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Pathophysiology 1 > Anemia > Flashcards

Anemia Flashcards

1
Q

What is the shape of RBCs?

A

Small Biconcave discs

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2
Q

What is in RBCs?

A

Cytoplasm- proteins, hemoglobin, electrolytes

No oraganelles

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3
Q

What are platelets?

A

Thrombocytes (fragments of megakaryoctyes)

Filled with chemicals for clotting rxn

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4
Q

Where do RBCs originate in fetus?

A

Yolk sac, then move to liver/ spleen

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5
Q

Where do RBCs originate in the adult?

A

Bone marrow - reticular tissue

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6
Q

What is hematopoiesis?

A

Blood cell formation

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7
Q

What is erythropoiesis?

A

Hemocytoblast to RBC

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8
Q

What is leukopoiesis?

A

Hemocytoblast to WBC

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9
Q

List the stages of hemocytoblast –> Erythrocyte

A

Hemocytoblast –> Proerythroblast –> Erythroblast –> Normoblast –> Recitulocyte –> Erythroctye

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10
Q

What are the two stages of hematopoiesis?

A 
Mitotic division (proliferation)
Maturation (Differentiation)
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11
Q

In erythropoiesis, where does the production of hemoglobin come from?

A

Ribosomes

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12
Q

What does erythropoiesis involve?

A

Loss of organelles, production of hemoglobin, loss of nucleus (forms reitulocyte)

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13
Q

When does the reticulocyte lose mitochondria and ribosomes?

A

When it leaves the bone marrow and enters blood

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14
Q

What do the mitochondria form the reticulocyte from?

A

Porphyrin ring

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15
Q

What makes up 90% of the dry weight of RBC?

A

Hemoglobin

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16
Q

What is the shape of hemoglobin?

A

Tetramer- 2 pairs of globin chains

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17
Q

What is attached to each globin?

A

Heme

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18
Q

How many O2s can be bound per hemoglobin?

A

4 O2

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19
Q

Where does the oxygen bind in the RBC?

A

Directly to the heme group

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20
Q

Where does CO2 bind on the RBC?

A

Directly to proteins

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21
Q

Each time O2 binds to the Heme group- what happens?

A

Conformational change so it is easier for O2s to hop on

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22
Q

What O2 is the easiest to take off the Heme group?

A

The first O2

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23
Q

If resting, what is the lowest normal O2 saturation your Heme will be at?

A

75% (loss of one O2)

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24
Q

What vitamins are needed for erythropoiesis?

A

Fe, B12, folate B6, riboflavin, pantothenic acid, niacin, ascorbic acid, Vitamin E (these are coenzymes for cellular metabolism)

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25
Q

What is required for vitamin B 12 absorption?

A

Intrinsic factor (why you need stomach- produces this factor so small intestine can absorb Vitamin B 12)

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26
Q

In the absence of vitamins there is no….

A

Erythropoiesis

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27
Q

What other nutrition is needed for erythropoiesis?

A

Proteins, vitamins, minerals

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28
Q

Are O2 and CO2 binding in erythrocytes energy dependent?

A

No

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29
Q

What energy source do RBCs use?

A

Glucose

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30
Q

What does the Rapoport-Leubering pathway form?

A

DPG (or BPG)

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31
Q

What does DPG (or BPG) facilitate in tissues?

A

Oxygen release

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32
Q

What produces 90% of glucose metabolism?

A

Embden-Meyerhof pathway

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33
Q

What produces 10% of glucose metabolism?

A

Hexose-monophasphate shunt

NADPH and GSH to reduce cellular oxidants

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34
Q

What is ATP needed for in erythrocytes

A

High intracellular K, low intracellular Na, low intracellular Ca, reduced hemoglobin, reduced GSH, membrane integrity and deformability

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35
Q

What is erythron?

A

Blood cells and precursors in marrow (describes blood as a single system)

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36
Q

What does EPO do?

A

Drives more cells through erythropoiesis

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37
Q

Where is EPO produced?

A

In the kidneys

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38
Q

Hypoxia can trigger…

A

Erythropoiesis

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39
Q

When is methemoglobin formed?

