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HEMATOLOGY > Anemia > Flashcards

Anemia Flashcards

1
Q

Normal RBC count

A

Females- about 4-5million/ul

Males- 4.3-5.7 million/ul

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2
Q

Hemoglobin females

A

12-16 gm/dl

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3
Q

Hemoglobin males

A

14-17 gm/dl

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4
Q

Anemic female Hgb and Hct

A

Hgb less than 12 gm/dl, Hct less than 37%

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5
Q

Anemic male Hgb and Hct

A

Hgb less than 13.5gm/dl, Hct less than 40%

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6
Q

Hct normal

A

About 45% (3 times the hemoglobin amount)

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7
Q

Mean corpuscular volume - definition

A

average size of RBC- 90 fL +/- 8

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8
Q

Mean corpuscular hemoglobin concentration

A

Amount of hemoglobin in each RBC- should be 33-37 g/dL. Should be 33% of the total cell weight

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9
Q

Reticulocytes in females

A

0.5-2.5%

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10
Q

Reticulocytes in males

A

0.5-1.5%

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11
Q

Platelet count

A

150-400,000/ul

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12
Q

WBC count

A

5,000-10,000/ul

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13
Q

Whole blood components

A

55% plasma, 45% formed elements, buffy coat

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14
Q

plasma components

A

92% water, proteins, and other solutes

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15
Q

Formed elements components

A

rbc, wbc’s, and platelets

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16
Q

WBC components

A

Neutrophils, lymphocytes (T cells, B cells, NK cells), monocytes, eosinophils, basophils

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17
Q

Where does RBC maturation occur in adults and kids?

A

Adults- shifts to vertebra, sternum, and ribs

Children- long bones

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18
Q

Where is the marrow taken from in BMT?

A

Iliac crests

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19
Q

Examples of chronic blood loss causing anemia?

A

GI bleeds, gynecalogic disturbances

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20
Q

Mild microcytic hypochromic anemia defined as…

A

MCV greater than 70 fl

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21
Q

Severe microcytic hypochromic anemia defined as…

A

MCV less than 70 fL

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22
Q

Patient presents with SOB, fatigue, increased heart rate, decreased BP, increased respiration, hypoxia, and admits many cravings for ice and sand. You order CBC- what do you find and what may be the cause?

A

CBC shows low hemoglobin and hematocrit- anemia. MCV is 72 fL, MCHC is below normal. Causes could be iron deficiency anemia (most common, associated with pica), thalassemia, sideroblastic anemia, anemia of chronic disease, lead toxicity

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23
Q

Which disorders are associated with MCV less than 70 fL

A

Microcytic hypochromic anemia caused often by iron deficiency or thalassemia

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24
Q

Difference between causes of macrocytic vs. microcytic

A

Microcytic usually associated with disorders of hemoglobin synthesis.
Macrocytic is associated with disorder with maturation of RBC

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25
Q

Total body iron

A

2-4 grams

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26
Q

How is iron absorbed in body from food?

A

10% from heme sources (red meat), and only 1% from non-heme sources (leafy vegetables, multivitamins)

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27
Q

Why do women tend to have lower iron levels than men?

A

because women lose 2-3mg/day when menstruating

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28
Q

How much iron in 1 ml of packed RBC’s?

A

I mg of iron

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29
Q

Fe2+ vs. Fe3+

A

Fe3+ is ferric, Fe2+ is ferrous. Iron needs to be reduced to ferrous form for it to be absorbed into epithelial cells in GI system

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30
Q

Apoferritin

A

Protein without iron

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31
Q

Lab values to check for if you think person has microcytic hypochromic anemia due to iron deficiency

A

Low ferritin levels (decreased iron stores in body), decreased serum iron, High indirect transferrin level or high total iron binding capacity, and low %age of saturated transferrin

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32
Q

Ferritin normal values

A

20-400 ng/ml

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33
Q

What can cause iron deficiency

A

Bleeding (thrombocytopenia or coag disorders), medications like motrin, NSAIDs, not getting enough in diet, or pregnancy- baby taking iron

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34
Q

Chronic bleeding leading to iron deficiency anemia is….

