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Heme > Anemia > Flashcards

Anemia Flashcards

1
Q

Hb in males with Anemia

A

<13.5 g/dl

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2
Q

Hb in females with Anemia

A

<12.5 g/dl

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3
Q

Microcytic

A

MCV<80

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4
Q

Normocytic

A

80<100

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5
Q

Macrocytic

A

100<MCV

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6
Q

TIBC

A

Total Transferrin in blood

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7
Q

% Saturation

A

% of transferrin that is bound to Fe

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8
Q

Serum Ferritin

A

How much iron present in storage sites

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9
Q

Fe + protoporphyrin =

A

Heme

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10
Q

Fe is absorbed in the

A

Duodenum

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11
Q

enterocytes transport Fe into blood via

A

Ferroportin

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12
Q

What transports iron and delivers it for storage

A

Transferrin

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13
Q

Where is iron stored

A

Liver and bone marrow macrophages

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14
Q

Folate enters the body as

A

Tetrahydrofolate

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15
Q

Folate enters the body and is quickly methylated. In order to participate in the synthesis of DNA precursors it has to lose its methyl group. What takes the methyl group from tetrahydrofolate (folate) to allow it to function

A

Vitamin B12

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16
Q

B12 passes the methyl group (taken from tetrahydrofolate) to what

A

Homocysteine

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17
Q

Methylated homocysteine is

A

Methionine

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18
Q

Folate is absorbed in the

A

Jejunum

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19
Q

How long does it take to develop folate deficiency

A

Only a few months becuase body stores are minimal

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20
Q

Salivary gland enzymes (IE amylase) liberate B12 from animal proteins B12 is then bound to what (also from the salivary gland) and carried through the stomach

A

R-binder

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21
Q

Pancreatic proteases in the duodenum detach B12 from R-binder. B12 binds intrinsic factor (made by stomach parietal cells) in the small bowel, and together, B12 and intrinsic factor are absorbed in the

A

Ileum

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22
Q

How long does it take to develop B12 deficiency

A

Years because of large hepatic stores

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23
Q

What helps distinguish between peripheral destruction of and underproduction of RBCs

A

Reticulocytes (Normal reticulocyte count is 1-2%)

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24
Q

A properly functioning marrow responds to anemia by increasing reticulocytes to

A

> 3%

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25
Q

reticulocyte count is corrected by

A

Multiplying it by Hct/45

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26
Q

A corrected reticulocyte count >3% indicates

A

Functional bone marrow >3% (<3% indicates poor marrow response: underproduction of RBCs)

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27
Q

Most common type of anemia

A

Iron Deficiency Anemia

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28
Q

Iron Deficiency Anemia is micro, normo, or macro-cytic

A

Microcytic (The initial stage of Fe deficiency anemia is normocytic)

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29
Q

4 phases of Iron Deficiency Anemia

A

Phase 1: Storage iron is depleted (Ferritin decreased, TIBC increased), Phase 2: Serum iron is depleted (Serum Fe decreased and % sat decreased), Phase 3: Bone marrow makes fewer but normal-sized RBCs, Phase 4: Microcytic, hypochromic anemia: Bone marrow makes smaller and fewer RBCs

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30
Q

What role could gastrectomy have in iron deficiency anemia

A

Acidity of stomach maintains Fe in the more bioavailable Fe2+ state

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31
Q

Clinical Features: Koilonychia (spoon shaped nails), Pica (psychological drive to eat or chew on dirt or other abnormal things)

A

Iron Deficiency Anemia

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32
Q

Lab Findings: Microcytic (MCV

A

Iron Deficiency Anemia

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33
Q

Anemia of Chronic Disease is micro, normo, or macro-cytic

A

Begins as a normocytic anemia and becomes microcytic as it becomes more severe

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34
Q

Most common type of anemia in hospitalized patients

A

Anemia of Chronic Disease

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35
Q

What is Anemia of Chronic Disease

A

There is enough iron but iron cannot be used because the patient has a chronic inflammatory disease and iron is being sequestered into storage sites by hepicidin. This prevents transfer of Fe from bone marrow macrophages to erythroid precursors. Hepcidin also suppresses erythropoeitin production

