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Pathophysiology 2.0 > Week 2 - Tutorial - Hypersensitivity > Flashcards

Week 2 - Tutorial - Hypersensitivity Flashcards

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?

A

Immune-complex-mediate hypersensitivity

19
Q

What is type III hypersensitivity mediated by?

A

mediated by Ag-Ab complexes

20
Q

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

A

a few hrs

21
Q

Describe the process of type III hypersensitivity.

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?

A

Delayed-type hypersensitivity

23
Q

Which Cell is type IV mediated by?

A

TH1 cells

24
Q

What two cells are involved in type IV hypersensitivity?

A

cytotoxic T cells (CD8+)

Th1 cells (CD4+)

25
Q

Which antibodies are involved in type IV hypersensitivity?

A

hahahhaha trick question lol

26
Q

Describe the steps of type IV hypersensitivity

A
  • antigen causes Th1 cells to release cytokines
  • causes accumulation & activation of macrophages
  • as well as activation of cytotoxic T cells
  • cause local damage
27
Q

How long after exposure does type IV reaction occur?

A

days to wks after challenge with allergen

28
Q

What % of worl suffers from allergies?

A

20%

29
Q

What is Atopy

A

a predisposition towards developing IgE-mediated hypersensitivity allergic reactions

30
Q

IgE is v. importento for the sensitisation stage of type I hypersensitivity.

How is IgE produced & what cytokines are involved?

Where is it localised?

A
  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
Q

How does IgE contribute to the activation stage of type I hypersensitivity?

A

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
Q

What are the two types of asthma?

A

allergic & non-allergic

33
Q

What is non-allergic asthma mediated by?

A

it is not IgE-mediated

is prompted by innate lymphoid cells (ILCs) specifically ILC2

34
Q

Describe how non-allergic asthma occurs.

A

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
Q

What are some diseases associated with type I hypersensitivity?

A

asthma

allergic rhinoconjunctivitis

anaphylaxis

36
Q

What is anaphylaxis?

A

Is an acute allergic reaction to an antigen

37
Q

Explain what happens in anaphylaxis.

A
  • 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
Q

What drug is used to reverse the effects of anaphylaxis

A

Typically is epinephrine or adrenalin

39
Q

What is the effects of adrenalin on the body during anaphylaxis?

A

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
Q

How does MS affect the Blood Brain Barrier?

A
  • Causes BBB to breakdown
  • BBB decreases the integrity of the tight junctions
41
Q

What does MS do the immune system?

A

Causes autoimmunity

aka immune system attacks the nervous system, forming plaques or lesions

commonly involves white matter

destroys oligodendrocytes = demyleniation

42
Q

What is the aetiology of MS

A

Is an interplay btw

environmental (migration, low vit d)

Genes (3-5% norm, 5% dizygotic twins & 30% monozygotic)

Infection (EBV, HHV6)

43
Q

What are the different classification of MS? descibe the tends of each one.

A
  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 (19 decks)

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