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Adv Pharm 1 > Anemia (pt 1/3) Iron, B12, Folic Acid, IL > Flashcards

Anemia (pt 1/3) Iron, B12, Folic Acid, IL Flashcards

1
Q

What is Hematopoiesis?

A

Process by which RBCs are made
-happens in the bone marrow

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2
Q

_____+ _____ = Hematopoietic Cell

A

Essential Nutrients + Growth Factors = Hematopoietic cells

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3
Q

What are the Essential Nutrients?

A

Iron
Vitamin B12
Folic Acid

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4
Q

What is a Hematopoietic Cell?

A

Immature cell that can develop into all types of blood cells

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5
Q

What is the most common cause of anemia?

A

Iron Deficiency

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6
Q

How do we get iron?

A

-Iron is recycled from damaged RBCs (don’t need a large intake usually)
-Only a small amount of iron is lost each day therefore dietary requirements are low

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7
Q

Iron requirements increase in what situations?

A

-Growing children
-Pregnant women
-Menstruating women

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8
Q

What is Hepcidin?

A

A peptide produced primarily by the liver.
-Regulates the absorption, transport and storage of iron.

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9
Q

How does low iron cause anemia?

A

-Iron forms the nucleus of the iron-porphyrin heme ring → hemoglobin
-↓iron = small RBCs with insufficient hemoglobin
-Microcytic (small) Hypochromic (less red) Anemia

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10
Q

What are S/Sx of Iron Deficiency?

A

-Fatigue, weakness
-pale/yellowish skin
-Dizziness/lightheadedness
-Irregular heartbeat
-Shortness of Breath
-Cold hands/feet
-Chest pain
-HA

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11
Q

What kind of anemia does low Iron cause?

A

Microcytic, Hypochromic

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12
Q

What are the laboratory abnormalities associated with Iron-deficiency anemia?

A

-Low serum Fe (<30 mcg/dl), increased transferrin iron-binding capacity
-% Transferrin saturation of <10%
-Low serum ferritin levels (stored iron) <20 mcg/L

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13
Q

What type of anemia occurs with Folic Acid Deficiency?

A

-Macrocytic Normochromic Anemia

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14
Q

What are the laboratory abnormalities associated with Folic Acid Deficiency Anemia?

A

Low Serum Folic Acid level
-< 4 ng/mL

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15
Q

What type of anemia occurs with Vitamin B12 deficiency?

A

-Macrocytic Normochromic Anemia

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16
Q

What are the laboratory abnormalities associated with Vitamin B12 deficiency anemia?

A

-Low Serum Cobalamin
-Increased Serum Homocysteine
-Increased Serum Methylmalonic Acid
-Increased Urine Methylmalonic Acid

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17
Q

What is Serum Homocysteine?

A

-Can be used to establish a diagnosis of Vit B12 deficiency.
-Methylcobalamin is required for the conversion of homocysteine to methionine.
-B12 deficiency decreases the formation of methylcobalamin, thereby increasing homocysteine levels (because it’s not being used to convert).

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18
Q

What is the stored form of Iron?

A

Ferritin

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19
Q

How is iron transported into the blood?

A

By Ferroportin (Fp)

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20
Q

How is iron actively transported in the blood?

A

By Transferrin (Tf)

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21
Q

In the blood, what are the two locations iron is transported to?

A

1) Erythroid precursors in the bone marrow for synthesis of hemoglobin
2) Hepatocytes for storage as Ferritin

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22
Q

How is iron reclaimed after it is used?

A

Macrophages that phagocytize senescent (old) erythrocytes (RBC) reclaim the iron (in the spleen or other tissues, macrophages) from the RBC hemoglobin and either export it or store it as ferritin.

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23
Q

What offers negative feedback by inhibiting ferroportin (the active transporter than pulls iron into the blood)?

A

High hepatic iron stores increase hepcidin synthesis, and hepcidin inhibits ferroportin (the active transporter)

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24
Q

What conditions require additional iron therapy?

