DISORDER
MECHANISM
CAUSES · FEATURES
LABS · TREATMENT
Aplastic anemia
stem-cell failure
Hematopoietic stem cells destroyed (often by autoreactive T cells) → pancytopenia.
Idiopathic (most); drugs (chloramphenicol, benzene, alkylators, carbamazepine); radiation; viruses (non-A–E hepatitis, EBV, HIV, parvovirus in some)
Hypocellular fatty marrow, low retic, no splenomegaly · ATG + cyclosporine, stem cell transplant
DNA crosslink repair defect (autosomal recessive mostly).
Short stature, absent/abnormal thumbs and radii, café-au-lait spots, pancytopenia in childhood
↑ AML and SCC risk; chromosome breakage test
Only erythroid precursors lost.
Thymoma, parvovirus B19 (in hemolytic patients), Diamond-Blackfan (congenital)
Anemia with retic ≈ 0; WBC and platelets normal
Myelophthisic anemia
crowded marrow
Marrow replaced by tumor, fibrosis or granulomas.
Metastatic breast/prostate cancer, myelofibrosis, TB, Gaucher disease
Leukoerythroblastic smear: teardrop cells, nucleated RBCs, immature WBCs
Plasma volume falls; RBC mass is normal.
Dehydration, burns, diuretics
Corrects with fluids
JAK2 V617F → RBC production without EPO.
Itching after a hot shower, plethora, erythromelalgia, splenomegaly, gout, thrombosis (Budd-Chiari)
↓ EPO; often ↑ WBC and platelets · phlebotomy, aspirin, hydroxyurea
Secondary — appropriate
hypoxia-driven
Low tissue O₂ → kidney ↑ EPO.
High altitude, COPD, sleep apnea, cyanotic heart disease, smoking (CO)
↑ EPO, ↓ SaO₂
Secondary — inappropriate
EPO made without hypoxia, or other stimulants.
RCC, HCC, hemangioblastoma, leiomyoma, pheochromocytoma; after kidney transplant; testosterone; EPO doping
↑ EPO, normal SaO₂