liveonearth (liveonearth) wrote,

ANEMIAS: Microcytic Hypochromic

types of micro-hypo: IDA, alpha or beta thalassemias, sideroblastic, ACD (some cases), pyridoxine responsive anemia, chronic blood loss, lead poisoning

--the most common type overall, and the most common micro-hypo
--ETIO: if iron deficient, decide if there is a chronic blood loss, dietary lack, high demand, or poor absorbtion
--Dx: serum iron and/or ferritin: low
--Dx: TIBC (total iron binding capacity): high
--Dx: HGB, HCT, RBC, MCV: low
--Dx: RDW: high in later stages
--Dx: PLT count may be increased dt BM stimulation
--Dx: RETICS decreased
--Dx: FEP (free erythrocyte protoporphyrin) increased in IDA but normal in thalassemia
--Dx: Mentzer Index = MCV/RBC, >13 is IDA, <13 is thalassemia
--Dx: no stainable iron in mononuclear phagocytic cells
--STAGES: initially will have normal transferrin saturation, HGB, MCV, RDW, HCHC
--STAGES: hyperchromicity first, ferritin drops as tissue stores are used to maintain MCHC
--STAGES: late: last to drop: transferrin, hemoglobin and MCV
--Tx: iron supplementation and optimization of absorption, monitor ferritin
-HGB should rise 1 gram%/mo with Tx, if it does not respond consider other ETIO for micro-hypo state
--IDA most common in developing countries where diet is vegetarian
--impaired absorption dt: celiac dz, sprue, other steatorrhea, chronic diarrhea, gastrectomy, diet
--dietary substances that inhibit the absorption of non-heme iron: phytates (grains, soy, nut hulls), tanmate (skins & fruit of plants), phosphates
--highest risk population: poor women with multiple, frequent pregnancies
--common causes of chronic blood loss: GI: PUD, gastritis, carcinoma, hemorrhoids, parasites, GU: renal, pelvic or bladder tumors, Gyn: menorrhagia, AUB, uterine carcinoma

--iron is absorbed from food in ferrous form, Fe2+, requires gastric acid
--heme iron (from animal products) is more easily absorbed than iron from non-meat sources
--absorption occurs in the duodenum and proximal ileum
--average western diet provides 10-30mg of iron daily
--absorption if 5-10% of intake, increases to 20-30% with deficiency
--total body iron is 3-4 grams, 70% in HGB, 15% in ferritin, 15% in hemosiderin
--hemosiderin is not bioavailable
--total absorption is 1-2 mg/day, same daily loss via skin desquamation and stool
--foods that interfere with iron absorption: phytates in cereal & vegetables (very high in soy), casein in milk, clay, tetracycline, pica in children
--transferrin tranports absorbed iron from intestine to bone marrow erythroblasts
--TIBC is an indirect measurement of transferrin
--some is stored by RE macrophages in ferritin form
--gastric bypass surgery reduces acid output and removes entire duodenum (RYGB = Roux-en-Y Gastric Bypass) dramatically reduces a body's ability to absorb iron and other vits/mins
--serum iron fluctuates with intake: TIBC and ferritin give better info on stores
--serum iron level decreases dramatically under severe stress (65%!!), also is low w/: dietary deficiency, chronic blood loss, malabsoption, late pregnancy, neoplasia
--serum iron increased: hemosiderosis, hemochromatosis, iron poisoning, hemolytic anemia, massive blood transfusions, liver disease, LEAD toxicity

--TIBC is an indirect measurement of transferrin
--increased: estrogen therapy, late preg, PCV, IDA
--decreased: malnutrition, hypoproteinemia, inflam dz, cirrhosis, hemolytic, pernicious and sickle cell anemias

--ferritin level may not necessarily exclude iron deficiency.
--many diseases, such as malignancy, liver disease and inflammatory diseases, cause a rise in ferritin independent of iron stores
--Normal levels does not exclude iron deficiency
--Falsely elevated in patients with chronic disease states
--Acts as acute phase reactant prot (incr 1-2 days after onset of acute, peaks @ 3-5 days)
--acute phase reactant protein (takes Fe away from microbes)
--Ferritin is the major iron-storage protein, primarily found in the liver.
--Good indicator of available iron stores in the body in healthy person
--1 ng/mL serum ferritin = about 8 mg of stored iron
--Levels below 12 mg/dL = diagnostic for Iron Deficiency Anemia (IDA)
--Levels rise persistently in males and post-menopausal females
--Severe protein depletion can decrease levels
--NORMAL: males 40-340 ng/ml
--NORMAL: females 14-150 ng/ml
--increased: hemochromatosis, hemosiderosis, megaloblastic anemia, hemolytic anemia, alcoholism, inflam dz, advanced cancer
--confounders/confusers: blood transfusions, high iron intake, dz of excess iron storage, hemolytic dz, menstruation
--decreased: IDA, severe prot deficiency, hemodialysis