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36
Q

Lab Findings: increased ferritin, decreased TIBC, decreased serum Fe, decreased % saturation, and increased FEP

A

Anemia of Chronic Disease

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37
Q

Treatment: Anemia of Chronic Disease

A

Treat inflammation to reduce production of hepcidin. Exogenous erythropoietin is useful in a subset of patients, especially those with cancer

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38
Q

What is Sideroblastic Anemia

A

decreased production of protoporphyrin = low heme = low Hb = microcytic anemia

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39
Q

Protoporphyrin is synthesized via a series of reactions: Methylmalonic acid gets converted to succinyl CoA by

A

B12

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40
Q

Protoporphyrin is synthesized via a series of reactions: What is the rate limiting step.

A

Aminolevulinic acid synthetase (ALAS) converts succinyl CoA to aminolevulinic acid (ALA) using vitamin B6 as a cofactor (rate-limiting step).

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41
Q

Protoporphyrin is synthesized via a series of reactions: Aminolevulinic acid dehydrogenase (ALAD) converts what to what

A

aminolevulinic acid (ALA) to porphobilinogen

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42
Q

Additional reactions convert porphobilinogen to protoporphyrin. What attaches protoporphyrin to Fe to make heme [and where does this final reaction occur]

A

Ferrochelatase (this final reaction occurs in the mitochondria)

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43
Q

Congenital defect of what gene most commonly causes Sideroblastic Anemia

A

Aminolevulinic acid synthetase (ALAS): Enzyme catalyzing the rate limiting step of protoporphyrin synthesis

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44
Q

What can denature ALAD and ferrochelatase, leading to Sideroblastic Anemia

A

Lead poisoning

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45
Q

What is required as a cofactor to ALAS (rate limiting step)

A

B6

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46
Q

Both alcoholism and Isoniazid can cause what kind of anemia

A

Sideroblastic Anemia

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47
Q

Iron-laden mitochondria form a ring around the nucleus of erythroid precursors in which anemia

A

Sideroblastic Anemia (they are known as Ringed sideroblasts)

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48
Q

Lab Findings: Prussian blue stain shows ringed sideroblasts. increased ferritin, decreased TIBC, increased serum Fe, increased % saturation

A

Sideroblastic Anemia

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49
Q

decreased SYNTHESIS of the globin chain of Hb = decreased Hb = microcytic anemia. This occurs in

A

Thalassemia

50
Q

Alpha-Thalassemia is Usually due to gene deletion of two or more of the 4 alpha alleles (one knockout is asymptomatic) that are present on what chromosome

A

16

51
Q

Cis deletion Alpha-Thalassemia is more common where and is it a better or worse prognosis

A

Asia and is worse for offspring becuase child could recieve the completely knocked out chromosome

52
Q

Trans deletion Alpha-Thalassemia is more common where and is it a better or worse prognosis

A

Africa and is better for offspring

53
Q

Clinical features of 2, 3, and 4 gene deletions in Alpha-Thalassemia

A

2 gene deletions present with mild anemia with slightly increased RBC count. 3 gene deletions result in severe anemia where beta chains form tetramers (HbH) that damage RBCs. 4 deletions is lethal in utero (hydrops fetalis: gamma chains form tetramers called Hb Barts that damage RBCs)

54
Q

Two beta genes are present on what chromosome

A

11

55
Q

Beta-Thalassemia Minor (Beta/Beta+)

A

The mildest form that is usually asymptomatic with increased RBC (microcytic and hypochromic ) count

56
Q

Beta-Thalassemia Major (Beta0/Beta0)

A

The most severe form of the disease that presents with severe anemia a few months after birth (HbF at birth is temporarily protective)

57
Q

Ineffective erythropoiesis and extravascular hemolysis as a result of alpha2, alpha2 tetramers damaging RBCs.

