Immune Not On Brainscape Flashcards
Which food allergy diagnoses screen for IgE
- serum specific IgE
- skin pin prick test
Correlate with likely hood of allergy
Hypersensitivity type 2 reactions caused by complement activation
- haemolytic disease of newborn
- transfusion reactions
Antigen HDN
Rhesus D
Antigen transfusion reaction
ABO
Antigen
- autoimmune haemolytic anemia
- immune thrombobytopenic purpura
- goodpastures
- red blood cells
- platelets
- collagen in GBM of lung and kidney
Examples of type 2 hypersensitivity caused by antibody dependent cell cytotoxicity
- autoimmune haemolytic anemia
- immune thrombobytopenic purpura
- goodpastures
Concequences HDN
Hydrops fetalis
Liver/splenomegaly
Severe hyperbilirubinemia
Kernicterus
What is given to prevent HDN
RhoGAM- solution of rhesus positive proteins that prevent the immune system from making Rh- antibodies
Or
Anti-D prophylaxis to neutralise RhD antigens from first babys’ RBC so the mother doesn’t produce RhD-
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
II disease caused by
- receptor stimulation
- receptor blockage
- protein blockade
Stimulation - graves
Receptor Blockade- MG
Protein blockade- pernicious anaemia
Antigen pernicious anemia
Intrinsic factor in gastric parietal cell
How to correct metabolism and give replacement therapy
Correct metabolism (graves)
- anti thyroid drugs
- thyroidectomy
Replacement therapy (MG/P anemia)
- pyridotygmine
- Vit B12
What is plasmapheresis used for
MG, goodpastures, graves
Type III immune mechanism
- intermediate size complex deposited
- complement activated
- neutrophil chemotaxis
- neutrophil adherence and degranulation
What is antigen rheumatoid arthritis, Lupus and glomerulonephtiris
RA- Fc portion of IgG
GN- infectious microbes
SLE- Ds DNA
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
