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Immune system > Lecture 2- Hypersensitivity 2 > Flashcards

Lecture 2- Hypersensitivity 2 Flashcards

1
Q

Type I hypersensitivity=

A

allergy ​

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2
Q

Allergy

A

Allergy is usually an immediate effect (<30 mins)that can affect different organs resulting in different clinical manifestations.

Allergy requires IgE and mast cells to be activated against an antigen that the host encounters.

Can occur as both local and systemic reactions.

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3
Q

local reaction

A

ingested or inhaled allergen

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4
Q

systemic reaction

A

insect sting or IV adminsitration

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5
Q

allergy antigens can be

A

environmental and non-infectious antens (proteins)

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6
Q

Insect sting

A
  • reaches systemic circulation- bad news- massive mast cell activation and degranulation- systemic reaction
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7
Q

Types of allergens

A
  • Seasonal exposure
    • Tree and grass pollens
  • Perennial exposure
    • House dust mite
    • Animal dander= cats and dogs
    • Fungal spores
  • Accidental exposure
    • Insect venom (wasp and be stings)
    • Medicines e.g. penicillin
    • Chemicals such as latex
    • Foods: milk, peanuts, nuts etc
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8
Q

Mechanisms of allergy

*

A
  • Abnormal adaptive immune response against the allergens
    • T helper 2 (TH2) response (IL-4, IL-5, IL-13)
    • IgE production
  • Mast cell activation (IgE dependent)
    • Sensitized individuals
    • Different clinical allergic disorders depending of on mast cell location
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9
Q

The development of allergy can be influenced two factors:

A

genetics and environmental exposure.

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10
Q

outline immune mechanism of an allergic response

A
  1. Upon first exposure to the allergen (sensitisation phase) a TH2 response is initiated and allergen specific IgE produced which binds to the mast cell via the FcRεRI.
  2. Upon repeated exposure to the antigen (effector phase) the allergen will crosslink with 2 IgE and activate the mast cells causing degranulation resulting in tissue reaction.
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11
Q

Why do people have allergies?

A
  • Hygiene hypothesis
    • This hypothesis suggests that the critical post-natal period of immune response is derailed by the extremely clean household environments often found in the developed world
  • “Old friends hypothesis” or “biodiversity hypothesis”
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12
Q
A
  • Trigger= bee
  • Timing = very acute
  • Symptoms
    • Respiratory
    • CV
    • Skin
    • Face
  • Therapy= epinephrine (2nd dose required)
  • Outcome= likely fatal

Probably had been stung before but didn’t get bad reaction- sensitisation reaction (no anaphylaxis)- however when he is stung again he is in the effector stage that drives hypersensitivity reaction (effector stage)

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13
Q

whyy are allegries increasing in prevalence in the western world

A

Western lifestyle associated with a reduced infectious burden

“Hygiene hypothesis”

  • Children exposed to animals, pets and microbes in the early postnatal period appear to be protected against certain allergic diseases
  • Strachan study (1989) found that children who grew up in large family had a lower risk of hay fever and eczema compared with children in small families
  • Illi study (2001) found in a prospective birth cohort study that infections of the upper respiratory tract before the age of 3 was protecting against allergic sensitisation and asthma later in life
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14
Q

The western lifestyle is associated with microbial dysbiosis

A

“Old friends hypothesis” or “biodiversity hypothesis”

  • Western lifestyle induces alteration of the symbiotic relationships with parasites and bacteria leading to “dysbiosis” of the microbiome at mucosal surfaces (gut)
    • Dysbiosis = compositional and functional alterations of microbiome
    • Microbiome = The complete genetic content of all the microorganisms that typically inhabit in the body, such as the skin or the gastrointestinal tract.
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15
Q

The culprit of allergic reactions

A

Content of mast cell granules will drive allergic reaction- triggered by IgE

Mature mast cell has:

  • FceRI
  • IL-3R
  • react to SCF
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16
Q

Origin of mast cell and tissue distribution

A
  • Strategic location
    • Most mucosal and epithelial tissue = GI tract, skin, resp epithelium
    • In connective tissue surrounding blood cells
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17
Q

