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PHRM 864 Module 3 > Anemia > Flashcards

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
Q

Oral iron for iron deficiency anemia

A

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
Q

Why might every other day dosing be better?

A

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
Q

Oral iron products

A

ferrous fumarate (100mg elemental iron), ferrous sulfate (65mg), ferrous gluconate (30mg), polysaccharide iron complex (100%)
no iron product is superior

28
Q

Oral iron counseling points

A

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
Q

Keep oral iron in a safe place!

A

looks like candy
overdose in children can be fatal

30
Q

IV iron

A

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
Q

Vitamin B12 deficiency anemia

A

decreased Hgb
macrocytic
increased RDW
decreased serum B12
increased homocysteine/methylmalonic acid

32
Q

Causes of vitamin B12 deficiency

A

diet: vegan/vegetarian, alcoholism
lack of intrinsic factor –> pernicious anemia
decrease absorption (ex. Crohn’s)
medication (PPIs, metformin)

33
Q

Consequences of B12 deficiency

A

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
Q

Vitamin B12 deficiency treatment

A

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
Q

Folic acid deficiency anemia

A

decreased Hgb
macrocytic
increased RDW
decreased serum folate (<5 ng/mL)
increased homocysteine

36
Q

Causes of folic acid deficiency

A

malabsorption
malnutrition - found in green vegetables, orange juice, cereal, flour, milk
alcoholism
medications: methotrexate, phenytoin, sulfasalazine, sulfamethoxazole/trimethoprim)

37
Q

Folic acid deficiency treatment

A

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
Q

FDA mandated that all enriched wheat flour was to be fortified with folic acid to prevent

A

neural tube defects in pregnancy

39
Q

Never replace folic acid without…

A

checking vitamin B12 first!
folic acid supplements will correct anemia, but neurologic deficits of vit B12 deficiency remain

40
Q

Anemia of chronic disease

A

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
Q

Anemia of CKD

A

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
Q

Anemia of chronic kidney disease treatment

A

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
Q

Anemia of CKD - erythropoiesis stimulating agents (ESA)

A

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
Q

Heart failure

A

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
Q

Blood loss anemia

A

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
Q

Hemolytic anemia

A

RBCs are destroyed before 120 days
types of hemolytic anemia: inherited - sickle cell anemia, G6PD deficiency; acquired: drug induced

47
Q

Sickle cell anemia

A

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
Q

Sickle cell anemia treatment

A

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
Q

Sickle cell anemia treatment: immunizations and pain control

A

immunizations: impaired splenic fx - risk of infection from encapsulated organisms; influenza, pneumococcal, and meningococcal
pain control: acetaminophen/NSAIDs; opioids in pain crisis (PCA)

PHRM 864 Module 3 (9 decks)

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