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27 Cards in this Set

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definition of anemia

inadequate circulating RBCs/hemoglobin/blood oxygen carrying capacity to meet physiological needs or any hemoglobin < 2 S.D. from age specific norms; inadequate circulating blood oxygen carrying capacity to meet physiological needs

RDW definition

red blood cell distribution width (measure of red cell MCV variability)

MCV definition

mean cell volume

MCH definition

mean cell hemoglobin

MCHC definition

mean cell hemoglobin concentration


pale --> short of breath --> fatigue and exercise intolerant/cramping --> dizzy, fainting --> palpatations, increased HR --> bounding pulses (hyperdynamic cardiac function)

classifications of anemias by RBC size

microcytic (MCV<80), macrocytic (blastic) (MCV>100), and normocytic (MCV=80-100)

microcytic anemias: size, causes, and names

MCV<80; these are hemo/globin problems; heme problem= not enough iron or a porphysin problem (including a smidge too much lead); globin chain problem= thalessemias; but why are they small? think shrink to fit

macrocytic (blastic) anemias: size, causes

aka megaloblastic anemias; MCV>100; are vitamins (that help with DNA formation)/DNA problems; vitamin B12; folic acid; but why are they big? nucleus slow to divide but cytoplasm keeps growing; dysjunction/asynchrony of cell growth because nucleus is stuck in S phase due to impaired DNA synthesis while cytoplasm continues to make proteins and RNA and increase in amount

normocytic anemias: size, causes

MCV=80-100; are problems of another day

where does the heme come from

heme is made in the mitochondria; early step in heme formation is PROTOPORPHYRIN 9; we use B TYPE HEME

common causes of macrocytosis

vit B12 deficiency; folate deficiency; DRUGS esp those that interfere with DNA synthesis= METHOTREXATE, SULFAMETHOXAZOLE, TRIMETHOPRIM, PHENYTOIN (ANTICONVULSANT), AND ZIDOVUDINE; THIS IS A BOARD QUESTION ALLERT; alcoholism

macrocytic anemia: vit B12 deficiency: where do we get B12, what does B12 look like, heat reaction?, dialyzable?

VIT B12 ONLY MADE BY CERTAIN BAC; many different forms; not synthesized by animals of plants; must come from diet= meat, dairy, egg; NONTRIVIAL ISSUE FOR STRICT VEGANS but for some reason, fewer adults affected than you'd thing (MAY AFFECT INFANT OF VEGAN MOM); yeast have no B12 unless its fed to them; corrin ring; cobalt atom; nucleotide; R=variable side chain; HEAT STABLE; NOT DIALYZABLE

macrocytic anemia: vit B12 deficiency: what are the R chains

DEOXYADENOSYLCOBALAMIN (AdoCbl)- human active; METHLYCOBALAMIN (MeCbl)- human active; hydroxocobalamin aka aquocobalamin- supplemental; cyanocobalamin- supplemental

clinical and subclinical vit B12 deficiency: is it stored in the body?, how long before anemia?, what can you see in this anemia? (besides anemia)

body stores mainly in LIVER; total STORAGE POOL in healthy adult is large= 3000-5000 MCG; normal american diet= 5-30 mcg of which 1-5 are absorbed; only need 2-4 mcg per day; SO TAKES YEARS TO DEVELOP OVERT CLINICAL DEFICIENCY SYMPTOMS; macrocytic megaloblastic anemia= hypercellular marrow, hypersegmented neutrophils with decreased WBCs and platelets, GI symptoms like anorexia, nausea, emesis, diarrhea, hunter's/atrophic glossitis or beefy tongue, cheilosis; nerve demyelination= subacute combined degeneration of spinal cord (demyalination of dorsal and lateral columns), paresthesias of extremities, ataxia, deteriorating coordination, hyperreflexia, NEUROCOGNITIVE= DEPRESSION/MOODINESS/MEMORY LOSS/DEMENTIA, osteoporosis

vita B12 (aka cobalamin) absorption (how does it work and where does it work and what is involved)

