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Inflammation > Inflammatory diseases > Flashcards

Inflammatory diseases Flashcards

1
Q

What is atopy?

A

genetic predisposition to developing these allergies

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2
Q

how do allergies happen?

A

The body produces IgE against innocuous substances e.g. peanuts

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3
Q

What is anaphylaxis?

A

is the airways being constricted until suffocation occurs.

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4
Q

Is an allergy the breakdown or delay of tolerance?

A

yes

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5
Q

the antibody IgE binds to what cell?

A

mast cells

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6
Q

How does the mast cell release granules when IgE binds?

A

the allergen crosslinks the IgE

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7
Q

What do mast cell granulomas release?

A

histamine

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8
Q

What does histamine do if the allergy is in the blood stream?

A

will cause fluids to go into the skin and you will get hives or anaphylaxis.

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9
Q

If allergens enter through the skin what does histamine do?

A

will cause a wheel (swelling) and flair (redness) response.

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10
Q

What does histamine do when you inhale allergens?

A

sneezing, nasal irritation and increased production of mucus. You might get asthma

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11
Q

what does histamine do if you ingest an allergen?

A

– diarrhea and vomiting or can diffuse into the bloodstream.

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12
Q

Is childhood exposure to possible allergens good?

A

yes

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13
Q

How do you treat a peanut allergy?

A

Avoidance, epi-pen, hospital treatment or oral immunotherapy.

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14
Q

What does an epi-pen do?

A

inject and the adrenaline can reverse the effects of histamine, increases blood pressure, increased heartrate, relaxes smooth muscle.

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15
Q

What do antihistimines do?

A

prevent the action of histamine of various histamine receptors

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16
Q

What can antihistimines be used for apart from stopping histamine?

A

Antiemetic (car and sea sickness – relax smooth muscle of the gut which reduces the chances of vomiting), sedation

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17
Q

what causes rheumatoid arthritis?

A

unsure, could be genetic, could be smoking, could be stress

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18
Q

What membrane in the small joints is inflammed in rheumatoid arthritis?

A

synobial membrane

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19
Q

What enters the synobial membrane tissue when inflammed during arthritis?

A

T-cells

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20
Q

After entering the cell in arthritis the T-cell responds to what dispalyed by the macrophages?

A

autoantigens

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21
Q

What does the T-cell release when responding to autoantigens?

A

interferon-gamma

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22
Q

what does interferon-gamma make macrophages do?

A

release pro-inflammatory cytokines

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23
Q

What do pro-inflammatory cytokines target in rheumatoid arthiritis?

A

fibroblasts

24
Q

what do fibroblasts release?

A

MMP (proteases) and RANK ligand

25
Q

What do MMPs do?

A

break down proteins such as soft tissues

26
Q

what does RANK ligand do?

A

triggers osteoclasts which break down bone

27
Q

How do you treat rheumatoid arthritis?

A

steroids and aTNF antagonists

28
Q

Examples of TNF antagonists: How does the antagonist Etanercept work?

A

TNFR receptor fuses to the IgG antibody which competes with TNF receptor in the tissue and mops up TNFalpha meaning the cytokine will be less so less inflammation.

29
Q

How does the antagonist infliximab work?

A

monoclonal antibody which can bind to TNFalpha

30
Q

What happens when you get infected with TB?

A

Macrophages will ingest and phagocytose the mycobacteria, some of which is destroyed but others will remain within cytoplasm of the macrophage.

31
Q

what happens to the TB in the cytoplasm of macrophages?

A

CD4 T cells release interferon gamma which activates infected macrophages to release TNF alpha

32
Q

what does the macrophage releasing TNF-alpha do to itself

A

Activates macrophages further and develop protective structures called granulomas

33
Q

what are granulomas surrounded by and what does this do?

A

T-cells which secrete interferon gamma to make macrophages more activated so it can keep the mycobacteria within.

34
Q

what happens to granulomas if you take infliximab?

A

break down releasing microbacteria making TB active once more and form new granulomas outside of the lungs

35
Q

ulcerative colitis: what do dendritic cells do?

A

sample the contents of the gut lumen.

36
Q

What recognises bacteria?

A

Pattern recognition receptors (PRR)

37
Q

In normal circumstances what does PRR signalling trigger?

A

anti-inflammatory responses.

38
Q

Why would bacteria be able to breakdown the gut barrier?

A

some bacteria can use mucus as a form of energy or something from the gut will go into the gut lumen and cause inflammation.

39
Q

What happens if the gut barrier is broken down?

A

bacteria can flood into another area of the body

40
Q

What do T-cells do in the inflammatory response to commensals being in the wrong place?

A

increasing pro-inflammatory cytokines.

41
Q

What happens if people have genetic mutations in PRR?

A

anti-inflammatory response to make a pro-inflammatory respons

42
Q

How do lymphocytes enter microbial tissue?

A

MAdCAM1 adhesion.

43
Q

What are some targets for ulcerative colitis?

A

target TNF-alpha, IL-6 receptor inhibition etc.

44
Q

What are signs of SIRS and Sepsis?

A

Temp more than 38 and lower than 36
Tachycardia
Hypo or hyperventilation
Low or high White blood count

45
Q

What is SIRS?

A

Systemic Inflammatory response syndrome (SIRS)

46
Q

What is sepsis?

A

SIRS due to infection

47
Q

What occurs during sepsis? (what gets into the blood stream and what happens from there?)

A

bacteria get into blood and disseminate through the body. lots of macrophages in the spleen releases TNF-alpha which acts on small blood vessels in the body

48
Q

What does TNF-alpha do to small blood vessels?

A

vasodilaton,
increased premeability - leak of all fluids,
diseminated intravascular coagulation –clots,
vascular collapse,
reduced prefusion of organs leading to organ failure and death

49
Q

How do you treat sepsis list?

A

Early recognition

Supportive therapies – ventilation, perfusion, fluids

Regular blood monitoring

Broad spectrum antibiotic – early stages of sepsis – but you want to identify the infection quickly.

Remove source of infection e.g. infected joint, peritoneal abscess, appendix.

50
Q

Examples of steroidal anti-inflammatory drugs?

A

Hydrocortisone, prednisolone, dexamethasone

51
Q

Do steroidal anti-inflammatory drugs decrease diapedesis and inflammatory cell activation?

A

yes

52
Q

Do steroidal anti-inflammatory drugs increase T-cell activation?

A

No they decrease it

53
Q

Do steroidal anti-inflammatory drugs decrease fibroblast function?

A

yes

54
Q

Do steroidal anti-inflammatory drugs decrease expression of COX-2 (prostaglandins)?

A

yes

55
Q

Do steroidal anti-inflammatory drugs decrease release of anti-inflammatory mediaters?

A

yes

56
Q

Do steroidal anti-inflammatory drugs increase release of anti-inflammatory cytokines?

A

yes

57
Q

Whats the best NSAID for inflammation?

A

ibroprofen

Inflammation (2 decks)

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