850- Anemia Flashcards

1
Q

Anemia Definition:

A

• Decreased hemoglobin (Hgb) concentration or red blood cell (RBC) volume/mass
• World Health Organization defines anemia as:
o Hgb <13 g/L in males
o Hgb <12 g/L in females

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2
Q

Anemia Pathophysiology:

A
  1. Hypoproliferative
  2. Maturation Disorders
  3. Hemorrhage/hemolysis
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3
Q

Hypoproliferative

A
  1. Bone marrow damage
  2. Iron deficiency
  3. Decreased stimulation
    • Chronic kidney disease
    • Inflammation
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4
Q

Maturation Disorders

A
  1. Cytoplasmic defects
    o Thalassemia
    o Iron deficiency
  2. Nuclear maturation defect
    o Folate deficiency
    o Vitamin B12 deficiency
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5
Q

Hemorrhage/hemolysis

A
  • Blood loss
  • Intravascular hemolysis
  • Autoimmune disease
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6
Q

Anemia Signs:

A
  1. Tachycardia
  2. Pale appearance
  3. Decreased mental acuity
  4. Increased intensity of some cardiac valvular murmurs
  5. Diminished vibratory sense or gait abnormality in vitamin B12 deficiency
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7
Q

Anemia Symptoms:

A
  1. Decreased exercise tolerance
  2. Fatigue
  3. Dizziness
  4. Irritability
  5. Weakness
  6. Palpitations
  7. Vertigo
  8. Shortness of breath
  9. Chest pain
  10. Neurologic symptoms in vitamin B12 deficiency
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8
Q

Signs and symptoms specific to cause of anemia:

Sudden blood loss = cardiorespiratory symptoms

A
  1. Chest pain
  2. Angina
  3. Fainting
  4. Palpitations
  5. Tachycardia
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9
Q

Signs and symptoms specific to cause of anemia:

Iron Deficiency Anemia

A
  1. Glossitis (tongue to swell in size, change in color)
  2. Koilonychias (spoon nails)
  3. Pica (craving and chewing ice, clay, soil, or paper)
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10
Q

Signs and symptoms specific to cause of anemia:

Vitamin B12 deficiency- Neurologic symptoms including

A
  1. Neuropathies (numbness, paresthesia-abnormal sensation of the skin)
  2. Movement disorders (ataxia, diminished vibratory sense, decreased proprioception, imbalance)
  3. Visual disturbances
  4. Psychiatric symptoms (irritability, personality changes, memory impairment, depression)

Proprioception: sense of self-movement and body position

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11
Q

Steps to assessing patient for anemia:

A
  1. First assess hemoglobin
    - Is Hgb concentration low?
  2. Next assess signs and symptoms
    - Is the patient exhibiting signs and symptoms consistent with anemia?
  3. Then assess MCV
    - Low Hgb, low MCV
    - Low Hgb, high MCV
    - Low Hgb, normal MCV
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12
Q

Low Hgb, low MCV

A

Microcytic anemia – consider iron deficiency

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13
Q

Low Hgb, high MCV

A

Macrocytic anemia – consider vitamin B12 and/or folic acid (folate) deficiency

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14
Q

Low Hgb, normal MCV

A

Normocytic anemia – consider:

  • Chronic kidney disease
  • Chronic Infection
  • Chronic Inflammation
  • Malignancy
  • Acute blood loss (surgery, trauma)
  • Bone marrow failure (aplastic anemia)
  • Hemolysis
  • Sickle cell anemia
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15
Q

Microcytic Anemia – Iron Deficiency Anemia (most common)

What are the common causes of iron deficiency?

A
  1. Inadequate Dietary Intake
  2. Decreased Iron Absorption
  3. Increased Iron Requirements
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16
Q

Microcytic Anemia – Iron Deficiency Anemia

Inadequate Dietary Intake

A
  1. Iron poor diets (vegan/vegetarian)
  2. Malnutrition
  3. Disease-related (dementia, psychosis)
  4. Blood Loss
    - Acute (e.g. GI hemorrhage)
    - Chronic (e.g. heavy menses, blood donations, PUD, IBD, intestinal cancer, hemorrhoids)
    - Drug-induced bleeding (e.g. NSAIDs, steroids, antiplatelets, anticoagulants)
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17
Q

