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Feb 8th
The diagram shows a cross-section of normal human skin. Pemphigus vulgaris patients suffer from production of autoantibodies against which of the following labeled layers in this image?
A. A
B. B
C. C
D. D
E. E
Feb 4th
Case 14 – A 68-year-old man with lower abdominal pain
A 68-year-old man presents to the emergency department with severe lower abdominal pain. He has a constant desire to urinate but can only produce a small amount of urine. His past medical history is unremarkable, but he says he has experienced hesitancy before the onset of urination and decreased strength of his urinary stream for several months. Physical examination is significant for trace pedal edema, and his blood pressure is 140/86 mm Hg, with no orthostatic changes. He has marked tenderness in the suprapubic region and dullness to percussion to the level of the umbilicus. Rectal examination reveals a large, smooth, firm, midline mass located anteriorly. Laboratory tests show:
Sodium: 142 mEq/L
Potassium: 6.0 mEq/L
Chloride: 113 mEq/L
Bicarbonate: 17 mmol/L
Blood urea nitrogen: 110 mg/dL
Creatinine: 7 mg/dL
Hemoglobin: 15 g/dL
Hematocrit: 45%
What is the most likely cause of this patient’s lower abdominal pain?
This is an example of post-renal (obstructive) acute renal failure. The patient’s early symptoms are suggestive of a partial bladder outlet obstruction. His current symptoms suggest that the obstruction is essentially complete. The suprapubic tenderness and dullness to percussion are due to a distended bladder. These signs and symptoms in elderly men are most commonly caused by benign prostatic hyperplasia, but prostate cancer must also be considered.
How do the laboratory findings help to confirm the diagnosis?
The elevations in blood urea nitrogen (BUN) and creatinine levels indicate a significant reduction in glomerular filtration rate (GFR). This is due to the increased tubular hydrostatic pressure from the obstruction, which offsets glomerular capillary hydrostatic pressure. The BUN:creatinine ratio is increased because of decreased flow through the collecting duct, which causes enhanced urea reabsorption. The normal hemoglobin and hematocrit levels indicate that this is acute and not chronic renal failure, which almost always causes a hypoproliferative anemia.
How could this diagnosis be confirmed?
A catheter bypassing the obstruction may be placed in the bladder. This is sometimes difficult to do when the prostate is very enlarged. An ultrasound of the kidneys would show dilated renal collecting ducts and bilateral ureteral dilatation. A bladder scan would show a markedly enlarged bladder.
What is the most appropriate management for this patient?
Temporary relief may be achieved with a transurethral catheter, if possible. A suprapubic catheter should be considered if the prostate is too large to pass a catheter by. A transurethral prostatectomy is the definitive procedure. In addition, a work-up to distinguish benign from malignant prostatic disease should be conducted.
What are potential consequences of the treatment?
A postobstructive diuresis is typical after the relief of prolonged urinary tract obstruction. The magnitude of the diuresis can reach several liters per day. One mechanism for this is due to the elimination of sodium and water retained during the period of obstruction. Once the obstruction is removed, GFR increases and the excess sodium and water can be eliminated, which is a self-limiting process. Another mechanism is osmotic diuresis from retained urea, which is eliminated as GFR recovers.
By Kristen Vierregger, University of Pennsylvania School of Medicine, Class of 2008; in association with Le TT, Schabelman E, Shivaram A, and Klein J, eds: First Aid Cases for the USMLE Step 2 CK. New York: McGraw-Hill, 2007.
Feb 3rd
A 30-year-old woman presents to a primary care physician for a new patient visit. She reports recurrent episodes of pneumonia, bronchitis, and otitis over the past 4 years. Although her vaccinations were up to date, she developed tetanus following a foot laceration last year. Her lymph nodes and tonsils are enlarged. Laboratory testing reveals low IgG, IgA, and IgM levels. After referral to a hematologist, who rules out other acquired and genetic causes of her hypogammaglobulinemia, she is diagnosed with common variable immunodeficiency. This woman is at the highest risk of developing which of the following condition?