Mast cell activation in: the epidermis

A

=Urticaria

18
Q

mast cell activation: Deep dermis

A

= Angioedema

19
Q

Mast cell mediators

A
20
Q

Immune mechanism of allergic reaction

A
  • First exposure= sensitisation phase
    • TH2 response
  • TH2 stimulates B cells to produce IgE
  • IgE binds to FC receptor on the mast cell
  • When antigen (e.g. re-exposed to allergic) mast cells already have antibodies - Effector phase
  • 1 allergen activated 2 antibodies attached to mast cell and cause degranulation of the mast cell
    • release of Histamine and chemokines
21
Q

Histamine and chemokines

A
  • Increased vascular permeability
  • Vasodilation
  • Bronchoconstriction (unwanted function)
22
Q

skin manifestations of allergic reaction : urticaria

A

Caused by mast cell activation within the epidermis (mediators= histamine and leukotrienes/cytokines)

- prloned and chronic exposure= atopic dermatitis and eczema

23
Q

Skin manifestation of allergic reactions: angiodema

A
  • In the deep dermis
    • Angioedema
      • medical emergency due to airway obstruction risk e.g. swollen tongue or pharynx
24
Q

Systemic manifestations of allergic reaction: Anaphylaxis

A

anaphylaxis

systemic release of histamine and chemokines:

  • increased vaslar permeability- hypotension, cvs collapse, generalised urticaria
  • vasodilation- angiodema
  • bronchial constriction- breathing problems

Lose 30% of circulating blood in 10 mins

25
Q

summary of anaphylaxis

A

Anaphylaxis Systemic mast cell activation resulting in:

  • Hypotension
  • Cardiovascular collapse
  • Generalised Urticaria
  • Angioedema
  • Breathing problems
26
Q

treatment of anaphylaxis

A

IM adrenaline (give second dose sometime after to prevent reaction continuing)

27
Q

how to deliver IM dose of adrenaline via epipen

A
28
Q

Type I hypersensitivity therapy

A
  • Abnormal adaptive immune response against the allergens
    • TH2 response = Allergen desensitization (oral immunotherapy)
    • Omalizumab = Anti-IgE monoclonal antibody
    • Mepolizumab – Anti-IL5 monoclonal antibody
  • Mast cell activation
    • Anti-histamine
    • Leukotriene receptor antagonists
    • Corticosteroids (most important anti-inflammatory drugs
29
Q

Allergen desensitization or immunotherapy

A
  • “It involves the administration of increasing doses of allergen extracts over a period of years, given to patients by injection or drops/tablets under the tongue (sublingual)”
    • 90% effective in patients with bee and wasp venom anaphylaxis
    • Potential mechanisms
      • CD4+CD25 Regulatory T cells
      • Shift from TH2 to TH1
      • Inhibitory anti-inflammatory cytokines

Allergen specific blocking

30
Q

Other allergic disease

A
  • Anaphylaxis is the worst
31
Q

Blood Groups

A

The major blood types, A, B, O, and AB, are based on the presence or absence of carbohydrate antigens on the RBC surface. Type A blood has the “A” antigen, type B blood has “B” antigen, type AB has both antigens, and individuals with type O blood have neither of these antigens. Individuals have “naturally” occurring antibodies in their serum (stimulated by the environment) directed against the AB antigen(s) that are not found on their red cells. For example, a person who has type B blood has anti-A in her plasma.

32
Q

What are the main blood groups defined by the ABO system?

A
  • blood group A – has A antigens on the red blood cells
  • blood group B – has B antigens
  • blood group O – has no AB antigens blood group
  • AB – has both A and B antigens

Antibodies present in plasma according to blood group

  • blood group A subjects – have anti-B antibodies in the plasma
  • blood group B subjects – have anti-A antibodies in the plasma
  • blood group O subjects – have both anti-A and anti-B antibodies in the plasma
  • blood group AB subjects – have NO antibodies in the plasma
33
Q

blood transfusions

A

Red cell products must be transfused only to recipients who lack the corresponding AB antibody in their plasma. Plasma products containing AB antibodies must be transfused only to recipients who lack the corresponding antigen on their red cell membranes. Since group O individuals lack any A or B antigens on their red cells, they are considered universal blood donors. Group AB individuals are universal plasma receivers, as they lack AB antibodies.