A

Beta-Thalassemia

58
Q

Microcytic anemia with massive erythroid hyperplasia. Expansion of hematopoeisis into marrow of skull and facial bones. Extramedulary hematopoiesis with HSM, and risk of aplastic crisis with parvovirus B19. Chronic transfusions are necessary which increases the risk for secondary hemochromatosis

A

Beta-Thalassemia Major

59
Q

Lab Findings: Target cells on blood smear, slightly decreased HbA, increased HbA2 to 5% (normal is 2.5%), and increased HbF to 2% (normal is 1%).

A

Beta/Beta+ (Beta-Thalassemia Minor)

60
Q

Lab Findings: Microcytic, hypochromic target cells and nucleated red blood cells. Electrophoresis will show little or no HbA, increased HbA2, and increased HbF

A

Beta0/Beta0 (Beta-Thalassemia Major)

61
Q

HbF

A

alpha2, gamma2

62
Q

HbA

A

alpha2, beta2

63
Q

HbA2

A

alpha2, delta2

64
Q

HbH

A

beta4 (damages RBCs)

65
Q

Hb Barts

A

gamma4 (damages RBCs)

66
Q

Megaloblastic anemia with hypersegmented neutrophils (>5 lobes), megaloblastic change in all rapidly-dividing cells in the body.

A

Folate Deficiency Anemia(Megaloblastic anemia)

67
Q

Causes: Folate Deficiency Anemia(Megaloblastic anemia)

A

Deficiency in folate inhibits DNA synthesis and can be a result of poor diet, increased demand (pregnancy, cancer, hemolytic anemia), and folate antagonists (methotrexate: inhibits dihydrofolate reductase)

68
Q

Clinical Features: Glossitis (due to decreased turnover of cells of the tongue)

A

Folate Deficiency Anemia(Megaloblastic anemia)

69
Q

Lab Findings: Macrocytic RBCs and hypersegmented neutrophils on blood smear. decreased serum Folate, increased serum homocysteine. Normal methylmalonic acid

A

Folate Deficiency Anemia(Megaloblastic anemia)

70
Q

Most commonly due to autoimmune destruction of parietal cells in the stomach leading to intrinsic factor deficiency (pernicious anemia)

A

B12 Deficiency Anemia (Also can be caused by pancreatic insufficiency, damage to the terminal ileum due to Crohn disease of Diphyllobothrium latum, and dietary deficiency rare, except in vegans)

71
Q

Clinical Features: Glossitis (due to decreased turnover of cells of the tongue), increased risk for thrombosis (due to elevated homocysteine), subacute combined degeneration of the spinal cord (high levels of methylmalonic acid impairs the spinal cord myelinization) leading to poor proprioception and vibratory sensation (posterior column) and spastic paresis (lateral corticospinal tract)

A

B12 Deficiency Anemia

72
Q

Lab Findings: Macrocytic RBCs and hypersegmented neutrophils on blood smear. decreased serum B12, increased homocysteine, and increased methylmalonic acid

A

B12 Deficiency Anemia(methylmalonic acid is increased because it cant be converted to succinyl CoA without B12)

73
Q

Lacks hypersegmented Neutrophils, and is caused by alcoholism, liver disease, or drugs (5-FU)

A

Macrocytic anemia

74
Q

Membrane blebs are formed and lost over time: loss of membrane renders cells round (spherocytes instead of disc-shaped). Spherocytes are less able to maneuver through splenic sinusoids and are consumed by splenic macrophages -> anemia

A

Hereditary Spherocytosis (Normocytic, Extravascular)

75
Q

Causes: Hereditary Spherocytosis (Normocytic, Extravascular)

A

Inherited defect Of RBC cytoskeleton-membrane tethering proteins (most commonly spectrin, ankyrin, or band 3.1)

76
Q

Clinical Features: Normocytic anemia with splenomegaly, jaundice with unconjugated bilirubin, increased risk for bilirubin gallstones (extravascular hemolysis), and increased risk for aplastic crisis with parvovirus B19 infection of erythroid precursors

A

Hereditary Spherocytosis (Sickle Cell Disease is associated with a shrunken fibrotic spleen)

77
Q

Lab Findings: Spherocytes with loss of central pallor, increased RDW and mean corpuscular hemoglobin concentration (MCHC). Diagnosed by osmotic fragility test, which reveals increased spherocyte fragility in hypotonic solution.

