immune disease 1 (W12) Flashcards

1
Q

innate lymphocytes features?

A

fast response
not adaptive - born with them and haven’t changed

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2
Q

innate lymphocytes function?

A

respond quickly to alert signals from sentinel cells near surfaces, and shape the subsequent adaptive immune response with cytokines

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3
Q

what life history factors can predispose you to different types of immunological tuning

A

nutrition (eg high salt = more inflammatory)
pollutants
chronic infection
sex hormones
immune ageing

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4
Q

2 types of harmful immune reactions

A

hypersensitivity (allergy)
autoimmunity (intolerance of self antigens that drives tissue damage)

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5
Q

how do we lose self-tolerance enough to cause disease?

A

neoantigen - self antigens become modified
molecular mimicry - microbe antigens resemble self
damage exposes hidden antigens (eg histones in dna)

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6
Q

majority of autoimmune diagnoses in men or women?

A

women (80%)

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7
Q

serum autoantibodies?

A

just having serum autoantibodies alone doesn’t mean disease. low level autoantibodies common with age, some produced after damage may help clear disease

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8
Q

susceptibility genes for autoimmunity?

A

risk alleles - MHC alleles, affect peptide binding for antigen presentation

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9
Q

why are most autoimmune diseases more common in women

A

sex steroids
X-chromosome influence autoimmunity

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10
Q

sex steroids and immune system/inflammation

A

oestrogen usually pro-inflammatory
progesterone usually anti-inflammatory
testosterone immunosuppression

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11
Q

pregnancy effects on RA and SLE (lupus)

A

RA flares improve
SLE flares worsen

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12
Q

post-partum effects on RA and SLE (lupus)

A

SLE and RA flares worsen

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13
Q

menopause effects on RA and SLE (lupus)

A

SLE flares improve, RA flares worsen

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14
Q

what is converted to oestrogen and why in inflamed tissues

A

androgen converted to oestrogen.
cytokines increase aromatase which cause this. makes tissue more inflammatory

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15
Q

what inhibits conversion of androgen to oestrogen

A

TNF (cytokine) inhibitors

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16
Q

atopy?

A

predisposition to become IgE-sensitised to innocuous environmental Ag (allergen)

17
Q

unwanted anti-parasite immune response to innocuous antigen?

A

exposure to antigen in skin/mucosa, ILC2 react, dendritic cells migrate and present antigen in node. naive T cells polarise to TH2 cells that induce B cells to switch to IgE production and mature

18
Q

IgE-mediated mast cell reactions

A

mast cells collected IgE. Synthesis of PG, LT, cytokines, chemokines. degranulation (histamine, proteases)
immediate and late effects

19
Q

immediate effects of IgE-mediated mast cell reactions

A

skin- itch, oedema, redness
airway- mucosal oedema, bronchospasm
gut- colic, diarrhoea, vomiting
blood- anaphylaxis

20
Q

late effects of IgE-mediated mast cell reactions? what can these be treated with

A

more oedema
inflammatory cells
glucocorticoids

21
Q

symptoms of anaphylaxis

A

difficulty breathing
vascular shock (low bp, tachycardia)
skin- evolving redness, itch, swelling
mucosal oedema
gut spasm

22
Q

treatment of anaphylaxis

A

early i.m. adrenaline (+ oxygen, antihistamine, corticosteroid

23
Q

non-allergen causes of mast cell degranulation?

A

radiocontrast medium, opiates, NSAID, anaphylotoxins (C3a, C5a), physical (heat/cold/vibration)

24
Q

chronic example of igE-mediated allergic diseases?

A

chronic allergic asthma

25
Q

chronic allergic asthma?

A

would healing scarring response - airway remodelling. goblet cell metaplasia, fibrosis of sub-epithelial collagen, hypertrophy of smooth muscle, chronic inflammation

26
Q

rhinovirus infection significance in chronic allergic asthma patients

A

patients airways are permanently narrowed therefore increased risk to irritants such as rhinovirus