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PT: Hematology & Pulmonary > Anemia > Flashcards

Anemia Flashcards

1
Q

What is anemia?

A
  1. Decreased Hgb and RBCs =

2. Decrease in oxygen carrying capacity of blood

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2
Q

What causes anemia?

A
  1. Decreased RBC productions
  2. Increased RBC loss
  3. Increased RBC destruction
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3
Q
  1. Decreased RBC productions
  2. Increased RBC loss
  3. Increased RBC destruction
A
  1. Hgb < 13 g/dL for men
  2. Hgb < 12 g/dL for women
  3. “Sign of disease”
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4
Q

What is the 2nd most prevalent and costly public health issue?

A

Anemia

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5
Q

How can you monitor or screen for anemia?

A

With NO chronic conditions check CBC every 5 years, if Hgb 11-12 g/dL consider further workup
With chronic conditions check CBC yearly

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6
Q

What is the clinical presentation of acute anemia?

A
  1. Tachycardia
  2. Angina
  3. Lightheadedness
  4. SOB
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7
Q

What is the clinical presentation of chronic anemia?

A
  1. Fatigue
  2. Weakness
  3. Headache
  4. Dizziness
  5. Pallor
  6. Sensitivity to the cold
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8
Q

What is the normal clarification of RBC size/Hgb content?

A

Normochronic and normocytic

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9
Q

Define Macrocytic

A

an abnormally large red blood cell

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10
Q

Define Microcytic

A

an abnormally small red blood cell

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11
Q

Define Hyperchromic

A

the red blood cells have more hemoglobin than normal

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12
Q

Define Hypochromic

A

the red blood cells have less hemoglobin than normal

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13
Q

What is the initial evaluation of anemia?

A
  1. CBC-Complete blood count (RBC indices)
  2. Reticulocyte Index
  3. Supporting labs (iron, folate, B12, etc.)
  4. Fecal occult blood stool cards
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14
Q

What is hemoglobin and what are the normal values?

A
  1. Estimates oxygen carrying capacity
  2. Men: < 13 g/dL
  3. Women: <12 g/dL
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15
Q

Where is hemoglobin made?

A

in RBCs

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16
Q

What happens with Hgb in anemia?

A
  1. Decreased Hgb per RBC

2. Decreased number of RBCs

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17
Q

What is hematocrit?

A

The % of RBCs in unit volume of whole blood

usually 3x the Hgb value

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18
Q

What happens to happens to hematocrit in anemia?

A

Decreased (increase in plasma volume)

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19
Q

What is the red blood cell count?

A
  1. Number of RBCs per unit of blood (millions/mcg)
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20
Q

What is the lifespan of a RBC?

A

120 days

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21
Q

What happens to RBCs in anemia?

A

Decreases

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22
Q

In what special populations do normal values vary?

A
  1. High altitude
  2. Smokers
  3. Elderly
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23
Q

What are the three RBC indices?

A
  1. MCV
  2. MCH
  3. MCHC
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24
Q

What are special facts about RBC indices?

A
  1. Describe size and Hgb content or RBCs

2. Do not express variation between cells

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25
Q

What is MCV?

A

Mean Cell Volume

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26
Q

What happens to MCV in macrocytic RBCs?

A

Increases

ALSO, folic acid and B12 deficient

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27
Q

What happens to MCV in microcytic RBCs?

A

Decreases

ALSO, Iron deficiency

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28
Q

What is Mean Cell Hemoglobin (MCH)?

A

The amount of Hgb in a RBC

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29
Q

What are false elevations of MCV referred to as?

A

Reticulocytosis

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30
Q

What happens to MCH in macrocytosis? microcytosis?

A
  1. Increases
  2. Decreases
    * You actually can’t distinguish between microcytosis and hypochromia*
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31
Q

What is the Mean Cell Hemoglobin Concentration (MCHC)?

A

Weight of Hgb per volume of cells (concentration)

-Independent of cell size

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32
Q

What occurs when a patient has a low MCHC and MCH?

A

Hypochromia

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33
Q

What occurs when there is normal MCHC and a decreased MCH?

A

Microcytosis

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34
Q

What is a reticulocyte?

A

young red blood cell

-indicates new RBC productions

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35
Q

What happens when total reticulocyte count is low? High?

A
  1. problem with bone marrow production

2. increased erythropoietic response to hemolysis or blood loss

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36
Q

What is the RBC distribution width?