A

Hereditary Spherocytosis (Normocytic, Extravascular)

78
Q

Treatment: Hereditary Spherocytosis (Normocytic, Extravascular)

A

Splenectomy; anemia resolves but spherocytes persist and Howell-Jolly bodies (fragments of nuclear material in RBCs) emerge on blood smear

79
Q

Causes: Sickle Cell Anemia (Normocytic, Extravascular)

A

Autosomal recessive mutation in Beta chain of hemoglobin; a single amino acid change replaces normal glutamic acid (hydrophilic) with valine (hydrophobic). Sickle cell disease arises when two abnormal Beta genes are present; results in >90% HbS in RBCs. HbS polymerizes when deoxygenated; polymers aggreagate into needle-like structures, resulting in sickle cells.

80
Q

Aggravating/Alleviating factors of sickling in Sickle Cell Anemia (Normocytic, Extravascular)

A

Increased risk of sickling occurs with hypoxemia, dehydration, and acidosis. HbF protects against sickling

81
Q

The presence of one mutated and one normal Beta chain and results in < 50% HbS in RBCs (HbA is slightly more efficiently produced than HbS).

A

Sickle Cell Trait

82
Q

Metabisulfite screen

A

Causes cells with any amount of HbS to sickle; positive in both sickle cell disease and trait.

83
Q

Lab Findings: 90% HbS, 8% HbF, 2% HbA2, no HbA

A

Sickle Cell Anemia (Normocytic, Extravascular)

84
Q

Lab Findings: 55%HbA, 43% HbS, 2% HbA2

A

Sickle Cell Trait

85
Q

Clinical features: Massive erythroid hyperplasia, Dactylitis, Autosplenectomy, Renal papillary necrosis, extramedullary hematopoiesis with hepatomegaly, increased risk of aplastic crisis with parvovirus B19 infection

A

Sickle Cell Anemia (Normocytic, Extravascular)

86
Q

Autosomal recessive mutation in the Beta chain of hemoglobin. Normal glutamic acid is replaced by lysine.

A

Hemoglobin C Anemia (Normocytic, Extravascular)

87
Q

Acquired defect in myeloid stem cells resulting in absent glycosylphosphatidylinositol (GPI) that renders cells susceptible to destruction by complement

A

Paroxysmal Nocturnal Hemoglobinuria (Normocytic, Intravascular)

88
Q

In Paroxysmal Nocturnal Hemoglobinuria (Normocytic, Intravascular), hemolysis occurs episodically, often at night during sleep becuase

A

Mild respiratory acidosis with shallow breathing during sleep that activates complement

89
Q

Clinical features: RBCs, WBCs, and platelets are lysed. Intravascular hemolysis leads to hemoglobinemia & hemoglobinuria. Hemosiderinuria is seen days after hemolysis.

A

Paroxysmal Nocturnal Hemoglobinuria (Normocytic, Intravascular)

90
Q

What is the main cause of death in Paroxysmal Nocturnal Hemoglobinuria (Normocytic, Intravascular)

A

Thrombosis of the hepatic, portal, or cerebral veins (Destroyed platelets release cytoplasmic contents into circulation, inducing thrombosis)

91
Q

Lab Findings: Sucrose test is used to screen for disease (confirmatory test in the acidified serum test or flow cytometry to detect lack of CD55 (DAF) on blood cells.

A

Paroxysmal Nocturnal Hemoglobinuria (Normocytic, Intravascular)

92
Q

X-Linked recessive disorder resulting in reduced half-life of G6PD renders cells susceptible to oxidative stress

A

Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency (Normocytic, Intravascular)

93
Q

Clinical presentation: Presents with hemoglobinuria and back pain hours after exposure to oxidative stress.