A

losing 2-4 ml/day

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35
Q

Why is TIBC increased in iron deficiency anemia?

A

Because body thinks liver needs more protein to carry iron, so starts to produce more transferrin, levels increase. But saturation of transferrin goes down because the problem is not that there’s a deficiency of iron-carrying protein, problem is there is not enough iron

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36
Q

Deficiency of of iron in stages

A

Iron stores are depleted first (takes a long time for lab values to get low), iron deficiency erythropoiesis- more RBC’s made because body senses low partial pressure of oxygen, and because of decreased iron have decreased Hg content (Low MCHC) and small RBC’s getting made (low MCV)

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37
Q

Tx of iron deficient microcytic hypochromic anemia

A

Ferrous sulfate PO 325 mg TID. In 2 months, normal levels. (F/U in 1 month- should be halfway to normal). Continue for 3-6 months to replenish iron stores.

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38
Q

If give ferrous sulfate to patient 325 mg TID. During follow up in 1 month, there iron levels are still low. What may be the problem and what is next plan?

A

May have chronic GI disease like chrome’s or diarrhea causing them to lose iron that is given to them (iron absorbed in epithelial cells in GI tract- if GI problem, not retaining the nutrients in body). IV sodium ferric gluconate 1.5-5 gm

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39
Q

What inhibits absorption of iron and what helps?

A

Ascorbic acid, like Vitamin C. Avoid antacids.

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40
Q

What prescription iron medications are well tolerated than iron salts?

A

Carbonyl iron or polysaccharide complex

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41
Q

Systemic manifestations of iron deficient microcytic hypochromic anemia

A

Neuropsychiatric - RLS, pica, plummer vinson syndrome, esophageal webs and strictures, koilonychia, angular stomatitis, glossitis

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42
Q

Cause of sideroblastic anemia

A

Hereditary or acquired deficiency (of Vitamin B6 if acquired) causing hemoglobin synthesis disorder because of failure of heme to get incorporated into porphyrin molecule

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43
Q

How to distinguish whether someone has sideroblastic or iron deficient anemia?

A

Both have low MCV and MCHC. But sideroblastic anemia has increased or normal iron levels, and increased % of transferrin saturated, increased ferritin levels, normal TIBC

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44
Q

Why do thalassemias produce a double whammy?

A

Because you get impaired RBC production, and also increased destruction becaues of defects in globin synthesis- recognized and destroyed by macrophages in spleen

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45
Q

What chromosomes are alpha and beta thalassemias associated with?

A

Alpha- chromosome 16 (4 genes)

Beta- chromosome 11 (2 genes)

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46
Q

Mutations in beta thalassemias

A

Point mutations commonly

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47
Q

What are target cells and basophilic stippling associated with?

A

B-Thalassemia minor

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48
Q

Diagnosis of beta thalassemia minor anemia

A

Microcytic, hypochromic anemia, so decreased Hgb, Hct, MCV, and MCHC. Characteristics- target cells, basophlic stippling, normal or increased reticulocytes. R/O iron deficient anemia and sideroblastic anemia (if don’t see ringed sideroblasts). Enlarged spleen, liver- extramedullary hematopoiesis, erythroid hyperplasia. HEMOCHROMATOSIS, BONE ISSUES

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49
Q

Why do patients with beta thalassemia major need to be transfused?

A

because without transfusion, their hemoglobin is 3-6 gm/dL

50
Q

Do you see manifestations in someone with both beta chains mutated in thalassemi?

