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Immunology > Hypersensitivity Reactions > Flashcards

Hypersensitivity Reactions Flashcards

1
Q

What is a hypersensitivity reaction

A

An antigen specific immune response that is either inappropriate or excessive and results in harm to the host

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2
Q

What are the types of hypersensitivity reactions

A

Type I - immediate, antibody dependent. Allergy. IgE drives reaction

Type II - antibody mediated. IgG or IgM drives reaction. Triggered by self-antigen

Type III - immune complex mediated. IgG or IgM drives reaction. Triggered by self-antigen

Type IV - cell mediated. Delayed. Triggered by self-antigen

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3
Q

Describe the two phases in a hypersensitivity reaction

A

Sensitisation phase - first encounter with antigen. Have activation of APCs and memory effector cells. No clinical manifestation

Effector phase - pathological reaction upon re-exposure to same antigen. Activation of memory cells of adaptive immunity. Clinical manifestation

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4
Q

Describe what causes type I hypersensitivity reactions

A

Type I is caused by an antigen/allergen. Either local or systemic reaction. Antigens are enviromental

Have abnormal, adaptive immune response against allergens

Have TH2 activation instead of TH1 activation against the allergen whihc results in TH2 sending signals to produce IgE against the antigen

IgE causes mast cell activation - sensitisation

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5
Q

Describe the immune mechanism in type I hypersensitivity reactions

A

On first exposure to the allergen, there is production of IgE specfiic antigen by plasma cells

IgE binds to mast cells, arming them for re-exposure

Upon re-exposure of the antigen, the antigen cross links the IgG bound to the mast cell which stimulates signals in the cell to cause degranulation

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6
Q

What does the release of inflammatory mediators from mast cells

A

Increased vascular permeability

Vasodilation

Bronchial constriction

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7
Q

Name some manifestations of an allergic reaction

A

Urticaria - ithcy, raised wheals surrounded by erythema. Caused by mast cell activation within the epidermis

Angioedema - caused by mast cell activation deep in the dermis

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8
Q

What is anaphylaxis and what are some signs and symptoms

A

Anaphylaxis - systemic manifestation of an allergic reaction

Sudden and rapid progression and involves more than 2 body systems

Signs and symptoms: hypotension, cardiovascular collapse, angioedema, breathing difficulty, generalised urticaria

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9
Q

How does adrenaline help to treat anaphlyaxis and what mechanisms does it act by

A

Reverses peripheral vasodilation, reduces oedema and allervaites hypotension by acting on alpha-1 receptors

Reverses airway obstruction/bronchospams - beta-2 receptors

Increases force of heart contraction - beta-1 receptors

Inhibits mast cell activation and degranulation

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10
Q

What is the treatment for type I hypersensitivty

A

Anti-IgE monoclonal antibody

Immunotherapy - inhibit TH2 response

Anti-histamines, leukotriene receptor antagonists, corticosteriods - inhibit mast cell activation

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11
Q

What are the two outcomes from type II hypersensitivity reactions and name some conditions in each outcome

A

Tissue/cell damage

  • Exogenous - haemolytic disease of newborn, transfusion reaction
  • Endogenous - autoimmune haemolytic anaemia, thrombocytopenia purpura, Goodpasture’s disease

Physiological changes

  • Receptor stimulation - Grave’s disease
  • Receptor blockade - Mysathenia gravis
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12
Q

How does tissue/cell damage occur with type II hypersensitivity reactions

A

Antibody (IgG/IgM) binds to the antigen to cause complement activation

This causes cell lysis via membrane attack complexes, neutrophil recruitment/activation and opsonisation

There is also antibody-dependent cell cytotoxicity by natural killer cells

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13
Q

What is haemolytic transfusion reaction

A

Life threatening condition caused by incompatibility in the ABO or rhesus D antigens that results in RBCs being destroyed by the recipients immune system

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14
Q

Describe haemolytic disease of the foetus and newborn

A

A condition where the mother is rhesus negative while the father is rhesus positive

The Rh -ve mother carrys a Rh +ve foetus and then during delivery, Rh antigens from developing foetus enter mother’s blood