Microcytic Anemia – Iron Deficiency Anemia

Decreased Iron Absorption

A
  1. High gastric pH (e.g. PPI, achlorhydria)

2. Gastrointestinal diseases (e.g. celiac disease, IBD, gastrectomy, gastric bypass)

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18
Q

Microcytic Anemia – Iron Deficiency Anemia

Increased Iron Requirements

A
  1. Pregnancy
  2. Lactation
  3. Infants
  4. Rapid growth (e.g. adolescence)
19
Q

Microcytic Anemia – Iron Deficiency Anemia

Iron Deficiency Anemia - Lab Findings

A

o LOW

  • Hgb, MCV
  • Reticulocyte count
  • Serum iron, ferritin, TSAT

o HIGH
- TIBC

20
Q

Microcytic Anemia – Iron Deficiency Anemia

Food recommendations:

A

• Heme iron in meat, fish, and poultry is 3x more absorbable than nonheme iron found in vegetables, fruits, dried beans, nuts, grain products, and dietary supplements

21
Q

Microcytic Anemia – Iron Deficiency Anemia Treatment drugs

A
  1. Oral Iron

2. Parenteral Iron

22
Q

Oral Iron (Microcytic Anemia - Iron Deficiency)

A
  1. Can adequately treat most patients with IDA
  2. Recommended dose: 100 to 200 mg elemental iron daily (typically in divided doses)
  3. No evidence that one oral formulation in better than another
  4. Iron absorption
  5. Continue oral iron for 3-6 months after anemia has resolved to allow for iron store to return to normal
  6. Drug interactions
23
Q

Oral Iron (Microcytic Anemia - Iron Deficiency)

Iron Absorption

A
  • Food decreases absorption (by as much as 50%), best to take on an empty stomach (1h before/2h after meals) – however many patients experience GI symptoms with oral iron products
  • Increase absorption in acidic environment – ascorbic acid/vitamin C may enhance absorption to minimal extent
  • Slow release/Sustained release/Enteric-coated – less GI irritation, but decreased absorption, therefore not recommended as initial therapy
24
Q

Oral Iron (Microcytic Anemia - Iron Deficiency)

Drug Interactions

A
  1. Drugs that DECREASE iron absorption:
    - Antacids, H2RAs, PPIs
    - Tetracycline & doxycycline
    - Cholestyramine
  2. Iron DECREASE absorption of:
    - Quinolone and tetracycline
    - Bisphosphonates
    - Levothyroxine
    - Levodopa
25
Q

Parenteral Iron (Microcytic Anemia - Iron Deficiency)

IV Iron preparations

A
  1. Iron dextran (INFeD)
  2. Iron sucrose (Venofer)
  3. Ferric carboxymaltose (Injectafer)
  4. Ferric pyrophosphate citrate (Triferic)
  5. Ferumoxytol (Feraheme)
  6. Sodium ferric gluconate (Ferrlecit)
26
Q

Parenteral Iron (Microcytic Anemia - Iron Deficiency)

Adverse Effects

A
  1. Fatal anaphylactic reactions (although rare) have been reported with all formulations of IV Fe
    - Highest rates observed with iron dextran
    » Require 25 mg test dose prior to first dose
    - Observe patients during and immediately following administration for at least 30 minutes (60 minutes for iron dextran) and until stable
    - Crash cart and personnel available to provide treatment
  2. Arthralgias, arthritis, lower back pain
  3. Hypotension
    - Slow infusion rate
    - Decrease dose
  4. Iron overload
    - Excess iron can deposit in the tissues → heart, pancreas, and liver dysfunction
    - Evaluate holding iron when ferritin >500 ng/mL
  5. Avoid administering IV iron during active systemic infections
27
Q

Macrocytic Anemia

  1. Cyanocobalamin (B12) deficiency
A

3 major causes:
1. Inadequate intake: may occur in strict vegans (and their breast-fed infants), chronic alcoholics, and elderly patients who consume a “tea and toast” diet
2. Malabsorption syndromes: loss of intrinsic factor (which is required for B12 absorption in small intestines) by autoimmune mechanisms (pernicious anemia), chronic atrophic gastritis, stomach surgery
» Metformin use for 2 or more years – intestinal bacterial overgrowth
» PPI use for 2 or more years
3. Inadequate utilization

