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

Block 4: Anemia Med Chem Flashcards

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
Q

How do you treat microcytic, macro, pernicious anemia?

A
  1. Iron
  2. Vitamin B12
  3. Folic Acid
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26
Q

How do you treat hemolytic anemia?

A

Steroids (methylprednisolone)
Rituximab

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27
Q

How do you treat sickle cell?

A
  1. Hydroxyurea, Oxbryta
  2. Crizanlibumab, L-Glutamine
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28
Q

What is this?

A

Normal RBC: 1/3 central pallor

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29
Q

What is the common cause for Hypochromic Microcytic Anemia?

A

Iron deficiency (lack of nutrition)

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30
Q

What is this?

A

Hypochromic Microcytic Anemia: RBC are smaller with increased central pallor

31
Q

What are the functions of iron?

A
  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
Q

Identify the components?

A
33
Q

What is the the difference between ferrous and ferric?

A

Ferrous: Better oral absorbtion
Ferric: Better IV

34
Q

What are the salts of ferrous?

A

Sulphate (Slow Fe and Slow Fe + Folic acid)
Gluconate (Fergon)
Fumarate (Iron)

35
Q

What are the ADRs of PO iron?

A
  1. Nausea
  2. Gastric discomfort
  3. Contipation
  4. Diarrhea
36
Q

How do you avoid side effects when using PO Iron?

A

Start patients on small doses and increase gradually

37
Q

What is INFeD?

A

Liquid complex of ferric hydroxide and dextran for IV or IM use

38
Q

What are are the components of INFeD?

A
  1. Iron dextran
  2. Sodium ferric gluconate
  3. Iron Sucrose
  4. Ferumoxytol
  5. Ferric carboxymaltose
39
Q

ADRs of using INFeD?

A

Anaphylactic shock

40
Q

What are the uses of parenteral iron? Down sides?

A
  1. Renal failure
  2. Short bowel
  3. Celiac disease

Doesn’t necessarily provide a faster response than PO

41
Q

What is this?

A

Megaloblastic (Macrocytic) Anemia: RBC are large as WBC, fewer RBCs

42
Q

What causes Megaloblastic anemia?

A

Lack of Vit B12 (cyanocobalamin) or folic acid

43
Q

Why is Megaloblastic anemia problematic?

A
  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
Q

Why is B12 and folic acid important?

A
  1. Helps with DNA synthesis
45
Q

What are symptoms of B12 and folic acid deficiency?

A
  1. Megaloblastic anemia, abnormal macrocytic RBCs, severe anemia
  2. B12 def → neurological symptoms
46
Q

How is B12 synthesized?

A

Basic structure is from bacteria, fungi, and algae, but conversion takes place in the body

47
Q

Is cyanocobalmin a nature product?

A

Used as a supplement and additive due to its stability → converted by biochem reactions

48
Q

What is another name for B12?

A

Extrinsic factor

49
Q

What is the function of extrinsic factor?

A

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
Q

What is an example of vitamin B12 def caused by autoimmunity?

A

Inability to absorb due to destruction of parietal cells of the stomach

51
Q

What are the causes of pernicious anemia?

A
  1. Defective secretion of intrinsic factors
    2.Gastrectomy
  2. Damaged distal ileum (IBD/IBS)
  3. Chronic pancreatitis, thyroid disease, bacterial overgrowth in SI
52
Q

What are the symptoms of B12 def?

A
  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
Q

How does B12 def present differently in adults and children?

A

Adults: anemia
Infants: slow growth rate

54
Q

What can replace B12?

A

Folic acid

55
Q

What is the function of folic acid?

A
  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
Q

What is the active coenzyme for of folic acid?

A

tetrahydrofolate (THF): 2 successive reductions of folate by dihydrofolate reductase

57
Q

Describe the R groups of folate molecules?

A

1-7 glutamate units bound in g-carboxyl amide linkages

58
Q

Describe the conversion of folate to THF?

A
59
Q

Describe methyl transfer with folate?

A
60
Q

When would the synthesis of DNA bases be rapid and fast?

A
  1. Developmental stages of pregnancy (NTDs)
  2. Formation of new blood cells
61
Q

What is dUMP? How is it synthesized?

A

B12 substrate necessary for DNA synthesis and cell division

DTMP → dUMP

62
Q

What are the presentations of autoimmune hemolytic anemia?

A
  1. Mixed thermal range of autoantibodies

Autoantibodies that target self RBC

63
Q

What is the treatment for AIHA?

A
  1. CCS
  2. Rituximab +/- splenectomy (2nd line when steroid fails or relapse occurs)
64
Q

What is Rituximab?

A

Chimeric monoclonal antibody against CD20 protein of B cells surface → Binds to CD20 → triggers cell death

65
Q

What is hemoglobin S?

A

RBC substitution of glutamic acid with valine at the 6th residue of the beta chain subunit of Hg

66
Q

What happens to HbS during low O2?

A

HbS aggregates and distorts into a sickle shape → cells become rigid, fragile, lose O2 carrying capacity

67
Q

What occurs during Vaso-occulusive crisis?

A

Endothelium activated recruits leukocytes → E-selectin/P-selectin on endothelium generate signals activating MAC1→ Crawling macrophage captures normal and sickle cell RBCs

68
Q

What are the ScA treatments?

A
  1. Hydroxyurea
  2. Voxelotor (Oxybryta)
  3. Crizanilzumab (Adakveo)
  4. L-glutamine
69
Q

What is the MOA of hydroxyurea?

A
  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
Q

What is the MOA of Voxelotor?

A

Binds to deoxygenated HbS to lessen polymerization and increase oxygen affinity

71
Q

What is the MOA of crizanliumab?

A

Targets P-selectin blocking it’s interaction with RBC, platelets, WBCs, and endothelial cells

72
Q

What is L-glutmaine?

A

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
Q

What is the dose of L-glutamine?

A

0.3g/kg

10-30g/day

Drug Action I (32 decks)

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