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Heme 2 > Intro to Anemia > Flashcards

Intro to Anemia Flashcards

1
Q

What is anemia?

A

Decreased circulating RBC mass–>

decreased hemoglobin concentration of blood–>

decreaed O2 carrying capacity of blood–>

decreaesd O2 delivery to tissues

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2
Q

Compensatory mechanism in anemia

A
  • Increased red cell production
  • Increased 2,3-DPG
  • Shunting of blood from non-vital to vital areas
  • Increased cardiac output
  • Increased pulmonary function
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3
Q

What causes a right shift or for O2 to offload faster?

A

Decreased pH, increaed H+

increased BPG

increased temp

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4
Q

Weakness, malaise, easy fatigability are dt:

Marrow expansion with potential bony abnormalities dt:

Pallor:

Tachycardia; cardiac ischemia:

Dysnpea on exertion:

A

Tissue hypoxia

Increased RBC production

Shunting of blood

Increased CO

increaed pulmon fnx

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5
Q

• Anemia is not a disease, it is a symptom ofother diseases thus:

A

• All anemias need to be explained

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6
Q

Three functional classes of anemia

A

Functional Classification of Anemia
• Blood Loss
• Decreased Production
• Accelerated Destruction

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7
Q
  • Iron deficiency–early
  • Thalassemia trait
  • (Anemia of chronic disease)*
  • Some hemoglobinopathies

examples of

A

Microcytic , normochormic anemia

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8
Q
  • Iron deficiency
  • Thalassemia trait
  • Sideroblastic anemia
  • (Anemia of chronic disease)*

examples of:

A

Microcytic, hypochromic anemia

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9
Q
A
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10
Q

– B12 and folate deficiency
– Liver disease
– Myelodysplastic syndromes
– Blood loss**
– Hemolysis**
– Some drugs

all cause:

A

MACROcytic anemia

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11
Q

– Anemia of chronic disease
– Anemia of renal failure
– Marrow infiltration
– Aplastic anemia
– Blood loss**
– Hemolysis**

examples of:

A

Normochromic/Normocytic

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12
Q

Key considerations when investigating anemia:

A
  • Clinical history
  • Physical exam
  • Complete blood count (CBC)
  • Reticulocyte count
  • Examination of peripheral blood smear
  • Specific diagnostic tests
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13
Q

– Most important parameter for assessment of O2
-carrying capacity of blood

A

• Hemoglobin concentration (Hb; g/dL or g/L)
– Hemoglobin in lysed sample reacted with proprietaryreagents
– Resulting complexes measured spectraphotometrically

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14
Q

What does Hematocrit (Hct; %) measure?

A

– Packed cell volume (percentage of blood volume
comprised by RBCs)
• Centrifugation (old method)
• Currently calculated as MCV x RBC

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15
Q

Hematocrit is usually ____ hemoglobin–does not add
independent information in vast majority of cases

A

3 times

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16
Q

– Direct measure of # of RBCs per unit volume
– Generally correlates well with Hb and hematocrit,
adds little independent information

A

Red blood cell count (RBC; # x 109/L)

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17
Q

– Measured directly based on either electrical
impedence or light scatter
– Very useful in the differential diagnosis of anemia
(e.g., microcytic, normocytic, and macrocytic anemias)

A

• Mean cellular (corpuscular) volume (MCV; fL)

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18
Q

Pt comes in with Microcytic anemia, what is on your DDx?

A
  • Iron deficiency
  • Thalassemia
  • Anemia of chronic disease
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19
Q

Patient comes in with Macrocytic anemia, what is on your DDx?

