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Heme Causes

clin med

Hypoproliferative Anemia 90% production problem (bone marrow fails to respond to anemia)
Hyperproliferative Anemia bone marrow is not able to compensate for blood loss or destruction by ramping up rbc production
Microcytic Anemia decreased rbc production ; severe due to either iron deficiency or thalassemia (also chronic inflammation or sideroblastic)
Normocytic Anemia decreased rbc production
Macrocytic Anemia decreased rbc production; severe is either B12 or folate deficiency or occ MDS
Thalassemia hereditary disorders which affect the production of globin chains (alpha or beta)
Alpha Thalassemia due to gene deletion causing a reduction in alpha chain synthesis (severity depends on how many deletions)
Beta Thalassemia due to gene mutations which cause rbc membrane damage which can lead to hemolysis
Iron Deficiency Anemia most common cause of anemia; diet (foods, caloric intake, absorptive capacity, increased loss*, increased requirements)
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)
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
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)
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
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
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*
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
Hereditary Spherocytosis inherited abnormality of rbc membrane (molecular defect in spectrin protein)
Paroxysmal Nocturnal Hemoglobinuria acquired stem cell disorder making rbc membrane prone to lysis by complement (due to lack of special proteins)
Glucose 6 Phosphate Dehydrogenase Deficiency hereditary enzyme defect causing episodic hemolytic anemia related to oxidative stress; X linked recessive (200 million affected worldwide)
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
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
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
Neutropenia bone marrow disorder or peripheral disorders
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..
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
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
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
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
Monoclonal Gammopathy of Unknown Significance (MGUS) IgG spike; M spike stable
Waldenstrom's Macroglobulinemia malignancy of B cells; causes overproduction of monoclonal macroglobulin (IgM)
Chronic Lymphocytic Leukemia most common leukemia; clonal proliferation and accumulation of mature-appearing B cells in blood and lympoid tissue
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
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
Acute Myelogenous Leukemia can be associated with exposure to toxins (benzenes, radiation, chemo)
Hodgkin's Lymphoma usually arises in single area and spreads to contiguous
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
Infectious Mononucleosis EBV
Ehrlichiosis tick-borne Ehrlichiae bacteria
Histoplasmosis intracellular fungus Histoplasma capsulatum
Acute Thrombocytopenia decrease in plt count due to: decreased production (bone marrow), increased destruction (meds, immune mediated), sequestration (splenomegaly)
Idiopathic (Immune) Thrombocytopenic Purpura antibodies form and destroy plts (underlying illness: lupus, lymphoma,etc); increased bone marrow production but cannot keep up with destruction
Heparin Induced Thrombocytopenia transient decrease in plt count (type I) or immune mediated (type II, is subset of ITP)- dev'p antibodies to FIV
Thrombotic Thrombocytopenic Purpura disorder of von Willebrand Factor processing; causes intra-vascular plt aggregation; leads to systemic manifestations (CNS, renal, cardiac, hematologic)
Hemolytic Uremic Syndrome related to TTP; associated with infectious diarrhea; rbcs destroyed and kidneys stop function
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
Liver Disease (prolonged PT) liver is where you make all of your factors except for FVIII
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
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
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
Glanzmanns thrombasthenia rare autosomal recessive disorder; have enough plts but not functioning properly; plts unable to aggregate due to defect in IIb/IIIa receptors
Bernard-Soulier have enough plts but not functioning properly; reduced or abnormal plt vWF receptor
Acquired Thrombopathy have enough plts but not functioning properly; drugs ASA, NSAIDS, cephalosporins; renal disease; alcohol and end-stage liver disease
Prothrombin 20210A Mutation elevated levels of prothrombin; leads to a modest increase in hyper-coaguability; second most common inherited cause of hypercoaguability
anticoagulation disorders Protein C or S deficiency; anti-phospholipid syndrome;
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
Hemophilia A low FVIII; X-linked recessive only in males; most common severe bleeding disorder
Hemophilia B low FIX; X-linked recessive only in males
Created by: ac202