Anti Anemic Drugs Flashcards
(103 cards)
1
Q
What is hematopoiesis?
A
Formation of blood elements
2
Q
- cytosis
A
Too many cells
3
Q
-penia
A
too few cells
4
Q
Anemia=
A
Reduced circulating RBCs and/or hemoglobin concentration
5
Q
Leukopenia =
A
Reduced circulating WBCs or other possible immune cell type
6
Q
Thrombocytopenia =
A
reduced circulating platelets
7
Q
What are the classes of anti-anemics?
A
- Erythroid stimulating agents
- Iron preperations
- Vitamin B12 deficiencies
- Folic acid preperations
8
Q
What is the most common cause of chronic anemia?
A
Iron deficiency
9
Q
A patient that is iron deficient can have
A
Pallor, fatigue, dizziness, exertional dyspnea and tissue hypoxia
10
Q
The reduction in RBCs will decrease blood viscosity and lower vascular resistance. This will
A
increase venous return and promote and increase in cardiac output
11
Q
What anemias develop with an iron deficiency?
A
Microcytic, hypochromic
12
Q
Iron deficiency from malabsorption can be because of what?
A
GI disease, overuse of antacids, surgery
13
Q
What does Hepcidin do?
A
Block the absorption and release of iron from liver (prevents iron overload)
14
Q
What will block the production of hepcidin?
A
Low iron stores
15
Q
What is transferrin responsible for?
A
transporting iron throughout the circulatory system.
16
Q
Transferrin can be taken up by
A
bone marrow RBC precursor to help in the production of RBCs
17
Q
Where is iron stored and how is it released?
A
In liver and can be released through ferroportin
18
Q
In the spleen, what do tissue macrophages do?
A
Engulf dead RBCs and recycle the iron
19
Q
Very little iron is lost from the body and because of recylcing the requirments of iron can be achieved in most individuals through
A
balanced diet
20
Q
Where is iron absorbed?
A
In the lumen of GI through the DMT-1 channel. Iron can also be transported through heme carrier protein
21
Q
Oral iron therapy is only for those with
A
adequate GI absorption and do NOT have CKD and are recieving hemodialysis and treatment with erythropoietin
22
Q
For oral iron therapy, what is preferred?
A
Ferrous salts
23
Q
Pharmakokinetics of oral iron therapy
A
Iron stores could be depleted as well, therefore oral iron should be continued for 3-6 months after correction
24
Q
What are adverse effects of oral iron therapy?
A
- Hypersensitivity, GI distress, nausea, vomiting
- Black stools
- MUST keep out of reach for children (could cause necrotizing gastroenteritis, shock, metabolic acidoses)
25
Parenteral iron therapy should be reserved for what type of patients?
Those that cannot tolerate oral iron and for any pt with extensive anemia that cannot be maintained with oral iron alone
26
What are adverse effects of iron dextran?
Headache, fever, flushing, arthralgias, nausea, vomiting, staining of skin if given IM, possible anaphylazis
27
What are adverse effects of Ferumoxytol?
Hypotension, nausea, vomiting and abdominal discomfort, may interfere with MRI imaging (done prior to therapy). can also cause fatal allergic reactions (BLACK BOX)
28
What are adverse effects of iron sucrose?
Leg cramps, hypotension, nausea, vomiting and abdominal discomfort
29
Ferumoxytol has carbohydrate shell which is removed where?
by the reticuloendothelial system (allows iron to be stored as ferritin or released to transferrin)
30
Is test dose neeeded for ferumoxytol?
No
31
Is test dose needed for ferric gluconate?
Only for those with a possible hypersensitivity to iron
32
Dosing for ferric gluconate
125-250 mg IV over 60min; multiple doses repeated weekly
33
Max dose of ferric gluconate
1000 mg
34
What are adverse effects of ferric gluconate?
Transient hypertension, tachycardia, GI disturbances, muscle cramps, local site reactions
35
What is dose for ferric carboxymaltose?
750mg IV followed by second 750mg dose in >7days
36
Is test dose required for ferric carboxymaltose?
No
37
What are adverse effects of ferric carboxymaltose?
Nausea, transient hypertension, flushing, transient hypophosphatemia, dizziness, skin discoloration at injection site
38
Vitamin C is an
antioxidant that helps keep iron in the Fe2+ state (reduced state)
39
Vitamin C is a water-soluble vitamin that is a cofactor for
Proline hydroxylation and in collagen synthesis
40
What does Vitamin C assist in
absorption of iron
41
How is vitamin C given?
Only orally
42
What are drugs that decrease iron absorptions (therefore interact with Vit C)?
- Aluminum, magnesium and calcium-containing antacids
- Tetracycline and doxycycline
- histamine 2 antagonists
- Proton pump inhibitors
- Cholestyramine
43
What are drugs affected by iron?
- Levodopa (chelates with iron)
- Levothyroxine (decreases efficacy)
- Pencillamine (chelates with iron)
- Fluroquinolone (forms ferric ion quinolone complex)
- Tetracyclines (chelates with iron)
44
What are symptoms of acute iron toxicity?
GI damage, shock or cardiovascular collapse, hematochezia, liver failure, neurotoxicity
45
Who does acute iron toxicity tend to occur in?
children and infants (due to ingestion of iron tablets)
46
What should be done for an Acute iron toxicity?
Whole bowel irrigation to flush out unabsorbed pills
47
Would activated charcoal help in acute iron toxicity?
