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36 Cards in this Set

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microcytic anemias: what is the MCV, what is the problem

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

active heme form

ferrous= Fe2+

storage and transport form of iron


where do we get iron?

iron is everywhere; too much can kill you; so body has restricted uptake but also restricted daily losses; highly regulated; much NON MEAT IRON (aka plant) is tightly bound to PHYTATES (storage phosphorous) in the inactive Fe3+ form which is hard to absorb but acids (especially ascorbate) can help; FENTON REACTION= Fe2+ + H2O2 --> OH- + Fe3+ AND THEN FE3+ +H2O2 --> HOO+ +H+ + FE3+ AND THIS CAN GO ROUND AND ROUND IN A CIRCLE which isn't what your cells want (CAN KILL THEM) (THIS IS A BOARD QUESTION)

how do we absorb iron?

HE SAID YOU NEED TO STUDY THIS FOR YOURSELF AND PAY ATTENTION TO DMT1 (TRANSPORTER FOR THE IRON), APO FERRITIN (AF) AND FERRITIN, TRANSFERRIN RECEPTORS, AND FERROPORTIN (HE SAID TO GO OVER A FEW TIMES BEFORE TEST SO IT'S DEF GOING TO BE A TEST QUESTION); intestinal cells actively absorb INORGANIC IRON via the DIVALENT METAL TRANSPORTER 1 (DMT1) and HEME IRON via the HEME CARRIER PROTEIN 1 (HCP1); in intestine HEME IRON is ACTIVELY TRANSPORTED INTO THE BLOOD BY FERROPORTIN (FP) OR COMPLEXED WITH APOFERRITIN (AF) and STORED AS FERRITIN (F); in blood IRON transported by TRANSFERRIN (Tf) to erythroid precursors in the marrow for synthesis of hemoglobin (Hgb) or to HEPATOCYTES FOR STORAGE AS FERRITIN; the TRANSFERRIN IRON COMPLEX binds to transferrin receptors (TfR) in erythroid precursors and hepatocytes and internalized; after release of iron the TfR-Tf complex is recycled to the plasma membrane and Tf is released; macrophages that phagocytize senescent erythrocytes (RBC) reclaim the iron from the RBC hemoglobin and either export it or store it as ferritin; hepatocytes use several mechanisms to take up iron and store the iron as ferritin; FO, FERROXIDASE, AKA HEPHAESTIN

where do we absorb the iron? and how much do we need in diet? and what are the hemoglobin iron contents and ferritin levels in men and women

DIET= 10-15 mg elemental iron/day; absorb 5-10% so 0.5-1 mg but this can increase with demand; absorbed in DUODENUM AND PROXIMAL JEJUNUM; hemoglobin level in men= 3000 and women= 1700; storage (ferritin) in men= 750 and in women=300

some signs/symptoms of iron deficiency anemia

koilonychias= spoon like curving of the nails; cheilitis= soreness of mouth with cracks at corner of lips; glossitis= soreness/swelling of tongue (saw this with B12 as well); restless leg syndrome= unclear etiology; plummer-vinson syndrome= esophageal web, dysphagia (THIS IS A TEST QUESTION**); PICA= UNGER FOR STRANGE SUBSTANCES SUCH AS DIRT, BRUSSEL SPROUTS ETC (BOARD QUESTION)(HE CONSIDERS THIS PSEUDO SCIENCE GARBAGE); pagophagia= eating ice

serum iron definition

ferritin iron (minor+ transferrin bound iron (major)

serum ferritin definition

usually in pretty good equilibrium with total body stores so if it is down your total body stores are probably down too

transferrin definition

usually about 30% occupied; main blood carrier of iron

% iron saturation definition

saturation state of transferrin

total iron binging capacity (TIBC) definition

transferrin surrogate; transferrin= 0.8xTIBC-43

zinc protoporphysin (ZPP) definition

aka free erythrocytes protoporphyrin (FEP)

lab findings in iron deficiency

decreased MCV, decreased serum iron and iron saturation of transferrin, decreased serum ferritin, increased TIBC and RDW, increased zinc protoporphyrin

what is zinc protoporphryin? and the effects of Pb2+ poisoning on heme synthesis

iron is linked to protoporphyrin 9 to form heme in the mitochondria; if you don't have iron, or you have lead which blocks the enzyme, you get a build up of protoporphyrin 3 which then binds to zinc and gets pushed into the blood; so normally don't have any zinc protoporphyrin unless deficient in iron or Pb poisoning

differential diagnosis (BOARD ALERT)

