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Microcytic anemias
| Question | Answer |
|---|---|
| Microcytic anemia have MCV of? | <80 |
| Size of RBC | small |
| how are RBC s formed? | Progenitor cell=Erythroblast. It divides to make RBC. |
| why does microcytosis occur? | Erythroblasts undergo one extra division than they are supposed to make microcytic RBC. This is because of DECREASED production of Hb. They divide to keep the concentration of Hb maintained. But results in smaller RBC |
| What is Hb made up of? | Hb=heme+globin; Heme= Fe+Protopophoryin. |
| What is the cause of microcytic anemia? | 1)Low Fe; low heme; low Hb (THUS IRON DEFICIENCY ANEMIA) 2)UNAVAILABLE Fe; low heme; low Hb(ANEMIA OF CHRONIC DISEASE) 3)Low prot; low heme;lowHB(SIDEROBLASTIC) 4)Decreased globin=low HB(THALASSEMIA) |
| How is Iron absorbed? | Enterocytes(line the duodenum)-> Fe+ferroprtin into blood. Transderrin takes Fe to Liver and bone marrow macrophages to store. It is bound to ferritin to avoid free radicals. |
| How do you measure Fe in the blood? | serum iron |
| how would you measure the transferrin molecules in the blood(bound and unbound) | TIBC- total FE binding capacity |
| How would measure just bound trasferrin | percent saturation |
| How would you measure the amoun of iron stored in macrophages in the liver and bone marow | serum ferritin |
| Fe deficiency is age based sooo... in infants? | breast feeding- has little Fe |
| Fe deficiency is age based sooo... in children? | poor diet |
| Fe deficiency is age based sooo... in adults? | peptic ulcers in males menorrhagia or pregnancy in females |
| Fe deficiency is age based sooo... in elderly? | colon polyps/ carcinoma(West) hookworms(EAST) |
| Fe deficiency can be caused due to malabsorption? | ciliac disease disrupts the cilia of the duodenum. |
| Fe deficiency can be caused due to gastrectomy? | iron is in Fe2+ and Fe3+. Fe2+ more easily absorbed. Acid maintains Fe2+ state. Gastrectomy looses part of the tummy and acid=so less Fe2+ |
| What are the stages of iron def in loss of blood? | make RBC using stored Fe. Thus low ferritin & high TIBC as liver tries to maintain the stored transferrin. Then low serum Fe & % saturation. Due to low Fe normocytic anemia happns.(Body wants to make good RBC but less). Then microcytic, hypochromic RBC. |
| What are the clinical features of Fe def? | anemia, koilonychia(spoon shaped nails), and pica(chew on things- dirt, ice). |
| Laboratory finding for Fe def anemia? | Microcytic, hypochromic RBCs with high red cell distribution width(RDW) 2. low ferritin; high TIBC; low serum iron; low % saturation 3. high Free erythrocyte protoporphyrin (FEP) |
| What is RDW? | red blood cell distribution width. Spectrum of size. If the spectrum is the same= RDW is low. If spectrum has a large variety then RDW is high. In anemia its high. |
| what is Free erythrocyte protoporphyrin (FEP)? | Heme = Fe + protophophorin Fe is low. proto is normal. but some will be free as there is no Fe to bind it. |
| What is the treatment for Fe def anemia? | Supplemental iron in ferrous sulfate |
| what is Plummer~Vinson syndrome | Plummer~Vinson syndrome is iron deficiency anemia with esophageal web and atrophic glossitis; presents with anemia, dysphagia, and beefy-red tongue |
| What is esophageal web? | mucosal protrution causing dysphagia |
| What is Anemia of Chronic disease? | Anemia associated with chronic inflammation (e.g., endocarditis or autoimmune conditions) or cancer; most common type of anemia in hospitalized patients |
| Mechanism behind Anemia of Chronic Disease? | Chronic inflammation = high acute phase reactants like hepcidin that locks Fe in storage sites. Thus low Fe, low heme = microcytic anemia. ALSO SUPPRESSES EPO production. Body produces more hepcidin to lock Fe from preassumed bacterial infection. |
