So You Think You Can Diagnose? Vol. 1

On May 20, 2010, in SYTYCD, by NYIT College of Osteopathic Medicine SGA

So You Think You Can Diagnose?

By Eric Steinberg, OMS III

Time to step it up… get all 5 of these right and you’ll get the residency of your choice… just make sure you get everything right on your Step 1 too.

  1. I have a jar full of gram positive bacteria.  I add penicillin, and nothing happens…. the bacteria laugh in my face and call me names.  I add gentamicin, and they stop growing, but are not dead.  I’m not happy.  Then, my 4yr old cousin, who can barely tie his shoelaces, dumps both penicillin and gentamicin in the jar and all the bacteria die.  Why did they die?
  2. A 35 year old woman with Beta-thalassemia has received 12 blood transfusions over the past 5 years.  She comes to NYCOM for an OMM treatment. As you prepare for the pelvic rock test, you notice that her belly is full of fluid.  Being an astute physician, you ask her to say ‘ahhh’ and notice a yellowish discoloration beneath her tongue.  You also do a comprehensive structural exam and as you palpate shoulder height, you notice a weird ‘spider-like’ rash on her shoulder.  Since you are super-doctor, you finger-stick her and her glucose is 300.  What’s going on?
  3. You are doing an ER consult at a busy hospital in Brooklyn and the nurse tells you that some crazy guy says his hat doesn’t fit anymore and is slowly losing his hearing.   Your disheveled ER attending tells you to do a dementia workup. As a NYCOM student, you have strong suspicion of another cause. What tests do you order?
  4. An 80 yr old strong man competitor had never been sick in his life.  He comes into your office wearing his USA Olympics weightlifting spandex telling you that ‘his bones hurt.’ You order a CBC and BMP.  CBC shows a hematocrit of 22 and hemoglobin of 6.5.  BMP shows a calcium level of 12, and a creatinine of 5.5.  Two years ago, all his lab values were normal.  What should you order next?
  5. Your favorite patient had a heart attack 6 weeks ago and he comes back to you because he has chest pain again, but this time, it feels different.  It gets worse when he takes deep breaths, and feels better when he sits up and leans forward.  On auscultation, you notice a friction rub.  You get an EKG, which shows PR-depression in all leads except for V1 and aVR.  What is the most likely mechanism of his chest pain?


  1. Penicillin binds and breaks down the bacteria cell wall, while gentamicin binds to ribosomes and inhibits protein synthesis.  Penicillin helps the gentamicin get into the bacteria; they share a synergistic relationship. As a result of bacteria’s resistance to penicllins (altered penicillin-binding proteins), it is harder to kill the bacteria alone.  Penicillin barely binds to the bacteria cell wall, but it makes a small hole.  This hole enables the gentamicin to come in, bind to the ribosome, and kill the bacteria.  Synergistic effect is due to the increase in bactericidal effect and the increase in the rate of killing.
  1. This woman has developed secondary hemochromatosis secondary to multiple blood transfusions for the treatment of her underlying disease, beta-thalassemia.  Secondary hemochromatosis is simply an overload of iron that accumulates in tissues.  This excess iron can deposit in the liver, skin, heart, brain, and pancreas.  In this case, she shows signs of cirrhosis (jaundice, which first shows up in the tongue/ascites/spinder angioma) from deposition in the liver, and glucose intolerance due to beta cell destruction secondary to iron deposition in the pancreas.  These patients are also known as ‘the bronze diabetics’, so look out for someone who has tan skin and diabetes.  The definitive diagnosis is to look at tissue, in this case, get a liver biopsy.  Treatment for most patients is phlebotomy. However, if multiple blood transfusions are absolutely necessary, as in this patient, you can use iron chelating agents.  Also, be aware that almost 1/3rd of hemachromatosis patients with liver symptoms can develop hepatocellular carcinoma.  You remember the serum marker for that?  AFP.
  1. Skeletal survey, alkaline phosphatase, calcium, phosphate, and aminotransferase levels. You will have an elevated level of alkaline phosphatase in the blood in combination with normal calcium, phosphate, and aminotransferase levels in an elderly patient.  Paget’s disease of the bone (Osteitis Deformans) is a chronic disorder results in enlarged and deformed bones.  Initially, the rate of bone resorption is increased due to the large and numerous osteoclasts. These localized areas of osteolysis are seen radiologically as an  advancing lytic wedge in long bones or osteoporosis circumscripta in the skull. On Step 1, the loss of hearing/increase in hat size are very common complaints for Paget’s disease. After osteolysis, a compensatory increase in bone formation is induced by osteoblasts recruited to the area. This results in accelerated deposition of lamellar bone in a disorganized fashion. This intense cellular activity produces a chaotic picture of trabecular bone (“mosaic” pattern), rather than the normal linear lamellar pattern. The resorbed bone is replaced and the marrow spaces are filled by an excess of fibrous connective tissue with a marked increase in the number of blood vessels (hypervascularity). The bone appears as  dense “pagetic bone,” also known as  burned-out Paget disease.
  1. Request protein electrophoresis of the blood and urine, which might show the presence of a paraprotein (monoclonal protein, or M protein) band, with or without reduction of the other (normal) immunoglobulins (USMLE will show you the “M SPIKE picture”). You are suspecting multiple myeloma.  One type of paraprotein is the Bence Jones protein, which is a urinary paraprotein composed of free light chains. Quantitative measurements of the paraprotein are necessary to establish a diagnosis and to monitor the disease. The paraprotein is an abnormal immunoglobulin produced by the tumor clone.  Skeletal surveys will show punched-out bone lesions. Remember the CRAB mnemonic—calcinosis, renal disease, anemia, bone lesions.
  2. Autoimmune. Dressler’s syndrome is an autoimmune pericarditis that occurs 2-10 weeks post-MI.  Step 1 loves this.  Just remember, MI +few weeks later + signs of pericarditis = autoimmune pericarditis.

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