An anemia is a decrease in number of red blood cells (RBCs) or less than the normal quantity of hemoglobin in the blood.[2][3] However, it can include decreased oxygen-binding ability of each hemoglobin molecule due to deformity or lack in numerical development as in some other types of hemoglobin deficiency.[citation needed]
Anemia is the most common disorder of the blood. There are several kinds of anemia, produced by a variety of underlying causes. Anemia can be classified in a variety of ways, based on the morphology of RBCs, underlying etiologic mechanisms, and discernible clinical spectra, to mention a few. The three main classes of anemia include excessive blood loss (acutely such as a hemorrhage or chronically through low-volume loss), excessive blood cell destruction (hemolysis) or deficient red blood cell production (ineffective hematopoiesis). Based on 2005-2006 estimates, the Centers for Disease Control and Prevention has stated that approximately 5.5 million Americans a year are either admitted to a hospital or seen by a physician, with some form of anemia as their primary diagnosis.[4]
Symptoms of anaemia include Plummer–Vinson syndrome, candidal infections. Altered taste sensation, smooth, red painful burning sensation of tongue, filiform followed by fungiform papillae atrophy may also be seen. Others include generalized stomatitis, angular cheilitis and gingivitis.[citation needed]
Oral manifestation of anemia include angular cheilitis, generalized stomatitis, candidiasis and gingivitis. There will be pallor of lips and oral mucosa. Patients might have a smooth, red painful tongue, experience burning sensation of tongue or disturbed taste sensation. Atrophy of filiform and fungiform papillae may also occur.[citation needed]
Nutritional anemias
A nutritional anemia is a type of anemia that can be directly attributed to either a nutritional disorder or a nutritional deficiency.
Iron-deficiency anemia (or iron deficiency anaemia) is a common anemia that occurs when iron loss (often from intestinal bleeding or menses) occurs, and/or the dietary intake or absorption of iron is insufficient. In such a state, hemoglobin, which contains iron, cannot be formed.[5]
Vitamin B12 deficiency anemia occurs when a "lower-than-normal" amount of the vitamin B12 is available within the body, leading to a decreased production of healthy red blood cells.[7]
Pernicious anemia (also known as macrocytic achylic anemia, congenital pernicious anemia, juvenile pernicious anemia, and Vitamin B12 deficiency) is one of many types of the larger family of megaloblastic anemias. It is caused by loss of gastric parietal cells, and subsequent inability to absorb vitamin B12. Pernicious anemia is the result of inadequate production of the protein intrinsic factor needed by the body to absorb vitamin B 12, causing a reduction of new red blood cells.[8]
Vitamin B 12 deficiency anemia due to selective vitamin B 12 malabsorption with proteinuria (also known as Imerslund-Gräsbeck syndrome) is a rare autosomal recessive disorder which requires the indefinite administration of Vitamin B12 injections.[9]
Megaloblastic anemia (or megaloblastic anaemia) is an anemia (of macrocytic classification) that results from inhibition of DNA synthesis in red blood cell production.[10]
Transcobalamin II deficiency (TCII) (also known as hereditary transcobalamin II deficiency) is a rare autosomal recessive disorder that results in neurological dysfunction.[11] Transcobalamin II are a type of carrier proteins which bind with plasma vitamin B12 (cobalamin) in the production of red blood cells.[12]
Folate-deficiency anemia (also known as dietary folate-deficiency anemia) is a condition that develops when the body does not have the adequate supply of folic acid available that is needed for the production of new healthy blood cells.[13]
Nutritional Megaloblastic anemia is an anemia (of macrocytic classification) that results from inhibition of DNA synthesis in red blood cell production.[10]
Acanthocytosis can refer generally to the presence of this type of crenatedred blood cell, such as may be found in severe cirrhosis or pancreatitis,[16]: 150 but can refer specifically to abetalipoproteinemia, a clinical condition with acanthocytic red blood cells, neurologic problems and steatorrhea.[17]: 2464 This particular cause of acanthocytosis (also known as abetalipoproteinemia, apolipoprotein B deficiency, and Bassen-Kornzweig syndrome) is a rare, genetically inherited, autosomal recessive condition due to the inability to fully digest dietary fats in the intestines as a result of various mutations of the microsomal triglyceride transfer protein (MTTP) gene.[18]
Acute posthemorrhagic anemia (also known as acute blood loss anemia) is a condition in which a person quickly loses a large volume of circulating hemoglobin. Acute blood loss is usually associated with an incident of trauma or a severe injury resulting in a large loss of blood. It can also occur during or after a surgical procedure.[19]
