RBC Pathology 2 Flashcards

1
Q

(T/F) Humans are totally dependent on dietary Vitamin B12

A

True

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2
Q

Vitamin B12 is absorbed in what part of the small intestine?

A

Ileum

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3
Q

Intrinsic factor is secreted by parietal cells in the _______ muscosa of the stomach

A

Fundic

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4
Q

Vitamin B12 takes the _____ group from methyltetrahydrofolate and transfers a carbon to homocysteine to form __________

A

Methyl; methionine

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5
Q

___________ delivers vitamin B12 to the liver and other cells of the body

A

Transcobalamin II

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6
Q

2 pathways where vitamin B12 is used

A

1) Conversion of homocysteine to methionine

2) Isomerization of methylmalonyl CoA to Succinyl CoA

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7
Q

In ________ deficiency, both homocysteine and methylmalonic acid are elevated while in ________ deficiency, only homocysteine levels are increased

A

B12; Folic acid

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8
Q

In Vitamin B12 deficiency, accumulation of methylmalonic acid causes demyelination of the _________ and ________ tract of the spinal cord

A

dorsal and lateral

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9
Q

In Vitamin B12 deficiency, provision of folate will improve s/s of _________ but not _______

A

anemia; neurologic symptoms

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10
Q

Enumerate anemias d/t diminished erythropoesis

A

Megaloblastic anemia, pernicious anemia, iron deficiency anemia

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11
Q

Why does folic acid and B12 deficiency cause megaloblastic anemia?

A

B12 and folic acid are needed in nuclear maturation and DNA synthesis causeing nuclear-cytoplasmic asynchrony

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12
Q

Enumerate the common causes of megaloblastic anemia

A

1) Decreased intake (vegan diet, alcoholics)
2) Impaired absorption
3) Fish tapeworm (competitive uptake)
4) Increased requirements (pregnancy, thyrotoxicosis, cancer, infants)
5) Medication: folic acid antagonists like methotrexate
6) Increased losses (hemodialysis)

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13
Q

In PBS of megaloblastic anemia what type of RBC is seen? Which cells are affected?

A

Macrocytic, hyperchromic RBCs; RBCs, Platelets, WBCs

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14
Q

In PBS of megaloblastic anemia what type of neutrophils are seen?

A

hypersegmented (macropolys)

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15
Q

The reticulocyte count is _________ in megaloblastic anemia. What is seen 5 days after IV administration of B12 / folic acid

A

decreased; striking reticulocytosis

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16
Q

In megaloblastic anemia there is bone marrow ___________ that is hypercellular

A

hyperplasia

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17
Q

In the BM of megaloblastic anemia, what is the erythroid:myeloid ratio?

A

1:1

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18
Q

In megaloblastic anemia, MCHC is always elevated (T/F)

A

false, may be normal to elevated

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19
Q

In pernicious anemia, there are autoantibodies against?

A

Intrinsic factor and/or parietal cells

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20
Q

Describe Type I of autoantibodies to intrinsic factor-type of pernicious anemia

A

Blocks attachment of B12 to IF

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21
Q

Describe Type II of autoantibodies to intrinsic factor-type of pernicious anemia

A

Blocks attachment of B12-IF complex to ileal receptors

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22
Q

Describe Type III of autoantibodies to intrinsic factor-type of pernicious anemia

A

Antibodies recognize the alpha and beta subunits of the gastric proton pump

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23
Q

Autoantibodies to gastric parietal cells leads to _____ and __________

A

Chronic atrophic gastritis; gastric atrophy

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24
Q

Enumerate the changes seen in pernicious anemia NOT seen in megaloblastic anemia

A

1) Achlorhydria
2) Serum antibodies
3) Atrophy of the stomach
4) Beefy red tongue (atrophy of the tongue)

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25
Q

Most common nutritional disorder in developing countries

A

Iron deficiency anemia (IDA)

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26
Q

Causes of IDA

A

1) Low dietary intake (elderly, infants and the mamamayan who cant afford meat =P)
2) Poor absorption
3) Increased demand (pregnancy, children)
4) Chronic blood loss

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27
Q

Which type of heme is more well-absorbed?

A

Heme iron

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28
Q

What are the functional forms of iron?

A

Heme, myoglobin, catalase

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29
Q

What is the storage form of iron? Where are they stored?

A

Ferritin; bone marrow & macrophages (RES)

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30
Q

(T/F) Free iron is highly toxic

A

True

31
Q

What is ferritin? Where is it found? Where is it MAINLY found?

A

Iron-protein complex; liver, spleen, BM, skeletal muscle; Macrophages

32
Q

Where is the storage form of iron in macrophages derived from?

A

breakdown of RBCs

33
Q

Where is hepatocyte iron derived from?

A

plasma transferrin

34
Q

(T/F) Iron is actively excreted

A

False, there is very limited iron excretion

35
Q

What is the only way that iron can be removed from the body?

A

Chelation

36
Q

Protein that ihibits absorption of iron in the gut

A

Hepcidin

37
Q

Hepcidin is increased in these situations

A

Anemia of chronic disease

Untreated infections

38
Q

PBS in IDA shows _______ ________ RBCs

A

hypochromic, microcytic

39
Q

If you see hypochromic, microcytic anemia in adults, what do you check for? In children?

