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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
What are the common causes of Vit B12 deficiency?
pernicious anemia partial or total gastrectomy (effectign distal ileum) Rare: bacterial overgrowth, chronic pancreatitis, thyroid disease, congenital deficiency of IF or IF receptor sites)
26
What are the treatments for Vit B12 deficiency?
Parenteral therapy (IM) with cyanocobalamin hydroxocobalamin
27
Which Vit B12 drug is preferred and why?
hydroxocobalamin more highly protein-bound remains longer in circulation
28
What forms of Folic Acid are used for essential biochemical rxns?
reduced forms
29
What does folic acid give precursors for?
sysnthesis of amino acids, purines and DNA
30
Where is folic acid deficiency found and is it common?
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
What are the oral therapies for folic acid deficiecny?
- high absorption even in pts with malabsorption - -1mg folic acid daily - continue therapy until the underlying cause of folate deficiency is repaired
32
What are the drug induced folate deficiencies caused by?
Methotrexate - trimethoprim (antimicrobial) - pryimethamine (anitmalarial) - phenytoin (antiepileptic agent)
33
What drug can reverse the folate deficiency caused by MTX? and what else dose it do?
Leucovorin; also modulates the effect of fluorouracil,
34
What is the importance of folate and depression relationship??
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
what is levomofolate and what does it do?
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
What is eopetin alpha?
an EPO receptor agonist, and stimulated erythroid proliferation and differentiation and induces the release of reticulocytes from the BM
37
What id darbepoetin alpha?
the long acting glycosylated form of epoetin alpha administered weekly
38
what is methoxy polethylene glycol-epoetin beta?
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
What is the EPO receptor properties?
a member of JAK/STAT superfamily of cytokine receptros, and use protein phosphorylationa dn transcription factor activation to regulate cellular function
40
What are the effects of erythropoietin?
to stimulate erythroid proliferation adn differnetation by interacting with EPO R on RBC progenitors induces release of reticulocytes from bone marrow
41
Where is EPO produced and why?
in the kidney in response to tissue oxygenation levels (hypoxic conditions)
42
That is different about the response of EPO in renal failure pts?
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
What are some of the BM disorders?
aplastic anemia, leukemias, myeloproliferative adn myelodysplastic disorders
44
What are the toxcites of EPO?
- 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
What are the non-life threatening AE of EPO?
- most likely: - - Hypertension - -Headache - -Arthralgias - -Nausea - Less likely: - -Edema - -Fatigue - -Dirarrhea - -Vomiting - Asthenia - -Chest Pain - -Disxxiness - -Skin rxns at injection site - -Seizures
46
Why is EPO banned by the international Olympic committee?
the use of RPO by athletes is bsed on that it could ^ RBC concentration and will ^ o2 delivery to muscels and improve performace
47
What is the relationship of EPO and zidovudine>
EPO helps to off set the anemia produced by zidovudine in HIV infected pts
48
What is the myeloid growth factors?
G and GM-CSF
49
What does G-CSF do?
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
What does GM-CSF do?
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
Where is GM-CSF active?
locally active factor at the site of inflammation
52
What growth factor stimualtes PBSCS mobilization best?
G-CSF > GM-CSF
53
How does the myeloid growth factors stimulate T-cell proliferation?
acting together with IL-2
54
What affect does G-CSF have on neutrophils?
accelerates the rate of neutorphil recovery after dose-intensive myelosuppressive chemotherapy
55
What is the drug names for G-CSF?
``` filgrastim pegfilgrastim (the long-acting from of filgrastim that is covalently liked to a type of polyethylene glycol) ```
56
What is the drug names for GM-CSF?
Sargramostim
57
What are the clinical utilities of G-CSF?
• 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
What are the toxcicities for G-CSF, pegfilgrastim and GM-CSF?
• 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
What are the kegakaryocyte growth factor drugs?
Oprelvkin (IL-11)
60
What does oprelvkin do?
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
What are the toxicites of oprelvekin?
• 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
What is Romiplostin?
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
What are the properties of romiplostin??
• 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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