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OD2 Semester 1 - Applied Clinical Training > M: Immunopathology 1 - Week 5 > Flashcards

M: Immunopathology 1 - Week 5 Flashcards

1
Q

How does the adaptive immune system rely on the innate?

A

relies on the innate immune system to facilitate T cell signals, that are required to mature the APCs

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2
Q

Explain in 4 steps the process of recognising and removing an infectious agent

A
  1. Resident APCs within peripheral tissue recognise or endocytose small peptides of foreign antigent (macrophages or other innate cells might also engulf pathogen)
  2. APC (and macrophages) mediate the activation of T cells
  3. Antigen presented to T cells activates them and in turn activates B cells to produce antibodies
  4. Depending on the antibody, a particular range of mechanisms will be used to fight off the infection
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3
Q 
What mechanisms are used to fight off infection when the following antibodies are produced?
A) IgM and IgG
B) IgG
C) IgA
D) IgA, IgG, IgM
A

A: C” activation
B: Opsonisation
C: Block adherence
D: Toxin neutralisation

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4
Q

How can T cells affect host tissue?

A

Some of the T-cell responses can cause cytotoxicity to the resident host cells (epithelial cells)

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5
Q

What T-cell enables chemotaxis of inflammatory cells to the site of infection/injury?

A

T-helper cells secrete cytokines and chemokines that enable the chemotaxis

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6
Q

What T-cell can dampen down the immune response?

A

Treg (Regulatory T cell)

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7
Q

Describe 2 broad ways immunopathology can occur, and provide an example for each

A
  1. Failure of all or part of the immune system
    - e.g. immunodeficiency
  2. Abnormal or unwanted responses
    - e.g. allergies, autoimmune disease, graft rejection
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8
Q

Compare Primary vs Secondary Immunodeficiency for the following:
A) Cause
B) Rarity

A

A:
Primary - results from “inherent congenital defect” in the immune system. Caused by either genetic or intrauterine environment
Secondary - caused by “external agents” or alterations in other body systems that can compromise the immune system

B: Secondary is more common than Primary (primary is rare)

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9
Q

List 6 predisposing factors for secondary immunodeficiency

A
  • age
  • malnutrition
  • tumours
  • cytotoxic drugs/irradiation (cancer drugs can kill immune cells)
  • other diseases incl. diabetes
  • infections incl. malaria, HIV
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10
Q

Name 4 common environmental antigens or normal flora that you could have a secondary immunodeficiency to

A
  1. candida albicans
  2. scedosporium species
  3. fusarium species
  4. pseudomonas aeruginosa
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11
Q

Diseases related to secondary immunodeficiencies are often due to re-activation of latent infection. Name 6 microorganisms that could achieve this

A
  • pneumocystis carinii
  • toxoplasma gondii
  • herpes simplex virus (HSV)
  • cytomegalovirus (CMV)
  • varicella zoster virus (VSV)
  • mycobacteria
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12
Q

What 3 ways are hypersensitivities recognised clinically as?

A
  • allergies
  • autoimmune disease
  • graft rejection
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13
Q

How many types of hypersensitivity classifications are there? Briefly explain them

A

Type 1: involves inflammatory response to allergens mediated by IgE

Type 2: where you have IgG and IgM antibodies that react with host cell antigens (particularly antigens expressed on host surface)

Type 3: is immune complex mediated

Type 4: is cell-mediated hypersensitivity or “delayed type”

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14
Q

What type of local (3) and systemic (1) responses can you get with type 1 hypersensitivity? Which is more common? local or systemic?

A

local: (common)
- rhinitis
- bronchoconstriction
- conjunctivitis
systemic; (rare)
- anaphylaxis

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15
Q

Describe the responses to type 1 hypersensitivity [in regards to time and phases]

A

They have both an immediate and delayed phase

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16
Q

Describe in 2 steps how a type 1 hypersensitivity occurs

A
  1. innocuous environmental antigens (e.g. pollens) stimulate the production of IgE antibodies which bind to local mast cells
  2. allergen becomes bound to mast cell by the IgE antibody on subsequent exposure
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17
Q

What type of cell mediates IgE mediated reactions?

A

TH2 lymphocytes

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18
Q

Name the 2 phases of a type 1 hypersensitivity reaction

A
  1. Sensitization phase

2. Elicitation phases

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19
Q

Describe in 3 steps the sensitization phase of type 1 hypersensitivity reactions

A
  1. In the presence of IL-4 and IL-33, the APCs will drive differentiation of T cells into TH2 cells
  2. TH2 activates the production of basophils
  3. TH2 also activates B cells to become plasma cells and start secreting IgE antibodies
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20
Q

Describe in 6 steps the elicitation phase of type 1 hypersensitivity reactions [continuing on from sensitization phase]

A
  1. IgE binds to mast cells in tissues via high affinity FceR
  2. Allergens cross-link the IgE on the surface of mast cells in tissues
  3. The cross link causes mast cell degranulation
  4. Rapid release of granules containing things like histamine
  5. 10-30 mins later, leukotrienes and prostaglandins are released from mast cells
  6. more than 10-30 mins: cytokines (TNFa and IL-4) are released from mast cells to exacerbate the allergic reaction
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21
Q

What does degranulation of the mast cell result in? What is contained within granules? (5)

A

results in the rapid release of preformed granules that contain: histamine, heparin, tryptase, chymase, TNFalpha

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22
Q

Name 4 typical allergic responses to hypersensitivity reactions. Are types of allergic responses tissue dependent?