A

-Infants especially premature infants
-Children during rapid growth periods
-Pregnant and lactating women
-Chronic Kidney Disease (2/2 RBC loss during hemodialysis)
-Inadequate absorption: Malabsorption post-gastrectomy for pts with severe small bowel disease; Normal process of iron function occurs in intestinal epithelial cells.
-Blood loss (Most common cause of iron deficiency anemia in adults):
Menstruating women lose 30 mg of iron with each menstrual period. Those with heavy bleeding can lose much more.

In men/post-menopausal women, the most common site of bleeding is the GI tract.

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25
Q

Describe the facts regarding the Ferrous Salts (Sulfate/Gluconate/Fumarate)?

A

-Oral or IV iron preparations
-PO corrects anemia just as rapidly and completely as parenteral IF iron absorption from the GI tract is normal (malabsorption issues = use IV form)
-Continue for 3-6 months so we don’t rapidly go back to anemia (replenishes iron stores)
-For patients on dialysis, IV therapy is preferred

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26
Q

What are the adverse effects associated with the Ferrous Salts (Sulfate/Gluconate/Fumarate)?

A

Dose related:
-Lower the dose
-Take with/after meals
-Change preparations

Nausea, epigastric discomfort, ABD cramps, constipation, diarrhea

Black stools:
-Not clinically significant
-May obscure GI bleed

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27
Q

What is Parenteral Iron Therapy (Iron Dextran) reserved for?

A

Reserved for patients with documented iron deficiency who are unable to tolerate or absorb oral iron.
-Pts with extensive chronic anemia who cannot be maintained with oral iron alone
-Advanced chronic kidney disease on requiring hemodialysis
-Post-gastrectomy patients
-Inflammatory bowel disease of the small bowel
-Malabsorption Syndromes

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28
Q

Why is the IV route preferred over IM for iron therapy?

A

IV is preferred – eliminates pain, tissue staining and allows full dose administration (absorb 100% of the dose).

IM is painful, stains tissue, and has limits in dosing.

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29
Q

What are the adverse effects associated with Parenteral Iron therapy?

A

HA
dizziness
fever
arthralgias
nausea, vomiting
back pain
flushing
urticaria
bronchospasm
anaphylaxis
death

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30
Q

What are two formulations in clinical use for Parenteral Iron therapy?

A

Low Molecular Weight Form
-INFed

High Molecular Weight Form
-Dexferrum

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31
Q

Inorganic free ferric iron has serious ______ _____________ toxicity.

A

Inorganic free ferric iron has serious dose dependent toxicity.

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32
Q

What are the special formulations of parenteral iron therapy?

A

-Colloid containing particles
-Iron Dextran: Risk of hypersensitivity reaction
-Sodium Ferric Gluconate Complex
-Iron-sucrose Complex

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33
Q

What is important to know about the Colloid containing particles (Parenteral Iron therapy)?

A

Colloid containing particles = stability and slow release of bioactive iron
Core of Oxyhydroxide surrounded by a core of Carbohydrate

34
Q

What is important to know regarding Iron Dextran?

A

-Risk of hypersensitivity reaction increases with repeated treatments or strong history of allergy
-Clinical anecdotal evidence indicates that the risk of anaphylaxis is largely associated with the HIGH Molecular Weight Forms!!

35
Q

Why do you need to monitor iron STORAGE levels during parenteral Iron therapy? (Blue Box!!)

A

-Monitor Iron Storage Levels!
-IV therapy bypasses the regulatory mechanism provided by instestinal uptake.
-IV can deliver more iron than can be safely stored.

36
Q

How can acute Iron Toxicity occur?

A

Children that ingest iron tablets
-10 tablets of any of the oral iron preparation can be lethal to young children

37
Q

What are the S/Sx of ACUTE Iron Toxicity?

A

-Necrotizing gastroenteritis
-vomiting
-ABD pain
-bloody diarrhea
-shock
-lethargy
-dyspnea
-Metabolic acidosis
-coma
-death

38
Q

What is the antidote for acute iron toxicity?

A

Deferoxamine

39
Q

How does Deferoxamine work?

A

A binding agent usually administered IV.
-Binds to iron that has not been absorbed.
-Excreted in urine and feces

40
Q

What is the other name for chronic iron toxicity (iron overload)?

A

Hemochromatosis (Excess iron in the organs: heart, liver, pancreas, etc)

41
Q

How can chronic iron toxicity occur?

