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 -2  (step2ck_form8#38)

This was a poorly worded question – the underlying mechanism of the child's condition is narrowing of the aorta, causing backup into the heart and upper body. If they wanted to get at why it presented after 3 days instead of immediately, maybe just maybe they should've asked that instead.

Subcomments ...

submitted by step_prep(48),
  • Young woman presenting with neurological symptoms separated in time and space, including L’hermitte’s sign (electric-like sensation with neck flexion) and optic neuritis (unilateral painful vision changes/loss) with a brain MRI showing multifocal, ovoid subcortical white matter lesions in a periventricular distribution most consistent with multiple sclerosis
  • Key idea: Multiple sclerosis is treated chronically with immunosuppressants, but an acute MS flare (such as this patient) should be treated with glucocorticoids, interferon beta or plasmapheresis

spiroskeet  This patient is currently asymptomatic, which is why treatment for her should be IFN-β (or glatiramer or natalizumab). If she still had symptoms of an acute MS exacerbation, treatment would consist of corticosteroids (i.e., dexamethasone/methylprednisolone). If symptoms persist in spite of steroids, she should undergo plasmapheresis. +2  

submitted by step_prep2(17),
  • Infant with sickle cell disease presenting with sepsis (fever, clear rhinorrhea, lymphocytosis), which is most likely caused by Strep pneumo and can be effectively treated with ceftriaxone
  • Key idea: Sickle cell disease leads to functional asplenia, which leads to increased risk of encapsulated infections (SHiN: Strep pneumo, Haemophilus influenzae, Neisseria meningitidus)
  • Key idea: Although daily penicillin prophylaxis decreases the risk of Strep Pneumo infection, it does not completely eliminate the risk

seagull  I would make a different argument. Because the infant is covered by Penicillin the pneumonia is likely gram negative. We don't have imaging to see the lung parenchyma but I would like to cover pseudomonas (ceftriaxone has partial coverage). Lastly, Ciprofloxacin given orally isn't likely to be done for inaptient (it would need to be an IV medication here). Also Cipro isn't a respiratory floroquinolone unlike moxifloxacin, gemifloxacin and levofloxacin. +1  
spiroskeet  Also, fluoroquinolones are contraindicated in children (tendinopathy) +  

submitted by step_prep2(17),
  • Young man who presents with inflammatory back pain (worse in the morning but improves over course of the day) who has limited range of motion of the back (consistent with “bamboo spine” physiology), all of which is most consistent with ankylosing spondylitis that can be diagnosed with x-ray or MRI of the sacroiliac joints
  • Key idea: Indications for x-ray in setting of low back pain is (1) Osteoporosis or compression fracture (2) Suspected malignancy (3) Ankylosing spondylitis
  • Key idea: Indications for MRI in setting of low back pain is (1) Sensory/motor deficits (2) Cauda equina syndrome (3) Suspected epidural abscess or infection

seagull  THe question said initial step. I thought this was a clinical dx that required elevated ESR, CRP. In reality we would order these and have him get an x-ray. I'm not sure if we can reliably dx Ankylosing Spondylitis unless we have the ESR unless the x-ray clearly shows that bones are fusing. THis is a younger guy too. +  
kingfriday  There was a uworld question that mirrors this if you use the search function you can probably find it. The reasoning they had there said that acute phase markers are usually elevated in AS but they have low specificity for establishing the dx. BONE SCAN - not good for AS, but it is good for osteomyelitis, suspected fractures, and neoplasms > MRI indicated for neurological s/sx +  
spiroskeet  Just found that UWorld question – it asked which would be most likely to establish a diagnosis in the patient. In that case, X-ray of SI joints is the right answer. However, the NBME question asked for initial step. My first step would probably be to order an ESR. It's nonspecific, but ESR is pretty much always nonspecific, so why would you ever order it? +  

Clue cells = gardnerella = grayish discharge and does change pH (>4.5)


  • Ferning = pregnancy / rupture of membranes, but she does not have male partners, so less likely

  • Budding yeast = candida = grayish, but does not change the vaginal pH (<4.5)

  • leukocyte sheets = ? Maybe erosive lichen planus / lichenoid vaginitis ?

  • Trich = green discharge, does change pH (>4.5)[6]/0/

spiroskeet  Reason for pH >4.5 is that Gardnerella outcompete Lactobacilli fauna, which (as their name implies) pump out acid +  

submitted by russnels(14),

Anything else here pointing to Fat Embolism Syndrome other than the long bone fracture? Is "fluffy infiltrates" pathognomonic for FES? Why could it not also be ARDS?

hambone  two things: 1) petechial hemorrhages 2) will see respiratory alkalosis in fat embolism, and metabolic acidosis in ARDS +  
komodo  i was also torn on this one because their PaO2/FiO2 is low (267), which I think technically qualifies as ARDS, especially with the fluffy infiltrates. I think the petechiae is the main thing that points to fat embolism over ARDS +  
spiroskeet  Also worth keeping in mind that, according to UWorld, the petechial rash doesn't necessarily always present in fat embolism syndrome. However, if it does present along with the rest of the clinical picture, it's a dead ringer for FES. +