A

• Megaloblastic (impaired DNA synthesis)
– B12 and folate deficiency
– Some drugs
– Myelodysplastic syndromes
• Non-megaloblastic (other mechanisms)
– Reticulocytosis
– Liver disease
– Hypothyroidism
– Some drugs

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20
Q

Causes of Megaloblastic anemia

A

type of MACROcytic anemia:

(impaired DNA synthesis)
– B12 and folate deficiency
– Some drugs
– Myelodysplastic syndromes

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21
Q

Causes of non-megaloblastic Macrocytic anemia:

A

– Reticulocytosis
– Liver disease
– Hypothyroidism
– Some drugs

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22
Q

– Measure of average amount of hemoglobin per RBC
– Calculated as Hb/RBC
– High correlation with MCV

A

Mean corpuscular hemoglobin (MCH; pg)

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23
Q

– Measure of “chromicity” of RBCs
– Calculated as Hb/(MCVxRBC)

A
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24
Q

Mean corpuscular hemoglobin concentration (MCHC; g/dL)

A
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25
Q

MCHC is:

–____ in hypochromic anemias
–______ in a few “hyperchromic” states (e.g., hereditary
spherocytosis, hemoglobin CC disease

A

Decreased

Increased

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26
Q

– Measure of variability of red cell volume

Useful for the separation of anisocytotic anemias
(e.g., Fe deficiency) from non-anisocytotic
anemias (e.g., anemia of chronic disease

A

Red cell distribution width (RDW)

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27
Q

Poikilocytosis refers to:

A

reb blood cell shape

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28
Q

Descirbe the abnormal RBC and when we see it in pts

A

Spherocytes
Round, Smaller Diameter, More densely staining, Lack of central palllor

hereditary spherocytosis, autoimmune hemolytic anemia

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29
Q

Describe cell and when we see it:

A

Target cells
Examples: Liver dz, splenectomy,
hemoglobinopathies

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30
Q

Describe cell and when we see it:

A

Elliptocytes (ovalocytes)
Examples: Hereditary elliptocytosis, megaloblastic anemia,

iron deficiency, myelofibrosis

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31
Q

Describe the cell and when we see it:

A

Teardrop cells
Examples: Megaloblastic anemia, myelofibrosis,
extramedullary hematopoiesis

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32
Q

Describe cell and when we see it

A

Fragments (schistocytes)
Examples: TTP, DIC, HUS
malignant hypertension

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33
Q

Describe Cell and when we see it

A

“Bite” cells
Example: Oxidant hemolysis
(e.g., G6PD deficiency)

34
Q
  • Red cell size variability =
  • Average red cell size =
A

(anisocytosis)

(microcytosis, macrocytosis)

35
Q

Hemoglobinization can be normal or too little

(below is normal)

A

(hypochromia,
normochromia)

36
Q

What’s with these weird cells in the PB smear?

A

Polychromasia: presence of reticulocytes = larger cells that look purple, sign of increased reticulocytes

37
Q

What the fudge are those things?

A

Howell-Jolly Bodies (nuclear
fragments)
Examples: Splenectomy,
megaloblastic anemia

38
Q

What are those little nugglets? why are they in there?

A

Pappenheimer bodies (iron
granules)
Examples: Splenectomy, iron
overload

39
Q

It looks like that poor cell has the chicken pox, whaaaaa?

A

Basophilic stippling (coarse)~ defect of hemoglobin synthesis
Examples: Thalassemias,
MDS, lead poisoning

40
Q

What is that? Why? Why is it there, WHY?

A
41
Q

what is it called when RBC stack like coins and why does this occur?

A

Rouleaux
Decreased repulsive forces between RBCs
Examples: Increased serum proteins (Ig,
fibrinogen)

42
Q

Why do RBC clump up in this image?

A

Agglutination
Examples: IgM RBC
antibodies (cold agglutinins) that are xlinking

43
Q

Anemia of Blood Loss–Acute

What happens initially?

When do we see signs of anemia?

A
  • Initially no anemia by CBC parameters despite decrease in blood volume
  • Anemia develops as tissue fluid enters vascular space to restore blood volume, producing dilution of cellular elements
44
Q

In anemia of acute blood loss: Reticulocyte count increases after ____days and peaks after _____

A

2-3

7-10 days

45
Q

Anemia of Blood Loss–Chronic
• No anemia initially because:
• Slight reticulocytosis

A

marrow is able to compensate

46
Q

In anemia of chronic blood loss, what occurs eventually?

