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Kidneys > Immunopath > Flashcards

Immunopath Flashcards

1
Q

What is type II hypersensitivity?

A

Antiobody mediated

IgM and IgG against cell-bound or extracellular matrix Ag

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2
Q

What is type III hypersensitivity?

A

Immune complex

IgM and IgG immune complex deposition

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3
Q

What is type I hypersensitivity?

A

Immediate type

IgE, mast cells and lipid mediators

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4
Q

What is type IV hypersensitivity?

A

Delayed type

CD4 mediated delayed type hypersensitivity

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5
Q

Which complement pathway are we interested in with regard to hypersensativities?

A

Classic

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6
Q

Complement pathway?

A

a

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7
Q

What does C3b do?

A

Binds to C3b receptor on phagocytes, opsonisation,! removal of immune ! complexes!

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8
Q

What does C5a do?

A

mediators of inflammation, phagocyte recruitment

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9
Q

What do C5b, C6, C7, C8, C9 do?

A

Membrane attack complex (MAC). Lysis of microbes and infected cells

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10
Q

What happens in type II hypersensitivity?

A

Binding of Abs to host antigens

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11
Q

What are the outcomes of type II hypersensitivity?

A

Injury due to activation of effector mechanisms

Abnormal physiological response (Graves & MG)

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12
Q

What does injury due to activation of effector mechanisms involve?

A
  •   C’activation
  •   Recruiment of inflammatory cells
  •   Activation via Fc Receptor
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13
Q

what does abnormal physiological response (Graves & MG) involve?

A
  •   Binding to receptors or proteins interfering with function
  •   Activation or inhibition.
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14
Q

What is the classic type II hypersensitivity?

A

Type II hypersensitivity responses often target erythrocytes

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15
Q

What are ABO blood group antigens?

A

Carbohydrate antigens,

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16
Q

What happens if you transfuse the wrong blood type?

A

Cause lysis, shock and potentially dath

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17
Q

What is a less common type II hypersensitivity?

A

Type II mediated drug allergies (rare)

eg penicillin, quinidine, methyldopa

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18
Q

What happens in type II drug allergies?

A

The drug becomes bound to red blood cells or platelets, which are then the target of anti-drug antibodies

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19
Q

Where are cells which are bound to drugs lysed in type II drug sensativity?

A

Splenic macrophages phagocytose the cells, resulting in haemolytic anaemia or thrombocytopenia

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20
Q

What happens if a mother is rhesis negative and she has a child which is rhesus positive?

A

Maternal antibodies can target foetal blood.

Can be a particularly big problem form the second child

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21
Q

How do we prevent against the development of an immune response against a rhesus +ve foetus?

A

Anti-Rh antibodies within 24 hrs of delivery remove fetal RBC’s in maternal circulation
Haemolytic

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22
Q

Can type II hypersensitivity responses can target tissues?

A

Yes

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23
Q

What is Goodpasture’s syndrome?

A

Antibodies are made against a variant of collagen type IV, a major component of basement membranes

24
Q

How does Goodpasture’s syndrome present?

A

Nephritis

slowing down of movement of antibodies allow them to activate against collagen in the nephron

25
Q

what does the thyroid gland do?

A

Thyroid gland essential for regulating metabolism through the production of thyroid hormones

26
Q

What does the thyroid gland do?

A

It produces thyroid hormones in response to thyroid stimulating hormone

27
Q

What happens in graves disease?

A

Antibodies bind to the thyroid gland and stimulate the production of thyroid hormones. This shuts down the pituitary,
Get hyperthyroidism

28
Q

What is myasthenia gravis?

A

Autoantibodies inhibit receptor function at muscle nerve interfaces
antibodies block the binding site of AcH and destroy the receptors

29
Q

What is the outcome of myasthenia gravis?

A

Muscle wasting and eventually death

30
Q

What happens in type III hypersensatvity?

