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633 > Moskovitz Immune system > Flashcards

Moskovitz Immune system Flashcards

1
Q

Physiologic Roots of Inflammation

A controlled inflammatory response is generally considered? But?

Acut inflammatory response:

Delivery of?

Triggered by?

Production of?

____ killing of pathogens

If neutrophils fail?

A
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2
Q

The cyclooxtgenase pathway

The COX pathway produces? 2 things

COX isoforms?

COX-1 activity is typically present and expressed by? Produces what with “housekeeping” function

Examples of these function 4 things

A
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3
Q

Prostaglandins

What common chemical structure is shared?

4 bioactive ones?

Each cell type generates one or two dominant producted which act as?

Prostaglandin production is typically?

When is production increased?

A
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4
Q

Glucocorticoids

Name some

Inhibit the action of ____ in what 3 ways?

used to treat patients with?

A
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5
Q

PGE2

One of the most? During inflammation what is it responsible for 3?

What do some of these stem from?

What about the other response?

Clinical relevance? Plays a role in the development of?

A
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6
Q

Case study continued NSAIDs and GI Toxicity

Which factors are important in determining the risk for the development of NSAID induced GI bleeding?

What has been developed to prevent this?

A
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7
Q

Oxicams

Meloxicam- kinetics?

Selective for?

Fenamates

Meclofenamate

Tx of?

High incidence of?

A
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8
Q

Microbial Inducers and Sensors

Exogenous inducers can be microbial or non microbial

Pathogen-associated molecular patterns (PAMPs)? What are they who carries them?

Virulence factors:

Unlike PAMPs they are not?

These factors cause what two negative affects which in turn causes?

Inflammasome

What is the inflammasome sensitive to?

A
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9
Q

Case study NSAIDs and GI toxicity

A
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10
Q

Endogenous Inducers: clinical relevance

Advanced glycation end products (AGEs)

The glycation of long lived proteins, such as collagen can result in?

AGEs are recognized alone by the receptor?

What situation would you expect the accumulations of AGEs?

A
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11
Q

Propanoic Acids

Naproxen (Aleve) and Ibuprofen (Advil)

High doses may have less?

Ibuprofen has a short? Naproxen?

A
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12
Q

Prostaglandins as therapeutic targets

THe NSAIDs

What do they do?

Prevent generation of?

Limits?

A
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13
Q

SEs associated with chronic glucocorticoid use

A

• Given the vast array of biological effects mediated by prostaglandins, the use of prostaglandins blocking drugs should be considered based on the individual condition

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14
Q

Lipid Mediators: Arachidonic Acid

Comes from what precursor? Only obtained?

Released from phospholipids by what enzyme?

This enzyme is stimulated by?

What type of drugs inhibit this?

Lipocortins? Another family? Suppression of?

____ supresses phospholipase A2 and?

A
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15
Q

Overview of Eicosanoid Functions

Examples of their function?

Regulation of what 3 things?

A
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16
Q

Inflammatory Mediators Overview

Mediators can be classified into 7 groups according to their biochemical properties

Vasoactive amines (_____)

  • Secreted in what manner and when?
  • What 2 things can it cause?

Vasoactive molecules (_____)

  • Stored in what form or generated by?
  • Cause what 2 things?

Complement proteins

  • Produced by?
  • ___ promotes ____ recruittment and Induce what type of degranulation? This affects?

Inflammatory cytokines

  • What are 3 examples?
  • Produced by many cell types but what are the two important ones?
  • Have many roles but activation and induction of what is the example?

Chemokines

  • Produced by? Control what 2 things towards the affected tissue?

Proteolytic Enzymes

  • Degrades what things?
  • Important roles in what 3 things?

Lipid Mediators

  • Derived from?
  • Why are these important?