A. Cardiovascular disease
B. Lymphoma
C. Miscarriage
D. Renal disease
E. Splenic autoinfarction
Feb 2nd
A 70-year-old man with type 2 diabetes mellitus (DM) and benign prostatic hyperplasia (BPH) is rushed to the emergency department after being found by his weekly visiting nurse to be lethargic, disoriented, and barely conscious. She found that his pill box was full of last week’s diabetes and BPH medications. On physical examination, the patient has a Glasgow Coma Scale score of 8 (out of 15), a fever of 38.9°C (102° F), hypotension, and tachycardia. Abdominal examination reveals suprapubic fullness. The physician is unable to elicit costovertebral angle tenderness secondary to his poor mental status, but Foley catheterization reveals 2 L of cloudy, putrid urine. Initial chemistries on venous blood sampling reveal serum glucose of 1100 mg/dL and pH of 7.4.
What is the most likely diagnosis?
Urinary tract infection/pyelonephritis complicated by hyperosmolar hyperglycemic nonketotic coma (HHNK), secondary to medication noncompliance and possible sepsis. HHNK frequently occurs in elderly patients taking oral hypoglycemic agents who are inadequately monitored, or patients with previously undiagnosed type 2 DM. This hyperglycemic crisis is a medical emergency, with a 10%–20% mortality rate.
What are the primary features of this condition?
Severe hyperglycemia; serum glucose is frequently >1000 mg/dL, unlike diabetic ketoacidosis (DKA) (<800 mg/dL) (see comparison below)
What are some symptoms associated with this condition?
Patients with HHNK often present late, with symptoms of hyperosmolality. It is not uncommon for a person to present in coma. Other neurologic derangements include:
Patients with DKA often present earlier than patients with HHNK do, as they develop symptoms of ketoacidosis (ie, Kussmaul’s respirations and abdominal pain).
Why is the patient not acidotic (pH <7.4)?
Patients with type 2 diabetes have sufficient insulin production to prevent ketoacidosis from occurring first. Conversely, in DKA extremely low insulin causes triglycerides to be converted to fatty acids, which are then converted to ketoacids in the liver.
What treatment is most appropriate for this condition?
The primary goal of therapy is rehydration and correction of electrolyte abnormalities. Patients may need over 10 L of intravenous fluids, but be careful in the elderly! Insulin is administered to promote normal glucose metabolism. It is also important to treat the underlying condition (in this case, urinary tract infection and pyelonephritis). Remember, the elderly are very sensitive to infection, but rarely present typically. An elderly patient presenting with acute mental status changes should be worked up fully for an infectious cause, among others (eg, cerebrovascular accident). Patient education is crucial, as is access to social services (ie, more frequent Visiting Nurse Association services versus placement in a managed care facility).
Comparison of DKA With HHNK:
Diabetic Ketoacidosis (DKA):
Hyperosmolar Hypoglycemic Non-Ketotic Coma (HHNK):
Feb 1st
After a brain tumor resection, a right-handed patient comes to the office with this wife. The wife reports that her husband can no longer balance his checkbook or count his money. Recently he has also had difficulty identifying individual fingers and confuses his left and right sides. Additionally, she reports that although he can read without effort, he has extreme difficulty writing. The damage can be localized to which of the following areas of the brain?
