Sweatman Drugs to treat Anemia Flashcards

1
Q

erythrocyte factors

A

B12
folate
ESA’s

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2
Q

granulocyte factors

A

Sargramostatin GM-CSF

Filgrastim G-CSF

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3
Q

Thrombocyte factors

A

IL-11 (Oprelvekin)

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4
Q

stimulates production of neutrophils specifically

A

Filgrastim–>G-CSF

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5
Q

stimulates all granulocytes

A

GM-CSF–> Sargramastin

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6
Q

seondary hemochromatosis is common in

A

beta thal

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7
Q

Megaloblastic anemia due to

A

B12 or folate

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8
Q

microcytic anemia

A

IDA
ACD
Sideroblastic anemia
Thalassemia

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9
Q

cause of pernicious anemia

A

defect in synthesis of Intrinsic factor to where you can’t absorb b12

  • either anti-parietal or anti IF ab’s
  • or surgical gastrectomy
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10
Q

regulation of totaly body iron is through

A

modulation of intestinal (duodenal) absorption HEPCIDIN

*no real good way to get rid of iron

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11
Q

only indication for iron administration

A

prevention or tx of Iron Deficiency Anemia

  • overload is highly toxic
  • bag of blood=bag of iron
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12
Q

IDA treated with dietary iron supplementation

A

ferrous sulfate, ferrous gluconate, ferrous fumarate

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13
Q

Special cases of IDA tx

Parenteral iron

A

iron dextran, sodium ferric gluconate, and iron sucrose

*colloid conatining a core of iron oxyhydroxide surrounded by core of carbohydrate

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14
Q

Iron intoxication

A

occurs most commonly via accidental ingestion of iron supplements by children

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15
Q

Describe the coure of iron inxication

A

necrotizing gastritis, shock, metabolic acidosis, and death

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16
Q

tx of acute iron intoxication

A

deferoxamine–> parenteral chelates circulating iron

*also remove undigested tabs and correct electrolyte abnormalities

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17
Q

iron overload occurs in

2 types

A

hemochromatosis
primary-> genetic defect in HFE gene–> cant turn off hepcidin
secondary–> chronically transfused as in beta thalassemia

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18
Q

symptoms of Hemochromatosis

A

free iron deposits in Heart, Liver and pancreas and other adrenal glands

gives you *cirrhosis and diabetes

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19
Q

tx of chronic iron overload

A

usually phlebotomy except if anemia

*deferasirox–> chelates free iron–> oral

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20
Q

With phlebotomy for Iron overload–> iron is first depleted from

A

ferritin stores first

then plasma iron

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21
Q

B12 defiency causes build up of

A

homocystein and methylmalonic acid

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22
Q

folate deficiency seen in

A

pregnancy

*lack of it causes NTD

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23
Q

causes CNS problems

A

b12–> methylmanolic acid build up

b12 required to conver methylmanolic acid into succinyl coa

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24
Q

Tx of megaloblastic anemia with folate only leaves the risk of

A

not getting rid of CNS defects–> you will correct the anemia and think the pt is doing better–> but not
–> must make sure it is a pure folate deficicneyc before you just administer folate

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25
Q

describe B12 absorption

A

first bound to haptocorin (r binder) present in salive which travels to the jejunum where B12 is released from haptocorin by degrdation of pancreatic proteases–> then it is bound to IF in the jejunum (but IF is produced by the pareital cells in the stomach–> them Cobalamin + IF travel to the distal illeum where they are taken up by transcobalamin II

26
Q

tx of B12 deficiency

A

cyanocobalamin and hydroxocobalamin

27
Q

which b12 tx has longer half life

A

hydroxocobalamin

28
Q

B12 is stored in the

A

liver–> large reserve–> enough to last a vegan 5 years

29
Q

b12 defiiency causes folate to accumulate as

A

N methyl THF

  • folate is depleted over time
  • production of RBC’s slows
30
Q

B12 replacement therapy should always be

A

parenteral–> bc lack of it is usally due to malabsorption such as in pernitious anemia

31
Q

why is folate important–>

A

DNA SYNTHESIS–> converted to dTMP–> THYMINE eventually–> without it DNA synthesis stops and cell become megaloblastic

32
Q

Folate is stored

A

modest amounts in the body–> run out in a few months

33
Q

DHFR

A

converts folate to DHF–>THF

34
Q

folic acid is different than dietary folate how?

A

dietary folate must be demethylated

35
Q

toxicity associated with folic acid/ b12

A

none

36
Q

ESA’s used for anemias associated with

A
renal failure
primary bone marrow failure
anemia of cancer or chemo
HIV/AIDS
BMT
37
Q

EPO is produced by the

A

kidney

*renal failure= anemia

38
Q

list ESA’s

A

Epoietin alfa (recombinant human EPO)
darbepoietin alfa
Methoxy polyethylene glycol-epoitein beta
–>long-lasting EPO adminstered 2 x monthly

39
Q

ESA with longest half life

A

darbepoitein alfa

*glycosylated form of EPO

40
Q

most common ADE’s of ESA are

A

hypertension and thrombosis

41
Q

HGB concentration of ppl undergoing ESA tx should not exceed

A

12–> any higher and you get adevrse CV events

42
Q

Used to accelerate recovery of neutrophils after chemo

A

Gcsf- neutrophils specifically and majorly HSC’s

GMCSF–> all granulocytes and minimally Hematopoietic Stem Cells

43
Q

What should you give a pt who has just gotten autologous stem cell transplant

A

Gcsf–. reduces tim to engraftment and increases neutrophils

44
Q

Hematopoietic stem cell mobilozer

A

plerixafor–> inhibitor of CXCR4

May be combined with GCSF in myeloma pt.s who do not respond well to just GCSF

45
Q

used to mobilize HSC’s prior to allogenic or autologous HSCT

A

GCSF

46
Q

side effects of GSCF

A

minimal bone pain

47
Q

side effects of GMCSF

A

fever, arthralgias, capillary damage

48
Q

GCSF formulation with with longer

A

pegfilgrastim

49
Q

Stimulates growth of megakryocytes

A

Oprevelkin IL-11

50
Q

indications for Oprevelkin

A

pt.s with thrombocytopenia following chemo–> reduces need for platelet transfusions

51
Q

TPO receptor agonist

A

romiplastin

eltrompobag

52
Q

TPO receptor

A

c-MPL

53
Q

ROute and indication for Romiplastin

A

Sub-Q

*pt’s with ITP who have responded poorly to conventional tx

54
Q

Route and indication for eltropobag

A

oral

*ITP with poor response to conv. tx

55
Q

major toxicity of eltropbag

A

hepatotoxicity

56
Q

TPO is made in the

A

liver and kidney

57
Q

EPO WORKS THROUGH

A

jak2 signaling cascade

58
Q

ESAs should be used only in patients with cancer

A

–>treating anemia specifically caused by chemotherapy, and not for other causes of anemia. Further, it states that ESAs should be discontinued once the patient’s chemotherapy course has been completed.

59
Q

ESA’S SHOULD NOT BE USED

A

for anemia that exists outside of the chemotherapy given to the pt.

60
Q

darbepoietin contraindicated in

A

pt.’s with preexisting HTN