No- it does not bind iron and would be ineffective
48
Describe chronic iron toxicity
- Hemochromatosis- treat with phlebotomy
- Thalassemia, sickle cell disease
49
Pharmacotherapy for iron toxicity includes
Oral deferasirox or parenteral deferoxamine
50
What are the pharmacodynamics of Deferasirox?
Selective affinity for ferric iron, chelates in a 2:1 ratio (iron: drug)
51
What are the pharmacokinetics of deferasirox?
Peak concentration after oral administration is 0.5-1hr
urinary excretion of iron-deferasirox complex
t1/2=8-16hrs
52
What are adverse effects of deferasirox?
Mild GI issues, skin rash
53
What are the pharmacodynamics of deferoxamine?
Selective affinity for ferric iron, chlates in a 1:1 ratio
54
What are the pharmacokinetics of deferoxamine?
- Half life is biphasic
- urinary excretion of iron deferoxamine complex
55
What are adverse effects of deferoxamine?
Gi issues, rash, imparts orange/red color to urine, hypotension with rapid infusion, renal oto and pulmonary toxicity with long term therapy
56
Vitamin B12 helps in the formation of
tetrahydrofolate
57
Vitamin B12 helps in the conversion of
methylmalonate CoA to succinyl CoA needed for ATP production
58
Where can dietary sources of vit B12 be found?
liver, eggs, and dairy products
59
Folate consists of
pteridine ring, PABA and glutamate residue
60
For elderly patients, deficiency of vit B12 can be from
Inadequate absorption
61
Where is storage of Vit B12?
In the liver
62
Vit B12 is transported in the body by
transcobalamin I, II and III
63
Vit B12 deficient patients can display with what type of anemia?
Megaloblastic, macrocytic anemia with associated leukopenia or thrombocytopenia
64
Vit B12 deficient patients can display
paresthesias in peripheral nerves and muscle weakness. Can progress to ataxia and other CNS dysfunction
65
In order to get folate to tetrahydrofolate, you require
Cobalamin
66
If Vit B12 is deficient, then folates will go into the
Methyl-folate trap
67
The methyl folate trap causes for a
buildup of homocysteine
68
How can you override a vit B12 deficiency?
High amounts of folic acid and using DHFR to form THF (helps the macrocytic anemia but not the peripheral neuropathy
69
Vit B12 absorption is dependent on what?
Intrinsic factor (because it binds to a receptor called culinary)
70
Lack of intrinsic factor is
pernicious anemia
71
What are etiologies of pernicious anemia?
- Gastric parietal cell disease, chronic use of proton pump inhibitor
- GI surgery
- Anti-IF antibodies (autoimmune)
- Disease of ileum (IBD or surgical resection)
- Diet
72
What is treatment for pernicious anemia?
Parenteral Vit B12 (hydroxocobalamin or cyanocobalamin)
73
Why is hydroxocobalamin preferred for parenteral Vit B12 therapy?
It is more highly protein ound and will remain in the circulation longer
74
Once pernicious anemia is in remission, then B12 therapy can be given as
nasal spray or gel
75
Absorption of folic acid occurs though what?
Proton coupled folate transporter
76
Total body stores of folic acid
10-30mg
77
Folic acid undergoes
enterohepatic recycling (200 micrograms per day)
78
Body stores of folate are relatively low and what can develop within 1-6 months after the intake of folates has stopped?
Megaloblastic anemia
79
What are etiologies of folate deficiency?
- Inadequate diet (alcohol dependence and liver disease)
- Malabsorption or renal dialysis
- Enhanced requirement
- Vitamin B12 deficiency
- Antifolate drugs (methotrexate, trimethoprim/pyrimethamine)
80
What measurements can diagnose a patient with a folate deficiency
Measurement of serum folate or red blood cell folate
81
What is used to treat acute toxicity of methotextrate?
Leucovorin (folinic acid)
82
What organ makes erythropoietin?
kidney
83
Who is at risk to being Epo deficient?
Pts with kidney disease or renal failure
84
Stem cells undergo what type of renewal?
self renewal
85
During destruction of RBCs, what is released?
Hemoglobin
86
How does the body deal with increase in Hb from destruction of RBCs?
Goes to spleen and makes bilirubin, so you will see hyperbilirubinemia and jaundice
87
Medication indeced decreased production of RBCs, such as chemo, damages the
bone marrow
88
In anemia of inflammation, the body responds by
turining down availability to absorb iron
89
Ir reticulocye is low, could be due to
Blood loss, early stage iron deficiency, aplastic anemia, renal disease, malignancy
90
If reticulocyte count is high, could be either
intrinsic or extrinsic
91
Someone with iron deficiency can experience
Hypotension and tachycardia (need to correct it to prevent further problems)
92
What does hepcidin do?
Blocks the absorption and release of iron from the liver. Done to prevent iron overload
93
Low iron stores will block the production of
hepcidin
94
How is hemochromatosis treated?
Phelbotomy
95
Hemachromatosis is an
iron overload
96
Low EPO can lead to a
reduction in RBCs and hemoglobin levels
97
In cases of low EPO, what can be given to help treat these?
Giving recombinant EPO
98
Epoetin alpha must be administered
IV
99
Why must epoietin alpha be administered IV?
Because it is a glycoprotein
100
How often is Epoietin alpha given?
3 times per week
101
Darbepoetin alpha is given how often?
once a week
102
Use of rHUEPO in anemia of inflam may also require supplementation with
iron or folate
103
What are adverse effects of epoietin alpha?
- Hypertension and thrombosis
- Hypersensitivity reactions since it is a recombinant protein
- Potential for abuse by athletes
