Anemia Flashcards
What is anemia?
decrease in RBC or hemoglobin (piece of RBC carrying oxygen)
How do I know if my patient has anemia?
hemoglobin (can diagnose with this)
signs/symptoms
bloodwork
Signs and symptoms
caused from not enough oxygen carried on RBCs
s/s: exertional dyspnea, angina (chest pain from not enough O2 to heart tissue), tachycardia (pump faster, compensate for low blood), fatigue, pallor (pale),
may be asymptomatic, especially if develops slowly
Bloodwork - hemoglobin (Hgb)
oxygen carrying capacity
male: 13.5-18 g/dL
female: 12-16 g/dL
Bloodwork - hematocrit (Hct)
volume of RBCs per unit of blood
male: 38-50%
female: 36-46%
Bloodwork - mean corpuscular volume (MCV)
avergae volume of RBCs, helps point in direction of what’s causing anemia
80-100mm^3
Bloodwork - RBC distribution width (RDW)
variation in size of RBCs
11.5-14.5%
True or false - iron supplementation is the first line treatment of anemia
false - depends on the cause of anemia
Causes of anemia
decreased RBC production
increased RBC destruction
increased RBC loss
Decreased RBC production
chronic disease: chronic kidney disease, cancer, CHF
nutritional deficiencies: iron, folic acid, vit B12
Increased RBC destruction
not lasting as long as they should
drugs (hemolytic anemia)
sick cell anemia/thalassemia
Increased RBC loss
acute blood loss
chronic NSAIDs/ASA
Classification - size of RBC
microcytic: MCV < 80 - iron deficiency, sickle cell, thalassemia
normocytic: MCV 80-100 - anemia of chronic disease, blood loss, hemolysis
macrocytic: MCV >100 - folic acid and or B12 deficiency
Consequences of anemia
impaired cognitive function
falls (especially with elderly)
heart failure
atrial fibrillation
cardiovascular events (MI)
mortality
Goals of therapy
increase Hgb
relieve sx (decrease fatigue)
reduct morbidity (HF, cognitive impairment)
improve QOL
reduce mortality
NOT JUST NORMALIZE LAB VALUES
Iron deficiency anemia
decreased Hgb
microcytic
normal or increased RDW
decreased ferritin
increased TIBC/transferrin
normal or decreased serum iron
decreased transferrin saturation (TSAT)
Ferritin
iron stores *acute phase reactant - elevated in acute inflammation or chronic disease (so sometimes can look higher than what it truly reflects)
normal value: 15-200 ng/mL *iron deficiency is still likely for ferritin <45 ng/mL
Normal transferrin values
200-360 mg/dL
Normal total iron binding capacity (TIBC) values
250-400 mcg/dL
Transferrin saturation (TSAT)
amount of iron ready for erythropoiesis
normal values: 20-50%
Causes of iron deficiency
blood loss: menstruation, blood donation
decreased absorption: maximal absorption in the duodenum, ex - celiac disease, gastric bypass
vegetarian diet: dietary iron, heme (from meat), non-heme (from plants or dairy); non-heme iron not well absorbed
increased consumption (pregnancy)
drug causes are unlikely
Additional s/s only for iron deficiency
spoon-shaped nails (koilonychias)
inflamed tongue (glossitis)
pica craving substances that do not have nutritious value: pagophagia (ice), geophagia (dirt, soil, clay)
How do I treat iron deficiency anemia?
iron supplements
Iron deficiency anemia - treatment
oral or IV iron?: oral is preferred (chepear + easier)
exceptions: cannot tolerate (side effects), cannot absord, end stage renal disease, heart failure
need to address the underlying cause
Oral iron for iron deficiency anemia
65mg of elemental iron every other day
120-200mg of elemental iron per day (often divided BID or TID)
often takes 3-6 months to replete stores
Why might every other day dosing be better?
hepcidin: hormone released after taking iron, harder to absorb oral iron
iron-regulating peptide hormone produced in liver that decreases dietary iron absorption and iron transfer to the plasma
hepcidin is increased after a dose of oral iron for ~24 hours and normalizes within 48 hours
hepcidin is also elevated during inflammation
Oral iron products
ferrous fumarate (100mg elemental iron), ferrous sulfate (65mg), ferrous gluconate (30mg), polysaccharide iron complex (100%)
no iron product is superior
Oral iron counseling points
taken every other day to three times daily
increased absorption on empty stomach
causes stomach upset - can take with food or split up doses (can also try taking at bedtime)
absorption increased by ascorbic acid
causes constipation: increase fluids, activity, and fiber
causes dark stool: may be mistaken for GI bleed
Keep oral iron in a safe place!
