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CMD Block 2 > Anti-Inflammatory's > Flashcards

Anti-Inflammatory's Flashcards

1
Q

Why should glucocorticoids be avoided in the elderly?

A

Their bones are already thinned
Their skin is already thin
They already bruise easily
***

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2
Q

What is a Sweatman-mentioned way to increase the likelihood of proving that your drug works (in clinical trials)?

A

Carefully select your patient population for the trial based upon their genetic makeup

This eliminates those who will not respond to anything, for example

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3
Q

MOA of anti-histamines:

A 
Inverse agonists 
(shifts the receptor into an inactive state)
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4
Q

How can the negative effects of chronic steroid use be avoided in asthmatics?

A

Inhalers

applied directly in small doses

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5
Q

What does a phosphodiesterase inhibitor do, in general terms?

A

Suppresses immune and inflammatory activity

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6
Q

What is the drug of choice for immuno suppression in connection with renal transplantation?

A

Thyroglobulin

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7
Q

What are the long term effects if immunosuppressant drugs?

A

Not yet determined…

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8
Q 
Grafts in order of immunogenicity (most to least): 
Heart
Kidney 
Liver 
Lung
A

Lung > heart > kidney > liver

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9
Q

What drives variation in the selection of maintenance drugs following transplant?

A

Risk (of rejection?)

Type of transplant (due to graft immunogenicity)

Medication related toxicities

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10
Q

Effects of corticosteroids on neutrophils:

A

Neutrophilia:
Increase production
Decrease apoptosis

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11
Q

Effect of corticosteroid on eosinophils:

A

Increase apoptosis (eosinopenia)

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12
Q

Effects of corticosteroids on monocytes:

A

Monocytopenia:
Decrease production
Decrease differentiation

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13
Q

What is the difference between 1st and 2nd generation anti-histamines?

A

1st is able to cross the blood brain barrier

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14
Q

What is the benefit of 1st generation anti-histamines?

A

Can treat Parkinson’s, insomnia, vertigo, etc

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15
Q

What is the benefit of 2nd generation anti-histamines?

A

They don’t cause drowsiness

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16
Q

What are inflammatory reactions often difficult to control?

A

There are usually many overlapping cytokine reactions mediating them

(Symptoms may be due to different cytokines or different reaction to a cytokines)

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17
Q

3 Ways to alter cytokines effects: (general)

A
  1. Block the action at the source
  2. Block action once it has been released
  3. Black action at/within the target cell
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18
Q

2 Ways to block cytokines at the source:

A
  • Block transcriptional regulation

* Inhibit synthesis

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19
Q

3 Ways to block cytokine action after its released:

A
  • Blocking monoclonal antibody (soak up the cytokine before it reaches its target tissue)
  • Fake soluble receptor (attracts cytokine and binds so it never reaches the correct tissue)
  • Cytokine antagonist (binds to surface receptor on target cell)
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20
Q

2 Ways to block cytokine action in target cell:

A
  • Inhibit the transcription factor

* Interrupt transcriptional regulation to diminish the consequences of the cytokine

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21
Q

What are the treatment goals in early vs late phase of asthma attack?

A
  • Early phase: controlling the bronchospasm

* Late phase: controlling the inflammation

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22
Q

2 important rules for glucocorticoid use in asthma therapy:

A
  1. only use systemically for a short duration (due to adverse effects)
  2. Use inhaled glucocorticoids (instead) to control long term
    - local/direct application
    - no systemic dose of meds = no adverse
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23
Q

2 important rules for glucocorticoid use in asthma therapy:

A
  1. only use systemically for a short duration (due to adverse effects)
  2. Use inhaled glucocorticoids (instead) to control long term
    - local/direct application
    - no systemic dose of meds = no adverse
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24
Q

This drug binds to importin-alpha to gain access to the cell.

A

glucocorticoid

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25
Q

This drug decreases production of inflammatory cytokines.

A

glucocorticoid

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26
Q

6 Possible reasons that a patient is not responding to glucocorticoids.

A
  1. Defective histone acetylation
  2. Efflux via active pumps
  3. Differences in ratio/distribution of α and β receptor types
  4. Familial resistance
  5. Receptor is modification
  6. Other inflammatory mediators are involved that are not acted on by glucocorticoids
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27
Q

Glucocorticoid MOA?

A

Inhibition of transcription factors –> Inhibits production of inflammatory mediators (T cell: IL2, etc)

28
Q

Corticosteroid MOA?

A

Inhibit phospholipase activity, which converts phospholipids → arachidonic acid

this blocks prostaglandins, thromboxane, leukotrienes

29
Q

What are 2 results of glucocorticoid transactivation by DNA binding?

A
  1. Side effects

2. Upregulation of lipocortins (anti-inflammatory proteins)

30
Q

What is cholchicine used to treat?

A

gout

31
Q

When is inhibited by NSAIDS, what is often occurs instead?

A

there is a tendency for the pathway to be shunted to

*this produces leukotrienes and inflammatory mediators

32
Q

How can NSAIDS affect asthma?

