Immunity Flashcards
What types of hypersensitivity are there
Type 1 - igE antibodies
Type 2 -igG
Type 3 -immune complex formation
Type 4 -cell mediated (delayed)
Describe type 1 hypersensitivity
Atopic allergy
Mast cells activated (de granulation and release of mediators) by binding of 2 igE on allergens
What is the mechanism behind type 1 hypersensitivity
Antigen presenting cell uptake and present via MHC class ii
TH2 cell interact with CD4 T cell via cytokines
T cell produces igE antibodies
They bind to the antigen on second exposure and activate the mast cell
What do the mediators released by mast cells do
Pharmacological- blood vessels, airways, cell infiltration and accumulation
Clinical effects- hay fever, asthma, eczema, anaphylaxis
Define atopic
Allergy due to hypersensitivity- Have higher evens of igE in serum- genetically predisposed
What do mast cells release
Preformed mediators- histamine, heparin and tryptase
Newly formed- arachiodonic acid (mins)
Prostaglandins, leukotrienes, cytokines (hours)
What are the types of hypersensitivity in terms as what things are recognised
Foreign- self damaging-allergy/hypersensitivity
Self- self damaging-autoimmunity/ hypersensitivity
Name five type 1 hypersensitivity responses and what is the response in each
Systemic anaphylaxis- oedema, tracheal occlusion and increased vascular permeability, circulatory collapse, death
Acute urticaria- local increase in blood flow increased vascular permeability, itch
Allergic rhinitis- oedema of nasal muscosa and irritation
Asthma- bronchial construction and increased mucus production, airway inflammation
Food allergy- vomiting diarrhoea, pruritis, urticaria, anaphylaxis
What are be staged reactions to skin tests
Immediate- igE
Immediate and late- igE and T cells
Delayed- TH1 cells
Eczematous- igE and TH2 cells
What is type 2 hypersensitivity
Cell of membrane reactive- igG igA and igM - neutrophils and complement
Name some type 2 allergies
Allergic haemolytic anaemia blood transfusion reactions
Haemolytic disease of the newborn
Name some type 2 autoimmunities
Autoimmune he's militia anaemia Autoimmune thrombocytopenia Pemphigold Good pastures disease Myasthenia gravis Graves' disease
Explain rhesus haemolytic disease of the newborn
Rhesus d negative mother has a rhesus d positive fetus
Rhesus d antigens mix with mothers blood ( at birth?)
Mother makes igG antibodies against them
New rhesus d postitive baby, igG antibodies cross the placenta and attack babies red blood cells
How is rhesus haemolytic disease avoided
Mother given rhesus prophylaxis- anti- d antibodies
What is type 3 hypersensitivity
Antibody mediated- ineffective removal of immune complexes
Involved igG igA igM, neutrophils and complement
Give examples of type 3 allergy and type 3 autoimmunity
Allergy- dermatitis, herpetoformis, allergic alveolitis
Autoimmunity- systemic lupus, erythematosus, rheumatoid arthritis
Explain normal removal of immune complexes
Usually removed via liver ( hepatic macrophages) too many produced- not removed or can become lodged in parts of the body
What is type 4 hypersensitivity
Cell mediated Involved T cells Th cells Macrophages Cytotoxic T cells
Give examples of type 4 allergy and type 4 autoimmunity
Allergy- contact dermatitis, acute graft rejection, Tb, leprosy
Autoimmunity- thyroiditis, adrenalitis (addisons) gastritis ( pernicious aneamia) type1 diabetes melluitis
What do macrophages become in type 4 hypersensitivity
Multincleated giant cells
What are the three types of leprosy
Tuberculoid, borderline and lepromatous
Define autoimmunity
Damage to self tissues triggered by an adaptive immune response to the bodies own tissue components ( auto antigens)
How can autoimmunity be categorised
Organ specific eg MS
Systemic disease eg rheumatoid arthritis
What hypersensitivities can be autoimmune
2 3 and 4
What is Graves’ disease
Type 2 hypersensitivity autoimmunity.
Autoimmune B cells make Autoantibodies that stimulate TSH receptors- overstimulation of thyroid follicular cells without any negative feedback control
= hyperthyroidism, goitre, weight loss, nervousness, palpitations and irritable
What is the danger of someone with Graves’ disease when they are pregnant
What is the treatment
Anti-TSHR antibodies cross the placenta and cause the newborn to also suffer from Graves’ disease
Anti-TSHR antibodies cures the disease
What is graves ophthalmopathy
Inflammation of connective tissue behind eyes= swelling
Production of mucopolysaccharides
Protrusion of eyeballs
What is pre-tibial myxoedema
Swelling of ankles
What is Hashimoto’s thyroiditis
Autoimmune destruction of thyroid tissue
Massive infiltration of lymphocytes to the thyroid
Causes hypothyroidism- weight gain/depression/fatigue
How can you detect Hashimoto’s thyroiditis
Autoantibodies produced to thyroid per oxidase and thyroglobulin, can be detected in blood/serum samples
Explain pernicious anaemia
Autoimmune destruction of gastric parietal cells type 4 autoimmunity.
