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Semester 1 > Pharm Exam 3 > Flashcards

Pharm Exam 3 Flashcards

1
Q

What are the 6 mechanistic approaches or immune suppression

A
  1. Inhibition of gene expression to modulate inflammatory responses
  2. Cytotoxic agents to deplete expanding lymphocyte populations
  3. Inhibition of lymphocyte signaling to block activation and expansion of lymphocytes
  4. Neutralization of cytokines essential in mediating the immune response
  5. Use of antibodies to deplete the immune system of specific cells
  6. Blockade of co-stimulation to induce anergy
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2
Q

What 2 classes of cytotoxic agents are utilized in immunosuppression

A

Antimetabolites and Alkylating agents

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3
Q

What is the goal of cytotoxic agents?

A

To eliminate undesirable cells

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4
Q

What are nucleosides derived from?

A

Derivatives of purines and pyrimidines that are conjugated to ribose or deoxyribose

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5
Q

What are the 3 sets of reactions is nucleotide synthesis?

A
  1. Synthsis of the ribonucleotides.
  2. Reduction of ribonucleotides to deoxyribonucleotides
  3. Conversion of deoxyuridylate (dUMP) to deoxythyridylate (dTMP)
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6
Q

What is the function of ribonucleotide reductase?

A

To reduce ribonucleotides to deoxyribonuccleotides. Thus catalyzing the formation of DNA.

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7
Q

In what ways do steroids act as Immune suppressors?

A
  1. Inhibition of cytokine release
  2. Decrease the activity to pattern receptors
  3. Decrease Th cells
  4. Decrease NK cell activity
  5. Inhibit inflammatory gene expression
  6. Inhibit phospholipase A2
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8
Q

What are the side effects of steroid use?

A 
Hyperglycemia
weight gain
central obesity
 severe swelling,
psychiatric symptoms,
gastric and duodenal bleeding,
adrenal suppression
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9
Q

What is the contraindication for steroid use?

A

Serious infection

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10
Q

How do alkylating agents produce their effects?

A

By adding a hydrocarbon group such a CH3. They interfere with DNA replication and gene expression.

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11
Q

What are the two types of antimetabolites?

A

Purine and pyrimadine analogs

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12
Q

Which nucleotide bases are Purines?

A

Adenine and Guanine

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13
Q

Which nucleotide bases are pyrimidines?

A

Thymine, Cytosine and Uracil

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14
Q

A nucleoside plus a phosphate group makes what?

A

A nucleotide

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15
Q

What are the functions of antimetabolites?

A

Antimetabolites are molecules that compete with essential components of metabolic processes thus inhibiting them.

  1. Act to inhibit enzymes of nucleotide synthesis
  2. The cell cannot replicate its genetic material
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16
Q

Examples types of antimetabolites

A

Purine analogs and pyrimidine analogs

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17
Q

Uses of antimetabolites

A

Antibacterial
Antifungal
Antiparasitic
Antineoplastic

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18
Q

4 categories of MOA by which antimetabolites produce their effects.

A
  1. Inhibitors of folate metabolism
  2. Inhibitors of purine metabolism
  3. Inhibitors of ribonucleotide reductase
  4. Nucleotide analogs
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19
Q

Cyclophosphamide

A

A highly toxic alkylating agent. It crosslinks DNA to itself by binding to DNA twice

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20
Q

What are the two Specific Lymphocyte Signaling Inhibitors

A

Calcineurin inhibitors and mTOR inhibitors

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21
Q

What is the end result of Specific Lymphocyte Signaling

A

Activated T cells which increase the production of IL-2

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22
Q

What is NFAT

A

Nuclear factor of activated T-cells

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23
Q

Steps in Specific Lymphocyte Signaling

A
  1. Calcineurin dephosphorylates NFAT
  2. Dephosphorylated NFAT moves into the nucleus
  3. Dephosphorylated NFAT stimulates the transcription of IL-2
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24
Q

What is Calcineurin

A

A phosphatase enzyme which dephosphorylates NFAT

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25
Q

Example of a Calcineurin inhibitor

A

Cyclosporine

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26
Q

MOA of Cyclosporine

A

Cyclosporine binds to cyclophilin which inhibits the phosphatase activity of Calcineurin and prevents NFAT from entering the nucleus. Thus inhibits the production of IL-2.

