1.Hemochromatosis arthritis presents clinically like RA but radiographically like OA
- Clinically: affects MCP, wrist, hip, knee (MCP and wrist are rarely affected in OA)
- Radiographically: osteophytes and join space narrowing (not seen with RA)
2. Inclusion body myositis
- ANA negative asymmetric inflammatory myositis in a middle aged man - think this
- affects distal and proximal muscles.
- usually symmetric but asymmetric in up to 15% of cases
- chronic and insidious course
- usually do not have extramuscular/systemic manifestations or symptoms.
- almost always ANA negative
3. Polymyositis
- Weakness of proximal muscles
- Acute or subacute course
- Frequently has extramuscular manifestations
- usually ANA+
4. Joint aspirate white count
<200 : normal
200-5000: gout
5,000-50,000: pseudo gout
>50,000: septic joint until proven otherwise, start broad spectrum antibiotics
5. Fluids in sickle cell patients

This quote below is from a “consult the expert column” in the Sickle Cell Newsletter for December 2008  http://listserv.emory.edu/cgi-bin/wa?A2=ind0812&L=sicklecell&T=0&P=70  (The Sickle Cell Information Center, PO Box 109, Grady Memorial Hospital, 80 Jesse Hill Jr Drive SE, Atlanta, GA 30303). 

“evidence comes from the 60, 70, and 80s…The principle is simple and based on the biochemistry of sickle hemoglobin polymerization and physiology. The rate of hemoglobin polymerization (sickling) is strongly dependent on the concentration of hemoglobin in the solution. This is exponential with the rate changing with the 25th to 35th power of the hemoglobin concentration. This means that sickling of intact sickle cells is very dependent on the concentration of hemoglobin within the red cell (MCHC)…..

         There are many other very important considerations. Almost all adults and most children with sickle cell anemia have renal tubular damage which prevents them from retaining free water. They cannot concentrate their urine so the loose large volumes of free water in the kidneys every day. The kidneys handle sodium normally and because of the anemia, they then to hold on to sodium they take in. When the patient becomes ill, they often decrease their intake of fluids and become free water dehydrated which greatly increases the sickling of their red cells and the potential for complications...sodium level will be 145 or higher when they come in crisis and 130 to 135 is ideal for reducing sickling without side effects.

             [a possible complication of normal saline?]  The third problem is the misconception about blood volume. Normal saline is used is a rehydrating solution because most dehydrated patients have reduced blood volume. Because of the chronic life-long anemia, the blood volume in sickle cell patients is normal or increased. This has been measured but the studies are old.  Administration of normal saline is potentially very dangerous in sickle cell patients during complications. Their plasma volume is increased, they have high cardiac demand from the anemia, and we are administering opiates that decrease cardiac output. Sodium will be retained and normal saline may precipitate heart failure.

             Very young children and individuals with Hb SC and Sbeta thalassemia may have less renal damage and be better able to retain water. Individuals with renal disease also may become hyponatremic with D5W. The best solutions for them are d5w ¼ normal or 1/3 normal saline.  I feel the best approach is to use one of the three and monitor the serum sodium, rather than to give a physiologically inappropriate replacement fluid (normal saline).

            There is no large clinical trial that directly addresses the issue.  The first reference is Guy et al In vitro and In vivo effect of hypotonic saline on the sickle phenomenon. Amer J Med Sci 266:267-277, 1973. It is also addressed indirectly in the article by Rosa et al in New Engl J Med 303:1138-1143, 1980. I don't think there will be further studies because people either believe the dogma and would consider it unimportant and unethical or such a small benefit off low cost so it is not important enough to spend the money required to test the hypothesis. There are recent attempts to capitalize on this effect by chronically decreasing the MCHC: chlotrimazole, Magnesium, and others. The studies on this are in process…"

