Download Free Medical RBC and Bleeding Disorders PowerPoint Presentation

RBC and Bleeding Disorders PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "RBC and Bleeding Disorders”.

This medical PowerPoint presentation is about RBCs (red blood cells) which are essential components of blood that carry oxygen from the lungs to the bodys tissues and remove carbon dioxide from those tissues. Bleeding disorders are conditions that affect the bodys ability to stop bleeding. Several types of bleeding disorders can impact RBCs, including Hemophilia, Von Willebrand disease, Thrombocytopenia, Sickle cell anemia, and Iron-deficiency anemia.

Tags : RBC, Bleeding Disorders, red blood cells, Hemophilia, Von Willebrand disease, Thrombocytopenia, Sickle cell anemia, Iron-deficiency anemia, Hematology, Hematology PowerPoint presentation

Published on : May 29, 2023 | Views : 1493 | Downloads : 3

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

RBC and BLEEDING DISORDERS
Slide 2-

RBC and Bleeding Disorders NORMAL Anatomy, histology Development Physiology ANEMIAS Blood loss: acute, chronic Hemolytic Diminished erythropoesis POLYCYTHEMIA BLEEDING DISORDERS
Slide 3-

ppt slide no 3 content not found
Slide 4-

ppt slide no 4 content not found
Slide 5-

ppt slide no 5 content not found
Slide 6-

ppt slide no 6 content not found
Slide 7-

ppt slide no 7 content not found
Slide 8-

WHERE is MARROW? Yolk Sac: very early embryo Liver, Spleen: NEWBORN BONE CHILDHOOD: AXIAL SKELETON & APPENDICULAR SKELETON BOTH HAVE RED (active) MARROW ADULT: AXIAL SKELETON RED MARROW, APPENDICULAR SKELETON YELLOW MARROW
Slide 9-

MARROW FEATURES CELLULARITY 50% MEGAKARYOCYTES at least 1-2/hpf M:E RATIO  3:1 MYELOID MATURATION  1/3 bands or more ERYTHROID MATURATION  nucleus/cytoplasm LYMPHS, PLASMA CELLS  small percentage STORAGE IRON, i.e., HEMOSIDERIN present “FOREIGN CELLS”
Slide 10-

MARROW “DIFFERENTIATION”
Slide 11-

ppt slide no 11 content not found
Slide 12-

ANEMIAS* BLOOD LOSS ACUTE CHRONIC IN-creased destruction (HEMOLYTIC) DE-creased production * A good definition would be a decrease in OXYGEN CARRYING CAPACITY, rather than just a decrease in red blood cells, because you need to have enough blood cells THAT FUNCTION, and not just enough blood cells.
Slide 13-

Features of ALL anemias Pallor, where? Tiredness Weakness Dyspnea, why? Palpitations Heart Failure (high output), why?
Slide 14-

ppt slide no 14 content not found
Slide 15-

HEMOLYTIC HEREDITARY MEMBRANE disorders: e.g., spherocytosis ENZYME disorders: e.g., G6PD deficciency HGB disorders (hemoglobinopathies) ACQUIRED MEMBRANE disorders (PNH) ANTIBODY MEDIATED, transfusion or autoantibodies MECHANICAL TRAUMA INFECTIONS DRUGS, TOXINS HYPERSPLENISM
Slide 16-

IMPAIRED PRODUCTION Disturbance of proliferation and differentiation of stem cells: aplastic anemias, pure RBC aplasia, renal failure Disturbance of proliferation and maturation of erythroblasts Defective DNA synthesis: (Megaloblastic) Defective heme synthesis: (Fe) Deficient globin synthesis: (Thalassemias)
Slide 17-

MODIFIERS MCV, microcytosis, macrocytosis MCH MCHC, hypochromic RDW, anisocytosis
Slide 18-

HEMOLYTIC ANEMIAS Life span LESS than 120 days Marrow hyperplasia (M:E), EPO+ Increased catabolic products, e.g., bilirubin, serum HGB, hemosiderin, haptoglobin-HGB
Slide 19-

HEMOLYSIS INTRA-vascular (vessels) EXTRA-vascular (spleen)
Slide 20-

M:E Ratio normally 3:1
Slide 21-

HEREDITARY SPHEROCYTOSIS Genetic defects affecting ankyrin, spectrin, usually autosomal dominant Children, adults Anemia, hemolysis, jaundice, splenomegaly, gallstones (what kind?)
Slide 22-

Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency A- and Mediterranean are most significant types
Slide 23-