Alpha-thalassemia (α-thalassemia) is a form of thalassemia involving the genes HBA1[20] and HBA2.[21] It is condition that causes a reduction of hemoglobin production. There are two types of Alpha-thalassemia, named hemoglobin Bart hydrops fetalis syndrome (also known as Hb Bart syndrome) and HbH disease.[22]
Anemia is a type of medical condition that results in a decrease in the number of red blood cells (RBCs) or less than the normal quantity of hemoglobin in the blood.[2]
Anemia of chronic disease (ACD) (also known as anemia of inflammatory response) is a condition where the body converts iron into unused ferrin, causing a drop in hemoglobin production, and as a result; decreased red blood cell production and count. This is caused by a natural defense mechanism initiated by an inflammatory response in response to the underlying chronic disease.[23]
Anemia in kidney disease and dialysis results from the diseased kidney's inability to produce enough of the hormone erythropoietin. Erythropoietin is used to stimulate an adequate production of red blood cells from the bone marrow.[24]
Beta-thalassemia (β-thalassemia) is an autosomal dominant blood condition that results in the reduction of hemoglobin production. The cause for the disorder is related to a genetic mutation of the HBB gene. This gene is responsible for providing the instructions to produce beta-globin; one of the major components of hemoglobin. The two classification types of beta thalassemia are thalassemia major (also known as Cooley's anemia) and thalassemia intermedia.[30]
Diamond–Blackfan anemia (DBA), (also known as Blackfan–Diamond anemia and Inherited erythroblastopenia) [31] is a congenitalerythroidaplasia that usually presents in infancy.[32]
Congenital dyserythropoietic anemia (CDA) is a generically inherited autosomal recessive (types I and II) or autosomal dominant (type III) blood disorder that affects the normal maturation process of red blood cell production. Mutations to the CDAN1 gene (type I), SEC23B gene (type II), and a currently unknown gene for type III causes a disruption in the normal formation of erythropoiesis, thereby causing a reduction of circulating healthy mature red blood cells.[33]
Drug-induced autoimmune hemolytic anemia is a type of hemolytic anemia in which a mediated immune response triggers IgG and IgM antibody production in regards to the presence of high doses of penicillin via the hapten mechanism causing the reduction of red blood cells in the spleen.[34]
Hemoglobinopathy is a kind of genetic defect that results in abnormal structure of one of the globin chains of the hemoglobin molecule.[35] Hemoglobinopathies are inherited single-gene disorders; in most cases, they are inherited as autosomal co-dominant traits.[36] Hemoglobinopathies imply structural abnormalities in the globin proteins themselves.[37] Hemoglobinopathy variants include sickle-cell disease.[38]
Hemolytic anemia (also known as haemolytic anaemia) is an anemia due to hemolysis, the abnormal breakdown of red blood cells. A number of different mediating factors can cause this condition; either from within the blood cell itself (intrinsic factors) or outside of the cell (extrinsic factors).[39]
Hereditary spherocytosis is a genetically transmitted (autosomal dominant) form of spherocytosis, an auto-hemolyticanemia characterized by the production of red blood cells that are sphere-shaped rather than bi-concave disk shaped (donut-shaped), and therefore more prone to hemolysis.[41]
Hereditary elliptocytosis (HE) (also known as ovalocytosis), is an inherited blood disorder in which an abnormally large number of circulating red blood cells are elliptical or cigar shaped rather than the typical biconcave disc shape. It is caused in part by mutations in the formation of specific spectrin tetramers or proteins responsible for giving the red blood cell its shape and elasticity causing continued deformation as the cell matures.[42] Subtypes of this condition include southeast Asian ovalocytosis and spherocytic elliptocytosis.
Hereditary pyropoikilocytosis (HPP) is an autosomal recessive form of hemolytic anemia which typically presents at infancy or early childhood, characterized by abnormal red blood cell morphology including "budding red cells, fragmented red cells, spherocytes, elliptocytes, triangular cells, and other bizarre-shaped red cells."[43]
Cold hemagglutinin disease (also known as cold agglutinin disease and autoimmune anemia due to cold-reactive antibodies)is an autoimmune disease characterized by the presence of high concentrations of circulating antibodies, usually IgM, directed against red blood cells.[44] It is a form of autoimmune hemolytic anemia, specifically one in which antibodies only bind red blood cells at low body temperatures, typically 28-31 °C.
