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Renal, Hematological, and Cardiovascular Organ Systems > Pharmacology- Anemia/ Hematopoietics (word document) > Flashcards

Pharmacology- Anemia/ Hematopoietics (word document) Flashcards

1
Q

What are the most common causes of Chronic anemia?

A

Iron Deficiency

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2
Q

What are the symptoms of iron deficiency?

A 
Pallor
fatigue
dizziness
exertional dyspnea
generalized symptoms of tissue hypoxia
cardiovascular adapatations
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3
Q

What are teh cardiovascular adaptations to chronic anemia?

A

tachycardia
increased cardiac output
vasodiliation

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4
Q

What is microcytic hypochromic anemia caused by?

A

inadequate iron, small hemoglobin-deficient erythrocytes are formed

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5
Q

What are the iron therapy drugs?

A

Ferrous Iron
Ferrous Sulfate
Ferrous Fumarate
Iron Dextran

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6
Q

What are the oral iron therapies?

A

ferrous Iron, Ferrous Sulfate, Ferrous Fumarate

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7
Q

What is the most efficiently absorbed oral iron therapies?

A

Ferrous Iron

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8
Q

What are the toxic effects of oral therapy?

A 
nausea, 
epigastric discomfort
abdominal cramps
constipation 
diarrhea
black stools
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9
Q

How can the adverse effects or oral iron be controlled?

A 
dose-related, so lower dose
take with food
change preparations (various iron salts)
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10
Q

What is the dosing regimen with oral iron?

A

200-400 mg given daily

continued for 3-6 mo after correction of CAUSE of iron deficiency

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11
Q

Why should you use parenteral iron therapy>

A

if a pts does not tolerate oral dosing or has extensive chronic anemia and is not able to maintain with oral iron alone

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12
Q

What are the treatment challenges for iron deficiency?

A

parenteral administration of inorganic free ferric iron produces serious dose-dependent toxicity (severly limits the does that can be used)

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13
Q

How is iron dextran given?

A

IV or IM

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14
Q

What are the toxic effects of parenteral therapy for iron deficiency?

A 
headache
light-headedness
fever
arthralgias
nausea 
vomiting
back pain
flushing 
urticaria
broncohospasm
rarely anaphyslaxis and death
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15
Q

What should always be done with iron dextran to prevent anaphylaxis?

A

small test does given

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16
Q

How can iron stores be estimated?

A

based on serum concentrations of ferritin and transferrinn saturation (TIBC)

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17
Q

What is acute iron toxicity and why does it occur in young children?

A

iron tablets look like candy and as few as 10 can be fatal!!

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18
Q

What are the detoxification that can be done for iron toxicity?

A

whole bowel irrigation

deferoxamine (a potent iron-chelating compound)

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19
Q

What can be done for chronic iron toxicity?

A

Deferasiorx (in OJ) to help with iron overload due to multiple transfussions

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20
Q

What symptoms are associated with deferasirox?

A 
diarrhea
nausea
abdominal pain 
headache
pyrexia
cough
increased serum creatinine and hepatic enzyme levels
auditory and visual disturbances
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21
Q

What is the most efficeint tx of chronic iron overal in the absence of anemia?

A

Phlebotomy- 1 unit of blood removed per week

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22
Q

What is Vit B12?

A

a cofactor for essential biochemical rxns (mbod relations MTHF rxns) methionine synthasze, methylomalonyl CoA to succinyl CoA

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23
Q

What does the deficiency of Vit B12 result in?

A

megaloblastic anemia gastrointestinal symptoms and neurological abnormalities

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24
Q

What are the symptoms of Vit B12 deficiency?

A

Megaloblastic
Macrocytic Anemia (mild or moderate leukopenia or thromobocytopenia)
neurological syndrome
hematologic anormalites

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25
Q

What are the common causes of Vit B12 deficiency?

A

pernicious anemia
partial or total gastrectomy (effectign distal ileum)
Rare: bacterial overgrowth, chronic pancreatitis, thyroid disease, congenital deficiency of IF or IF receptor sites)

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26
Q

What are the treatments for Vit B12 deficiency?

A

Parenteral therapy (IM)
with cyanocobalamin
hydroxocobalamin

27
Q

Which Vit B12 drug is preferred and why?

