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Anemia Flashcards

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1
Q

Describe the basic shape of RBCs

A

Anucleate biconcave discs

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2
Q

Ratio of RBCs:WBCs in the peripheral blood

A

About 1000:1

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3
Q

What is the first stage of a RBC released from the marrow into peripheral blood? Describe its appearance

A

Reticulocyte

Cytoplasm may be blue-pink due to residual RNA (polychromasia)

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4
Q

What is the normal life span of a RBC?

A

120 days

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5
Q

What is the function of an RBC membrane skeleton?

A

Control biconcave shape and cell deformability

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6
Q

List some basic components of the RBC membrane

A

Phospholipid bilayer with glycolipids and cholesterol

Integral proteins span the bilayer

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7
Q

Describe the basic structure of heme

A

4 pyrrole groups joined into a large ring with a ferrous ion (Fe2+) in the center

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8
Q

Describe the basic structure of globin chains

A

~150 amino acids per chain

Heme binds to a specific region of each chain

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9
Q

Describe the basic structure of hemoglobin. What si the structure of the most common form of adult hemoglobin?

A

Two globin dimers and heme form hemoglobin

Hemoglobin A has 2 alpha and 2 beta globin chains

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10
Q

What organ removes aging RBCs from the circulation? How?

A

Spleen

Monouclear phagocytic engulfment

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11
Q

When hemoglobin is broken down, what are the elements it is broken into and how are they used?

A

Heme is divided into iron (gets recycled) and porphyrin rings (eliminated as bilirubin)

Globin is dismantled into amino acids

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12
Q

Accelerated RBC destruction is known as….

A

Hemolysis

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13
Q

Define anemia

A

Reduced O2 carrying capacity of the blood

Reduction below normal limits of total circulating RBC mass by either reducing volume of packed cells or reducing hemoglobin concentration

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14
Q

What are three general causes of anemia?

A

Blood loss
Hemolysis
Reduced RBC production

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15
Q

Some intrinsic abnormalities of RBCs that may lead to hemolysis are…

A

Membrane disorder
Enzyme deficiency
Hemoglobin synthesis disorder
Acquired disorder

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16
Q

Some extrinsic abnormalities of RBCs that may lead to hemolysis are…

A 
Antibody mediated
Mechanical trauma
Infections
Chemical injury
Sequestration
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17
Q

Microcytic anemia may be seen in what diseases?

A

Iron deficiency
Thalassemias
Anemia of chronic disease

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18
Q

Macrocytic Anemia may be seen in what diseases?

A

Vitamin B12 or Folate deficiency (megaloblastic anemia)

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19
Q

What is the MCV in microcytic anemia? Macrocytic? Normocytic?

A

Normocytic - 80 - 100 fL
Microcytic - below 80 fL
Macrocytic - above 100 fL

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20
Q

List some general pathological characteristics of hemolytic anemias

A

Shortened RBC life span
Accumulation of hemoglobin catabolism products
Compensatory increase in erythropoiesis in marrow

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21
Q

Describe what intravascular hemolysis is and what it may lead to

A

RBCs are destroyed within the vascular compartment

May cause hemoglobinemia, hemoglobinuria, and hemosiderinuria

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22
Q

What should you look for in blood samples of anemic patients to detect potential hemolysis?

A

Haptoglobin

If haptoglobin levels are low, you know there is some kind of hemolysis occuring. Free hemoglobin will form complexes with haptoglobin and be removed by the liver.

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23
Q

Describe what extravascular hemolysis is and what is might lead to

A

RBCs are destroyed primarily by tissue macrophages

May cause splenomegaly

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24
Q

Hereditary Spherocytosis

What is the basic pathological problem?

A

Hereditary (autosomal dominant mostly) problem with intrinsic defect in RBC membrane

Results in spheroid RBCs that are less deformable and more vulnerable to splenic sequestration and destruction

