clin med
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| Hypoproliferative Anemia | 90% production problem (bone marrow fails to respond to anemia)
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| Hyperproliferative Anemia | bone marrow is not able to compensate for blood loss or destruction by ramping up rbc production
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| Microcytic Anemia | decreased rbc production ; severe due to either iron deficiency or thalassemia (also chronic inflammation or sideroblastic)
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| Normocytic Anemia | decreased rbc production
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| Macrocytic Anemia | decreased rbc production; severe is either B12 or folate deficiency or occ MDS
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| Thalassemia | hereditary disorders which affect the production of globin chains (alpha or beta)
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| Alpha Thalassemia | due to gene deletion causing a reduction in alpha chain synthesis (severity depends on how many deletions)
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| Beta Thalassemia | due to gene mutations which cause rbc membrane damage which can lead to hemolysis
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| Iron Deficiency Anemia | most common cause of anemia; diet (foods, caloric intake, absorptive capacity, increased loss*, increased requirements)
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| Anemia of Chronic Disease | liver disease, acute or chronic infection (HIV), chronic inflammation, hypothyroidism, renal disease(hypertensive/diabetic), cancer (could be result of reduced erythropoietin stimulation)
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| Sideroblastic Anemia | Enzyme disorder in which body has adequate iron, but is unable to incorporate it into Hgb (iron accumulates in mitochondria of rbc); can be inherited, acquired or idiopathic
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| B12 Deficiency | B12 must come from diet (2000-5000mcg of stored B12 in liver so takes 3+ yrs to become deficient); inadequate intake, malabsorption* (intrinsic factor, gut or Rx); pernicious (familial)
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| Folate Deficiency | total body stores are 5-20mg so deficiency can occur in a matter of months; inadequate intake*, increased requirements, malabsorption, impaired metabolism; Rx interactions
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| Pure Red Cell Aplasia | rare; either idiopathic or acquired; autoimmune disease mediated by T cells or rarely IgG antibody; thymoma, lymphoid malignancies, solid tumors, SLE, RA, infections, medications
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| Aplastic Anemia | bone marrow failure bc of injury or suppression of hematopoietic stem cell; acquired (Rx, chemo, radiotherapy, chemicals, viruses, preggers, lupus, gvhd); hereditary rare; idopathic*
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| Hemolytic Anemias | rbcs are destroyed either episodically or continuously; anemia results when bone marrow is not able to keep up with rate of destruction; cause of destruction is either due to an intrinsic defect or some external factor
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| Hereditary Spherocytosis | inherited abnormality of rbc membrane (molecular defect in spectrin protein)
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| Paroxysmal Nocturnal Hemoglobinuria | acquired stem cell disorder making rbc membrane prone to lysis by complement (due to lack of special proteins)
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| Glucose 6 Phosphate Dehydrogenase Deficiency | hereditary enzyme defect causing episodic hemolytic anemia related to oxidative stress; X linked recessive (200 million affected worldwide)
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| Sickle Cell Disorders | Hgb S; autosomal recessive; onset in first year of life when Hgb F levels fall; avg life expectancy 40-50 yrs; trait have no anemia
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| Autoimmune Hemolytic Anemia | acquired disorder which IgG autoantibody formed that binds to rbc membrane and causes destruction in spleen and liver; 50% idiopathic; occurs at all ages
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| Cold Agglutinin Disease | acquired hemolytic anemia due to IgM autoantibody; only reacts at temperature lower than 37degreesC; IgM binds with complement which causes destruction of rbc within liver; most idiopathic
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| Neutropenia | bone marrow disorder or peripheral disorders
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| Polycythemia Vera (PCV) | myeloproliferative disorder; increased rbcs resulting from a clonal multipotent hematopoietic stem cell defect; primary: true increase, secondary: increase due to another condition such as hypoxia, renal disease, MI's, dehydration..
