Hematology Exam 3 COPY Flashcards

1
Q

What is one of the largest organs in the body?

A

Bone marrow

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2
Q

What percentage of our body weight is bone marrow?

A

4%

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3
Q

Where is bone marrow found in infants?

A

All bones

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4
Q

Where is bone marrow found in adults?

A

Flat bones

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5
Q

Where are RBCs located in bone marrow?

A

Inside the sinus around a macrophage

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6
Q

Where are megakaryocytes located in bone marrow?

A

Near the sinus wall

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7
Q

Ratio of fat to tissue in normal bone marrow

A

50:50

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8
Q

Job of macrophages in bone marrow

A

To incorporate iron into the red cells

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9
Q

What forms the foundation or support of bone marrow?

A

Meshwork of stromal cells

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10
Q

Cells unique to bone marrow

A

Osteoclasts - bone destroying/breakdown

Osteoblasts - bone forming

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11
Q

Name the cells

A

Osteoblasts

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12
Q

Name the cells

A

Osteoclasts

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13
Q

What is circled? (BM)

A

Spicules in bone marrow

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14
Q

What does seeing spicules tell you?

A

You have a good aspirate

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15
Q

Where does the core biopsy go in the lab?

A

Histology

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16
Q

Lifespan of RBCs

A

120 days

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17
Q

Lifespan of WBCs

A

anywhere from 7 hours to 20 days depending on the type of WBC

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18
Q

Function of bone marrow

A

Supplies mature cells for circulation in steady state or for increased demand

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19
Q

What maintains the self-renewal of bone marrow?

A

Pluripotential stem cells

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20
Q

What are some examples of stimuli received to create cells in the bone marrow?

A
  • Thrombopoietin
  • Erythropoietin
  • Colony stimulating factors
  • Interleukins
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21
Q

What is produced by stromal cells, fibroblasts, endothelial cells, and macrophages?

A

Growth factors

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22
Q

What colony stimulating factors go in to the myeloid line?

A
  • CSF-Spleen
  • CSF-GEMM
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23
Q

Anemia, polycythemia, leukopenia, and thrombocytopenia are all diseases that affect what in bone marrow?

A

Blood production of bone marrow

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24
Q

How do the following systemic diseases affect bone marrow?:

  • Solid metastasizing tumors that spread to the marrow such as cancer and Hodgkin’s lymphoma
  • Fever of Unknown Origin (FUO)
A

They affect blood production in bone marrow

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25
Q

Type of hereditary diseases that can affect bone marrow

A

Storage pool diseases such as Gauchers

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26
Q

Usual location a bone marrow aspirate is performed on adults

A

Posterior superior iliac crest

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27
Q

Usual location a bone marrow aspirate is done on children and infants

A

Top of tibia below the knee

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28
Q

Type of needle used for bone marrow aspirate

A

Jamshidi needle

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29
Q

Amount needed for bone marrow aspirate

A

0.5 - 1.5mL for hematology and an additional 5cc for other departments

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30
Q

2 diseases that could cause a “dry tap” (no aspirate)

A
  • Myelofibrosis
  • Aplastic anemia
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31
Q

Reasons an aspirate may not be collected

A
  • Dry tap (Myelofibrosis or aplastic anemia)
  • Not in the bone marrow
  • Tumor
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32
Q

Preservative used for biopsy

A

Formalin

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33
Q

Marrow slide examination:

Childhood cellularity percentage

A

80%

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34
Q

Marrow slide examination:

Age 30-70 cellularity percentage

A

50%

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35
Q

Marrow slide examination:

How do you calculate the cellularity percentage for ages >70?

A

100 - patient age = cellularity +/- 10%

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36
Q

Bone marrow cellularity

What would be the expected cellularity for an 82 year old patient?

A

100 - 82 = 18

8 - 28%
(18 +/-10%)

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37
Q

Under oil immersion, how many cells are counted during a bone marrow differential? What cells are counted?

A

500 to 1000 both red and white cells

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38
Q

What cells are not included in the M:E ratio?

A

Lymphs, monos, and plasma cells

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39
Q

What percentage of the bone marrow differential count will be comprised of neutrophilic myelocytes, metamyelocytes, bands, and segmented neutrophils?

A

50%

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40
Q

M:E Ratio:

350 neutrophilic blasts >segs, eos, baso

75 lymphs, monocytes, and plasma cells

75 erythroid cells (blasts>meta)

What is the M:E ratio?

A

350 / 75 = 4.7:1

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41
Q

Normal M:E ratio

A

3:1

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42
Q

How would myeloid hypoplasia effect the M:E ratio?

A

Myeloid cells would be decreased causing the M:E to be < 3:1

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43
Q

How would erythroid hyperplasia effect the M:E ratio?

A

Erythroid hyperplasia would increase the red cells count causing the M:E ratio to be 1:1

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44
Q

What stains are performed on each bone marrow aspirate?

A
  • Wright’s stain
  • Iron stain
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45
Q

Iron that is stored in the bone marrow is in what form?

A

Hemosiderin

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46
Q

What is hemosiderin composed of?

A

Iron and protein

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47
Q

Stain used to stain iron

A

Prussian Blue

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48
Q

Symptoms of anemia

A
  • Tachycardia
  • Shortness of breath
  • Headaches
  • Pallor
  • Fatigue
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49
Q

TRUE or FALSE

Typical CBC results in anemia include:

-Decreased hemoglobin, hematocrit, and RBC count

A

TRUE

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50
Q

TRUE or FALSE

With most anemia, the M:E ratio is 1:1

A

TRUE

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51
Q

What MCV classifies as microcytic anemia?

A

< 80fL

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52
Q

What MCV classifies as a macrocytic anemia?

A

> 100 fL

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53
Q

What MCV classifies as a normocytic anemia?

A

80 - 100 fL

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54
Q

What is the cause of Microcytic, hypochromic anemias?

A

Inadequate production of some part of hemoglobin (iron, heme, globin)

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55
Q

Thalassemias have what abnormality?

A

Globin abnormality

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56
Q

2 Etiologic categories of macrocytic anemias

A
  • Megaloblastic
  • Non-Megaloblastic
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57
Q

Cause of megaloblastic anemias

A

Abnormal DNA synthesis

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58
Q

Cause of non-megaloblastic anemia

A

Increase in membrane lipids

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59
Q

TRUE or FALSE

Non-megaloblastic anemia will have an MCV > 110

A

FALSE

Non-megaloblastic anemia will have an MCV > 100 fL but < 110 fL

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60
Q

This anemia is due to a slowdown in DNA synthesis in developing cells causing a shorter life span in the deficient cells

A

Megaloblastic anemia

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61
Q

What causes the defect in DNA replication that is seen in megaloblastic anemia?