Lower membrane stability and loss of membrane fragments

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25
Hereditary Spherocytosis | Autosomal dominant form is primarily a defect in...
Ankyrin gene Less synthesis of ankyrin leads to less synthesis of spectrin
26
Hereditary Spherocytosis | Autosomal recessive form is primarily a defect in...
alpha-Spectrin gene
27
Hereditary Spherocytosis | What will improve their symptoms?
Spenectomy | Spherocytes will persist, but the anemia will improve
28
Hereditary Spherocytosis | What is seen on the peripheral blood smear?
Spheroidal RBCs that are abnormally small and do not have a central zone of pallor
29
Hereditary Spherocytosis | Clinical Symptoms/Features
Anemia Splenomegaly Jaundice May be asymptomatic in 20-30% of people
30
Hereditary Spherocytosis | How is it diagnosed?
Family history Hematologic findings Increased mean cell hemoglobin conc. Lab evidence of increased osmotic fragility
31
G-6-PD Deficiency | What is the inheritance?
X linked, so mostly males are affected
32
G-6-PD Deficiency | What is the normal function of G-6-PD?
Converts NADP to NADPH, allowing for the conversion of GSSG (oxidized glutathione) to GSH (reduced glutathione)
33
G-6-PD Deficiency | What are the symptoms?
Usually asymptomatic until they have some infection, oxidative stress, exposure to certain drugs or toxins
34
G-6-PD Deficiency | What is the characteristic finding on histology?
Heinz bodies
35
G-6-PD Deficiency | How are Heinz bodies formed?
Due to H2O2 accumulating and oxidizing sulfhydryl groups of globin chains. This denatures the hemoglobin and forms Heinz bodies, which attach to the RBC memrbane and cause damage and decreasing deformability
36
G-6-PD Deficiency | What is a characteristic finding on peripheral blood smear? How are they formed?
Bite cells Formed as the RBCs+Heinz bodies pass through spleen. Macrophages bite the Heinz bodies and lead to loss of membrane and formation of spherocytes
37
What are two problems with hemoglobin synthesis that may lead to hemolytic anemia?
Structually abnormal globin synthesis (sickle cell) Deficient globin synthesis (thalassemia)
38
Sickle Cell Disease | What is the mutation that causes this disorder?
Mutation in 6th position of the beta-globin gene (substitute Val->Glu)
39
Sickle Cell Disease | What is the pathogenesis?
Hemoglobin S molecule is formed, which will aggregate and polymerize RBC becomes distorted into the sickle shape
40
Sickle Cell Disease | What are some factors that may induce sickling in these patients?
More HbS synthesis MHC increase Fall in pH
41
Sickle Cell Disease | What are the two major clinical consequences of this disease?
Chronic hemolytic anemia Occlusion of small blood vessels
42
Sickle Cell Disease | How is the spleen involved in the pathogenesis?
Spleen may play a role in the hemolysis (rigid sickled RBCs may become sequestered there) Over time, hypoxic tissue damage may occur and the spleen may become small and fibrotic ("auto-splenectomy")
43
Sickle Cell Disease | What is is the clinical outcome of occlusion of small blood vessels?
Widespread microvascular obstruction from rigid red cells may result in ischemic damage Intermittent, sudden episodes are called vasoocclusive crises
44
Sickle Cell Disease | How may this be diagnosed?
Ordinary peripheral blood smear can show sickled cells Blood sample may be induced to show sickling Usually diagnosed by hemoglobin electrophoresis
45
Sickle Cell Disease | What group of people is this more commonly seen in?
African Americans
46
Thalassemia | What is the general pathological problem?
Genetic disorder characterized by decreased synthesis of either alpha or beta chains of hemoglobin A. The consequences derive from diminished synthesis of one globin chain leading to low intracellular hemoglobin or excess of the other kind of chain
47
Alpha Thalassemia | Where are the alpha globin chain genes?
There are two alpha genes on chromosome 16.
48
Alpha Thalassemia | 4 degrees of this disease may result. List them
Silent carrier -a/aa Alpha thalassemia trait --/aa or -a/-a HbH disease --/-a Hydrops fetalis --/--
49
Beta Thalassemia | What causes the anemia?
Reduced synthesis of beta-globin, leading to inadequate Hgb A formation Hemolysis is caused by excess alpha chains, which form insoluble aggregates
50
What is the major difference between Thalassemia major and Thalassemia minor?
Major - severe disease with reliance on transfusions Minor - asymptomatic, mild, or absent anemia and some RBC abnormalities
51
Beta Thalassemia Major | What are some clinical observations?
Marrow space expanding into skull (hair on end appearance of the Xray) Hepatosplenomegaly Multiple transfusions necessary
52
Beta Thalassemia Minor | What are the clinical associations?
Minor microcytic hypochromic anemia "Target" cell - central pallor with a dot in the middle RBCs have "bell" shape
53
