hypersensitivity

Question 1

Dust

Answer 1

can mimic parasite and stimulate antibody response
if dominant is IgE- allergy symptoms
if stimulate IgG -different kind f hypersensitivity, eg farmer’s lung

Question 2

haptens

Answer 2

Smaller molecules sometimes diffuse into the skin triggering a delayed hypersensitivity reaction.
small molecule irritants that bind to proteins and elicit an immune response
Contact dermatitis caused by nickel.
Drugs administered orally, by injection, or onto the surface of the body can elicit hypersensitivity

Question 3

type 1 hypersensitivity

Answer 3

Mediated through the degranulation of mast cells and eosinophils.
The effects are felt within minutes of exposure.
Immediate hypersensitivity, allergy
IL-4 (TH2 cells)production induces Ig E antibody

Question 4

Atopy

Answer 4

Immediate hypersensitivity reaction to environmental antigens mediated by IgE.
Develops within minutes of exposure
Family history with atopy traits.
Anaphylaxis
Angioedema
urticaria
rhinitis

Question 5

Allergens

Answer 5

Peanut allergy is the most common cause of severe allergic reactions.
Allergy to peanut protein Ara h2, Ara h8, cross reactivity with other foods.
latex
Penicillin allergy, the allergen is β-lactam

Question 6

degranulating cells

Answer 6

release of mediators
mast cells
eosinophils migrate
basophils stay in circulation appear like mast cells
MCs initiate allrgic symptoms
-receptors for IgE and FcεRI (high affinity IgE receptor)

Question 7

skin allergy

Answer 7

urticaria
angioedema
atopic eczema

Question 8

genetics of allergies

Answer 8

Filaggrin is expressed by keratinocytes and involved in maintaining epithelial barriers and moisturizing surfaces and controlling pH.
Polymorphisms in the gene encoding is established as a cause of allergy and implicated in 50% of severe eczema.
Exposure to environmental factors
timing

Question 9

hygiene hypothesis

Answer 9

: increase in allergies in the developed world is caused by reduced exposure to microorganisms in early life

Question 10

polymorphisms

Answer 10

variants of different alleles in the same gene

Question 11

anaphylaxis

Answer 11

vasodilation and increased vascular permeability
shift fluids from vascular to extra vascular space resulting in a fall in vascular tone
severe drop in blood pressure
in skin, mast cells release histamine- fluid shift and oedema

Question 12

allergic rhinitis

Answer 12

inhaled allergens stimulate mast cells in the nasal mucosa.
Subsequent vasodilation and oedema in the nose causes nasal stuffiness and sneezing.
Leukotrienes increase mucus secretion,

Question 13

Asthma

Answer 13

Increased mucus secretion and contributes to the airflow obstruction.
In the lungs, leukotrienes cause smooth muscle contraction, which has the most dramatic effects on airflow reduction
Several hours after the acute episode, the airflow in the bronchi may deteriorate again, reflecting the migration of leukocytes into the bronchi in response to chemokines

Question 14

drug treatment

Answer 14

β2-adrenergic agonists, mimic the effects of the sympathetic nervous system and work mainly by preventing smooth bronchial muscle contraction in asthma
Epinephrine (adrenaline) lifesaving where blood pressure falls dramatically. Epi­nephrine stimulates bothα- andβ-adrenergic receptors, decreases vascular permeability, increases blood pressure, and reverses airway obstruction
Antihistamines block histamine receptors and have allergies that affect the skin, nose, and mucus membranes.
Specific receptor antagonists block the effects of leukotrienes. Montelukast reduces airway inflammation in asthma
Corticosteroids can prevent the immediate hypersensitivity reaction, the late phase, and chronic allergic inflammation

Question 15

type II hypersensitivity

Answer 15

Antibody mediated hypersensitivity 
IgG or IgM reacting with antigen present on the surface of cells. 
The bound Ig interacts with complement or with Fc receptor macrophages. 
Opsonisation of target cells
Immune mediated haemolysis.
Takes several hours.
Drug-induced haemolysis.
Rhesus ABO

Question 16

immune mediated haemolysis

Answer 16

Alloimmune Haemolysis
Rhesus antigen (IgG develops during pregnancy and crosses the placenta and causes haemolytic disease).
Incompatibility in the ABO system

Autoimmune Haemolysis
systematic autoimmune disease (SLE)
Autoantibodies produces by malignant B cells

Type II Autoimmune Hypersensitivity Against Solid Tissue
Goodpasture syndrome, IgG autoantibodies bind a glycoprotein in the basement membrane of the lung and glomeruli. Anti–basement membrane antibody activates complement, which can trigger an inflammatory response

Question 17

graves disease

Answer 17

Most common cause of hyperthyroidism
Mainly young women
Family history
HLA allele DR3
Thyroid is stimulated with an autoantibody that binds into the THS receptor

Question 18

type III hypersensitivity

Answer 18

Immune complex disease
IgG is also responsible
Immune complexes of antigen and antibody form and cause damage at the site of production or circulate and cause damage elsewhere.
Immune complexes take some time
form complexes must by polyvalent.
Present long enough to start an antibody response
At low levels of antibody, each antigen molecule binds several immunoglobulin molecules.
When antibody and antigen levels are approximately equal, or antibody levels are slightly in excess, large complexes can form.
When antibody exceeds antigen, small complexes form.

Question 19

clearance of complexes

Answer 19

Complement breaks down large complexes

Complement Receptor 1 Transfers Complexes to Phagocytes

Question 20

immune complex disease in kidney

Answer 20

Glomerulonephritis
Nephrotic syndrome (protein leaks into urine) with gradual development of renal failure
Nephritis with rapid onset renal failure, blood and protein in the urine and hypertension

Question 21

type IV hypersensitivity

Answer 21

This can take 2 to 3 days to develop
Delayed hypersensitivity
Delayed hypersensitivity reactions are initiated when tissue macrophages recognize danger signals and initiate an inflammatory response.
Dendritic cells loaded with antigen migrate to local lymph nodes, where they present antigen to T cells.
Specific T-cell clones proliferate in response to antigens, which migrate to the site of inflammation.
Tumour necrosis factor (TNF) is secreted by both macrophages and T cells and stimulates much of the damage in delayed hypersensitivity

Question 22

Rheumatoid arthritis

Answer 22

Many features of delayed hypersensitivity with persis­tent TH1 and TH17 reactions and TNF secretion.
antigens that drive RA appear to be citrullinated proteins. Citrullination is the conversion of the amino acid arginine to the amino acid citrulline.
Autoreactive T cells and B cells can recognize citrullinated proteins. The result is production of antibodies against citrullinated protein. These are referred to asanti–cyclic citrullinated peptide(CCP) antibodies
The synovium becomes infiltrated by T cells (TH1 and TH17) and macrophages.
TNF and IL-17 attract and activate neutrophils that cause damage to the synovium.
Osteoclasts are activated and destroy bone at the joint margins, creating erosions.
Persistent IL-6 secretion triggers an acute-phase response.
Family history.
Association with HLA-DR4.

Question 23

MS

Answer 23

Chronic, disabling neurologic disease.
Initially in MS, acute attacks occur during which inflammatory lesions consisting of TH1 and TH17 cells and macrophages develop in the affected nervous tissue.
The inflammatory lesions cause the reversible, relapsing disability typical of early MS.
Although active inflammation is present in the vicinity, myelin loss impairs the ability of neurons to conduct impulses, resulting in neurologic symptoms.
Once the inflammation settles, the disability improves.
Between attacks, there is usually good recovery of function, at least early in the disease.
The chronic disability that usually occurs later results from axonal loss.