HE SAID STUDY THIS TABLE PLEASE; THIS IS A TABLE TO STUDY SO DO THAT AND DON'T RELY ON THESE NOTES -->; PAY ATTENTION TO TIBC AND SERUM FERRITIN LEVELS IF YOU ARE SEEING ZINC PROTOPORPHYRIN LEVELS (TIBC INCREASED AND SERUM FERRITIN DECREASED MEANS IRON DEFICIENCY AND TIBC DECREASED AND SERUM FERRITIN INCREASED MEANS LEAD POISONING); keep in mind that you can have issues with false levels of TIBC due to liver failure and pregnancy and false levels of serum ferritin because of infection (this is why you need to look at both of these levels at the same time to determine lead poisoning versus iron deficiency)


iron def= MCV/RBC>13 (number of RBC numbers decrease faster than the cells shrink); thal minor=MCV/RBC<13 (cells shrink faster than the RBC number decreases; (SAID THIS IS NO REALLY IMPORTANT TO KNOW)--> the principle= in iron deficiency the marrow cannot produce as many RBCs so the RBC count in usually much less and as a result the index will be greater than 13 whereas in thal the RBC count is more normal so the index will be less than 13 and in practice the MCV has to be unusually low and/or the RBC atypically high for a thal minor to produce an index of less than 13

what do you do if a pt has MCV<80

it has to be a defect in hemoglobin synthesis; check serum iron and iron binding capacity; if serum iron is high or normal and iron binding capacity is low or normal then the defect must be in prophysin, heme, or globin so do hemoglobin electrophoresis; if abnormal then defect in globin synthesis and interpret; if normal then defect in porphyrin heme (lead poisoning, hereditary sideroblastic anemia, acquired sideroblastic anemia, or pyridozine response anemia); if serum iron is low and iron binding capacity is high then you are in an iron deficiency state; AND NOTHING SAYS THAT YOUR PT CAN'T HAVE BOTH FE DEFICIENCY AND PB POISONING WITH A CONCURRENT THALASSEMIA MINOR (IN KIDS ITS NOT UNCOMMON) (BOARD QUESTION)

treatment of iron deficiency anemia

GIVE IRON; ORAL IRON is cheap and usually works; also is nauseating, tastes nasty, and relies on pt compliance (BOARD QUESTION); STOOLS CAN TURN BLACK (MELANOTIC) can hide GI bleeding that caused iron deficiency in the first place; VIT C can help increase absorption; ORAL IRON PREPARATIONS (200-400 MG ELEMENTAL IRON PER DAY ABOUT 25% ABSORBED FOR 3-6 MONTHS)

treatment of iron deficiency anemia: other options

GIVE PARENTAL IRON IF= can't tolerate oral, defective uptake, chronic renal dialysis, bowel resection or any GI disorder decreasing absorption, oral just doesn't work; FORMULATIONS OF PARENTAL IRON (most need a total of 1000-2000 mg elemental divided into 2-3 doses)= IRON DEXTRAN (IV or deep IM (Z track)= headache, lightheadedness, fever, arthralgias, nausea, back pain, flushing, hives, PESKY ANAPHYAXIS AND DEATH (BOARD QUESTION) (TAKEAWAY=DON'T GIVE THIS), InFeD is lower molecular weigh so maybe more less anaphylaxis and DexFerrum is higher molecular weight so maybe more anaphylaxis), SODIUM FERRIC GLUCONATE COMPLEX (IV only), IRON SUCROSE (venofer) (IV only), ferumoxymaltose (injectafer) (IV only and bigger doses (750 mg) x2 separated); ALWAYS GIVE A TEST DOSE FIRST; NEVER EVER EVER GIVE IV IRON AT 3 AM

treatment of iron deficiency anemia: iron dextran dosing

iron needed (mg) = (2.2(HgbD-HgbO)wt) + 13(wt); HgbD= desired, Hgbo=observed; HE DIDN'T GO OVER THESE AT ALL SO I'M NOT SURE IF WE NEED TO KNOW THEM OR NOT

in replacing blood loss: iron dextran dosing

assumption= 1 mL of normocytic, normochromic erythrocytes (i.e. packed RBC) contains i mg of elemental iron; my iron needed= estimated blood loss (in mL) x HCT (as decimal fraction)