Arachidonic Acid

  • Synthesized from? Linked to?
  • Different pathways can form different?
A
  • – Vasoactive amines (histamine)
    • Secreted in all-or-none manner when mast cells and platelets degranulate
    • Can cause vasodilation and increased vascular permeability –
      • Vasoactive molecules (serotonin)
    • Stored in active form in secretory vesicle or generated by proteolytic processing of inactive precursors
    • Cause vasodilation and increased vascular permeability
  • Complement proteins
    • Complement fragments are produced by several pathways
    • C5a promotes leukocyte recruitment and induce mast-cell degranulation, affecting the vasculature
  • Inflammatory cytokines
    • Examples include tumor-necrosis factor-α (TNF-α), IL-1, IL-6, and many others
    • Produced by many cell types, but most importantly by macrophage and mast cells
    • Have several roles, including activation of the endothelium and leukocytes and induction of the acute-phase response
  • Chemokines
    • Produced by many cell types, and controls leukocytes extravasation and chemotaxis towards the affected tissues
  • Proteolytic enzymes
    • Degrades the extracellular matrix and basement-membrane proteins
    • Have important roles in host defense, tissue modeling, and leukocyte migration
  • Lipid mediators:
    • These are derived from phospholipids that are present in cellular membranes
    • These mediators represent an important focus of discussion, as they represent current targets of anti-inflammatory therapies
  • Arachidonic Acid (AA)
    • AA is synthesized from fatty acids, and is linked to membrane phospholipids
    • Different pathways can form different metabolites of AA, as shown on the next slide
17
Q

PGD2

Sythesized in? What 2 things does it regulate?

What other places?

Involved in what type of reponse?

Clinical relevance?

A
18
Q

Salicylates (nonacetylated)

Diflunisal and Salsalate

No significant effect on?

Less frequent?

Generally tolerated by?

Relatively slow?

A
19
Q

The Inflammatory Pathway

Inducers

Sensors

Mediators

A
20
Q

Non Microbial Inducers and Sensors

Exogenous Examples? Think of? The sensors for allergens?

Asbestos

Endogenous inducers of inflammation- Signals are produced by? Sensors are able to detect?

How are cells and tissues able to distinguish between normal and stressed, damaged, or dysfunction states? What can they detect?

“separation strategy”

Examples supporting the things

A
21
Q

Acetic Acids

Diclofenac (Voltaren) and Indomethacin (indocin)

Diclo

Available as? When would this be useful?

Indomethacin?

Useful for the tx of?, potently? SEs?

A
22
Q

Nonacidic- Nabumetone only drug in class

Kinetics? Selective for?

Celecoxib?

Reduction in? Why is this?

What risks are dose related?

A
23
Q

PGF2a

Acts in the female?

Important role in?

Recent studies show important activity in 4 things?

Leads to? Suppressed by?

Clincial relevance in 3 disease states?

A
24
Q

Inflammasome case

Given the preceding information, what molecule(s) could be acting like inducers of inflammation (DAMPs or PAMPs) in the setting of atherosclerosis?

A
25
Q

Endogenous Inducers: Clinical relevance

Example of an inducer involved in chronic inflammation:

____ is cause by a build up of _______ crystals in joints, bones, and soft tissue

Hyperuricemia?

At higher concentrations?

When urate crystals reach a certain size, they are?

Phagocytosis triggers activation of?

A
26
Q

Inflammasome case

Activation of the inflammasome has been strongly linked to Know this one you can answer the rest?

Inflammation is thought to promote?

Where would you expect inflammation to take place?

What might be inducers of the inflammation?

A
27
Q

Case Study the Inflammasome

Inflammasomes are systems of innate immune receptors/ sensors: That are responsible for?

Inflammasomes have been linked to a variety of diseases?

A
28
Q

Thromboxane

TXA2 is an unstable metabolite of? Half life?

TXA2 functions?

Mediates platelet?

Mediates smooth muscle?

Activates?

Clinical Relevance?

A
29
Q

PGI2

Important regulator in?

What are 3 major sources of PGI2

PGI2 is an important mediator of? Associated with acute inflammation

CLincial relevance:

A
30
Q

Mediators and Effectors of Inflammation

Inducers trigger? What can these be derived from? Many of these affect?

Cellular Mediators? Produced by? Some are stored in?

Other mediators?

A
31
Q

Salicylate

Aspirin

High doses are limited by?

Used infrequently for?

What is different compared to other NSAIDs?

A
32
Q

Cyclo pathyway

COX-2

Expression is?

As inflammation progresses what happens?

Both isoforms generate? who cares?

A
33
Q

Common themes of all NSAIDs

Most have the option of?

Have a dose and age related risk of?

Can cause or worsen?

Avoided in what patients?

Use with caution in?

A
34
Q

From Atachidonic Acids

_____ are lipid signalling molecules derived from?

AA can be enzymatically metabolized by what 3 pathways?

A

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