.
What should be done next in the management of this patient?
Fomepizole. The patient in this vignette appears to have alcohol intoxication with flank pain, hematuria, and calcium oxalate crystals on urinalysis. In addition, he has an anion gap metabolic acidosis and a high serum osmolal gap, which are all important signs of ethylene glycol intoxication. Methanol intoxication may mimic this presentation, but the metabolic byproducts of methanol cause optic nerve damage (causing an afferent pupillary defect) whereas the metabolic byproducts of ethylene glycol are more likely to cause renal failure. The presence of calcium oxalate crystals may be seen in ethylene glycol intoxication, but it is a nonspecific finding and should not be relied upon to make the diagnosis. Fomepizole is a competitive aldehyde dehydrogenase inhibitor that prevents the breakdown of methanol and ethylene glycol into their toxic byproducts. (Note: ethanol is another effective competitive inhibitor that was used historically, but fomepizole is preferred.) Other important treatments are bicarbonate and hemodialysis, especially if the patient has significant acidemia. (A, B) Activated charcoal is not beneficial with any type of alcohol intoxication; however, it should be used in acetaminophen toxicity followed by N-acetylcysteine (if the patient meets criteria based on serum levels plotted on the nomogram). (C, E) Glucagon is used for β-blocker toxicity, and flumazenil is used for benzodiazepine toxicity.
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