A

• Eventual development of iron deficiency with
resultant iron deficiency anemia

47
Q

Sites of RBC production
– Embryo: ____
– Fetus (3 months gestation until birth):
– Shortly after birth through adult life:

A

Yolk sac

Liver

BM

48
Q

How is RBC production regulated in terms of oxygen delivery and EPO?

A

– Decreased oxygen delivery induces the production of
erythropoietin by kidney
– Erythropoietin causes proliferation and differentiation
of committed progenitor cells

(EPO–>CFU-E to inducte Erythroblasts to become RBC)

49
Q

Normoblastic Maturation
• Normoblasts (nucleated RBC precursors) obtain
iron from _______ for hemoglobin
synthesis

A

plasma transferrin

50
Q

Up to _____ produced from each pronormoblast (earliest morphologically recognizable erythroid precursor)

A

16 reticulocytes

**• Roughly equal numbers of reticulocytes and
normoblasts in marrow

51
Q

As we go vrom Stemcell to RBC in the normoblastic maturation, what happens to Hemoglobin and RNA?

A

Hemoglobin INCREASES

RNA DECREAES

*cells shrink and will lose nucleus

52
Q

What is pictured below?

A

pronormoblast (earliest morphologically
recognizable erythroid precursor)

very roud regular nuclei with concentric ring of cytoplasm

***basophilic normoblasts are more basophilc and look simular

53
Q

Admix of RNA and proteins, just note polychromatophilcl and basophilic thing

A

look at picture before

54
Q

Earliest anucleate erythroid form
• Larger than mature RBCs
• Contain residual RNA which gives cytoplasm a
blue tinge on routinely stained blood smears
(polychromasia)

A

Reticulocytes

55
Q

How long to reticulocytes reside in marrow and what do they do there?

A

Stay in marrow for 1 to 2 days synthesizing
hemoglobin before being released into
circulation

56
Q

Reticulocytes:

• Normally circulate for approximately ____before
losing residual ribosomes, mitochondria, and other
organelles to becoming _______
• Normally __% of peripheral erythrocytes

A

one day , mature erythrocytes

1%

57
Q

How can we detect reticulocytes?

• Used as measure of marrow RBC production
– Cleaves anemias broadly into those with decreased red cell
production and those with adequate marrow response to
blood loss or increased RBC destruction

A

Can be detected using RNA stains to obtain a
“reticulocyte count”
– Expressed as % of total RBCs

58
Q

Used as measure of marrow RBC production
– Cleaves anemias broadly into those with decreased red cell
production and those with adequate marrow response to
blood loss or increased RBC destruction

A

Reticulocytes

59
Q

The Reticulocyte Count
• Problem:
• Solution: Corrected reticulocyte percentage
– Retic% x (patient HCT/45)
• Better Solution:

A

Reticulocyte % varies depending on
total RBC count

Absolute reticulocyte count

60
Q

Decreased RBC Production
leads to what 3 problems

A

• Ineffective erythropoieis
• Decreased RBC precursors (marrow failure)
• Anemia of chronic disease (anemia of
inflammation)

61
Q

Decreased red cell production despite increased RBC precursors in marrow
• Characterized by defects in maturation

A

Ineffective Erythropoiesis

62
Q

Three examples of Ineffective erythropoiesis

A

– Iron deficiency (cytoplasmic maturation defect)
– Megaloblastic anemia (nuclear maturation defect)
– Myelodysplastic disorders

63
Q

Features of Ineffecitve Erythropoiesis:

Ineffective Erythropoiesis:
General Features
• Prominent______ abnormalities of erythrocytes due to disordered mutation
•______ of erythroid precursors in marrow
• Decreased_____ count despite increased erythroid mass in marrow

