Pathophysiology 2.0 > Week 2 - Tutorial - Hypersensitivity > Flashcards

Week 2 - Tutorial - Hypersensitivity Flashcards

(43 cards)

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1
Q

What is type I hypersensitivity?

A

Immediate hypersensitivity

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2
Q

What is type I hypersensitivity mediated by?

A

mediated by IgE antibodies

thus, mast cells & basophils

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3
Q

How long after exposure does type I hypersensitivity occur?

A

~30 mins after exposure

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4
Q

What type of reaction does type I hypersensitivity cause?

A

Allergic Reaction

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5
Q

What are the 3 steps in the allergic reaction?

A
  1. Sensitisation
  2. Activation
  3. Effector step (early & late phase)
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6
Q

What occurs during Sensitisation?

A

SENSITISATION

  • TH2 cells release interleukins in response to the presence of antigens or allergens (<1μg/year)
  • the ILs cause the plasma cells to produce IgE antibodies that are specific to that allergen
  • the new Ab will bind to the FcεR1 on Mast cells & basophils
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7
Q

What occurs during the Activation phase of the Allergic Reaction Response?

A

ACTIVATION

  • re-exposure to the SAME ALLERGEN
  • the Ag induces the cross-linking of the IgE to the FcεR1 on the Mast cell or basophil
  • causes degranulation of the mast cell or basophil
  • causes release of chemical mediators into tissue site
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8
Q

What are the two phases in the effector step in the Allergic reaction response?

A
  1. Early phase
  2. Late Phase
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9
Q

What Occurs in the Early Phase of the Effector step in the allergic reaction response?

A

Early phase

  • occurs immediately
  • caused by the direct effects of chemical mediators on blood vessels & smooth muscle
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10
Q

What Chemical Mediators are secreted by the TH2 cells and are involved in the Allergic Reaction Response?

A

IL-2, IL-10, IL-13

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11
Q

What Chemical Mediators are released by Mast Cells during the Allergic Reaction Response?

A
  • Interleukotriens
    • IL-4, IL-5, IL-6, IL-8 & IL-9
  • Cytokines
    • TNFα
    • GM-CSF
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12
Q

What Chemical Mediator is in the plasma & cause the activation of what cell? This cell then secretes what?

A

Platelet Activating Factor (PAF) causes platelets to aggregate at site of injury

causes mast cell, macrophage & basophils to accumulate

above cells degranulate & release histamine

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13
Q

What occurs in the Late Phase of the Effector step in the allergic reaction response?

A
  • occurs 6-10 hrs after the initial response
  • infiltration of eosinophils, neutrophils, macrophages Th2 & basophils
  • Mainly Eosinophils
    • migrate to site via IL-4 & chemokines
    • cause expression of the FcR (for IgG) & FcεR1 on the eosinophil
    • when both the IgG & IgE bind to the FcR & FcεR1 causes degranulation
  • release of inflammatory mediators
    • leukotrienes, major basic protein, eosinophilic cationic protein, eosinophilic peroxidase & PAF
  • Causes extensive tissue damage
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14
Q

What are the physiological or pharmacological effects during the effector step?

A

Pharmacological Effect

  • Thru the release of histamine, it binds to;
    • H1R on smooth muscle = constriction
    • H1R on endothelial cells = increase permeability
    • H2R on respiratory mucosa = increase mucus secretions
    • H2R on gut mucosa = release of stomach acid
  • Thru release of cytokines & chemokines
    • causes chemotaxis & activation of inflammatory cells
    • makes process continue & worsen
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15
Q

What is type II hypersensitivity?

A

Cytotoxic or Cytolytic Hypersensitivity

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16
Q

What is Type II hypersensitivity mediated by?

A

IgG or IgM mediated

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17
Q

Describe the steps of type II hypersensitivity.

A
  1. Immunoglobin binds to antigen (Ab-Ag or Ab-IgG) forms immune complex
  2. immune complex triggers activation of complement or ADCC
  3. causes damage
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18
Q

What is type III hypersensitivity?

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A

Immune-complex-mediate hypersensitivity

19
Q

What is type III hypersensitivity mediated by?

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A

mediated by Ag-Ab complexes

20
Q

How long after exposure does type III hypersensitivity’s reaction occur?

21
Q

Describe the process of type III hypersensitivity.