A

hydroxocobalamin
more highly protein-bound
remains longer in circulation

28
Q

What forms of Folic Acid are used for essential biochemical rxns?

A

reduced forms

29
Q

What does folic acid give precursors for?

A

sysnthesis of amino acids, purines and DNA

30
Q

Where is folic acid deficiency found and is it common?

A

it is common
-alcoholics and pts with liver disease
-poor hepatic storage of folate
pregnant women and pts with hemolytic anemia have increased requirements
-pts with malabsorption syndromes
-renal dialysis removes folate from the plasma

31
Q

What are the oral therapies for folic acid deficiecny?

A
  • high absorption even in pts with malabsorption
  • -1mg folic acid daily
  • continue therapy until the underlying cause of folate deficiency is repaired
32
Q

What are the drug induced folate deficiencies caused by?

A

Methotrexate

  • trimethoprim (antimicrobial)
  • pryimethamine (anitmalarial)
  • phenytoin (antiepileptic agent)
33
Q

What drug can reverse the folate deficiency caused by MTX? and what else dose it do?

A

Leucovorin; also modulates the effect of fluorouracil,

34
Q

What is the importance of folate and depression relationship??

A

the results demonstrate an association b/n the dietary intake of folate, magnesium and zine and depressive illnesses, although reverse causality and or confounding cannot be rule out as explanation.

35
Q

what is levomofolate and what does it do?

A

9methylenetetrahydorfolate reductase) is bioactive form of folate found in circulation after MTHFR enzymatic reduction and it is then able to be transported across cell membranes and receptors-mediated endocytosis
-it can cross BBB and moulate the formation of monamine serotonin, and norepinephrine and dopamine

36
Q

What is eopetin alpha?

A

an EPO receptor agonist, and stimulated erythroid proliferation and differentiation and induces the release of reticulocytes from the BM

37
Q

What id darbepoetin alpha?

A

the long acting glycosylated form of epoetin alpha administered weekly

38
Q

what is methoxy polethylene glycol-epoetin beta?

A

the long-acting form administered 1-2x a mo

it is PEGelated… it extends the PKs of the drug and reduce the need for so frequent a re-dosing

39
Q

What is the EPO receptor properties?

A

a member of JAK/STAT superfamily of cytokine receptros, and use protein phosphorylationa dn transcription factor activation to regulate cellular function

40
Q

What are the effects of erythropoietin?

A

to stimulate erythroid proliferation adn differnetation by interacting with EPO R on RBC progenitors
induces release of reticulocytes from bone marrow

41
Q

Where is EPO produced and why?

A

in the kidney in response to tissue oxygenation levels (hypoxic conditions)

42
Q

That is different about the response of EPO in renal failure pts?

A

they have v EPO levels

  • most likely to respond to tx with exogenous EPO
  • ^ EPO levels in most BM dissorders adn nost nutritional and secorndary anemias
  • folate and or iron supp. may be necessary
43
Q

What are some of the BM disorders?

A

aplastic anemia, leukemias, myeloproliferative adn myelodysplastic disorders

44
Q

What are the toxcites of EPO?

A
  • Chronic Kidney Disease
  • use lowest dose sufficient to reduce the need for RBS transfusions
  • Cancer!!
  • increase the risk of tumor progression in some clinical pts.
  • duet o increased risk of DVT– DVT prophylaxis recommended!!!!
45
Q

What are the non-life threatening AE of EPO?

A
  • most likely:
    • Hypertension
  • -Headache
  • -Arthralgias
  • -Nausea
  • Less likely:
  • -Edema
  • -Fatigue
  • -Dirarrhea
  • -Vomiting
  • Asthenia
  • -Chest Pain
  • -Disxxiness
  • -Skin rxns at injection site
  • -Seizures
46
Q

Why is EPO banned by the international Olympic committee?

A

the use of RPO by athletes is bsed on that it could ^ RBC concentration and will ^ o2 delivery to muscels and improve performace

47
Q

What is the relationship of EPO and zidovudine>

A

EPO helps to off set the anemia produced by zidovudine in HIV infected pts

48
Q

What is the myeloid growth factors?

A

G and GM-CSF

49
Q

What does G-CSF do?

