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Disease Mechanisms > Immunology - Hypersensitivity Reactions > Flashcards

Immunology - Hypersensitivity Reactions Flashcards

1
Q

What are hypersensitivity reactions?

A

Immune response that results in bystander damage to self, usually an exaggeration of normal immune response

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2
Q

What are the four types of hypersensitivity reactions?

A

Type I - immediate hypersensitivity

Type II - direct cell killing

Type III - immune complex mediated

Type IV - delayed type hypersensitivity

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3
Q

Define allergy

A

IgE-mediated antibody response to external allergen

(Type I hypersensitivity)

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4
Q

How quickly do type I hypersensitivity reactions occur?

A

minutes to 1-2 hours

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5
Q

What may affect the threshold for allergic reaction?

A

cofactors such as exercise, alcohol and infection

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6
Q

What are specific features of allergic disease?

A

asthma

urticaria

angioedema

allergic rhinitis

allergic conjunctivitis

diarrhoea and vomiting

anaphylaxis

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7
Q

Which cells are involved in allergy?

A

B lymphoctes - recognise antigen, produce IgE

T lymphocytes - helper for B cells

Mast cells - release vasoactive substances

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8
Q

Which substances are preformed in mast cells?

A

histamine

tryptase

heparin

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9
Q

Which substances do mast cells synthesize on demand?

A

leukotrienes

prostaglandins

cytokines (including IL4, TNF)

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10
Q

What is the function of mast cells?

A

defense against parasites

wound healing

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11
Q

What role do mast cells play in the inflammatory cascade?

A

increase blood flow

increase vascular permeability

contraction of smooth muscle

increase secretions at mucosal surface

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12
Q

How long do hives normally last?

A

appear within 1 hour

last 2-6 hours, occasionally 24 hours.

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13
Q

What is angioedema?

A

Self-limited, localised swelling of subcutaneous tissues or mucous membranes

non-pitting oedema

often without clear demarkation

generally not itchy

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14
Q

What are the clinical features of anaphylaxis?

A

Angioedema of lips and mucous membranes

Laryngeal obstruction, stridor

Hypotension

Wheeze

Itch of palms, soles of feet, genitalia

Flushing

Urticaria

Oral itching

Vomiting, diarrhoea, abdominal pain

Loss of consciousness

Death

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15
Q

What are non allergic causes of mast cell degranulation?

A

Drugs: morphine & other opiates; aspirin and NSAIDS

Thyroid disease

Idiopathic

Physical urticaria - pressure & heat

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16
Q

What is Samter’s triad?

A

Asthma

Nasal Polyps

Severe end of aspirin sensitivity spectrum

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17
Q

What are the general features of allergic reaction?

A

Reaction occurs quickly

Responses are often consistent

Often associated with more than one organ system

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18
Q

What are the investigations for allergy?

A

Skin prick tests

Quantitive IgE to putative allergen

Challenge test

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19
Q

What investigation would you perform during an acute anaphylactic episode?

A

Serum mast cell typtase levels - evidence of mast cell degranulation

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20
Q

What drugs need to be stopped for skin prick tests?

A

Antihistamines for 48 hours

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21
Q

How does the sensitivity and specificity of IgE RAST test compare with that of skin prick testing?

A

70-70%

22
Q

What are common causes of elevated total IgE?

A

Allergic disorders

Vasculitis

Lymphoma

Drugs

23
Q

What are the pitfalls of measuring total IgE in allergy?

A

Many other causes of elevated IgE

Significant allergic disease can exist in absence of elevated IgE

24
Q

When does tryptase reach its peak concentration during anaphylaxis? When does it return to baseline?

A

Peak 1-2 hours

Baseline 6 hours

25
Q

How do adrenalin injection pens work in anaphylaxis?

A

β2-adrenoreceptors

Constrict arterial smooth muscle - increases blood pressure, reduces vascular leakage

Dilates bronchial smooth muscle

26
Q

What is immunotherapy?

A

Controlled exposure to increasing amounts of allergen

27
Q

What are the risks of immunotherapy?

A

Anaphylaxis

28
Q

What are the key features of Type II hypersensitivity reactions?

A

Antibody to cell surface antigens

resulting in

activation of complement

antibody mediated phagocytosis

29
Q

What type of hypersensitivity reactions are transfusion reactions?