A

Chronic blood loss; thalassemia or IDA

40
Q

BM in IDA shows __________ sideroblasts

A

decreased

41
Q

In IDA, serum ____ and _____ are decreased and ______ is increased

A

Fe and ferritin; TIBC

42
Q

What is the response to treatment in IDA

A

Reticulocytosis in 3 days

43
Q

Give s/s of IDA

A

koilonychia, pica, alopecia, atrophic glossitis, atrophic gastritis

44
Q

What constitutes the Plummer Vinson Syndrome?

A

Esophageal webs + atrophic gastritis + IDA with depressed Hb, Hct, MCV, serum Fe, ferritin

45
Q

Anemias d/t BM failure

A

aplastic anemia

46
Q

Aplastic anemia is a syndrome of?

A

chronic primary hematopoetic failure and attendant pancytopenia

47
Q

In the diagnosis of aplastic anemia, the BM shows? PBS shows? and the reticulocyte count is (decreased / increased)?

A

hypocellular with fat and no hematopoetic elements; Pancytopenia; Decreased

48
Q

2 treatments for aplastic anemia

A

transplant, immunosuppressive therapy

49
Q

Causes of aplastic anemia

A

hereditary (Fanconi’s anemia)
Idiopathic (Stem cell defects)
Acquired

50
Q

Give some acquired causes of aplastic anemia

A

Drugs (chloramphenicol, phenytoin, carbamazapine), Chemicals, infections (CMV, parvovirus, etc), Whole body irradiation

51
Q

The normal histology of the bone marrow shows ___ % fat and ___% hematopoetic cells

A

50%; 50%

52
Q

How do you histologically differentiate tumoral BM vs BM in aplastic anemia?

A

Tumoral is hypocellular with no fat while Aplastic anemia is hypocellular with more fat (than hematopoetic cells)

53
Q

Enumerate the clinical features of aplastic anemia

A

1) Pancytopenia
2) Progressive weakness, pallor, dyspnea
3) Thrombocytopenia
4) Splenomegaly
5) RBCs are slightly macrocytic, normochromic

54
Q

What is a primary BM disorder wherein only the erythroid progenitors are suppressed? What is it usually associated with?

A

Pure red cell aplasia; neoplasms, thymoma, large granular lymphocytic leukemia

55
Q

Give other causes of anemia

A

Myelophtisic anemia, chronic renal failure, diffuse liver disease, neoplasia, hypithyroid disease

56
Q

What type of RBC is diagnostic of myelophthisic anemia

A

teardrop shaped RBC

57
Q

Give the anemias associated with decreased MCHC, MCV and MCH

A

IDA, thalassemia, Anemia of chornic inflammation

58
Q

Give the anemias associated with increased MCHC, MCV and MCH

A

Pernicious anemia, B12 deficiency, Folate deficiency

59
Q

Give the anemias associated with normal MCHC, MCV and MCH

A

Hemolytic anemia, aplastic anemia, Polycythemia

60
Q

Which anemia has an increase in color (MCHC) but a decrease in size (MCV)?

A

Spherocytosis

61
Q

Polycythemia is an increase in _____ with a corresponding increase in ______

A

RBCs; Hemoglobin

62
Q

What are the 3 types of polycythemia? What is the difference between them?

A

Relative ( Volume is decreased but RBC not actually increased); Absolute (increase in total RBC); Stress polycythemia (individuals are usually hypertensive, obese & anxious)

63
Q

Primary absolute polycythemia results from?

A

An intrinsic abnormality oh hematopoetic precursors, neoplastic condition

64
Q

Secondary absolute polycythemia results from?

A

Increased erythropoetin secretion that may be compensatory or pathologic

65
Q

Give some tumors that produce erythropoetin

A

renal cell CA, hepatocellular CA, cerebellar hemangioblastoma

66
Q

How do you differentiate between primary and secondary absolute polycythemia?

A

Primary has decreased erythropoetin which is increased in secondary

67
Q

Type of polycythemia where there is an increase in marrow production of myeloid progenitors but lymphocytes are not increased

A

Polycythemia vera

68
Q

Polycythemia vera is d/t a mutation of ______ causing erythropoetin receptors to become ______

A

JAK2 tyrosine kinase; hypersensitive

69
Q

In the laboratory diagnosis of polycythemia vera, what are the values of: RBC, WBC, Platelets, Hct; What is seen in the PBS?

A

RBC (6M); WBC (12000 - 50000); Platelets (=/> 500000); Hct (=/> 60%); PBS shows Panmyelosis

70
Q

Incidence of polycythemia vera is higher in?

A

Males, middle aged to elderly

71
Q

S/S of polycythemia vera

A

Cyanosis, pruritus, peptic ulcer, plethoric headache, dizzines, hypertension

72
Q

Complications of polycythemia vera

A

Thrombosis, Bleeding, Hyperuricemia, Myelofibrosis

73
Q

Treatment for polycythemia vera

A

Regular phlebotomy