Can cause neurologic dysfunction: cognitive impairment, peripheral neuropathy

28
Q

Macrocytic Anemia

  1. Folate Deficiency
A
  1. Results in tongue and oral ulcerations, changes to skin hair and fingernail pigmentation
  2. Causes:
    - Inadequate intake – poor eating habits, making more common in elderly, teenagers (whose diets consist of “junk food”), alcoholics, food faddists, impoverished, and those who are chronically ill or demented
    - Decreased absorption – malabsorption syndromes or those who have received certain drugs
    - Increased folate requirements – pregnant women, patients with hemolytic anemia, malignancy, chronic inflammatory disorders (Crohn’s, RA, psoriasis) patients undergoing long-term dialysis, burn patients, adolescents and infants during growth spurts
29
Q

Macrocytic Anemia

  1. Folate Deficiency (Drug Induced)
A
  • Inhibit DNA synthesis: azathioprine, 6-mercaptopurine, 5-fluoruacil, hydroxyurea, zidovudine
  • Folate antagonist – methotrexate, pentamidine, trimethoprim
  • Decreased folic acid absorption – phenytoin, phenobarbital, primidone
30
Q

Macrocytic Anemia

  1. Lab Findings
A
  1. LOW hemoglobin and HIGH MCV

2. LOW serum levels of B12 and/or folate

31
Q

Macrocytic Anemia

  1. Treatment (treat the underlying deficiency)
A
  1. Vitamin B12 Deficiency

2. Folic Acid

32
Q

Macrocytic Anemia

  1. Treatment (Vitamin B12 Deficiency)
A
  1. Early treatment is paramount, if not corrected within months, neurologic effects may be irreversible
  2. Oral vitamin B12 (1000 – 2000 mcg) as effective as parenteral IM injections
  3. Oral vitamin B12 supplementation is effective in patients with pernicious anemia due to presence of alternate passive absorption pathway for B12 that is independent of intrinsic factor. Patients with pernicious anemia need lifelong vitamin B12 supplementation
  4. Dose: B12 1000 to 2000 mcg po daily for 1-2 weeks then 1000 mcg po daily
  5. B12 injections first line for patients with severe deficiency or neurological symptoms
    - Dose 1000 mcg IM daily x 1 week, then weekly for 1 month, then monthly for maintenance.
    - Daily oral cyanobalamin may be administered after symptoms resolve and hematologic indices have normalized
  6. Intranasal B12 spray (Nascobal®) efficacy has not been well studied, therefore should only be used for maintenance therapy after hematologic parameters have normalized and absence of nervous system symptoms
  7. Adverse effects rare
33
Q

Macrocytic Anemia

  1. Treatment (Folic Acid)
A
  • 1 mg po daily, deficiency related to malabsorption 1-5 mg po daily
  • Parenteral folic acid available, rarely necessary
  • Therapy continued for about 4 months, long-term folate administration may be needed with chronic conditions or if underlying cause of deficiency cannot be identified/corrected
  • Adverse effects – not reported, considered nontoxic at high doses, rapidly excreted in urine
  • Folic acid supplementation in women (who may become/plan to become pregnant) – minimum of 0.4 mg (400 mcg) po daily
34
Q

Normocytic Anemia

  1. Anemia of Chronic Kidney Disease
A

Primarily due to deficiency in erythropoietin (EPO):

  1. Hormone produced by kidneys that stimulates bone marrow to produce RBC
  2. Assess iron labs first, if low administer iron supplement
  3. KDIGO guidelines recommend iron therapy if TSAT is ≤30% and ferritin levels are ≤500 ng/mL
  4. Erythropoiesis- Stimulating Agents (ESAs) may be considered in patients with Hgb < 10 g/dL
35
Q

Normocytic Anemia

  1. Anemia of Chronic Kidney Disease (Erythropoiesis)
A
  1. Optimize iron first to improve ESA response
  2. Epoetin alfa = Epogen, Procrit
  3. Darbepoetin alfa = Aranesp
  4. Methoxy polyethylene glycol epoetin beta = Mircera
  5. May be administered SC/IV
  6. Adverse effects
    - Common: hypertension, headaches
    - Serious: increased risk of mortality MI, stroke, and thromboembolism; seizures; pure red cell aplasia
    - CKD: increase risk of death, serious cardiovascular events and stroke when target Hgb >11 g/dL; use lowest effective dose to reduce the need for blood transfusion
    - Cancer: Shortened overall survival and/or increased risk of tumor progression or recurrence (especially solid tumors); not indicated when the anticipated outcome is cure
36
Q