bound to food proteins and haptocorrins (aka R binders); released with chewing and binds to salivary haptocorrins (ex. transcobalamin 1= R binder); in stomach mucosa, PARIETAL CELLS make ACID and INTRINSIC FACTOR (IF) (rate limiting); in stomach, acid and trypsin and pepsin hlep further release VIT B12 (aka EXTRINSIC FACTOR) from dietary proteins and haptocorrins and it further binds to salivary R proteins; IN DUODENUM, pancreatic enzymes degrade R proteins to release vit B12 and allow BINDING TO INTRINSIC FACTOR; in jejunum excess vit B12 not bound to TF absorbed passively but inefficiently (1:1000); IN ILEUM IF-vit B12 COMPLEX BINDS TO SPECIFIC RECEPTOR FOR INTERNALIZATION and release; vit B12 enters circulation to transcobalamin (aka transcohalamin II) and there is some entero-recirculation

vit B12 absorption: important notes (what can you have that prevents absorption)

receptors IN ILEUM not uniformly distributed= MODEST ILEAL RESECTION OR CROHN'S CAN PERTURB UPTAKE; METFORMIN (diabetes med) can block IF-vitB12 complex receptor in the ileum; any decrease in stomach area (GASTRECTOMY) decreases acid production (PROTON-PUMP, H2-BLOCKERS) can preturb uptake; GASTRIC ATROPHY (helicobacter pyloris) can decrease parietal cells and ability to make acid and intrinsic factor; PERNICIOUS ANEMIA is an AUTOIMMUNE CELLULAR REACTION TO PARIETAL CELLS AND SO REDUCES BOTH IF AND ACID AND USUALLY HABE CIRCULATING ANTIBODIES TO IF but usually a disease of older age; ALCOHOLICS usually have poor diets and decreased intake of all B vits, can have gastric atrophy, bleeding varices etc and can be prone to B12 deficiency neuro changes as well as thiamine deficiency neuro changes and also livers are usually shot so unable to store in liver as well as a healthy person; it takes 8-12 hrs for IF mediated vitB12 to enter blood; and every board question writer's favorite= TAPEWORMS!

so what happens in the cell in B-12 megaloblastic anemias?

both folate and B12 are needed for the synthesis of purines and this is a cyclic process; if you don't have any B12 then the process can stop after the addition of folate and it can no longer progress (stuck in N5 methyltetrahydrofolate); addition of B12 allows the production of METHIONINE (from HOMOCYSTEINE) and tetrahydrofolate which can then go around the cycle and make purines; you can overcome the trap if you add FOLIC ACID but the problem with doing this instead of giving them what they need (B12) is that you also need B12 to convert METHYLMALONYL-COA --> SUCCINYL COA so without it you build up methylmalonyl CoA which has an odd number of fatty acids which is terrible and causes nerve problems; so, this is why big time FOLIC AICD (he has folate on the slide but he said folic acid) can rescue the anemia but not the neuro problems and so CAN MASK THE TOTAL B12 DEFICIENCY PROBLEM= progressive nerve degeneration in the absence of an anemia; HE SPENT A LOT OF TIME ON THIS SLIDE SO I'D KNOW IT

what are the major folates

dihydrofolic acid; tetrahydrofolic acid; 5-methyltetrahydrofolic acid= FOLATE TRAP; 5,10 methylenetetrahydrofolic acid; HE SAID I DOUBT ANYONE WILL EVER ASK YOU TO IDENTIFY THESE (he has diagrams on the slide) BUT JUST REMEMBER THE FOLATE TRAP

when you first test them and see MCV>100 what do you do

look at B12 levels and if low do a shilling test= take radioactive cobalt which is linked to vit B12 and give it to pt and see if they can take some up, if low then maybe INADEQUATE INTRINSIC FACTOR to bring and take up B12 or there is something wrong with their ileum, if normal (they take it up) then DIETARY DEFICIENCY or lack of B12 binding protein in plasma; if you find that the B12 levels are very low then you expect to also see HIGH HOMOCYSTEINE (HA) LEVELS, HIGH SERUM AND URINE METHYLMALONIC ACID (MMA) (remember this leads to neural issues), AND MAYBE ANTI IF ANTIBODIES; if the B12 serum levels were normal to begin with we start thinking folate but we'll talk about that later

what are the states of N12 in the blood (what do you find it bound to?)

