DIAG 2735 7 - Blood Pathologies

DIAG 2735 7 - Blood Pathologies - Blood Disorders Blood Red...

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Unformatted text preview: Blood Disorders Blood Red Blood Cells White Blood Cells Platelets Erythrocyte Disorders Erythrocyte Anemia (too few) a Polycythemia (too many) a Anemia a 3 Categories • • • Blood Loss Impaired production Hemolysis (destruction) Symptoms common to all anemias anemias a a a a a a Increased cardiac Increased output output Increased Increased respiration rate respiration Chronic fatigue Dyspnea upon Dyspnea exertion exertion Faintness Pallor a a a a a a a Vertigo Palpitation Headaches Fever Slight edema Systolic murmurs Weak, bounding Weak, pulse pulse Blood Loss Anemia Blood a Acute blood loss • May be internal, into GI, or external • Results in hypovolemia (decreased blood Results volume) volume) • Blood volume is restored 1-2 days • Once volume is restored HCT and Hb drop Blood Loss Anemia Hematology Hematology Decreased platelets a Increased neutrophils w/ shift to left a • Shift to the left means more band cells than Shift the usual 10% the a Changes in RBC morphology • • • • Anisocytosis poikilocytosis macrocytosis nucleated RBCs Blood Loss Anemia Blood a Chronic blood loss (slow bleeding) • Symptoms do not appear until stored Fe is Symptoms depleted depleted • RBC morphology – Normocytic – Hypochromic • Elevated platelets • Leukopenia Impaired Production Anemia Impaired IDA Iron Deficiency Anemia a Megaloblastic Anemia a • Pernicious anemia • Folate deficiency anemia a Other • • • • • Renal Insufficiency Immune related Liver disease Endocrine disorders Bone marrow infiltration Iron Deficiency Anemia Iron Results when loss exceeds intake and Results stored Fe is depleted (see blood loss) stored a Cells are hypochromic and microcytic a May result from increased need ie. May Growth spurt Growth a • Most common anemia in infants and Most toddlers toddlers • Starts age 6 months when fetal Fe is Starts depleted depleted Iron Deficiency Anemia Iron a Other causes • Partial or total gastrectomy impairs Partial absorption absorption • Sprue (malabsorption syndromes of gut) – Nontropical - autoimmune – Tropical - parasite or vitamin deficiency induced Very rare to not be able to absorb iron a Average adult male has 3-4 year supply Average stored stored a Iron Deficiency Anemia Iron a Three stages • Iron depletion - loss exceeds intake • Iron deficiency eryhthropoeisis - plasma Iron concentration of Fe falls, transferrin saturation is less than 15%, possibility of symptoms symptoms • Iron deficiency anemia - RBC morphology Iron changes (hypochromic, microcytic) and symptoms Iron Deficiency Anemia Iron a Other symptoms • Paresthesias • Burning tongue (epithelial atrophy) • Angular stomatitis (cracking at mouth Angular corners) corners) • Gastritis • Pica (craving non-food) • Other (very rare) – spooning nails (koilonychia) – Difficulty swallowing (dysphagia) Iron Deficiency Anemia Iron a Blood values • • • • • MCV (size) is low MCHC is low (less hemoglobin in cells) HCT is low (microcytes) Hb is low (no Fe to make it) Leukocytes uneffected Megaloblastic Anemia Megaloblastic Results from B12 or Folate deficiency a These vitamins responsible for These maturation of RBCs maturation a RBC morphology is large (macrocytic) RBC ovalocytes ovalocytes a Other hematology finding Other hypersegmented neutrophils hypersegmented a B12 Deficiency B12 B12 is called the maturation factor a B12 is present in all animal tissues a • Inadequate intake: only vegans a B12 is manufactured by microbes Symptoms Symptoms a a a a Anemia with jaundice Atrophic glossitis (sore smooth or pale Atrophic tongue) tongue) Acute glossitis ( red raw tongue) Abdominal pain • Alternating diarrhea and constipation a Posterior and lateral column demyelination • paresthesia, pallesthesia, UMNL signs a Emotional lability (personality changes) Pernicious Anemia Pernicious Results from lack of intrinsic factor a Intrinsic factor (IF) is made by parietal Intrinsic cells of stomach cells a IF binds to B12 for absorption a Patient may either have decreased IF Patient production, or autoimmune attack of parietal cells or IF a Pernicious Anemia Pernicious a Other causes • • • • • a Gastrectomy Sprue Diphyllobothrium Lataum (fish tapeworm) Congenital Endocrine disorder Cure is intramuscular injection B12 Folate Deficiency Folate a Due to inadequate intake Body only stores three month supply Rare in US because milk is high in Folate Alcoholic liver disease causes deficiemcy