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Hemolytic Anemia

Clinical Medicine II

What is hemolytic anemia increased RBC destruction (5%) all anemia worldwide
What happens w/ hemolytic anemia low RBCs, Hgb released from RBC
What happens w/ ↑ Hgb release in blood ↑breakdown of it: jaundice, ↑indirect bilirubin, gallstones, ↓haptoglobin
What does ↑ destruction cause ↑ RBC production: ↑reticulocytes, skeletal changes d/t over-active bone marrow
What does a reticulocyte >2.5% suggestive of hemolytic anemia, also higher in acute blood loss w/ erythroid compensation, also, adding a deficient molecule show up to 20% increase
How do we screen/monitor Hemolytic anemia monitor haptoglobin and retic count
Why does haptoglobin decrease with HA ↑ release of Hb d/t destruction of RBCs, Hp binds to the free Hb ↓ the free Hp
Retic count for deficiency anemia .5-2.0 (>1.5 would be d/t compensation but not significantly high)
Signs of extravascular hemolysis splenic hypertrophy/meagly, iron overload
Signs for intravascular hemolysis ↑free Hgb in plasma, ↑hemosiderin, ↑ met Hgb, no haptoglobin, hemoglobinuria (dark urine) ↑LDH
Common triad of hemolytic anemia normocytic or microcytic anemia, ↑ retic count >2,5, hyperbillirubinemia
Defect of Structural protein of RBC membrane (Na/K ATPase) hereditary spherocytosis, forms spherocytes ↑osmatic fragility, cells can’t pass thru spleen: hemolysis
Presentation of hereditary spherocytosis ↑MCH and MCHC, jaundice, splenomegaly, gallstones, (hyperchromic)
Tx hereditary spherocytosis control anemia, splenectomy, pneumococcal vaccine
Defect in structural protein forming weak elliptical cells hereditary elliptocytosis (less severe) d/t able to pass through spleen
How does RBC get ATP glycolysis
Where is glucose-6-phosphate dehydrogenase deficiency seen Africa, mediterranean, middle east, south east asia
What is G6PD protective of malaria
Patho G6pd can’t convert to 6phosphate gluconate, so ↓ NADPH, ↓ glutathione, no protection against oxidation, RBC’s destroyed
induce G6PD def antimalarials, nitrofurantoin, NSAIDS, quinidine, quinine, sulfonamides, aspirin and infx, fava beans
Acute sxs of G6PD def malaise, weakness, abd/back pain, ↑bilirubin, jaundice, dark urine/hemoglobinuria
Diagnosis of G6PD normochromic/cytic anemia, During attack blood smear shows bite cells, ↑free Hb, so ↓Hp, ↑reticulocytes, ↑LDH, ↑billirubin, G6PD screening, DNA analysis
Sxs of G6PD malaise, weakness, abd/back pain, ↑bilirubin, jaundice,
Complications of G6PD Acute: renal railure, aplastic crisis Chronic: bilirubin gallstones, splenomeagaly
Problem with PKD loses 2 ATP production
Metabolic defect of PKD no PK to conversion to pyruvate (PEP) which loss of ATP→↓ATP causes RBC rigidity: hemolysis: removed by spleen
Presentation and Dx of PKD neonatal jaundice, ↑ reticulocytes, splenomegaly (broad anemia signs), dx: enzyme and DNA analysis
Tx of PKD supportive, ↑ folic acid, avoid transfusions if not severe, iron chelation? Splenectomy?
Where is thalassemia commonly seen Mediterranean
Genetic varience of alpha-thalassemia 1-4 gene deletion (seen in Asians)
Signs for 2-3 gene mutation microcytic anemia, ↑ reticulocyte, splenomegaly,
1 gene mutation is what asymptomatic and a carrier trait
Pathology of thalassemia imbalance f a and b chain production: ineffective erythropoiesis, hemolysis of mature RBCs
What is often mistaken for iron def thalassemia minor, heterozygous, mild anemia, nl life-expectancy
How does b-thalassemia major usually present 1st 2nd yr, failure to thrive
Tx b-thalassemia severe anemia needs transfusions q4-6wks
Dx of thalassemia for mild to severe ↓Hgb, HCT, MCV, MCH and ↑ reticulocytes Hgb eectophoresis
Growth findings of thalassemia growth retardation, bone deformities d/t ↑bone marrow production, no room, splenomegaly
Fxns of transfusions for tx thalassemia ↑nl Hgb corrects anemia, suppressing ineffective erythropoiesis
Dx b/w iron def and thallasemia thalassemia is ↑ reticulocytes
Issue w/ concurrent transfusions iron overload, will need to tx eventually
What causes fatality of thalassemia iron overload→CHF, infection, liver failure
Pathotphys of sickle cell anemia adenine is replaced by thymine (single substitution): glutamic acid replaced by valine, Hgb loses –charge
When hgb is – what happens O2 can’t bind, causes hgb to polymerize into rigid bundles: sicke shaped
Problem with sickle cell shape ↓ O2 carrying, impair blood flow →tissue ischemia cause death
Genetic inheritance of sickle cell , protective against what autosomal recessive, malaria with both
Complications and symptoms of sickle cell fatigue, anemia, recurrent painful vaso-occlusive crisis could result in acute/chronic multisystem organ failure
What are sickle cell crisis precipitated by infection, dehydration, cold, acidosis, hypoxia,
Set test for dx sickle cell hemoglobin electrophoresis, blood smears, but will have these vaso-occlusive episodes
Tx sickle cell hydroxyruria, transfusions, folic acid supplements, iron chelation, prompt tx of infxs
Why do we give hydroxyuria ↑Hgb fetal, (more nl and resistant to sickling) and also ↓ WBC and reticulocytes
Why do we give transfusions proportion of Hgb S and sickling
What do we do for a sickle cell crisis IV fluids, O2, rest, pain med, alagesics (narcs/nsaids) transfuse to maintain adequate Hgb concentration, organ management, splencecomy?
Most life threatening hemolytic anemia B-thalassemia and sickle cell
Purpose of transfusions “normalize” Hgb, O2 delievery, and suppress ineffective erythropoiesis
Attracting macrophages and neutrophils chemotaxis
Enhancing phagocytosis of antignes opsonization
Rupturing of membranes of foreign cless - cell lysis
AG-bearing agents clumping
Direct antiglobulin AG added to pt’s RBCs detects IgG and compliments bound to RBC membrane Agglutination-+test
Indirect AG test detects autoantibodies and alloantibodies induced by transfustions ( mixing blood)
Created by: becker15
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