A

This person is homozygous, so have beta thalassemia major. Normal at birth because of HbF, which has 2 alpha and 2 gamma chains. Will see manifestations after 6-9 months and require transfusions

51
Q

Hemochromatosis

A

Iron overload occuring in transfusions of more than 100 units of blood, seen in (beta) thalassemias

52
Q

Diagnosis of beta thalassemias

A

Electrophoresis- can look at migration of alpha and beta chains

53
Q

Tx for beta thalassemia minor

A

Screen- genetic testing of common genes, esp if family history or of mediterranean descent

54
Q

Tx for beta thalassemia major

A

Blood transfusions with iron chelation (taking iron out to avoid hemochromatosis), BMT, agents to increase HgF (hydroxyurea)

55
Q

Hydroxyurea

A

agent that increases HbF, and therefore oxygen carrying capacity. Can be prescribed in beta thalassemia major

56
Q

Mutation in alpha thalassemia usually caused by…

A

gene deletion (in contrast to beta thalassemias caused by POINT mutation)

57
Q

alpha thalassemias can cause non-alpha chains to be unpaired resulting in

A

gamma tetramers in newborns, and beta tetramers in children and adults

58
Q

What is HgH disease

A

alpha thalassemia with only 1 normal alpha gene, resulting in beta 4 tetramers

59
Q

In which type of alpha thalassemia would you expect to see high levels of bilirubin and LDH?

A

Hemoglobin H disease- only 1 normal alpha gene, resulting in chronic hemolytic anemia

60
Q

classifications of alpha thalassemias

A

silent carrier, alpha thalassemia trait, hemoglobin H disease, and 0 normal genes in fetus that is stillborn

61
Q

What do you expect the RBC count to be in alpha thalassemia

A

Normal or increased. Even though RBC’s are being destroyed, there is increased hematopoiesis to try and get the count up

62
Q

Diagnosis of alpha thalassemias

A

electrophoresis- will be normal for thalassemia trait or mild anemia, but abnormal in hemoglobin H disease

63
Q

You would expect to see target cells in…

A

alpha and beta thalassemias

64
Q

Tx for alpha thalassemias

A

Transfusions

65
Q

Microcytic hypochromic Anemia of chronic disease most commonly associated with

A

Infections, autoimmune diseases, cancer, and chronic solid organ rejection

66
Q

Patient with viral infection, causing them to be very tired. Have SOB, fatigue, pale conjunctiva, tachycardia. You suspect anemia. What does CBC and bone marrow smear tell you?

A

May possibly be anemia of chronic disease due to viral infection. Have decreased Hgb, Hct, low MCV (or normal), and low MCHC. Bone marrow sluggish due to infection, so low EPO level, low reticulocyte count. WBC count may be elevated if infection, otherwise normal. Platelets normal. Ferritin levels increased, but body not using iron- so decreased TIBC, % transferrin saturated decreased, low serum iron

67
Q

How to treat anemia of chronic disease

A

Treat chronic disease. Give EPO 30,000 units/week to stimulate bone marrow to produce more RBC’s

68
Q

Deficiencies in folic acid and Vitamin B12 can cause….

A

Ineffective megakaryopoiesis- bone marrow not working well resulting in poor production of platelets (thrombocytopenia) and poor production of RBC’s (macrocytic normochromic anemia)

69
Q

What effects does liver disease have in causing macrocytic normochromic anemia?

A

Liver produces cholesterol, so in liver disease cholesterol esterification is defective. So the cell membrane is no longer able to hold its shape, and stretches out more resulting in huge cells (macrocytic)

70
Q

Why do nutiritonal defects in vitamin B12 and folate cause cells to become huge?

A

Because both those nutrients necessary for nuclear development (DNA synthesis). If deficient, nuclear development is slow, and cytoplasmic development becomes huge (asynchrony between nuclear and cytoplasmic development).

