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Intro Anemia Flashcards

1
Q

What is anemia? (i.e. what leads to the final physiologic consequence)

A
  1. Decreased circulating red cell mass ⇒
  2. Decreased hemoglobin concentration of blood ⇒
  3. Decreased O2-carrying capacity of blood ⇒
  4. Decreased O2 delivery to tissues (final physiologic consequence)
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2
Q

What are the physiologic compensatory mechanisms for 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 are signs/symptoms of anemia? What mechanisms lead to these?

A
  • Weakness, malaise, easy fatigability ⇒ Tissue hypoxia
  • Marrow expansion with potential bony abnormalities ⇒ Increased red cell production
  • Pallor ⇒ Shunting of blood from non-vital to vital areas
  • Tachycardia; cardiac ischemia in severe cases ⇒ Increased cardiac output
  • Dyspnea on exertion ⇒ Increased pulmonary function
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4
Q

What kind of disease is anemia?

A

Anemia is NOT a disease

  • it is a symptom of other diseases and must be explained!
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5
Q

What is the functional classification of anemia?

A
  • Blood Loss
  • Decreased Production
  • Accelerated Destruction
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6
Q

What are the morphologic categories of anemia?

A
  • microcytic
    • normochromic
    • hypochromic
  • normochromocytic/normocytic
  • macrocytic
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7
Q

What causes microcytic anemias?

A
  1. Normochromic
    • Iron deficiency–early
    • Thalassemia trait
    • (Anemia of chronic disease)*
      • Most commonly normochromic/normocytic
    • Some hemoglobinopathies (e.g., hemoglobin E)
  2. Hypochromic
    • Iron deficiency
    • Thalassemia trait
    • Sideroblastic anemia
    • Anemia of chronic disease*
      • Most commonly normochromic/normocytic
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8
Q

What causes normochromic/normocytic anemias?

A
  1. Anemia of chronic disease
  2. Anemia of renal failure
  3. Marrow infiltration
  4. Aplastic anemia
  5. Blood loss**
    • normocytic or macrocytic, depending on degree of blood loss
  6. Hemolysis**
    • normocytic or macrocytic, depending on degree of blood loss
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9
Q

What causes **macrocytic **anemias?

A
  1. B12 and folate deficiency
  2. Liver disease
  3. Myelodysplastic syndromes
  4. Blood loss**
    • normocytic or macrocytic, depending on degree of blood loss
  5. Hemolysis**
    • normocytic or macrocytic, depending on degree of blood loss
  6. Some drugs
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10
Q

Investigation of anemia:

A
  • Clinical history
  • Physical exam
  • Complete blood count (CBC)
  • Reticulocyte count
  • Examination of peripheral blood smear
  • Specific diagnostic tests (guided by above)
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11
Q

What can be assessed on a peripheral blood smear?

A
  • Red cell shapes (poikilocytosis)
  • Red cell size variability (anisocytosis)
  • Average red cell size (microcytosis, macrocytosis)
  • Hemoglobinization (hypochromia, normochromia)
  • Polychromasia (reticulocytes)
  • Red cell inclusions
  • Red cell arrangement
  • White cell and platelet morphology
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12
Q

What CBC parameters are used to evaluate anemia?

this is a really long card, sorry :/

A
  1. Hemoglobin concentration (Hb; g/dL or g/L)
    • Most important parameter for assessment of O2-carrying capacity of blood
  2. Hematocrit (Hct; %)
    • Packed cell volume (percentage of blood volume comprised by RBCs)
    • Usually 3 times hemoglobin–does not add independent information in vast majority of cases
  3. Red blood cell count (RBC; # x 109/L)
    • Direct measure of # of RBCs per unit volume
    • Generally correlates well with Hb and hematocrit, adds little independent information
  4. Mean cellular (corpuscular) volume (MCV; fL)
    • Very useful in the differential diagnosis of anemia (e.g., microcytic, normocytic, and macrocytic anemias)
  5. Mean corpuscular hemoglobin (MCH; pg)
    • Calculated as Hb/RBC
    • Measure of average amount of hemoglobin per RBC
    • High correlation with MCV
  6. Mean corpuscular hemoglobin concentration (MCHC; g/dL)
    • Measure of “chromicity” of RBCs
    • Calculated as Hb/(MCVxRBC)
    • Decreased in hypochromic anemias
    • Increased in a few “hyperchromic” states (e.g., hereditary spherocytosis, hemoglobin CC disease)
  7. Red cell distribution width (RDW)
    • Measure of variability of red cell volume
    • Coefficient of variation of red cell volumes = svolume/MCV)
    • Useful for the separation of anisocytotic anemias (e.g., Fe deficiency) from non-anisocytotic anemias (e.g., anemia of chronic disease)
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13
Q

What is the differential diagnosis for a microcytic anemia?

