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Flashcards in Anemia Deck (63):
1

Most of the iron in the body is in (1)

1. hemoglobin.

2

What are the two forms of iron available in the diet?

heme iron (found in meat, fish & poultry), which has the greatest bioavailability and nonheme iron (found in vegetables & dietary supplements)

3

Absorption of nonheme iron is affected by?

(a) phosphates which decrease absorption; and,
(b) ascorbic acid and meat which increase absorption.

4

Iron is best absorbed in its (1) form, however, dietary iron is in the (2) form which is not absorbed. (2) is ionized by stomach acid and then reduced to the (1) form.

1. ferrous (Fe2+)
2. ferric (Fe3+)

5

The ferrous form is actively taken up primarily in the (1) but absorptive processes of the mucosa limit the amount of iron absorbed.

1. duodenum

6

Within the mucosal cells, ferrous iron is oxidized to ferric iron which forms a complex with (1), a ß1-glycoprotein with two binding sites for ferric iron.

1. transferrin

7

This complex binds to specific receptors in the plasma membrane and is taken up by receptor-mediated endocytosis.

ferric iron and transferrin complex

8

If iron is plentiful, then there are fewer (1) on the surface of cells. This prevents iron-replete cells from
receiving excess iron

1. transferrin receptors

9

combination of ferric iron with apoferritin

ferritin

10

aggregated ferritin

hemosiderin

11

Sites of iron storage include:

(1) the reticuloendothelial system
(2) hepatocytes.

12

Storage forms of iron include:

hemoglobin, myoglobin, enzymes, ferritin, hemosiderin

13

Symptoms of iron deficiency anemia

a. Feelings of weakness and lassitude
b. Headache
c. Dizziness
d. Palpitations; chest pain
e. Decreased exercise tolerance; shortness of breath

14

Iron deficiency diagnosis

quantitation of transferrin saturation,
and plasma ferritin

15

Adverse effects of oral iron

(a) heartburn
(b) constipation or diarrhea
(c) nausea (more prevalent at higher doses)
(d) upper abdominal pain (more prevalent at higher doses)

16

hemoglobin recovers in 1–2 months

ferrous sulfate

17

Contraindications of oral iron

antacids, proton-pump inhibitors, H2-
receptor antagonists decrease absorption

18

replenishment of iron stores may require many (3–6) months

ferrous sulfate

19

can interfere with absorption of many drugs; Avoid
concurrent administration, separate doses by >2 hours.

ferrous sulfate

20

Clinical uses of parenteral iron

(a) Patients in whom GI absorption is prevented by disease
(b) Patient who cannot tolerate orally administered iron
(c) Hemodialysis patients (Sodium ferric gluconate and iron
sucrose)

21

complex of ferric oxyhydroxide with polymerized
dextran

Iron dextran

22

The complex must be phagocytized by reticuloendothelial
cells before iron becomes available

Iron dextran

23

Can cause anaphylaxis

Iron dextran

24

Lower risk of anaphylactic reactions

Sodium Ferric gluconate and iron sucrose

25

Delivered to transferrin more readily

Sodium Ferric gluconate and iron sucrose

26

Signs and symptoms of iron poisoning

i) abdominal pain
ii) diarrhea
iii) vomiting brown or bloody stomach contents with pills
iv) lassitude & drowsiness
v) pallor or cyanosis
vi) hyperventilation (due to acidosis)
vii) cardiovascular collapse
viii) Death can occur within 6 hours or be delayed 12-24 hours
with a period of apparent recovery in between

27

Iron poisoning treatment

Treatment includes emesis & lavage with sodium bicarbonate to precipitate iron

28

If plasma concentration of iron > 3.5 mg/L, (1) (IM or IV) is indicated.

1. deferoxamine

29

has a high affinity for ferric iron. Once bound with iron, excreted in the urine

Deferoxamine has a high affinity for ferric iron. Once bound with iron, feroxamine is excreted in the urine

30

Deferoxamine contraindications

Contraindicated in renal insufficiency and anuria

31

can cause allergic reactions (pruritus, wheals,
rash, anaphylaxis)

Deferoxamine

32

Without vitamin B12, folate is trapped as (1),
and subsequent steps in folate metabolism that require (2) are deprived of substrate. This provides the common basis for the development of (3) with deficiency of either vitamin B12 or folic acid

1. methylTHF
2. THF
3. megaloblastic anemia

33

Deficiency in either of these substances results in defective synthesis of DNA in any cell attempting chromosomal repair or division.