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| Thrombocytosis | increased sensitivities to cytokines which stimulate bone marrow cell proliferation and growth; decreased inhibition of plt inhibiting factors; defects in cellular microenvironment; JAK-2 mutations
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| Myelofibrosis | cause unknown; bone marrow is replaced with scar tissue, leading to anemia and eventually marrow failure; an abnormal myeloid precursor is believed to give rise to dyplastic megakaryocytes that produce increased fibroblast factors
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| Myelodysplastic Syndrome | acquired clonal disorders of the hematopoietic stem cell; affect one or more cell lines; occurs b/c blood cells do not develop into mature cells so they are not released into blood and accumulation of immature cells occur in bone marrow
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| Multiple Myeloma | etiology unknown; plasma cells crowd out other cells in bone marrow; collection in bone marrow = myeloma, multiple collections seen as multiple bone lesions = multiple myeloma
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| Monoclonal Gammopathy of Unknown Significance (MGUS) | IgG spike; M spike stable
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| Waldenstrom's Macroglobulinemia | malignancy of B cells; causes overproduction of monoclonal macroglobulin (IgM)
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| Chronic Lymphocytic Leukemia | most common leukemia; clonal proliferation and accumulation of mature-appearing B cells in blood and lympoid tissue
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| Chronic Myelogenous Leukemia | too many wbcs/granulocytic cells made in bone marrow (esp myeloid cells); 3 phases defined by the # of blasts in marrow (chronic, accelerated, acute); blast crisis when blasts compromise >30% of bone marrow cells; accounts for 7-20% of leukemia
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| Acute Lymphoblastic Leukemia | neoplasm of immature lymphoblasts w markers of B or T cell lineage; bone marrow (>20%) and peripheral blood (>10%) and frequently in the liver, spleen, lymph nodes and other organs; common in children
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| Acute Myelogenous Leukemia | can be associated with exposure to toxins (benzenes, radiation, chemo)
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| Hodgkin's Lymphoma | usually arises in single area and spreads to contiguous
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| Non-Hodgkin's Lymphoma | 5th most common malignancy in the US; arise from cells residing in lymphoid tissue (90% of cases arise from B cells); incidence higher in pts with immunodeficiences
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| Infectious Mononucleosis | EBV
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| Ehrlichiosis | tick-borne Ehrlichiae bacteria
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| Histoplasmosis | intracellular fungus Histoplasma capsulatum
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| Acute Thrombocytopenia | decrease in plt count due to: decreased production (bone marrow), increased destruction (meds, immune mediated), sequestration (splenomegaly)
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| Idiopathic (Immune) Thrombocytopenic Purpura | antibodies form and destroy plts (underlying illness: lupus, lymphoma,etc); increased bone marrow production but cannot keep up with destruction
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| Heparin Induced Thrombocytopenia | transient decrease in plt count (type I) or immune mediated (type II, is subset of ITP)- dev'p antibodies to FIV
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| Thrombotic Thrombocytopenic Purpura | disorder of von Willebrand Factor processing; causes intra-vascular plt aggregation; leads to systemic manifestations (CNS, renal, cardiac, hematologic)
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| Hemolytic Uremic Syndrome | related to TTP; associated with infectious diarrhea; rbcs destroyed and kidneys stop function
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| Coagulation: prolonged PT | deficiency in FVII and common pathway factors (FI, FII, FV, FX); caused by liver disease, warafin therapy, vitamin K deficiency, inhibitor to FVIIa
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| Liver Disease (prolonged PT) | liver is where you make all of your factors except for FVIII
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| Vitamin K deficiency (prolonged PT) | have to have vitamin K in liver to make clotting factors (esp II, VII, IX, X) and Protein C and S (these are naturally occuring anticoagulants in body); causes of deficiency: biliary tract disease, Rx, malnutrition
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| Coagulation: prolonged aPTT | deficiency in intrinsic (HMWK, PK, FXII, FXI, FIX. FVIII) and common pathway factors; caused by heparin and DTI therapy, inhibitors to coagulation factors
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| von Willebrand Disease | most common hereditary bleeding disorder (1%); mucocutaneous bleeding; deficient in vWF quantity or quality (defect in plt adhesion); have enough plts but not functioning properly
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| Glanzmanns thrombasthenia | rare autosomal recessive disorder; have enough plts but not functioning properly; plts unable to aggregate due to defect in IIb/IIIa receptors
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| Bernard-Soulier | have enough plts but not functioning properly; reduced or abnormal plt vWF receptor
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| Acquired Thrombopathy | have enough plts but not functioning properly; drugs ASA, NSAIDS, cephalosporins; renal disease; alcohol and end-stage liver disease
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| Prothrombin 20210A Mutation | elevated levels of prothrombin; leads to a modest increase in hyper-coaguability; second most common inherited cause of hypercoaguability
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| anticoagulation disorders | Protein C or S deficiency; anti-phospholipid syndrome;
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| Disseminated Intravascular Coagulation | excessive and uncontrolled thrombosis leading to bleeding manifestations; circulating plasma turns into serum; "consumptive coagulopathy" - forming clots and consuming all of the products needed to form clots
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| Hemophilia A | low FVIII; X-linked recessive only in males; most common severe bleeding disorder
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| Hemophilia B | low FIX; X-linked recessive only in males
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