6/20/16: Multiple Sclerosis

  • Recognize the risk factors for MS:
    • Age: typically younger (20-40 years old)
    • Female > Male (3:1)
    • Family History of MS
    • Infections (EBV)
    • Race – white, northern European decent
    • Smoking
    • Autoimmune disease
    • Northern hemispheres (potentially related to lack of sunlight / vitamin D deficiency)
  • Remember the THREE TYPES OF MS:
    • Primary progressive (Green)
    • Relapsing/Remitting (Blue)
    • Secondary progressive (Red)


Lhermitte Sign: a shock-like sensation radiating down the spine or limbs induced by neck movements.

Uhthoff Phenomenon: worsening MS symptoms with increased body temperature.

  • Diagnosis requires the evidence of CNS demylenation in BOTH SPACE AND TIME.
  • Remember the common eye findings with MS:
    • Optic neuritis: occurs in 50% of MS patients and is the presenting symptom in 20-30%
    • MLF syndrome: inability to adduct the affected eye; opposite eye can experience nystagmus
    • Marcus Gunn Pupil (afferent pupillary defect): inability of the affected eye to constrict when light is shown
  • Oligoclonal bands IgG on LP
  • Treatment regimen:
    • Routine: physical activity, vitamin D/calcium, routine vaccinations, smoking cessation
    • Acute: high dose steroids (typically 1 g/day for 3-5 days)

6/15/16: Acid/Base Problems

For Acid Base Disorders:

  • Check for internal consistency
  • Use pH to determine the primary disorder
  • Calculate the AG
  • Determine the presence of additional disorders
  • Calculate the expected pCO2 for any metabolic acidosis to evaluate for additional respiratory acidosis.

Winter’s Formula: expected pCO2 = 1.5 (HCO3) + 8 +/-2

  • Remember vagal maneuvers for SVT: carotid massage, valsalva, diving reflect
  • Remember the trial of DKA:
    • Hyperglycemia
    • Anion Gap Metabolic Acidosis
    • Ketonemia
  • DKA management:
    • Fluids: usually 3-6L deficient
    • Insulin: 0.1 U/kg bolus followed by a rate of 0.1 U/kg/hr; adjust as needed
    • Electrolytes: watch for K and phosphate – typically appear normal initially, but are actually “total body” deplete – likely to drop quickly with insulin administration

6/1/16: Adrenal Insufficiency

  • Remember the layers of the adrenal anatomy and the corresponding hormones produced:

Glomerulosa: Mineralcorticoids (i.e. aldosterone)

Fasciculata: Glucocorticoids (i.e. cortisol)

Reticuloaris: Adrenal Androgens (i.e. testosterone

Chromuffin Cells: Epinephrine

  • Remember the ANTERIOR products of the pituitatry gland: (FLATPEG)








  • Remember the two hormones of the POSTERIOR pituitary:



06/30 Neutropenic fever Morning Report



>38.3 fever or >38 sustained for one hour
-ANC<500 or ANC expected to decrease <500 within 48 hours

Empiric therapy (give as soon as possible for neutropenic fever, <30-60 minutes)

1)Cefepime 2 gm IV q8h
2)Meropenem 1 gm q8h (or other carbapenem but NOT Ertapenem as misses pseudomonal coverage)
3)Zosyn 4.5 g IV q6-8h
4)Ceftazidime 2 gm IV q8h (less often used due to resistance patterns)

*If concern for anerobic infection, can add Flagyl to Cefepime or if suspecting C.diff
*No proven benefit to one empiric therapy over another

When to add Vancomycin to empiric therapy

1)Severe sepsis/HD unstable
3)MRSA colonization
4)Suspected CVC related infection
5)Previously on Quinolone prophylaxis
6)Skin/soft tissue infections
7)+ BC for GPC

*Can consider discontinuing Vancomycin if negative cultures x 48 hours

How long to treat for with empiric therapy?

-(generally) continue antibiotics until ANC>500 and afebrile if no culture data
-If culture data, treat x 14 days

06/27/16 Morning Report-Factor 8 inhibitor


How do approach elevated PT/INR, or PTT of unknown etiology

-Do Mixing study to see if it corrects (deficiency) or doesn’t correct (inhibitor)
-PT=Play Tennis OUTSIDE=Extrinsic pathway
-PTT=Play Table Tennis INSIDE=Intrinsic pathway
-Most common inhibitor is Factor 8 inhibitor causing elevated PTT

Causes of elevated PTT

-Involves Factor 8, 9, or 11
-Iatrogenic causes include heparin, LWMH
-Lupus anticoagulant (usually presents with thrombosis)

Risk factors for developing a Factor inhibitor

-Pregnancy, post-partum, RA,  malignancy, SLE, some drug reactions (Phenytoin/Penicillin)


-Control bleeding (done via activated prothrombin complex concentrate like FEIBA or recombinant human factor VIIA)
-Eliminate inhibitor via immunosuppression (steroids +-rituximab +-Cytoxan)