| Lab findings for Anemia of chronic disease? | high ferritin(locked up Fe), low TIBC(pile up transferrin bound Fe), low serum iron(macrophages steal from serum rather than the stores), low saturation % (macrophages steal from serum rather than the stores)and high FEP. |
| treatment for Aniemia of chronic disease? | Treatment involves addressing the underlying cause; exogenous EPO is useful in a subset of patients, especially those with cancer |
| What is sideroblastic anemia? | Anemia due to defective protoporphyrin synthesis 1. low protoporphyrin ~ low heme ~ low hemoglobin ~ microcytic anemia |
| How is Protoporphyrin synthesized? | Aminolevulinic acid synthetase(ALAS)+B6(rate-limiting step)converts succinyl CoA to aminoevulinic acid(ALA). Aminolevulinic acid dehydrogenase (ALAD) converts ALA to porphobilinogen.More steps Ferrochelatase attaches protoporphyrin+iron=heme(MITOCHONDR |
| what is a ringed sideroblasts? | Fe is transfered from the storage sites to- mitochondria thru macrophages. if protoporphyrin is defective then Fe stays trapped in the mitochondria. All mitochondria get loaded and for a ring around the nucleus |
| Causes of Sideroblastic anemia? | 1. Congenital defect most commonly involves ALAS (rate-limiting enzyme). 2. Acquired i. Alcoholism-mitochondrial poison ii. Lead poisoning-inhibits ALAD and ferrochelatase iii. Vitamin B6 deficiency-a side effect of isoniazid treatment for TB |
| Laboratory findings of Sideroblastic anemia? | high ferritin, low. TIBC, high serum iron, and high% saturation. So erythroid precursor has high Fe kill cell. Leak of Fe. increasin serum iron. MO are storing the Fe from erythroid precursors so high ferritin. Low TIBC. |
| What is Thalaseemia? | nemia due to decreased synthesis of the globin chains of hemoglobin |
| What are thalasemic pts protected against? | Inherited mutation; carriers are protected against Plasmodium falciparum malaria. |
| Types of Thanlaseemia? | alpha and beta |
| Normal types of Hemoglobin are? | HbF (a2gamma2) , HbA (a2b2), and HbA2 (a2 delta2). |
| cause of alpha thalasemia? | gene deletion; usually there are 4 alpha chains on the ch16 |
| one gene of aplha thalessia is knocked out? | no symptoms |
| two gene of aplha thalessia is knocked out? | Mild animia and slight rise in RBC. cis- when deletion on the same chromosome. if on opp then trans. Cis-is worse. |
| three gene of aplha thalessia is knocked out? | When the baby is the mothers womb:-he has fetal blood and the one alpha keeps it normaal. When the baby is born-HbA/HbA2. thne beta joins with another beta and forms a tetramer(HbH) which damages RBC |
| four gene of aplha thalessia is knocked out? | lethal in utero (hydrops fetalis); gamma chains form tetramers (Hb Barts) that damage RBCs; |
| What is beta thalamemia? | It is due to geneMUTATION 2 beta genes are on ch 11 Mutation results in abdent Beta naut or diminished B+ |
| What is Beta thalaseeimia minor | mildest form asymptomatic with high RBC Microcytic hypochromic RBC one normal and one diminished beta chains a red bleb in the center low HbA HIGH HbA2 HIGH HbF |
| What is Beta thalaseeimia major | sever, beta naut beta naut. Fetus no problems when fetal blood goes away- sever anemia no beta, alpha chains dimerize= tetramers of alpha Precipitation of RBC and damage of the RBC. spleen will destroy it. Massive erythroid hyperplasia. |
| what is massive erythroid hyperplasia? | expansion of hematopoiesis into the skull (reactive bone formation leads to 'crewcut'appearance and facial bones ('chipmunk facies'), hepatosplenomegaly, aplastic crisis w/ parvovirus infection of erythroid precursors. |
| treatement for B thalamesia? | chronic transfusion of RBC but can lead to hemochromatosis |
| Blood smear of B thalaemia? | microcytic, hypochromic, target cells, nucleated RBC no HbA with increased HbA2 and HbF. |
| what is a target cells? | it is an area in the bi concave area that is filled with blood. presenting a target like appearance. |
Created by:
atayal
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