A

Variation in RBC size
-Increased % = greater variation in size
This is useful for Dx of mixed anemia

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37
Q

What is meant by ‘serum iron’?

A

Concentration of iron bound to transferrin

Transferrin = binds and transports iron (normally 1/3)

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38
Q

What is the total iron binding capacity (TIBC)?

A

Measures the iron binding capacity of transferrin

DOES NOT FLUCTUATE

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39
Q

What does it mean when a patient has high TIBC and low serum iron?

A

Iron deficiency

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40
Q

What does it mean when a patient has low TIBC and low serum iron?

A

Anemia of chronic disease

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41
Q

What is transferrin saturation?

A

indicates the extent to which iron binding sites on transferrin are vacant

Serum Iron / TIBC X 100 = % ~33%

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42
Q

What is ferritin?

A

storage iron

it is proportional to total iron stores in the body

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43
Q

What does it mean when a patient has low ferritin?

A

Virtually diagnostic for IDA–chronic disease

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44
Q

What do low levels of folic acid and vitamin B-12 mean?

A

Vitamin deficiencies

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45
Q

What is important about homocysteine?

A

Folic acid and b-12 are needed to convert homocysteine to menthinoine
If there are high levels of homocysteine there may be vitamin deficiencies

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46
Q

What is methylmalonic acid (MMA)?

A

Vitamin B-12 is needed to convert MMA to succinyl Co-A

If there is an increase in urinary secretion of MMA usually before there is a decrease in serum b-12

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47
Q

What is erythropoietin?

A

it stimulates RBC production and maturation

increases 100 to 1000 fold during hypoxia or anemia

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48
Q

What are the three reasons iron is important?

A
  1. Transports O2 to tissue as part of Hgb
  2. Cell’s energy metabolism
  3. Facilitates O2 use and storage in muscles
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49
Q

What causes IDA-the most common nutritional deficiency and type of anemia?

A
  1. Inadequate dietary intake (3rd world)
  2. Inadequate absorption (Gastrectomy)
  3. Increased Iron needs (blood donations)
  4. Blood loss (GI tract)
  5. Other chronic illnesses (malabsorption)
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50
Q

What is the clinical presentation of IDA?

A

Don’t appear until Hgb <8-9

  1. Glossal pain
  2. Decreased salivary flow
  3. Pica/parophagia
  4. Psychomotor/mental devalopment
  5. “spoon” shaped nails
  6. Guaiac stool
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51
Q

How does the lab dx a patient with depletion of storage iron?

A
    1. Decreased serum ferritin*

2. Normal serum iron and Hbg/Hct

52
Q

How does the lab dx a patient with a decrease in transport iron?

A
    1. Decreased Serum iron*
    1. Increased TIBC*
    1. Decrease transferrin saturation*
      1. Normal Hgb/Hct
53
Q

How does the lab dx a patient with decreased Hgb production?

A
    1. Decrease Hgb/Hct*
      1. increased RDW
      2. decreased MCV
      3. decreased reticulocytes
54
Q

What are the goals of treatment in IDA?

A
  1. Replenish iron stores
  2. Treat any underlying disease
  3. Normalize Hgb/Hct
55
Q

What are is the preferred treatment of IDA?

A

Oral iron therapy

56
Q

What is the recommend iron dosage in a patient with IDA?

A

200 mg elemental iron in 2-3 daily doses
Start with smaller doses and gradually increase
Treat for 3-6 months AFTER anemia is resolved

OR
Every other day

Younger 325 bid-tid
Old 325 qd

57
Q

What form of iron is better absorbed?

A

Ferrous (Fe++) is better absorbed than Ferric (Fe+++), Fe+++ needs ionized and reduced in the stomach first

58
Q

Where is iron absorbed?

59
Q

How can a patient increase the absorption of iron?

A

heme iron in meats, poultry, fish better than non-heme iron veggies and grains

60
Q

What can decrease the absorption of iron?

A
  1. Calcium
  2. Slow release preparation/enteric coating
  3. Tea
  4. Food (1 hour before means 2 hours after)
61
Q

What are disadvantages of oral iron preparation?

A

Poor absorption and low compliance

62
Q

Where is oral iron preparations best absorbed?

A

In an acidic medium, needs to be non-enteric coated

63
Q

What is the recommended dosages of oral iron preparation?

A
  1. Younger: 325 mg ferrous sulfate BID-TID

2. Elders: 325 mg ferrous sulfate daily

64
Q

What are notable side effects of oral iron preparations?