A

Can be inherited or develop in pts who receive a lot of RBC transfusions over a long period of time (Beta thalassemia)
-Can lead to organ failure and death

42
Q

What is the treatment for chronic iron toxicity?

A

-Intermittent phlebotomy is used for patients with chronic iron overload in the absence of anemia (remove 1 unit blood/week)
-For patients with refractory anemia (Ex. Thalassemia major, sickle cell, aplastic) chelation therapy is the better option: More complicated, expensive and hazardous

43
Q

What are the drugs used in Iron Chelation Therapy?

A

-Deferoxamine (IV)
-Deferasirox (PO)
-Deferiprone (PO)

44
Q

What is Vitamin B12?

A

-Also called Extrinsic Factor
(Intrinsic Factor is a protein secreted by the stomach that is required for GI uptake of Vit B12)
-Cofactor for several essential biochemical reactions in humans
-Deficiency leads to megaloblastic anemia, GI symptoms and neurologic abnormalities

45
Q

What are the symptoms of Vitamin B12 Deficiency?

A

-Often associated with mild to moderate leukopenia or thrombocytopenia

Neuro symptoms: (unique)
-Paresthesias in peripheral nerves
-Weakness progressing to spasticity, ataxia, other CNS dysfunction
-Treatment will stop the progression of neuro symptoms but may not reverse it

46
Q

What are the causes of Vitamin B12 deficiency?

A

Usually malabsorption.
-Deficiency due to inadequate diet (less common, can occur in older adults)
-Inadequate absorption
-Gastrectomy: Needs therapy for life

Common Causes:
-Pernicious anemia – caused by defective secretion of Intrinsic Factor from gastric mucosal cells
-Partial or Total gastrectomy
-Malabsorption Syndrome
-Inflammatory Bowel Disease
-Small Bowel Resection
-Strict Vegan Diet
-Congenital deficiency of intrinsic factor

47
Q

What are the chief dietary sources of Vitamin B12?

A

Meat
Eggs
Dairy products

48
Q

What are the Vitamin B12 options administered as treatment?

A

Cyanocobalamin
Hydroxycobalamin

49
Q

Which form of Vitamin B12 is preferred?

A

-Hydroxycobalamin
-Preferred b/c highly protein bound = longer circulation time

50
Q

Why is Folic Acid necessary?

A

Folic Acid = Pteroylglutamic Acid (Vit B9)
-Required for essential biochemical reactions that provide precursors for the synthesis of amino acids, purines and DNA.

51
Q

What are sources of Folic Acid?

A

-Various forms of folic acid are present in a wide variety of plant and animal tissues.
-Richest sources are yeast, liver, kidney and green vegetables.
-5-10 mg of folates is stored in the liver and other tissues
-Excreted in the urine/stool, and destroyed by catabolism → serum levels fall within a few days when intake is diminished

52
Q

What are causes of Folic Acid Deficiency?

A

Common and easily corrected. Often the result of poor diet, inadequate intake or diminished hepatic stores.
-Pregnancy
-Alcohol dependence
-Liver disease
-Renal dialysis patients
-Malabsorption syndromes
-Methotrexate therapy (deficiency of folate cofactors)

53
Q

T/F: PO Folic Acid therapy is not absorbed in patients with Malabsorption.

A

False; PO folic acid is well absorbed, even in pts with malabsorption.

54
Q

What does Folic Acid Deficiency cause?

A

-Causes megaloblastic anemia that is microscopically indistinguishable from that caused by Vit B12 deficiency
-Does not cause the neuro symptoms seen in Vit B12 deficiency
-Definitive cause determined by labs especially RBC folate levels

55
Q

What is the treatment for Folic Acid Deficiency (Megaloblastic Anemia)?

A

-1mg PO daily → reverse Megaloblastic Anemia
-Restore serum folate levels & replenish stores
-Prevention therapy with oral supplementation is recommended for high-risk patients

56
Q

T/F: We store a lot of Folic Acid in our bodies, so it never really becomes deficient.

A

False; Stores are relatively low compared to the high daily requirement = folic acid deficiency and anemia can develop within 1-6 months after ↓intake

57
Q

What are Hematopoietic Growth Factors?