71
Q

What kind of synthesis are vitamin b12 and folate required for

A

thymidine synthesis

72
Q

Cellular characteristics in megaloblastic anemia

A

macrocytic normochromic cells, ovalocytes, low reticulocyte count, anisocytosis, pokilocytosis, hypersegmented neutrophils

73
Q

Reticulocyte count in megaloblastic anemia

A

Low because bone marrow not working right, so can’t produce them as much - don’t have necessary ingredients for production

74
Q

What disorder could you expect to see hypersegmented neutrophils in?

A

megaloblastic anemia

75
Q

3 types of antibodies related to pernicious megaloblastic anemia

A

Type I antibody- blocks Vitamin B12 binding to intrinsic factor
Type II antibody- Prevents Intrinsic factor-Vitamin B12 binding to receptor in ileum so no absorption
Type III antibody- antibody to gastric parietal cell, so intrinsic factor cannot be produced because of parietal cell damage

76
Q

How is pernicious megaloblastic anemia caused?

A

Caused due to lack of intrinsic factor, causes included Chronic atrophic gastritis which causes loss of parietal cells, failure of intrinsic factor production, surgery in gastric bypass patients (absoption problems), dietary problems

77
Q

Do you see neurological manifestations in pernicious anemia or folate deficiency anemia?

A

Vitamin B12 only- needed by neurons. Will see demyelination of lateral and posterior columns of spinal cord causing vibration, abnormal proprioception- irreversible process

78
Q

Megaloblastic anemia with numbness, tingling, and decreased proprioception- what do you suspect?

A

Vitamin B12 deficiency, NOT folate deficiency

79
Q

Diagnosis of pernicious megaloblastic anemia

A

Decreased Vitamin B12 levels, elevated methylmalonic acid levels, and Schiling Test

80
Q

What acid levels would be increased in pernicous anemia?

A

Methylmalonic because Vitamin B12 normally converts this into succinyl CoA. If reduced levels, buildup of methylmalonic acid

81
Q

Tx of pernicious megaloblastic anemia

A

Vitamin B12 injections 1000 mcg * 7 days, then once a week, then 1 a month

82
Q

mcg is what

A

micrograms

83
Q

Body store of folic acid and daily requirement

A

5,000 mcg, need 50-100 mcg/day

84
Q

Diagnosis of megaloblastic anemia caused by folic acid deficiency

A

Red cell folate decreased (better indicator than folic acid levels), R/O pernicious anemia- normal VB12 levels and methylmalonic acid levels. Ovalocytes, hypersegmented neutrophils, elevated MCV, anisocytosis, poikiolocytosis

85
Q

Tx for megaloblastic anemia caused by folic acid deficiency

A

Folic acid supplements

86
Q

How is hereditary spherocytosis inherited?

A

75% autosomal dominant

87
Q

Why does hereditary spherocytosis cause increased destruction of RBC’s?

A

Because the RBC’s become spheroidal in shape, causing spleen sequestration and destruction

88
Q

Where is hereditary spherocytosis most commonly found?

A

Northern Europe

89
Q

RBC life span in hereditary spherocytosis

A

10-20 days

90
Q

2 types of crises that hereditary spherocytosis can cause

A

Aplastic crisis- certain infections, like acute parvovirus infection causes shutdown of RBC production
Hemolytic crisis- can occur if person also has mono- enlarged spleen, so now person has even more destruction of RBC’s

91
Q

Diagnosis of HS

A

Low Hgb, Hct, MCV will be decreased, MCHC will be ELEVATED due to cellular dehydration, inc destruciton of RBC’s leading to increased bilirubin (possibly jaundice), reticulocytes possibly, SPHEROCYTES, OSMOTIC FRAGILITY TEST

92
Q

What does osmotic fragility test test and why is it ordered?

A

To see how fragile RBC’s- how likely it is to burst. Can order if suspect HS- defect in membrane cytoskeleton causes it to be less flexible and more fragile

93
Q

Tx in HS

A

Splenectomy will decrease destruction, folic acid (not curative)

94
Q

How is G6PD deficiency inherited?

