Pathology of Anemia Flashcards

1
Q

Anemia

  1. Blood Loss - Acute vs. Chronic (examples)
A

Acute: trauma

Chronic: GI disturbance (ulcer, tumor) or Gynecological disturbance

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2
Q

Anemia

  1. Decreased RBC Production (4 reasons)
A
  1. Inherited Genetic Defects
    - Fanconi Anemia (defects in stem cells depletion)
    - Thalassemias (defects in erythroblast maturation)
  2. Nutritional Deficiencies
    - Vitamin B12/Folate (defective DNA synthesis)
    - Iron deficiency (defective Hb synthesis)
  3. Erythropoietin (EPO) Deficiency
    - Renal Failure, Anemia of chronic disease
  4. Immune-mediated Injury to Progenitors
    - Aplastic anemia, pure red cell aplasia
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3
Q

Other Causes of Anemia via Decreased RBC Production

(4 of them)

A
  1. Inflammation-induced iron sequestration (Anemic of chronic disease)
  2. Primary Hematopoietic Neoplasms (Acute Leukemia, Myelodysplasia, Myeloproliferative disorders)
  3. Space-occupying Marrow Lesions (Metastatic neoplasms, Granulomatous disease)
  4. Infection of RBC progenitors (Parvovirus B19 infection)
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4
Q

Anemia

  1. Increased RBC Destruction (Inherited - 3 examples)
A
  1. RBC membrane disorders (Hereditary spherocytosis, hereditary elliptocytosis)
  2. Enzyme deficiencies (HMP shunt - G6PD and glutathione reductase; Glycolytic Enzymes - pyruvate kinase/hexokinase)
  3. Hemoglobin abnormalities (Thalassemia, Hemoglobinopathies, Sickle Cell anemia, Unstable Hb)
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5
Q

Anemia

  1. Increased RBC Destruction (Acquired - 3 types)
A
  1. Deficiency of PIGA
  2. Antibody Mediated

***3. Mechanical Trauma to RBCs

-Microangiopathi Hemolytic Anemia –> Disseminated Intrvascular Coagulation (DIC)

-Chemical Injury –> Lead poisoning (any house before 1978)

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6
Q

What other cell is comparable to the size of a RBC?

A

The nucleus of a lymphocyte

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7
Q

What are the 4 things you look for in a PBS?

A
  1. Normochormic (normal amt of Hb; whtie dot ~1/3 of diameter)
  2. Minimal Poikilocytosis (most are nice and round in shape)
  3. Minimal Anisocytosis (most are pretty much the same size)
  4. Nothing weird going on (e.g. no nucleated RBCs, no infectious orgnaisms within RBCs (e.g. malarial organisms), no iron aggregates, no Howell-Jolly bodies, etc.)
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8
Q
A

Anisocytosis

(Variation in size)

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9
Q
A

Anisocytosis

(Variation in size)

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10
Q
A

Poikilocytosis

(Variation in shape)

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11
Q
A

Poikilocytosis

(Variation in shape)

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12
Q

Hyper- vs. Hypochromic

A
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13
Q
A

Hypochromasia (increased central pallor)

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14
Q

Polychromasia (RBCs with more than one color)

  1. How will a reticulocyte present?
A

Larger, bluish gray (as it is H&E stained and has RNA still, so stains bluish-gray)

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15
Q
A

Polychromasia

(sign of cellular immaturity)

-Polychromatic RBCs are characterized by their large size and bluish hue due to their RNA content

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16
Q

What is Normoblastemia?

What conditions will it be found in?

A
  1. Presence of nucleated RBCs in PBS
  2. Hemolytic Anemias
17
Q
A

Normoblastemia

(Seen in hemolytic anemia)

18
Q

What kind of cell is this, and what disorders can you find it in?

A

Spherocytes

Hereditary Spherocytosis

Autoimmune Hemolytic Anemia

19
Q

What kind of cell is this, and in what disorders will you find it?

A

Schistocyte

Microangiopathic Hemolytic Anemia (DIC, TTP, HUS - Hemolytic Uremic Syndrome)

Other Hemolytic Anemias

20
Q

What does a PBS look like in a patient with lead poisoning?

A

Coarse, basophilic stippling

21
Q

What does this slide show and what causes it?

A

Punctate Basophilia/Basophilic Stippling

Causes:

-Severe anemia, LEAD POISONING, Severe infection, Drug exposure, Alcoholism

22
Q
A

Basophilic Stippling

23
Q

What are these and what do they indicate?

A

Howell-Jolly Bodies (H-J Bodies)

  • Purple nuclear remnants
  • Larger than basophilic stippling

***Indicate absence of spleen/post-splenectomy or hemolysis

24
Q
A

Reticulocyte

25
Q

What is a normal vs. abnormal Retic Count?

A
26
Q

What is hemoglobin composed of?

A

Hb = heme + globin chains

27
Q

Defects in Synthesis of Hb

  1. Defects in Heme Synthesis (3)
A
  1. Iron Deficiency
  2. Anemia of Chronic Disease
  3. Sideroblastic Anemias
28
Q

Defects in Synthesis of Hb

  1. Defects in Synthesis of Globin Chains (a/B)
A

alpha and Beta thalassemias

29
Q
A

Microcytic Anemia

30
Q
A

Microcytic Hemochromic Anemia

(Iron Deficiency Patient)

31
Q

What are the 4 common cause of Macrocytic (MCV > 100 fL) Anemia?

A
  1. Vitamin B12/Folate Deficiency
  2. Alcohol Use
  3. Liver Disease
  4. Reticulocytosis
32
Q

What are 2 uncommon causes of Macrocytic Anemia?

A

Myelodysplastic Syndrome

Hypothyroidism

33
Q

Macrocytic Anemia

  1. Pathogenesis
A

Defective DNA Synthesis (B12/Folate deficiency)

Increased RBC Membrane (From lipid alterations associated with alcohol use)

34
Q

Normocytic Anemia (MCV = 80-100 fL)

  1. Reticulocyte Count < 3%
  2. Reticulocyte Count > 3%
A
  1. Acute blood loss (<7 days), Aplastic Anemia, Anemia of Chronic Disease, Renal Disease, Early Iron Deficiency

2.

Intrinsic RBC Defect –> Membrane Defects, Abnormal Hb, Defective Enzyme

Extrinsic RBC Defect –> Autoimmune hemolytic anemia, PNH, Microangiopathic Hemolytic Anemia

35
Q

What happens if the patient survives an acute blood loss?

A
  • Intravascular shift of water from interstitial fluid compartment
  • Hemodilution - low PCV

Reduced oxygen –> stimulates EPO –> stimulated erythroid hyperplasia –> Reticulocytes appear in peripheral blood after 5 days

36
Q

Acute Blood Loss

  1. Clinical Effects (depends upon…)
A
  • Rate of hemorrhage
  • Whether bleeding is external or internal

External (e.g. peptic ulcer) –> may result in iron deficiency

Internal (e.g. ruptured AAA) –> iron is recaptured