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Drug Action I > Block 4: Anemia Med Chem > Flashcards

Block 4: Anemia Med Chem Flashcards

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1
Q

What is hematopoiesis?

A

Continual replacement of mature blood cells

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2
Q

What nutrients are required for hematopoiesis?

A

Iron, Vitamin B12, folic acid

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3
Q

What growth factor increases hematopoiesis?

A

Erythropoeitin

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4
Q

What gives rise to all types of blood cells?

A

Pluripotent stem cells

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5
Q

What is anemia?

A

A deficiency of RBC or Hg

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6
Q

What factors does a CBC test measure?

A
  1. Number of RBC
  2. Number of WBC
  3. Total amount to Hg
  4. Hematocrit
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7
Q

What is hematocrit?

A

Total fraction of blood that is made up of RBC and its size

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8
Q

T/F Anemia is a disease.

A

An indication of a disease process/alteration in body function

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9
Q

What are the outcomes of prolonged anemia?

A
  1. Tissue hypoxia
  2. Physical fatigue
  3. Angina
  4. Cramps
  5. DZ
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10
Q

How does CV system compensate for anemia?

A
  1. Increased CO
  2. Tachycardia
  3. Vasoconstriction and dilation
  4. Complications in patients with CV disease
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11
Q

What are the causes of anemia?

A
  1. RBC loss w/o destruction
  2. Deficient RBC porduction
  3. Increased RBC destruction over production
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12
Q

In what ways can RBC loss w/o RBC destruction?

A
  1. Hemorrhage
  2. Menstrual flow
  3. Gynecological disorders
  4. Pregnancy
  5. Parasites (hook worm)
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13
Q

In what ways can there be a deficiency in RBC production?

A
  1. Neoplasia
  2. Myelofibris
  3. Pernicious anemia
  4. Iron deficiency anemia
  5. Aplastic anemia
  6. Renal disease (Increased RBC destruction over erythropoiesis)
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14
Q

What is are some of the causes of hemorrhages?

A
  1. Trauma
  2. Surgery
  3. Disorders: cancer, ulcers, TB, DVD, IBS
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15
Q

What is neoplasia?

A
  1. Leukemia
  2. Metastasis to bone marrow
  3. Osteogenic sarcoma
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16
Q

What is pernicious anemia?

A

Caused by a lack of intrinsic factor, a substance needed to absorb Vit B12 from the GIT

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17
Q

What is aplastic anemia?

A

Bone marrow doesn’t produce enough or any new cells to replenish the blood cells

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18
Q

In what ways can there be increased RBC destruction over production?

A

Intrinsic and extrinsic abnormalities

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19
Q

What are intrinsic abnormalities?

A
  1. Thalassemia
  2. G6PD- glucose-6-phosphate dehydrogenase defficiency
  3. Sickle cell anemia
  4. Hereditary sperocytosis
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20
Q

What are extrinsic abnormalities?

A
  1. Infections (malaria, mycoplasma)
  2. Lead poisoning
  3. Disseminated intravascular coagulation
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21
Q

What is thalassemia?

A

Genetic defect results in reduced rate of synthesis of normal global chains

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22
Q

What is sickle cell anemia?

A

RBC that contain mostly hemoglobin S, difficulty passing through small capillaries and die faster

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23
Q

What is hereditary sperocytosis?

A

Defective RBC membrane (smaller, spherical, fragile)

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24
Q

How do you treat myelosupression?