Normocytic Anemia

  1. Anemia of Inflammation
A

o Newer term used to describe anemia of chronic disease and anemia of critical illness
o Inflammation underlying etiology
o Common in elderly
o Diagnosis usually one of exclusion
o Anemia of chronic disease observed in patients that lasts longer than 1-2 months
o Common causes of anemia of inflammation
o Treatment of Anemia of Inflammation

37
Q

Normocytic Anemia

  1. Anemia of Inflammation (Common causes of anemia of inflammation)
A
  1. Chronic infections:
    - Tuberculosis
    - HIV
    - Osteomyelitis
  2. Chronic inflammation
    - Rheumatoid arthritis
    - Systemic lupus erythematosus
    - Inflammatory bowel disease
  3. Malignancies
38
Q

Normocytic Anemia

  1. Anemia of Inflammation (Treatment of Anemia of Inflammation)
A
  1. Treat underlying cause
  2. RBC transfusion
    - Typically considered for patients with severe anemia (Hg <7-8 g/dL)
    » Risks: blood-borne infections, development of autoantibodies, transfusion reactions, iron overload
39
Q

Normocytic Anemia

  1. Aplastic Anemia
A
  1. Bone marrow fails to make enough RBC, WBCs, and platelets
  2. Causes:
    - Drugs (Chemotherapeutics – alkylating agents, antimetabolites, antimitotics); some antibiotics, carbamazepine, methimazole, propylthiouracil
    - Infectious diseases
    - Autoimmune disorders
  3. Risk of developing life-threatening infections or bleeding
40
Q

Normocytic Anemia

  1. Aplastic Anemia Treatment
A
  1. Immunosuppressants
  2. Blood transfusions
  3. Stem cell transplant
  4. Eltombopag (Promacta) = thrombopoietin nonpeptide agonist
    - Approved for treatment of severe aplastic anemia in patients unresponsive to immunosuppressive therapy
41
Q

Normocytic Anemia

  1. Hemolytic Anemia
A
  1. RBC destroyed and removed from bloodstream before their normal lifespan of 120 days
  2. Acquired: drug-induced, associated with immune disorder
  3. Inherited (sickle cell disease, glucose-6-phosphate dehydrogenase deficiency)
  4. Drug induced hemolytic anemia
    - One mechanism involved medication binding to RBC surface and triggering development of antibodies that attack the RBC
    - This autoimmune reaction can persist for several weeks even after the medication has been discontinued
  5. Direct Coombs test is used to detect antibodies stuck to the surface of RBCs
42
Q

Normocytic Anemia

  1. Hemolytic Anemia (Drugs-Induced)
A
  • Beta-lactamase inhibitors
  • Cephalosporins
  • Levodopa
  • Methyldopa
  • Penicillins: since 2008, piperacillin is the single most common drug to cause drug-induced hemolytic anemia
  • Platinum-based chemotherapy agents (carboplatin, cisplatin)
  • Quinidine
  • Quinine
  • Rifampin
  • Ribavarin
43
Q

Normocytic Anemia

  1. Hemolytic Anemia (Glucose-6-Phosphate dehydrogenase deficiency)
A
  • X-linked inherited disorder
  • G6PD is an enzyme that protects RBCs from harmful substances (for example reactive oxygen species)
  • With G6PD deficiency RBCs hemolyze 24-72 h after exposure to oxidative stress
  • Infections, certain foods (fava beans) severe stress, certain drugs are factors that can increase risk of hemolysis
  • When hemolysis is severe – patients present with weakness, tachycardia, jaundice, hematuria
  • Symptoms self-limiting and usually resolve after 8-14 days
  • High risk medications (if used, should be monitored closely and discontinued if hemolysis develops.)
44
Q

Normocytic Anemia

  1. Hemolytic Anemia (Glucose-6-Phosphate dehydrogenase deficiency: High risk meds)
A
  1. Chloroquine
  2. Dapsone
  3. Methylene blue
  4. Nitrofuantoin
  5. Primaquine
  6. Probenecid
  7. Sulfonamides