Malabsorption syndromes may cause Malabsorption deficiency deficiency Increased need like pregnancy a Cure is Folate and often antimicrobial agent a a a a a Aplastic Anemia Aplastic Pancytopenia (all blood cells Pancytopenia decreased) decreased) a Due to shut down of bone marrow a May be rapid onset and proceed quickly May to death to a May be slow and chronic a Causes of Aplastic Anemia Causes 70 % is idiopathic a Infection - hepatitis, Epstein-Barr virus, Infection parvovirus parvovirus a Damage or destruction of stem cells a • Radiation • Drugs- anticonvulsives, sulfonamides, Drugsantihistamines, some analgesics, • Chemicals- mustard gas, DDT, urethane, Chemicalsgold, bismuth, mercury gold, Aplastic Anemia Aplastic Pregnancy will magnify problem a May even be congenital a Thymoma usually only blocks RBC Thymoma production production a Sideroblastic Anemia Sideroblastic Due to increase in serum Iron a Elevated saturated % of transferrin a Demonstrates siderotic granules in RBC a Primary form is idiopathic a Secondary comes from drugs - anti TB, Secondary Lead poisoning, alcoholism, Iron inhalation inhalation a Other Sources of Impaired Production Production a a a a a Chronic inflammation (Rheumatoid) Renal insufficiency (kidneys stop making Renal erythropoeitin ) + uremia leads to hemolysis erythropoeitin Liver disease causes normal production but Liver diminished life span < 120 days, leads to jaundice, reticulocytosis, and spur cells jaundice, Endocrine - decreased production except Endocrine parathyroid which shows increased production production Bone marrow infiltration - leukemia, Bone Hemolytic Anemias Hemolytic Increased RBC destruction due to Increased shorter life span shorter a Intrinsic form - involves a membrane, Intrinsic metabolic, or hemoglobin disorder metabolic, a Extrinsic form - involves factors outside Extrinsic the RBC the a Often lead to gall stones a Intrinsic Hemolytic Anemias Intrinsic Hereditary spherocytosis a Sickle cell disease a Thalassemia a Metabolic hemolysis a Hereditary Spherocytosis Hereditary 1: 5000 of Northern European descent a RBC morphology is spherical not RBC biconcave biconcave a Biconcave cells bend to get through Biconcave spleen spleen a Spheres do not a Spleen destroys the cells a Jaundice results, with brown stools, Jaundice increased urobilinogen in urine increased a Sickle Cell Disease Sickle .1-.2% of black population a Serious and chronic a Often fatal by age 30 Often a Happens due to substitution of Valine Happens for Glutamine at the 6th position on the beta chain beta a Sickle Cell Disease Sickle In high O2 environments cells are normal normal a In low O2 environments cells undergo reversible sickling reaction, Hb forms a rigid sickle shaped crystal deforming the RBC RBC a Rigidity of sickles leads to hemolysis in Rigidity RE system in spleen and complications RE a Sickle Cell Disease Sickle a External signs • hand feet syndrome aka sickle cell dactilitis hand swelling of dorsum of hands and feet with periostitis (prior to age 4) periostitis a Spleen triad • Sequestration -blood pooling • Splenomegaly and hypovolemic shock • Functional asplenia (due to RE filters becoming Functional blocked) blocked) a RBC morphology • Target cells, sickle cells, Howell Jolly Target Thalassemia Thalassemia Aka Medterranean anemia aka Cooley’s Aka a Labeled by which hemoglobin chain is Labeled effected (alpha and beta most common) effected a One chain is not made at the same rate One as the others as a Destabilizes the RBC Destabilizes a Thalassemia Thalassemia Morphology - hypochromic, microcytic, Morphology extreme poikilocytosis, target cells, ovalocytosis, Cabot rings, Howell Jolly bodies bodies a Minor form is heterozygous (one parent) a Major form is homozygous (both Major parents) parents) a Thalassemia Thalassemia Asymptomatic (alpha and beta minor Asymptomatic forms) to severe (beta major) forms) a Beta major symptoms a • Bone marrow expansion - honeycomb, hair Bone on end skull on • Iron overload • Jaundice • Leg ulcerations • Splenomegaly Thalassemia Thalassemia Minor forms need no treatment a Major form requires blood transfusions, Major need decreases post splenectomy need a Metabolic Hemolysis Metabolic a Internal metabolic processes do not Internal work, weaken cell work, • lack of mitochondria • lack of glucose-6-phosphate lack dehydrogenase dehydrogenase • lack of pyruvate kinase • lack of glycolytic enzymes • lack of pyramidine-5-nucleotidase Extrinsic Hemolytic Anemias Extrinsic Chemical a Physical a Autoimmune a Infection a Erythroblastosis