A

Type II

Anti-blood group antibodies bind to surface of circulating donor erythrocytes

30
Q

What are the features of immediate haemolytic transfusion reaction?

A

Overwhelming systemic response occuring after only 1ml blood transfused

Pyrexia and rigors

tachycardia/tachypnoea

hypotension/dizziness

headaches, chest or lumbar pain

May be fatal

31
Q

Give some examples of Type II hypersensitivity.

A

Transfusion reactions

Autoimmune haemolytic anaemia

Idiopathic thrombocytopaenic purpura

Goodpasture’s syndrome (kidney)

Myasthenia gravis (nervous system)

Guillan Barre (nervous system)

Grave’s disease (TSH receptor - hyperthyroidism)

Pemphigus vulgaris (skin)

32
Q

What is the management for type II hypersensitivity?

A

Plasmapheresis

(limited by rebound antibody production)

Immunosuppression

(switch of B cell production of antibody)

33
Q

What causes Type III hypersensitvity reactions?

A

Deposition of antigen-antibody immune complexes in small vessels causing complement activation and infiltration of macrophages and neutrophils

34
Q

What are the clinical features of acute hypersensitivity pneumonitis (type III)?

A

wheezing and malaise, 4-8 hours after exposure

Dry cough, pyrexia, breathlessness

Examination often normal

Cell accumulation and inflammation within alveoli

35
Q

What type of hypersensitivity reaction is Systemic Lupus Erythematous?

A

Systemic Type III

Antibodies produced against contents of cell nuclei

Immune complexes deposited in small vessels in skin, joints, kidneys

Complement activation, recruitement of immune cells.

36
Q

How are Type III hypersensitivity reactions diagnosed?

A

Specific IgG to putative antigen

Complement

37
Q

How are Type III hypersensitivity reactions managed?

A

Avoidance

Corticosteroids to reduce inflammation

Immunosuppression to decrease antibody production

38
Q

What are the anti-inflammatory effects of corticosteroids?

A

Inhibits Phospholipase A2 - blocks formation of inflammatory mediators:

Prostaglandin formation

Platelet Activating Factor

Arachidonic Acid

39
Q

What is the effect of corticosteroids on phagocytes?

A

Decreased expression of adhesion molecules on endothelium - transient increase in neutrophil counts because they don’t leave the bloodstream for the tissues

Decreased release of proteolytic enzymes

40
Q

What are the effects of corticosteroids on the number of circulating lymphocytes?

A

Decreased numbers of lymphocytes because:

lymphocytes are sequestered in lymphoid tissue and spleen

high dose is cytotoxic to lymphocytes

41
Q

How is the function of lymphocytes blocked by corticosteroids?

A

Inhibition of cytokine expression

Inhibiting of antigen-induced T cell proliferation

Decreased antibody production by plasma cells

42
Q

What are the metabolic side effects of corticosteroids?

A

diabetes

central obesity

protein catabolism (muscle wasting)

lipid abnormalities

adrenal suppression

43
Q

What are the non-metabolic effects of corticosteroids?

A

Cataracts

Glaucoma

Peptic ulceration

Pancreatitis

Osteoporosis

Hirsutism

Acne

Moon face

44
Q

How is Type IV hypersensitivity mediated?

A

T cells

Primed T cells are produced by initial sensitization to antigen

Subsequent exposure activates previously primed T cells causing

recruitment of macrophages, lymphocytes, neutrophils

Inflammatory cascade

Granuloma

45
Q

Give examples of autoimmune Type IV hypersensitivity reactions.

A

Type I diabetes

Psoriasis

Rheumatoid Arthritis

46
Q

Give examples of non-autoimmune Type IV hypersensitivity.

A

Nickel hypersensitivity

Tuberculosis

Leprosy

Sarcoidosis

Cellular rejection of solid organ transplant

47
Q

What is characteristic of sarcoidosis?

A

Granuloma formation

Multi system disease

48
Q

How is sarcoidosis managed?

A

Watchful waiting - many patient have spontaneous remission

NSAIDS (acute onset)

Systemic corticosteroids

49
Q

Which occupational diseases are characterised by Type IV hypersensitivity and granuloma formation?

A

Beryllosis

Silicosis

Other dust diseases

50
Q

What type of hypersensitivity reaction is the chronic stage of hypersensitivity pneumonitis?

A

Type IV

Disease Mechanisms (9 decks)

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