Antigen - autoimmune haemolytic anemia - immune thrombobytopenic purpura - goodpastures

- red blood cells - platelets - collagen in GBM of lung and kidney

Immune Not On Brainscape Flashcards by Amy Healey

Which food allergy diagnoses screen for IgE

serum specific IgE
skin pin prick test

Correlate with likely hood of allergy

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Hypersensitivity type 2 reactions caused by complement activation

haemolytic disease of newborn

- transfusion reactions

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Antigen HDN

Rhesus D

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Antigen transfusion reaction

ABO

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Antigen

autoimmune haemolytic anemia
immune thrombobytopenic purpura
goodpastures

red blood cells
platelets
collagen in GBM of lung and kidney

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Examples of type 2 hypersensitivity caused by antibody dependent cell cytotoxicity

autoimmune haemolytic anemia
immune thrombobytopenic purpura
goodpastures

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Concequences HDN

Hydrops fetalis
Liver/splenomegaly
Severe hyperbilirubinemia
Kernicterus

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What is given to prevent HDN

RhoGAM- solution of rhesus positive proteins that prevent the immune system from making Rh- antibodies

Anti-D prophylaxis to neutralise RhD antigens from first babys’ RBC so the mother doesn’t produce RhD-

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How to test for HDN

Indirect Coombs- tests for Anti-D antibody in plasma of mother and needs RhD antigen and Coombs reagent to be added

Direct coombs- looks at RBC from baby for Anti-D. Needs RhD antigens and Coombs reagent

+ve test = agglutination of RBCs

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II disease caused by

receptor stimulation
receptor blockage
protein blockade

Stimulation - graves
Receptor Blockade- MG
Protein blockade- pernicious anaemia

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Antigen pernicious anemia

Intrinsic factor in gastric parietal cell

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How to correct metabolism and give replacement therapy

Correct metabolism (graves)

anti thyroid drugs
thyroidectomy

Replacement therapy (MG/P anemia)

pyridotygmine
Vit B12

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What is plasmapheresis used for

MG, goodpastures, graves

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Type III immune mechanism

intermediate size complex deposited
complement activated
neutrophil chemotaxis
neutrophil adherence and degranulation

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What is antigen rheumatoid arthritis, Lupus and glomerulonephtiris

RA- Fc portion of IgG
GN- infectious microbes
SLE- Ds DNA

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3 subtypes of granulomatous inflammation

contact
tuberculin
granulomatous

Diseases caused by type Iv

Hashimotis, diabetes mellitus

Antigen hashimotis and DM

H- thyroid gland

DM- pancreatic island cell

How is anaphylaxis treated

Adrenaline

reverses peripheral vasodilation and reduces oedema
reversed airway obstruction
inhibits mast cell activation

Mechanism type 1 hypersensitivity

TH2 response
IgE production
causes mast cell activation and degranulation

4 chemical mediators for anaphylaxis

tryptase-remodel connective tissue matrix
histamine- increase vascular permeability
leukotrieone- increase vascular permability
platelet activating factor- activate neutrophils/eosinohils and platelets

key points epi pen

Properly remove the safety cap
• Place device against mid-anterolateral thigh
• Correct injection with a click heard
• Hold device in place for 10 seconds
• Massage injection site for 10 seconds

systemic anaphylaxis symptoms

RESPIRATORY:
• Upper airway obstruction with Stridor
• Lower airway obstruction with wheeze
• Cyanosis
CVS:
• Palpitations, tachycardia, bradycardia
CNS:
• Dizzy, Confusion, unconscious
ABDOMEN:
• nausea and vomiting,
• Abdominal pain

RA xray signs

Narrowing of joint space
osteoporosis localized at the MCP joints of both hands (Periarticular osteopenia}

small erosions (proximal phalanges)

Juxta-articular bony erosions (in non-cartilage protected bone)

soft tissue swelling involving all fingers,

In severe and advanced cases you will see Subluxation and gross deformity

antibodies RA

Fc portion IgG (rheumatod factor) ACPA

extra articular features RA

dry eyes, pericarditis, splenomegaly, renal inbolvement

autoimmune pathophysiologu SLE

* Self antigens and failure of the immune system to inactivate B cells and T cells that recognize these self antigens (i.e. a breakdown of tolerance) * Development of autoantibodies that either form circulating complexes or deposit by binding directly to tissues. * Activation of complement * Influx of neutrophils, causing inflammation in those tissues. * Abnormal cytokine production

4 key points SLE diagnosis

joint problems, renal problems, malar rash, ANA antibodis

treatment SLE

DMARDS- azathioprine education- suncream use steroids- prednisolone

symptoms anaphylaxis

``` Angioedema Urticaria Loss of consciousness Confusion Abdo pain/vomiting/diarrhoea ```

mechanism anaphylaxis

Type 1 hypersensitivity reaction A sensitized individual is re-exposed to an antigen The antigen binds to IgE bound to mast cells – cross-linking of IgE This leads to mast cell degranulation & release of granular contents and synthesis of new mediators

Give two differences between IgE mediated and Non-IgE mediated food allergy (2 marks):

Onset for Ige = immediate, onset for Non-IgE = delayed Age for IgE is variable & depends on age of contact, Non IgE = infancy & early childhood Non-IgE tends to resolve much sooner than IgE mediated (which may never resolve)

Explain the underlying pathology causing rheumatoid arthritis (4 marks)

Type 3 hypersensitivity reaction Antibodies bind to the antigen (often Fc portion of IgG) forming immune complexes Immune complexes (intermediate sized) deposit in the joints Complement system is activated recruiting neutrophils to the area There is neutrophil adherence to the tissue and degranulation leading to destruction of the tissue causing pain and inflammation

what pescribed alongside methotrexate

folic acid

Briefly describe the mechanism of the type IV hypersensitivity reaction (2 marks):

Sensitization phase APCs present the antigen to TH1 cells. | Effector phase TH1 cells bind with resting macrophages to activate them leading to an inflammatory response

Give 4 side effects of long-term steroid use (2 marks):

``` Skin thinning Immunosuppression Water retention Osteoporosis Cushing syndrome ```