A

Glycoprotein hormones that regulate the proliferation and
differentiation of hematopoietic progenitor cells in the bone marrow.

58
Q

What eventually becomes RBCs?

A

Erythropoietin (epoetin alfa & epoetin beta)

59
Q

What eventually becomes WBCs?

A

Granulocyte Colony-Stimulating Factor (G-CSF)

60
Q

What eventually becomes platelets?

A

Interleukin-11 (IL-11)

61
Q

What is Recombinant DNA Technology?

A

-Uses enzymes to cut and paste together DNA sequences of interest. For creation of blood component growth factors.
-The recombined DNA sequences can be placed into vehicles called vectors that ferry the DNA into a suitable host cell where it can be copied or expressed.

62
Q

What was the first human hematopoietic growth factor to be isolated?

A

Erythropoietin

63
Q

What is Erythropoietin?

A

-Originally purified from the urine of patients with severe anemia
-Glycoprotein that promotes RBC production
-Endogenous erythropoietin is produced in the kidney
-Inverse relationship between Hct/Hgb levels and serum erythropoietin levels
-Normal serum erythropoietin < 20 IU/L
-Mod-severe anemia = 100-500 IU/L
-Severe anemia can be in the 1000s
-Kidney disease is the exception to the inverse relationship
-Binds to specialized receptors on red cell progenitors
-Induces release of reticulocytes (immature RBCs) from the bone marrow
-Commonly used by endurance athletes to enhance performance

64
Q

What is Recombinant Human Erythropoietin?

A

(rHu-EPO, epoetin alpha)

Produced by mammalian cell expression system.

65
Q

What are the uses for Erythropoietin Stimulating Agents (ESAs)?

A

-Treat anemia secondary to chronic kidney disease
-↓RBC transfusion in myelosuppressive cancer treatments
-Myelodysplastic Syndrome
-Anemia requiring blood transfusions
-Pts with serum erythropoietin levels < 100 IU/L have the best response

66
Q

What are the toxicity effects associated with Erythropoietin Stimulating Agents (ESAs)?

A

-HTN
-Thrombotic complications ↑ with Hgb > 11 g/dL (makes blood viscous)
-Allergic reactions are rare
-Long term SQ administration can cause pure red cell aplasia (PRCA)

67
Q

What are the 3 example drugs of the Erythropoietin Stimulating Agents (ESAs)?

A

1) Epoetin Alpha (3 x’s per week)
-Half-life 4-13 hours in CRF Pts
-Not cleared by dialysis

2) Darbepoetin Alpha (weekly)
-Modified erythropoietin
-↑ glycosylation
-2-3 times longer half-life

3) Methoxy Polyethylene Glycol-Epoetin Beta (every 2 wks or monthly)
-Isoform of erythropoietin
-Extensive half-life
-IV or SQ

68
Q

What are the effects of the Erythropoietin Stimulating Agents (ESAs)? (Blue Box!)

A

Blue Box:
-Reticulocyte counts ↑ in 10 days
-Hgb & Hct ↑in 2-6 wks
-Target Hgb is pt specific (No greater than 10-12 g/DL)
-CKD Pts require PO or parenteral Iron supplements
-Folic Acid supplements PRN

Not in Blue box:
-Conservative use in cancer patients with Hgb < 10 and not to exceed 11g/dL in CKD pts.
-Hgb should kept at the lowest dose necessary to avoid transfusion (don’t overcorrect)
-Do not use when cancer therapy is curative

69
Q

What is the MOA of the G-CSF and GM-CSF?

A

Cause differentiation and proliferation by agonism of myeloid progenitor cells.

70
Q

What are Myeloid Growth Factors?

A

-Myeloid = bone marrow
-Subclass of Hematopoietic Growth Factors
-Includes Granulocyte Colony Stimulating Factor (G-CSF) and Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF)
-Originally purified from cultured human cells
-Currently recombinant
-Half-lives are 2-7 hours
-Admin either IV or SQ
-Recombinant human G-CSF (rHuG-CSF, Filgrastim or Tbo-Filgrastim) is produced in a bacterial suspension system
-Pegfilgrastim = conjugation product of Filgrastim with polyethylene glycol has a longer half-life
-Lenograstim = used in Europe
-Recombinant human GM-CSF (rHuGM-CSF, Sargramostim) is produced in a yeast expression.