A
  1. Iron deficiency
  2. Thalassemia
  3. Anemia of chronic disease
  4. Other (rare)
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14
Q

Macrocytic Anemia: Differential Diagnosis

  • Megaloblastic:
  • Non-megaloblastic:
A
  • Megaloblastic:
    • B12 and folate deficiency
    • Some drugs
    • Myelodysplastic syndromes
  • Non-megaloblastic:
    • Reticulocytosis
    • Liver disease
    • Hypothyroidism
    • Some drugs
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15
Q

What measures ‘‘chromicity” of RBCs?

A

Mean corpuscular hemoglobin concentration (MCHC)

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16
Q

What CBC parameter would be used to differentiate between Fe deficiency anemia (anisocytosis) vs. anemia of chronic disease (non-anisocytosis)?

A

Red cell distribution width (RDW)

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17
Q

What CBC parameter is used to differentiate between microcytic, normocytic and macrocytic anemias?

A

**Mean cellular (corpuscular) volume **(MCV)

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18
Q

Type of cell and associations?

A

Spherocytes

  • Round
  • Smaller Diameter
  • More densely staining
  • Lack of central pallor
  • Associations:
    • hereditary spherocytosis
    • autoimmune hemolytic anemia
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19
Q

Type of cell and associations?

A

Bite cells

  • Oxidant hemolysis (G6PD deficiency)
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20
Q

Type of cell and associations?

A

Target cells

  • liver dz
  • splenectomy
  • hemoglobinopathies
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21
Q

Type of cell and associations?

A

Elliptocytes (ovalocytes)

  • hereditary elliptocytosis
  • megaloblastic anemia
  • iron deficiency
  • myelofibrosis
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22
Q

Type of cell and associations?

A

Schistocytes (fragments)

  • TTP
  • DIC
  • HUS
  • malignant hypertension
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23
Q

Type of cell and associations?

A

Teardrop cells

  • megaloblastic anemia
  • myelofibrosis
  • extramedullary hematopoiesis
24
Q

Type of cell and associations?