    James Eckman, MD and Lewis Hsu, MD PhD

6. Coag negative staph

-Considered low virulence organisms
-Coagulase binds prothrombin and forms staphylothrombin, which is capable of cleaving fibrinogen to fibrin (just like thrmobin...) This fibrin coats the bacteria and makes them resistant to phagocytosis, which is why they are believed to be more virulent.
7. Staph hemolyticus: 
-Coag negative staph (CONS)
-More virulent than other CONS, perhaps because they make hemolysin (hemolysins are able to lyse RBCs to gain iron, often a rate-limiting nutrient for bacterial growth. An in vitro study of e.coli a-hemolysin from the early 1980s was shown to cripple leukocytes, significantly reducing phagocytosis and chemotaxis). http://www.ncbi.nlm.nih.gov/pmc/articles/PMC347633/
-Can cause meningitis, cellulitis, prosthetic joint infections, bacteremia, and rarely, endocarditis (http://www.ncbi.nlm.nih.gov/pubmed?cmd=retrieve&list_uids=17141458&dopt=abstract).
-Known for their remarkable resistance patterns-- commonly R to methicillin, clindamycin, cephalosporins, macrolides, tetracyclines, sulfonamides, fluroquinolones, and even glycopeptide antibiotics (vanc, teicoplanin), which most staph bacteria are susceptible to.
-From a Japanese group that sequenced the entire genome: "A comparative analysis of the genomes of S.haemolyticus, S.aureus, and S.epidermidis elucidated differences in their biological and genetic characteristics and pathogenic potentials. We identified as many as 82 insertion sequences in the S.haemolyticus chromosome that probably mediated frequent genomic rearrangements, resulting in phenotypic diversification of the strain. Such rearrangements could have brought genomic plasticity to this species and contributed to its acquisition of antibiotic resistance." Takeuchi F et al, Whole-genome sequencing of staphylococcus haemolyticus uncovers the extreme plasticity of its genome and the evolution of human-colonizing staphylococcal species. J Bacteriol. 2005 Nov;187(21):7292-308.
 8. Interstitial lung disease DDx: 
- Idiopathic
- Sarcoid
- Pneumonitis (birdkeeper's lung, etc)
- Occupational: beryllium, coal dust,
- Rheum: mixed connective tissue disease!! (hence why people need regular PFTs after this diagnosis) scleroderma
9. Other facts about ILD: 
- Hear fine rales on exam "velco rales"
- Aspergillus balls can grow in the spaces left over after honeycombing
10. Basal Bolus insulin > sliding scale 
Umpierrez GE, et al Randomized study of basal-bolus insulin therapy in the inpatient management of patients with type 2 diabetes (RABBIT 2 trial). Diabetes Care. 2007 Sep;30(9):2181-6.
RESEARCH DESIGN AND METHODS:
We conducted a prospective, multicenter, randomized trial to compare the efficacy and safety of a basal-bolus insulin regimen with that of sliding-scale regular insulin (SSI) in patients with type 2 diabetes. A total of 130 insulin-naive patients were randomized to receive glargine and glulisine (n = 65) or a standard SSI protocol (n = 65). Glargine was given once daily and glulisine before meals at a starting dose of 0.4 units x kg(-1) x day(-1) for blood glucose 140-200 mg/dl or 0.5 units x kg(-1) x day(-1) for blood glucose 201-400 mg/dl. SSI was given four times per day for blood glucose >140 mg/dl.
RESULTS:
The mean admission blood glucose was 229 +/- 6 mg/dl and A1C 8.8 +/- 2%. A blood glucose target of <140 mg/dl was achieved in 66% of patients in the glargine and glulisine group and in 38% of those in the SSI group. The mean daily blood glucose between groups ranged from 23 to 58 mg/dl, with an overall blood glucose difference of 27 mg/dl (P < 0.01). Despite increasing insulin doses, 14% of patients treated with SSI remained with blood glucose >240 mg/dl. There were no differences in the rate of hypoglycemia or length of hospital stay.
CONCLUSIONS:
Treatment with insulin glargine and glulisine resulted in significant improvement in glycemic control compared with that achieved with the use of SSI alone. Our study indicates that a basal-bolus insulin regimen is preferred over SSI in the management of non-critically ill, hospitalized patients with type 2 diabetes.