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Anemia Odesa National Medical University Anemia Odesa National Medical University

Anemia Odesa National Medical University - PowerPoint Presentation

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Anemia Odesa National Medical University - PPT Presentation

Department of internal medicine 1 with course of cardiovascular pathology Complete blood count CBC RED BLOOD CELL COUNT M 4555 10 12 F 3545 10 12 HEMOGLOBIN M 130160 gl 1316 mgdl ID: 1033128

iron anemia deficiency hemoglobin anemia iron hemoglobin deficiency blood cell cells rbc treatment hemolytic severe disease due liver index

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1. AnemiaOdesa National Medical UniversityDepartment of internal medicine 1with course of cardio-vascular pathology

2. Complete blood count (CBC)RED BLOOD CELL COUNTM – 4,5-5,5 *1012; F – 3,5-4,5 *1012 HEMOGLOBINM – 130-160 g/l (13-16 mg/dl); F – 120-140 f/l (12-14 mg/dl)HEMATOCRIT (HCT)34-46%PLATELET COUNT180-400 *109MCV80 – 100 flMCH26 – 34 pgMCHC30 – 370 g/lCOLOR INDEX0,85 – 1,05RETICULOCYTES 0,2 – 1,2% ESRM – 2-10 mm/hour; W – 5-15 mm/hourRDWc11.5-14.5%

3. MCV (Mean corpuscular volume) – size of the RBCRDW (Red Cell Distribution Width) - this indicator tells how much red cells differ in sizeMCH (Mean corpuscular hemoglobin) – shows how much hemoglobin is contained in one erythrocyteMCHC (Mean corpuscular hemoglobin concentration) – shows as erythrocyte is saturated with hemoglobin

4. Anisocytosis - the content of macro- and microcytes is more than 15% of all red blood cellsPoikilocytosis - different forms of red blood cells Spherocytes- erythrocytes have a spherical shape, a greater thickness, they have no central illumination. Spherocytes - cells, ready to hemolysis. Spherocytosis observed in hemolytic anemia, septicemia, blood incompatibility AB0 system, DIC syndrome, with implantation of artificial blood vessels, heart valves, burns, autoimmune disease. Microspherocytosis is a pathognomonic sign for anemia Minkowski–Chauffard (hereditary microspherocytosis). In a small number microspherocytes may occur in other hemolytic anemias. Ovalocytes - cell oval or elongated form due to the anomaly of the membrane or hemoglobin. It occurs in hereditary elliptocytosis, thalassemia, megaloblastic anemia, iron deficiency anemia, liver cirrhosis, anemia associated with deficiency of G-6-PDG, glutathione, sickle-cell anemia. It may occur as an artifact (in the thickest part of the drug).

5. acanthocytes (sheet-like cell, spur-like cell) – RBC with protrusions of various sizes, arranged at different distances from each other. Occur in severe liver disease (chronic hepatitis, cirrhosis, alcoholic liver disease), hereditary deficiency of pyruvatekinase, hereditary spherocytosis (severe), in violation of lipid metabolism, treatment with heparin. A small number of acanthocytes can be found in patients after splenectomy. codocytes (target cells) - flat pale colored periphery of RBC with accumulation of hemoglobin in a center as a target. Codocytes have an increased surface area due to excess of cholesterol. Typical for thalassemia, hemoglobinopathies S, C, D and E, iron deficiency anemia, lead poisoning, liver disease, especially accompanied by obstructive jaundice, after removal of the spleen. drepanocytes (sickle cell) - the cells like a sickle or holly leaves. Typical for sickle cell anemia and other hemoglobynopathies stomatocytes (mouth cells) – remind the mouth. Typical for hereditary spherocytosis and stomatocytosis, tumors, alcoholism, cirrhosis and obstructive liver disease, cardiovascular diseases, after transfusions, when taking certain medications. Can be revealing as artifacts.

6. Echinocytes (Burr cells) - cell has spikes of the same size and symetrical localization. It occurs in uremia, a transfusion of blood containing the old RBC, gastric cancer, peptic ulcer, complicated by bleeding, hypophosphatemia, hypomagnesemia, in hereditary deficiency pyruvate kinase, phosphoglycerate. It often occurs as an artifact. Degmacytes ("bitten cell") - a cell looks like it took a bite. Occurs in G-6-PDG deficiency, unstable hemoglobin Bubble cells - cell looks as though on the surface there is a bubble or blister. The mechanism of formation is not clear. It occurs at a the immune hemolytic anemia. Schistocytes - cells similar to the helmet, cocked hat, splinters. Observed in a microangiopathy, hemolytic anemia by physical factors, malignant hypertension, uremia, complications with prosthetic valves and vessels, DIC, sepsis, tumor, when taking certain medications, exposure to toxins. Dacrocytes (Teardrop Cells) - cells remind drop or a tadpole. Observed in a myelofibrosis, myeloid metaplasia, hypoplastic anemia due to tumor, granuloma, lymphoma and fibrosis, thalassemia, severe iron deficiency, toxic hepatitis.