looks like candy
overdose in children can be fatal
IV iron
indications: end stage renal disease, heart failure, failed oral iron, malabsorption
SEs: hypotension during infusion, skin tattooing
products: sodium ferric gluconate, iron sucrose, ferumoxytol, ferric carboxymaltose, iron dextran (risk of anaphylaxis)
Vitamin B12 deficiency anemia
decreased Hgb
macrocytic
increased RDW
decreased serum B12
increased homocysteine/methylmalonic acid
Causes of vitamin B12 deficiency
diet: vegan/vegetarian, alcoholism
lack of intrinsic factor –> pernicious anemia
decrease absorption (ex. Crohn’s)
medication (PPIs, metformin)
Consequences of B12 deficiency
our bodies cannot make vitamin B12 - must absorb it from diet (fish, dairy, eggs, meat)
consequences of B12 deficiency: neurologic - weakness, numbness, cognitive dysfunction
Vitamin B12 deficiency treatment
vitamin B12 replacement
IM or deep SC: 100-1000 mcg (daily, weekly, monthly - regimens vary); often daily for 1-2 weeks, then weekly or monthly as maintenance
oral: 1000-2000 mcg/day; oral as effective as parenteral *may not be as effective in pernicious anemia; water soluble vitamin (if have too much, just pee out extra)
Folic acid deficiency anemia
decreased Hgb
macrocytic
increased RDW
decreased serum folate (<5 ng/mL)
increased homocysteine
Causes of folic acid deficiency
malabsorption
malnutrition - found in green vegetables, orange juice, cereal, flour, milk
alcoholism
medications: methotrexate, phenytoin, sulfasalazine, sulfamethoxazole/trimethoprim)
Folic acid deficiency treatment
oral folic acid supplement
1-5 mg daily until Hgb normalizes
well absorbed, rarely need IV
treat underlying cause or continue to supplement
water soluble vitamin
FDA mandated that all enriched wheat flour was to be fortified with folic acid to prevent
neural tube defects in pregnancy
Never replace folic acid without…
checking vitamin B12 first!
folic acid supplements will correct anemia, but neurologic deficits of vit B12 deficiency remain
Anemia of chronic disease
one of the most common causes of anemia
pts with chronic diseases lasting months to years; common in inflammatory or infectious diseases - CKD, CHF, cancer, HIV/AIDS
Anemia of CKD
erythropoietin is produced in kidneys and stimulates production of RBCs - so when kidneys aren’t working well, not producing the hormone
anemia occurs because of: decreased erythropoietin production; chronic inflammatory state which causes anemia of chronic disease; nutritional deficiencies (iron, folate, vit B12)
Anemia of chronic kidney disease treatment
avoid blood transfusions: especially for pts eligible for kidney transplantation (risk of allosensitization)
correct nutritional deficiencies: folate/B12; iron - oral iron in stage 3-5 CKD if possible, use IV iron in hemodialysis pts; target transferrin saturation (TSAT) above 30%
Anemia of CKD - erythropoiesis stimulating agents (ESA)
ESAs help prevent blood transfusions
DO NOT target normal Hgb levels: use minimum dose to maintain Hgb > 10 to prevent an increase risk of cardiovascular events, stroke, and death
only start ESA after replenishing iron stores
do not titrate dose up for at least 4 weeks after initiating or increasing dose
Heart failure
pts that may benefit from IV iron (especially with reduced EF): NYHA class II and III HF and iron deficiency (ferritin < 100 or 100-300 if TSAT <20%)
decreased HF hospitalizations, but no mortality benefit
oral iron supplementation has not showed benefit
ESAs should not be used: increased risk of thromboembolic events
Blood loss anemia
stop the bleeding
transfuse packed RBCs when Hgb < 7: each use of PRBC contains ~250 mg iron
meds may be indicated for specific indications: pantoprazole infusion for upper GI bleed
Hemolytic anemia
RBCs are destroyed before 120 days
types of hemolytic anemia: inherited - sickle cell anemia, G6PD deficiency; acquired: drug induced
Sickle cell anemia
RBCs are irregular shaped (sickles)
RBCs collect in spleen and are destroyed faster than they can be produced
inherited: sickle cell trait - asymptomatic; sickle cell anemia - both genes are sickle cell hemoglobin (homozygous)
Sickle cell anemia treatment
folic acid: 1mg/day; increased need due to accelerated eryhtropoiesis
blood transfusions: symptomatic episodes of acute/chronic anemia; caution with iron overload
hydroxyurea: fetal hemoglobin inducer, decreases sickling; 10-15 mg/kg/day
Sickle cell anemia treatment: immunizations and pain control
immunizations: impaired splenic fx - risk of infection from encapsulated organisms; influenza, pneumococcal, and meningococcal
pain control: acetaminophen/NSAIDs; opioids in pain crisis (PCA)
