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Year 1 > Hypersensitivity and Autoimmunity > Flashcards

Hypersensitivity and Autoimmunity Flashcards

1
Q

What is the cause of hypersensitivity?

A

Allergens, pathogens or environmental substances. These can lead to overexcessive immune response following its entry into the body.

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2
Q

What is type 1 hypersensitivity?

A

IgE binds to allergen and preloaded onto mast cell via its Fc region which initiates a potent response of degranulation of inflammatory mediators such as histamine. Effects last mins

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3
Q

What is type 2 hypersensitivity?

A

IgG/IgM antibody binds to cell surface antigens and initiates cytoxic action of WBC or complement cascade via its Fc domain. Effects last mins to hours

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4
Q

What is type 3 hypersensitivity?

A

IgG binds to soluble antigen and forms an immune complex which is deposited and intiates the complement cascade to induce inflammation. Effects last hours

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5
Q

What is type 4 hypersensitivity?

A

Delayed hypersensitvity where Th1/Th2 bind to soluble antigens to intiate Type1/2 immunity. Cytoxic T cell binds to cell surface antigen to intiaite lysis. Effects last hours

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6
Q

What are allergens?

A

An antigen which promotes the allergic response.

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7
Q

What is an allergic reaction?

A

Driven by IgE type 1 hypersensitivity in response to repeated exposure to an allergen.

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8
Q

What is atopy?

A

Predisposition to an IgE mediated allergic response.

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9
Q

What are the characteristics of IgE antibodies?

A

IgE antibodies are preloaded onto mast cells which increases the potency of degranulation and has a longer half life.

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10
Q

What do mast cells release during allergic hypersensitivity?

A

Histamine, heparin, cytokines, generates infalmmatory mediators such as arachidoinc acid, leukotriene and prostaglandin.

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11
Q

What is the immediate reaction?

A

CHarcaterised by the degranulation of mast cells and release of inflammatory mediators.

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12
Q

What is the effect of histamine?

A

Vasoconstriction, itching and smooth muscle contraction in the gut and lungs.

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13
Q

What is the effect of tryptase?

A

Activation of the complement system.

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14
Q

What is the effect of mast cell cytokines?

A

TNF induces pro-inflammation.

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15
Q

What is the effect of leukotrienes?

A

Chemotaxis of eosinophils and bronchial and gut contraction.

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16
Q

What is the effect of prostaglandins?

A

Smooth muscle contraction of the gut and lungs, vasodilation and increased vascular permeability.

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17
Q

What are the mast cell mediators involved in the immediate reaction?

A

Histamine, cytokines such as TNF, leukotrienes, prostaglandins and tryptase

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18
Q

How do eosinophils destroy pathogens?

A

They release enzymes such as eosinophils which degrade helminths and promote inflammation.

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19
Q

What is the late response?

A

Hours after exposure where WBC such as eosinophils and lymphocytes are recruited to clear pathogens.

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20
Q

What cells are invovled in the late reaction?

A

Primarily eosinophils.

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21
Q

What is the effects of IgE-mediated mast cell degranulation on the GI tract?

A

Increased peristalsis (contraction) and fluid secretion for the expulsion of gut contents through diarrhoea or vomiting.

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22
Q

What is the effects of IgE-mediated mast cell degranulation on the BV?

A

Vasodilation and increased vascular permeability to increase blood flow to the lymph nodes and recruit more lymphocytes and WBC however this can cause hypotension and lead to anaphylactic shock.

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23
Q

What is the effects of IgE mediated mast cell degranulation on the GI eye and airways?

A

Causes decreased diameter and increased mucus secretion.

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24
Q

What is allergic rhinitis?

A

IgE mediated hypersensitivity to an allergen that causes inflammation of the nose and post nasal drip and other cold-like symptoms. When this is seasonal caused by pollen, this is hayfever, which has symptoms even without exposure.

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25
Q

How can allergic rhinitis be treated?

A

Intranasal corticoids, reducing exposure to allergen or immunotherapy.

26
Q

What is allergic asthma?

A

IgE mediated hypersensitivity to allergen such as dust which causes release of inflammatory mediators via mast cell degranulation which promotes the smooth muscle contraction of the airways.

27
Q

How is asthma treated?

A

Treatment using salbutomol B2 agonist, preventative with a corticosteroid, leukotriene receptor antagonsits and theophyllines which inhibit leukotriene synthesis.

28
Q

What is eczema?

A

Caused by genetic mutation of the filaggrin protein in the epidermis which allows entry of allergnes. IgE-mediated hypersensitvity and TH2 responds by releasing cytokines to recruit TH1 which characterises it as an autoimmune condition. Eosinophils are recruited which induce inflammation. Keratocytes in the skin release TSLP which contribute to itching. Eczema leads to thickening of the dermis and red patches caused by inflammation.