A

morphologic

Dysmaturation

reticulocyte

64
Q

Proliferation Defect characterized by an absolute decrease in the marrow mass of erythroid precursors

A

Decreased RBC precursors

65
Q

Cause of absolute decrease in the marrow
mass of erythroid precursors seen in Decreased RBC Precursors

A

– Decreased erythroid progenitors available for RBC
production or
– Decreased proliferative capacity of numerically adequate
erythroid progenitor

66
Q

– Usually normochromic/normocytic
– Usually little anisopoikilocytosis (compared to maturation
defects/ineffective erythropoiesis)
– Decreased reticulocyte counts

A

General features of Decreased RBC precursors:

67
Q

Decreased RBC Precursors
• Stem cell defects with adequate erythropoietin: 3 causes

A

Red cell aplasia (pure) vs. pan-aplasia (aplastic anemia)
– Congenital
– Acquired

68
Q

Diamond-Blackfan syndrome (pure red cell aplasia)
• Fanconi’s anemia (pan-aplasia)

both examples of:

A

congenital Stem cell defects with adequte erythropoietin

(see decreased RBCs)

69
Q

In Decreased RBC precursors we can see marrow replacement caused by what?

A

– Leukemias/lymphomas
– Metastatic carcinoma
– Fibrosis
– Storage disease

70
Q

Decreased EPO could case decreased RBC precursors, when would we see that?

A

Anemia of renal failure

71
Q
  • Inflammatory block in erythropoiesis
  • Thought to be mediated by IL-1, TNF-alpha, and IFN gamma
  • Probably multiple mechanisms
A

Anemia of Chronic Disease

72
Q

General properties of RBCs

A

• Biconcave disc
– 7.5-8.7 m in diameter
– Average volume of 90 fl
• Special membrane structure which provides
durability, flexibility, and tensile strength
– Can swell to a volume of 150 fl
– Can get through a 2.8 m diameter capillary
– Springs back to original shape after distortion

73
Q

Key in RBC membrane cytoskeleton

A

ankyrin

Beta spectrin

Alpha spectrin

***RBC should be able to do red cell

74
Q

Accelerated RBC Destruction
(Hemolysis)
• Red cells normally circulate for ~120 days
• Increased destruction results in

A

increased marrow production
– 8 times normal in ideal circumstances
• Enough iron
• Enough folate
• Otherwise good health

75
Q

• When rate of destruction exceeds bone marrow’s ability to
compensate,_____ develops
– we see a new steady state at _____

A

anemia

lower hemoglobin level

76
Q

Predominates in most forms of hemolytic anemia
• Final common pathway: Decreased RBC
deformability

A

Extravascular Hemolysis

77
Q

What results from decreased RBC deformability seen in Extravascular hemolysis?

A

– Rigid, non-deformable cells have trouble traversing
narrow slits between splenic cords and sinusoids
– Cells are damaged further with prolonged exposure to
splenic cordal environment
– Damaged cells phagocytized by cordal macrophages

78
Q

What is the fate of Hemoglobin in the Intravascular pathway?

A

Hemoglobin + Haptoglobin –> to the liver

1/2 = 10-30 mins

79
Q

What is the fate of Hemoglobin in the extravascular pathway?

A

taken up by splenic macrophage and combines with lysosome–> get lipid + protein + heme breakdown

80
Q

Heme –> Biliveridin how?

Biliveriden –> Bilirubin how?

A

via Heme oxygenase

Biliveridin Reductase

81
Q

Features of Hemolysis

  • _____ indirect bili from heme metabolism
  • _____ LDH released from destroyed RBCs
  • _____ haptoglobin
A

Increased

Increased

Decreased

82
Q

Features of hemolysis:
• Splenomegaly in ____ cases
• Bony abnormalities in _____ hemolytic
anemias

A

chronic

severe chronic

Heme 2 (14 decks)

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