Hypersensitivty- type II, III, IV Flashcards

1
Q

What does the term hypersensitivity mean?

A

The antigen specific immune response that are either inappropriate or excessive and result in harm to host

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2
Q

How can you trick the immune system?

A

Believe that have the disease so causes an immune response

- vaccination

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3
Q

What are exogenous substances?

A

Non infectious substances (allergy)
Infectious microbes
Drugs e.g. Penicillin

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4
Q

What are intrinsic antigens?

A
Infectious microbes (mimicry- autoimmune- has parts that are like hosts microbes) 
Self antigens
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5
Q

What is type I or immediate

A

Allergy
Environments non infectious antigen
IGE

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6
Q

What is type II hypersensitivity?

A

AntiBody mediated

IGM

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7
Q

What is type III hypersensitivity?

A

Immune Complexes mediated

IGG

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8
Q

What is type IV hypersensitivity?

A

Cell mediated- Delayed

Environmental infectious agents and self antigens

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9
Q

What mechanisms cause hypersensitivity?

A

The immune repossess that are employed to fight host infection
However too much- overreaction

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10
Q

What is the difference between type II and III?

A

Type III is against soluble

Membrane bound type II

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11
Q

What is sensization phase?

A

First encounter with the antigen

Activation of APC and memory effector cells

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12
Q

If an individual has been previously exposed to an antigen what are they said to be?

A

Sensitised

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13
Q

What is the effector phase?

A

Pathological reaction upon re exposure to the same antigen and activation of the memory cells of the adaptive Immunity

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14
Q

When does type II hypersensitivity develop?

A

5-12 hours after exposure

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15
Q

What kind of antibodies does hypersensitivity type II involve?

A

IGM or IGG

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16
Q

What does hypersensitivity type II target?

A

Cell bound antigens

E.g. Blood group antigens, Rhesus D antigen,self antigens

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17
Q

What does type II hypersensitivity cause?

A

Tissue or cell damage

Change in cell function

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18
Q

How can type II sensitive cause cell damage?

A

by antigen dependant cells when in natural killer cells bind to antibody through FRC receptor and release toxic radicals through to the cell itself
Self antigen- usually present in red blood cells, activate complement and destroyed, also happens in platelets

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19
Q

What can complement act on?

A

Many cells in innate immunity, adaptive immunity and disposal system

20
Q

What is an example of a disease caused by type II hypersensitivity? IGM

A

Haemolytic transfusion reaction

21
Q

What is haemolytic transfusion reaction?

A

Life threatening condition
Shock
Kidney failure
Circulatory collapse and death

22
Q

What is the Immune mechanism of haemolytic transfusion reaction?

A

Incompatible in the ABO of rhesus D antigens
Donor red blood cells destroyed by recipients Immune system
Red blood cell lysis induced by type II hypersensitivity by the naturally occurring antibodies

23
Q

What is an example of type II sensitivity? IGG

A

Rhesus posture father and Rhesus negative mother
In response the mother will produce anti Rhesus antibodies
If pregnant again her antibodies will cross the placenta and damage fatal red blood cells
Causes haemolytic disease of the newborn- anaemic

24
Q

What is treatment for problems with Rhesus positive father and negative mother?

A

Give Rhesus d immune globulin human

Prevents mother getting sensitised

25
Q

What is Graves’ disease?

A

Increased thyroid activity

Antigen is TSH receptor

26
Q

What is myasthenia gravis?

A

Impaired neuromuscular signalling

Antigen=acetylcholine receptor

27
Q

What are the therapeutic approaches for type II hypersensitivity tissue cell damage?

A

Immune suppression
Plasmapheresis
Splenectomy
Intravenous immunoglobulin

28
Q

What are the therapeutic approaches for type II hypersensitivity physiological damage?

A

Correct metabolism

Replacement therapy

29
Q

What is plasmapheresis therapy?

A

Plasma is filtered and discarded and serum is given

Short term relief and allows healing of damaged tissue

30
Q

When is plasmapheresis therapy used?

A

Myasthenia gravis
Goodpastures syndrome
Graves’ disease

31
Q

When does type III hypersensitivity develop?

A

Within 3-8 hours

32
Q

What does type III hypersensitivity target?

A

Soluble antigens e.g. Foreign infection or endogenous (self antigens)

33
Q

What does type iii hypersensitivity cause?

A

Tissue damage

34
Q

What are the key factors affecting IC pathogenesis ?

A

Complex size
Host response- low affinity antibody or complement deficiency
Local tissue factors

35
Q

What is type iii hypersensitivity efffect?

A

Multiststem disease

36
Q

What are the two main diseases that type III hypersensitivity cause?

A

Rheumatoid arthritis

Glomerulonephritis

37
Q

What are the features of rheumatoid arthritis?

A

Rheumatoid factor antigen IGG

Episodes of inflammtion and remission

38
Q

What is glomerulonephritis?

A

Infectious
Bacterial endocarditis
Hepatitis b infection

39
Q

What is systemic lupus erthematosus?

A

Every patient unique
Do-DNA antigen
Mainly women
Repeated miscarriage

40
Q

What are the features of type IV hypersensitivity?

A

Develops within 24-72 hours

Involves lymphocytes and macrophages

41
Q

What are the subtypes of type IV hypersensitivity?

A

contact hypersensitivity- eczematous rash
Tuberculin hypersensitivity- induration and swelling
Granulomatous- tissue damage, granuloma- walls off infected cells

42
Q

What diseases are caused by type IV hypersensitivity exogenously?

A

Granulomatous hypersensitivity- tuberculosis, leprosy, schistosomiasis, sarcoidosis

Contact hyoersensitiy- nickel, poison ivy, organic chemicals

43
Q

If someone has beeen infected with tuberculosis how would you find out if they are sensitised?

A

Antigen injected and processed by antigen presenting cells
T cells recognise antigen and release cytokines which react on endothelium
Pathogocytes and plasma to site and causes visible lesion

44
Q

What diseases are caused by type IV hypersensitivity endogenously?

A

Autoimmune disease e.g. Pancreatic islet cells- insulin dependant diabetes mellitus
Thyroid gland- Hashimoto’s thyroiditis (cd8+ T cells and antibodies)
IGG- rheumatoid arthritis

45
Q

What are the therapies for type iii and IV hypersensitivity?

A

Anti inflammatory drugs e.g. Non steroid, corticosteroids, second drugs of steroid sparing agents

Monoclonal antibodies
B cells and T cells
Will have more as time goes on