prophylaxis for chronic renal failure with dialysis

erythropoetin to replace deficient production; IRON TO REPLACE PRIMING LOSSES FOR THE DIALYSIS (MONITOR STORES)

iron poisoning: symptoms

ACUTE, ORAL= necrotizing gastroenteritis, emesis, abdominal pain, bloody diarrhea, shock, lethargy and dyspnea, severe metabolic acidosis, coma, and death

iron poisoning: treatment: determining stage

HE ONLY DESCRIBED FIRST STAGE AND SAID THAT IF YOU SURVIVE IT YOU CAN HAVE MULTIPLE PROBLEMS; diagnose stage; first stage= GI toxicity (30 mins to 12 hrs (after ingestion)) so nausea, vomiting, diarrhea, abdominal pain, ematemesis, melena and rarely shock, seizures, and coma; second stage= latent period (8-36 hrs) with improvement but no resolution; third stage= systemic toxicity (12-48 hrs) with hepatic injury or failure, hypoglycemia, metabolic acidosis, bleeding, shock, convulsions, death; fourth stage= late complications (4-8 weeks) with pyloric/antral stenosis, CNS sequelae; DETERMINE SERUM IRON CONCENTRATION 2-6 HRS AFTER INGESTIONS (peak varies with formulation level>350 mcg/dl associated with systemic toxicity; SERUM IRON LEVELS obtained at any time after ingestion MAY BE NORMAL EVEN IN THE PRESENCE OF SEVERE POISONING so treatment should be determined by clinical symptoms

iron poisoning: treatment

if dose <20 mg/kg then no treatment needed; for unknown dose of >20 mg/kg if no symptoms in first 6 hrs then no treatment= other than that induce emesis and take xray and lavage of stomach and maybe clean out bowel (with golytely); GIVE DEFEROXAMINE IV AT 15 MCG/KR/HR IN ALL CASES OF SERIOUS POISIONING (BOARD QUESTION)(ON TEST) and if urine is red before therapy started then continue for 24 hrs after producing adequate volume of normal colored urine, when AXR clear and all signs and symptoms resolved; large IV fluid volumes should be given for first 24 hrs ; note= activated charcoal does NOT bind iron so no need to give

iron poisoning treatment if chronic iron overload

deposition in tissues has happened (HEMOCHROMATOSIS) in heart, liver, pancreas, others; can lead to severe organ dysfunction and death; common in chronic transfusion dependent; most effectively treated by INTERMITTENT OR REGULAR PHLEBOTOMY (drain their blood) one unit/week; if phebotomy contraindicated (sickle cell, thal major, aplastic anemias) chelate WITH IV DEFEROXAMINE OR ORAL DEFERASIROX but these are less efficient and usually chelate out other metals causing deficiencies

lead poisoning: who do you see it in, symptoms

usually in small children living in OLDER houses painted with LEAD PAINT; but can be from any environment/occupational source (pottery, toys etc); lead paint chips are slightly sweet but can also be lead paint dust; much more common in NORTHERN MIDWEST TO EAST COAST IN CENTRAL CITIES; less common in southwest but family could have moved there; symptoms= emesis, constipation, ataxia, irritability, microcytic anemia, seizures, altered consciousness, xrays may show chips in GI tract or lead lines in metaphyeal regions of bones, CAN RESULT IN PERMANENT COGNITIVE DEFICITS, ABDOMINAL PAIN, LEARNING DIASBILITIES, LOWER IQ SCORES, DELAYED GROWTH AND DEVELOPMENT, IMPAIRED HEARING

lead poisoning: treatment

chelation therapy for blood lead levels>45 ug/dL; oral dimercaptosuccinic acid (SUCCIMER, DMSA)= absorbed rapidly but incompletely, most is protein (mainly albumin) bound, only very small amount present as free drug, it is not known whether protein bound DMSA can chelate lead, excreted in urine, chelation may occur principally if not exclusively in the kidney; dose=DMSA 30 mg/kg/day; duration= REPEATED COURSES OF AT LEAST 5 DAYS if a treatment free period of AT LEAST 1 WEEK BETWEEN COURSES is included TO ALLOW REDISTRIBUTION OF LEAD FROM BONE TO SOFT TISSUES AND BLOOD; INTRAVENOUS= ethylenediaminetetraacetic acid (EDTA); INTRAMUSCULAR= dimercaprol or british anti lewisite (BAL) GIVEN IM q4h; BAL IS THE MOST HORRIBLE STUFF IMAGINABLE (THE PAIN IS UNBEARABLE)

