Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

What three inflammatory mediators are produced from arachidonic acid from phospholipids, and which enzymes are involved?

A

Leukotrienes
Thromboxane A2 (vasoconstictor and platelet agonist) - cyclooxygenase enzyme
Prostaglandins (bronchodilator, vasodilator) - cyclooxygenase enzyme
[Lipoxins (anti-inflammatory mediator) - 15-lipoxygenase]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the three effects of NSAIDs (3 As)?

A

Anti-inflammatory
Analgesic
Antipyrexic
[except paracetamol, which isn’t anti-inflammatory]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is aspirin?

A

Irreversible antagonist of COX-1 and COX-2.

inhibition of COX-2 upregulates production of lipoxins from arachidonic acid which have anti-inflammatory effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the side effects of aspirin?

A

Hearing loss, petechia, peptic ulceration, MI, vomiting blood (haememesis), blood in stool (melena), tachycardia and dyspnoea, urticaria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the two isoforms of cyclooxygenase, and where are they found?

A

1) Constitutive = COX-1, found in stomach, intestines, platelets, endothelial cells
2) Induced = COX-2, found in cells at inflammatory sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why does ibuprofen have less severe side effects than aspirin?

A

It is a reversible cyclooxygenase antagonist, not irreversible like aspirin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do NSAIDs block cyclooxygenase?

A

They bind to an allostearic site which blocks the “channel of access” so arachidonic acid can’t reach the catalytic site and produce prostaglandins, superoxide, proteases, thromboxane A2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is different about 2nd generation NSAIDs, but what is the problem with them?

A

They specifically inhibit COX-2, but they carry a risk of myocardial infarction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some examples of second generation NSAIDs?

A

celecoxib, etoricoxib

[all end in -coxib]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are NO-NSAIDs?

A

Nitric oxide secreting NSAIDs which have a gastro-protective effect and increased anti-inflammatory activity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the major inflammatory cytokines?

A

Tumour necrosis factor (TNF), IL-1, IL-3, IL-4, IL-5, Granulocyte macrophage colony stimulating factor (GM-CSF), CXCL8 (chemokine).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are SAIDs?

A

Glucocorticoids, based on the body’s own endogenous hormones (cortisol produced from cholesterol).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the problem with using glucocorticoids?

A

They are very efficacious, so they are good for topical, acute use, but have severe side effects with chronic use.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do glucocorticoids work?

A

They diffuse into the cell and bind to the receptor in the cytosol, this complex then diffuses into the nucleus and acts as a transcription factor, binding to the promotor of an inflammatory gene. They downregulate the transcription of inflammatory genes (which produce the inflammatory cytokines).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which genes are downregulated by glucocorticoids?

A

Nitric oxide synthesase
COX and phospholipase A2 (involved in the production of prostaglandins)
Adhesion molecules, so reduce diapedesis
[upregulate endonucleases so cause apoptosis in lymphocytes and eosinophils]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the side effects of chronic use of glucocorticoids?

A

Osteoporosis
Iatrogenic Cushing’s syndrome
Susceptibility to infections
Suppression of endogenous glucocorticoid synthesis
Affecting carbohydrate and protein metabolism

17
Q

Which are the complement proteins that are anaphylotoxins (strong pro-inflammatory factors) and what are their effects?

A

C3a and C5a

Cause increased permeability of capillaries, vasodilation, chemotaxis, Mast cell activation

18
Q

What are the effects of histamine receptor activation?

A 
Stimulation of gastric acid secretion
Bronchoconstriction
Vasodilation
Positive chronotropy
Increased permeability of capillaries
19
Q

What is a side effect of antihistamines?

A

Sedation

20
Q

What is the term used to describe tissue rejection?

A

Graft vs. Host disease.

21
Q

What is the effect of cyclosporin A and tacrolimus?

A

Inhibit production of IL-2 by stopping the transcription in T cells. This has an anti-inflammatory effect because IL-2 promotes T-cell differentiation.

22
Q

What is the effect of rapamycin?

A

Binds to FK-binding protein (receptor) and blocks signal transduction of IL-2 in T cells so stops clonal selection.

23
Q

What is Basiliximab?

A

A monoclonal antibody which can be used as an immunosuppressant because it targets the IL-2 receptor.

24
Q

Which structures allow lymphocytes to directly enter lymph nodes from the blood?

A

High Endothelial Venules

25
Q

What is the Lewis Triple Response, and which compound is involved in each effect?

A

Histamine is involved in each
Flair - histamine acting on nerve endings
Wheal - oedema due to histamine
Reddening - vasodilation due to histamine

Immunology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions