Common definitions:

Dysphagia: difficulty swallowing

Odynophagia: pain with swallowing

Globus sensation: lump in throat; non-painful

• Remember the breakdown between OROPHARYNGEAL and ESOPHAGEAL

• 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)

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

• 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)

FSH

LH

ATCH

TSH

PROLACTIN

ENODORPHINS

GH

• Remember the two hormones of the POSTERIOR pituitary:

Oxytocin

ADH

TAKE HOME POINTS 

Diagnosis

>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
2)Pneumonia
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

TAKE HOME POINTS 

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)

Treatment

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

Teaching Pearls

• Aeromonas is a Gram Negative Rod and is the third leading cause of SBP in Korea
• It causes a warm season diarrheal disease
• Remember the three indications for SBP prophylaxis:
  • History of SBP, lifelong prophylaxis
  • Cirrhosis with GI Bleed, 7 days of prophylaxis
  • Ascitic protein < 1, prophylax while inpatient
• Don’t forget to give Albumin 1.5grams/kg on Day 1 and 1.0gram/kg on Day 3 for patients with SBP
• Remember to think about secondary bacterial peritonitis (from intestinal perforation, PUD) in the differential for SBP
• Check out this review on AeromonasSBP!

• Cryptococcosis is treated with Flucytosine, Ambisome for 2 weeks of Induction, and the Fluconazole for maintenance
• Include Bacillary angiomatosis on the differential for Kaposi’s Sarcoma
• Fungal infections can be due to Yeasts, Molds, or Dimorphic Fungi
  • Yeast: Think Single Celled Organisms, Candida and Cryptococcus
  • Mold: Think Filamentous with Hyphae. Aspergillus,  Mucor
  • Dimorphic Fungi: Can be both yeast or molds depending on the Temperature. Includes Histo, blasto, cocci
• We didn’t get to this today, but here is a framework for organizing anti-fungal medications!

• Think about calciphylaxis in your ESRD patients with non-healing ulcers in areas of adiposity (abdomen, buttocks, thighs, legs)
• Biopsy shows arterial calcifications without vasculitis
• Often associated with elevated PTH levels and elevated calcium-phosphorous product, hypoalbuminemia
• Check out this UCSF resident hand-out on calciphylaxis!
• We had a great review of features of chronic venous stasis including lipodermatosclerosis (inverted champagne bottle), atrophie blanche, telangiectasias, ulcerations on the medial ankles.
• See the table below for comparison/contrast of arterial versus venous ulcers

Teaching Pearls

• Think TB and malignancy in the differential for lymphocytic exudative pleural effusions
• Right sided unilateral exudative effusion in a foreigner/traveler – consider entameoba histolytica, echinococcus, paragonimus
• Pleural Color
  • Pale Yellow –> Transudate
  • Red/Bloody –> Malignancy
  • White –> chylothorax
  • Brown –> long standing bloody effusion, amoebic liver rupture “anchovy paste”
  • Black –> fungal infections
  • yellow-green –> Rheumatoid pleurisy
• Rheumatoid pleurisy and complicated parapneumonic effusions cause the lowest pleural glucose
• The yield of pleural fluid culture is low, pleural biopsy yield for TB is ~90%