A. Left angular gyrus
B. Left posterior inferior frontal lobe
C. Left posterior superior temporal gyrus
D. Left sylvian region
E. Left temporoparieto-occipital junction
Jan 28th
Case 13 – A 70-year-old man with narcotic overdose
A 70-year-old man with a history of chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF), myasthenia gravis, and chronic back pain is recovering after a motor vehicle accident. The patient fractured both tibiae and multiple ribs, but remains without serious internal organ injury. His problem during this hospitalization has been pain control. He has recently been transitioned to oral oxycodone, but morphine injections are still being used for breakthrough pain. At the 4 a.m. vital sign check, the night nurse notes the patient is unarousable. He has a respiratory rate of 5/min and an oxygen saturation of 80% by pulse oximetry. His heart rate is 80/min and blood pressure is 130/80 mm Hg. He has pinpoint pupils, a normal cardiac examination, and clear lung fields. Arterial blood gas analysis shows a pH of 7.02, partial pressure of carbon dioxide of 90 mm Hg, partial pressure of oxygen of 45 mm Hg, and bicarbonate of 15 mEq/L. Administration of 100% oxygen via a non-rebreather mask raises the oxygen saturation to 95%. Review of the medication logs shows that the patient accidentally got two morphine boluses in addition to his maximum oxycodone dosage.
What is the most likely diagnosis?
Acute hypercarbic respiratory failure secondary to narcotic overdose. Opiates depress the central drive to breathe, first causing hypercarbia and then hypoxia. Some of the other causes suggested by the patient’s history include COPD or asthma exacerbation, flash pulmonary edema secondary to CHF, or respiratory muscle weakness due to myasthenia gravis. However, the clinical picture of decreased mental status, depressed respiratory rate, and overmedication suggest narcotic overdose.
How is the diagnosis approached?
The first step should be an arterial blood gas analysis. This will differentiate between hypercarbic or hypoxemic respiratory failure. Pure inhaled oxygen should also be administered. If this improves oxygenation, the pathology is due to ventilation/perfusion (V/Q) mismatch. If oxygenation does not improve, a shunt physiology is suggested.
How is the A-a gradient calculated and what is its significance?
The A-a gradient is the difference between alveolar and arterial oxygenation. It is calculated as:
[(PATM ? 47) × FIO2] ? [(PAO2 ? PACO2 / 0.8)]
A normal A-a gradient is 5-10 mm Hg. An increased gradient indicates a problem getting alveolar oxygen into the bloodstream. Hypoventilation alone results in hypoxemia with a normal A-a gradient.
What other conditions should be included in the differential diagnosis?
The differential list for acute respiratory failure is very broad and can be divided into two categories: hypercarbic and hypoxemic. Hypercarbia is caused by decreased ventilation, due to loss of central drive (secondary to toxins or brain stem injury) or respiratory muscle failure (due to myasthenia gravis, Guillain-Barré syndrome, or botulism). Hypoxemia that corrects with oxygen therapy can be due to V/Q mismatch, often due to intrinsic lung disease such as COPD, asthma, interstitial lung disease, or a pulmonary embolus. Hypoxemia due to shunt physiology can be the result of a true vascular or intracardiac shunt; severe alveolar filling as seen in pneumonia, pulmonary edema, or hemothorax; or alveolar collapse as seen in COPD or asthma.
What is the most appropriate management for this patient?
The underlying disease process must be addressed; in this case, naloxone should be given to reverse the effects of the narcotics. Oxygenation can be improved by increasing FIO2 and adding positive end-expiratory pressure in a mechanically ventilated patient. Hypercarbia is controlled by changing minute ventilation (increasing respiratory rate and/or tidal volume).
By Melissa Rosenstein, MD, Resident in Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco Medical Center; in association with Le TT, Schabelman E, Shivaram A, and Klein J, eds: First Aid Cases for the USMLE Step 2 CK. New York: McGraw-Hill, 2007.
Jan 27th
A 32-year-old man is stabbed in the left chest and presents to the emergency department in distress. His pulse is 130/min, blood pressure is 70/50 mm Hg, and respiratory rate is 39/min. The stab wound is in the left fifth intercostal space in the midaxillary line. On examination his trachea is deviated to the right, jugular veins are distended bilaterally, and he has absent breath sounds and hyperresonance to percussion on the left side. Subcutaneous emphysema is palpated on the left thoracic wall. What is the best next step in management?
