HLB - allergy and hypersensitivity

what is hypersensitivity

an immune disorder caused by inappropriate response to antigens that are not necessarily pathogens

how many categories of hypersensitivity are there

4

what is an allergy

a damaging immune response by the body to an allergen to which it has become hypersensitive to

what does an allergic response trigger an increase in

vascular permeability and inflammation

what is meant by a local allergic response

when symptoms are restricted to the site where the antigen interacts with the body

what is meant by anaphylaxis

a system wide allergic response

what is type I hypersensitivity

allergy and atopy/ immediate hypersensitivity

what is atopy

a genetic disposition to develop an allergic reaction

which antibody is type I hypersensitivity driven by

igE

what do individuals without allergies generally only produce IgE antibodies in response to

parasitic infections

what processes, apart from the action of IgE, are involved in type I hypersensitivity

degranulation of mast cells, basophils, and eosinophils

in type I hypersensitivity, what receptor do mast cells, basophils and eosinophils express

Fc3RI

what does FcεRI act as

a main mediator of allergy symptoms

what can FcεRI be cross linked via

igE complexes

what does the cross linkage of FcεRI initiate

a signalling cascade, resulting in mast cell and basophil degranulation, with the release of inflammatory mediators

when does the degranulation and secretion of molecules occur in type 1 hypersensitivity

after Fc3RI binds to IgE and triggers the signalling cascade

what lipid mediators are released in type 1 hypersensitivity

prostaglandins and leukotrienes

what do prostaglandins and leukotrienes cause

vasodilation and smooth muscle contraction

what is responsible for inflammation in type 1 hypersensitivity

cytokines

what does exocytosis of the granule cause in type 1 hypersensitivity

vasoactive amines and proteases

what are vasoactive amines responsible for

vascular dilation and smooth muscle contraction

what are proteases responsible for

tissue damage

how does the gradient differ between the immediate reaction and the late phase reaction

the immediate reaction has a higher peak

in the asthmatic response, what does histamine initially cause

the contraction of the bronchial and tracheal smooth muscles

what does histamine bind to

the H1 receptor

in the asthmatic response, what occurs when histamine binds to the H! receptor

there is an increase in vascular permeability and mucus secretion

asthma is an example of what type of hypersensitivity

type I

what releases phospholipase in the asthmatic response

degranulation

what does phospholipase cause in the asthmatic response

enzymatic breakdown of phospholipids in the plasma membrane

the breakdown of phospholipids in the plasma membrane leads to?

the release of leukotrienes and prostaglandins

how much more active are leukotrienes and prostaglandins than histamine

about 1000 times more active

how long after the release of the leukotrienes and prostaglandins does further bronchoconstriction occur in the asthmatic response

within 30 to 60 seconds

in the asthmatic response, what does further bronchoconstriction trigger

an increase in vascular permeability and mucous secretion

what is thought to contribute significantly to prolonged bronchospasm and mucous build up

leukotrienes

what do cytokines increase the expression of

adhesion molecules on the surface of endothelial cells

what is the function of adhesion molecules on endothelial cells

to facilitate the influx of neutrophils, eosinophils, and helper t cells

how can type II hypersensitivity be described

antibody mediated

what antibody drives type II hypersensitivity

IgG and also sometimes IgM

how is destruction caused in type II hypersensitivity

via the antibody binding to the target, triggering either the complement cascade, ADCC, or opsonization

what is ADCC

antibody dependent cell-mediated cytotoxicity

what is opsonization

the process of coating antigens with opsonins to enhance phagocytosis

what type of hypersensitivity are transfusion reactions

type II

what type of hypersensitivity is haemolytic disease of newborn

type II

what type of hypersensitivity is malaria

type II

what type of hypersensitivity is drug induced haemolytic anaemia

type II

what is haemolytic disease of newborn

when an Rh- mother has hypersensitivity to Rh antigens on fetal blood

in haemolytic disease of newborn, where does the baby recieve the Rh antigen from

its father

what is drug induced haemolytic anaemia

when red blood cells are destroyed faster than bone marrow can replace them due to a metabolite triggering antibody responses

how could type III hypersensitivity be described

immune complex-mediated

what are immune complexes formed from

clusters of antibodies and antigens that were formed during immune response, and remain as they cannot be cleared by phagocytes

what can immune complexes induce

degranulation of mast cells, inflammation triggered by complement activation, and attraction and activation of neutrophils at the site

what can occur if immune complexes are deposited in the tissues and capillary beds

can induce more innate immune activity,, vasculitis, and tissue damage

what is vasculitis

blood vessel inflammation

what type of hypersensitivity is the arthus reaction

type III

what is the arthus reaction triggered by

insect bites, or inhalation of fungal or animal proteins

what can the deposition of immune complexes in the kidney lead to

glomerulonephritis

what can deposition of immune complexes in the joints lead to

arthritis

which complement system do immune complexes typically trigger in type II hypersensitivity

c3b

what does c3b attract

neutrophils

what do neutrophils try, but fail to do to c3b

phagocytose

what is type IV hypersensitivity

cell mediated

what two phases are involved in type IV hypersensitivity

the sensitisation phase and the effector phase

what is the sensitisation phase in type IV hypersensitivity

when the initial contact with the APC triggers activation, clonal expansion, and differentiation of t helper cells

what is the effector phase in type IV hypersensitivity

when re-exposure to the antigen causes the sensitised T cells to produce cytokines and chemokines

in type IV hypersensitivity, what is the function of the produced cytokines

to attract and activate macrophages that perpetuate the immune response

what are the 8 red flag symptoms for coughing

persistent cough, pleuritic chest pain, dyspnoea, haemoptysis, persistant nocturnal cough, wheeze, recurrent chest infections, plegm, unintentional weight loss, night sweats

how long has a cough been occuring if it is said to be persistant

more than three weeks

what is meant by pleuritic chest pain

chest pain due to inflammation of the pleurae

what is dyspnoea

laboured breathing

what is haemoptysis

coughing up blood

how long must a patient be coughing up phlegm consistently in the morning for it to be considered a red flag symptom

more than three months