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UofG Medicine Question Bank 2020 > Autoimmunity > Flashcards

Autoimmunity Flashcards

1
Q

What is a break in Tolerance?

A

The immune system mistakenly attacks itself, and fails to tolerate self-cells

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2
Q

Does autoimmune disease primarily affect males or females?

A

Females

Not sure why, possibly related to sex hormones or how the immune system functions in different sexes

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3
Q

What causes autoimmunity?

A

Genetics (several polymorphisms) in combination with infection and environmental exposures

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4
Q

How is nature of autoimmune disease determined?

A

Type of dominant immune response

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5
Q

Over time, how does the response to self change?

A

Changes from autoimmune response with a little inflammation, to low autoimmune response with lots of inflammation

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6
Q

What is central tolerance?

A

Development and education of the immune system (bone marrow, and thymus- B cells, T cells formation and education)

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7
Q

What is peripheral tolerance?

A

Where mature Immune cells can leave and go to Secondary lymphoid organs, and we have mechanisms here that can suppress autoimmune responses that can be lost (Treg).

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8
Q

What is molecular mimicry in relation to autoimmunity?

A

Bacterial epitope looks similar to something we have within ourselves.
So if we generate a response to a foreign bacteria that looks similar to our self cells, it may result in mounting an autoimmune response.

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9
Q

What is inappropriate activation of the immune system?

A

When a response is mounted by the immune system and said target is not appropriate, i.e. a response to self-cells

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10
Q

What type of regulation occurs within the central thymic centre in relation to limiting risk of autoimmunity?

A

Positive and negative selection of T cells

Killing of T cells that are self reactive, or not reactive enough

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11
Q

What type of regulation occurs within the peripheral

centre in relation to limiting risk of autoimmunity?

A 
Regulatory T and B cells 
Dendritic cells and danger
Co-stimulation
Ignorance 
Privilege
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12
Q

What genes are related to autoimmune disease?

A 
HLA genes (T cell communication) 
AIRE
CTLA4
FOXP4
FAS
C1q
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13
Q

Are most gene-related predispositions to autoimmunity monogenic or polygenic?

A

Polygenic

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14
Q

What is the hygiene hypothesis?

A

Too clean of an environment.
If we aren’t exposed to enough bacteria/viruses, our immune system wont be educated enough to effectively fight infection

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15
Q

What is the pathogenesis of autoimmunity?

A

Susceptibility gene -> Failure of self-tolerance -> persistence of functional self-reactive lymphocytes (they are there, but don’t drive pathology) -> Trigger event (can be environmental, stress, injury) -> activation of self-reactive lymphocytes -> immune response against self tissue

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16
Q

What cells are responsible for autoimmunity?

A

T cells and B cells forming autoantibodies

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17
Q

What is an autoantibody

A

Antibody that reacts to the epitope of a self-antigen.

May or may not be pathogenic

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18
Q

What are some autoimmune diseases involving autoantibodies? Name the target of the abs.

A

Graves Disease (TSH receptor)
Myasthenia Gravis (Acetyl choline receptor)
Idiopathic Thrombocytopenic purpura ITP (platelets)
Guillain-Barre Syndrome (Gangliosides within plasma membrane)
Multiple Sclerosis (related to demyelination)

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19
Q

How is Grave’s Disease caused?

A

Autoantibodies to TSH produced that can bind the TSH receptor stimulating thyroid synthesis.
Removes self-regulation of thyroid hormone to pituitary gland.

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20
Q

How is Myasthenia Gravis caused?

A

Autoantibody to acetylcholine receptor, binding to Ach receptor helping to induce internalisation and degradation of the receptor (therefore no response to Ach).
Can also bind to Ach receptor and block Ach interaction.
No/weakened muscle contraction

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21
Q

In autoimmune diseases involving autoantibodies, do T cells play a role?

A

Yes

T cell specific for auto–antigen may help generate anti-host response

22
Q

What are some organ specific autoimmune diseases?

A 
Hashimoto Thyroiditis
Thyrotoxicosis
Guillain-Barre Syndrome
T1 Diabetes
Multiple Sclerosis
Atrophic Gastritis
Addison's Disease
Grave's Disease
23
Q

What are some non-organ specific autoimmune diseases?

A 
Systemic Lupus
Rheumatoid Arthritis
Scleroderma (attacks collagen)
Dermatomyositis
Mixed connective tissue disease
Sjogren's Syndrome (attacks secretions- dry eyes/mouth)
24
Q

What is organ specific autoimmunity?

A

Autoimmune attack against the self antigens of a specific organ

25
Q

What is Guillain-Barre Syndrome?

A

A transient autoimmune disease
Auto-antibody mediated autoimmune disease to gangliosides of peripheral nerves
Infection with C. jejuni -> antibody formation for bacteria (similar to gangliosides in self- cell membranes). -> Can result in stripping of myelination from cells, inappropriate nerve firing, and lack of muscle innervation.
B cells response is tied to the infection, and B cells will stop producing the antibodies, but the other pre-existing antibodies will prolong and can cause the listed damage.