A
  1. GI
    diarrhea, nausea, constipation, dark stools
    Need to titrate, and increase compliance
    If you don’t see SE’s there may be noncompliance
65
Q

How should you counsel a patient with GI intolerance when taking oral iron preparations?

A
  1. Lower dose
  2. Take with food
  3. Use a different formulation
  4. Attempt parenteral iron therapy
66
Q

What is notable about toxicity in children?

A
  1. Use child resistant containers

2. 10-15 tablets can be LETHAL AND AN EMERGENCY

67
Q

What is the iron chelator?

A

Dexferoxamine

68
Q

What drugs decrease iron absorption?

A
  1. Al, Mg, Ca containing antacids
  2. Tetracycline
  3. Doxycycline
  4. H2-antagonists
  5. PPIs
  6. Cholestyramine
69
Q

What results in a treatment failure of anemia?

A
  1. Noncompliance
  2. Incorrect diagnosis
  3. Continued bleeding
  4. Inability to absorb iron
70
Q

When should PN iron be used?

A
  1. Sig. intolerance
  2. Noncompliance
  3. Malabsorption
  4. Achlorhydria
  5. Renal failure, TPN, Cancer, Dialysis
71
Q

What is the preferred IV form of iron?

A

Iron dextran

Black Box Warning: anaphylactic reactions

72
Q

What are local reactions to iron dextran?

A

Pain, atrophy, brown skin staining, abscesses, necrosis

73
Q

What are the immediate reactions to iron dextran?

A
  • Mild:* malaise, nausea, headache, itching, sweating

* Anaphylactic:* dyspnea, chest pain, flushing, urticaria, dizziness, hypotension

74
Q

What are delayed reactions to iron dextran?

A

myalgia, arthralgia, phlebitis, fever, chills, dizziness, headache, n/v

75
Q

Ferric Gluconate:

A
  1. IV only
  2. approved for hemodialysis patients
  3. NO test dose required
  4. less anaphylaxis
76
Q

Iron Sucrose:

A
  1. hemodialysis patients
  2. NO test dose required BBW
  3. Well tolerated: leg cramps, hypotension
77
Q

Ferumoxytol (feraheme):

A
  1. Initial dose followed by 2nd 3-8 days later (510)
  2. Approved in CKD
  3. No test dose required
  4. Well tolerated
  5. MRI procedures
78
Q

Ferric Caboxymaltose (Injectafer)

A
  1. Two doses of 750 mg
  2. 15 min infusion
  3. Hypophosphatemia
79
Q

How do you differentiate between megaloblastic and non-megaloblastic anemias?

A

Peripheral blood smear

80
Q

What is a megaloblast?

A

retarded DNA synthesis, unbalanced cell growth

81
Q

What are the two types of megaloblastic anemias?

A
  1. Vitamin B-12 Deficiency

2. Folic Acid Deficiency

82
Q

What does vitamin B-12 do?

A
  1. Essential for DNA synthesis
  2. Maintains neurological system
  3. Needed for metabolic rxns involving folic acid
83
Q

What are the (3) causes of B-12 deficiency?

A
  1. Inadequate intake (vegans)
  2. Malabsorption syndromes (no intrinsic)
  3. Inadequate utilization (overgrowth of bacteria)
84
Q

What drugs can cause B-12 deficiency?

A
  1. Metformin
  2. H2-antagonists
  3. PPIs
85
Q

What are the clinical findings behind vitamin B-12 anemia?

A
  1. Pale loss of appetite, glossitis, weakness

2. Neurological

86
Q

What lab findings are associated with vitamin B-12 anemia?

A

Low: Hgb, HCT, RBCs
High: homocysteine, MMA, MCV, MCHC
Peripheral Blood Smear: macrocytosis

87
Q

What are the goals of therapy in vitamin B-12 anemia?

A
  1. Replace body stores of b-12
  2. Reverse hematological manifestations
  3. Prevent/reverse neurological problems
88
Q

What is the early treatment for vitamin B-12 anemia?

A
  1. VERY IMPORTANT
  2. Neurological damage can be irreversible after 6-12 months
  3. Range from numbness to psychosis/memory loss
89
Q

What is the oral vitamin B-12 anemia therapy?

A

Cyanobalamin (1-2 mg daily)

–> Can be used for pernicious anemia

90
Q

What is the PN vitamin B-12 anemia therapy?

A

Preferred with neurological symptoms

IM Cyanobalamin

91
Q

How can you evaluate the treatment of vitamin B-12 anemia therapy?