A

X linked recessive

95
Q

Distinguish between spur cells and burr cells

A

Burr cells or echinocytes: RBC’s with multiple spikes around them as a result of increase in uric acid.
Spur cells or acanthocytes- RBC’s with spiked cell membrane appearance, common in liver disease

96
Q

What does a “dry tap” signify

A

That bone marrow is hypocellular with mostly fat- in aplastic or fanconi anemia

97
Q

What will aplastic or fanconi anemia lab show

A

Pancytopenia, Normal MCV, and normal MCHC.

98
Q

Disease associated with ashkenazi jews

A

hemophilia C

99
Q

Disease endemic in mediterranean basin

A

Thalassemia

100
Q

The 2 most severe forms of G6PD deficiency are seen in…

A

African americans and meditarranean individuals

101
Q

What is protective against oxidants?

A

G6PD

102
Q

What exposures can cause oxidative stress?

A

Drugs (tylenel, sulfonamids), infections, and fava beans

103
Q

Heinz bodies

A

Result when globin chains denature forming precipitates that cause intravascular and extravascular hemolysis (seen in G6PD deficiency)

104
Q

Tx for acute and chronic G6PD deficiency

A

acute- treat irritant, remove stressor

chronic- splenectomy, folic acid

105
Q

Diagnosis of G6PD deficiency

A

Decreased Hgb, Hct, normal MCV and MCHC, increased bilirubin

106
Q

Inheritance of sickle cell disease

A

Autosomal recessive, Point mutation- valine for glutamic acid in beta chain

107
Q

Population most affected by sickle cell trait

A

African americans (10%) and 30% africans because protective against malaria

108
Q

What does low partial pressure of oxygen cause in sickle cell disease?

A

RBC gets deoxygenated, causing HbS molecules to polymerize and herniate through membrane causing efflux of water and leading to sickle cell shape change

109
Q

Effects of sickle cells in circulation and spleen

A

Can get caught up in narrow capillaries because of inflexible shape causing death of tissue (infarction) distal to vessel obstruction in circulation and spleen. In spleen, recognized and lysed leading to enlarged spleen initially, then tiny spleen because of infarction and fibrosis

110
Q

What inhibits polymerization of HbS molecules?

A

HbF inhibits sickling and HbA inhibits polymerization only in people with Sickle cell trait

111
Q

How does hgb content in cell affect sickling?

A

Decreased MCHC increases polymerization of HbS molecules

112
Q

How do acidic conditions affect sickling?

A

Low pH decreases oxygen affinity to hemoglobin, causing desaturation–so sickling more likely to occur

113
Q

Sickling confined to microvascular beds with ___ transit times

A

slow

114
Q

Manifestations of sickle cell anemia

A

Chronic hemolytin anemia causing jaundice, pigmented gallstones, and splenomegaly (eventually splenic infarction and fibrosis) and infarction due to vessel occlusions- pain crisis in kidney, heart, liver, lungs, and GI tract

115
Q

Manifestations of sickle cell anemia in children

A

Bone crisis, sequestration crisis, aplastic crisis if parvovivus B19 infection, impaired growth and developement due to chronic hypoxia, and susceptibility to infection due to altered splenic function

116
Q

Why should you encourage vaccinations of pneumococcus pneumonia and H influenza esp. in kids with sickle cell anemia

A

because spleen has altered function, more susceptible to infection

117
Q

Diagnosis of sickle cell anemia

A

Electrophoresis to identify abnormal beta chain

118
Q

What do target cells represent in sickle cell anemia?

A

dehydration

119
Q

Tx of sickle cell anemia

A

avoid triggers and hydroxyurea 500-750 mg/day which increases HbF levels, inhibits WBC production, and inhibits DNA synthesis

120
Q

Tx in crisis situations in sickle cell anemia

A

Fluids, pain management (morphine)

HEMATOLOGY (5 decks)

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