(12/7) Pop Lecture: Nutritional Anemia Anemia: This condition is defined by the decreased oxygen-carrying capacity of the blood

- Labs: Decrease in Hemoglobin < 13 (males) or < 12 (females) Decrease in Hematocrit < 41% (males) or < 36% (females)

- RBC Morphology: Can be used to help determine the cause of Anemia o Microcytic (small): Related to Iron-deficiency. Iron is a dietary component needed to produce RBC o Normocytic: Anemia is likely related to recent blood loss or chronic disease. o Macrocytic (big): B12 or Folic Acid deficiency. These are needed for DNA synthesis

Nutritional Anemia: This is a variety of Anemia specifically related to inadequate intake or malabsorption of an essential nutrient. Essential nutrients include: Iron (largely dependent on Vit-C normality), Vit-B12, and Folic Acid.

- S/Sx: Acute: Tachycardia, SoB, Dyspnea, Angina Chronic: Fatigue, HA, Weak, Pallor - High Risk Cohort: Children (nutrition), Elderly (cognitive effects, poor intake), Pregnancy, Boozers, Obesity

surgery – Anything affecting intake or absorption Iron-Deficiency Anemia: This is the Leading cause of anemia worldwide, AND the most common nutritional deficiency

- S/Sx: Initially presents as asymptomatic. May exist with normal Hg, normal Hct (even if 15%ß in RBC mass)… Deficiency takes a while to show. However, eventually you’ll see glossal/tongue pain, reduced salivary flow, pica (eat werid shit) and pagophagia (chewing ice)

- Labs: Serum Ferritin is the strongest indicator we have, earliest and most sensitive. In iron deficiency, it is LOW o Total Iron Binding Capacity (TIBC): In iron-deficiency, it will be HIGH because of the extra availability

to bind iron o Transferrin: Normally 30% saturated with iron, it is responsible for delivering extra iron as necessary.

Lower than 30, we notice an iron-deficiency - High Risk Cohort: Mainly children <2yo, menstruating females, pregnancy, elderly - Absorption: Absorption occurs in the ferrous state (Fe2+). Ferric (Fe3+) is ionized in the stomach to Fe2+, absorbed

in the duodenum and jejunum, and transferred across cells into the plasma. o Factors: Iron intake ¹ Iron absorbed. Absorption depends on the storage, rate of RBC production, diet,

and substances that enhance or inhibit absorption. But the body normally compensates, as internal levels decrease, GI absorption increases

- Intake: Depends on the individual. 27mg if pregnany, 18mg if menstruating, 8mg if a dude or menopause. o Dietary Heme-Iron: Meat, fish, poultry. Heme Iron is 3x more absorbable than non-heme o Dietary Non-Heme Iron: Veges, fruits, beans, nuts, grains. This is poorly absorbed, but can be improved

by having good supplies of gastric acid. Vitamin C supplementation can improve non-heme absorption, so go tell your menstruating vegetarian friends to get some C. (naturally in red peppers, oranges)

§ Why is it poorly absorbed? Non-heme iron forms insoluble complexes. These insoluble complexes develop more readily with tea (tannins) or coffee

o Calcium intake inhibits absorption of HEME and NON-HEME - Oral Supplementation: Iron-replacement therapy depends on the patient’s ability to tolerate it. Start low.

o Pregnancy: 30mg/Qdaily o At risk children: Ferrous sulfate 1mg/kg/day o Adults: 200mg elemental iron daily in divided doses. o AE: Discoloration of stool (dark), constipation, NVD. o DDI: PPI, H2RA, Tetracyclines will decrease the absorption of the iron product. o Counseling: Take it 1 hour before meals, may benefit from taking concurrent Vit-C. GI complications

Take it with food, though empty stomach is recommended. Constipation? Drink water and stool softener. Wait 2 hours before/after to take a calcium supplement, it can bind to iron and reduce its availability.

- IV Supplementation: Reserved for those who are intolerant to PO, Malabsorption, long-term non-adherence o Preferred: Iron Dextran. Do a test dose and observe for 1 hour (BBW – Anaphylaxis)

Vitamin B12 Deficiency: Rare deficiency with low prevalence, usually due to malabsorption - S/Sx: Neurologic: Numbeness, Ataxia, Tingly, Bad vision Psychiatric: Irritability, depression, psychosis - Labs: [B12]ß, HomocysteineÝ - (Folate conversions), Methylmalonic AcidÝ (specific indicator) - Malabsorption factors: Gastric-acid suppressing agnets, H. pylori, Auto-immune mechanisms (pernicious anemia) - Intrinsic Factor Pathway: A story of cobalamin being carried to the distant ileac lands by Intrinsic factor

o Ingested Cobalamin (B12) binds to R-protein complex of the parietal/salivary cells. o The duodenum degrades that complex, releasing free cobalamin- which binds to intrinsic factors o Cobalamin-Intrinsic Factor attaches to the mucosal cell receptors in the distal ileum

o Intrinsic factor is discarded, and cobalmin binds to transcobalamin I and III o In pernicious anemia, there is a problem with the Intrinsic Factor pathway

- Intake: Generally has the same sources as iron – makes it easy! Only 33-50% is absorbed due to its solubility o High [B12] Foods: Clams, Beef liver, breakfast cereal, SOCK EYE SALMON

- Treatment: Indicated for B12 Deficiency presenting with: o Megaloblastic Anemia: Huge RBC being made by bone marrow o Hematological Abnormalities o Neurological Disease

- Supplementation: PO is just as effective as IM. PO is preferred. o PO: 1000mcg for 1 to 2 weeks, with a maintenance of 1000mcg daily [OTC] o IM: PO is preferred. IM is only indicated in cases of Hematologic or Oral issues.

§ 100mcg daily x6-7 days, then maintenance 100mcg/qmonthly o IN: PO is preferred. Intranasal is only for long-term maintenance patients. Qweekly

Folic Acid Deficiency: Common in the US, due to boozers and pregnant women - S/Sx: Fatigue, gray hair, mouth sores, growth problems, tongue swelling, pallor

o Symptoms resolve when you replace folate UNLESS there is an underlying B12 deficiency (fix that first) - Labs: Folateß, B12~, Mean Cell VolumeÝ, HomocysteineÝ, Methylmalonic Acid~

o Use the labs to rule out B12 deficiency (MMA) - Cx: Due to inadequate intake (booze, socioeconomic, fad), malabsorption, or increased requirements (preg)

o Anticonvulsant medications are major contributors to reduced folic acid intake - Absorption Pathway: Folic acid is polyglutamated, degraded to monoglutamate, absorbed in SI, converted to

tetrahydrofolate via cobalamin-dependent rxn - Intake: In 1997, the US started fortifying a lot of foods with folic acid, helped improve neural tube defects

o Foods high in Folate: Beef liver, cereal, lentils, chick peas - Supplementation:

o Oral: 0.4 – 0.8mg Qdaily for maintenance of women in childbearing age (Higher if deficient) o In cases of malabsorption, may require 1-5mg Qdaily

During Pregnancy, The goals for IRON and FOLIC ACID,,,,,, not B12,,, are increases exponentially during pregnancy