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Year 1 > Hematopoiesis Nutrition > Flashcards

Hematopoiesis Nutrition Flashcards

1
Q

Enzyme used in the rate limiting step converting dUMP to dTMP

A

Thimidylate synthase

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2
Q

Both of these nutrients are required for DNA synthesis

A

Folate and Vitamin B12

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3
Q

Cobalmin

A

Vitamin B12

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4
Q

Vitamin B9

A

Folate

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5
Q

What is the structural change when converting RNA dUMP to DNA dTMP

A

addition of one methyl grop

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6
Q

Source of methyl groups

A

Folate

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7
Q

Also involved in purine biosynthesis

A

Folate

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8
Q

Co-enzyme for recycling folate

A

Vitamin B12

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9
Q

After folate is taken in from diet, what are the two successive reduction steps?

A

Folate»DHF»THF

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10
Q

THF trap

A

If don’t have B12, can’t convert N5 methyl THF back to THF

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11
Q

The name of B12 or folate deficiency which results in fewer, but larger blood cells

A

Megaloblastic anemia

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12
Q

3 important consequences of B12 or folate deficiency

A
  1. DNA synthesis impaired
  2. Cell division impaired
  3. Cytoplasm matures faster than nucleus (cytoplasm can still undergo maturation so can make hemoglobin, gets larger, but won’t divide)
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13
Q

What are visual signs of megaloblastic anemia?

A

Multilobed PMNs (normal are 3-4), macrocytic RBCs

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14
Q

Why are fortified foods with folic acid more stable?

A

Doesn’t contain/form a polygluconate conjugate

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15
Q

Why can hemolytic anemia cause an increased demand and use of folate?

A

Hemolytic anemia is due to RBC destruction, have to keep up with loss of RBCs, so requires a lot of cell division

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16
Q

Term for reduction of all types of blood cells (RBC, WBC, platelets)

A

Pancytopenia

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17
Q

Why is neural tube defect a symptom of folate deficiency?

A

Highest proliferation during embryogenesis, need high folate levels. Neural tube defect

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18
Q

Major component of VB12 structure

A

Corrin ring

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19
Q

Source of VB12

A

Made by bacteria, found in meats/animal biproducts

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20
Q

Two direct steps involving VB12 that are important in neuronal function

A

Homocysteine —*—->Methionine (—>SAM)

Methylmalonyl CoA —*—> Succinyl CoA

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21
Q

This breakdown product of methylmalonyl CoA will accumulate if B12 deficient

A

methylmalonic acid (MMA)

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22
Q

What produces haptocorrin?

A

Salivary glands in the mouth

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23
Q

2 other names for haptocorrin

A

Transcobalamin I, R factor

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24
Q

Vitamin B12 is not readily available because it is bound to proteins. Where does VB12 get digested and liberated from proteins?

A

Stomach

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25
Q

After liberated from proteins, VB12 binds to this molecule to protect it from the hydrochloric acid found in stomach

A

Haptocorrin

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26
Q

Instrinic Factor (IF) is made by?

A

Parietal cells (stomach epithelial cells)

27
Q

VB12 disassociation from haptocorrin occurs where? What chews up haptocorrin?

A

Duodenum, pancreatic enzymes

28
Q

When released from haptocorrin, VB12 binds to what? Where?

A

Intrinsic factor in the dudodenum

29
Q

Where is B12/IF absorbed?

A

Terminal Ileum by ileal cells

30
Q

Storage of B12

A

liver and muscle

31
Q

This glycoprotein binds and transport VB12 through the blood once it has been absorbed by terminal ileum

A

Transcobalamin II (TC-II)

32
Q

List 4 conditions that prevent VB12 absorption

A
  1. Loss of intrinsic factor (IF)
  2. Achlorhydria (not making enough HCL that maks up gastric acid)
  3. Pancreatic insufficiency
  4. Malabsorption in terminal ileum
33
Q

Gastric acid in the stomach favors binding to?