A

A depletion of thymidine triphosphate, an immediate DNA precursor

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62
Q

If there is an increase in _______________ , it tells us there is possibly a B12 deficiency

A

Methylmalonyl Coenzyme A

(MMA)

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63
Q

Being deficient in this causes slowed nuclear maturation and mitosis resulting in asynchrony in cells

A

Thymidine triphosphate

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64
Q

When the nucleus of a cell is immature and the cytoplasm is matured, this is referred to as what?

A

Asynchrony

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65
Q

Another name for B12

A

Cyanocobalamin

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66
Q

How is B12 absorbed in the body?

A

Through the intestine by Intrinsic Factor (IF)

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67
Q

Where is Intrinsic Factor produced?

A

Parietal cells of the stomach

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68
Q

What do the IF-B12 complexes attach for absorption?

A

To receptors on the ileal mucosal cells

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69
Q

What does B12 attach to after being absorbed?

A

Transcobalamin II

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70
Q

Where does the B12-transcobalamin II complex go?

A

Bone marrow

or

Liver for storage

(large amount is stored)

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71
Q

Where do we get B12 from in our diet?

A

Meat

Eggs

Dairy products

Liver

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72
Q

Where does folic acid come from in our diets?

A
  • Leafy greens
  • Meat
  • Some fruits
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73
Q

What carries folate after it is absorbed?

A

Albumin

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74
Q

Where does albumin take folate in the body?

A

Bone marrow

or

Liver

(only a small amount is stored)

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75
Q

Once absorbed and transported, what 2 cofactors play an important role in DNA synthesis?

A

Folate and Vitamin B12

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76
Q

Any cell actively dividing or replicating will have a defective nucleus when either of what 2 cofactors are deficient?

A

B12 and Folate

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77
Q

A lack of intrinsic factor causes what anemia?

A

Pernicious Anemia

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78
Q

What tapeworm can cause a B12 deficiency?

A

Diphyllobothium latum - fish tapeworm

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79
Q

TRUE or FALSE

In pernicious anemia, folate cannot be absorbed

A

FALSE

Vitamin B12 cannot be absorbed properly due to a lack of intrinsic factor

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80
Q

An autoimmune disorder with autoantibodies produced by parietal cells causes what type of anemia?

A

Pernicious anemia

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81
Q

Pernicious anemia is typically found in which descent of people?

A

Northern European

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82
Q

How is pernicious anemia treated?

A

Vitamin B12 injections

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83
Q

Which is more common and why?

B12 deficiency

or

Folate deficiency

A

Folate deficiency because little to none is stored in the body

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84
Q

Clinical features of megaloblastic anemia

A
  • Typical signs of anemia
  • Lemon-yellow pallor

-Smooth, sore tongue

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85
Q

Clinical features of B12 deficient megaloblastic anemia

A

Neurologic manifestations from degeneration of myelin:

  • tingling and numbness of extremities
  • gait abnormalities
  • psychosis due to defective methyl group metabolism
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86
Q

Key diagnostic features seen in the peripheral blood smear of megaloblastic anemia

A
  • Hypersegmented neutrophils
  • Macro-ovalocytes
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87
Q

Identify the anemia:

  • Decreased retic
  • Hypercellular bone marrow
  • MCV >110
  • Decreased RBC, WBC, and PLT counts
  • Macro-ovalocytes
  • Hypersegmented neutrophils
A

Megaloblastic anemia

-either B12 or Folate deficiency but cannot distinguish without further testing

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88
Q

What is the term for a pyknotic cell causing a fragmented nucleus?

A

Karyorrhexis

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89
Q

Giant bands and giant metamyelocytes are a key findings in the bone marrow of which anemia?

A

Megaloblastic anemia

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90
Q

What is the term used to describe the cell the arrow is pointing to?

A

Karyorrhexis

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91
Q

What chemistry tests are elevated due to hemolysis with megaloblastic anemia?

A

LD and Bilirubin

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92
Q

Test that is used to differentiate between Pernicious Anemia and other B12 deficiencies

A

Schilling Test

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93
Q

Non-megaloblastic conditions (3)

A
  • Liver disease
  • Alcoholism
  • Reticulocytosis
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94
Q

MCV will increase 1 fL for each ___% of retics

A

MCV will increase 1 fL for each 1% of retics

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95
Q

What can cause the MCV to appear macrocytic?

A
  • Cold agglutinin
  • High WBC count
  • High glucose causing cells to swell
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96
Q

The following morphologic characteristics are seen in what class of anemia?:

  • MCV <80
  • MCH and MCHC are decreased
  • RDW is generally normal
A

Microcytic, hypochromic anemia

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97
Q

Where does most of the iron required by the cells come from?

A

Broken down RBCs

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98
Q

How much iron is needed for each mL of RBCs?

A

1mg

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99
Q

What regulates the absorption of iron in the body?

A

Mucosal cells in the GI tract

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100
Q

How much of the daily intake of iron from diet is actually absorbed?

A

10%

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101
Q

What enhances iron absorption?

A

Ascorbic acid (vitamin C) and using cast iron pots/skillets

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102
Q

What decreases iron absorption in the body?

A

Antacids

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103
Q

All of the following affect what?

  • Type of iron in the food
  • Other food that is ingested
  • Acidity of stomach
  • Availability of iron stores
A

Absorption of iron

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104
Q

Iron is transported from mucosal cells to the blood in what state?

A

Ferrous state (Fe2+)

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105
Q

What is the dietary form of iron?

A

Ferric (Fe3+)

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106
Q

What protein transports the ferric iron?

A

Transferrin

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107
Q

Number of iron atoms that transferrin can bind to at once

A

2 iron atoms per 1 transferrin molecule

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108
Q

Where are the 2 places transferrin will transport iron?

A
  • Bone marrow
  • Liver
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109
Q

Iron is stored as this in the liver

A

Ferritin

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110
Q

Transferrin can bind ____ - ____ mg of iron

A

240 - 280 mg

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111
Q

About what percentage of transferrin is bound with iron?

A

30%

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112
Q

How does celiac disease cause iron deficiency?

A

Celiac disease doesn’t allow iron to absorb properly

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113
Q

What is significant about having an inherited mutation with matripase 2 protein?