A

Sickled cells

  • Sickle cell disease
25
Describe this peripheral blood smear:
**Macrocytosis**
26
Describe this peripheral blood smear:
**Microcytosis**
27
Describe this peripheral blood smear:
**Normochromic**
28
Describe this peripheral blood smear:
**Hypochromic**
29
Describe this peripheral smear: What type of cell is this?
**Polychromasia = Reticulocytes**
30
What is this? What are the associations?
**Howell-Jolly Bodies** (nuclear fragments) * splenectomy * megaloblastic anemia
31
What is this? What are the associations?
**Pappenheimer bodies** (iron granules) * splenectomy * iron overload
32
What is this? What are the associations?
**Basophilic stippling** (coarse) * Thalassemias * MDS * Lead poisoning
33
What is this? What are the associations?
**Hemoglobin C crystals** * Hb CC disease * Hb SC disease
34
What is this pattern? Causes?
**Rouleaux** * _Decreased repulsive forces between RBCs_ * **Examples:** Increased serum proteins (Ig, fibrinogen)
35
What is this pattern?
**Agglutination** * IgM RBC antibodies (cold agglutinins)
36
What can cause anemia?
* Blood Loss * Decreased Production * Accelerated Destruction
37
What are the changes seen in **acute blood loss**?
* **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 * **Reticulocyte count increases after 2-3 days** * peaks after 7-10 days
38
What are the changes seen in **chronic blood loss**?
* **No anemia initially because marrow is able to compensate** * Slight reticulocytosis * **Eventual development of iron deficiency** ⇒ iron deficiency anemia
39
**RBC Production:** * **Sites of Production** * **Regulation of RBC Production**
* **Sites of RBC production** * Embryo ⇒ **Yolk sac** * Fetus (3 months gestation until birth) ⇒ **Liver** * Shortly after birth through adult life ⇒ **Bone Marrow** * **Regulation of RBC production** * **Decreased oxygen delivery** ⇒ **production of erythropoietin** by kidney * **Erythropoietin** ⇒ proliferation and differentiation of committed progenitor cells
40
**Normoblastic Maturation** * What is their function? * How many reticulocytes are produced from 1 pronormoblast? * What is the normal reticulocytes:normoblasts?
* Normoblasts (nucleated RBC precursors) **obtain iron from plasma transferrin** for hemoglobin synthesis * Up to **16 reticulocytes produced from each pronormoblast** * Roughly equal numbers of reticulocytes and normoblasts in marrow
41
* What are reticulocytes? * How do they appear morphologically? * How long are they normally in the marrow?
* **Earliest anucleate erythroid form** * Larger than mature RBCs * **Contain residual RNA** which gives cytoplasm a blue tinge on routinely stained blood smears **(polychromasia)** * **Stay in marrow for 1 to 2 days** **synthesizing hemoglobin** before being released into circulation
42
* How long are reticulocytes normally in the peripheral blood? * What is the normal % of reticulocytes in the peripheral blood?
* **Normally circulate for approximately one day** before losing residual ribosomes, mitochondria, and other organelles to becoming mature erythrocytes * **Normally 1%** of peripheral erythrocytes
43
* What is the reitculocyte count? * Why do we use this? * How can anemias be classified based on the reticulocyte count?
* Can be detected using RNA stains to obtain a “reticulocyte count” * Expressed as **% of total RBCs** * **Used as measure of marrow RBC production** * **Cleaves anemias broadly:** * decreased red cell production * adequate marrow response to blood loss * increased RBC destruction
44
* What are the potential drawbacks of the reticulocyte count? * How is this overcome?
* **Problem:** Reticulocyte % varies depending on total RBC count * **Solution:** Corrected reticulocyte percentage * Retic% x (patient HCT/45) * **Better Solution:** Absolute reticulocyte count
45
What can cause **decreased RBC production**?
* Ineffective erythropoieis * Decreased RBC precursors (marrow failure) * Anemia of chronic disease (anemia of inflammation)
46
* Define **ineffective erythropoeisis****:** * Give examples of ineffective erythropoeisis
* Definition: **Decreased red cell production despite increased RBC precursors in marrow** * Characterized by defects in maturation * **Examples:** * **Iron deficiency** (cytoplasmic maturation defect) * **Megaloblastic anemia** (nuclear maturation defect) * _Myelodysplastic disorders_
47
**Ineffective Erythropoiesis:** General Features
* **Prominent morphologic abnormalities of erythrocytes due to disordered maturation** * **Dysmaturation of erythroid precursors** in marrow * **Decreased reticulocyte count** despite increased erythroid mass in marrow
48
What can cause **decreased RBC precursors**?
* **Proliferation defect** * Characterized by an **absolute decrease in the marrow mass of erythroid precursors:** * Decreased erythroid progenitors available for RBC production **or** * Decreased proliferative capacity of numerically adequate erythroid progenitors
49
**Decreased RBC precursors:** General features
* Usually **normochromic/normocytic** * Usually **little anisopoikilocytosis** (compared to maturation defects/ineffective erythropoiesis) * **Decreased reticulocyte counts**
50
**Decreased RBC precursors:** * What is casued by **stem cell defects with adequate erythropoietin**?
* **Red cell aplasia** (pure) vs. **pan-aplasia** (aplastic anemia) * **Congenital** * Diamond-Blackfan syndrome (pure red cell aplasia) * Fanconi’s anemia (pan-aplasia) * Others * **Acquired** * Idiopathic * Drugs and toxins * Autoimmune * Infections * Paraneoplastic
51
**Other causes of decreased RBC precursors:** * Marrow replacement * Decreased erythropoeitin
* **Marrow replacement** * Leukemias/lymphomas * Metastatic carcinoma * Fibrosis * Storage disease * **Decreased erythropoietin** * Anemia of renal failure
52
What is the RBC structure?
* 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
53
**Accelerated RBC destruction (hemolysis)****:** * How does this affect the bone marrow? * When will anemia develop? * What will cause anemia not to develop?
* Red cells normally circulate for ~120 days * **Increased destruction results in increased marrow production** * _8 times normal in ideal circumstances_ * Enough iron * Enough folate * Otherwise good health * **When rate of destruction exceeds bone marrow’s ability to compensate, anemia develops** * New steady state at lower hemoglobin level * **Can have hemolysis without anemia if bone marrow is able to compensate**
54
How is hemolysis classified?
* Intravascular * Extravascular * Combination
55
**Extravascular Hemolysis** * What is it? * Describe the final common pathway:
* **Predominates** in most forms of hemolytic anemia * **Final common pathway: Decreased RBC deformability** * 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**
56
Fate of Hemoglobin
57
**Hemolysis:** General Features
* **Reticulocytosis** * **Increased indirect bili** from heme metabolism * **Increased LDH** released from destroyed RBCs * **Decreased haptoglobin** * _Morphologic abnormalities_ of red cells characteristic of specific disorders * _Splenomegaly_ in chronic cases * _Bony abnormalities_ in severe chronic hemolytic anemias

Heme/Lymph (18 decks)

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