A

By blocking the COX pathway, products are pushed down the lipoxygenase pathway instead–this yields leukotrienes and proinflammatory mediators

33
Q

2 things that result from leukotrienes, in normal system?

A
  1. chemotaxis of inflmm cells

2. bronchoconstriction

34
Q

Why would we want to inhibit leukotrienes, specifically?

A
  1. treat bronchospasm
  2. prevent related inflammation

*asthma

35
Q

This medication is given prophylactically to prevent cold air from inducing asthma symptoms?

A

Cromolyns

36
Q

This drug blocks chloride channels on mast cells, which prevents degranulation

A

Cromolyn

37
Q

This drug “soaks up” IgE so it isn’t free to bind/trigger degranulation

A

Anti-IgE Antibody: Omalizumab

38
Q

What receptor is involved in the wheal response, vasodilation (and anaphylaxis), and bronchoconstriction?

A

H1 histamine receptor

39
Q

How does a histamine inverse agonist work?

A

binds to receptor and shifts the conformation into an inactive form

40
Q

What is the benefit of sustaining cAMP levels in the cell?

A

Suppress inflammatory and immune activity

41
Q

Roflumilast blocks recruitment of:

and dampens:

A
  1. inflammatory cells (mast, T cells, etc)

2. cholinergic activity

42
Q

How can you improve the results of your drug trial?

A

Select patients with the correct profile (likely to respond to drug)

43
Q

How do TNF-alpha receptors affect the results of TNF-alpha inhibition?

A

The balance of the type 1 and 2 receptors relates to the response

44
Q

What are the 2 types of TNF-alpha receptors?

A

–Cell-surface: receptor for incoming signals on original cell

–Soluble receptor: Binds to target receptor and initiates action in target tissue

45
Q

6 ways that drugs inhibit TNF-alpha:

A
  1. Mediate CDC/ADCC
  2. Neutralization
  3. Bind transmembrane TNF-alpha
  4. Inhibit transmembrane cytokine cleavage
    (TNF-alpha can’t solubilize)
  5. Apoptosis
  6. PMN death (??)
46
Q

Big concern regarding TNFalpha inhibitors

A

Ab-bound TNF-α components may line up on surface of cell, converting drug to superagonist

47
Q

T/F: Inhibiting a cytokine is an easy way to prevent symtpoms.

A

F: Not easy–Patients may have different patterns of cytokine activity!

48
Q

Introduction of this drug resulted in the use of immunosuppressants and organ transplantation.

A

Cyclosporine

49
Q

Uses of immunosuppressive drugs:

A
  1. Organ transplantation
  2. Inflammatory conditions
  3. Immuno dysfunctional conditions (RA, myasthenia gravis, lupus, diabetes, etc)
50
Q

Cytokine responsible for T cell proliferation and clinal expansion.

A

IL2

51
Q

7 targets for immunosuppressive therapy

A
  1. Inhibition of gene expression
  2. Selective attack on clonally expanding cells
  3. Inhibition of intracellular signaling
  4. Neutralization of cytokines/receptors needed for t cell activ
  5. Selective depletion of immune cells
  6. Inhibition of co-stim from APCs
  7. Inhibition of lymphocyte:target interactions
52
Q

Immunosuppressant drug targets on the surface of T cells

A

Block response to IL2
Block T cell activation
Target T cell for degradation

53
Q

Why are immunosuppressant regimens not given long term at large doses?

A

Toxicity

54
Q

What is induction (therapy)?

A

Drug regimen given at time of transplant

Relatively intense dosing

55
Q

What are alternatives to induction drug regimens?

A

Transfusion

Irradiation

56
Q

What is a maintenance drug regimen?

A

Lower potency immunosuppressant drugs

Chronic use

57
Q

What is a rescue immunosuppressant drug regimen?

A

Intense, effective doses given in response to rejection episode

58
Q

What is determined by the patients medical history, which dictates the selection of immunosuppressant drugs?

A

Potential severity of rejection

59
Q

3 drugs commonly involved in maintenance therapy

A

Calcineurin inhibitor
Anti-proliferative
Steroid

60
Q

Mechanisms by which drugs can prevent T cell activation:

A 
Block CD3
Block CD28 (no B7)
61
Q

What is calcineurin? What happens if inhibited?

A

Phosphatase that controls nuclear access of transcription factor NFAT

Inhibition = no IL2 upregulation

62
Q

How do glucocorticoids act on the cell?

A

Inhibit transcriptional regulation of of pro-inflammatory genes (can’t produce IL2)

63
Q

How do drugs inhibit T cell activation?

A
  1. Block CD25, which is the IL2 receptor that allows adjacent T cells to become activated
  2. Inhibiting mTOR, which is normally activated by IL2 within the TCell
64
Q

How does one immunosuppressant eliminate T cells?

A

Ab binding to CD52, inducing lysis via ab-mediated cytotoxicity and complement-mediated cytotoxicity

65
Q

How do immunosuppressants deplete T cells?

A

Via IgG against T cell

CMD Block 2 (38 decks)

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