A. Needle thoracostomy
B. Chest tube thoracotomy
C. Pericardiocentesis
D. Surgical exploration
E. Diagnostic peritoneal lavage
Jan 26th
A 35-year-old nurse presents to the emergency department complaining of heart palpitations. She has also been jittery, hot, and sweaty for several hours. She has lost 15 lb (6.8 kg) in the past 2 months, missed her period in the last month, and has had frequent bouts of diarrhea ever since her fiancé cheated on her 3 months ago. She has no past medical history and denies medication or drug use. Physical examination reveals an anxious, warm, and diaphoretic woman with increased deep tendon reflexes and a fine tremor. Head and neck examinations are unremarkable. Her laboratory findings are as follows:
Serum thyroxine (T4): 30 µg/dL (normal 4–12 µg/dL)
Free thyroxine (FT4): 4.8 ng/dL (normal 0.7–1.9 ng/dL)
Serum triiodothyronine (T3): 270 ng/dL (normal 80–180 ng/dL)
Thyroid-stimulating hormone (TSH): 0.04 µU/mL (normal 0.5–6 µU/mL)
Thyroxine-binding globulin (TBG): 2 µg/dL (normal 12–20 µg/dL)
What is the most likely diagnosis?
Self-administration of thyroxine to induce factitious hyperthyroidism. This condition is seen in people with factitious disorders (feigning illness to play the sick role), malingering (feigning illness to achieve secondary gain), or those trying to lose weight. Health care workers and caretakers of chronically ill patients are at risk of abusing regularly prescribed drugs, particularly pain medication, insulin, and thyroid hormone.
How is thyroid hormone synthesis regulated?
The hypothalamus secretes thyroid-releasing hormone (TRH), which acts on the anterior pituitary gland to secrete TSH. TSH stimulates the thyroid gland to release T3 and T4. T4 is secreted in greater abundance, whereas T3 is the more active form. T4 is converted to T3 in the periphery. In the circulation, thyroid hormones are bound to TBG, a protein produced by the liver. Only free/unbound thyroid hormone is active. Levels of T3 and T4 in the periphery negatively feedback on the hypothalamus and pituitary, to suppress TRH and TSH, respectively.
What is a possible explanation for the patient’s laboratory results?
The patient has increased levels of free thyroid hormone (T3/T4) through ingestion. (Synthetic thyroid hormone is available in different combinations of T3 and T4.) She has decreased TSH levels, due to the negative feedback by the elevated levels of T3 and T4. She has decreased free TBG levels, as the binding sites have been saturated by the increased thyroid hormones.
How do the physical examination findings aid in diagnosing this condition?
While this patient is clearly displaying signs and symptoms of hyperthyroidism, the fact that she has no goiter, no exophthalmos, and no pretibial myxedema, makes Graves’ disease less likely.
How can this condition be distinguished from a panic attack?
There clearly is a psychological component to this patient’s disorder. However, on the boards, anxiety attacks are typically short-lived, peak within 5–10 minutes, and normally resolve within 30 minutes.
What would be expected on a radioactive iodine (RAI) scan?
Decreased RAI uptake. The normal hypothalamic-pituitary-thyroid axis is intact in this case. Endogenous thyroid function is suppressed by negative feedback, and therefore will not take up the RAI as avidly. In contrast, in Graves’ disease the RAI would show increased uptake, as the negative feedback mechanism is perturbed secondary to thyroid-stimulating immunoglobulins against the TSH receptor.
Jan 25th
As a result of its review, the Step 1 Committee decided to raise the three-digit score recommended to pass Step 1 from 185 to 188. The new minimum passing score will be applied to Step 1 examinations for which the first day of testing is on or after January 1, 2010.
Jan 25th
A 3-year-old boy is brought to the pediatrician because of decreased vision and pain in his right eye. Past medical history is significant for the diagnosis of glaucoma shortly after birth that has been refractory to standard medical therapies. Focused physical examination reveals iris hamartomas. Which of the following additional signs is most likely on physical examination?
A. Bilateral acoustic neuromas
B. Bilateral renal cell carcinomas
C. Cystic medial necrosis of the aorta
D. Leptomeningeal angioma
E. Scoliosis