--NORMAL: males 215-365, females 250-380 mg/dl
--transferrin saturation = serum iron / TIBC
--transferrin saturation describes how many binding sites are occupied by iron

--inherited disorder of globin chain synthesis
-->globin deficiency-->not enough HGB-->hypochromic and microcytic, mb increased RBC numbers
--heterozygous = carrier or symptomatic, homozygous = major dz
--alpha or beta chain
--alpha globins four genes if all four defective: fatal (just one, silent carrier)
--beta globins two genes, either carrier or diseased
--B-thal major: micro-hypo w/ basophilic stippling, target cells, NRBC's
--Dx: serum iron increased, TIBC decreased or normal, % saturation increased
--Dx: ferritin increased or normal, retics increased, LDH mb increased w/ hemolysis
--Dx: haptoglobin reduced dt hemolysis
--Dx: FEP normal in thal, high in IDA
--Dx: HGBE
--complications: repeated transfusions-->increased iron load-->risk of hemochromatosis treated by iron chelation
--S/Sx: tissue anoxia-->kidneys increase EPO output-->marrow expansion: heavy brow
--an old post on thalassemia and vampirism from when I was first studying biochemistry

--four genes code for each alpha globin chain, so four different levels of dz
--deletion of one gene-->silent carrier state
--deletion of two-->trait
--deletion of three-->>alpha thal major and Hgb H Dz
--HbH = tetramer of excess beta-globin, has high affinity for oxygen and does not deliver O2 to tissues, is prone to oxidation-->Heinz bodies and bite cells, causes moderate anemia
--Asians have most alpha thal major
--all 4 deleted = hydrop fetalis-->death before birth without intrauterine tranfusions
--alpha thalassemia: alpha globin gene is missing, not defective
--alpha thalassemia DECREASES sickle cell symptoms when pt has both, because the lower globin synthesis reduces the MCHC

--most common cause of thalassemia = defect in production of beta globin-->beta thalassemia
--population w/ lion's share of beta thalassemia genes: Mediterraneans
--beta thal major arises at 5-6 months when fetal hemoglobin is no longer produced
--beta thal major pt gets transfusions, survives past childhood-->rare to survive past 30
--free alpha globin chains (w/ beta chain deficit-->insoluble inclusions in normoblasts-->cell membrane damage-->apoptosis
--which kind is Cooley's anemia???

--pyridoxine = vitamin B6
--B6 needed to make gamma-ALA for heme production
--acquired form more common, hereditary very rare
--acquired assoc w/ isoniazid therapy for TB

--inadequate/abnormal utilization of marrow iron
--usu microcytic hypochromic (mb normochormic) with high RDW
--acquired or hereditary
--two RBC populations, one normochromic and one hypochromic
--DX: by BM biopsy, find "rings" of Fe in RBC
--marked anisocytosis w/ siderocytes
--high serum iron, transferring & ferritin
--Dx: ringed sideroblasts, erythroid hyperplasia in bone marrow
--if cause unknown check serum lead
--siderocyte = polychromatophilic, stippled, targeted RBC

--defect in heme synthesis dt Pb obstructing two enzymes
--significant lead intoxication will occur before micro-hypo anemia
--Dx: basophilic stippling in RBC's
--Dx: low retics

--the 3rd most common form worldwide
--found in SE Asians?
--Hgb AE heterozygotes are asx
--Hgb EE homozygotes exhibit mild microcytic anemia and target cells)

--anemia in 30-50% of pts
--morphology ranges from macro to microcytic
--decreased thyroid hormone has a direct effect on erythropoiesis since hormone administration corrects both anemia and hypothyroid condition
Tags: anemia, biochemistry, blood, diagnosis, hemochromatosis, iron, lead, nutrition, thalassemia

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