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Clin Med hematology > Anemia > Flashcards

Anemia Flashcards

1
Q

What is a CBC

A

Complete blood cell count

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2
Q

What does hemoglobin (Hgb) measure

A

Total amount of hemoglobin in the peripheral blood

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3
Q

What is the job of hemoglobin

A

carry oxygen

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4
Q

What is an immature RBC

A

Reticulocyte

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5
Q

What is Hematocrit (Hct)

A

Measures total blood volume

made up of RBCs

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6
Q

How is Hct expressed with lab results

A

percentage

*can also be called packed cell volume

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7
Q

What values are included with a CBC

A

MCV (mean corpuscular volume)
MCH(Mean corpuscular hemoglobin)
MCHC (mean corpuscular hemoglobin concentration)
RDW( red cell distribution width)

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8
Q

What does the reticulocyte level tell us on labs

A

Bone marrow function

*reticulocytes increase in response to anemia = competent BM

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9
Q

Which cells are acute phase reactants

A

WBC

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10
Q

If there is an elevation in WBC, what is it indicative of

A

Infection
trauma
malignancy
leukemias
tissue necrosis

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11
Q

What is a Diff on lab work helpful with

A

ID underlying cause of leukocytosis

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12
Q

What are neutrophils responsible for

A

nom-nom Spiderman

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13
Q

If there is an increase in neutrophils, what is it indicative of

A

Bacterial infection

“the left shift”

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14
Q

What are examples of lymphocytes

A

T and B cells

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15
Q

What will cause an increased lymphocyte count

A

Immune response, chronic bacterial, viral infection

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16
Q

What oxygen deprivation effects can occur with anemia

A

Fatigue
Dyspnea on exertion
Headache
Dyspnea at rest (more severe)

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17
Q

What symptoms can occur with hypovolemia

A

Lethargy
confusion
Angina
Arrhythmias
MI
CHF

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18
Q

What is the textbook diagnosis of Anemia

A

Low number of circulating RBCs

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19
Q

What is MCV

A

Size of RBC

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20
Q

What is MCH

A

Average Hgb per RBC (color or redness in RBC)

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21
Q

If there is low MCH, what does it indicate

A

Hypochromia (paler RBC)

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22
Q

If someone presents with a B12 or folate deficiency, what will be seen with their blood smear

A

Megaloblastic process

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23
Q

What is another word for fragmented RBCs

A

Schistocytes (helmet cells)

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24
Q

What are abnormally shaped RBCs known as

A

Poikilocytosis

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25
Q

What diseases will you see hypochromia

A

Thalassemia
Iron deficiency
Sideroblastic

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26
Q

What diseases cause Target RBCs

A

Liver disease
Thalassemias

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27
Q

What disease causes Speculated cells

A

Liver disease
Uremia

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28
Q

What are speculated cells

A

Disorganization in cell membrane (spiky)

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29
Q

What are burr cells indicative of

A

uremia

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30
Q

What are acanthocytes indicative of

A

Liver disease

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31
Q

What are Howell-jolly bodies

A

Nuclear remnants

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32
Q

What diseases will cause Howell-jolly bodies

A

Aplenia
Hyposplenia (sickle cell)

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33
Q

What type of stain is Howell-jolly bodies seen on

A

Wright giemsa stain

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34
Q

What are Heinz bodies

A

denatured hemoglobin

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35
Q

What will you see on a smear when there is oxidative injury to the RBC

A

Heinz-bodies

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36
Q

What is basophilic stippling

A

precipitation of ribosomes

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37
Q

What can cause basophilic stippling

A

Lead / heavy metal poisoning
Thalassemias
ETOH abuse

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38
Q

What are the types of microcytic anemia

A

Thalassemias
Iron deficiency
Chronic disease
Sideroblastic

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39
Q

What is one of the most common autosomal recessive conditions in the world

A

Thalassemias

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40
Q

What happens to the RBCs in thalassemia

A

RBC destruction in bone marrow
or
intravascular hemolysis due to damaged red cell membranes

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41
Q

What is hemoglobin Barts

A

Error in the alpha chains early in life causing more gamma chains to form and is not compatible with life

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42
Q

What allows hemoglobin to be exchanged between mom and baby

A

Gamma chains… has a higher affinity for O2

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43
Q

what nationality is Alpha thalassemia most common in

A

African Americans

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44
Q

When is Alpha Thalassemia detected

A

Generally less than 6 months of age

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45
Q

What nationality is beta thalassemia common in

A

African american
AND
Mediteranean

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46
Q

When is beta thalassemia diagnosed

A

Around 6+ months of age

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47
Q

What may occur anatomically in someone who has thalassemia

A

Bone expansion (chipmunk facies)