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27
Q

Cyclosporine is extensively metabolized by

A

CYP3A

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28
Q

Side Effects of Cyclosporine

A 
Opportunistic infection
     (EBV and CMV)
Nephrotoxicity 
Kidney damage
Hypertension
CNS problems
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29
Q

Cyclosporine is effective in suppressing T cell immunity if the T cells are still inactive or activated

A

Still inactive

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30
Q

What does mTOR stand for

A

Mammalian Target of Rapamycin

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31
Q

What is another name for Rapamycin

A

Sirolimus

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32
Q

What is the MOA of Rapamycin (sirolimus)?

A

It binds to FKBP 12 protein in the cytoplasm which then inhibits mTOR

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33
Q

What are the cellular level effects of Rapamycin?

A

Suppressor of RNA translation
Blocks the activation of IL-2
Inhibits the activation of T and B cells

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34
Q

Example of an mTOR inhibitor

A

Sirolimus (AKA Rapamycin)

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35
Q

What are the tissue level effects of mTOR inhibitors?

A
  1. Impede vascular endothelial cell stimulation by vascular endothelial growth factor.
  2. Reduce abnormally increased proliferation of endothelial cells and vascular smooth muscle cells
  3. Alter the growth and proliferation of cancerous lymphocytes
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36
Q

Advantage of mTOR inhibitors over Calcineurin inhibitors?

A

mTOR inhibitors are not nephrotoxic.

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37
Q

Side effects of mTOR inhibitors?

A
  • Mucositis (canker sores) *
  • Anemia, thrombocytopenia or neutropenia *
  • Interstitial Pneumonitis
  • Infection
  • Hyperglycemia
  • Hyperlipidemia
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38
Q

Contraindications of mTOR inhibitors

A

None. can be a drug interaction with Calcineurin inhibitors

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39
Q

Tumor Necrosis Factor Alpha (TNF-a) does what

A

Initiates acute phase response.
Vasodilates venules, increasing blood flow.
Increases vascular permeability
Increases endothelial adhesiveness.
Increases synthesis of cytotoxic metabolites.

40
Q

Tumor Necrosis Factor Alpha (TNF-a) is what kind of cell signaling protein?

A

A cytokine

41
Q

Uses of TNF-a inhibitors

A

Auto immune diseases such as

  • Crohn’s
  • Ulcerative colitis
  • Psoriasis
  • Ankylosing Spondytis (fusion of the axial skeleton)
42
Q

Contraindications of TNF-a inhibitors.

A
  • Latent TB
  • Immunocompromise
  • Active infection
43
Q

Side effects of TNF-a inhibitors

A
  • Injection site irritation
  • Acute inflammatory infection
  • Delayed inflammatory infection
  • Heart failure
  • liver failure
  • demyelination of the CNS
  • Cancer
44
Q

MOA of TNF-a inhibitors?

A

Inhibition of the inflammatory process by inhibition of TNF-a. mAbs antagonize TNF-a by competitively binding to it’s receptors. Fusion Proteins bind to free TNF-a in the blood inhibiting it from binding to its receptor.

