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Pathology > Red Blood Cells > Flashcards

Red Blood Cells Flashcards

1
Q

Which type of hemaglobin is most common in adults?

A

HgbA is at 97% (two alpha chains and two beta chains)

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2
Q

Which hemaglobins are increased in beta-thalassemia?

A

HgbA2 (otherwise only 1.5-3%)
and
HgbF (50-90% at birth, <1% in adults)

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3
Q

Normal adult hemoglobin levels for men and women?

A

Men: 13
Women: >11.5

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4
Q

Hematocrit

A

Volume of RBCs

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5
Q

Which organs are susceptible to hypoxia?

A
  1. Kidney tubules
  2. myocardium
  3. brain
  4. hepatic cells
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6
Q

Locations of extramedullary hematopoiesis?

A
  1. Liver
  2. Lymph nodes
  3. Spleen

*these sites create RBCs in fetus up until 8 weeks gestation

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7
Q

Pancytopenia

A

Destruction of all stem cells of WBC, RBC, and platelets

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8
Q

Anisocytosis

A

Variation in the size of RBC (ex. microcytic, normocytic, macrocytic)

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9
Q

Poikilocytosis

A

Variation in the shape of RBCs (ex. burr cells, spur cells, sickle cells)

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10
Q

Which two anemias are associated with microcytic cells?

A
  1. Iron deficiency

2. Thalassemia

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11
Q

Which two anemias are associated with macrocytic cells?

A
  1. Vitamin B12 deficiency (cyanobalmin)

2. Folate deficiency

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12
Q

Pathologic classification of anemias are based on what 3 things?

A
  1. Peripheral blood smears
  2. Measurement of Hg content
  3. Chemical analysis of hemoglobin
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13
Q

What are the 3 causes of normocytic anemias (diminished marrow capacity)?

A
  1. Acute blood loss
  2. Myelophthitic
  3. Aplastic
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14
Q

What characterizes the blood smear for acute blood loss?

A

normochromic, normocytic with increased reticulocytes in recovery phase

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15
Q

Myelophthitic anemia: etiology

A

space-occupying lesion that destroys bone marrow productive capacity of all formed elements (pancytopenia)

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16
Q

MC cancer causes of myelopthtic anemia

A
  1. Breast
  2. Lung
  3. Prostate
  4. Thyroid
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17
Q

Myelopthitic blood smear

A
  • moderate to severe normocytic anemia
  • anisopoikilocytosis
  • tear drop cells
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18
Q

What is the most common cause of aplastic anemia

A

idiopathic (2/3)

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19
Q

Name 4 secondary causes of aplastic anemia

A
  1. Cytotoxic drugs (NSAIDS, alkylating chemo, insecticides, arsenicals, anticonvulsants)
  2. Viral infection (CMV, EBV, HIV, Parvo B19, Hep C)
  3. Radiation therapy
  4. Benzene
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20
Q

As marrow regenerates, what changes would you expect to see in the blood?

A

reticulocytes reaching 10-15% after 7 days

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21
Q

What would you expect to see on bone marrow biopsy for aplastic anemia?

A
  • fibroblasts
  • fat cells
  • scattered lymphocytes

-NO hematopoietic stem cells

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22
Q

What is the most common form of anemia?

A

iron-deficiency anemia

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23
Q

What do the RBCs look like in iron-deficiency anemia?

A

hypochromic, microcytic

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24
Q

MC clinical signs of each gender in iron deficiency anemia

A

Female - menstrual blood loss

Male - GI (colon cancer, bleeding hemorrhoids)

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25
Q

Iron-deficiency anemia: histology

A

bone marrow is hyperplastic with small normoblasts with absent Fe staining (Prussian blue stain)

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26
Q

What is the treatment for iron deficiency anemia

A

Ferrous sulfate + vitamin C

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27
Q

What do RBCs look like in thalassemia?

A

hypochromic, microcytic with target cells

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28
Q

What is the etiology of Thalassemia?

A

No abnormal hemoglobin is produced. Problem stems from not enough hemoglobin being made

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29
Q

Thalassemia: Clinical manifestations

A
  • Hemolytic anemia: elevated serum FE and indirect bilirubin
  • Jaundice
  • Splenomegaly
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30
Q

Decreased synthesis of beta chain.

Alpha chains unstable and easily precipitate in erythroid cels, from blasts to mature erythrocytes causing destruction of phagocytes in the bone marrow and causing erythropoiesis

A

Beta thalassemia

31
Q

What would you expect to find in the bone marrow of iron-deficient anemia and Thalassemia

A

erythroid hyperplasia

32
Q

What does normal hemoglobin A contain?

A

4 chains:
2 alpha
2 beta

33
Q

Where are the 2 genes for beta chain synthesis?

A

chromosome 11

34
Q

Where are the 4 genes for alpha chain synthesis?

A

chromosome 16

35
Q

How can the beta chain deletion be partially compensated for in Thalassemia?

A

The gamma chain may combine with the alpha chain resulting in the formation of fetal hemoglobin HgbF

36
Q

Which is more common Beta thal or alpha thal

A

Beta thalassemia

37
Q

Is Thalassemia minor or major more common?

A

Thal-minors are more common than Thal-majors

38
Q

Besides decreased beta chains what else can you see in Beta Thal?

A

increased alpha chains that precipitate in erythroid cells which leads to their destruction by phagocytes in the bone marrow. If they make it to the blood stream they are destroyed by the spleen–> hemolytic anemia

39
Q

What is the consequence of hemolysis of immature erythrocytes?

