To Do

  • Hypermobility disorder
  • AS and TNF inhibitors (Ms Reed - Enbrel, Humira, and now on simponi)
  • CD - ab to all TNF and now on ustezimumabn ? (ms fens) also had psoriasis 
  • SLE and LN ; cyclophosphamide vs cellcept for LN - PLN vs MLN (ms cole)
  • SLE when to stop cell cept (ms cole)
  • SLE flare up vs infection 

  • Procal to differentiate gout vs infectious cellulitis  arthritis  

  • As good as the TNF inbibitors and other biological disease modifying drugs are, when these drugs are stopped, disease flare up. Impying, these are not curative treatment. Better understanding of trigger and stopping it there and then is the curative while we look to check the inflammation with the intervention via TNF inhibitors or other such treatment. 
  • Important to read and understand, why are these intervention curable and take disease to remission in Hematological malignancies. 

Research Questions related to SLE
  • SLE and Immunopathophysiology: Why CRP is increased in few patients and not in others, are they different immuno-pathophysiology i.e end-type vs phenotype? or additional disease process ongoing that we do not recognize fully?
  • SLE and trigger! SLE, not all patients have all ab, some ab confer worse prognosis? is there a different trigger in instances that leads 
  • Do they respond well?
  • Research topic: On patients with Lupus, folks with increased CRP and normal CRP, do they behave similarly on treatment? 
  • TNF inhibitors, presumed mechanisms for DILE is due to blockage of Th1 pathways, and may cause switch to TH2 pathways? What is the mechanism for Pracainamde, Hydralazine?
  • Why SLE, RA, SS cause Fibromyalgia, and not so much in others like SSc, Spondyloarthritis?
  • SLE grants? 
  • How to gain trust?
  • 4 corners
    1. Patient
    2. Disease course
    3. Medicine
    4. Doctor
  • Starting point: Current state 
  • End point : DORIS
  • To reach an endpoint is a not one path, but multiple path with potential for bumpy ride due to 1, 2, 3. Role of doctor is to help navigate the disease 
  • Videos to empower patient about knowledge of SLE 
  • Because C1q directs immune complex to monocyte, if this is defective, then it goes to dendritic cells instead. Hence, malfunction of the C1q to direct immune complex to monocyte may be one of the underlying mechanism of Lupus. By appropriately boosting this interaction, one may be able to CURE Lupus
  • Drugs affecting IFN could selectively target patients by IFN signature or by low complements 
  • Complement medicated disease process like vasculitis have very high CRP, then why in SLE will it be low. Is it to actually do with periodic low complement levels cause more disease flare up than the consumption of complement. ---argument against, competent is deposited in the tissue 

From my reading so far, complement and Lupus are related in so many ways. However, when it comes to complement and CRP, two plausible mechanism exists.

1) One of the ligands that C1q attaches to is CRP (others being surface-bound immunoglobulin (Ig)M and complexed IgG being the main ligands, DNA, microbial components, and apoptotic and necrotic cells). This may be the direct way by which both CRP response and complement pathway may be related in Lupus patients. I will do more reading on this.

3) Various cell that are recruited to the site of complement activation by C3a and C5a may contribute to CRP response.... *** Complement in LN ****

Additional mechanism in Lupus for sure exists in looking for underlying pathogenesis in select patients.

1) C1q also binds to apoptotic and necrotic cells as additional ligands to activate classical pathway to help in opsonization and phagocytosis of these dead cells. By this disposal hypothesis, deficiency of C1q or early complement pathway protein can explain why SLE is so common.