A
  1. Neurological Complications

2. Failure to respond (incorrect dx, other cause)

92
Q

What is important about folic acid?

A

Necessary for DNA/RNA

93
Q

What can occur in folic acid deficiency?

A

Increased risk for neural tube defects with pregnancy

94
Q

What can cause folic acid deficiency?

A
  1. Inadequate intake
  2. Decreased absorption
  3. Hyperutilization
  4. Drug induced
95
Q

What is the clinical presentation of folic acid anemia?

A

Similar to B-12 anemia without neurological symptoms, must rule out B-12

96
Q

What are the lab presentation in folic acid anemia?

A

Same as B-12 with low serum folic acid

Homocysteine elevates

97
Q

What is the treatment of folic acid anemia?

A

Oral folic acid therapy

98
Q

What is ACD?

A

anemia of chronic disease

99
Q

How does ACD occur and what diseases can result in it?

A
  1. > 1-2 months
  2. HIV, RA, Malignancy, Heart failure
    (Coexist with other anemias)
100
Q

What happens during ACD?

A
  1. Shortened RBC lifespan
  2. Impaired bone marrow response (decreased EPO)
  3. Change in iron metabolism
101
Q

What are the lab manifestations in ACD?

A
  1. No definitive test
  2. Decreased serum iron
  3. Ferritin normal or increased
  4. normocytic and normochromic
102
Q

How can you treat ACD?

A
  1. Anemia = poorer prognosis
  2. Treat underlying disease!!
  3. Iron therapy alone = typically ineffective
  4. Blood Transfusions
  5. Epoetin, Darbepoetin
103
Q

What are the erythropoietic agents?

A

Epoetin and Darbepoetin

  1. Stimulates RBC production and maturation
  2. IV/SQ
  3. Supplement with iron therapy
104
Q

What is the most common ADE of EPO?

A

Hypertension

105
Q

What is the target Hgb level in ACD patients?

A

11-12 mg/dL

106
Q

What are the contributing factors to anemia of critical illness?

A

sepsis, blood draws, surgical blood loss, immune mediated functional iron deficiency, GI bleeds

107
Q

What are the lab findings in a patient with anemia of critical illness?

A

Low serum iron and TIBC

Ferritin normal to high

108
Q

What is the treatment plan in a patient with anemia of critical illness?

A
  1. Supplemental iron
  2. Mixed findings with epoetin/darb
  3. Blood transfusions
109
Q

What is the process of Anemia of chronic kidney disease

A
  1. Diseased kidney cannot produce as much EPO
  2. Bone marrow produces fewer
  3. RBCs produced have shorter life span due to uremic environment
  4. Less oxygen available to organs leading to complications
    - -Onset and severity related to GFR–
110
Q

When would you discontinue erythropoietic agent?

111
Q

When should you discontinue erythropoietic agent?

A

failure to respond in 1st 8-12 weeks

112
Q

Deleterious effects of anemia of critical illness

A
  • cardiac morbidity and mortality

- reduced oxygen carrying capacity to organs

113
Q

Anemia in elderly

A
  • 12% of those >60

- more common in hospitalized or nursing home

114
Q

Underlying cause of anemia in elderly can be identified in ____ % of cases. What is it generally?

A

80%

chronic blood loss

115
Q

Contributing factors of anemia in elderly

A
  • progressive decrease in hematopoietic reserve
  • declining renal function
  • potentially lower Hgb in males
116
Q

Anemia in elderly labs

A
  • check nutritional status

- lab same as other anemia

117
Q

Two peak periods of children at risk of anemia

A
  • late infancy/early childhood

- adolescence

118
Q

When is the 1st anemia screening for infants?

A

6-12 months

119
Q

When do iron stores during gestation run out?

120
Q

T/F anemia in pediatrics leads to significant morbidity and mortality worldwide

121
Q

Anemia of prematurity treatment

A

RBC transfusions

122
Q

When does anemia of prematurity occur?

A

3-12 weeks after birth in infants with <32 weeks gestation

123
Q

What are the drug induced causes of folic acid deficiency?

A 
Anticonvulsants* (phenytoin, primidone, phenobarb)
Oral contraceptives
Methotrexate*
TMP
Triamterene
124
Q

Anticonvulsants cause folic acid deficiency how?

A

Interfere with folate abs

125
Q

Methotrexate causes folic acid deficiency how?

A

Block dihydrofolate reductase

126
Q

ADE of oral folic acid

A

Virtually none

PT: Hematology & Pulmonary (8 decks)

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