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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
This drug decreases production of inflammatory cytokines.
glucocorticoid
26
6 Possible reasons that a patient is not responding to glucocorticoids.
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
27
Glucocorticoid MOA?
Inhibition of transcription factors --> Inhibits production of inflammatory mediators (T cell: IL2, etc)
28
Corticosteroid MOA?
Inhibit phospholipase activity, which converts phospholipids → arachidonic acid this blocks prostaglandins, thromboxane, leukotrienes
29
What are 2 results of glucocorticoid transactivation by DNA binding?
1. Side effects | 2. Upregulation of lipocortins (anti-inflammatory proteins)
30
What is cholchicine used to treat?
gout
31
When is inhibited by NSAIDS, what is often occurs instead?
there is a tendency for the pathway to be shunted to *this produces leukotrienes and inflammatory mediators
32
How can NSAIDS affect asthma?
By blocking the COX pathway, products are pushed down the lipoxygenase pathway instead--this yields leukotrienes and proinflammatory mediators
33
2 things that result from leukotrienes, in normal system?
1. chemotaxis of inflmm cells | 2. bronchoconstriction
34
Why would we want to inhibit leukotrienes, specifically?
1. treat bronchospasm 2. prevent related inflammation *asthma
35
This medication is given prophylactically to prevent cold air from inducing asthma symptoms?
Cromolyns
36
This drug blocks chloride channels on mast cells, which prevents degranulation
Cromolyn
37
This drug “soaks up” IgE so it isn’t free to bind/trigger degranulation
Anti-IgE Antibody: Omalizumab
38
What receptor is involved in the wheal response, vasodilation (and anaphylaxis), and bronchoconstriction?
H1 histamine receptor
39
How does a histamine inverse agonist work?
binds to receptor and shifts the conformation into an inactive form
40
What is the benefit of sustaining cAMP levels in the cell?
Suppress inflammatory and immune activity
41
Roflumilast blocks recruitment of: | and dampens:
1. inflammatory cells (mast, T cells, etc) | 2. cholinergic activity
42
How can you improve the results of your drug trial?
Select patients with the correct profile (likely to respond to drug)
43
How do TNF-alpha receptors affect the results of TNF-alpha inhibition?
The balance of the type 1 and 2 receptors relates to the response
44
What are the 2 types of TNF-alpha receptors?
--Cell-surface: receptor for incoming signals on original cell --Soluble receptor: Binds to target receptor and initiates action in target tissue
45
6 ways that drugs inhibit TNF-alpha:
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
Big concern regarding TNFalpha inhibitors
Ab-bound TNF-α components may line up on surface of cell, converting drug to superagonist
47
T/F: Inhibiting a cytokine is an easy way to prevent symtpoms.
F: Not easy--Patients may have different patterns of cytokine activity!
48
Introduction of this drug resulted in the use of immunosuppressants and organ transplantation.
Cyclosporine
49
Uses of immunosuppressive drugs:
1. Organ transplantation 2. Inflammatory conditions 3. Immuno dysfunctional conditions (RA, myasthenia gravis, lupus, diabetes, etc)
50
Cytokine responsible for T cell proliferation and clinal expansion.
IL2
51
7 targets for immunosuppressive therapy
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
Immunosuppressant drug targets on the surface of T cells
Block response to IL2 Block T cell activation Target T cell for degradation
53
Why are immunosuppressant regimens not given long term at large doses?
Toxicity
54
What is induction (therapy)?
Drug regimen given at time of transplant | Relatively intense dosing
55
What are alternatives to induction drug regimens?
Transfusion | Irradiation
56
What is a maintenance drug regimen?
Lower potency immunosuppressant drugs | Chronic use
57
What is a rescue immunosuppressant drug regimen?
Intense, effective doses given in response to rejection episode
58
What is determined by the patients medical history, which dictates the selection of immunosuppressant drugs?
Potential severity of rejection
59
3 drugs commonly involved in maintenance therapy
Calcineurin inhibitor Anti-proliferative Steroid
60
Mechanisms by which drugs can prevent T cell activation:
``` Block CD3 Block CD28 (no B7) ```
61
What is calcineurin? What happens if inhibited?
Phosphatase that controls nuclear access of transcription factor NFAT Inhibition = no IL2 upregulation
62
How do glucocorticoids act on the cell?
Inhibit transcriptional regulation of of pro-inflammatory genes (can't produce IL2)
63
How do drugs inhibit T cell activation?
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
How does one immunosuppressant eliminate T cells?
Ab binding to CD52, inducing lysis via ab-mediated cytotoxicity and complement-mediated cytotoxicity
65
How do immunosuppressants deplete T cells?
Via IgG against T cell

CMD Block 2 (38 decks)

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