A

Immune complexes composed of self antigen or foreign antigen
Occurs if complexes are excessively produced, and inefficiently cleared

31
Q

What is the pathology of type III?

A

Pathology depends entirely upon where these complexes deposit

32
Q

How is complement usually removed?

A

Immune complexes are usually removed in the spleen by resident macrophages

33
Q

What makes up immune complexes?

A

RBC, C3b Receptors, antigens, antibodies

34
Q

What is needed for immune complex formation?

A

High affinity IgG, need to fix C’

35
Q

Why are large complexes good?

A

Large complexes not only activate complement better, they are better at binding FcR, so are removed from the circulation more efficiently by RBCs

36
Q

What happens when there is a large amount of complex formed?

A

The mononuclear phagocyte system may be overloaded when large amounts of complex are formed, leading to a rise in circulating complexes

37
Q

What is equivalence?

A

Large lattices, good complement activation

38
Q

When are immune complexes not cleared/

A

–  Ag excess
–  Low affinity Ab
–  Inefficient C’ activation

39
Q

What happens to complexes over time?

A

Get deposition on vessel walls Increase in concentration over time results in eventual C’ activation

40
Q

What are the downstream effects of complement?

A
  •   Generate anaphylotoxins (C5a, C3a) –  neutrophil, mast cell degranulation
  •   Induce macrophage cytokine release
  •   Immune complexes directly activate platelets, basophils and mast cells
  •   Vasoactive amines –  increased vascular permeability
41
Q

Where does type III hypersensitivity form/

A

Small tissues

Slow blood flow

42
Q

What are common outcomes of Type III Hypersensitivity?

A

Vasculitis (deposition in blood vessel walls)

  •   Glomerulonephritis (deposition in glomerular basement membranes)
  •   Arthritis (deposition in joint synovium and vessels)
43
Q

Farmers lung?

A
  •   serum sickness,
  •   nephritis in chronic hepatitis,
  •   rheumatic fever and endocarditis,
  •   autoimmune conditions including rheumatic fever and systemic lupus erythematosis (SLE)
44
Q

Diseases resulting from immune complex deposition

A

Persistant infection
Autoimmunity
Inhaled antigen

45
Q

What casues farmers lung?

A

Farmers lung is caused by localised immune complex formation in the lungs due to exposure to hay dust or bacteria resulting in alveolitis

46
Q

What agent specifically causes farmers lung?

A

Actinomyces, a Gram positive environmental bacterium, found in mouldy hay, that stimulates production of IgG antibodies.
IgG containing immune complexes are formed in the alveoli, leading to inflammation and fibrosis

47
Q

Who is affected more by lupus?

A

Females

48
Q

What triggers lupus?

A

Unknown, thought to be UV damage

49
Q

What happens in lupus?

A

Numerous autoantigens are involved and these are widely expressed

Multiple systems involved

50
Q

How is lupus diagnosed?

A

Presence of anti-DNA autoantibodies and immune complex deposition in kidney

51
Q

What causes the damage in lupus?

A

Immune complex deposition on basement membranes of the kidney

Activation of the complement cascade

Tissue injury is the result of leukocyte activation and inflammation

52
Q

Why do patients with lupus present with red rashes?

A

Antibodies target the skin as well.

UV light causes cell death which can in turn trigger immune response

53
Q

How do we create antibodies against self?

A

Immune system has inbuilt randomness. The immune system has developed mechanisms to remove self antibodies

54
Q

What is negative selection?

A

if an immune self can bind to a self anitigen it is destroyed

55
Q

What is central tolerance?

A

–  Occurs during development in primary lymphoid organs

–  Removes self-reactive lymphocytes during development

56
Q

What other mechanisms (aside from central tolerance) prevent immunological tolerance?

A

Peripheral Tolerance
–  Occurs in the periphery
–  Controls self-reactive lymphocytes

Kidneys (15 decks)

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