Mother produces anti-Rh antibodies - IgG

If women becomes pregnant with another Rh +ve foetus then her anti-Rh antibodies can cross the placenta and damage the foetal RBCs causing cell lysis so baby is born with HDFN

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15
Q

What is given to mothers to prevent HDFN

A

RhoGam/Anti-D is given to mothers after their baby is born

Anti-D isolates the Rh D antigen and clears it away by activating the innate immune system against the Rh D antigen so the body clears it before an acquired immune response can develop

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16
Q

What is the treatment for type II hypersensitivity reactions

A

Tissue/cell damage - anti-inflammatory drugs, IVIG, plasmapheresis, splenectomy

Physioloical change - correct metabolism and replacement therapy

17
Q

Describe type III hypersensitivity reactions

A

Usually develop within 3-8hrs and is caused by immune complexes between IgG/IgM and antigens

Complexes circulate in the blood and are deposited in host tissue resulting in tissue damage and inflammation

The immune complexes are deposited in tissues, activating complement which causes neutrophil chemotaxis, adherence and degranulation

18
Q

Name some factors affecting the pathogenesis of type III hypersensitivity reactions

A

Immune complex size - intermediate complexes cannot be cleared by the body so have increased risk of causing type III hypersensitivity reaction

Host response - low affintiy antibodies favour production of intermediate immune complexes

Local tissue factors - complexes often deposited in areas with high blood flow

19
Q

Name some conditions caused by a type III hypersensitivity reaction

A

Rheumatoid arthritis - rheumatoid factor which deposits everywhere

Glomerulonephritis

Systemic lupus erythematosus - antigen is Ds-DNA. Have multi-organ inflammation

20
Q

Describe type IV hypersensitivity reactions

A

Usually develops within 24-72hrs

Involves lymphocytes and macrophages

Different subgroups - contact, tuberculin and granulomatous hypersensitivity

In sensitisation phase there is production of TH1 cells against trigger/antigen and then upon re-exposure, TH1 cells recognise trigger and produce inflammatory factors that trigger macrophage activation which then causes localised tissue damage

21
Q

What is contact hypersensitivity and give some examples

A

Type IV hypersensitivity reaction where there is an epidermal reaction in response to haptens that bind to endogenous proteins to cause a reaction

E.g. nickel, poision ivy, organic chemicals

22
Q

What is granulomatous hypersensitivity and give some examples of some diseases of this type

A

Occurs 21-48 days post exposure where there is tissue damage as a result of a large number of granuloma formation in the tissue

E.g. TB, schistosomiasis, sarcoidosis

23
Q

What is the treatment for type III and type IV hypersensitivity reactions

A

Anti-inflammatory drugs - non-steriodals corticosteroids

Monoclonal antibodies - against B and T cells, cytokine network or APCs

24
Q

What is myasthenia gravis and describe the pathophysiology behind it

A

An autoimmune neuromuscular condition characterised by skeletal muscle weakness

There are antibodies against AChR produced which bind to nicotinic receptors on muscle end plates and prevent ACh binding so the end plate cannot be activated

This means no action potential can occur in the muscle so there is no muscle contraction

New-borns will have symptoms if mother has myasthenia gravis as anti-AChR antibodies from mother can cross placenta during pregnancy

25
Q

What is given to treat myasthenia gravis and how does it work

A

Pyridostigmine

It is an acetylcholinesterase inhibitor that binds to AChesterase to reduce degradation of ACh so its levels in the synaptic cleft can rise high enough to cause an AP in the muscle

26
Q

Name some signs and symptoms of myasthenia gravis

A

Droopy eyelids

Muscle fatigue quickly during exercise

Symmetrical weakness with normal muscle tone

Normal sensation and normal tendon reflexes

Difficulty chewing and swallowing

Slurred speech

Shortness of breath

27
Q

Name some signs and symptoms of systemic lupus erythematosus

A

Butterfly rash and red patches on skin

Endocarditis

Pleuritis

Haematuria

Anaemia

Hypertension

Muscle and joint pain

Swollen joints

Severe abdominal pain

Alopecia

High fever

Headache

Immunology (6 decks)

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