Fetalis a Erythroblastosis Fetalis Erythroblastosis Happens due to Rh (-) Mom and Rh (+) Happens Dad Dad a They have an Rh (+) baby a The Rh factor in Baby’s blood sensitizes The Mom’s immune system Mom’s a Baby is born a Next Rh (+) baby is conceived a Mom makes antibodies, destroys baby’s Mom blood blood a Erythroblastosis Fetalis Erythroblastosis Baby may die in utero a Baby will develop hyperplastic bone Baby marrow to keep up with destruction marrow a Bone marrow kicks out immature RBCs Bone (erythroblasts) to make room for more to be made to a Erythroblastosis Fetalis Erythroblastosis Treatment is to load up Mom with anti Treatment Rh antibodies with every pregnancy to destroy fetal blood in Mom’s circulation before Mom gets sensitized before a May require immediate transfusion at May birth for baby with Rh (-) blood birth a Polycythemia Polycythemia Increased HCT with normal MCV a Absolute polycythemia more cells a Relative polycythemia less plasma Relative (dehydration) (dehydration) a Absolute Polycythemia Absolute a Appropriate form • Increased erythropoeitin due to low O2 levels in tissues levels – physiologic - due to living at high altitudes – secondary - due to heart and lung problems a Inappropriate form • Increased erythropoeitin level due to: renal Increased tumor, kidney ischemia (hydronephrosis, hepatic mass), familial form (high Hb affinity) affinity) Polycythemia Vera Polycythemia a Cancerous overproduction of all blood Cancerous cell types cell Leukemia Leukemia Results from malignant degeneration of Results the WBC stem cells the a Blood and marrow shows Blood nondifferentiated cells in great numbers nondifferentiated a Often squeeze out the RBC and platelet Often producing cells producing a Acute forms life < 3 months untreated a Chronic forms life > 1 year untreated a Types of Leukemia Types a a a a ALL - Acute Lymphocytic (lymphatic) ALL Leukemia Leukemia AML - Acute Myelocytic Leukemia CLL - Chronic Lymphatic (lymphocytic) CLL Leukemia Leukemia CML - Chronic Myelocytic Leukemia Acute forms of Leukemia Acute a Classified on the FAB system • • • French-American-British L1, L2, L3, M1, M2, M3, M4, M5, M6 Based upon the stage of maturation when Based cancer begins cancer Acute forms of Leukemia Acute a Symptoms • • • • • • Nonspecific Fatigue, Fever, Malaise Anorexia - weight loss Secondary infection Excessive bleeding or bruising Excessive Anemia Acute Lymphocytic Leukemia Acute Happens in young children a Cure rate is good a Relapse tends to occur in CNS, testes, Relapse or bone marrow or a May involve joint pain and bone pain a Blood shows undifferentiated Blood lymphocytes (blueberries) lymphocytes a Acute Myelocytic Leukemia Acute Occurs in adults a Arises in bone marrow a May result from other chemotherapy a Cure rate is much less a Chronic Leukemias Chronic Insidious onset a Nonspecific symptoms a • • • • Fatigue Weight loss Pallor (anemia) Bacterial, Viral, Fungal infection due to Bacterial, immunosupression immunosupression • Dyspnea on exertion Chronic Lymphatic Leukemia Chronic Occurs in people over 60 a Lymphocytes accumulate in bone Lymphocytes marrow marrow a Lymphocytes accumulate in lymphoid Lymphocytes tissue (lymph nodes and splenomegaly) tissue a Immune deficiency is present a Usually involves the B cells a Chronic Lymphatic Leukemia Chronic Onset is insidious a Often found by accident when checking Often lymphadenopathy lymphadenopathy a Feeling of fullness due to splenomegaly a Lab shows increased lymphocytes a • differentiated from Viral infection by the fact differentiated that the cells are recognizable but abnormal abnormal Chronic Myelocytic Leukemia Chronic Increased numbers of granulocytes in Increased bone marrow, spleen, lymph nodes, and blood blood a May involve megakaryocyte and May erythroblasts erythroblasts a Blood smear shows varying degrees of Blood granulocyte differentiation granulocyte a Basophils and eosinophil levels way up a Lymphoma Lymphoma Hodgkins or non-Hodgkins a Occurs in adolescence and early Occurs adulthood adulthood a Shows Reed- Sternberg cells a • binucleated cells in lymph nodes Hodgkin’s Lymphoma Hodgkin’s a Signs and symptoms • • • • Adenopthy without systemic complaint Adenopthy Intense itching Occasional high fever (days to weeks) Increased pain in effected areas with Increased alcohol use alcohol More Signs and Symptoms More Bone involvement -asymptomatic ivory Bone vertebra leads to pancytopenia vertebra a Spinal cord compression- paraplegia a Horner’s syndrome a Jaundice from bile duct obstruction a