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Pharm test 3 > anemias and hematinic agents > Flashcards

anemias and hematinic agents Flashcards

1
Q

most common blood disorder is what

A

anemia

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2
Q

anemia results from what

A

defect in RBC formation or function- tissue does get enough O2

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3
Q

what is needed from the liver to make RBC

A

erythropoietin

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4
Q

do erythrocytes have nucleus?

A

no, they lose it during formation

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5
Q

what is nutritional anemia called

A

microcytic anemia (iron deficiency anemia) (tired blood)

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6
Q

cause of microcytic anemia

A

relative lack of iron- RBC are small, pale looking

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7
Q

does the body have mechanisms to eliminate iron?

A

no

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8
Q

iron is broken down in stomach by what

A

HCL

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9
Q

iron is absorbed as what form

A

Fe2+ ferrous iron

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10
Q

iron is transported as what form

A

Fe3+ feric iron

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11
Q

what converts Fe2+ to Fe3+

A

transferrin

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12
Q

what carrier iron throughout body

A

transferrin

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13
Q

T/F transferrin increases during times of anemia

A

True

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14
Q

excess iron is stored as what and where?

A

ferritin in liver

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15
Q

excess loss of iron leads to what?

A

chronic blood loss

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16
Q

ecology of iron deficiencies

A
  1. not enough in diet
  2. decreased absorption if HCL is very low or other GI dysfunctions
  3. increased requirements- pregnancy, body growth.
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17
Q

drug of choice of microcytic anemia

A

iron, speciccaly FeSO4-, orally, cheap, effective

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18
Q

SE of iron intake

A

GI upset

nausea

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19
Q

can you take iron via parenterally?

A

yes, severe deficiency

20
Q

can taking iron orally be toxic?

A

yes, in small children, lethal dose could be little as 3. grams/ 10 tablets

21
Q

acute iron toxicity

A 
nausea
abdominal pain
drowsiness
cardio collapse
convulsions or death
22
Q

treatment of acute iron toxicity

A

iron chealators, deferoxamine

23
Q

chronic toxicity of iron and treatment

A

hemochromatosis (too much stored), treatment is phlebotomy- bleeding somebody

24
Q

macrocytic anemias

A

large RBC precursors. due to inhibition of DNA synthesis

25
Q

___ ____ is needed for DNA replication

A

folic acid

26
Q

symptoms of folic acid deficiency

A

macrocytic RBC precursors

27
Q

etiology of folic acid deficiencies

A

intake deficiency

drugs can inhibit synthesis of active form

28
Q

folic acid deficiency in pregnancy can caused what

A

neural tube defects

29
Q

folic acid deficiency leads to deficiencies to what other molecules

A

methionine and dTMP (don’t make enough thimadine which is needed for RBC synthesis)

30
Q

therapy of folic acid deficiency

A

oral therapy is usually sufficient

31
Q

therapy if there is an absorption abnormality.

A

parenteal therapy. no toxicities, no contraindications

32
Q

function of B12

A

essential for DNA synthesis and methionine

33
Q

symptoms of B12 deficiency

A
  • megaloblastic anemic,
  • lack of methionine causes decrease in myelin synthesis –> neuronal damage, weakness, ataxia, opacity, irreversible spinal cord damage
34
Q

etiologies of B12 deficiency

A

mainly decrease in absorption, most common

35
Q

what does parietal cells make that B12 requires to get absorbed

A

Gastric inrinsic factor (G.I.F)

36
Q

pernicious anemia

A

pt. lacks ability to make G.I.F, can’t absorb B12 which is needed for RBC synthesis, so low RBC’s

37
Q

in pernicious anemia how is B12 given?

A

by injection

38
Q

if B12 deficiency isn’t due to pact of GIF how to you correct deficiencies?

A

orally

39
Q

anemias due to chronic renal failure or chemo. list or drugs

A

epoietin alfa
darbepoietin
peginesatide

40
Q

why does anemia happen in chronic renal failure or chemo?

A

liver isn’t making erythropoietin like it should be.

41
Q

hemolytic anemia is what

A

abnormal lysis of RBC. iron not generally helpful, erythropoietin useful though

42
Q

toxicities of drugs used with chronic renal failure are due to what

A

due to excess of RBC, increase BP, increase clotting, stroke

43
Q

sickle cell anemia

A

abnormal flow of RBC- change shape, hard to get thoruhg caps

44
Q

drug used for sickle cell anemia

A

hydroxyurea

45
Q

hydroxyurea

A

increase formation of fetal hemoglobin which does not sickle.

46
Q

SE of hydroxyurea

A

mutagenic

preg category D

Pharm test 3 (4 decks)

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