1. Upper lobe lesions in the lungs
– Aspiration while supine: rapid onset, very sick patients
– TB: chronic course
– Primary cancer: usually one lesion
– Mets: uncommon, these tend to occur more in the lower lobes where there is better more blood
– Histo, blasto.
– Aspergillus fungal ball.
2. Rheum to grow: 
– Ankylosing spondylitis: primarily involves the apophyseal (= facet) joints.
– Arthritis pain that occurs in a young person, symptoms occur at night, and improve with exercise => think inflammatory arthritis. (most injury or degenerative arthritis is worse with exercise, improve with rest and doesn't have nighttime symptoms)
– Manage lupus with limited skin and joint involvement with hydroxychloroquine. Do eye exams q6 months as this drug may cause retinopathy or corneal damage.
– Dermatomyositis is associated with an increased risk of internal malignancy. Up to 10% of people with adult onset DM will develop malignancy. DM is six times more common in women than men. The most common cancers are ovarian, breast, lung, uro-gyn malignancies
– Treat inflammatory polymyopathies with high dose steroids
– Treat reactive arthritis with NSAIDs

- Stills disease: maculopapular rash that occurs on the trunk and extremities that coincides with fever and joint pain

3. Complications of rheumatologic disease 
– Aortic aneurysm: behcets, Takayasu, giant cell, the seronegative spondyloarthropathies notably AS, RA
– Renal failure: Wegener's, lupus, Goodpasture's, HSP, PAN, Scleroderma
– Alveolar hemorrhage: churg Strauss, Goodpasture's, wegners, behcet
– Pulmonary fibrosis: dermatomyositis, scleroderma
– Carpal tunnel: sarcoid, amyloidosis, RA (can also happen in hypothyrodism)
– Mononeuritis multiplex: Churg Straus, PAN, Wegener's, lupus, amyloid,sarcoid,  cryoglobulinemia, RA
4. Amyloidosis
– Primary AL, secondary AA - Chronic Inflammatory state like RA, IBD, chronic infections (Bronchiectasis, osteomyelitis, TB), Cancer, vasculitis
Manifestations:
– Cardiac - hypertrophy without change in chamber diameter
– Renal: nephrotic syndrome
– Neuropathy : Autonomic (orthostatic hypotension), peripheral neuropathy (carpal tunnel syndrome)
– Hepatomegaly
– Other organ enlargement like macroglossia
– Waxy skin
– Easy bruising/bleeding diathesis
– Colchicine is used in the prophylaxis and treatment of AA amyloidosis
5. Stuff that crystallizes in your kidney tubules 
- Acyclovir
- Protease inhibitors (indinavir)
- Ethylene glycol (ca-oxylate crystals - envelope shaped crystals)
- Sulfa drugs
- Methotrexate
- Stuff that gives you AIN - B lactams, PPIs, usually takes 7-10 days
6. More renal stuff 
– Nephrotic GN: Membranous, diabetes, IgA, Amyloidosis, minimal change, FSGS
– Mild Nephritic GN: thin basement membrane syndrome, IgA, lupus
– Moderate/severe Nephritic GN: Post strep/infectious, membranoproliferative, lupus, vasculitis,  RPGN
– If a patient with pyelo does not respond after 48-72 hours of appropriate antibiotics, urologic imaging (CT or ultrasound) is indicated to look for complicating pathology like an obstruction or abscess
– Hypertensive nephropathy: characterized by increased pressures, leading to nephrosclerosis, that is, fibrosis of the renal arterioles, progressing to sclerosis of the glomerular capillaries
– Diabetic nephropathy: characterized by increased filtering, leading to increased extracellular matrix, thickening of the glomerular basement membrane, and mesangial proliferation
– Analgesic abuse nephropathy: characterized by focal glomerulosclerosis. Its a tubulointerstitial disease. Additionally analgesia mediated vasospasm of the vasa recta => papillary necrosis resulting in painless hematuria. On UA the red cells appear normal, in contrast with glomerular sources of bleeding where the red cells appear dysmorphic. The bleed can be significant to where the blood clots will cause renal colic.

- Acetylcysteine has been shown to decrease IV contrast nephropathy, perhaps because of its antioxidant and vasodilatory properties 

- Goodpasture's disease: you make anti-glomerular basement membrane antibodies. Treat with immediate plasmapheresis to prevent renal injury. 

- Treat Wegener's with cyclophosphamide and steroids

- Prednisone can cause fluid retention in people with renal failure 

7. Everybody loves ID 
- Treat bartonella henselae with five days of Azithro
- Influenza can cause proteinuria and leukopenia - there's data that h5n1 virus destroys lung epithelial cells and leukocytes in replication.
- Viruses that cause myocarditis: Coxsackie B, adeno, entero, parvo, HHV-6
- Colitis and pneumonia one month post bone marrow transplant: think CMV. Diarrhea and other GI symptoms caused by ulcers.
- Hepatitis B initially goes through an immune tolerant phase where the virus replicates; AST and ALT are low, HBV DNA and E Antigen are high. Then there is an immune clearance phase where the body starts to attack infected hepatocytes. ALT rises, biopsy shows inflammation in the liver, and markers of Hep B Infection ( E antigen and viral load) fall during this. Follow ALT and HBeAg q3-6 months to ensure total clearance.
Palm and sole rash:
- syphillis secondary and congenital (copper)
- RMSF (outside in) and typhus
- Kawasaki, TSST, measles (peeling)
- coxsackie A / hand foot mouth
Others: contact dermatitis, lupus, erythema multiforme
8. Measles (rubeola) vs rubella  
- both have same prodrome - cough, conjunctivitis, coryza, lymphadenopathy
- measles has higher fever > 40
- rash moves from head down, fast in rubella, slow in measles
- rubella associated with arthritis in women older than adolescent age (not men or children)
9. CML versus leukemoid reaction
– Both = leukocytosis with marked left shift
– Leukemoid reaction is a response to severe infection / Inflammation
– Leukocyte alkaline phosphatase is the critical distinguishing factor. It will be elevated in leukomoid but decreased in CML
– CML blast crisis is where CML behaves like AML: > 20% blasts on peripheral smear
10. GI stuff 
– Melanosis coli: Brown Stained colon with white patches representing Lymphoid tissue, 2/2 Dulcolax/Bisacodyl (ab)use
– GI angiodysplasias are often diagnosed in the setting of acquired coagulopathy, such as acquired von Willebrand disease (aortic stenosis => shearing of large VWF multimers) or uremic platelet dysfunction 2/2 ESRD
– Hemolytic anemia + acute onset transaminitis and ascites: think PNH. PNH predisposes to venous clots, particularly in hepatic veins.

- Chronic portal vein thrombus can present as varices