Paroxysmal cold hemoglobinuria (PCH) (also known as Donath-Landsteiner syndrome) is a rare condition characterized by the sudden presence of hemoglobin in the urine (called hemoglobinuria), typically after exposure to cold temperatures.[45]
Hereditary stomatocytosis is a classification of inherited autosomal dominant human conditions which affect the red blood cell, in which the membrane or outer coating of the cell 'leaks' sodium and potassium ions, causing cell lyses and eventual haemolytic anaemia.
Hexokinase deficiency (also known as human erythrocyte hexokinase deficiency) is an anemia-causing condition associated with inadequate hexokinase.[47]
Hypochromic anemia is any type of anemia in which the red blood cells (erythrocytes) are paler than normal.[48] This is caused by a proportionally reduced amount of hemoglobin present in relation to the size of the red blood cell.
Ineffective erythropoiesis is an anemia caused by the premature apoptosis of the body's mature red blood cells [49] and subsequent reduction in an adequate production and full maturation of new healthy red blood cells.[50]
Megaloblastic anemia (or megaloblastic anaemia) is an anemia of macrocytic classification that results from inhibition of DNA synthesis in red blood cell production.[10]
Myelophthisic anemia (also known as myelophthisis) is a severe kind of anemia found in some people with diseases that affect the bone marrow. Myelophthisis is the displacement of hemopoietic bone-marrow tissue into the peripheral blood,[51] either by fibrosis, tumors or granulomas.
Neuroacanthocytosis (also known as Levine-Critchley syndrome) is a group of rare, genetic conditions that are characterized by movement disorders and acanthocytosis.[52]
Chorea-acanthocytosis (ChAc)(also known as Levine-Critchley syndrome, acanthocytosis with neurologic disorder, neuroacanthocytosis, and choreoacanthocytosis)[53] is a rare hereditary disease caused by a mutation of the gene that directs structural proteins in red blood cells. It belongs to a group of four diseases characterized as neuroacanthocytosis.[54]
Paroxysmal nocturnal hemoglobinuria (also known as Marchiafava-Micheli syndrome) is a rare, acquired, life-threatening blood disease, with anemia due to red blood cell destruction, red urine, and thrombosis.
Pyruvate kinase deficiency, also called erythrocyte pyruvate kinase deficiency,[55] is an inheritedmetabolic disorder of the enzyme pyruvate kinase which affects the survival of red blood cells and causes them to deform into echinocytes on peripheral blood smears.
Rh deficiency syndrome is a type of hemolytic anemia that involves erythrocytes whom membranes are deficient in Rh antigens. It is considered a rare condition.[56]
Sickle cell disease is a group of inherited blood disorders, caused by a genetic abnormality in the oxygen-carrying protein haemoglobin found in red blood cells.[57] Under certain circumstances, this leads to the red blood cells adopting an abnormal sickle-like shape; with this shape, they are unable to deform as they pass through capillaries, causing blockages and consequent tissue damage. Sickled cells are quickly eliminated from the bloodstream, causing anemia.[57]
Southeast Asian ovalocytosis (also known as stomatocytic ovalocytosis, stomatocytic elliptocytosis, and Melanesian ovalocytosis) is a form of hereditary elliptocytosis common in some communities in Malaysia and Papua New Guinea, as it confers some resistance to cerebral falciparum malaria.[60]
Spur cell hemolytic anemia is a form of hemolytic anemia that results when free cholesterol binds to the red blood cell's membrane increasing its surface area, causing later deformities such as rough or thorny projections on the erythrocyte named acanthocytes. This condition is caused by the deceased liver's decreased ability to esterificate cholesterol.[61]
Thalassaemia is an inherited blood disorder which is caused by genetic mutations that causes the body to make fewer healthy red blood cells and less hemoglobin due to lack of protein chains.
