Nutritional+Anemias

specifics of types/causes of anemias

nutriotnal anemia...decreased hemoglobin due to

nutrients Iron Folci acid B6 B2 C ita E Niacin COpper CObalt Vitamin A protein amino acids B12 (cobalamin) calories

lack of any of these can cause impairment of RBC manufacure

most common aquired anemia: iron deficiency prepare to be blasted with iron metabolism normal body content 3-4g level of RBCs maintained some flows aroudn freely most moved by transferrin... less than 0.2 in body is in plasma

70% is hemoglobin, rest myoglobin

30% is in storage forms: ferritin, hemosiderin

metabolism levels vast majority from iron metabolism good recycling

some used for non-heme protein and tissue heme protin...cytochromes, myoloin recycling take iron through GI tract some in palmsa most boudn to transferin small amt goes to liver, sotrage, cell use, majority to bone marrow normoblasts, reitcs ost go to circlating RBCs removed from ciculation....RES store cycles over again

typical american diet has 7mg/100kcal per day heme iron is absorbed intact non-heme iron is affected by number of factors...reduced by castric acdid from Fe+3 to FE+2 presence of absorption inhibtors...grain, tea, egg yolks or enhancers

ferrous iron aborbed in duodenum, proximal jejunum only 10% f ingested iron is typcially absorbed however aborsprtion is dependent on level of body iron stores

Hepcidin believed to be 'master regulator' thought to be 'master regulator' of iorn homeostasis reduction of hepcidin secretion is seen in most of iron overload syndromes
 * limits GI iron absorption...inhibits iron absorption, iron recycling by macrophages

transferrin purpose is to transoport iron capacity is 300ug Fe/DL transports iorn to cells increased with iron deficiency, pregnancy, estrogen therapy decreased with inflammation, malignancy, lvier diease, menrphrotic syndrome, malnutiriton tranferrin saturation: proportion of the available iron binidng sights that are occupied.... serum iron/TIBC

transfer is bound deliverd to RBC b y bidning to transferrin receptors transferin-transferin receptor compelxes are endocytoesed transferrin is then released into plasma once more

There is no physiological mechanism for Fe secretion iron lost for epiutheilai cells fort he GI teract, skin and renal tubules RBC loss form bleeding Iron lost frombody only when cels are lost

Since there is lilttle control of excretion....< >

Presenation of iron deficient ot
> fatigue > paloor > weakness > exertional dyspnea > lightheadedness
 * asymptimatic
 * symtoms of anema

> bleeding
 * symptoms and sighs of underlying cause of iron defiicency > GI symptoms

> glossitis > angular cheilosis > esophageal webs > kilonycha (spoon shaped fingernails) > blue slcerae > gastric atrophy > pica < >
 * effects of iron deficiency opn nonhematooietic tissues

Evaluation 1) CBC Hematocrit > MCV > RDW
 * Hb
 * RBC indices

Need ot be able ot calculate MCV

2) serum iron 3) total iron binding capacity
 * transferrin saturation

4) serum ferritin therefor,e level> 12 ug/L does NOT rule out iron deficiency
 * reflects total body iron stores
 * less than 12 ug/L is diagnostic of iron defiiciency
 * levlels can be elevatied in inflammation, ifnection, malignancy, and hemoolysis...

smear of someone with iron deficiency anemia microcytic anisocytosis rdw is elevated hypochromic cells....central pallor... normall central paollor should be about 1/3 of total diameter of cvell also pencil cells

preadolescent: similar male vs female androgens drive up RBCs

first deplete stores then deplete plasma ferritin need fair amount of time

Treatment Treat dunderlying associated ocnditions Oral iron replacement is the therapy of choice ferrous sulfate other iron alts parentral iron dextran or other iron formualtions

megaloblasic anemias a gorup o fidsordres characteriZed by a sdistinct morpholoigcal pattern of in the hematopoeitic cells that reulsts from a defect in DNA synthesis As there are typcailly only minor defects in RNA and protein synthesis, the affeected cells are the result of a state of unbalanfed cell grwth and impaired cell division. Cells are 'immature'-appearing nucleus with 'mature' appearing cyotplasm and large cell volume mgagloblastic hematopoiesis is usually manifest as anemia vitamin B12/cobalamin and oflic acid ar ethe two most common casues of megalobalstosis

hematologic manifestations of megalobalsic anemia peripheral blood smear no morphological differences in appearance of peripheaal blood cells in megaloblasosis due to vitamin B12 or folic acid RBCs Increased MV Anisocytosis Poikilocytosis

