1. Reactive thrombocytosis 
- Platelets are an acute phase reactant - you will see them up in infection, inflammation
- Bleeding - platelets generally go up in bleed; they only go down in profound hemorrhage s/p many many units of transfusion
- Iron deficiency
- Cancer
- Splenectomy (transiently will go up over 1,000.000) - sickle cell patients tend to run high because of autoinfarction of spleen, 5 or 600,000
- These conditions rarely push your platelets above 1,000,000
2. Primary thrombocytosis 
- You will see numbers >1-1.5 million
- Essential thrombocythemia
- Polycythemia vera
3. RBC mass 
- 71 mL/kg is the normal blood volume.
- 29-33 mL/kg is the normal RBC mass
- Fick principle - take aliquot of blood label with chromium 51, inject back, then take another aliquot, measure chromium 51, then you can determine the total rbc mass.
4. Reactive erythrocytosis
- You expect to see decreased epo
- Chronic hypoxemia (COPD, R to L cardiac shunt etc)
- Renal (RCC, PCKD)
- Hepatocellular CA that makes epo
- Chronic carbon monoxide poisoning (ie smokers) - can get a CO test
- Some inherited Hb mutations that cause left shift of your oxyhemoglobin disassociation curve, so you've got a relative hypoxemia.
5. Primary erythrocytosis 
- Expect to see increased epo
- P.Vera (High rbc, wbc, platelets, big spleen)
6. Reactive left shift (i.e. infection)
- Reminder cell line progeny: Blasts -> promyelocytes -> myelocytes -> metas -> bands -> polys
- Polys and bands will be way up, occasionally metas and myelocytes will be up a bit but you will almost never see promyelocytes or blasts.
- NO changes in eos and basos.
- Changes you will see in the polys-- toxic granulation, vacuolated neutrophils, dhole bodies (typically sepsis, sometimes G-CSF recipients)
7. CML left shift
- You'll see a more disorderly left shift
- Some polys, less bands, few metas, tons of myelocytes, lots of basos, increased eos, some promyelocytes and blasts.
- Neutrophils are pale, NOT toxic granulations. Work perfectly well, no infection risk so long as you have enough polys.
8. Myelodysplastic vs myeloproliferative
- Myeloproliferative - you make more cells, but the cells are functional. Look in the BM- all wbc, its CML, all cell lines up, its P.vera. Myelofibrosis ia type of myeloproliferative-- clonal production of megakaryocytes that elaborate cytokines (particularly FGF) induce filling of the marrow with fibroblasts, collagen.
- Myelodysplastic- you make a lot of cells, but the cells don't work well; your marrow is full of wbc but you're still getting infections. <20% blasts is MDS, >20% blasts is AML.
9. Phosphodiesterase inhibitors
- Nonselective: caffeine, theophylline, IBMX
- PDE 3 inhibitors: milrinone, cilastazol, imarinone, enoximone.
- PDE 4 inhibitors: rolipram, ibudilast, roflumilast
*PDE4 is in immune cells, so PDE4-I are often used as anti-inflammatories esp in people with inflammatory lung diseases (asthma, copd)
- PDE 5 inhibitors: dipyridamole aka persantine, all the viagra-type drugs (sildenafil, tardalafil, etc)
- PDE 10 inhibitors: papaverine (opium alkaloid antispasmotic). Treats GI/ureter spasm, can induce smooth muscle relaxation in coronary and cerebral vessels (has been used to treat subarachoid hemmorhage, angina). Can be directly applied to blood vessels in microsurgery to relax them to facilitate vascular anastomoses.
- Also, forskolin is an Adenylyl cyclase activator.
10. Prinzmetal's angina
- Tends to occur at the same time every day; often between the hours of midnight and 8 AM.
- Diagnosed clinically but can also be diagnosed with ergonovine infusion in cath lab
- Tx with calcium channel blockers