A

It causes impaired absorption of iron leading to iron deficiency anemia

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114
Q

Most common cause of iron deficiency anemia

A

Increased blood loss

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115
Q

Sequence of development of iron deficient anemia

A
  1. Iron storage depleted
  2. Transport iron depleted
  3. Functional iron depletion
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116
Q

Iron is required for _____ synthesis

A

Iron is required for heme synthesis

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117
Q

Stage of Iron depletion:

  • Normal hemoglobin
  • Normal serum iron
  • Normal TIBC
  • Decreased ferritin
A

Stage 1

Storage Iron Depletion

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118
Q

Stage of Iron depletion:

  • Normal hemoglobin
  • Decreased serum iron
  • Increased TIBC
  • Decreased ferritin
A

Stage 2

Transport Iron Depletion

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119
Q

Stage of Iron depletion:

  • Decreased hemoglobin
  • Decreased serum iron
  • Increased TIBC
  • Decreased ferritin
A

Stage 3

Functional Iron Depletion

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120
Q

Normal range for serum iron

A

50 - 160 ug/dL

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121
Q

Normal range for TIBC

A

250-400 ug/dL

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122
Q

What is TIBC?

A

Total Iron Binding Capacity = transferrin related test

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123
Q

Normal range for % transferrin saturation

A

20 - 55%

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124
Q

Normal range for ferritin for males

A

40 - 400 ng/mL

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125
Q

Normal range for ferritin for females

A

12 - 160 ng/mL

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126
Q

Classify the type of anemia

(size and pallor)

A

Hypochromic, microcytic

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127
Q

What is iron overload also known as?

A

Hemosiderosis

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128
Q

The following may cause what?:

  • Hemolytic anemia with massive transfusions
  • Disorders of erythropoiesis where cells cannot be made and iron builds up
A

Hemosiderosis

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129
Q

What is the term for a more severe form of hemosiderosis

A

Hemochromatosis

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130
Q

What is the cause of Hereditary hemochromatosis?

A

A gene mutation (hereditary iron or transferrin receptor protein)

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131
Q

The following results are seen in what disorder?

  • Abnormal AST and ALT (LFTs)
  • Increased serum iron
  • Increased % transferrin saturation
  • Increased serum ferritin
  • Increased hgb
  • Increased HCT
A

Hemochromatosis

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132
Q

How is hereditary hemosiderosis treated?

A

Therapeutic phlebotomy

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133
Q

How is transfusion related hemosiderosis treated?

A

Chelation therapy

Patient is given desferrioxamine which binds to iron and gets excreted in urine

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134
Q

Thalassemia, Anemia of Chronic Disease/Inflammation, Lead poisoning, and Sideroblastic Anemia are all examples of what type of anemia?

A

Microcytic anemia

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135
Q

An inherited disorder in which the globin chain is not produced in adequate amounts

A

Thalassemia

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136
Q

This is the most common anemia among hospitalized patients

A

Anemia of Chronic Disease/Inflammation

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137
Q

This hormone is an acute phase reactant that regulates the absorption of iron in the intestines and also the release of iron from macrophages.

A

Hepcidin

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138
Q

What produces hepcidin?

A

The liver

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139
Q

This acute phase reactant is an iron binding protein located in the granules of neutrophils. It is involved in preventing phagocytized bacteria from using intracellular iron for their own metabolic processes

A

Lactoferrin

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140
Q

The following lab results are seen with which type of anemia?:

  • Decreased serum iron
  • Decreased TIBC
  • Increased serum ferritin
  • normal soluble transferrin receptors (sTfRs) - newer test
A

Anemia of Chronic Disease/Inflammation

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141
Q

Treatment of Anemia of Chronic Inflammation

A
  • Treat with erythropoietin, given with iron b/c the body’s stored iron remains unavailable
  • Alleviate the causative condition
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142
Q

Lead poisoning is caused by lead blocking the production of what in several spots?

A

Lead poisoning blocks heme production

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143
Q

This microcytic anemia causes:

-Interference in the conversion of aminolevulinic acid (ALA) to porphobilinogen (PBG)

and

-Interference in the incorporation of iron into protoporphyrin IX by ferrochetalase

A

Lead poisoning

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144
Q

This microcytic anemia will interfere with the breakdown of ribosomal RNA creating coares basophilic stippling and a low MCV

A

Lead poisoning

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145
Q

TRUE or FALSE

Basophilic stippling is diagnostic for lead poisoning

A

FALSE

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146
Q

In this microcytic anemia the following occurs:

  • Cells cannot use available iron
  • The iron is trapped in the cell
  • Iron will form pappenheimer bodies in mature cells
A

Sideroblastic anemia

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147
Q

This picture depicts a hallmark representation of what microcytic anemia?

A

Sideroblastic anemia

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148
Q

What is considered “hallmark” for sideroblastic anemia?

A

Dimorphic RBCs and ringed sideroblasts

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149
Q

MCV, MCH, and MCHC are lowest with which microcytic anemia?

A

Thalassemia

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150
Q

Will the RDW be normal, elevated, or decreased with iron deficiency anemia?

A

Elevated

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151
Q

Will RDW be normal, elevated, or decreased with Thalassemia?

A

Normal

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152
Q

What is included in iron studies?

A
  • Serum iron
  • Total Iron Binding Capacity (TIBC)
  • % Transferrin Saturation
  • Serum Ferritin
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153
Q

What is measured in serum iron?

A

The amount of iron bound to transferrin in circulation

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154
Q

What does TIBC measure?

A

The amount of transferrin bound and unbound with iron

It is measuring the binding ability of transferrin

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155
Q

How is % transferrin saturation calculated?

A

Serum iron / TIBC x 100

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156
Q

Normal range for soluble transferrin receptors

A

1.15 - 2.75 mg/L

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157
Q

The amount measured in this test is based on intracellular iron and is an indicator of functional iron available in cells

A

Soluble transferrin receptors (sTfR)

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158
Q

TRUE of FALSE

sTfR is increased in Anemia of Chronic Inflammation

A

FALSE

Normal in Anemia of Chronic Inflammation

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159
Q

TRUE or FALSE

sTfR is increased in IDA

A

TRUE

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160
Q

When does free erythrocyte protoporphyrin accumulate?

A

When iron is NOT available

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161
Q

Free erythrocyte protoporphyrin will be increased, decreased, or normal in IDA?

A

Increased

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162
Q

With which anemia is knowing the value of free erythrocyte protoporphyrin is most valuable?

A

Lead poisoning due to ferrochelatase impairment

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163
Q

Normal value of free erythrocyte protoporphyrin

A

< 80 ug/dL

164
Q

A storage form of iron mostly found in bone marrow

A

Hemosiderin

165
Q

Red cells having a “shaggy” cytoplasm is seen with what anemia?

A

Iron deficiency anemia

166
Q

Name the hypochromic, microcytic anemia

A

Iron Deficiency Anemia

167
Q

Name the hypochromic, microcytic anemia

A

Thalassemia

168
Q

Name the hypochromic, microcytic anemia

A

Anemia of Chronic Inflammation/Disease

169
Q

Name the hypochromic, microcytic anemia

A

Sideroblastic anemia

170
Q

Name the hypochromic, microcytic anemia

A

Lead poisoning

171
Q

Free erythropoietin is also known as

A

Zinc protoporphyrin (ZPP)

172
Q

What are the 3 types of normocytic, normochromic anemia?