FEATURES of G6PD Defic. Genetic: Recessive, X-linked Can be triggered by foods (fava beans), oxidant substances drugs (primaquine, chloroquine), or infections HGB can precipitate as HEINZ bodies Acute intravascular hemolysis can occur: Hemoglobinuria Hemoglobinemia Anemia
Slide 24-

Sickle Cell Disease Classic hemoglobinopathy Normal HGB is α2 β2: β-chain defects (Val->Glu) Reduced hemoglobin “sickles” in homozygous 8% of American blacks are heterozygous
Slide 25-

Clinical features of HGB-S disease Severe anemia Jaundice PAIN (pain CRISIS) Vaso-occlusive disease: EVEREWHERE, but clinically significant bone, spleen (autosplenectomy) Infections: Pneumococcus, Hem. Influ., Salmonella osteomyelitis
Slide 26-

ppt slide no 26 content not found
Slide 27-

THALASSEMIAS A WIDE VARIETY of diseases involving GLOBIN synthesis, COMPLEX genetics Alpha or beta chains deficient synthesis involved Often termed MAJOR or MINOR, depending on severity, silent carriers and “traits” are seen HEMOLYSIS is uniformly a feature, and microcytic anemia, i.e, LOW MCV (just like iron deficiency anemia has a low MCV) A “crew cut” skull x-ray appearance may be seen in severe erythroid hyperplasia.
Slide 28-

ppt slide no 28 content not found
Slide 29-

Hemoglobin H Disease Deletion of THREE alpha chain genes HGB-H is primarilly Asian HGB-H has a HIGH affinity for oxygen HGB-H is unstable and therefore has classical hemolytic behavior
Slide 30-

HYDROPS FETALIS FOUR alpha chain genes are deleted, so this is the MOST SEVERE form of thalassemia Many/most never make it to term Children born will have a SEVERE hemolytic anemia as in the erythroblastosis fetalis of Rh disease: Pallor (as in all anemias), jaundice, kernicterus Edema (hence the name “hydrops”) Massive hepatosplenomegaly (hemolysis)
Slide 31-

Paroxysmal Nocturnal Hemoglobinuria (PNH) ACQUIRED, NOT INHERITED like all the previous hemolytic anemias were ACQUIRED mutations in phosphatidylinositol glycan A (PIGA) Note: It is “P” and “N” only 25% of the time! GlycosylphosPhatidylInositol (lipid rafts)
Slide 32-

Immunohemolytic Anemia All of these have the presence of antibodies and/or compliment present on RBC surfaces NOT all are AUTOimmune, some are caused by drugs Antibodies can be WARM (IgG) COLD AGGLUTININ (IgM) COLD HEMOLYSIN (paroxysmal) (IgG)
Slide 33-

IMMUNOHEMOLYTIC ANEMIAS WARM AGGLUTININS (IgG), will NOT agglutinate at room temp Primary Idiopathic (most common) Secondary (Tumors, especially leuk/lymph, drugs) COLD AGGLUTININS: (IgM), WILL agglutinate at room temp Mycoplasma pneumoniae, HIV, mononucleosis COLD HEMOLYSINS: (IgG) Cold Paroxysmal Hemoglobinuria, hemo-LYSIS in body, ALSO often follows mycoplasma pneumoniae
Slide 34-

COOMBS TEST DIRECT: Patient’s CELLS are tested for surface Ab’s INDIRECT: Patient’s SERUM is tested for Ab’s.
Slide 35-

HEMOLYSIS/HEMOLYTIC ANEMIAS DUE TO RBC TRAUMA Mechanical heart valves breaking RBC’s MICROANGIOPATHIES: TTP Hemolytic Uremic Syndrome
Slide 36-

NON-Hemolytic Anemias:i.e., DE-creased Production “Megaloblastic” Anemias B12 Deficiency (Pernicious Anemia) Folate Deficiency Iron Deficiency Anemia of Chronic Disease Aplastic Anemia “Pure” Red Cell Aplasia OTHER forms of Marrow Failure
Slide 37-

MEGALOBLASTIC ANEMIAS Differentiating megaloblasts (marrow) from macrocytes (peripheral smear, MCV>94) Impaired DNA synthesis For all practical purposes, also called the anemias of B12 and FOLATE deficiency Often VERY hyperplastic/hypercellular marrow
Slide 38-

ppt slide no 38 content not found
Slide 39-

Vit-B12 Physiology Oral ingestion Combines with INTRINSIC FACTOR in the gastric mucosa Absorbed in the terminal ileum DEFECTS at ANY of these sites can produce a MEGALOBLASTIC anemia
Slide 40-