45
Q

What do B Cell biologics do

A

Target B cells for destruction or interfere with ability to mount an immune response

46
Q

What are the 2 B Cell targets

A

CD20 and CD22

47
Q

What is the function of CD20

A

It is present at all stages of B Cell differentiation Except the first and the last. It regulates the early steps in the activation of B Cell differentiation

48
Q

MOA of B Cell biologics

A
  1. As a B Cell depleting agent they inhibit the expression of CD20 which results in apoptosis of B Cells
  2. As an immunomodulator they block the cytokines required for B cell;
    - Maturation
    - Memory induction
    - Activation
    - Proliferation
49
Q

Uses of B Cell Biologics

A
  • B Cell tumors
  • Inflamatory Autoimmune Diseases
  • Transplants
50
Q

Contraindications of B Cell Biologics

A
  • Active infection

- Latent infection (Hep C)

51
Q

Early Side Effects of B cell Biologics

A 
Common and Mild
- Hyper/ Hypotension
- chills
- Scratchy throat
- bronchospasm
- Mucocutaneous reactions
Rare and Severe
- Hypoxia
- MI
- Stroke
- ARDS
- Death
52
Q

Late Side effects of B Cell Biologics

A
  • Immunosuppression leading to infection
  • Progressive multifocal leukoencephalopothy
    (Inflammation of the white matter)
53
Q

What are the targets for T cell biologics?

A

CD3, CD25 and CD28

54
Q

Important functions of CD3 on T Cells

A
  • All T cells express CD3.
  • Nonspecific, influence all subtypes of T cells.
  • Induce selective apoptosis of activated T cells after binding to CD3.
55
Q

Important functions of CD25 on T Cells

A
  • IL-2 receptor.
  • Suppression of IL-2 receptor decreases inflammation.
  • Suppress autoreactive T cells.
56
Q

Uses of T Cell biologics

A
  • T Cell Tumors
  • Inflammatory Autoimmune diseases
  • Transplant medicine
57
Q

Contraindications of T Cell Biologics

A

Active infection

58
Q

MOA of T Cell Biologics

A

Inhibit the expression of CD3 and CD25 proteins which are important for T Cell function leading to improper function or apoptosis

59
Q

Side Effects of T Cell biologics

A

Immunosuppression

  • N/V
  • Diarrhea
  • Hypotension
  • SOB
  • Headache
60
Q

How are polyclonal antibodies produced?

A

Immunization of rabbits or horses with lymphoid cells.

61
Q

What 2 things are required for T Cell activation

A
  1. The antigen

2. The costimulator

62
Q

Example of a T Cell costimulator

A

CTLA- 4 is a costimulator and is up regulated in activated T Cells. It is inhibited by CTLA-4Ig

63
Q

MOA of Glatiramoids

A
  • Binds major histocompatibility cells (MHC class II) on Antigen presenting cells (APS’s)
  • Increases Th2 suppressors
64
Q

What can Th 2 cells do

A

May cross the Blood Brain Barrier and secrete anti-inflammatory cytokines

65
Q

Indication for Glatiramoids

A

Treatment of MS

66
Q

Contraindications of Glatiramoids

A

None

67
Q

Side Effects of Glatiramoids

A
  • Chest Pain
68
Q

Inhibition of cytokines by steroids leads to inhibition of what?

A

IL 1,2, 6 and TNF-a

69
Q

Folate is an essential cofactor in what?

A

Purine Ribonucleotide synthesis and cTMP

70
Q

Which cells secrete TNF-a

A

Macrophages
Mast Cells
Activated Th cells

71
Q

Example of a Fusion protein which binds TNF-a

A

Enteracept

72
Q

MOA of AGI

A

Starch Blockers .
They bind to Glycosidase with a greater affinity than carbohydrates. This slows the absorption of carbohydrates in the GI tract. Also they stimulate GLP-1.

73
Q

MOA of Biguanides

A
  • Decrease in gluconeogenesis by activation of AMP Kinase
  • Increase the action of insulin
  • Delay GI absorption of glucose
  • Stimulation of glycolysis
  • Reduce plasma glucagon
  • Enhance transcription of GLUT-4
74
Q

MOA of Glucagon

A
  • Stimulated by the sympathetic NS
  • In the liver it binds to a G Protein receptor
    • This increases cAMP which then Protein Kinase A
  • Increase Glycogenolysis increasing glucose
  • Decreases Glycogen synthesis which increases available glucose
  • increased Glycolysis (the use of glucose)
75
Q

