Autoimmunity Flashcards

1
Q

Distinguish between immunity, hypersensitivity/allergy, and autoimmunity

A

foreign material recognised and damaged - immunity
foreign material recognised and self material damaged - allergy/hypersensitivity
self material recognised and self material damaged

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2
Q

explain the 4 types of hypersensitivity

A

ATOPIC (type I) - involves IgE, sensitive to an allergen and triggers inflammatory response on 2nd exposure

CELL/MEMBRANE REACTIVE (type II) - bind IgG to IgM/IgA antibodies on cells surface antigens cause destruction (haemolytic transfusion reaction)

IMMUNE COMPLEX (type III) - forms immune complexes that precipitate and deposit. Body’s attempt to remove can cause damage

CELL MEDIATED (type IV) - T-cell mediated, exposure to antigen triggers inflammatory response

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3
Q

Broadly, explain Grave’s disease. What is seen at the neck?

A

autoimmune hyperthyroidism

swelling in neck where thyroids are found

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4
Q

What kind of thyroidism is Graves’?

A

hyperthyroidism

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5
Q

Explain the pathophysiology of Graves’ disease

A

auto-reactive b cells make anti-TSH antibodies that bind to receptors and thyroid stimulating antibodies which switches off TSH but no effect on b cells
=low TSH but high TH

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6
Q

Consdiering TSH and thyroid hormones, what would be their levels?

A

low TSH

high TH

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7
Q

How can babies get Graves from their mothers?

A

IgG can cross the placenta
baby can be born with symptoms of Graves’ disease but as they aren’t making it antibodies are removed by body’s natural degradation or plasmapheresis and then symptoms disappear

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8
Q

What happens to the eyes in Graves’?

A

Grave’s opthalmopathy
inflammatory process of orbital tissue - affects ct and muscle surrounding the eyes
Retraction of lower eyelid
this can all cause protrusion of eyeballs

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9
Q

Explain the pathophysiology of Graves’ ophthalmopathy

A

some expression of TSH on the CT of the eyes means autoimmune process translates onto orbital tissue
stimulates cytokines -> triggers GAGs -> brings mucinous substances that cause oedema

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10
Q

What do TSHR-antibodies cause

A

autoimmune hypothyroidism

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11
Q

Explain Hashimoto’s thyroiditis

A

swelling of thyroid tissue on the neck (goiter) caused by destruction of thyroid tissue as a result of proliferation of thyroid lymphocyte infiltrating the tissue

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12
Q

Explain pernicious anaemia. What’s the cell under attack, and what are the 2 ways in which Abs bind to a target

A

B12 malabsorption and antibiotics attack stomach wall
Parietal cell is targeted - these cells secrete IF which help absorbs B12

B cells secrete antibiotics that bind IF to themselves - bind to either the part that would bind to B12 or to ileum

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13
Q

Explain type 1 DM

A

beta cells specific T cells recognise peptides from insulin or glutamic acid decarboxylase and target beta cells in islets

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14
Q

Explain autoimmune haemolytic anaemia

A

destruction of mature RBCs
antibodies bind to surface of RBC and opsonise (makes it more susceptible to phagocytosis) the surface which then bind to FCR on phagocytes and get destroyed or activates the complement pathway to form the membrane attack complex

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15
Q

What is Goodpasture’s disease and what kind of hypersensitivity is it?

A

type II hypersensitivity

binds directly to glomerular basement membranes (type II collagen) - eventual kidney failure

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16
Q

What happens in Lupus?

A

As cells die in patient’s body, those released constituents then form immune copmlexes with the antibodies, which then deposit and damage tissue.
Vasculitis. Damage to muscle, joints, CNS, kidneys etc. Pic on left shows kidney damage.
and damage to skin by UK which releases contents which then form immune comple