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Heme Pharm > Anemia > Flashcards

Anemia Flashcards

1
Q

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

A
  1. hemoglobin.
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2
Q

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

A

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

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3
Q

Absorption of nonheme iron is affected by?

A

(a) phosphates which decrease absorption; and,

(b) ascorbic acid and meat which increase absorption.

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4
Q

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.

A
  1. ferrous (Fe2+)

2. ferric (Fe3+)

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5
Q

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

A
  1. duodenum
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6
Q

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.

A
  1. transferrin
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7
Q

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

A

ferric iron and transferrin complex

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8
Q

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

A
  1. transferrin receptors
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9
Q

combination of ferric iron with apoferritin

A

ferritin

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10
Q

aggregated ferritin

A

hemosiderin

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11
Q

Sites of iron storage include:

A

(1) the reticuloendothelial system

(2) hepatocytes.

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12
Q

Storage forms of iron include:

A

hemoglobin, myoglobin, enzymes, ferritin, hemosiderin

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13
Q

Symptoms of iron deficiency anemia

A

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

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14
Q

Iron deficiency diagnosis

A

quantitation of transferrin saturation,

and plasma ferritin

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15
Q

Adverse effects of oral iron

A

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

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16
Q

hemoglobin recovers in 1–2 months

A

ferrous sulfate

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17
Q

Contraindications of oral iron

A

antacids, proton-pump inhibitors, H2-

receptor antagonists decrease absorption

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18
Q

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

A

ferrous sulfate

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19
Q

can interfere with absorption of many drugs; Avoid

concurrent administration, separate doses by >2 hours.

A

ferrous sulfate

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20
Q

Clinical uses of parenteral iron

A

(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)

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21
Q

complex of ferric oxyhydroxide with polymerized

dextran

A

Iron dextran

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22
Q

The complex must be phagocytized by reticuloendothelial

cells before iron becomes available

A

Iron dextran

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23
Q

Can cause anaphylaxis

A

Iron dextran

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24
Q

Lower risk of anaphylactic reactions

A

Sodium Ferric gluconate and iron sucrose

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25
Q

Delivered to transferrin more readily

A

Sodium Ferric gluconate and iron sucrose

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26
Q

Signs and symptoms of iron poisoning

A

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
Q

Iron poisoning treatment

A

Treatment includes emesis & lavage with sodium bicarbonate to precipitate iron

28
Q

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

A
  1. deferoxamine
29
Q

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

A

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

30
Q

Deferoxamine contraindications

A

Contraindicated in renal insufficiency and anuria

31
Q

can cause allergic reactions (pruritus, wheals,

rash, anaphylaxis)

A

Deferoxamine

32
Q

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

A
  1. methylTHF
  2. THF
  3. megaloblastic anemia
33
Q

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

A

Vitamin B12 and folic acid

34
Q

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

A

Methylcobalamin (CH3B12)

one of the two active coenzyme forms of B12

35
Q

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

A

Deoxyadenosylcobalamin

one of the two active coenzyme forms of B12

36
Q

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

A

B12

37
Q

Intrinsic factor, secreted from

(1) binds B12

A
  1. parietal cells
38
Q

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

A
  1. ileal

refers to IF-B12 complex

39
Q

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

A
  1. transcobalamin II (TcII)

2. liver

40
Q

Most circulating cobalamin is bound to ?

A

transcobalamin I and III

41
Q

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.

A
  1. passive diffusion
42
Q

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

A

vitamin B12

43
Q

Effects of B12 deficiency

A

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
Q

Diagnosis of B12 deficiency

A

a. Determination of the plasma concentration of B12

b. Examination of blood smear for macrocytosis and hypersegmented polymorphonuclear leukocytes

45
Q

Clinical use: patients with pernicious anemia or ileal disease

A

Cyanocobalamin parenteral

46
Q

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

A

Cyanocobalamin (oral)

47
Q

Plasma becomes normoblastic after 7 days

A

Cyanocobalamin

48
Q

Are neuropsychiatric signs of B12 deficiency reversible?

A

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
Q

Inadequate secretion of intrinsic factor

A

pernicious anemia

50
Q

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

A

folic acid

51
Q 
Polyglutamates in food are hydrolyzed, reduced, & then
methylated by (1). (2) is transported to tissues and is taken up by receptor-mediated endocytosis
A
  1. dihydrofolate reductase

2. methyl-THF

52
Q

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

source of THF

A

Methyl-THF

53
Q

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

A
  1. liver

2. CH3THF

54
Q

Folate is stored within cells as (1)

A
  1. polyglutamates
55
Q

The principal effect of folic acid deficiency is:

A

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
Q

Diagnosis of folic acid deficiency

A

a. Determining plasma concentration of folate

b. Examination of blood smear

57
Q

prophylactic administration when there is

increased utilization such as in pregnancy and lactation

A

folate

58
Q

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

A

Leucovorin (folinic acid)

59
Q

Folate deficiency during pregnancy is associated with ?

A

congenital

neural tube defects

60
Q

High doses counteract the effects of antiepileptic drugs

A

Folic acid

61
Q

Acute or chronic alcoholism

A

causes of folic acid deficiency

62
Q

Inhibitors of dihydrofolate reductase (methotrexate, trimethoprim)

A

causes of folic acid deficiency

63
Q

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

A

causes of folic acid deficiency

Heme Pharm (13 decks)

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