MOA of Insulin

A
  • Up regulates GLUT-4
  • Inhibits gluconeogenesis (reduces glucose)
  • Facilitates uptake of amino acids thus increasing protein synthesis
  • Inhibits lypolysis
76
Q

MOA of Incretins

A

Two types

  • DPP-4 inhibitors (Gliptins)
  • Block DPP-4 enzymes from breaking down incretins GLP-1 and GIP leading to seduction in glucose
  • Incretin mimetics
  • are GLP-1 mimetics which cannot be degraded by DPP-4
77
Q

MOA of Meglitinides

A

Bind to the SUR1 subunit (ATP sensitive K channel) it closes the K channel, thus depolarization which activates the Ca channel and exocytosis Insulin

78
Q

MOA of Sulfonylureas

A

Bind to the SUR1 subunit (ATP sensitive K channel) it closes the K channel, thus depolarization which activates the Ca channel and exocytosis Insulin. Simmilar action to meglitinides but a different site on the SUR1.

79
Q

MOA of Thiazolidinediones

A
  • Decreases glucose by increasing glucose uptake by muscle and adipose cells.
  • Also decrease of gluconeogenesis in the liver.
  • Increase fatty acid storage (FFA leads to insulin resistance)
80
Q

MOA of Somatostatin Analogs

A
  • Produced by delta cells
  • Binds to G Proteins and decreases cAMP
  • Inhibits Hormones
  • GH
  • Insulin
  • Glucagon
  • Gastrin
  • VIP
  • Pancreatic Enzymes
81
Q

MOA of GH Antagonists

A
  • Blocks GH from coupling to its receptor in the liver

- GH in the liver releases IGF-1 thus GH Antagonists bloc the release of IGF-1

82
Q

MOA of ACTH

A
  1. Released from the AP
  2. Binds to ACTH G protein receptors in the ZF
  3. Increases cAMP
  4. Activates PKA
  5. Increase CA++
  6. Synthesizes Cortisol
83
Q

MOA of TH replacements

A
  • Act similarly to steroids in that the mediate transcription
  • Replace deficient endogenous T3 and T4
  • Typically T4 because of 7 day half life vs. T3 1 day half life
84
Q

MOA of antithyroids

A

2 types

  • Thioamides
  • Block iodine oxidation
  • Block the coupling of iodinated tyrosines MIT and DID
  • Do not block the uptake of iodine by the thyroid
  • Radioactive Iodine 131I
  • Destroys the thyroid by radiation
85
Q

Second messenger action of Muscarinic receptor subtypes M1, M3 and M5 action

A

Formation of IP3 and DAG, increased intracellular calcium

86
Q

Second messenger action of Muscarinic receptor subtypes M2 and M4 action

A

Opening of potassium channels, inhibition of adenylyl cyclase. Decreased cAMP

87
Q

Alpha 1 receptor second messenger action

A

Formation of IP3 and DAG, increased intracellular calcium.

88
Q

Alpa 2 receptor second messenger action

A

Inhibition of adenylyl cyclase, decreased cAMP.

89
Q

Beta 1,2,and 3 second messenger action

A

Stimulation of adenylyl cyclase, increased cAMP.

90
Q

Dopamine receptor subtypes D1 and D5 second messenger action

A

Stimulation of adenylyl cyclase, increased cAMP.

91
Q

Dopamine receptor subtypes D2, D3 and D4 second messenger action

A

Inhibition of adenylyl cyclase, decrease in cAMP

92
Q

Cholioceptors respond to

A

Receptors (both muscarinic and nicotinic) that respond to ACh.

93
Q

Adrenoceptors respond to

A

Receptors that respond to catecholamines, such as NE and Epi.
Can be further divided into alpha and beta

94
Q

Nicotinic receptors are located where?

A

The ganglion of the sympathetic and parasympathetic NS

95
Q

Nicotinic receptors function by?

A

Opening of sodium, potassium channels leading to depolarization.

Semester 1 (15 decks)

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