A

As RBC ages (when iron oxidizes)

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40
Q

What removed aging RBCs?

A

MPS (mononuclear phagocytic system) in liver and spleen

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41
Q

What is globin broken down into?

A

Amino Acid and Fe is recycled

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42
Q

What happens to porphyrin as cell ages?

A

Reduced to bilirubin (to liver) –> pigments that are part of feces

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43
Q

What is jaundice due to?

A

Increased bilirubin in blood (increased RBC destruction)

44
Q

What is saturation?

A

The amount of Hb bound to O2 relative to total Hb

45
Q

What is the percentage of saturation of venous blood?

A

60-80%

46
Q

What is the arterial saturation?

A

95%-100%

47
Q

What is this equation? Co X (CaO2 - Cv)2) X10

and what does it show?

A

Fick equation- shows gas transport acid-base balance

48
Q

The bulk of CO2 is in what form?

A

Bicarbonate

49
Q

Bicarbonate acts as what type of buffer?

A

pH

50
Q

What factors stimulate EPO release?

A

Hb mass (anemia) and decreased SaO2 (hypoxia)

51
Q

What disorder is an actual decrease in RBC number?

A

Absolute anemia

52
Q

What type of anemia has normal total RBC mass but disturbances in regulation of plasma volume?

A

Relative anemia

53
Q

Clinically, what is anemia?

A

Reduced O2 carrying capacity

54
Q

What are compensatory mechanisms of anemia?

A

Increased HR, CO, circulatory rate, preferential organ related blood flow

55
Q

Why is there an increase in DPG as a compensatory mechanisms for anemia?

A

DPG allows O2 to dissociate easier

56
Q

What are 4 types of anemia due to decreased RBC production?

A

Aplastic anemia
Anemia of chronic renal failure
Anemia related to Vitamin B12 or folate deficit
Iron deficit anemia

57
Q

What type of anemia is a stem cell disorder?

A

Aplastic anemia- reduction of hematopoietic tissue

58
Q

What is pancytopenia?

A

Decrease in RBCs, WBcs, and platelets

59
Q

Besides familial causes, what can cause aplastic anemia?

A

Radiation, immunologic injury, mycobacteria, viral infection, pregnancy

60
Q

What type of onset does aplastic anemia have?

A

Insidious

61
Q

The magnitude of what is important for aplastic anemia?

A

Granulocytopenia

62
Q

What type of penia has fever, chills, bacterial infections?

A

Neutropenia

63
Q

What type of penia involves petecia, brusing, nose bleeds?

A

Thrombocytopenia

64
Q

Why is there anemia with chronic renal failure (primarily)

A

Impaired EPO production due to renal endocrine failure

65
Q

What are secondary causes of anemia from chronic renal failure?

A

Hemolysis, bone marrow cell depression, blood loss (all from failure of excretory function)

66
Q

Will WBC and platelet values be abnormal in anemia of chronic renal failure?

A

No- they will be normal

67
Q

What will the RBCs look like in anemia of chronic renal failure?

A

Normal but with spikes on the outside surface

68
Q

How do RBCs look in aplastic anemia?

A

Normal

69
Q

What causes anemia in Vitamin B 12 or Folate deficiency?

A

Disruption of DNA synthesis in blast cells of bone marrow

70
Q

What do Vitamin B12 and Folate contain that is needed for RBC synthesis?

A

Coenzymes for DNA synthesis

71
Q

What is the difference b/w symptoms of pernicious anemia and folate deficiency anemia?

A

Pernicious anemia shows neurologic defects due to lack of Vitamin B12

72
Q

What can cause a folate deficiency?

A

Dietary deficiency, alcoholism, cirrhosis, pregnancy, infancy

73
Q

What type of anemia has RBCs that are smaller and paler than normal (hypochromic, microcytic)?

A

Iron deficiency anemia , thalassemia

74
Q

What are the 4 types of anemia related to inherited disorders of the RBC?

A

Thalassemia
Sickle-cell anemia
hereditary spherocytosis
Glucose-6-phosphate dehydrogenase deficiency

75
Q

What is a result of Thalassemia?