7. AnemiaDefinition: Low oxygen carrying capacity in the blood due to low erythrocyte mass.We use the hematocrit or hemoglobin as surrogate markers for the erythrocyte mass because that it too difficult to measure.Hemoglobin of < 12 g/dL in women or a Hemoglobin of <13 g/dL in men is considered abnormal (WHO criteria).The hematocrit is approximately 3 x the hemoglobin.

8. Classifications of anemia (1)1. Posthemorrhagic (acute / chronic)2. Due to the formation of RBC disorders(iron deficiency, deficiency of vitamin B12 and folic acid, hypo/aplastic)3. Hemolytic (congenital/ acquired)4. Mixed

9. Classifications of anemia (2)Macrocytic (MCV>100 fl)Microcytic (MCV<80 fl)Normocytic (MCV 81-99 fl)

10. Classifications of anemia (3)Hypochromic (color index <0.8) Normochromic (color index 0.85-1.05)Hyperchromic (color index >1.05)

11. Classifications of anemia (4)Severity of anemiaMild (Hb >90 g/L or 9.0 mg/dl)Moderate (Hb 90-70 g/L or 9.0-7.0 mg/dl)Severe (Hb <70 g/L or 7.0 mg/dl)

12. Posthemorrhagic anemia

13. Acute posthemorrhagic anemiaEtiology – bleeding Symptoms – (depends on the duration and volume of blood loss) severe weakness, shortness of breath, dizziness, syncope, ringing in the ears, darkening of the eyes, dry mouth, cold sweat, paleness of skin and mucose membranes, tachycardia, arrhythmias, hypotension, tachypnea

14. Lab diagnostics Reflex-vascular phase (1-2 days) – normal level of RBC, Hb; possible ↑WBC, Plt;Hydremic phase (2-3 days) - ↓ RBC, Hb; N color index;Bone marrow phase (5-6 days) - ↑ reticulocytes; presence of young WBCNormalization in 2-3 weeksTreatment - Stop the bleeding- Replenishment of circulating blood volume- If needed - the transfusion of blood or its components

15. Chronic posthemorrhagic anemiaEtiology – Repeated and prolonged bleeding Symptoms, diagnosis is similar to iron-deficiency anemia

16. Anemia due to RBC and Hb formation disorders

17. Iron is a part of hemoglobin, myoglobin, cytochrome, catalase enzymes , lactateperoxidase; ferritin, hemosiderin, transferrin and other enzymes.

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19. Iron-deficiency anemia (sideropenic anemia)EtiologyChronic bleedings (hyperpolymenorrhea, GIT diseases, hematuria, epistaxis, lung diseases, iatrogenic blood loss) Increased need for iron (pregnancy, childbirth, lactation, puberty, intense exercise)Insufficient intake of iron from foodMalabsorption syndrome Violation of transport (reducing amount of transferrin)CongenitalHypoproteinemiaPresence of antibodies to transferrin and its receptors

20. Symptoms and sings Anemic syndrome Sideropenic syndromeTaste perversionAddicted to spicy, salty, sour, spicy foodSmell perversion Severe muscle weakness and fatigue, muscle atrophyDegenerative changes in the skin and its appendages (skin is dry, flaking; hair is thin, faint, rapidly fall and turning gray; koilonychia)Angular stomatitisGlossitisAtrophic gastritis and enteritisa symptom of the "blue sclera“sideropenic subfebrilitetmoderate immunosuppressionreduction of reparative processes of the skin, mucous membranes

21. Conjunctival rim pallor

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23. Lab diagnostic CBC (↓ RBC and Hb, ↓MCH, ↓color index, ↓MCV, anisocytosis, poikilocytosis, N reticulocytes, moderate ↑ ESR)Checking iron (↓ferritin, ↓serum iron (FE), ↑total iron-binding capacity (TIBC), ↓iron saturation, ↓test with desferal)Puncture of the bone marrow (↓ sideroblast cells)

24. Treatment Treatment of etiological factorsDietTreatment with iron-consist drugsElimination of iron deficiency(100-300 mg BID/TID per os, rarely – IM or IV) 6-8 weeksRestocking (1/2-1/3 from main dose) 3 monthPreventive treatment (if necessary)

25. Iron redistribution anemias (Anemia in impaired iron reutilization,Anemia of chronic disease) anemia caused by disturbance of movement of iron into the plasma and into bone marrow from the depot.