34
Q

The Rh system

A

Another type of blood grouping is the Rh system. Of the numerous antigens in the Rh system, the D antigen is the most important. Rh-positive blood denotes the presence of the D antigen on the red cells of an individual’s blood. The D antigen is strongly immunogenic, and anti-D (anti-Rh) antibodies are the leading cause of haemolytic disease of the newborn.

35
Q

haemolytic disease of the newborn.

A

When an Rh-negative pregnant woman carries an Rh-positive fetus, small amounts of D-positive red cells can enter her circulation. Her body can then produce anti-D IgG antibodies. If she becomes pregnant in the future with an Rh-positive fetus, the antibodies can cross the placenta and attack the red cells of the fetus.

36
Q

how is haemolytic disease of newborn prevented

A

Rh-negative pregnant women are given a small amount of Rh immunoglobulin (anti-D), RhoGAM, which prevents their own formation of antiD antibodies

37
Q

Haemolytic disease of the newborn – clinical features

A

Destruction of red blood cells causes elevation of bilirubin level in the bloodstream. After delivery of baby with Haemolytic Disease of the Newborn (HDN), bilirubin present in the neonate’s blood is no longer cleared via the placenta, leading to the accumulation of bilirubin in the baby’s bloodstream (called hyperbilirubinemia) and other tissues/fluids resulting in JAUNDICE.

38
Q

*Explain the type of hypersensitivity reaction responsible for the HDN

A

This is an example of type II hypersensitivity reaction leading to loss of function (cytotoxicity). HDN is caused by the presence of maternal IgG directed against the rhesus D antigen, which has crossed the placenta and opsonised foetal red cell blood cells. These red cells with antibody attached are cleared from the circulation by the liver and spleen macrophages.

39
Q

steps in neuromuscular transmission

A

(i) An action potential is propagated down the motoneuron until the presynaptic terminal is depolarized.
(ii) Depolarization of the presynaptic terminal causes voltage-gated Ca2+ channels to open, and Ca2+ flows into the nerve terminal.
(iii) Uptake of Ca2+ into the nerve terminal causes exocytosis of stored acetylcholine (ACh) into the synaptic cleft.
(iv) ACh diffuses across the synaptic cleft to the muscle end plate, where it binds to nicotinic ACh receptors (AChRs).
(v) The nicotinic AChR is also an ion channel for Na+ and K+ . When ACh binds to the receptor, the channel opens.
(vi) Opening of the channel causes both Na+ and K+ to flow down their respective electrochemical gradients. As a result, depolarization occurs.
(vii) This depolarization, called the end plate potential, spreads to the neighboring regions of the muscle fiber.
(viii) Finally, the muscle fibers are depolarized to threshold and fire action potentials.

Through this elaborate sequence of events, an action potential in the motoneuron causes an action potential in the muscle fibers that it innervates

40
Q

pathophysiology opf myasthenia gravis

A

abnormal antibodies to AChR (AChR-ab) are produced, circulate in the blood, and bind to nicotinic receptors on the muscle end plates. When antibodies are bound to AChR, the receptors are not available to be activated by the ACh that is released physiologically from motoneurons. Thus, while normal action potentials occur in the motoneurons and ACh is released normally, the ACh cannot cause depolarization of muscle end plates. Without depolarization of muscle end plates, there can be no action potentials or contraction in the muscle

41
Q

how is Ach recycles in normal neuromuscular transmission

A

After ACh binds to and activates AChR on the muscle end plate, it is degraded by acetylcholinesterase, an enzyme that is also present on the muscle end plate. This degradative step, whose byproducts are choline and acetate, terminates the action of ACh on the muscle fiber. Choline is taken up into the motoneuron terminal and recycled into the synthesis of more ACh.

42
Q

MG treatment

A

Pyridostigmine is an acetylcholinesterase inhibitor that binds to acetylcholinesterase and thereby reduces binding and degradation of ACh at the muscle end plate. In the treatment of myasthenia gravis, pyridostigmine prevents the degradation of ACh, increasing its synaptic concentration and prolonging its action. The longer the muscle end plate is exposed to high concentrations of ACh, the greater the likelihood that action potentials and contraction in the muscle will occur

Immune system (7 decks)

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