2) C3a, C5a also activate innate immune cells either directly or indirectly

3) Regulation of adaptive immune response: Affects B cells by binding to Complement Receptor (CR2) in the B cells . In addition, CR2 helps to present the antigen to the dendritic cells - and we know dendritic cells are responsible for the IFN signature seen in most of Lupus patients. Additionally, can affect T cells activation by affecting dendritic cells - T cell interaction. Also,

Research in RA
  • Facts: TNF, GM-CSF, and IL-6 can be expressed by Th1 and Th2 cells and are abundant in synovial fluid and produced by RA synovial tissue. However, the primary sources of these cytokines in the rheumatoid joint are macrophages and fibroblasts.
  • Hypothesis: Why TNF inhibitors may not have 100% success and even if had initial success, could fail as other pathway are activated. 
  • Research option: 
    • Sequential treatment option: Guided by genetic signature of these markers.  Initially, the treatment should be focused on the pathway that is expressed most abundantly. Follow up should be towards finding when additional pathways are more pronounced due to one pathway being blocked. When inflammation starts then, direct treatment for that pathway. Which means, initially failed therapy may still be relevant down the line. 
    • Combined treatment: Instead of the high dose of one cell type, combined use of TNF inhibitor + anti- IL 6 and GM-CSF inhibitor may prevent the disease flare up. 
      • This can actually be studied in the labs with use of various dose of TNF-inhibtor and IL-6 combination 
  • Hypothesis: However, so long as the trigger is present, by treating the effector cells response, the autoimmune disease cannot be treated. Treatment should be guided along with this as above towards identifying what the trigger for given patient is and avoid the exposure to it. Only then the inflammatory pathway can be halted. 
  • As good as the TNF inbibitors and other biological disease modifying drugs are, when these drugs are stopped, disease flare up. Impying, these are not curative treatment. Better understanding of trigger and stopping it there and then is the curative while we look to check the inflammation with the intervention via TNF inhibitors or other such treatment.
  • Early aggressive Treatment of TNF inhibitor leads to remission in limited number of patients. Is it because if prevents the continues feedback look for chronic synovitis rightaway or is it because those patients had temporary trigger. Remains unclear.
  • Patients with an inadequate response to a TNF inhibitor can still respond to either rituximab or abatacept, which supports the notion that multiple independent pathways can contribute to the pathogenesis of RA and the heterogeneous nature of the disease. Identifying, right pathway by signature etc could help treat disease rightaway and can prevent damage accrual. 
  • Surprisingly, patients with little or no clinical improvement still have significant delay or arrest of joint damage. This observation supports the concept that inflammation and destruction have distinct pathogenic mechanisms.

To Do:
Association between CPPD and OA  fo
  • CPPD in the absence of OA
  • CPPD in the presence of OA
OA in the setting of 
  • Other inflammatory diseases Gout, CPPD
  • Prior trauma, infection 
  • In the absence of above 
Need to understand 
  • Hyaline articular cartilage 
  • Fibrocartilage 
  • Chonrocytes 
  • Osteoblasts 
  • Osteoclasts 
  • Joint anatomy (RA, OA, Gout, CPPD, BCP etc)

Research topic 

1) Relapsing-remitting, long quiescent, chronic active , mono-phasic - identify the patient in each group 
2) Study the Type 1 IFN signature in each group 
3) Study the CRP level in each group 
4) tnf use in high CRP 


1) How would you build a DDx for Thrombocytopenia?
2) When should BM biopsy be done?
3) What are the 5 causes of increased platelet consumption / destruction? What are the three DDx that requires urgent eval? HIT TTP DIC 
4) Pathophysiology of TTP, HIT, DIC - common to all these three? 
5) Pathophysiology of ITP?  

I) Clinical Practice
1) Pathophysiology 
alcohol metabolism, 
2) Physical Examination 
3) Disease Specific 
Ischemic colitis vs mesenteric ischemia; Leucocoria; Strep gonnadi; Krukunburg tumor; Nausea; Penetrating Ulcer in CD; 
4) Pharmacology 
Risperidone; Seroquel; Steroids; 

II) Research 
1) Medical Student Research
2) Resident Research 


Tenure application MERCER

Pneumonia: Urinary Test
COPD: Not recognizing and starting treatment
Magnesium replacement and recheck
Syncope: No orthostatics BP
Anemia of Bleeding: Stopping Plavix, Ongoing IV fluid
Abdominal Pain: No pelvic exam

EPIC inbasket

  • Heme: Anemia, CLL, AML, Hypereiosinophilic syndrome, 

  • MKSAP Gout: Q 48 BPP, Q59 Duraiton of Colchicine, 93 CPPD diseases causing osteoarthritis  