A

Haptocorrin

34
Q

How would pancreatic insufficiency affect VB12 absorption?

A

Need pancreatic enzymes to chew up haptocorrin and release B12

35
Q

How would gastritis, gastrectomy, or antibodies to parietal cell antigens affect VB12 absorption?

A

Loss of intrinsic factor= pernicious anemia

Pareital cells in stomach make intrinsic factor, haptocorrin hands off VB12 to IF in duodenum

36
Q

Blind loop, bacterial overgrowth, fish tape worm, and IBS all would affect

A

VB12 absorption in terminal ileum

37
Q

How does B12 deficiency specifically cause neurological impairment?

A

Affect myelination

38
Q

Where is folic acid absorbed?

A

Duodenum/jejunum (middle section of small intestine)

39
Q

Synthesis of heme and hemoglobin occur in these two cites

A

Mitochondria and cytoplasm (heme is made in mitochondria and joins with globin chains in the cytoplasm to make hemoglobin)

40
Q

What is the rate limiting step in heme synthesis? What enzyme?

A 
ALA synthetase (aminolevulinic acid)
converts succinyl CoA---> dALA
41
Q

Iron deficiency only affects

A

RBCs

42
Q

size of RBCs when iron deficient

A

microcytic, small because not enough hemoglobin

43
Q

Iron deficiency shows these three signs

A
  1. microcytic
  2. hypochromic (less hemoglobin, expanded area, thinner hemoglobin, pale looking)
  3. Insufficient hemoglobin
44
Q

Why does iron cause insufficient hemoglobin?

A

Fe2+ gets incorporated into heme to make hemoglobin; incorporation is complex

45
Q

What is the most common cause of iron deficiency? Rare cause?

A

Bleeding bleeding bleeding. Rare cause is renal/pulmonary syndrome (kidney failure)

46
Q

Why might pulmonary syndrome cause iron deficiency?

A

Kidney responsible for EPO synthesis, so no reticulocyte response, and red blood cell survival decreases

47
Q

Eating, craving weird things; a symptom of iron deficiency

A

Pica

48
Q

Are platelets and WBCs affected by iron deficiency?

A

NO, ONLY RBCs

49
Q

4 iron parameters for deficiency diagnosis

A
  1. Serum Iron
  2. Transferrin saturation
  3. TIBC (total iron binding capacity)
  4. Ferritin
50
Q

Type of anemia in B12 and folate

A

Hypoproliferative

51
Q

Type of anemia in Iron

A

hypoproliferative (if don’t have enough heme, body sense that and slows down proliferation)

52
Q

Size of RBCs in B12 and folate deficiency

A

macrocytic (large, because not enough DNA synthesis but still can make hemoglobin)

53
Q

Size of RBCs in iron deficiency

A

microcytic (small, because not enough hemoglobin)

54
Q

Most common cause of deficiency in B12 and folate

A

Reduced absorption or intake

55
Q

2 key points about deficiency treatment

A
  1. should be rapid and complete

2. folate will partially correct the hematologic manifestations of B12 deficiency but NOT the neurologic

56
Q

This metal is involved in iron transport, heme synthesis, and RBC membrane

A

Copper

57
Q

This metal is involved in DNA synthesis, and in excess inhibits copper absorption

A

Zinc

58
Q

This metal is the corrin core of cobalamin

A

Cobalt

59
Q

This metal blocks iron absoprtion and heme synthesis

A

Lead

60
Q

This vitamin is involved in iron absorption

A

Vitamin C (ascorbic acid)

61
Q

This vitamin is involved in heme synthesis

A

Vitamin B6, pyridoxine

62
Q

This vitamin is involved in iron absorption and mobilization

A

Vitamin A

63
Q

Autoimmune version of VB12 deficiency

A

pernicious anemia

Year 1 (48 decks)

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