A
  • Hemolytic
  • Aplastic Anemia
  • Acute Blood loss
173
Q

In this category of N/N anemia cells are not made. The building blocks are present and RBCs look normal but there just aren’t enough of them.

A

Aplastic anemia

174
Q

In this category of N/N cells are broken down at an increased rate

A

Hemolytic anemias

175
Q

N/N anemia:

  • Cellular areas of bone marrow are replaced by fat cells
  • Caused by toxic, radiant, or immunologic injury to pluripotential cells
A

Aplastic anemia

176
Q

Normocytic/Normocytic anemias are categorized based on increased, decreased, or normal ______

A

Reticulocyte count

177
Q

TRUE or FALSE

Aplastic anemia is always permanent and requires a bone marrow transplant - but this may not always work

A

FALSE

It can be permanent but only if all of the pluripotential cells are damaged.

178
Q

Types of congenital aplastic anemia

A
  • Fanconi anemia
  • Dyskeratosis Congenita
  • Scwachman-Bodian-Diamond Syndrome
179
Q

This inherited aplastic anemia is an autosomal recessive chromosomal instability disorder

A

Fanconi Anemia

180
Q

In this aplastic anemia you will see:

-Pancytopenia, a decrease in reticulocytes, hypocellular bone marrow

as well as

-Skin pigmentation, short stature, and hypogonadism

A

Fanconi Anemia

181
Q

This inherited aplastic anemia is a bone marrow failure disease

A

Dyskeratosis Congenita

182
Q

With this inherited aplastic anemia you will see:

  • Abnormal skin pigmentation (dark spots with white dots in them)
  • Dystrophic nails (look almost like a fungal infection)
  • Oral leukoplakia (very white thrush-looking tongue)
  • Bone marrow failure
A

Dyskeratosis Congenita

183
Q

This inherited aplastic anemia resembles cystic fibrosis

A

Shwachman-Bodian-Diamond Syndrome

184
Q

Name the inherited aplastic anemia:

  • Pancreatic insufficiency
  • Cytopenia
  • Skeletal abnormalities
  • Predisposition for hematologic malignancies
  • Neutropenia and immune dysfunction
  • Normal sweat chloride (will differentiate it from cystic fibrosis)
A

Shwachman-Bodian-Diamond Syndrome

185
Q

What percentage of aplastic anemia is diagnosed as idiopathic?

A

50-75%

186
Q

Secondary aplastic anemia accounts for what percentage of cases?

A

25%

187
Q

Causes of secondary aplastic anemia

A
  • Chloramphenicol, an old antibiotic
  • Industrial chemicals such as benzene
  • Insecticides such as DDT
188
Q

What can cause acquired aplastic anemia?

A
  • Radiation exposure
  • Infections such as hepatitis, HIV, Epstein-Barr, or TB
189
Q

TRUE or FALSE

You will see pancytopenia and increased infections with aplastic anemia

A

TRUE

190
Q

What is the survival rate for aplastic anemia after bone marrow transplant?

A

80%

191
Q

What anemia is this bone marrow indicative of?

A

Aplastic anemia

192
Q

This is a selective decrease in the red cell commited stem cells resulting in a temporary reduction in RBC production. It often follows a parvovirus infection.

A

Pure Red Cell Aplasia

193
Q

What does parvovirus infection cause in children?

A

Fifth Disease

194
Q

What is due to clonal proliferation of pluripotential stem cells with incomplete maturation of marrow precursors?

A

Myelodysplastic syndromes

195
Q

These disorders are due to a chromosomal defect in stem cells from oncogenes, environmental elements, or secondary to chemotherapy and radiation from previous cancers

A

Myelodysplastic disorders

(MDS)

196
Q

In ____, apoptosis appears to be increased early in the disease

A

MDS

197
Q

This anemia is usually resistant to any therapy. Pancytopenia including reticulocytopenia, is present. The bone marrow is normo- or hypercellular with increased iron stores.

A

Refractory anemia

198
Q

In this anemia, erythroid hyperplasia with nuclear budding in erythroid precursors can be seen in the bone marrow

A

Refractory Anemia

199
Q

TRUE or FALSE

Refractory anemia can be cured with hematopoietic stem cell transplant

A

TRUE

200
Q

The cause of this NC/NC anemia is mostly due to decreased erythropoietin

A

Anemia of renal disease

201
Q

How is anemia of renal disease treated?

A

Erythropoietin therapy

202
Q

What other organs may contribute to anemia of renal disease disorder?

A

Thyroid and liver

203
Q

Anemia of chronic disorders is the most common anemia of what type of people?

A

Hospitalized patients

204
Q

What anemia is observed with infections, autoimmune disorders (SLE, RA), and malignancies?

A

Anemia of chronic disorders

205
Q

Name the anemia:

  • Cytokines are produced by the immune system in response to immune or tumor stimulus
  • Erythropoietin is inhibited
  • Macrophages become stimulated and will not release iron after normal RBC breakdown in the spleen
  • Hepcidin protein is involved
A

Anemia of chronic disorders

206
Q

Acute phase reactant that increases in inflammation/infection

  • Iron regulator produced by hepatocytes
  • Increased in anemia of chronic disorder
A

Hepcidin

207
Q

This anemia results from marrow infiltration with subsequent damage to hematopoietic microenvironment and replacement of normal cells.

-Due to metastatic carcinoma whereby primary cancer cells go to bone marrow and start to proliferate

A

Myelophthisic anemia

208
Q

Extramedullary hematopoiesis occurs with this anemia producing less functional cells.

A

Myelophthisic anemia

209
Q

What anemia is depicted in this picture?

  • Tear drop RBCs
  • Leukoerythroblastic cells
  • NRBCs
A

Myelophthisic anemia

210
Q

This NC/NC anemia leads to cardiovascular collapse and shock

A

Acute blood loss

211
Q

What percentage of blood loss will result in shock and death?

A

50%

212
Q

What percentage of blood loss with result in major symptoms?

A

30-40%

213
Q

What are the 2 major categories of NC/NC anemia?

A

Aplastic and hemolytic

214
Q

With normocytic/normochromic anemias, what CBC results are normal and what results are decreased?