Triosephosphate isomerase (TPI) deficiency is a genetically inherited autosomal recessive condition "characterized bychronic hemolytic anemia, cardiomyopathy, susceptibility to infections, severe neurological dysfunction, and, in most cases, death in early childhood."[62]
Warm autoimmune hemolytic anemia is an autoimmune hemolytic anemia (AIHA) characterized by formation of antibodies that attack the body's own red blood cells in a destructive immune system response.[63]
Blood cancers
A blood cancer or hematological malignancy is a type of malignant cancer that originates, affects, or involves the blood, bone marrow, or lymph nodes.[64] These cancers include leukemias, lymphomas, and myelomas. These particular types of cancers can arise as defected mature cell types that have differentiated from hematopoietic precursor cells (often in the bone marrow) and begin to quickly proliferate through the bloodstream where it can then often infiltrate other organs and tissues. Others can involve the formation of tumors from lymphoblasts from within the lymphoid tissue.[65] Incidence of affected people with a form of blood cancer has been steady increasing over recent years; however, due in part to early detection methods and subsequent advancements in the treatment of the diseases, mortality rates have continued to decrease.[66]
Angioimmunoblastic T-cell lymphoma (AILT) (also known as Angioimmunoblastic lymphadenopathy with dysproteinemia)[68]: 747 is a mature T-celllymphoma with systemic characterized by a polymorphous lymph node infiltrate showing a marked increase in follicular dendritic cells (FDCs) and high endothelial venules (HEVs) and systemic involvement.[69] It is also known as immunoblastic lymphadenopathy (Lukes-Collins Classification) and AILD-type (lymphogranulomatosis X) T-cell lymphoma (Kiel Classification).[69]
Hepatosplenic T-cell lymphoma is a systemic neoplasm comprising medium-sized cytotoxic T-cells that show a significant sinusoidal infiltration in the liver, spleen, and bone marrow.[70] It is a rare and generally incurable form of lymphoma.[71]
Follicular lymphoma (also known as indolent follicular lymphoma) is a type of non-Hodgkin's lymphoma that involves both large and small B-cell lymphocytes that spreads from the lymphatic system and into the blood, bone marrow, and internal organs. Approximately 20 to 30 percent of non-Hodgkin's lymphomas are diagnosed as follicular lymphoma, with a majority of cases involving those 60 years of age or older.[72]
Mucosa-associated lymphatic tissue lymphoma (as known as MALT lymphoma and extra-nodal marginal zone lymphoma) is a condition in which lymphatic tissue abnormally presents outside the lymphatic system (extra-nodular) and instead within the mucosa of the gastrointestinal tract, typically as a lesion in the stomach.[73]
B-cell chronic lymphocytic leukemia (also known as small cell lymphocytic lymphoma) is a blood cancer that involves the B-cell lymphocytes; responsible for the creation of antibodies. Of the two general types of chronic lymphocytic leukemias (the other involving T-cells), B-cell chronic lymphocytic leukemia accounts for approximately 95 percent of the diagnoses.[74]
Mantle cell lymphoma (MCL) is a type of B-cell lymphoma and one of the rarest forms of non-Hodgkin's lymphomas comprising approximately 6% of diagnosed cases.[75]
Burkitt lymphoma (also known as Burkitt's tumor or malignant lymphoma, Burkitt's type) is a type of B-cell lymphoma that is categorized into one of variant types. These variants are endemic (occurring in equatorial Africa), sporadic ("non-African"), and immunodeficiency-associated (usually associated with HIV).
Waldenström's macroglobulinemia (also known as lymphoplasmacytic lymphoma) is a lymphoproliferative disease that involves an abnormal increase of lymphocytes within the bone marrow, creasing disruption of normal red blood cell production.[76]
Splenic marginal zone lymphoma (SMZL) (also known as well-differentiated lymphocytic lymphoma, small lymphocytic lymphoma, and splenic lymphoma with circulating villous lymphocytes) is a lymphoma made up of small B-cells that replace the normal architecture of the white pulp of the spleen. The neoplastic cells are both small lymphocytes and larger, transformed blasts, and they invade the mantle zone of splenicfollicles and erode the marginal zone, ultimately invading the red pulp of the spleen. Frequently, the bone marrow and splenichilarlymph nodes are involved along with the peripheral blood.[77]
Leukemia is a malignancy producing of white blood cells in bone marrow. It can be a serious disease if not treated early.
Sometimes it can be cured by chemotherapy or stem cell treatment. It can affect our bloodstream, skin, lymph nodes, heart, and brain.
Acute megakaryoblastic leukemia (AMKL) is a form of acute myeloid leukemia where megakaryoblasts account for approximately 30% of the nucleated cells within the bone marrow.[81]
Acute panmyelosis with myelofibrosis (APMF) is a poorly defined disorder that arises as either a clonal disorder, or following toxic exposure to the bone marrow.
