Anemic Drugs Flashcards

1
Q

conditions associated with normocytic, microcytic, and macrocytic RBCs

A

normocytic RBC - acute blood loss
microcytic - iron deficiency anemia
macrocytic - B12 or folic acid deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

causes of iron deficiency

A

acute or chronic blood loss
insufficient intake esp in kids
heavily menstruating or preggo women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

type of anemia from iron deficiency

A

hypochromic, microcytic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

oral iron therapy

A

ferrous sulfate
ferrous gluconate
ferrous fumurate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

adverse effects of oral iron therapy

A
nausea
epigastric discomfort
abdominal cramps
constipation
diarrhea

black stool (no significance other than may obscure diagnosis of continued GI blood loss)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are parenteral iron therapy and when is it given

A

iron dextran, sodium ferric gluconate complex, iron sucrose

given to those who are unable to absorb or tolerate oral iron and extensive chronic anemia that cannot be maintained with oral iron alone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

when is acute iron toxicity usually seen

A

in children who accidentally swallow iron tablets and it is a medical emergency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what do kids with acute iron toxicity experience as in what are their symptoms

A

necrotizing gastreoenteritis, vomiting, abdominal pain, blood diarrhea

can be followed by shock, metabolic acidosis, coma, and death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how do you treat acute iron toxicity

A
  • whole bowel irrigation to flush out iron
  • Deferoxamine, an iron chelator, can systemically bind iron that has already been absorbed and get rid of it in urine or feces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

another name for chronic iron toxicity and what is it

A

hemachromatosis and when excessive iron is deposited in the heart, liver, pancreas, and other organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

who is hemachromatosis mainly seen in

A

pts with inherited hemachromatosis

those who receive many red cell transfusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

drugs used in pts with thalassemia major to get rid of iron

A

iron chelators - deferoxamine and deferasirox

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does deficiency in vit B12 lead to

A

megaloblastic anemia

neurological symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

active form of vit B12 found in humans

A

deoxyadenosylcobalamin and methylcobalamin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

forms of vit b12 found in foods that are converted to active form

A

cyanocobalamin, hydroxycobalamin, and other cobalamins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how long will it take to use up our storage of vit b12

A

5 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

relationship between vitamin B12 and folate

A

methylcobalamin (from vit B12) is an intermediate in transfer of methyl group from N5-methyltetrahydrofolate to homocysteine in order to form methionine and tetrahydrofolate (dTMP)

without vit B12, you have a build up of homocysteine and lack of tetrahydrofolate (needed for DNA synthesis)

called methylfolate trap

18
Q

what happens when you have lack of tetrahydrofolate due to lack of Vit B12 and what is treatment

A
  • lack of tetrahydrofolate means reduced DNA synthesis

- give folic acid to tx the anemia

19
Q

what leads to neurological symptoms in vit B12 deficiency

A

vit b12 is needed to convert methylmalonyl CoA to succinyl coA by methylmalonyl coA mutase so without it, you have a build up of methylmalonyl coA which accumulates as methymalonic acid which causes neurological problems

20
Q

characteristic manifestation of Vit B12 deficiency

A
  • megaloblastic, macrocytic anemia
  • mild or moderate leukopenia/thrombocytopenia
  • hypercellular bone marrow
  • accumulation of megaloblastic erythroids
  • parasthesia in peripheral nerves
  • ataxia and other CNS problems
21
Q

if megaloblastic anemia is diagnosed, why must it be determined if it is due to vit B12 or folic acid deficiency

A
  • treating with folic acid will reverse the hematological problems but the neurological symptoms of vit B12 will continue to get more severe
22
Q

common causes of vit b12 deficiency

A
  • pernicious anemia (no secretion of intrinsic factor by gastric mucosal cells)
  • partial or total gastrectomy
  • conditions that affect distal ileum
23
Q

what are the parenteral injections given for vit b12 deficiency and for how long

A

cyanocobalamin and hydroxocobalamin

for life if due to pernicious anemia especially

24
Q

drugs that cause folate acid deficiency

A

methotrexate
phenytoin
trimethoprim and pyrimethamine

25
Q

high risk patients that require folate supplementation

A
pregnant women
alcoholics
hemolytic anemia
liver disease
certain skin disease
pts on renal dialysis
26
Q

what are the hematopoietic growth factors

A
FrIEDS
Filgastrim
Interleukin 11
Erythropoietin
Darbepoetin
Sargramostim
27
Q

where is endogenous erythropoietin produced and what happens with it during tissue hypoxia

A
  • produced in the kidney

- increased transcription of erythropoietin in response to hypoxia hence correcting anemia

28
Q

relationship between hematocrit/hemoglobin levels and erythropoietin normally and in anemia of chronic renal failure

A
  • normally if hematocrit or hemoglobin levels are high then erythropoietin levels are low and vice versa
  • in those with anemia of chronic renal failure, erythropoietin levels are usually low because kidney is not able to produce it so they benefit from exogenous erythropoietin
29
Q

what is darbepoetin and how does it differ from erythropoietin

A

long acting version of erythropoietin that differs by an addition of two carb chain which improves it biological activity

it has decreased clearance and half life that is three times that of erythropoietin

30
Q

adverse effects of erythropoietin

A

hypertension

thrombotic complications

31
Q

what are the growth factors and what do they do

A

filgastrim (G-CSF –> granulocyte colony stimulating factor)
sargramostim (GM-CSF –> granulocyte-macrophage colony stimulating factor)

they both stimulate the production and function of neutrophils

GM-CSF stimulates production of myeloid and other megakaryocyte progenitors

32
Q

have receptors that are part of JAK-STAT pathway

A

erythropoietin
filgastrim
sargramostim

33
Q

what is filgastrim and sargramostim used for

A

accelerate recovery of neutrophil after cancer therapy and to treat other form of neutropenia

34
Q

what is erythropoietin used for

A

anemia in renal failure but also anemia of other forms

35
Q

adverse effects of filgastrim and sagrasmostim

A

G-CSF - bone pain

GM-CSF - fever, arthralgias, capillary damage with edema

36
Q

what does interleukin-11 do and what is it used to treat

A

stimulates growth of primitive megakaryocyte progenitors and increase number of peripheral platelets

used for patients with prior episodes of thrombocytopenia after a cycle of cancer chemo so they don’t have to get platelet transfusions

37
Q

used to treat sickle cell anemia

A

hydroxyurea

38
Q

what does hydroxyurea do

A

it increases the amount of fetal hemoglobin therefore diluting the amount of abnormal hemoglobin S (HbS)

39
Q

side effects of hydroxyurea

A

bone marrow suppression and cutaneous vasculitis

40
Q

what is hydroxyurea used to treat other than sickle cell

A

chronic myelogenous leukemia (CML)

polycythemia vera