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Pathology Final > Hematopathology > Flashcards

Hematopathology Flashcards

1
Q

What is hematopoiesis?

A

Production of blood cells and formed elements in blood

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2
Q

Where does hematopoiesis take place during the fetal period?

A

Liver and spleen

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3
Q

Where does hematopoiesis take place during the neonatal period and into adult life?

A

Bone marrow compartment

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4
Q

What is a committed stem cell?

A

Myeloid or erythroid

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5
Q

Where do committed stem cells come from?

A

Multipotent stem cells

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6
Q

What are some different methods to evaluate blood cells and the marrow compartment?

A

1) Peripheral blood collection and smear
2) Bone marrow biopsy, aspirate and smear
3) Flow cytometry

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7
Q

What is anemia?

A

A reduction below normal in the volume of packed red cells, as measured by the hematocrit, or the reduction in the hemoglobin concentration of the blood

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8
Q

What are some causes of macrocytic anemia? And what is it?

A

Macrocytic anemia is an enlargement of RBCs. This is usually due to the lack of B12 or folate. These cells get bigger and bigger to divide but because they are lacking these essential vitamins they cannot divide.

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9
Q

What are some causes of microcytic hypochromic anemia and what is it?

A

These cells are smaller and lack a certain amount of hemoglobin leading to the paler color in the RBC. These cells are usually caused by Fe (iron) deficiency, thalassemia, and ACD.

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10
Q

What is a normal range for iron content for women and men?

A

Women: 2-4 g
Men: 6g

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11
Q

What percentage of iron is found in hemoglobin, myoglobin and iron containing enzymes in the body?

A

80%

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12
Q

What percentage of iron is in storage pools?

A

20%

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13
Q

What are storage pools for iron?

A

Ferritin and hemosiderin

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14
Q

________ is a good indicator of the adequacy of body iron stores.

A

Ferritin

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15
Q

How is iron transported in the plasma?

A

By a protein known as transferrin. Absorbed iron is taken by portal blood to liver and bone marrow

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16
Q

Where is heme usually absorbed?

A

Duodenum

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17
Q

What are some indicators to diagnose iron deficiency anemia?

A

1) Hypochromia, polychromasia, and microcytosis on a peripheral smear
2) Decreased MCV
3) Decreased serum iron
4) Decreased ferritin (cell and plasma)
5) Increased total iron binding capacity (TIBC)

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18
Q

What are some clinical features associated with iron deficiency anemia?

A

1) Koilonychias - abnormally thin, flat nails
2) Cheliosis - inflammation of one or more corners of mouth
3) Glossitis - inflammation with depapillation of the dorsal surface of the tongue; sometimes soreness

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19
Q

What is pernicious anemia?

A

Anemia due to B12 deficiency - causes megaloblastic cells

20
Q

What is another word for B12?

A

Methylcobalamin

21
Q

What does B12 do?

A

Converts homocysteine to methionine and the reaction yields FH4 (tetrahydrofolic acid)

22
Q

How is B12 liberated?

A

From protein by pepsin

23
Q

What does B12 bind to in saliva?

A

R-binder

24
Q

R-B12 is broken down by pancreatic enzymes and is released then binds to ___________________which is produced by parietal cells.

A

Intrinsic factor

25
Q

IF-B12 complex travels to the __________ where receptors for IF are located.

A

ileum

26
Q

The IF-B12 complex is absorbed by mucosa and travels through blood by ______________________.

A

transcobalamin II

27
Q

What is the cause for Chronic Atrophic Gastritis?

A

The gastric mucosa is destroyed by a parietal cell antibody that blocks the B12-IF binding, so B12 can’t be carried to the ileum. This causes inflammation and loss of parietal cells

28
Q

What are some diagnostic features involving megalobastic anemia?

A

1) Leukopenia with hypersegmented granulocytes
2) Thrombocytopenia
3) Neurological changes associated with posterolateral columns
4) Inability to absorb and oral dose of cabalamin
5) Low serum B12

29
Q

If a patient has low serum B12 and is unable to absorb an oral dose of cobalamin, what might the patient have?

A

Megaloblastic anemia

30
Q

Folic acid deficiency is sometimes seen in ______________.

A

Alcoholics

31
Q

T/F - Humans are entirely dependent on dietary sources for folic acid.

A

True

32
Q

How can you tell the difference between pernicious anemia and folic acid deficiency?

A

Pernicious anemia shows neurological symptoms, poor balance, and problems with steriognosis. Folic acid deficiency has NO neurological symptoms.

33
Q

In order to diagnose Pernicious anemia, a ______________ test should be done. Folic acid levels should be tested for folic acid deficiency.

A

Schilling Test

34
Q

What is the major repository for mononuclear phagocytic cells?

A

Spleen - It is the recycling center for RBCs (iron), filtration organ of unwanted elements from the blood, a major secondary organ, reserve pool and storage site, and also a source of lymphoreticular cells.

35
Q

What disease is seen to have premature destruction of RBCs, accumulation of products of hemoglobin catabolism, and compensatory increase in erythropoiesis within bone marrow?

A

Hemolytic anemia

36
Q

_________________ hemolysis causes damage to RBCs be mechanical, immune, or toxic factors.

A

Intravascular

37
Q

_________________ hemolysis occurs whenever red cells are injured, rendered foreign or become less deformable and are sequestered by the spleen for destruction.

A

Extravascular

38
Q

What occurs in G6P dehydrogenase (G6PD) deficiency?

A

G6PD regenerates NADPH, which generates GSH, and H2O2 disposal is dependent on GSH. So, if G6PD is deficient, there is lack of GSH to dispose of the H202. This causes cell injury due to the oxidant free radicals (H2O2). Heinz bodies are seen due to the denatured globin within the cell.

39
Q

What are some key features seen in sickle cell anemia?

A
  • Hereditary
  • Abnormal hemoglobin
  • Beta-globulin gene
  • Substitution of Valine for Glutamic acid at 6th position Beta-globulin chain
40
Q

Sickle cell hemoglobin is also known as _____.

A

HbS

41
Q

What occurs to the RBCs of a patient with sickle cell anemia?

A

HbS molecules aggregate and polymerize upon deoxygenation leading to the formation of HbS fibers and distortion of the RBCs. Repeated episodes of sickling and unsickling, cause permanent damage, leading to irreversible sickled RBCs.

42
Q

Heterozygotes (sickle cell trait) RBCs sickle under conditions of severe __________.

A

Hypoxia

43
Q

Why don’t newborns manifest the sickle cell disease until they are about 5-6 months?

A

Fetal hemoglobin inhibits the polymerization of HbS

The reason that infants don’t show symptoms at birth is because baby or fetal hemoglobin protects the red blood cells from sickling. When the infant is around 4 to 5 months of age, the baby or fetal hemoglobin is replaced by sickle hemoglobin and the cells begin to sickle.

44
Q

What different things can be seen in sickle cell disease?

A
  • Splenomegaly (reticulocyte entrapment within the spleen due to deformed RBCs)
  • Autosplenectomy (damage to spleen is so vast that the organ becomes so small and non-functional)
  • Secondary Hemochromatosis
  • Gallstones
  • Legulcers
45
Q

What are the ways to test for Sickle cell anemia?

A
  • Peripheral blood smear
  • Hgb electrophoresis
  • Sickling test
46
Q

What is thalassemia?

A

Characterized by lack of or decreased synthesis of either alpha- or beta-globin chain of HbA

Pathology Final (1 decks)

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