Production of autoantibodies for intrinsic factor IF. Stops IF binding to vitamin b12 in ileum so can’t absorb.
B12 needed for nucleotide synthesis so no DNA = no replication especially important in fast replicating cells ie RBC
Explain type 1 diabetes
Insulting producing beta cells in islets of langerhans attacked and destroyed by autoreactive T cells. Leave alpha and gamma in tact
Explain myasthenia gravis
(Type 2) Autoantibodies inhibit Ach receptors expressed on muscle cells ( at neuromuscular junction) blocks binding and induces internalisation and degradation of receptors
Explain autoimmune haemolytic anaemia
Autoantibodies (type 2) opsonise erythrocytes, activating complement and flagging for destruction by phagocytes
What is good pastures disease
Autoantibodies ( type 2) bind to glomerular basement membranes, activate complement and neutrophils = tissue damage and eventually kidney failure
Can also be to alveoli basement membrane
What is pemphigus vulgaris
Autoantibodies bind to intracellular substance of epidermis of skin= blistering skin reaction
What is systemic lupus erythematosus
Immune complexes of DNA/ anti-DNA in blood are deposited in the glomeruli= irregular staining pattern
Tissue damage in the kidney glomeruli, skin, joints, CNS
explain rheumatoid arthritis
Immune complexes formed by rheumatoid factors
IgM and igG autoantibodies - joint damage
What is the classification of immune deficiency
Primary- inherited or congenital
Secondary- congenital or acquired
Component - adaptive (antibody/cell mediated/ combined)
Innate (complement/phagocytes/NK cells)
What are the different infections that can characterise immunodeficiency
Fungi and viruses- T cells
Bacteria - antibody, classical complement, terminal complement and phagocytes
Abscesses - phagocytes
Which antibody defect ( primary or secondary) is more common in adults
Primary
Which antibody deficiency (1• or 2• ) is lymphoproliferative
Secondary
Which antibody deficiency is underdiagnosed
Primary
What can antibody defects be secondary to
Lymphoproliferative
Renal/gut loss of igG
Malnutrition
Drugs
What are the primary causes of antibody deficiency
Hyper igM syndrome X limbed agammaglobulinaemia Common variable immune deficiency IgA deficiency IgG deficiency
What is common with and antibody deficiency
Bacterial infections ( ears, sinus, chest) Giardia gut infection Permanent damage esp. If diagnosis is delayed
What are other complications of antibody deficiency
Enteroviral infection
malignancy
Autoimmunity
What is Di George syndrome
T cell defect, primary immunodeficiency
Defective development of thymus and other tissue in face/neck/chest due to defective 3rd and 4th pharyngeal arches
= fungal and viral infections
What is AIDS defined as
HIV with appearance of opportunistic infections
How does HIV infect T cells
Bind to cd4 molecules
What are the early symptoms of HIV
Persistent generalised lymphadenopathy
How is HIV transmitted
Sexual/ blood contact
How is HIV diagnosed
Detection of anti-HIV antibodies in serum
What is sever combined immunodeficiency
Primary immunodeficiency inherited stem cell defect lack of function of b and T cells
Susceptible to essentially all types of infectious agents
Fatal is untreated ( bone marrow transplant)
What causes primary neutrophil defects
Kostmanns, cyclical neutropenia
What causes secondary neutrophil defects
Leukaemia
Cancer chemotherapy
Infections
What is leucocyte adages ion define u due to
Lack of production of integrins adhesion molecules
What is chronic granulomatous disease
Defects in enzymes involved in generation of reactive oxygen species ( needed to kill phagocytosed infection)
What is recurrent neisserial infections a feature of
Complement defieciency - alternative and membrane attack pathways
What are immunodeficiencies secondary to
Iatrogenic ( immunosuppressive treatment or radiation or surgery)
Malignancies ( leukaemia, lymphoma, myeloma)
Some infections- HIV, chronic malaria, measels
Malnutrition
Protein losing diseases
Chronic diseases ( renal)
Burns
What is acute appendicitis caused by
Lumen obstruction and bacterial infection
What does acute appendicitis spread to become when it perforates
General peritonitis
What are some outcomes of lobar pneumonia
Death in acute phase Death during resolution Successful resolution Abscess formation Organisation of exudate- lung fibrosis
What can neisserial infection cause
Meningitis
Septicaemia
Pneumonia
Arthritis
What is an acute superficial folliculitis
Zits
What are the signs of inflammation
Calor- heat
Pain- dolor
Rubor- redness
Tumor- swelling
What is osteomyelitis
Come infection almost always causes by bacteria and can destroy the bone
What do a high pulse and bp often indicate
Infection
What types of TB are there
Primary
Miliary ( spread in blood)
fibrocaseous
Tuberculosis bronchopneumonia
What are five causes of granulomatous infection
Mycobacterium infection
Insoluble organic material ( endogenous/ exogenous)
Insoluble inorganic material (endogenous (urate) exogenous (silica))
Sarcoidosis
Fungal infection
