Immune review - 7 Flashcards
this contains the bare bones immune system stuff for the exam - so is a good set of flash cards to recap
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be able to define the 4 types of hypersensitivity
give pathophysiology
timing
at least two/three clinical examples
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Type 1 - be able to answer these Q’s
• What is sensitization?
• Ig? production
- MAST CELL activation:
- Where are mast cells found?
- How are they activated?
- Mast cell mediators: - list up to 6.
- Link clinical findings to mediators →
- And link clinical findings to SITE of mast cells (e.g. in different layers of the skin, etc.)
- Treatment:
- Symptomatic:
- Desensitization: what is this ?
- Advice to patient: List at least 4 points regarding advice
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IgE production
Autoimmunity
• Definition …..
• Criteria for the diagnosis of a disease as autoimmune ….
- What triggers autoimmunity? Give some examples
- IgG can transfer from the mother to the foetus during pregnancy and cause a transitory autoimmune disease in the newborn. Give three examples
- Some microbial infections can trigger autoimmune diseases. Give one example
- Strategies for therapy: general approach
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8 Case studies - make a spider diagram on each of these from groupwork
Heamolytic disease of the newborn mysathenia gravis anaphylaxisis nut allergy Thyroid - graves Thyroid - Hasimotos SLE Rheumatoid Arthritis
case studies • Haemolytic disease of the newborn • ABO and RhD • D antigen is highly immunogenic. Which Hypersensitivity reaction? • Haemolytic anaemia → jaundice • 1st baby fine • Coombs test ? what is this ?
- Myasthenia gravis
- Clinical presentation
- Which autoantibodies? Which Hypersensitivity reaction?
- Basic pathophysiology
- Newborn infant of mother with myasthenia gravis….
- Neuromuscular junction
- Treatment with pyridostigmine
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Haemolytic disease of the newborn
• Rhesus (Rh) antigens: D is the most important. Can be + or –
• Rh D is highly immunogenic and will trigger an immune response in someone who is D negative.
• SO: if mother D negative and baby is D positive: what will happen?
- 1st pregnancy fine as mother not sensitised. If some of babies red cells leak into mother’s circulation mother will initially produce IgM antibodies which do not cross placenta.
- 2nd pregnancy with a RhD+ father and foetus, she will produce IgG antibodies which do cross placenta and cause damage.
treatment ?
TREATMENT - PREVENTION:
• Anti-D antibody given to RhD negative mothers during first pregnancy at 28 weeks and within 72 hours of giving birth.
• Causes destruction of fetal red cells that have crossed into mother’s circulation and prevents sensitization.
Nut allergy • IgE mediated symptoms • HISTORY ………….. • Screening test • Skin prick testing • Treatment advice
- Anaphylaxis
- What type of reaction:
- Systemic activation of mast cells: What are the consequences?
- Clinical features: List main features
- Treatment of anaphylaxis
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• THYROID: Graves’
disease
• THYROID: Hashimoto’s
disease
Clinical features – at least 4
- Type of hypersensitivity
- Autoantibody
- Basic pathology if relevant
- Treatment
• Newborn of mother with
Graves’
Rheumatoid arthritis • Main autoantibody? Other autoantibodies? • Key clinical features • Pathophysiology – brief • Non-articular manifestations • Lung …. • Two others • Treatment: give two medications
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• SLE • Type of hypersensitivity • Basic pathophysiology • Main autoantibody? Other autoantibodies? • Key clinical features • SKIN • What might blood count show? • Kidney • Treatment: principles
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do the examsoft quiz and other quizzes
do the SAQ formative on blackboard
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