A

Normal: indices (MCV, MCH, MCHC)

Decreased: Hgb, HCT, RBC count

215
Q

What are the classifications of hemolytic anemia? (6)

A
  • Intrinsic
  • Extrinsic
  • Acquired
  • Inherited
  • Acute
  • Chronic
216
Q

This classification of hemolytic anemia is intracellular - due to a defect of the cell

A

Intrinsic

217
Q

This classification of hemolytic anemia is extracellular - due to a defect outside the cell.

A

Extrinsic

218
Q

Classification of hemolytic anemia that is sudden and/or episodic

A

Acute

219
Q

Classification of hemolytic anemia that occurs over time and may not be evident if the bone marrow is able to compensate.

A

Chronic

220
Q

Classification of hemolytic anemia that is passed to offspring by parents and is due to a mutant gene

A

Inherited

221
Q

Hemolytic anemia classification that is developed in individuals who were previously normal but exposed to a chemical/agent/ or condition

A

Acquired

222
Q

Hemolytic anemias:

Most intrinsic defects are ______, while most extrinsic defects are _______.

A

Most intrinsic defects are inherited, while most extrinsic defects are acquired.

223
Q

What hemolytic anemia is intrinsic but acquired instead of inherited?

A

Paroxysmal Nocturnal Hemoglobinuria

224
Q

Examples of acute hemolytic anemia

A
  • Paroxysmal Nocturnal Hemoglobinuria
  • Hemolytic Transfusion Reaction
225
Q

Examples of chronic hemolytic anemia

A

-G6PD deficiency

226
Q

All of the following are examples of what classification of hemolytic anemia?:

  • Abnormalities of the RBC membrane
  • Defective enzymatic pathways
  • Defective hemoglobin molecule
A

Intrinsic hemolytic anemia

227
Q

All of the following are examples of what classification of hemolytic anemia?:

  • Malaria parasitic infection
  • Antibodies to an RBC antigen
A

Extrinsic hemolytic anemia

228
Q

Term that means the cell is destroyed by the spleen

A

Extravascular

229
Q

Term that means the cells is destroyed in the vessel

A

Intravascular

230
Q

Percentage of cell destruction that is intravascular

A

10%

231
Q

Percentage of cell destruction that is extravascular

A

90%

232
Q

Compensated or uncompensated?:

-Little to no anemia

A

Compensated

233
Q

Compensated or Uncompensated?:

Red cell life span is usually only 15-20 days

A

Uncompensated

234
Q

In compensated bone marrow response, the bone marrow is able to increase its output how much?

A

6x - 8x

(six-fold to eight-fold)

235
Q

-Autosomal dominant

  • Defects in proteins that disrupt the vertical interactions between transmembrane proteins and cytoskeleton proteins of red cells
  • Ankrin and Spectrin

-Results in a destabilization of the lipid bilayer allowing lipids to escape

A

Hereditary spherocytosis

236
Q

In this disorder the cell is not able to deform due to decreased surface-to-volume ratio so macrophages in the spleen will remove the cell.

The disorder is more common in northern European descent

A

Hereditary spherocytosis

237
Q

Clinical symptoms of this disorder include:

  • Mild jaundice
  • Anemia
  • Splenomegaly

Lab Findings:

  • MCV normal or slightly decreased
  • MCH elevated
  • MCHC >36% (hallmark)
  • Increased LD and Bilirubin
  • Increased osmotic fragility
  • Reticulocytosis
A

Hereditary spherocytosis

238
Q

Measures the surface-to-volume ratio of RBCs

  • Cells are placed in graded hypotonic salt (saline) solutions
  • Water enters cell, cell swells, and bursts
A

Osmotic fragility

239
Q

What is represented by A

A

Target cells and elliptocytes

240
Q

What does B represent?

A

Normal cells

241
Q

What does C represent?

A

Spherocytes

242
Q

Normal range of osmotic fragility

A

Hemolysis begins at 0.45% NaCl

100% hemolysis occurs between 0.35-0.30%

243
Q

When does hemolysis begin for hereditary spherocytosis in osmotic fragility?

A

0.65% NaCl

244
Q

Treatment for hereditary spherocytosis

A

Splenectomy in severe cases

245
Q

Autosomal dominant hereditary membrane defect involving the horizontal bonds on the skeleton of RBCs

A

Hereditary elliptocytosis

246
Q

This membrane defect is caused by an imbalance of cations and is more commonly acquired due to acute alcoholism, malignancy, or medications.

A

Stomatocytes

247
Q

This membrane defect condition is rare and usually inherited. Fragmentation, microspherocytosis, and elliptocytosis are seen. RBCs show a marked thermal sensitivity- incubated cells between 41C-45C will fragment.

A

Pyropoikilocytosis

248
Q

This membrane defect is observed in:

-Acquired liver disease

and

  • Congenital abetalipoproteinemia (rare)
  • No LDL/VLDL
  • Fat malabsorption, ataxia, neuropathy, retinitis pigmentosa, acanthocytosis
A

Acanthocytes

249
Q

This deficiency is transmitted a by sex-linked, mutant gene and is more common in males

A

G-6-PD Deficiency

250
Q

When this is deficient NADP cannot be converted to NADPH, glutathione is reduced, hemoglobin aggregates or precipitates (Heinz Bodies), and premature destruction of red cells occurs.

A

G-6-PD

251
Q

Relatively common disorder in African American males and Asians. Most people never suffer any clinical manifestations because the bone marrow will compensate.

A

G-6-PD deficiency

252
Q

If you have this, you will have a sensitivity to fava beans and primaquine (an anti-malarial drug) could induce a hemolytic episode

A

G-6-PD deficiency

253
Q

Qualitative test for G-6-PD deficiency

A

Fluorescent Spot Test

254
Q

Second most common enzyme deficiency

-Involved in Embden-Meyerhoff pathway

A

Pyruvate Kinase Deficiency

255
Q

Acquired intracellular defect with intravascular hemolysis

A

Paroxysmal Nocturnal Hemoglobinuria

256
Q

In PNH, what is deficient?

A

CD 55 - Decay Accelerating Factor

CD 59 - Membrane inhibiting of Reactive Lysis (MIRL)

These proteins prevent normal cells from complement destruction

257
Q

Screening test for PNH

A

Sugar Water Test

-promotes binding of complement to red cell membrane; complement-sensitive PNH red cells are lysed while normal cells are unaffected

258
Q

Confirmation test for PNH

A

Ham’s Test (Acidified serum lysis test)

259
Q

PNH treatment

A
  • Treat symptoms - support therapy
  • Treat complications
260
Q

Average survival period for PNH

A

10 years

-May become AML

261
Q

What causes autoimmune hemolytic anemia?