Please remember that ALL megaloblastic anemias are also MACROCYTIC (MCV>94 or MCV~100), and that not only are the RBC’s BIG and hyperplastic/hypercellular, but so are the neutrophils, and neutrophilic precursors in the bone marrow too, and even more so, HYPERSEGMENTED!!!
Slide 41-

PERNICIOUS ANEMIA MEGALOBLASTIC anemia LEUKOPENIA and HYPERSEGS JAUNDICE NEUROLOGIC posterolateral spinal tracts ACHLORHYDRIA Can’t absorb B12 LOW serum B12 Flunk Schilling test, i.e., can’t absorb B12, using a radioactive tracer
Slide 42-

FOLATE DEFICIENCY MEGALOBLASTIC AMEMIAS Decreased Intake: diet, etoh-ism, infancy Impaired Absorption: intestinal disease DRUGS: anticonvulsants, BCPs, CHEMO Increased Loss: Hemodialysis Increased Requirement: Pregnancy, infancy Impaired Usage
Slide 43-

Fe Deficiency Anemia Due to increased loss or decreased ingestion, almost always, in USA, nowadays, increased loss is the reason Microcytic (low MCV), Hypochromic (low MCHC) THE ONLY WAY WE CAN LOSE IRON IS BY LOSING BLOOD, because FE is recycled!
Slide 44-

Fe Transferrin Ferritin (GREAT test) Hemosiderin
Slide 45-

Clinical Fe-Defic-Anemia Adult men: GI Blood Loss PRE menopausal women: menorrhagia POST menopausal women: GI Blood Loss
Slide 46-

ppt slide no 46 content not found
Slide 47-

2 BEST lab tests: Serum Ferritin Prussian blue hemosiderin stain of marrow (also called an “iron” stain)
Slide 48-

ppt slide no 48 content not found
Slide 49-

Anemia of Chronic Disease* CHRONIC INFECTIONS CHRONIC IMMUNE DISORDERS NEOPLASMS LIVER, KIDNEY failure * Please remember these patients may very very much look like iron deficiency anemia, BUT, they have ABUNDANT STAINABLE HEMOSIDERIN in the marrow!
Slide 50-

APLASTIC ANEMIAS ALMOST ALWAYS involve platelet and WBC suppression as well Some are idiopathic, but MOST are related to drugs, radiation FANCONI’s ANEMIA is the only one that is inherited, and NOT acquired Act at STEM CELL level, except for “pure” red cell aplasia
Slide 51-

APLASTIC ANEMIAS
Slide 52-

APLASTIC ANEMIAS CHLORAMPHENICOL OTHER ANTIBIOTICS CHEMO INSECTICIDES VIRUSES EBV HEPATITIS VZ
Slide 53-

MYELOPHTHISIC ANEMIAS Are anemias caused by metastatic tumor cells replacing the bone marrow extensively
Slide 54-

POLYCYTHEMIA Relative (e.g., hemoconcentration) Absolute POLYCYTHEMIA VERA (Primary) (LOW EPO) POLYCYTHEMIA (Secondary) (HIGH EPO) HIGH ALTITUDE EPO TUMORS EPO “Doping” CVAC, the trendy California bubble pods
Slide 55-

P. VERA A “myeloproliferative” disease ALL cell lines are increased, not just RBCs
Slide 56-

BLEEDING DISORDERS(aka, Hemorrhagic “DIATHESES”) Blood vessel wall abnormalities √ Reduced platelets √ Decreased platelet function √ Abnormal clotting factors √ DIC (Disseminated INTRA-vascular Coagulation), also has ↓ plats.
Slide 57-

VESSEL WALL ABNORMALITIES(angiopathic thrombocytopenias)(NON-thrombotic cytopenic purpuras) Infections, especially, meningococcemia, and rickettsia Drug reactions causing a leukocytoclastic vasculitis Scurvy, Ehlers-Danlos, Cushing syndrome Henoch-Schönlein purpura (mesangial IgA deposits too) Hereditary hemorrhagic telangiectasia (Osler–Weber–Rendu syndrome, Autosomal Dominant) Amyloid
Slide 58-

THROMBOCYTOPENIAS Like RBCs: DE-creased production IN-creased destruction Sequestration (Hypersplenism) Dilutional Normal value 150K-300K
Slide 59-