29
Q

What are the characteristics of eczema?

A

Red patches of skin where there is thickened dermis and inflammation in the crooks of elbows or near ankles

30
Q

What is TSLP?

A

Thymic stromal lymphopoietin which induces inflammation and recruits lymphocytes, released by skin cells that contributes to the characteristic itching.

31
Q

How is eczema treated?

A

Emollients (moisturisers), gloves to prevent itching or topical corticosteroids.

32
Q

What is urticaria?

A

IgE mediated allergic response that leads to red whelts

33
Q

How is urticaria treated?

A

Ciclosporin, anti-histamines, corticosteroids, avoid triggers and omalizumab (anti-IgE therapy)

34
Q

What is anaphylaxis?

A

Severe allergic response where there is rapid synthesis of leukotrienes and prostaglandins.

35
Q

WHat are the symptoms of anaphylaxis?

A

Vomiting and diarrhoea, constricted airways, increased vascular permeabiltiy and vasodilation which causes oedema and hypotension, confusion and fainting

36
Q

What is type 2 hypersensitivity?

A

IgG or IgM mediated response where it binds to cell surface antigens to intiate lysis via interacting with cytoxic T cells via its Fc domain or complement cascade activation or cell receptor modification.

37
Q

What type of hypersensitvitiy is rhesus disease of newborns?

A

Type 2 hypersensitvitiy

38
Q

What is goodpasture syndrome?

A

IgG mediated hypersensitivity to collagen in the basement membrane of kidneys.

39
Q

What is myasthenia gravis?

A

IgG mediated hypersensitivity where the acetylcholine receptor is blocked that leads to muscle weakness.

40
Q

How is myasthenia gravis treated?

A

Using the acetylcholinesterase inhibitor pyridostigmine, corticosteroids, thyrectomy, B cell depleting therapy

41
Q

What is the mechanism of type 3 hypersenstvity?

A

IgG antibodies bind to soluble antigens and form immune complexes which can be deposited in areas of the body and induce the complement cascade that leads to tissue damage.

42
Q

Why do immune complexes form?

A

When there are equal levels of antibodies and the antigen to prevent damage in the body and recruit WBC.

43
Q

How are immune complexes removed?

A

Via the complement cascade by the body.

44
Q

What are the consequences of type 3 hypersensitvity?

A

Inflammation at the site of deposition due to the activation of the complement cascade. In the joints, this can cause arthritis.

45
Q

What is systemic lupus erythematosus?

A

Failure of removal of old autoantigens causes mediated IgG response to clear it. Characteristic rash across the cheeks, joint pain and attacking the organs.

46
Q

How is systemic lupus treated?

A

It is an autoimmune condition so there can’t be reduced via exposure, immunosuppressants are the general treatment.

47
Q

What is rituximab?

A

B cell depleting therapy.

48
Q

What are alkylating agents?

A

DNA synthesis inhibiton such as cyclophosamide.

49
Q

What is arthus reaction?

A

Vaccine is administered intradermally rather than intravenously which results in immune response that causes inflammation.

50
Q

What is serum sickness?

A

IgG mediated response to anti-venom that leads to large purpuric rashes

51
Q

What is type 4 hypersensitivity?

A

T cell mediated where TH1 recruits macrophages and TH2 recruits eosinopihls or CTL cause cytolysis of infected cells.

52
Q

What is sensitisation?

A

Caused by exposure to the antigen which promotes generation of memory cells. Used in vaccination.

53
Q

What is primary and secondary exposure?

A

Primary exposure occurs during first encounter with antigen which takes time to generate memory cells. Due to this, secondary exposure has greater rate of antibody production.

54
Q

Example of type 4 hypersensitivity?

A

Coeliac disease that leads to atropy of small intestine and malabsorption.

55
Q

What is the DTH response?

A

Delayed hypersensitivity 24-72hours after exposure driven by TH1 cell that releases cytokines to attract macrophages and WBCs to cause inflammation and TNF to initiate destruction.

56
Q

What is contact sensitisation?

A

Delayed hypersensitivity caused by contact with the allergen such as clothing.

57
Q

What is the tuberculin test?

A

Th1-mediated delayed hypersensitivity to TB bacterium for testing in school-aged children.

58
Q

What is rheumatoid arthritis?

A

Type 4 hypersensitivity where there is Immune cell mediated destruction caused by autoantiboides.

59
Q

What are the types of autoantibodies in rheumatoid arthritis?

A

Rheumatoid factor which recognises IgG. Anti-citrullinated peptide antigen antibodies.

60
Q

What is multiple sclerosis?

A

Th1-mediated destruction of the myelin in the spinal cord. Diagnosed via testing of CSF or neurological examination and treated with immunosuppressants or anti cytokine therapy.

Year 1 (191 decks)

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