71
Q

What does G-CSF do?

A

-Promotes differentiation of neutrophils
-Activates phagocytic actions of mature neutrophils
-Mobilizes peripheral blood stem cells (Allows for transplantation of peripheral blood stem cells vs. bone marrow)

72
Q

What does GM-CSF do?

A

-Broader actions than G-CSF
-Early & late granulocytic progenitors
-Erythroid & megakaryocyte progenitors
-Stimulates mature neutrophils
-Works with IL-2 on T-cells
-Mobilizes peripheral blood stem cells (↓efficacy & ↑ toxicity versus G-CSF)

73
Q

What does G-CSF therapy in Chemotherapy induced Neutropenia do?

A

-Accelerates the rate of neutrophil recovery after dose-intensive myelosuppressive chemotherapy
-Reduces the duration of neutropenia
-Raises the nadir (lowest neutrophil count seen following a cycle of chemotherapy.)
-↓ episodes of febrile neutropenia (not true with GM-CSF because it itself can cause a fever).
-↓ requirements for broad spectrum antibiotics
-↓ infections
-↓ days of hospitalization

Used as Preventative therapy for pt’s receiving regimens with high risk for febrile neutropenia.
However, Clinical trials did not show improved survival in cancer patients treated with G-CSF.

74
Q

What are the uses for G-CSF and GM-CSF?

A

-Congenital Neutropenia
-Cyclic Neutropenia
-Myelodisplasia
-Aplastic Anemia
-Autologous Stem Cell Transplant

75
Q

Do G-CSF or GM-CSF stimulate the formation of erythrocytes and platelets? (Blue Box!)

A

Neither G-CSF nor GM-CSF stimulates the formation of erythrocytes and platelets, they are sometimes combined with other growth factors for treatment of pancytopenia.

76
Q

What are the limits of use of G-CSF and GM-CSF?

A

-G-CSF and Pegfilgrastim are more used more frequently than GM-CSF. All have similar effects on neutrophil counts but G-CSF generally tolerated better
-G-CSF and Pegfilgrastim can cause bone pain. Clears when the drug is discontinued
-GM-CSF causes more severe side effects (Fever, malaise, arthralgias, myalgias and capillary leak syndrome (peripheral edema and pleural or pericardial effusions) )
-Allergic reactions are infrequent
-Splenic rupture is a rare but possible complication when G-CSF is given for autologous stem cell transplant

77
Q

What does Interleukin 11 (IL-11) do?

A

-Stimulates the growth of multiple lymphoid and myeloid cells
-Acts in conjunction with other growth factors: Stimulating the growth of megakaryocytic progenitors
-↑peripheral platelets
-↑neutrophils

78
Q

What is Megakaryocyte Growth Factor?

A

-Megakaryocyte are vital to the production of platelets
-Subclass of Hematopoietic Growth Factors
-Natural protein produced in the bone marrow by fibroplasts and stromal cells
-Oprelvekin = recombinant IL-11 produced by expression in Escherichia coli.
-Half-life 7-8 hours
-Administered SQ at 50 mcg/kg daily
-Given daily for 14-21 days or until the platelet count rises to more than 50,000/µL
-Use the smallest dose to keep platelets counts > 50,000/µL

79
Q

What are the uses of Interleuken-11 (IL-11)?

A

-Prevention of thrombocytopenia in chemotherapy pts (Only in non-myeloid cancers)
-↓Platelet transfusions between chemotherapy cycles (Started 6-24 hours after chemo)
-No benefit on leukopenia due to myelosuppressive chemotherapy

80
Q

What are the adverse effects associated with Interleuken-11 (IL-11)?

A

-Fatigue, headache, dizziness
-Anemia due to hemodilution
-Dyspnea due to fluid accumulation in the lungs
-Transient a-fib
-Hypokalemia
-All adverse effects are reversible!!

81
Q

T/F: The adverse effects associated with Interleuken-11 are irreversible.

A

False; All adverse effects with IL-11 are reversible!!

Adv Pharm 1 (28 decks)

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