A

Primary - idiopathic

Secondary to autoimmune disorder or cancer- SLE, RA, CLL, lymphoma

262
Q

2 types of autoimmune hemolytic anemias

A
  • Warm-reactive antibodies (IgG)
  • Cold-reactive antibodies (IgM)
263
Q

70% of all cases of autoimmune hemolytic anemias are due to this autoantibody

A

Warm-reactive (IgG)

264
Q

What will differentiate warm-reactive autoantibodies from spherocytosis?

A

Direct antiglobulin test

  • Positive with warm auto
  • Negative with spherocytosis
265
Q

When treating a patient with a warm autoantibody, what is done only as a last resort?

A

Transfusion

266
Q

Cold-reactive autoantibodies are most often observed when?

A

Secondary to an infection such as:

-Mycoplasma pneumonia
or
-Infectious mononucleosis

267
Q

Clinical findings of cold autoantibodies

A

Acrocyanosis- cyanosis in extremities

Anemia symptoms

268
Q

With this autoimmune hemolytic anemia the specimen will agglutinate as it cools to room temperature and you will observe agglutinated red cells on the peripheral blood smear

A

Cold autoantibody

269
Q

Non-immune hemolytic anemia also referred to as sports anemia. Caused by trauma to cells from physical disruptions

A

March hemoglobinuria

270
Q

This non-immuno hemolytic anemia is a serious life-threatening disease in which cells are fragmented by fibrin in the vessels or a defective heart valve.

A

Microangiopathic anemia

271
Q

Non-immune hemolytic anemia can be caused by what chemical or physical agents?

A
  • Copper
  • Water (drowning)
  • Insect venom
  • Drugs
  • Chemicals
  • Heat stroke
272
Q

What microorganisms can cause a non-immune hemolytic anemia?

A
  • Malaria
  • other bateria and viruses producing toxins
273
Q

This microorganism is the most common cause on non-immune hemolytic anemia in the world

A

Malaria

274
Q

Will the following be increased, decreased, or normal in hemolytic anemias?:

  • Unconjugated bilirubin
  • LD
  • Reticulocytes
  • MCV
  • Red cells
  • Haptoglobin
  • HCT
  • Urine urobilinogen
A

Increased:

  • unconjugated bilirubin
  • LD
  • Reticulocytes
  • Urine urobilinogen
  • Bone marrow red cells
  • MCV slightly if retic % is increased

Decreased:

  • Red cells in peripheral blood
  • Haptoglobin
  • HCT

Normal:

-MCV if retic % is normal

275
Q

Urine hemoglobin and hemosiderin are increased in what type of hemolysis?

A

Intravascular hemolysis

276
Q

What test is specific for autoimmune hemolytic anemia?

A

Direct antiglobulin test (DAT)

277
Q

What test is specific for hemoglobinopathies?

A

Hemoglobin electrophoresis

278
Q

What test is specific for G6PD deficiency?

A

Heinz bodies

and

G6PD assay when patient is not in a crisis

279
Q

Test that is specific for hereditary spherocytosis and elliptocytosis

A

Osmotic fragility

280
Q

What test is specific for PNH?

A

Sucrose hemolysis (screening)

and

Ham Test (confirmation)

281
Q

What is hemoglobin A comprised of?

A

2 Alpha chains and 2 Beta chains

282
Q

Percentage of adult hemoglobin that is Hgb A

A

95%

283
Q

What is Hemoglobin A2 comprised of?

A

2 Alpha chains and 2 Delta chains

284
Q

Percentage of hemoglobin that is A2

A

~3%

285
Q

What is hemoglobin F comprised of?

A

2 Alpha chains and 2 Gamma chains

286
Q

Percentage of hemoglobin that if F

A

~1%

287
Q

A chronic hemolytic anemia resulting from an inherited alteration of the globin chain.

Valine is substituted for glutamic acid on the sixth position of the Beta chain

A

Sickle Cell anemia

288
Q

Why do the red cells form sickle shapes in sickle cell anemia?

A

Valine is insoluble and hydrophobic
-so when the red cell is deoxygenated, polymerization occurs causing the hemoglobin molecules to combine and “flatten”

289
Q
  • Autosomal recessive
  • 7-8% of African Americans have the trait
  • .25% of African Americans have homozygous disease
  • Disease is found in Africa, Middle East, and USA
  • Associated with malaria
A

Sickle Cell Anemia

290
Q

Screening tool for Hemoglobin S

A

Solubility test

291
Q

A turbid result of the solubility test is _____ for hgb S

A

Positive

292
Q

What can cause a false negative on a sickle solubility test?

A
  • Increased levels of hgb F
  • If the patient is very anemic (<7.0 g/dL hgb)–add 50ul of blood to the reducing agent–
293
Q

False positive sickle solubility

A
  • Too much sample
  • Hyperlipidemia
294
Q

Order of movement for hemoglobin on cellulose acetate agar

(from cathode to anode)

A
  • (cathode)

origin

Hgb C

Hgb S

Hgb F

Hgb A

+ (anode)

295
Q

What is the pH of cellulose acetate agar?

A

8.4 pH

296
Q

pH of citrate agar

A

6.0-6.2 pH

297
Q

What is citrate agar used for in hemoglobin electrophoresis?

A

To verify Hgb S or C from other variants

298
Q

Mild chronic hemolytic anemia with splenomegaly resulting from glutamic acid being substituted by lysine on the sixth position of the Beta chain. Found in 2-3% of African Americans

A

Hemoglobin C

299
Q

What are the arrows pointing at?

A

Hemoglobin S - Sickle cells

300
Q

What is the arrow pointing to in the picture?

A

Hemoglobin C crystals

301
Q

What are the arrows pointing to?

A

Hemoglobin SC

302
Q

This hemoglobin variant causes a splice site, causing transcription of mRNA which results is both qualitative and quantitative defects. A mild chronic hemoltic anemia forms as a result.