Hematological disorders may be caused by a number of infection-related conditions involving the introduction of microorganisms into the host, such as bacteria, viruses, microfilaria, fungus and protozoa.[40]
^Saladin, Kenneth S.; Miller, Leslie (2004). "18". Anatomy & Physiology: The Unity of form and Function (3rd ed.). McGraw-Hill. p. 679. ISBN0-07-242903-8.
^Mayo Clinic staff (March 4, 2011). "Vitamin deficiency anemia". Mayo Foundation for Medical Education and Research. Mayo Clinic. Retrieved 5 March 2011.
^"Pernicious anemia". National Center for Biotechnology Information (NCBI). U.S. National Library of Medicine. November 23, 2008. Retrieved 1 March 2011.
^Kaikov, Y.; L. D. Wadsworth, C. A. Hall and P. C. J. Rogers; Hall, C. A.; Rogers, P. C. J. (1991). "Transcobalamin II deficiency: Case report and review of the literature". European Journal of Pediatrics. 150 (12): Volume 150, Number 12, 841–843. doi:10.1007/BF01955004. PMID1743216. S2CID11707936.
^"Folate-deficiency anemia". National Center for Biotechnology Information. U.S. National Library of Medicine. 31 January 2010. Retrieved 2 March 2011.
^Vorvick, MD, Linda (March 14, 2009). "Scurvy". Medline Plus. U.S. National Library of Medicine. Retrieved 1 March 2011.
^Hillman, RS; Ault, KA; Leporrier, M; Rinder, HM. (2011). Hematology in Clinical Practice (5th ed.). McGraw-Hill. ISBN978-0-07-162699-6.
^Longo, D; Fauci, AS; Kasper, DL; Hauser, SL; Jameson, JL; Loscalzo J. (2012). Harrison's Principles of Internal Medicine (18th ed.). McGraw-Hill. ISBN978-0-07174889-6.
^Haldeman-Englert, C; Zieve, D. (4 August 2011). "Bassen-Kornzweig syndrome". Pub Med Health. National Center for Biotechnology Information, U.S. National Library of Medicine.
^Turgeon, Mary (2005). "8". Clinical Hematology: Theory and Procedures (4th ed.). Philadelphia: Lippincott Williams & Wilkins. p. 117. ISBN0-7817-5007-5.
^"Anemia in Kidney Disease and Dialysis". The National Kidney and Urologic Diseases Information Clearinghouse. National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health. October 2008. Retrieved 28 March 2011.
^"Congenital dyserythropoietic anemia". Genetics Home Reference. U.S. National Library of Medicine, National Institutes of Health. July 2009. Retrieved 22 March 2011.
^Dhaliwal, Gurpreet; Cornett, Patricia; Tierney, Lawrence (2004). "Hemolytic Anemia". American Family Physician. 69 (11): 2599–2606. PMID15202694. Retrieved 28 March 2011.
^Reviewed by Vorvick, Linda J.; Chen, Yi-Bin (31 January 2010). "Hemolytic anemia". Pub Med Health. National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 24 March 2011.
^ abTurgeon, Mary Louise (2004). "12". Clinical Hematology (4th ed.). Lippincott Williams & Wilkins. p. 161. ISBN0-7817-5007-5.
^Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier Saunders. p. 625. ISBN0-7216-0187-1.
^"Paroxysmal cold hemoglobinuria (PCH) e". Medline Plus. U.S. Department of Health and Human Services, National Institutes of Health. March 28, 2010. Retrieved 28 March 2011.
^"Hemolytic Uremic Syndrome in Children". National Kidney and Urologic Diseases Information Clearinghouse. National Institutes of Health of the U.S. Department of Health and Human Services. January 2009. Retrieved 4 March 2011.
^McPhee, Stephen; Ganong, William (2003). "Chapter 5: Neoplasia". Pathophysiology of Disease (5th ed.). New York: Lange Medical Books/McGraw-Hill. pp. 106–110. ISBN0-07-144159-X.
^James, William D.; Berger, Timothy G. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ISBN0-7216-2921-0.
^ abJaffe E.S.; Harris N.L.; Stein H.; Vardiman J.W., eds. (2001). World Health Organization Classification of Tumors. Pathology and Genetics of Tumours of Haemopoietic and Lymphoid Tissues. Lyon: IARC Press. ISBN92-8322411-6.