A

it stimulates proliferationa nd differentiation of progenitors already committed to the neutrophil lineage

  • activated the phagocytic activity of mature neutrophils and prolongs their survival in the circulation
  • mobilizes hematopoietic stem cells, to increase their concentration in peripheral blood
50
Q

What does GM-CSF do?

A

has a broader biologic action than G-CSF, it has a mulitpotential hematopoietic growth factor, and stimulates proleration and diffenentiation of early and late granulocytic progenitor cells; erythroid an dmegakaryocyte progenitors
- also stimulates faction of mature neutrophils

51
Q

Where is GM-CSF active?

A

locally active factor at the site of inflammation

52
Q

What growth factor stimualtes PBSCS mobilization best?

A

G-CSF > GM-CSF

53
Q

How does the myeloid growth factors stimulate T-cell proliferation?

A

acting together with IL-2

54
Q

What affect does G-CSF have on neutrophils?

A

accelerates the rate of neutorphil recovery after dose-intensive myelosuppressive chemotherapy

55
Q

What is the drug names for G-CSF?

A 
filgrastim 
pegfilgrastim (the long-acting from of filgrastim that is covalently liked to a type of polyethylene glycol)
56
Q

What is the drug names for GM-CSF?

A

Sargramostim

57
Q

What are the clinical utilities of G-CSF?

A

• Neutropenia associated with congenital neutropenia, cyclic neutropenia,
myelodysplasia, and aplastic anemia
• In autologous stem cell transplantation for patients undergoing high-dose
chemotherapy
o High doses of chemotherapy are necessitated by the resistance of the tumor
cell population
o Myelosuppression is then counteracted by reinfusion of the patient’s own
hematopoietic stem cells (which are collected prior to chemotherapy)
• Mobilization of PBSCs
o PBSCs have largely replaced bone marrow as the hematopoietic preparation
used for autologous transplantation

58
Q

What are the toxcicities for G-CSF, pegfilgrastim and GM-CSF?

A

• All 3 factors (G-CSF, pegfilgrastim & GM-CSF) have similar effects on neutrophil
counts
o G-CSF, pegfigrastim are better tolerated
• Bone pain upon discontinuation
• G-CSF and pegfilgrastim are used more frequently
• More severe side effects with GM-CSF, particularly at higher doses
o Fever, malaise, arthralgias, myalgias, and a capillary leak syndrome
characterized by peripheral edema and pleural or pericardial effusions
o Allergic reactions may occur but are infrequent
o Splenic rupture is a rare but serious complication of the use of G-CSF for
PBSC

59
Q

What are the kegakaryocyte growth factor drugs?

A

Oprelvkin (IL-11)

60
Q

What does oprelvkin do?

A

stimulates megakaryocytopiesis and thromboipiesis

  • binds to IL-11 R on megakaryocytes and their progenitor cells (interact through a family of cytokin receptors with ar all capable of interacting with singnal transducing receptor gp130
  • induces megakaryocyte maturation resulting in increased platelet production
  • to increase platelet cound!!
61
Q

What are the toxicites of oprelvekin?

A

• Most commonly: fatigue, headache, dizziness
• Cardiovascular effects
o Anemia (due to hemodilution)
o Dyspnea (due to fluid accumulation in the lungs)
o Transient atrial arrhythmias
• Hypokalemia has also been seen in some patients
• All of these adverse effects appear to be reversible

62
Q

What is Romiplostin?

A

a genetically engineered protein from E. Coli that the Fc component of a human antibody is fused to two copies of a peptide that stimulates the throbopoietin receptros; approved for tx of idiopathic throbocytopenic purpua (ITP)

63
Q

What are the properties of romiplostin??

A

• Thrombopoietin-mimetic Fc-peptide fusion protein (peptibody)
• Contains two identical single-chain subunits, each consisting of human
immunoglobulin IgG1 Fc domain (constant region), covalently linked at the C-terminus to two identical peptide sequences that each bind and activate the TPO
receptor
• Fc component of the romiplostim peptibody extends the half-life
o Remains active in the circulation much longer than endogenous TPO
o Eventually removed by the reticuloendothelial system

Renal, Hematological, and Cardiovascular Organ Systems (9 decks)

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