misc anemias: anemia of chronic kidney disease (CKD): description and treatment

insufficient ERYTHROPOETIN; dialysis= loss of IRON, maybe FOLATE, so SUPPLEMENTS given; ERYTHROPOETIN REPLACEMENT THERAPY options may vary on patent status= recombinant erythropoetin (EPOETIN ALFA, EPOGEN, PROCRIT) IV, SQ, serum half life 4-13 hrs and not cleared by dialysis, given 3x PER WEEK, ARANESP glycosylated half life 8-36 hrs, IV, SQ, given WEEKLY, MIRCERA IV or SQ Q 2-4 WEEKS; all can cause HYPERTENSION; all can have rare PURE RED CELL APLASIA (neutralizing antibodies); KEEP Hgb<12 or INCREASED RISK OF STROKE, THROMBOSIS, and cardiovascular incident

erythropoetin replacement therapy

KNOW THIS CAPPED STUFF VERY WELL (ON TEST); is used in CERTAIN CANCERS but both hematopoetic malignancies and solid cancers can have EPO receptors, unclear if they are functional in solid cancers but decreased survival in solid cancer pts treated wiTh EPO, AVOID EOP IN CANCER PTS THAT YOU EXPECT TO GET A LONG TERM RESPONSE TO; is used in ANEMIA OF PREMATURITY; is used in AUTOLOGOUS BLOOD DONATION FOR ELECTIVE NONCARDIAC SURGERY; is used for ZIDOVUDINE ASSOCIATED ANEMIA IN HIV; is used in ANEMIA OF CHRONIC DISEASE if endogenous EPO is low; if endogenous EPO level <50-100 IU/L more likely to respond to exogenous ESAs

misc anemias: sickle cell: symptoms, treatment

VASO OCCLUSIVE CRISIS (pain, bone infarction, possible marrow emboli to chest), ischemic STROKE (long term treatment include chronic transfusion protocol), PRIAPISM (an erection that won't go down), splenic infarct FUNCTIONALLY ASPLENIC (STREP PNEUMONIAE SUSCEPTABILITY), acute sequestration event, long term CARDIAC AND RENAL DAMAGE (CAN'T CONCENTRATE URINE= dehydration and increased sickling), susceptibility to PARVOVIRUS B19 infection (can suppress marrow into APLASTIC CRISIS); risk of narcotics addition; HYDROXYUREA normally used in CML leukemia to inhibit ribonucleotide reductase and thereby deplete dNTPs but in SICKLE CELL ANEMIA 15-3 mg/kg, PO, daily (adjust to marrow suppression) and can increase fetal Hgb gamma (HbF) levels, may inhibit Hgb polymerization/precipitation, therefore sickling, may also keep cells more supple, fewer vaso occlusive crises



Awoman who livesalone and reported that she rarely cooked, relying on take-out food instead,most from local hamburger franchises. She states that she feels tired allthe time. Laboratory results: hemoglobin 10.3 g/dL (low), hematocrit 33% (low),MCV 70 fL (low), MCH 21.9 pg (low). What is the best treatmentfor this patient? a. folic acid plus iron b. oral ferrous sulfate c. parental ferric carboxymaltose d. 3 pounds of spinach per week e. vit B12 plus iron

b. oral ferrous sulfate, this is a microcytic anemia; a and e for microcytic anemias; c can do but not really ideal unless oral can't be done; d bioavalability won't be great

Awoman with inflammatory bowel disease has been diagnosed with macrocyticanemia. She wants to become pregnant. Which of the following is important forthe prevention of neural tube defects before she becomes pregnant? a. cyanocobalamin b. erythropoietin c. folic acid d. hydroxyurea e. oral ferrous sulfate

macrocytic anemia= B12 or folate deficiency, neural tube defects= folic acid=c; b. makes her red cell mass go up; d. sickle cell anemia; THIS ONE IS IMPORTANT TO KNOW

Achild with beta-thalassemia was unable to receive a bone marrowtransplantation. He has undergone chronic blood transfusion therapy to maintainhis hemoglobin at 9-10 g/dL. Currently his hemoglobin is 9.2 g/dL and his liveriron concentration is 6.5 mg iron/g dry weight (>3 mg requires treatment).Which of the following treatments is appropriate?a. deferoxamineb. folic acidc. hydroxyuread. more red meat in his diete. vit B12

a. deferoxamine (DE-FER getting rid of Fe)