A

Decreased RBC survival

76
Q

What classifies Thalassemia?

A

Chain of aberrant synthesis (alpha or beta)

77
Q

What is the alpha chain deficiency Thalassemia associated with?

A

Asian populations

78
Q

What is the beta chain deficiency of Thalassemia associated with?

A

Mediterranean, Middle east, India, Pakistan populations

79
Q

What type of thalassemia does not allow the child to survive?

A

Thalassemia major

80
Q

What is sickle cell anemia due to?

A

A genetic defect in HB synthesis (val replaces glu in 6th position of B-chain –> sickle cells

81
Q

When do cells sickle in sickle cell anemia?

A

When the person is oxygen stressed

82
Q

What is wrong with RBCs in hereditary spherocytosis?

A

They have defective membrane skeletons, altered membrane properties, and they are spherical which leads to their destruction

83
Q

What type of genetic disorder is hereditary spherocytosis?

A

Autosomal dominant

84
Q

There is an increase amount of what in RBC for individuals with hereditary spherocytosis.

A

Hemoglobin

85
Q

What population is hereditary spherocytosis found in?

A

Northern Europeans

86
Q

What is glucose-6-phosphate dehydrogenase deficiency caused by?

A

Enzyme deficiency –> altered glycolysis (can’t keep Na/K at normal levels)

87
Q

Membrane damage in glucose-6-phosphate dehydrogenase anemia causes what?

A

Early phagocytosis- anemia

88
Q

When does a person discover they have glucose-6-phosphate dehydrogenase anemia?

A

Drug challenge- example- primaquine (anti-malarial)

89
Q

What type of genetic condition is glucose-6-phosphate dehydrogenase anemia?

A

X-linked recessive

90
Q

What populations is glucose-6-phosphate dehydrogenase common in?

A

African Americans and Sephardic Jews

91
Q

What are the three types of anemia related to extrinsic RBC Destruction or Loss?

A

Hemolytic disease of the newborn
Antibody-mediated drug rxns
Acute blood lost

92
Q

What happens in hemolytic disease of the newborn to baby’s RBCs?

A

Destroyed by maternal anitibodies

93
Q

What will baby’s RBCs in hemolytic disease of the newborn have?

A

Nucleated RBCs in peripheral blood (reticulocytosis)

94
Q

What happens with antibody-mediated drug rxns?

A

Drug induced immune hemolytic anemia

95
Q

What are the 4 mechanisms of antibody mediated drug rxn

A

Hapten, neoantigen, membrane modification, autoantibody induction

96
Q

What occurs in hapten mechanisms of antibody-mediated drug rxns?

A

Drug attached to outside of RBC and immune system creates antibodies against that drug (only recognizes drug)

97
Q

What happens in neoantigen formation (antibody-mediated drug rxn)?

A

Drug binds to outside of RBC membrane- combination of drug and RBC produces a new antigen (antibodies attack RBC and drug at the same time)

98
Q

What happens in membrane modification (antibody-mediated drug rxn)?

A

drug alter proteins on RBC and immune system comes in and destroys cell

99
Q

What occurs in autoantibody induction (antibody-mediated drug rxn)?

A

Drug produces autoantibodies directed to RH antigen- triggers destruction of RBCs

100
Q

What drug is involved in autoantibody induction (antibody mediated drug rxn)?

A

Methyldopa

101
Q

Where is there anemia with acute blood loss?

A

Plasma is replaced before hemoglobin

102
Q

What percentage of blood loss leads to death?

A

50%

103
Q

What is polycythemia?

A

Excess of RBCs- increased whole blood viscosity and BV

104
Q

What is a clinical symptom of polycythemia?

A

Hypertension

105
Q

What is polycythemia vera due to?

A

Neoplastic transformation of stem cells in bone marrow; chronic panmyelosis (genetic)

106
Q

What happens with secondary polycythemia?

A

Chronic hypoxia with increased EPO production- due to a primary disease
No WBC or platelet increase

107
Q

What is relative polycythemia due to?

A

Dehydration, endocrine disorder

Pathophysiology 1 (11 decks)

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