Anemia Flashcards

1
Q

What is anemia?

A

decrease in RBC or hemoglobin (piece of RBC carrying oxygen)

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2
Q

How do I know if my patient has anemia?

A

hemoglobin (can diagnose with this)
signs/symptoms
bloodwork

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3
Q

Signs and symptoms

A

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

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4
Q

Bloodwork - hemoglobin (Hgb)

A

oxygen carrying capacity
male: 13.5-18 g/dL
female: 12-16 g/dL

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5
Q

Bloodwork - hematocrit (Hct)

A

volume of RBCs per unit of blood
male: 38-50%
female: 36-46%

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6
Q

Bloodwork - mean corpuscular volume (MCV)

A

avergae volume of RBCs, helps point in direction of what’s causing anemia
80-100mm^3

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7
Q

Bloodwork - RBC distribution width (RDW)

A

variation in size of RBCs
11.5-14.5%

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8
Q

True or false - iron supplementation is the first line treatment of anemia

A

false - depends on the cause of anemia

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9
Q

Causes of anemia

A

decreased RBC production
increased RBC destruction
increased RBC loss

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10
Q

Decreased RBC production

A

chronic disease: chronic kidney disease, cancer, CHF
nutritional deficiencies: iron, folic acid, vit B12

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11
Q

Increased RBC destruction

A

not lasting as long as they should
drugs (hemolytic anemia)
sick cell anemia/thalassemia

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12
Q

Increased RBC loss

A

acute blood loss
chronic NSAIDs/ASA

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13
Q

Classification - size of RBC

A

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

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14
Q

Consequences of anemia

A

impaired cognitive function
falls (especially with elderly)
heart failure
atrial fibrillation
cardiovascular events (MI)
mortality

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15
Q

Goals of therapy

A

increase Hgb
relieve sx (decrease fatigue)
reduct morbidity (HF, cognitive impairment)
improve QOL
reduce mortality
NOT JUST NORMALIZE LAB VALUES

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16
Q

Iron deficiency anemia

A

decreased Hgb
microcytic
normal or increased RDW
decreased ferritin
increased TIBC/transferrin
normal or decreased serum iron
decreased transferrin saturation (TSAT)

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17
Q

Ferritin

A

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

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18
Q

Normal transferrin values

A

200-360 mg/dL

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19
Q

Normal total iron binding capacity (TIBC) values

A

250-400 mcg/dL

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20
Q

Transferrin saturation (TSAT)

A

amount of iron ready for erythropoiesis
normal values: 20-50%

21
Q

Causes of iron deficiency

A

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

22
Q

Additional s/s only for iron deficiency

A

spoon-shaped nails (koilonychias)
inflamed tongue (glossitis)
pica craving substances that do not have nutritious value: pagophagia (ice), geophagia (dirt, soil, clay)

23
Q

How do I treat iron deficiency anemia?

A

iron supplements

24
Q

Iron deficiency anemia - treatment

A

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

25
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
26
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
27
Oral iron products
ferrous fumarate (100mg elemental iron), ferrous sulfate (65mg), ferrous gluconate (30mg), polysaccharide iron complex (100%) no iron product is superior
28
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
29
Keep oral iron in a safe place!
looks like candy overdose in children can be fatal
30
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)
31
Vitamin B12 deficiency anemia
decreased Hgb macrocytic increased RDW decreased serum B12 increased homocysteine/methylmalonic acid
32
Causes of vitamin B12 deficiency
diet: vegan/vegetarian, alcoholism lack of intrinsic factor --> pernicious anemia decrease absorption (ex. Crohn's) medication (PPIs, metformin)
33
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
34
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)
35
Folic acid deficiency anemia
decreased Hgb macrocytic increased RDW decreased serum folate (<5 ng/mL) increased homocysteine
36
Causes of folic acid deficiency
malabsorption malnutrition - found in green vegetables, orange juice, cereal, flour, milk alcoholism medications: methotrexate, phenytoin, sulfasalazine, sulfamethoxazole/trimethoprim)
37
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
38
FDA mandated that all enriched wheat flour was to be fortified with folic acid to prevent
neural tube defects in pregnancy
39
Never replace folic acid without...
checking vitamin B12 first! folic acid supplements will correct anemia, but neurologic deficits of vit B12 deficiency remain
40
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
41
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)
42
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%
43
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
44
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
45
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
46
Hemolytic anemia
RBCs are destroyed before 120 days types of hemolytic anemia: inherited - sickle cell anemia, G6PD deficiency; acquired: drug induced
47
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)
48
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
49
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)