  • Why does S4 sound occur
    • resulting from a forceful left atrial contraction and movement of blood into hypertrophied LV
  • Screen for secondary HTN
    • < 25  yr 
    • Resistant HTN
  • Low risk factor finding in Stress test
    • Medical management prior to Cath: ASA, Statin, and either BB or CCB and or long acting nitrate 
  • Use of DAPT in a Cardiac patients 

  • Antiplatelet on patient underoing non-cardiac surgery 
2016 ACC/AHA Guideline Focused Update Circulation 2016

  • HFrEF: NYHA 2 or more. If Cr < 2.5  in men and < 2.0 in women, and K < 5, start EPLERENONE 

Diagnosis and treatment of deep-vein thrombosis CMAJ 2006

  • Doxazosin is preferred not to be used in HTN as it makes HF worse as seen in ALLHAT Trial 
  • Pericardial Rub has 3 components 
    • Atrial Systole
    • Ventricular Systole
    • Rapid Ventricular fielding during early diastole 

Endo Topics to Read

1. Identify the causes of Adrenal Insufficiency related to normal aldosterone production?
2. What are the 8 symptoms, 5 signs, and 7 biochemical findings in adrenal insufficiency and their prevalence?
3. Identify the differences in the management of acute adrenal insufficiency vs chronic adrenal insufficiency?
4. What is adrenal escape mechanism?
5. What are the screening and confirmatory tests for conn's syndrome?
6. What are the precautions one should take in interpreting PRA tests results?
7. What are the 6 tests for Pheo, and what is the sensitivity and specificity of each tests and how to decide Possible, likely, unlikely pheo based on lab values?
8. Name drugs that interfere with Pheo assays and in what ways?
9. What is the typical radiological findings of Pheo?
10. Name 3 Pheo syndromes?
  1. Student and resident eval
  2. Complete EPIC deficiencies
  3. Green Card (follow up)
  4. Financial Planning 
  5. Research
Noon Conference Lecture Topics
  • Borderline Personality Disorder: Case example from EPIC
  • Insomnia: Case example from Epic
  • Cryptogenic Stroke
  • Any Stroke
  • CAD and CABG
  • HTN and Hyperlipemia
  • any Sepsis 
  • EBM 2 lecture series
  • Allergic Rhinitis 
  • Asthma 
  • postmenopausal symptoms 

HIV Study : To IRB

MKSAP and Boards Score, and ITE Performance: Nick

ME Prevention Study:Inhospital
H and P:

A and P:
Diagnostic Error: Outpatient including obesity
EBM study 
Patient focused paper, vs any good paper of the week 

Increased Globulin. Normal SPEP, S IFA increased IgG, Normal FLC 
ALP increase.
CRP, ESR increased. 
Decreased Testesterone, but normal hcg
RPR reactive, FTA-ABS reactive.
Resistant HTN 
Transverse Myelitis 
Rapidly progressive Dementia vs Pseudodementia vs Vasculitis (elevated CRP and ESR)
Salmonella Bacteremia (species unknown)
Multiple Sclerosis
Intractable N and V 
Fungal Calcification 

Mechanism of Polyuria with Hyperkalemia
MM - IL1 mediated osteoclast activation
Lymphoma - causes direct activation of 1,25 hydroxylase (unlike due to macrophages in granulomatous disease)
Where is 1-alpha hydroxylase located in Kidney that PTH acts on? 

NAFLD vs Hep to differentiate ?
PFT - bronchodilatation..Albuterol or anti-cholinergic combination?
Insomina - Ambien vs Restoril ?  
Leg Cramps 

Question to ask to any heme-onc physician?

What to order when doing Flow Cytometry?
1) in a patient with leukocytosis? 
  • Concern for CLL, 
  • Concern for AML, or ALL
2) in  a patient with M-spike present in SPEP, or FLC?

Live Vaccines
Adeno virus (military only)
Rota virus
MMRV (varicella)
Herpes Zoster 

Disease to be monitored in a patient with RA on treatment 
Skin cancer (non-melanoma)
Lymphoproliferative Disease
Hep B and Hep C