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A

antigen binds to immunoglobin

Ag-IgM or Ag-IgG complexes activate complement

granulocytes are attracted to site of activation

damage is caused by the release of lytic enzymes from granulocyte

22
Q

Type IV hypersensitivity is known as?

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A

Delayed-type hypersensitivity

23
Q

Which Cell is type IV mediated by?

24
Q

What two cells are involved in type IV hypersensitivity?

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A

cytotoxic T cells (CD8+)

Th1 cells (CD4+)

25
Which antibodies are involved in type IV hypersensitivity?
hahahhaha trick question lol
26
Describe the steps of type IV hypersensitivity
* antigen causes Th1 cells to release cytokines * causes accumulation & activation of macrophages * as well as activation of cytotoxic T cells * cause local damage
27
How long after exposure does type IV reaction occur?
days to wks after challenge with allergen
28
What % of worl suffers from allergies?
20%
29
What is Atopy
a predisposition towards developing IgE-mediated hypersensitivity allergic reactions
30
IgE is v. importento for the sensitisation stage of type I hypersensitivity. How is IgE produced & what cytokines are involved? Where is it localised?
1. IgE production * (a) Ag presenting cell (dendrocyte or macrophage) presents Ag to naive T cell * t cell binds to Ag & costimulates factor of Ag presenting cell * naive cell now becomes Th2 cell * (b) Th2 cause B cells to undergo Ab class switching (switches from IgM to IgE) 2. What cytokines are involved? * (a) occurs in presence of IL-4, IL05 & IL-10 * (b) Th2 cells release IL-4 & IL-13 for b cell & IL-5 for activation of eosinophils 3. Where is it localised? * (a)lymph node * (b) site of injury
31
How does IgE contribute to the activation stage of type I hypersensitivity?
IgE binds to FcεR1 on mast cells & forms crosslinkage crosslinkage is v hard to break up activation of mast cell causes its degranulation & thus release of histamine & other mediators into tissue
32
What are the two types of asthma?
allergic & non-allergic
33
What is non-allergic asthma mediated by?
it is not IgE-mediated is prompted by innate lymphoid cells (ILCs) specifically ILC2
34
Describe how non-allergic asthma occurs.
Irritant (smoke air pollution etc.) irritates lung epithelium triggers release of IL-33 from lung epithelium binds to IL-33R (ST2R) on ILC2 & activates it ILC2 secretes large amounts of IL-5 & IL-13 cytokines induce inflammatory cell infiltration, mucus production & airway hyperresponsiveness aka asthma
35
What are some diseases associated with type I hypersensitivity?
asthma allergic rhinoconjunctivitis anaphylaxis
36
What is anaphylaxis?
Is an acute allergic reaction to an antigen
37
Explain what happens in anaphylaxis.
* after a type I hypersensitivity reaction * IgE-mediated release of inflammatory mediated forms mast cells & basophils * IL-4, IL-5, IL-6, GM-CSF, TNFα ECF & PAF * Which cause the release of histamine from platelets * levels rise within 5 mins & stay elevated for 30 to 60 mins * causes; * increase vascular perm = urticaria (hives) & angioedema (swelling of skin, mucosa & submucosa) * increase HR * contraction of smooth muscle in brochiole & GIT *
38
What drug is used to reverse the effects of anaphylaxis
Typically is epinephrine or adrenalin
39
What is the effects of adrenalin on the body during anaphylaxis?
adrenaline causes the smooth muscle to relax reduces vascular permeability (thru reformation of the right junctions btw endothelial cells) improves cardiac output & causes changes in systemic BP (aka MAP rises)
40
How does MS affect the Blood Brain Barrier?
* Causes BBB to breakdown * BBB decreases the integrity of the tight junctions
41
What does MS do the immune system?
Causes autoimmunity aka immune system attacks the nervous system, forming plaques or lesions commonly involves white matter destroys oligodendrocytes = demyleniation
42
What is the aetiology of MS
Is an interplay btw environmental (migration, low vit d) Genes (3-5% norm, 5% dizygotic twins & 30% monozygotic) Infection (EBV, HHV6)
43
What are the different classification of MS? descibe the tends of each one.
1. Benign Multiple Sclerosis * stable with few acute relapses 2. Relapsing-Remitting Multiple Sclerosis * relatively stable but with each relapse gets worse 3. Secondary Chronic Progressive * more relapses with less stable plateaus & one relapse = progression 4. Primary-Progressive (10 - 20% of cases) * exponential increase in progression
Pathophysiology 2.0
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