26
Q

What is the evolving pathogenesis of rheumatoid arthritis (name the phases)?

A

Genetic predisposition + environmental factors
Pre-articular or lymphoid phase (RF, CCP-specific ab, collagen specific response, GF 39-specific response)
Transition phase (some sort of insult)
Articular phase (articular localization, CVD, osteoporosis, functional decline)

27
Q

How long to pre-clinical trials typically take?

A

3-5 years

28
Q

What is phase 1 clinical trials?

A

Study of effects on health human (20-50)

29
Q

What is phase 2 clinical trials?

A

Limited study of patients (50-100)

30
Q

What is phase 3 clinical trials?

A

Comparative studies on large number of patients (500-5000)

Cost millions by this point

31
Q

What is NDA phase of clinical trials?

A

Authorization process

32
Q

What is phase 4 clinical trials?

A

Continued comparative studies

Evaluate long term impacts

33
Q

How much do clinical trials cost, and how long do they typically last?

A

5-8 years

Costs over 150million

34
Q

What 3 symptoms do NSAIDs try to target?

A

Analgesic- pain
Antipyretic- reduce body temp
Anti-inflammatory- at higher disease- reduce inflammation

35
Q

What is the process of enzyme activation in creating inflammatory responses in the body?

A

Phospholipases create arachidonic acid
AA is converted by Cox2 to prostaglandin G2, and then into prostacyclin (PGI2), PGD2 and PGE2 (primary role in pyrogenics), which all contribute to vasodilation and inflammation.

36
Q

What does prostacyclin I and E do?

A

I- Causes vasodilation, inhibits platelet aggregation

E- Important mediator of inflammatory responses and causes fever and pain

37
Q

What does thromboxane do?

A

Causes vasoconstriction, promotes platelet aggregation

38
Q

How does Aspirin impact inflammation? Describe its mechanism of action.

A

Prevents prostacyclin/ thromboxane a2/prostaglandin production by inhibiting Cox1 and Cox2 non-selectively.
This inhibition prevents conversion of arachidonic acid into prostaglandin G2 (PGG2) and the listed products.

39
Q

What does Cox1 produce?

A

Thromboxane A2

40
Q

What does Cox2 produce?

A

PGE2, PGD2, and PGI2

Has a side pocket

41
Q

Do NSAIDs impact cox1 or 2?

A

Both

42
Q

What impact does paracetamol have within the body?

A

Analgesia
Anti-pyretic (via inhibiting pyrogens, like IL1 released from leukocytes, acts directly on thermoregulatory centre in hypothalamus)
Can be hepatotoxic

43
Q

What impact does aspirin have within the body?

A

Analgesia
Anti-platelet
Anti-inflammation (although not primary use)

44
Q

How do NSAIDs impact the gastric mucosa?

A

Prostaglandin (produced using Cox1) pushes mucosa out to protect the stomach lining
Aspirin will block prostaglandin preventing bicarbonate and mucosa production.
This means gastric lining can be damaged by acid, causing peptic ulcers, perforation and septicaemia

45
Q

What do exogenous corticoid drugs mimic within the body?

A

Drugs mimic endogenous hormones (glucocorticoids (immunosuppressants) and mineralocorticoids (salt and water metabolism)) that are normally produced by adrenals

46
Q

What is a side effect of exogenous corticoids?

A

They impact our metabolism as they are very close to the mineralocorticoids (which can impact electrolyte/fluid balance- aldosterone is a mineralocorticoid)

47
Q

How do exogenous corticoids work?

A

Increase transcription of anti-inflammatories (annexin-1) and decrease transcription of inflammatory mediators (cytokines, chemokines, adhesion molecules)

48
Q

What is annexin 1?

A

A protein that blocks the production of arachidonic acid by binding/inhibiting phospholipases
VERY strong, and more effective than NSAIDs
Used in many auto-immune diseases

49
Q

What are the side effects of annexin-1?

A 
Mess up metabolism (fat stomach, thin arms)
Cataracts 
Mood (euphoria then depression)
Poor wound healing
Osteoporosis
Tendency for hyperglycaemia
50
Q

What pathology commonly and safely utilizes corticosteroids for treatment?

A

Asthma via inhalers
Not a systemic use, it is direct in the lungs
There is some exchange into systemic circulation
There is a modified version that is inactivated via first-pass metabolism in the liver

51
Q

What are biological agents?

A

Monoclonal antibodies
They are biological drugs that are every specific
Problems: Increased risk of infection, expensive, intolerance/inadequate response in some patients

52
Q

What are immune-checkpoint inhibitor drugs?

A

Check point proteins block T cell activity, so inhibiting them will result in an immune boosting.
“They work by blocking checkpoint proteins from binding with their partner proteins. This prevents the “off” signal from being sent, allowing the T cells to kill cancer cells.”
Used in treating cancer- but have side effects with people with chronic inflammatory disorders

UofG Medicine Question Bank 2020 (42 decks)

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