A
  1. elevated serum Fe

2. elevated indirect bilirubin (unconjugated)

40
Q

Clincal manifestations of Beta Thalassemia Major

A
  1. Marked splenomegaly
  2. Hemochromatosis (due to frequent transfusions - increased hemosiderin and Fe in the phagocytic cells and hepatocytes)
  3. Hyperbilirubinemia–>jaundice
  4. Crew-cut hair on Xray
  5. Retarded growth in children, impaired brain development
41
Q

How is thalassemia major diagnosed?

A

Hemoglobin electrophoresis - decreased (or no) Alpha or Beta chains

42
Q

Where is Vitamin B12-intrinsic factor complex absorbed?

A

Terminal ileum

43
Q

Where are excess B12 and Folic acid stored?

44
Q

Essential cofactors for DNA synthesis and blood cell production

A

Folic Acid and Vitamin B12 (cyanocobalamine)

45
Q

Causes for B12 deficiency

A
  1. Decreased intake
  2. Pernicious Anemia
  3. Gastrectomy
  4. FIsh Tapeworm (Diphyllobothrium latum)
  5. Intestinal lymphoma
46
Q

What WBC changes are associated with megaloblastic anemias?

A

Hypersegmentation of neutrophils (5-7 segments instead of the normal 3-4 lobes)

47
Q

RBC pathology in megaloblastic anemia

A

mature and immature RBCs contain coarse blue inclusions called basophilic stippling (also seen in lead poisoning)

48
Q

What is the most common type of megaloblastic anemia?

A

pernicious anemia

49
Q

Who is most commonly affected by pernicious anemia?

A
  • Older people

- Scandinavians, English, or Irish

50
Q

Why do patients with pernicious anemia have difficulty absorbing B12?

A
  • Antibodies destroy parietal cells in the stomach so not enough intrinsic factor is produced
  • Antibodies to intrinsic factor inactivate it
51
Q

What are the clinical signs of Pernicious anemia

A
  • Lemon yellow skin (due to premature breakdown of erythroblasts
  • Raw, beefy, smooth tongue
52
Q

Neuro features of pernicious anemia

A
  1. CNS lesions in 3/4 of all cases
  2. Loss of myelin in upper thoracic and lower cervical spine (posterior and lateral column)
  3. Loss of vibratory sense and proprioception
  4. Loss of DTRs
  5. Patients can’t walk without looking at their legs
53
Q

Schilling test

A

measuring cobalamine absorption indirectly by administering radioactive cobalamine and measuring excretion in the urine.

54
Q

What will someone with untreated pernicious anemia die of?

A

heart failure

55
Q

Which is more common Folic acid deficiency or Vitamin B12 deficiency?

A

Folic acid

especially in alcoholics, pregnant women and malnourished pts.

56
Q

How does Folic acid deficiency differ with pernicious anemia?

A

Similar, except no neurologic symptoms associated with folic acid deficiency

57
Q

What is the inheritance pattern for Hereditary spherocytosis?

A

Autosomal dominant pattern

-Northern european descent

58
Q

What is the most common hereditary disease of RBCs in whites?

A

Hereditary spherocytosis

59
Q

What is the pathology of hereditary spherocytosis?

A

Deficiency of spectrins, major structural proteins, which cause RBCs to form spheres

60
Q

What is the consequence of spherical RBCs?

A

less deformable with rigid membranes, vulnerable to sequestration and destruction by the spleen

61
Q

Clinical signs of Hereditary spherocytosis

A
  1. Anemia with pallor
  2. splenomegaly
  3. Mild hepatomegaly
  4. Jaundice
62
Q

Hereditary spherocytosis: blood smear

A
  • round, dark red cells with no central pale zone.

- Marked anisocytosis

63
Q

How is hereditary spherocytosis diagnosed?

A

when spherocytes are put in hypotonic solution they will lyse sooner than normal RBCs would

64
Q

Treatment for hereditary spherocytosis

A

splenectomy, at age 5-6

65
Q

Genetic defect in synthesis of beta chain of hemoglobin

A

Sickle cell anemia

66
Q

What substitution is responsible for sickle cell

A

substitution of glutamic acid by valine at the 6th position of the beta chain

67
Q

What is formed by abnormal beta chain combining with alpha chains

68
Q

Dactylitis

A

tops of hands and feet are swollen and painful due to multiple infarcts

69
Q

What are two causes for sickling crisis

A
  1. Fever
  2. Respiratory disease

(other forms of hypoxia since sicklin is accelerated under low oxygen tension)

70
Q

Signs of Sickle cell disease (9)

A
  1. Hair on end Xray
  2. Neuro defects
  3. Visual problems (retinal infarcts)
  4. Bossing of frontal skull**
  5. Hyperbilirubinemia->bile stones (pigment stones)
  6. Cardiac hypertrophy and heart failure
  7. Pulmonary edema -> predisposition to PNA
  8. Fibrous scarring following foci of ischemic necrosis in all organs
  9. Shrunken spleen
71
Q

What is added to RBCs to induce low oxygen tension in a test tube to identify sickle cell

A

sodium metabisulfite

72
Q

What is the most common cause of macroangiopathic hemolytic anemia?

A

RBC trauma due to prosthetic heart valve or synthetic vascular graft

73
Q

What are the classic examples of microangiopathic hemolytic anemia

A
  1. Hemolytic Uremic Syndrome (HUS)
  2. Thrombotic Thrombocytopenic Purpura (TTP)
  3. Disseminated Intravascular Coagulation (DIC)

*all feature generalized thrombosis of smaller capillary vessels

Pathology (15 decks)

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