26. EtiologyAcute and chronic infection diseases Sepsis Tuberculosis Infective endocarditisChronic leukemiaSarcoidosis Rheumatoid arthritisChronic active hepatitisOncologyAlcoholic damaging of liver IHD

27. Lab diagnostic CBC (↓ RBC and Hb, ↓MCH, ↓color index)Checking iron (↑ferritin, N/↓ serum iron, ↓/N total iron-binding capacity (TIBC))Puncture of the bone marrow (↓ sideroblast cells)Clinical and laboratory sings of inflammation Treatment – mainly its treatment of main disease

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29. Megaloblast anemia/ macrocytic anemia

30. Folate deficiencyFound in: Fruits (e.g. citrus, melon, bananas), leafy green vegetables, and fortified grain productsCauses include: alcohol due to both a decreased ability to absorb folate and, frequently, decreased intake of folate rich foods Malabsorption (celiac disease, IBD)Diseases/conditions associated with rapid cell turnover such as sickle cell disease, psoriasis, pregnancyMedications: trimethoprim, phenytoin, methotrexate

31. B12 deficiency anemia Etiology:Problems with absorptionCompetitive consumption of vitamin B12 Increased consumption (multiple pregnancy, ch hemolytic anemia, myeloma, thyrotoxicosis)Violation of dietary intakeDecreasing of storage (liver cirrhosis)Violation of vitamin B12 transport

32. Symptoms Damaging of the digestive system (lack or loss of appetite, belching, pain and burning in the tongue. Development of glossitis, atrophic gastritis, atrophic changes of the intestinal mucosa)Damage of the hematopoietic system/ anemic syndrome (specificity - yellowness of the skin and sclera)Nervous system damage / funicular myelosis (violation of proprioceptive sensitivity, reduced reflexes, muscle atrophy of the lower extremities, pelvic organ dysfunction OR lower spastic paraparesis)

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34. Lab diagnostic CBC - ↓ Hb/RBC, ↑MCV, ↑ color index, anisocytosis, poikilocytosis, Howell-Jolly bodies, Cabot rings, ↓ reticulocytes, ↓ WBC, neutrophils, eosinophils, lymphocytes, platelets , hypersegmented neutrophils Myelogram - irritation red hematopoietic, appearance of the megaloblast type of hematopoesis, changing in myeloid cellsThe amount of folate, vitamin B-12 and vitamin C in blood antibodies to intrinsic factorMethylmalonic acid testPlasma Total Homocysteine

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36. Vitamin B12If levels are at the lower limits of normal (200-300), then consider checking methylmalonic acid and homocysteine levels, these will be elevated in the case of B12 deficiencyShould be given orally, IM in rare situationsOral dosing is 1000 – 2000 mcg po q dayIM dosing is 1000 mcg IM q day x 7 days, then q wk x 4 wks then q month

37. Criteria for of treatment effectiveness- Subjective improvement- Reticulocytosis in 5-7 days of treatment (20%)- Increase in hemoglobin and RBC from 2 week of treatment- Normalization of the CBC in 3-4 weeks

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39. Hemolytic anemiaLabs to order: reticulotye count, peripheral smear, haptoglobin, indirect bilirubin and LDHThe peripheral smear will help you differentiate between causes of hemolysis

40. Extravascular Hemolytic AnemiaEtiologies of extravascular hemolysis include:Congenital hemoglobin abnormalities: hemoglobinopathiesErythrocyte membrane abnormalities: hereditary spherocytosisErythrocyte metabolic abnormalities: G6PD deficiencyAuto-immune process: idiopathic, underlying malignancy, CVD, lymphoproliferative disorders, medications (PCN, cephalosporins, NSIADs)

41. Glucose 6-phospate dehydrogenase deficiencyX-linked enzyme deficiency that results in decreased glutathione levelsMost common form results in severe hemolysis with medications (primaquine, sulfa, dapsone), fava beans and some infxn.Dx: enzyme activity testing, may have false negative test in the setting of acute hemolysis, re-test at 2-3 months

42. Intravascular hemolytic anemiaEtiologies include:Microangiopathic hemolytic anemia – TTP, HUS, DIC, HELLPShearing due to malfunctioning mechanical heart valves

43. TransfusionsWhen to transfuse?General rule: Hct <21%, consider at <25% in pt’s with multiple medical problemsOther times to consider: on-going rapid blood loss, highly symptomatic patients, patient with low Hct and severe cardiovascular diseaseYou expect the Hct to increase 3% for each unit of blood transfused

44. Anemia of Chronic Kidney DiseaseHypoproliferative (low reticulocyte count), normocytic anemiaFor erythropoietin therapy to be effective need adequate iron stores – ferritin >100 and transferrin saturation >20%Treatment goal is hemoglobin of 11-12 (Hct 33-36%), higher levels are associated with increased morbidity and mortality – carries a Black Box warningCan use darbopoetin or epoetin

45. ThalassemiaThalassemia trait: mild anemia with pronounced microcytosis (MCV <70)Ethnicity: Mediterranean, Asian, AfricanPt are asymptomaticFamHx is often negative Dx thal trait: Hemoglobin electrophoresisThalassemia intermedia:Ineffective erythropoiesis, more severe anemia, often require frequent transfusions, at risk of development of iron overloadIron deficiency anemia: usually more pronounced microcytic anemia than thal trait