DE-CREASED PRODUCTION APLASTIC ANEMIA ACUTE LEUKEMIAS ALCOHOL, THIAZIDES, CHEMO MEASLES, HIV MEGALOBLASTIC ANEMIAS MYELODYSPLASTIC SYNDROMES (PRE-Leukemias)
Slide 60-

IN-CREASED DESTRUCTION AUTOIMMUNE (ITP) POST-TRANSFUSION (NEONATAL) QUINIDINE, HEPARIN, SULFA MONO, HIV DIC, “CONSUMPTIVE” TTP/HUS “MICROANGIOPATHIC”
Slide 61-

THROMBOCYTOPENIAS ITP (Idiopathic Thrombocytopenic Purpura) Acute Immune DRUG-induced HIV associated TTP, Hemolytic Uremic Syndrome
Slide 62-

I.T.P. ADULTS AND ELDERLY ACUTE OR CHRONIC AUTO-IMMUNE ANTI-PLATELET ANTIBODIES PRESENT INCREASED MARROW MEGAKARYOCYTES Rx: STEROIDS
Slide 63-

ACUTE ITP CHILDREN Follows a VIRAL illness (~ 2 weeks) ALSO have anti-platelet antibodies Platelets usually return to normal in a few months
Slide 64-

DRUGS Quinine Quinidine Sulfonamide antibiotics HEPARIN
Slide 65-

HIV BOTH DE-creased production AND IN-creased destruction factors are present
Slide 66-

Thrombotic Microangiopathies BOTH are very SERIOUS CONDITIONS with a HIGH mortality: TTP (THROMBOTIC THROMBOCYTOPENIC PURPURA) H.U.S. (HEMOLYTIC UREMIC SYNDROME) These can also be called “consumptive” coagulopathies, just like a DIC
Slide 67-

“QUALITATIVE” platelet disorders Mostly congenital (genetic): Bernard-Soulier syndrome (Glycoprotein-1-b deficiency) Glanzmann’s thrombasthenia (Glyc.-IIB/IIIA deficiency) Storage pool disorders, i.e., platelets mis-function AFTER they degranulate ACQUIRED: ASPIRIN, ASPIRIN, ASPIRIN
Slide 68-

BLEEDING DISORDERS due toCLOTTING FACTOR DEFICIENCIES NOT spontaneous, but following surgery or trauma ALL factor deficiencies are possible Factor VIII and IX both are the classic X-linked recessive hemophilias, A and B, respectively ACQUIRED disorders often due to Vitamin-K deficiencies (II, VII, IX, X) von Willebrand disease the most common, 1%
Slide 69-

von Willebrand Disease 1% prevalence, most common bleeding disorder Spontaneous and wound bleeding Usually autosomal dominant Gazillions of variants, genetics even more complex Prolonged BLEEDING TIME, NL platelet count vWF is von Willebrand Factor, which complexes with Factor VIII, it is the von Willebrand Factor which is defective in von Willebrand disease Usually BOTH platelet and FactorVIII-vWF disorders are present
Slide 70-

PTT PT/INR
Slide 71-

HEMOPHILIA A The “classic” HEMOPHILIA Factor VIII decreased Co-factor of Factor IX to activate Factor X Sex-linked recessive Hemorrhage usually NOT spontaneous Wide variety of severities Prolonged PTT (intrinsic) only Rx: Recombinant Factor VIII
Slide 72-

HEMOPHILIA B The “Christmas” HEMOPHILIA Factor IX decreased Sex-linked recessive Hemorrhage usually NOT spontaneous Wide variety of severities Prolonged PTT (intrinsic) only Rx: Recombinant Factor IX
Slide 73-

DIC, Disseminated INTRA-vascular, Coagulation ENDOTHELIAL INJURY WIDESPREAD FIBRIN DEPOSITION HIGH MORTALITY ALL MAJOR ORGANS COMMONLY INVOLVED
Slide 74-

DIC, Disseminated INTRA-vascular, Coagulation Extremely SERIOUS condition NOT a disease in itself but secondary to many conditions Obstetric: MAJOR OB complications, toxemia, sepsis, abruption Infections: Gm-, meningococcemia, RMSF, fungi, Malaria Many neoplasms, acute promyelocytic leukemia Massive tissue injury: trauma, burns, surgery “Consumptive” coagulopathy
Slide 75-

Common Coagulation TESTS PTT (intrinsic) PT INR (extrinsic) Platelet count, aggregation Bleeding Time, so EASY to do Fibrinogen Factor Assays
Slide 76-

RBC LAB http://www.chronolab.com/hematology/2_1.htm