A

Hemoglobin E

303
Q

A beta chain variant (a2B2)26Glu->Lys causes this hemoglobin variant which is commonly found in Southeast Asian descent

A

Hemoglobin E

304
Q

This is the most common single gene disorder in humans

A

Thalassemia

305
Q

Due to a reduced rate of a globin chain

A

Thalassemia

306
Q

What is the term used to describe the area in which thalassemia is most often found

A

“Thalassemia belt”

307
Q

Having a thalassemia minor means you’re ____________

(heterozygous/homozygous)

A

Heterozygous

308
Q

Thalassemia major is _______

(homozygous/heterogous)

A

Homozygous

309
Q

Genetic disorder resulting in abnormal amount or function of mRNA, producing reduced or absent beta globin chains

A

Beta thalassemia

310
Q

Found in people from Mediterranean region, Saudi Arabia, Southeast Asia, and Africa

A

Beta thalassemia

311
Q

Heterzygous state of beta thalassemia with no hematologic abnormalities or clinical symptoms

A

Beta thalassemia silent carrier

312
Q

Heterzygous state of beta thalassemia with mild hemolytic anemia, microcytic/hypochromic RBCs, no clinical symptoms

A

Beta thalassemia minor

313
Q

Homozygous state of beta thalassemia with severe hemolytic anemia, microcytic/hypochromic RBCs, severe clinical symptoms, and transfusion dependent

A

Beta thalassemia major

314
Q

Type of beta thalassemia: Mild to moderate hemolytic anemia, microcytic/hypchromic RBCs, moderate clinical symptoms, transfusion independence

A

Beta thalassemia intermedia

315
Q

This Thalassemia has:

  • No Hgb A
  • Most of the Hgb is Hgb F with increased Hgb A2
  • Hgb value is very low; 3-7 g/dL
  • Marked expansion of marrow spaces due to ineffective erythropoiesis
  • Extreme skeletal changes
  • Marked aniso, poik, mciro, and hypo
  • Target cells, NRBCs, and basophilic stippling are seen on peripheral blood smear
A

Beta Thalassemia Major

aka

Homozygous Beta Thalassemia

316
Q

What thalassemia is depicted in these pictures?

A

Beta Thalassemia Major

(Homozygous Beta Thalassemia)

317
Q

What is the treatment for Beta thalassmeia major?

A
  • Blood transfusions throughout lifetime
  • Hematopoietic stem cell transplant
  • Possible gene therapy
318
Q

This beta thalassemia causes a mild microcytic, hypochromic anemia with target cells and basophilic stippling. Patients have few symptoms except during pregnancy.

-May resemble IDA

A

Beta thalassemia trait/minor

319
Q

Which thalassemia is depicted in the picture?

A

Beta thalassemia trait/minor

320
Q

What chromosome contains the genes that control beta, gamma, and delta chains?

A

Chromosome 11

321
Q

What chromosome comtains the genes that control alpha chains?

A

Chromosome 16

322
Q

Number of genes on chromosome 11 that control beta, gamma, and delta chains

A

2

323
Q

Number of genes on chromosome 16 that control alpha chains

A

4

324
Q

Alpha Thalassemia:

What number of gene deletions has no clinical symptoms, normal hematology values, and affects 30% of all African Americans?

A

1 gene deletion

325
Q

Alpha Thalassemia:

What number of gene deletions has no clinical symptoms, creates a slight hypo, micro anemia, and affects Asians?

A

2 gene deletions cis

326
Q

This alpha thalassemia is a 2 gene deletion in which the deletions are on the same chromosome

A

2 gene deletion cis

327
Q

Alpha Thalassemia:

What number of gene deletions has no clinical symptoms, creates a slight hypo/micro anemia, and affects mostly Blacks?

A

2 gene deletion trans

328
Q

This alpha thalassemia is a 2 gene deletion in which the deletions are on opposite chromosomes

A

2 gene deletion alpha thalassemia trans

329
Q

Alpha Thalassemia:

This number of gene deletions causes:

  • Severe hemolytic anemia
  • Is name Hgb H disease, causes patients to have mostly Hgb H (tetramer of beta chains)
  • Is observed in Asians
A

3 gene deletions

330
Q

Alpha Thalassemia:

This number of gene deletions causes:

  • Hydrops Fetalis
  • Always fatal
  • No Hgb A, A2, or F
  • All Hgb is Bart’s Hgb (tetramer of gamma chains)
  • Observed in Asian descent
A

4 gene deletion

331
Q

With this disorder, there is no switch from fetal hgb to adult hgb. Beta chains are not produced. Homozygous individuals have 100% Hgb F. Carriers have 15-35% Hgb F.

A

Hereditary Persistence of Fetal Hemoglobin

HPFH

332
Q

This test is used to visualize Hgb F in peripheral smears

A

Kleihauer Betke Test

333
Q

In the Kleihauer Betke test, how will RBCs containing adult hemoglobin appear?

A

as “ghost” RBCs

334
Q

Constant Spring, M Hemoglobin, Hemoglobin Lepore, Hgb Hammersmith, and Hgb Gun Hill are all examples of what?

A

Abnormal hemoglobins

335
Q

Increased or Decreased:

This oxygen affinity is ovserved in erythrocytosis (such as PV) because hemoglobin does not released O2 to the tissues.
-Causes erythropoietin to be activated due to decreased oxygen tension in the blood

A

Increased oxygen affinity

336
Q

Increased or Decreased:

This oxygen affinity is due to more oxygen being released to the tissue so erythropoietin is not activated causing a slight anemia.

A

Decreased oxygen affinity

337
Q

Hgb Kempsey is an example of _________ oxygen affinity causing a left shift in the oxygen dissociation curve.

A

Increased

338
Q

Hgb Kansas is an example of ________ oxygen affinity causing a right shift in the oxygen dissociation curve.

A

Decreased

339
Q

What is caused due to an abnormality in the globin chains in the hemoglobin molecule?

A

Hemoglobinopathies

340
Q

How do we identify hemoglobinopathies?

A

Hemoglobin electrophoresis

341
Q

How do you calculate the relative reticulocyte count?

A
342
Q

Normal range for relative retic count

A

0.5 - 2.5%

343
Q

How do you calculate the absolute reticulocyte count?

A
344
Q

Normal range for absolute retic count

A

20,000 - 115,000/uL

345
Q

How do you calculate the corrected retic count to adjust for anemia?

A
346
Q

Patients with a hematocrit of 35% should have what corrected retic value?

A

2-3%

347
Q

Patients with a hematocrit < 25% should have what corrected retic value?

A

3-5%

348
Q

This calculation adjusts for prolonged peripheral maturation time for reticulocytes

A

Reticulocyte production index (RPI)

349
Q

What are the calculations for the reticulocyte production index?

A
350
Q

What RPI value indicates adequate bone marrow response?

A

RPI > 3

351
Q

What RPI value indicates inadequate erythropoietic response?

A

RPI < 2

352
Q

Fat to cell ration seen with aplastic bone marrow

A

90: 10
- normal = 50:50

353
Q

Most anemias will have what type of cell hyperplasia in the bone marrow?

A

Erythroid hyperplasia

(RBCs)

354
Q

What would you expect to see in a bone marrow smear for possible megaloblastic anemia?

A
  • Asynchrony
  • Hypersegmented neutrophils
  • Giant metamyelocytes and bands
355
Q

What tests will help distinguish the different microcytic anemias?