80% is B12+haptocorrin/transcobalamin I which is the inactive form; 20% is B12+transcobalamin II WHICH IS THE ACTIVE FORM (B12+transcobalamin= HOLOTRANSCOBALAMIN because it is the whole and useful form (just for mem not actually true))

treatment of B12 deficiency: first you half to figure out if it is a true deficiency

HE DIDN'T GO INTO THESE VERY MUCH JUST SAID can get false highs and false lows so you test them a few times and try to rely on homocysteine and MMA levels and then go ahead and treat and see if it is correcting the problem (obvi if it doesn't then you need to think other things); well it might have been a false low cobalamin level= folate deficiency, pregnancy, oral contraceptives, multiple myeloma, HIV infection, low haptocorrin levels; there can also be false low AND high homocysteine and MMA levels too; there might be a false high or normal B12 level too= high haptocorrin levels (myeloproliferative disease, renal disease), increased tissue release of B12 (liver disease), low or absent transcobalamin, low affinity treanscobalamin prolymorphism, inherited disorders of B12 metabolism, recent B12 therapy, cobalamin analogues (nitrous oxide therapy, high dose vit C, intestinal bac overgrowth)

treatment of vit B12 deficiency anemia

HYDROXYCOBALAMIN (AKA AQUACOBALAMIN) more protein bound, longer circulation; CYANOBALAMIN; likely you want to give some IM therapy to quickly replace a supply but especially IF THERE ARE NO NEURO SIGNS/SYMPTOMS; 100-1000 mcg, IM, daily or every other day for 1-2 weeks; if neuro sings then continue IM q 1-2 weekly for 6 months; then some say 1000 mcg IM q monthly for life; however remember that shots hurt, are more inconvenient, and costly so if no neuro signs and pt otherwise compliant then you can start with or switch over to oral; 1000-2000 mcg, PO, daily

folic acid deficiency: diet source and amount, storage, uptake location, how quickly do you see anemia development, reaction to heat, dialyzable?

average diet= 500-700 mcg daily (they come as poly-glutaminated so need to DE-POLYGLUTAMINATED THEN 50-200 MCG ABSORBED); increased need and uptake in pregnancy (your jejunum adjusts); uptake in PROXIMAL JEJUNUM (CLASSIC TEST QUESTION** COMPARING THE LOCATION OF UPTAKE OF B12 AND FOLATE (ILEUM)); STORED IN LIVER and other tissues= 5-20 MCG; unlike B12 BODY STORES DEPLETE FAIRLY QUICKLY AND SERUM LEVELS WILL DECREASE WITHIN DAYS; ANEMIA can develop WITHIN 1-6 MONTHS after folate intake stopped; HEAT UNSTABLE; DIALYZABLE; supplemented in foods (by gov) to prevent NEURAL TUBE DEFECTS (THIS IS A CLASSIC BOARD QUESTION**) (could hide B12 deficiency); sources= leafy veggies, fruit, meat; N5-methyltetrahydrofolate

what happens in the cell in folate deficiency megaloblastic anemia?

with folate deficiency there is an INCREASE IN HOMOCYSTERINE BUT NORMAL MMA and so there are NO NEURO SIGNS (GOOD WAY TO DISTINGUISH BETWEEN B12 AND FOLATE DEFICIENCY); anything that damages DHFR (enzyme) can also cause folate deficiency anemia (antimalarials)

ok so going bake to hey I have MCV>100 lets check B12 but B12 is normal then what next

you immediately suspect folate so check serum folate; if low then INADEQUATE ABSORPTION, liver disease, OR INCREASES REQUIREMENT; if normal then BLOCKED NUCLEIC AICD SYNTHESIS BY DRUGS, or deficiency in other nucleic acid precursors; if there is a folate deficiency then there will also be INCREASED HOMOCYSTEINE (HA), NORMAL SERUM AND URINE METHYLMALONIC ACID (MMA), RBC FOLATE MAY BE MORE ACCURATE THAN SERUM FOLATE; remember that people can easily have DEFICIENCIES OF BOTH VIT B12 AND FOLATE (BOARD QUESTION)

treatment of folate deficiency

1-5 MG FOLIC ACID, PO, DAILY; heme response should take 7-10 days, watch for development of iron deficiency anemia due to increased demand; prophylactic supplementation= PREGNANCY, ALCOHOLICS (BAD DIET, DAMAGED LIVER AKA CIRRHOSIS), HEMOLYTIC ANEMIA, LIVER DISEASE (DECREASED STORES), RENAL DIALYSIS, certain skin diseases (exfoliative dermatitis)