A

Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency (Normocytic, Intravascular)

94
Q

Variant with markedly reduced half-life of G6PD leading to marked intravascular hemolysis with oxidative stress.

A

Mediterranean variant Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency (Normocytic, Intravascular)

95
Q

Mildly reduced half-life of G6PD leading to mild intravascular hemolysis with oxidative stress.

A

African Variant Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency (Normocytic, Intravascular)

96
Q

Decay accelerating factor (DAF) on the surface of blood cells protects against complement-mediated damage by inhibitng

A

C3 convertase

97
Q

DAF is secured to the cell membrane by what

A

glycosylphosphatidylinositol (GPI), an anchoring protein

98
Q

An antioxidant that neutralizes H2O2, but becomes oxidized in the process

A

Glutathione

99
Q

What is needed to regenerate reduced glutathione

A

NADPH (a by-product of G6PD)

100
Q

Antibody-mediated (IgG or IgM) destruction of RBCs.

A

Immune Hemolytic Anemia (Normocytic, Intravascular)

101
Q

Type of hemolysis in Immune Hemolytic Anemia: IgG-mediated disease vs IgM-mediated disease

A

IgG-mediated disease (warm agglutinin) usually involves extravascular hemolysis. IgM-mediated disease (cold agglutinin) usually involves intravascular hemolysis.

102
Q

Most common cause of cold agglutinin hemolytic anemia

A

SLE

103
Q

Warm agglutinin hemolytic anemia is associated with

A

mycoplasma pneumoniae and infectious mononucleosis

104
Q

Anti-IgG is added to patient RBCs; agglutination occurs if RBCs are already coated with antibody. Confirms the presence of antibody-coated RBCs

A

Direct Coombs test

105
Q

Anti-IgG and test RBCs are mixed with the patient serum; agglutination occurs if serum antibodies are present. Confirms the presence of antibodies in patient serum.

A

Indirect Coombs test

106
Q

Occurs with microthrombi (TTP-HUS, DIC, HELLP), prosthetic heart valves, and aortic stenosis. Microthrombi produce schistocytes on blood smear

A

Microangiopathic Hemolytic Anemia (Normocytic, Intravascular)

107
Q

RBCs rupture as a part of the plasmodium life sycle, resulting in intravascular hemolysis and cyclical fever. Spleen also consumes some infected RBCs, results in mild extravascular hemolysis

A

Malaria (Normocytic, Intravascular)

108
Q

Infection of RBCs and liver with plasmodium is transmitted by what

A

Female anopheles misquito.

109
Q

daily fever

A

P Falciparum

110
Q

Fever every other day

A

P Vivax and P Ovale

111
Q

Parvovirus B19

A

Infects progenitor red cells and temporarily halts erythropoiesis, leading to significant anemia in the setting of preexisting marrow stress (IE sickle cell anemia).

112
Q

Treatment: Parvovirus B19 (Underproduction)

A

Treatment is supportive (infection is self-limited)

113
Q

Damage to hematopoietic stem cells, resulting in pancytopenia (anemia, thrombocytopenia, and leukopenia) with low reticulocyte count. Etiologies include drugs or chemicals, viral infections, and autoimmune damage.

A

Aplastic Anemia (Underproduction)

114
Q

Biopsy reveals an empty, fatty marrow

A

Aplastic Anemia (Underproduction)

115
Q

Pathologic process (ie metastatic process) that replaces bone marrow, impairing hematopoiesis, and resulting in pancytopenia

A

Myelophthisic Process (Underproduction)

116
Q

Inheritance of Sickle Cell Disease

A

Autosomal Recessive

117
Q

Inheritance of Hemoglobin C Disease

A

Autosomal Recessive

118
Q

Inheritance of G6P Deficiency

A

X-linked Recessive

119
Q

CD59

A

protectin: binds the membrane attack complex and prevents C9 from binding to the cell

120
Q

CD55

A

Decay-accelerating factor (DAF): disrupts formation of C3 convertase

Heme (7 decks)

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