A

-Hemoglobin electrophoresis to detect:
~Thalassemia, Sickle, Hgb C
~If no Hgb A, disease is homozygous
~Kleihauer Betke stain to detect increased fetal hgb in thalassemia or HPFH

-Ferritin, iron, TIBC to detect IDA

356
Q

Tests used to distingiush normocytic anemias

A
  • Sickle solubility test: cannot distinguish disease from trait
  • Direct antiglobulin test (DAT): for AIHA
  • Osmotic fragility: will diagnose hereditary spherocytosis or elliptocytosis
  • Enzyme deficienes: G6PD deficiency will have Heinz Bodies and a deficient G6PG screen
  • Sucrose hemolysis, Ham test, and Flow cytometry for PNH: lysis positive
  • Haptoglobin, urine hemosiderin, urine urobilinogen: determines intravascular vs extravascular hemolysis
  • Reticulocytes: indicates if hemolysis or hypoproliferative disorder
  • Bilirubin and LD: increased in hemolytic anemia
357
Q

Tests used to distinguish macrocytic anemia

A
  • B12 and folate levels
  • Erythropoietin level increased: intramedullary hemolysis
  • Schilling test: detects Pernicious Anemia
  • Liver enzymes increased in liver disease
  • Bone marrow for myelodysplasia: pre-leukemia
358
Q

Red cell inclusions:

  • DNA
  • Seen in post-splenectomy
  • Megaloblastic anemias and some hemolytic anemias
  • Small single, deep blue, round granule at periphery of cell
A

Howell Jolly Body

359
Q

Red cell inclusions:

  • RNA
  • Associated with decreased RBC survival/hemorrhage, erythroid hyperplastic marrow
  • Polychromasia with Wright’s stain
A

Reticulocyte

360
Q

Red cell inclusions:

  • Iron
  • Seen in sideroblastic anemia and thalassemia
  • Subtle pale dots near periphery of cell
A

Pappenheimer body

361
Q

Red cell inclusions:

  • Precipitated hemoglobin
  • Seen in G6PD deficiency
  • Can only be seen with supravital stain
A

Heinz Body

362
Q

Red cell inclusions:

-Crystallized hemoglobin

A

C crystal

363
Q

Red cell inclusions:

  • Iron
  • Nucleated red blood cell precursor with at least five granules that circle at least 1/3 of the nucleus
A

Ringed sideroblast

364
Q

Red cell inclusions:

  • RNA aggregates
  • Seen in thalassemia (fine) and lead poisoning (coarse)
A

Basophilic stippling

365
Q

Red cell inclusions:

  • DNA
  • Usually a metarubricyte
  • Always abnormal in adult peripheral blood
A

NRBC

366
Q

How do is the automated hematocrit calculated?

A
367
Q

Common cause for Folate deficiency

A

Diet

368
Q

What is increased in hemochromatosis?

A

Iron

369
Q

What anemia is found in mononucleosis?

A

Cold agglutinin (IgM)

370
Q

What globin chains are in Hgb A?

A

2 Alpha

2 Beta

371
Q

What globin chains are in Hgb A2?

A

2 Alpha

2 Delta

372
Q

What chains are in Hgb F?

A

2 Alpha

2 Gamma

373
Q

What chains are in Hgb H?

A

4 Beta

374
Q

What chains are in Bart’s Hemoglobin?

A

4 Gamma

375
Q

Percentage of transferrin bound to iron

A

30%

376
Q

How are intravascular and extravascular hemolysis distinguised?

A

Urine hemosiderin

(increased with intravascular)

377
Q

Tests utilized in the detection of hemolytic anemia

A
  • Bilirubin: increased
  • LD: increased
  • Haptoglobin: decreased
  • Urine hemosiderin: increased
378
Q

What is the reticulocyte value for hemolytic anemias?

A

Increased

379
Q

What is the reticulocyte value for anemias due to nutritional deficiencies?

A

Decreased until the nutritional need is met

380
Q

Which of the anemias are life threatening?

A
  • Alpha Thalassemia major (4 gene deletion)
  • Microangiopathic Anemia (DIC, HUS, TTP)
381
Q

How can Hgb A with Hgb S be confirmed?

A

Hemoglobin electrophoresis using citrate agar

382
Q

How can IDA and anemia of chronic disease be differentiated?

A

Ferritin and TIBC

IDA: Ferritin is decreased and TIBC is increased

Anemia of chronic disease: Ferritin and TIBC are decreased

383
Q

What’s the purpose of the Schilling test?

A

Detects malabsorption of B12 found in Pernicious Anemia

384
Q

What is the breakdown product of hemoglobin?

A

Urobilinogen

385
Q

What are the products of heme synthesis?

A
  • Protoporphyrin
  • Uroporphyrin
  • Coproporphyrin
386
Q

Which thalassemia is more serious?

A

Alpha thalassemia major

387
Q

What microscopic power is used to view bone marrow megakaryocytes?

A

10X, low power

388
Q

What do karyorrhexis and asynchrony indicate?

A

Defective DNA synthesis

389
Q

At what point do normal RBCs lyse in osmotic fragility?

A

~ 0.45 - 0.5% NaCl with complete hemolysis by 0.3%

390
Q

Which anemia type is found in liver disease?

A

Macrocytic

391
Q

Which chemistry tests are elevated in hemolytic anemia?

A

Bilirubin and LD

392
Q

Which group of anemias has the most polychromasia?

A

Hemolytic anemias

393
Q

Ringed sideroblasts on an iron stain indicate what?

A

Sideroblastic anemia

394
Q

Are hyper-segmented neutrophils reported?

A

Yes

395
Q

What is the bone marrow fat to cell ratio in aplastic anemia?

A

90:10

396
Q

If the wrong type of blood is transfused, what type of hemolysis is found?

A

Intravascular

397
Q

Fetal hemoglobin content for newborns

A

60-90%

398
Q

Fetal hemoglobin content for HPFH heterozygous

A

15 - 35%

399
Q

Fetal hemoglobin content for HPFH homozygous

A

100%

400
Q

Fetal hemoglobin content for sickle cell trait

A

Normal, ~1%

401
Q

What is the M:E ratio for erythroid hyperplasia?

A

1:1

402
Q

Calculate the M:E ratio-

-During a bone marrow analysis, 370 myeloid cells are counted, 130 erythroid cells are counted.

A

370 myeloid : 130 erythroid

2.8 : 1

403
Q

What is the normal M:E ratio?

A

3:1

404
Q

What is the M:E ratio in anemia?

A

1:1

405
Q

What percentage of white blood cells are the more mature cells in normal bone marrow?

A

50% of neutrophils are myelocytes, metamyelocytes, bands, and segs

406
Q

What is an advantage of using automated instruments?

A

Increased precision

407
Q

When is basophilic stippling observed?

A
  • Thalassemia
  • Lead poisoning
  • Megaloblastic anemia
  • Sickle Cell anemia