Vitamin B12 and folic acid

34

important for folate metabolism and for the formation of methionine and S-adenosylmethionine from homocysteine

Methylcobalamin (CH3B12)
one of the two active coenzyme forms of B12

35

required for the isomerization of L-methylmalonyl CoA to succinyl CoA.

Deoxyadenosylcobalamin
one of the two active coenzyme forms of B12

36

released from digested
protein by the actions of gastric
acid and pancreatic enzymes

B12

37

Intrinsic factor, secreted from
(1) binds B12

1. parietal cells

38

The complex interacts with
specific receptors on (1)
mucosal cells, is absorbed and
enters the circulation

1. ileal
refers to IF-B12 complex

39

Once absorbed, B12 binds with (1) for transport to tissues. The complex is preferentially distributed to the (2) (up to
90%)

1. transcobalamin II (TcII)
2. liver

40

Most circulating cobalamin is bound to ?

transcobalamin I and III

41

An alternate pathway for absorption exists which does not require intrinsic factor or an intact terminal ileum. The pathway involves (1) and accounts for 1% of ingested B12.

1. passive diffusion

42

Deficiency (takes several years to develop following vitamin deprivation due to enterohepatic circulation

vitamin B12

43

Effects of B12 deficiency

a. Megaloblastic anemia
b. Potentially irreversible nerve damage:
parethesias of the hands and feet, decreased vibration and position senses with resultant unsteadiness, decreased deep tendon reflexes
In later stages: confusion, moodiness, loss of memory, and loss of central vision.

44

Diagnosis of B12 deficiency

a. Determination of the plasma concentration of B12
b. Examination of blood smear for macrocytosis and hypersegmented polymorphonuclear leukocytes

45

Clinical use: patients with pernicious anemia or ileal disease

Cyanocobalamin parenteral

46

Clinical use: In patients with pernicious anemia high doses are used since it is absorbed via passive diffusion

Cyanocobalamin (oral)

47

Plasma becomes normoblastic after 7 days

Cyanocobalamin

48

Are neuropsychiatric signs of B12 deficiency reversible?

They can be reversible with cyanocobalamin treatment if they are LESS than 6 months duration. Will need to keep pt on Therapy for at least 6 months to see improvement

49

Inadequate secretion of intrinsic factor

pernicious anemia

50

reduced to tetrahydrofolic acid
which acts as an acceptor of
one-carbon units

folic acid

51

Polyglutamates in food are hydrolyzed, reduced, & then
methylated by (1). (2) is transported to tissues and is taken up by receptor-mediated endocytosis

1. dihydrofolate reductase
2. methyl-THF

52

acts as a methyl donor (for formation of CH3B12) and as a
source of THF

Methyl-THF

53

The (1) reduces & methylates folic acid (PteGlu) and transports (2) into the bile for reabsorption by the gut

1. liver
2. CH3THF

54

Folate is stored within cells as (1)

1. polyglutamates

55

The principal effect of folic acid deficiency is:

a. Megaloblastic anemia
b. Unlike B12 deficiency, neurological abnormalities are NOT common
c. Folate deficiency during pregnancy is associated with congenital neural tube defects

56

Diagnosis of folic acid deficiency

a. Determining plasma concentration of folate
b. Examination of blood smear

57

prophylactic administration when there is
increased utilization such as in pregnancy and lactation

folate

58

circumvents the action of inhibitors of dihydrofolate reductase and potentiates the cytotoxic effects of 5-
fluorouracil

Leucovorin (folinic acid)

59

Folate deficiency during pregnancy is associated with ?

congenital
neural tube defects

60

High doses counteract the effects of antiepileptic drugs

Folic acid

61

Acute or chronic alcoholism

causes of folic acid deficiency

62

Inhibitors of dihydrofolate reductase (methotrexate, trimethoprim)

causes of folic acid deficiency

63

Drugs which interfere with absorption and storage of folate (certain anticonvulsants and oral contraceptives)

causes of folic acid deficiency