Leg edema from groin lymph node Leg blockage blockage a Tracheal blockage causing dyspnea a Decreased immunity a Non-Hodgkin’s Lymphoma Non-Hodgkin’s More common than Hodgkin’s a Comes in low, medium, high, and Comes miscellaneous forms miscellaneous a Non-Hodgkin’s Lymphoma Non-Hodgkin’s May have asymptomatic May lymphadenopathy lymphadenopathy a Mediastinal and retroperitoneal Mediastinal adenopthy causes symptoms adenopthy a • edema of face from blockage of vena cava edema (not a sign of Hodgkin’s) (not • ureteral blockage from pelvic nodes ureteral leading to renal failure (also not Hodgkin’s) leading a Anemia results Anemia Non-Hodgkin’s Lymphoma Non-Hodgkin’s a Causes of anemia • • • a Bleeding in GI Hemolysis Bone marrow infiltration High grade lymphomas classified as High leukemic leukemic Non-Hodgkin’s Lymphoma a Differential list: • • • • Leukemia (acute and chronic) Mets Infectious mono TB Diagnosis confirmed by biopsy only a Prognosis better for milder forms a Coagulopathies Coagulopathies Coagulation factors a Platelets a Coagulation Factors Coagulation a Hereditary • Hemophilia a Acquired • Disseminated Intravascular Coagulation Disseminated DIC DIC • Circulating anticoagulants Hemophilia Hemophilia Hemophilia A is lack of factor VIII (80% Hemophilia cases) cases) a Hemophilia B is lack of factor IX a Need genetic assay to tell A from B a Is an X-linked trait a Effects males almost exclusively a Hemophilia Hemophilia a Signs and symptoms • • • • uncontrolled bleeding from minor trauma Usually discovered before 18 months Bleeding into tongue may close airway hemorrhage and hemarthrosis may lead to hemorrhage deformity deformity • severe form is only 1% of necessary factor • mild form is 5% necessary factor • patients at 10-30% need only fear surgeons and patients dentists dentists Hemophilia Treatment Hemophilia Identify problem a Measure factor levels a Add whole plasma to mild forms a Add distilled factors to severe forms a Disseminated Intravascular Coagulation (DIC) Coagulation Results from abnormal generation of Results fibrin circulating in blood fibrin a Initiated by: a • • • • • Complications of pregnancy Infection (Gram -) Malignancy Shock Head trauma DIC Signs and Symptoms DIC Subacute form - venous thrombosis, Subacute aortic valve thrombosis, emboli, thrombi may become serious most often in kidney leading to failure kidney a Acute massive DIC - thrombocytopenia Acute and depletion of clotting factors create severe bleeding tendency severe a DIC in the Laboratory DIC Subacute - thrombocytopenia, Subacute increased prothrombin time (PT) and partial thromboplastin time (PTT), reduced fibrinogen level, and increased fibrin split products fibrin a Acute Massive DIC- thrombocytopenia, Acute prolonged PT and PTT possible absence of clot formation, massive liver failure can mimic this form failure a DIC Treatment DIC Identify the cause Identify a Treat the cause a Circulating Anticoagulants Circulating Normally present substances inhibit Normally clotting clotting a Usually they are antibodies which bind Usually to prothrombin to a Lupus anticoagulant a • found in a variety of disorders • patients do not have increased risk of patients bleeding bleeding • patients do have increased risk of patients Platelet Disorders Platelet Thrombocytopenia a Caused by: a • drugs • bone marrow infiltration a Results in: • • • Petechiae ecchymosis mucosal bleeding Thrombocytopenia Thrombocytopenia a Heparin induced • heparin binds to platelet membrane • heparin inhibits platelet from functioning heparin with factors with • heparin as treatment for thrombosis works heparin in first five days -discontinue after that in Thrombotic Thrombocytopenic Purpura-Hemolytic-Uremic Syndrome Syndrome TTP-HUS TTP-HUS TTP-HUS Acute potentially fatal disorder a Symptoms a • • • • • severe thrombocytopenia Fragmented RBCs on blood smear Acute renal failure Fever Ischemic damage to multiple organs TTP-HUS TTP-HUS Most often appears suddenly, Most idiopathically idiopathically a Has been seen resulting from a • E.Coli infection • Pregnancy with severe preeclampsia or Pregnancy ecclampsia ecclampsia • Drugs use • Bone marrow transplant • Mets Other sources of Platelet Dysfunction Dysfunction a Hereditary disorders often have normal Hereditary count with prolongued bleeding times count • Von Willenbrand’s • disorders of platelet activation (most disorders common) either due to membrane defects or internal malfunction or a Acquired- aspirin and other drugs ...
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