Due to marrow working harder to make RBCs

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48
Q

How do you get a definitive diagnosis of thalassemia

A

Hemoglobin analysis
-electrophoresis
-Genotyping
-HPLC

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49
Q

What will be abnormal in labs with someone who has thalassemia

A

Significantly reduced MCV

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50
Q

How can you treat thalassemia

A

Folic Acid
Transfusions
Iron chelation therapy
NO IRON

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51
Q

What is the number 1 cause of anemia world wide

A

iron deficiency

52
Q

What are the main causes of iron deficiency anemia

A

Blood loss (most common)
inadequate dietary intake

53
Q

What are some signs of iron deficient anemia

A

Pica
Brittle nails
Spoon shaped nails
Smooth tongue
Esophageal webs
Cheilosis

54
Q

What is Ferritin

A

Protein cells that store iron

55
Q

What is transferrin

A

Protein that regulates Iron in the blood

56
Q

What is the best test for Iron deficiency anemia diagnosis

A

Low plasma Ferritin <30

57
Q

How often will you take PO iron with iron deficiency anemia

A

3 times a day (start 1x and slowly titrate up)

58
Q

How long should treatment last with iron deficiency anemia

A

minimum of 3 months but typically 6-12 months

59
Q

What in your diet do you need to avoid when taking iron

A

dairy- will prevent iron absorption

60
Q

What is anemia of inflammation

A

Anemia of chronic disease

61
Q

What are some etiologies of anemia of chronic disease

A

Chronic inflammation
Organ failure
Any active malignancy**
impaired marrow function

62
Q

What is the cause of aplastic anemia

A

bone marrow failure

63
Q

What is pancytopenia

A

Anemia plus reduction in all other cell lines

64
Q

What can you give to treat the anemia aspect of anemia of chronic disease

A

erythropoietin (Epo)

65
Q

Where is aplastic anemia most prevalent

A

Asia and middle eastern populations

66
Q

What are some causes of aplastic anemia

A

idiopathic
SLE
Chemo
Radiation
Toxins
Drug induced (chloramphenicol / ASM)
Hereditary

67
Q

How does aplastic anemia typically present

A

Increased incidence of infection
pupura / petechiae
Abnormal bruising

68
Q

What will be seen in a biopsy of aplastic anemia

A

Hypocellular marrow with fatty infiltration

69
Q

What criteria makes aplastic anemia severe

A

ANC<500
Plts <20,000
Reticulocytes <1%
Bone marrow cellularity <20%
*3 of 4 of these

70
Q

If someone has severe aplastic anemia, how do you treat them

A

<40 w/ compatible sibling donor = BMT

> 40 OR <40 with NO sibling donor = immunosuppression

71
Q

What is the prognosis of aplastic anemia

A

20% survive to 1 year without treatment

72
Q

What is Sideroblastic anemia

A

Impaired heme synthesis = iron accumulation

73
Q

What can cause Sideroblastic anemia

A

Myelodysplasia
Chronic alcoholism
Hereditary
Drug induced

Lead poisoning*** –> until proven otherwise

74
Q

What on labs will indicate lead poisoning

A

Basophilic stippling

75
Q

How do you get a definitive diagnosis for sideroblastic anemia

A

Bone marrow eval

76
Q

What causes normocytic anemia

A

Acute blood loss
Bone marrow failure
Chronic disease
Destruction (hemolysis)

77
Q

If a patient >50y/o with unexplained new anemia, what must be ruled out

A

Colon CA

78
Q

What is an intrinsic cause of hemolytic anemia

A

Problem with the RBC

79
Q

What is an extrinsic cause of hemolytic anemia

A

problem is outside of the RBC (often autoimmune)

80
Q

What will be seen on labs with hemolytic anemia

A

Elevated reticulocyte count

Elevated unconjugated bilirubin (leading to jaundice)

81
Q

If you have a positive combs test… what do you have

A

Autoimmune hemolytic anemia

82
Q

What is the most common genetic hemolytic anemia

A

hereditary spherocytosis

83
Q

What happens to RBC in hereditary spherocytosis

A

Shape changes from concave to spherical

84
Q

What is the treatment of choice for hereditary spherocytosis

A

Splenectomy

85
Q

What is G6PD deficiency

A

Hereditary X-linked recessive disorder

86
Q

Why is G6PD deficiency also called Favism

A

Also found in fava beans
*confers some protection from malaria

87
Q

What happens if you have G6PD deficiency

A

Episodic hemolytic anemia

88
Q

What can cause G6PD deficiency

A

Exposure to oxidative drugs (aspirin, quinidine, Dapsone), fava beans or infection