A

EPO

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25
How do you treat microcytic, macro, pernicious anemia?
1. Iron 2. Vitamin B12 3. Folic Acid
26
How do you treat hemolytic anemia?
Steroids (methylprednisolone) Rituximab
27
How do you treat sickle cell?
1. Hydroxyurea, Oxbryta 2. Crizanlibumab, L-Glutamine
28
What is this?
Normal RBC: 1/3 central pallor
29
What is the common cause for Hypochromic Microcytic Anemia?
Iron deficiency (lack of nutrition)
30
What is this?
Hypochromic Microcytic Anemia: RBC are smaller with increased central pallor
31
What are the functions of iron?
1. O2 transport (Hg) 2. Heme enzymes 3. Metalloflavoprotein enzymes 4. The mitochondrial enzyme alpha-glycerophosphate oxidase and other mitochondrial enzymes 5. Immune function 6. Brain function
32
Identify the components?
33
What is the the difference between ferrous and ferric?
Ferrous: Better oral absorbtion Ferric: Better IV
34
What are the salts of ferrous?
Sulphate (Slow Fe and Slow Fe + Folic acid) Gluconate (Fergon) Fumarate (Iron)
35
What are the ADRs of PO iron?
1. Nausea 2. Gastric discomfort 3. Contipation 4. Diarrhea
36
How do you avoid side effects when using PO Iron?
Start patients on small doses and increase gradually
37
What is INFeD?
Liquid complex of ferric hydroxide and dextran for IV or IM use
38
What are are the components of INFeD?
1. Iron dextran 2. Sodium ferric gluconate 3. Iron Sucrose 4. Ferumoxytol 5. Ferric carboxymaltose
39
ADRs of using INFeD?
Anaphylactic shock
40
What are the uses of parenteral iron? Down sides?
1. Renal failure 2. Short bowel 3. Celiac disease Doesn't necessarily provide a faster response than PO
41
What is this?
Megaloblastic (Macrocytic) Anemia: RBC are large as WBC, fewer RBCs
42
What causes Megaloblastic anemia?
Lack of Vit B12 (cyanocobalamin) or folic acid
43
Why is Megaloblastic anemia problematic?
1. Lack of B12 and folic → prevents DNA and RBC production 2. Macrolytic cells may have enough Hb but are not concave 3. Can't transport O2 4. Cells damage more easily
44
Why is B12 and folic acid important?
1. Helps with DNA synthesis
45
What are symptoms of B12 and folic acid deficiency?
1. Megaloblastic anemia, abnormal macrocytic RBCs, severe anemia 2. B12 def → neurological symptoms
46
How is B12 synthesized?
Basic structure is from bacteria, fungi, and algae, but conversion takes place in the body
47
Is cyanocobalmin a nature product?
Used as a supplement and additive due to its stability → converted by biochem reactions
48
What is another name for B12?
Extrinsic factor
49
What is the function of extrinsic factor?
Combined with intrinsic factor produced but the parietal glands of the stomach Combo enables binding to receptor and phagocytosis of the complex by the distal ileum cells
50
What is an example of vitamin B12 def caused by autoimmunity?
Inability to absorb due to destruction of parietal cells of the stomach
51
What are the causes of pernicious anemia?
1. Defective secretion of intrinsic factors 2.Gastrectomy 3. Damaged distal ileum (IBD/IBS) 4. Chronic pancreatitis, thyroid disease, bacterial overgrowth in SI
52
What are the symptoms of B12 def?
1. Diarrhea 2. Loss of appetite 3. Weight loss 4. Weakness 5. Sore tongue 6. HA 7. Heart palp 8. Irritability 9. Behavioral disorders
53
How does B12 def present differently in adults and children?
Adults: anemia Infants: slow growth rate
54
What can replace B12?
Folic acid
55
What is the function of folic acid?
1. Serve as an acceptor and donor of single carbon units in reactions requiring one-carbon transfer 2. Responsible for all oxidation levels of carbon except CO2 where biotin is the carrier 3. Important for the synthesis of thyamine
56
What is the active coenzyme for of folic acid?
tetrahydrofolate (THF): 2 successive reductions of folate by dihydrofolate reductase
57
Describe the R groups of folate molecules?
1-7 glutamate units bound in g-carboxyl amide linkages
58
Describe the conversion of folate to THF?
59
Describe methyl transfer with folate?
60
When would the synthesis of DNA bases be rapid and fast?
1. Developmental stages of pregnancy (NTDs) 2. Formation of new blood cells
61
What is dUMP? How is it synthesized?
B12 substrate necessary for DNA synthesis and cell division DTMP → dUMP
62
What are the presentations of autoimmune hemolytic anemia?
1. Mixed thermal range of autoantibodies Autoantibodies that target self RBC
63
What is the treatment for AIHA?
1. CCS 2. Rituximab +/- splenectomy (2nd line when steroid fails or relapse occurs)
64
What is Rituximab?
Chimeric monoclonal antibody against CD20 protein of B cells surface → Binds to CD20 → triggers cell death
65
What is hemoglobin S?
RBC substitution of glutamic acid with valine at the 6th residue of the beta chain subunit of Hg
66
What happens to HbS during low O2?
HbS aggregates and distorts into a sickle shape → cells become rigid, fragile, lose O2 carrying capacity
67
What occurs during Vaso-occulusive crisis?
Endothelium activated recruits leukocytes → E-selectin/P-selectin on endothelium generate signals activating MAC1→ Crawling macrophage captures normal and sickle cell RBCs
68
What are the ScA treatments?
1. Hydroxyurea 2. Voxelotor (Oxybryta) 3. Crizanilzumab (Adakveo) 4. L-glutamine
69
What is the MOA of hydroxyurea?
1. In ScA, HU induces an upregulation in the concentration of fetal hemoglobin through an imprecise mechanism. 2. Fetal hemoglobin does not polymerize or deform like HbS
70
What is the MOA of Voxelotor?
Binds to deoxygenated HbS to lessen polymerization and increase oxygen affinity
71
What is the MOA of crizanliumab?
Targets P-selectin blocking it's interaction with RBC, platelets, WBCs, and endothelial cells
72
What is L-glutmaine?
SS RBCs have ↑ levels of ROS → PO L-glutamine ↑ NAD redox potential and NADH level in sickle RBCs → Less damage, deformation, adhesion, decreased VOC
73
What is the dose of L-glutamine?
0.3g/kg 10-30g/day

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