Pathophysiology of Inflammation III Flashcards

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1
Q

In terms of regulation of inflammation, what are the 2 types?

A

Pro - Inflammatory

Anti - Inflammatory

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2
Q

What are the 2 main triggers of autoimmune disease?

A

Environment

Genetics

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3
Q

In terms of environmental triggers, name some examples.

A

Triggers // Infection // Microbiome // Tissue Injury

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4
Q

In terms of genetic triggers, name some examples.

A

Multiple genetic polymorphisms in immune related genes IMPAIR immune regulation.

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5
Q

In terms of auto reactive lymphocytes, what are the 2 types of cells?

A

Auto - reactive T - cells

Auto - reactive B - cells.

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6
Q

What are auto - reactive lymphocytes?

A

Reacts to NORMAL tissues -> attacks joints // pancreas

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7
Q

What does the auto - reactive T - cells do?

A

Attack the tissues directly.

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8
Q

What does the auto - reactive B - cells do?

A

Autoantibodies made which can attack your own tissue cells.

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9
Q

What are the stages of an autoimmune disease?

A
Initiation
Propagation 
Resolution 
Propagation 
Resolution
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10
Q

In terms of autoimmune diseases, what happens to the tissues and organs over time?

A

Over time, the progressive damage of the affected tissues and organs REDUCES.

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11
Q

Which type of inflammatory are T - Reg cells?

A

T - Reg cells are anti - inflammatory.

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12
Q

Which type of inflammatory are T - Pro cells?

A

T - Pro cells are pro - inflammatory.

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13
Q

What is the purpose of CCP - antibodies?

A

These attack the tissues in the body as it is acute inflammation and gives TISSUE DESTRUCTION.

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14
Q

Why when doing an x - ray can the hands look normal?

A

This is because the disease could be at the early stages and therefore, the symptoms could be minor // show up elsewhere.

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15
Q

What is the erythrocyte sedimentation rate (ESR)?

A

This the type of blood test which measures how quickly RBC’s settle at the bottom of a test - tube which contains a blood sample.

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16
Q

What is the units for ESR?

A

mm / hr

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17
Q

What indicates inflammation during an ESR?

A

A faster rate than normal indicates inflammation.

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18
Q

What happens when there is a negative charge on red blood cells?

A

Negative charge results in RBC’s repelling.

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19
Q

What happens when there is a positive charge on red blood cells?

A

Positive charge results in fibrinogen causing RBC’s to stick together.

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20
Q

In terms of chronic inflammation, what happens to the proteins?

A

There is a change in the proteins.

21
Q

What are the 2 main environmental triggers for CCP antibodies?

A

Smoking

Gum Disease

22
Q

What is the process triggered by gum disease // smoking?

A
Deamination of arginine. 
Releases PAD (protein arginine deaminase). 
Some of the arginine goes to the citrulline and this is when the amino acids change and thus, TRIGGER an anti - cc antibody. 
These attack the joints and thus, ARTHRITIS occurs.
23
Q

What is the purpose of PAD? (protein arginine deaminase.)

A

These catalyse the hydrolysis of peptides - arginine.

24
Q

What is the first stage of RA?

A

No damage -> inflammation symptoms arise.

25
Q

What is the second stage of RA?

A

Symptoms of inflammation causes DAMAGE to the joint cartilage.

26
Q

What is the third stage of RA?

A

Damage extends from the cartilage to the bones -> this is known as EROSION.

27
Q

What is the fourth stage of RA?

A

NO inflammation in the joints BUT the joints do not work.

28
Q

What is the aim of anti - inflammatory drugs?

A

Reduce symptoms.

29
Q

What is the aim of disease modifying drugs?

A

Prevent long term tissue damage.

30
Q

What is the aim of physiotherapy // occupational therapy?

A

Maintain function.

31
Q

What is hypersensitivity?

A

This is an excessive // immune reaction to a foreign substance not otherwise considered to be noxious.
“Undesirable reactions are produced”

32
Q

What is Type I hypersensitivity?

A

Immediate // Anaphylatic.

It is a form of an allergy and its exposure is via ingestion // infection // inhalation.

33
Q

What is anaphylaxis?

A

This is a combination of oedema and airway constriction. This prevents the tissues from getting oxygen.

34
Q

Give some examples of diseases caused by type I hypersensitivity.

A

Conjunctivitis // Angio - Oedema // Eosinophilia // Rhinitis

35
Q

What is the mechanism of action for type I hypersensitivity?

A

Plasma cells secrete IgE (immunoglobulin E) antibodies. Binds to the mast cells and thus, releases histamines.
Activates an immune memory when exposure to allergens causing inflammation at the site as the blood flow to the affected tissues is affected.

36
Q

What are the symptoms of life - threatening acute reaction?

A
Swelling = Angiodema 
Fast heartbeat 
Blood pressure can DROP. 
Collapsing 
Confusion 
Wheezing 
Clammy skin 
Restricts the airways.
37
Q

What are the ways of treating anaphylaxis?

A

Anti - Histamine
Adrenaline Injection
Corticosteroids

38
Q

Explain more about the adrenaline injection. (Known as an Epi - Pen).

A

Vasoconstrictor which is an injection which contains epinephrine.
This NARROWS the blood vessels and opens the airways in the lungs.

39
Q

What is the purpose of corticosteroids in treating anaphylaxis?

A

Used for the 2nd round of inflammation.

BLOCKS histamine = BLOCKS vasodilators.

40
Q

Why may an epi - pen NOT work?

A

May not have FULLY circulated around the body.

41
Q

How can chronic type - 1 hypersensitivity be triggered?

A

House Dust mite.
Fungal Spores.
Animal Dander.

42
Q

In terms of preventing type - 1 hypersensitivity what is done?

A

Maintaining immunosuppression = NO inflammation.

Give corticosteroids // desensitisation.

43
Q

In terms of treating type - 1 hypersensitivity what is done?

A

Control flares or attacks with corticosteroids.

44
Q

What is type II antibody dependent cytotoxic hypersensitivity?

A

Antibody mediated process in which IgM and IgG antibodies are directed AGAINST antigens on cells.

45
Q

What does high levels of IgM indicate?

A

Sign of a new infection.

46
Q

What is the most common type of immunoglobulin found in the body?

A

IgG.

47
Q

What is type III complex mediated hypersensitivity?

A

Reactions are characterised by tissue damage -> Caused by the activation of complement in response to antigen - antibody complexes which are deposited in the tissues.

48
Q

What is type IV cell mediated // delayed hypersensitivity?

A

This is when the response is mediated by effector t - cells // macrophages and leukocytes.
They infiltrate a site of the antigen exposure and induce a delayed form of inflammatory tissue damage.