What is the only acquired defect in the RBC membrane?
PNH | Paraoxysmal Nocturnal Hemoglobinuria
54
PNH | What is the pathogenesis?
Stem cell disorder that results from a mutation in the PIGA gene Leads to a deficiency of GPI anchor and lack of expression of GPI-linked proteins
55
List some important GPI-linked proteins.
CD55 CD59 C8 binding protein
56
PNH | Clinical Findings
Classic intravascular hemolysis Infections and venous thrombosis May occassionally evolve to aplastic anemia or leukemia
57
What are two causes of mechanical RBC hemolysis?
Prosthetic cardiac valves Narrowing of small vessels and fibrin deposition (Microangiopathic hemolytic anemia)
58
List some forms of Microangiopathic hemolytic anemia
TTP HUS DIC
59
How can you confirm Microangiopathic hemolytic anemia with a blood smear?
See schistocytes
60
In anemias from impaired RBC production, what are some general problems that can halt RBC production?
Deficient heme synthesis Deficient DNA synthesis Multiple mechanisms Disordered proliferation and maturation of the stem cells
61
What is the most common cause of iron deficient anemia?
Chronic blood loss, usually in the GI tract
62
Describe the pathogenesis of iron deficient anemia (what happens first, etc)
Stored iron (ferritin) is depleted first, the circulating iron goes low Hemoglobin eventually goes low and the RBCs become microcytic with reduced hemoglobin concentration
63
Symptoms of iron deficient anemia
Nails develop ridges, get spoon shape Tongue may become smooth Intestinal malabsorption Esophageal webs (rare)
64
What would the blood smear of iron deficient anemia look like?
RBCs have a larger central pallor than usual
65
What is the general problem in megaloblastic anemia?
Deficient DNA synthesis from a Vit B12 or Folate deficiency
66
Megaloblastic Anemia | What is seen in the proliferating cells?
Enlarged RBC precursors (megaloblasts) | Enlarged red cells (macrocytes)
67
Megaloblastic Anemia | How does impaired DNA synthesis cause enlargement?
Abnormal cell maturation and division
68
What could potentially cause a B12 deficiency?
``` Intrinsic Factor (IF) deficiency Pancreatitis Gastrectomy Ileal resection Parasites (Fish tapeworm) ```
69
What is pernicious anemia?
Vit B12 deficiency secondary to gastritis with underproduction of IF
70
What is the role of IF in B12 absorption?
Intrinsic Factor (IF) from the stomach needs to bind B12 for its absorption in the distal ileum
71
Why is Vitamin B12 necessary for humans?
Necessary cofactor in methionine synthesis (deficiency of B12 leads to less THF for the reaction) Isomerization of methylmalonyl CoA to succinyl CoA
72
What may be seen on peripheral blood smear in B12 deficiency?
Megaloblastic anemia Leukopenia with hypersegmented granulocytes
73
Describe the problems Megaloblastic Anemia may cause in the CNS
Subacute combined degeneration | -affects sensory and motor tracts
74
What are some symptoms of Megaloblastic Anemia from folate deficiency?
Megaloblastic anemia is identical to B12 deficiency, but there are no CNS symptoms in folate deficiency.
75
Anemia of Chronic Disease You may see high plasma levels of.... What does this compound do?
Hepcidin High levels of hepcidin may block transfer of iron from macrophages to RBC precursors
76
List the pathological consequences of Anemia of Chronic Disease
Microcytic anemia with low serum iron High ferritin Decreased total iron binding capacity Increased bone marrow iron stores
77
Aplastic Anemia | What will you find in the peripheral blood?
"Pancytopenia" Anemia Granulocytopenia Thrombocytopenia
78
Aplastic Anemia | What is the pathologic problem?
Failure or suppression of stem cells leading to a hypocellular marrow May be caused by defect in HSCs, bone marrow stroma, or suppression by T cell mediated immunity
79
Aplastic Anemia | What would you see in the bone marrow?
Hypocellular bone marrow | Increased fat
80
Aplastic Anemia | How should you treat?
Could use HSC transplant, but this is difficult and the morbidity/mortality is high
81
What is the MCH? How is it calculated?
Mean Corpuscular Hemoglobin MCH = (Hemoglobin x 10)/RBC
82
What is the MCHC? How is it calculated?
Mean corpuscular hemoglobin concentration Hemoglobin/Hematocrit = MCHC
83
In hypochromic anemias, how are the MHC and MCHC affected?
Both are decreased in hypochromic anemias (like iron deficiency or thalassemia)
84
Give an example of a hyperchromic anemia. | How are the MCH and MCHC affected?
Hereditary spherocytosis | MCHC will be increased
85
In macrocytic anemias, how is the MCHC affected?
It is normal. | MCH is high (hemoglobin is increased), but the cells themselves are also large.
86
What is RDW a measure of?
Red Cell Distribution | Measure of the variability in RBC size
87
What is anisocytosis?
Variation in RBC size, measured by RDW
88
What is poikocytosis?
Variation in RBC shape

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