89
Q

When do symptoms start in sickle cell anemia

A

around 6 months

90
Q

How does sickle cell anemia present

A

Vascular occlusion (painful crisis)
*sickle under stress

Delayed growth / puberty

Splenic sequestration (pooling of blood in spleen)

91
Q

What are sickle cell patients at risk for

A

Cholelithiasis
Splenomegaly
Leg ulcers
Retinopathy
Renal infarcts
priapism

92
Q

What are some treatments of sickle cell

A

Pain management
Prevention: Hydroxyurea
Prevention of complications
Possible BMT in kids
Prenatal testing

93
Q

Which hemoglobin is less likely to sickle and why

A

Hgb F because it binds more tightly to oxygen

94
Q

What happens to the RBCs with G6PD deficiency

A

bite cells

95
Q

What are 3 main causes of Vitamin B12 deficiency

A

Pernicious anemia
Dietary insufficiency
Malabsorption

96
Q

What are causes of Macrocytic anemias

A

Pregnancy
Alcohol abuse
Thyroid disease
Reticulocytosis
B12 / folate deficiency
Cirrhosis

97
Q

What are the primary sources for B12

A

Fish
Eggs
Dairy
Red meat
Poultry
Shellfish

98
Q

What is the average age of onset for pernicious anemia

A

70-80 y/o

99
Q

What is the common presentation with B12 deficiency

A

Normal anemia symptoms
Neuro symptoms
Psych symptoms

100
Q

What happens intracellularly with B12 deficiency

A

Cytoplasm continues to grow while DNA / nucleus matures = megaloblastic

101
Q

What will you see in labs for someone with B12 deficiency

A

Low serum B12
Elevated MMA
+/- elevated serum folate

102
Q

How can you treat pernicious anemia

A

IM B12 injections
*B12 and folate supplementation often initiated simultaneously

103
Q

What is the typical cause of a folate deficiency

A

Primarily due to nutritional deficiency

104
Q

Why is folate so important in pregnancy

A

neural tube defects

105
Q

What is required for folate absorption

A

Intrinsic factor

106
Q

How does a folate deficiency differentiate from B12 deficiency

A

No neurologic symptoms

107
Q

What is Myelodysplastic syndrome

A

Group of neoplasms involving hematopoietic cells

108
Q

What is the risk with someone who has myelodysplastic syndromes

A

High risk to transform into Acute myelogenous Leukemia

109
Q

How are Myeloblastic syndromes classified

A

Type and number of cell lines involved

Amount of blasts present

Chromosomal abnormalities

110
Q

What is pathognomonic in myelodysplastic syndromes

A

Pancytopenia

111
Q

What is Polycythemia vera

A

Myeloproliferative disorder
-neoplastic process

112
Q

What population is polycythemia vera seen in

A

Ashkenazi Jewish patients

113
Q

What is the average age of presentation for polycythemia vera

A

60
*median survival 15-20 years

114
Q

What can polycythemia vera progress too

A

CML
AML
Myelofibrosis

115
Q

What is the primary mutation in polycythemia vera

A

JAK2 (diagnostic)

116
Q

What is a secondary cause of polycythemia vera

A

Increased EPO activity

117
Q

What happens to the blood with polycythemia vera

A

Increased volume and viscosity

118
Q

How is polycythemia vera typically found

A

Increased HCT on routine lab exam

119
Q

What some clinical presentations of polycythemia vera

A

Ruddy complexion (plethora)

Redness in extremities

Engorged retinal veins

generalized pruritus after showering***

120
Q

What is the treatment for polycythemia vera in low risk patients

A

Serial phlebotomy

121
Q

What is the treatment for polycythemia vera in high risk patients (majority)

A

Myelosuppression w/ Hydroxyurea

OR

Bisulfran (inhibit JAK2)

122
Q

What qualifies a patient with polycythemia as high risk

A

Age >60

Hx of thrombosis

123
Q

What is hemochromatosis

A

Iron overload

124
Q

When do clinical symptoms generally present with hemochromatosis

A

After age 50

125
Q

What is the most common cause of hemochromatosis

A

inherited gene mutation
(reduced hepcidin levels)

126
Q

How does hemochromatosis generally present

A

Iron deposition
Fatigue
vertigo
Bronze skin
Hepatomegaly

127
Q

How do you treat someone with iron overload / organ injury with hemochromatosis

A

Regular therapeutic phlebotomy

Clin Med hematology (6 decks)

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