Neutrophils demonstrate hypersegmentation > 3 PMNs with 5 lobes 5% of PMNs with 5 lobes or one with 6 lobes mild to moderate leukopenia might be present Bone marrow is hyeprcellular wih hyperpalsia of all 3 hemaotoietic cell lines abnormal appearnace of hematopoeitic cells cells don't mature enough til can be released

differentiall diagnosis of megaloblastosis anything that interferes with DNA synthesis congenial dyserythropoietic anemias erythroleukemia exposure to drugs or toxins that intgerfere with DNA sytnehsis


 * chemotherapy
 * antibiotics
 * anticonvulsants
 * oral contraceptives
 * antiviral
 * arsenic, pesticides, herbicides

Macrocytosis
 * reticulocytiosis
 * [ost-splenectomy
 * alcoholism
 * COPD
 * Liver disease
 * alastic anemia
 * hypothyoridism
 * bengign familial macrocytosis

Artifactual
 * cold agglutinins ( cold can make RBCs clump together & trigger false positive on machine)
 * hyperglycemia

1) symptoms & signs of anemia 2) effects of imparied DNAA synthesis on a non-hemoatopoeitic tissues Epithelial tissues Glossitis-beefy red tongue ?loss of papillae neural itssue damage Korsakof optic atrophy dorsal column, peripheral neuropathy

B12 essentail for conversion of homocysteine to methionine by methyltransferase

required for DNA sythesis

Also L-methonyl to >>>succinlycoa adensylcobalamin mutase

din nature only bty vitain B12 producing microoganisms Humans obtain B12 only from diet Plants ocntaminated with B12...producing bacteria...(legumes) also organs, muscles

US diet contains 5-7 ug of B12 per day total body ontaent is 2-5mg 1 mg in liver well stored in coenzyme forms picture.... absorption nproceess

R protein in stomach w/pepsin B12 released in stomach binds to R protein from saliva along with intrinsic factor from stomach absorbed in distal ileum

produce strict vegetarian diset

lack fo gastir cacid or pepsin lack of intrinsic factor...pernicious anemia rediuced number of ileal receptors..... crohns disease, spruse

pancreatic insufficiency zollinger-ellison syrome...inactivation of pancrateic protesase by gastic acid hypserecretion.... 2 more

serum B12 level fairly reliable measure is serum B12 level falsly low/normal/elevated

serum hoocysteine and mehtylmalonic acid levels

if want to know where defect is, can use schilling test.. pt given radiolabelled vit B12 orally and inejction of unlabaelled B12

amount of labelled B12 in urine if intrinsic factor, cans upplement intrinsic factor if still not found, can give 7-10 d of antibiotics also supplement pancreatic enzymes treatment

intramuscular or IV injection oral route works in some pts cyanocobalamin various dosing schedules... pancreatic extract often monthyly basis for life if need pancreatic extract, may sppleent may precipiatte neurological problems
 * Do Not Give FOlic Acid Until B12 Fixed!!**

Last... Folic acid Body store 5-10 mg 2-4 months stored in liver

daily requirements 50-100ug child/adult pregnancy and lactation 300-400ug

diet is source: leafy green veggies yeast legumes fruits animal proteins, parenchymal organs

absorped in small intestine does not need transport protein free or nonspeicifcally bound enterohepatic recirclation ipmportant for folic acid metabolism and redistribution of folic acid from liver stores external biliary drainge can lead to decreases in serum folic acid levels > draining bile can cause deficiency

usually stays within cell throught cell's lifespan THF, tetrahydrofolate, is active form

Deficiency inadequate intake increased requirements...pregnancy, spsoriasis, lactation, pregnancy inetstinal malalbsorption drugs...ethanol, baribiturates, sfa drugs deffective cellular uptake--rare

Diagnosis Measure seru folic acid level very sensitive to intake more relabile is RBC folate level.... not readily influenced by recent oral intake mild hemolyssi can incease serum FA level serum homocystiene and methylmaolnic acid levels Pay attention ot reaction of blahblahblah

Treatment Usually oral supplementaiton (even if poorabsorption) continue until blood normal prophylactic adminstration for those who may become pregnant