A
  • vasodilation
  • increased permeability of blood vessels/capillaries in affected area
  • smooth muscle contraction
  • fluid secretion

Yes they are.

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23
Q

Describe the effects of an allergic response in the GI tract (2). What clinical symptoms can this result in? (2)

A
  • Increased fluid secretion
  • Increased peristalsis

Symptoms include:

  • diarrhea
  • vomiting
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24
Q

Describe the effects of an allergic response in the Skin (2). What clinical symptoms can this result in? (3)

A
  • increased fluid secretion
  • increased vasodilation

Symptoms include:

  • swelling
  • itching
  • urticaria (hives)
25
Q

Describe the effects of an allergic response in the Airways (2). What clinical symptoms can this result in? (4)

A
  • decrease in bronchial smooth muscle
  • increase in mucous

Symptoms include:

  • nasal blockage
  • coughing
  • phlegm
  • asthma
26
Q

Describe the effects of an allergic response in the blood vessels (2). What clinical symptoms can this result in? (3)

A
  • increase in blood flow
  • increase in permeability

Symptoms include:

  • increase in tissue fluid
  • increase in cell infiltrate
  • anaphylactic shock
27
Q

Name 4 examples of a type 1 hypersensitivity in the eye (4)

A
  1. Allergic (seasonal) conjunctivitis: hayfever conjunctivitis, SAC
  2. Vernal Keratoconjunctivitis (VKC): assoc. with warm climates, males, family history, other allergies
  3. Giant papillary conjunctivitis: assoc. with CL wear
  4. Atopic keratoconjunctivitis (AKC): assoc, with cool climates, older px’s
28
Q

What cytokines are implicated in atopic keratoconjunctivitis (AKC)?

A

TH1 and TH2 cytokines

29
Q

What are the 2 main outcomes of type 2 hypersensitivity?

A
  1. Cytotoxicity of host cells

2. Functional modification of host cells

30
Q

What does cytotoxicity of host cells involve?

A

Cells can be lysed and tissue injury due to:

  • excessive complement activation
  • excessive phagocyte activation leading to phagocytosis or extracellular enzyme and oxygen radical release
31
Q

Provide two examples of a type II hypersensitivity that can occur or affect the eye

A
  • Cicatricial pemphigold - it causes tissue cytotoxicity

- Myaesthenia Gravis

32
Q

What is the outcome of late stage Cicatricial Pemphigold? (2)

A

Corneal keratinisation and scarring following trichiasis

33
Q

Describe the process/mechanism behind Cicatricial Pemphigold. How does this lead to impairment of corneal/conjunctival stroma?

A

IgG antibodies target B4 integrin on either the corneal or conjunctival epithelium – at the level of the hemidesmosome-epithelial membrane complex

Antibody and complement are deposited on the basement membrane – this means the hemidesmosomes are interrupted and thus the adhesion between the epithelium and the stroma of either the cornea or conjunctiva is iimpaired

34
Q

What symptoms does Cicatricial Pemphigold lead to? (4)

A
  • chronic blistering
  • scarring
  • severe ocular dryness
  • eyelid and eyelash abnormalities
35
Q

How can scarring in the conjunctiva affect the normal anatomy of the lids?

A

every time you blink, the eyelids will scratch the surface of the cornea

36
Q

T/F: Cicatricial Pemphigold only affects the cornea or conjunctiva

A

False. Other mucous membranes can be affected

37
Q

What does a conjunctival biopsy reveal for a patient with late stage Cicatricial Pemphigold? (6)

A
  • loss of epithelium polarity
  • squamous cell metaplasia
  • epithelial thickening
  • vascularisation
  • macrophages
  • absence of goblet cells
38
Q

How can we treat Cicatricial Pemphigold? (3)

A
  • difficult; blister cleansing
  • systemic corticosteroids, other immunosuppressives
  • removal of eyelashes, tear film management, surgery
39
Q

Describe Myasthenia Gravis

A

Is where autoantibodies are produced against the ACH receptor, which inhibit the receptor’s function
– this reduces the number of ACH receptors available to receive NTs in the synapse

40
Q

How does myasthenia gravis result in loss of muscle function

A

complement components induce cell destruction and loss of muscle function

41
Q

Name a type of muscle that is notably affected in Myasthenia Gravis (1), and state the outcomes of this change (3)

A

Extraocular muscles, particularly the Levator muscle.
Results in:
- lid ptosis of affected eye
- difficulty to sustain gaze
- affect binocular vision – leading to diplopia

42
Q

How is type III hypersensitivity mediated? Explain the process that occurs to immune complexes in NORMAL (non-hypersensitivity) conditions

A

is immune complex mediated.

  • IgG and IgM containing complexes activate the complement cascade and become coated with C3b
  • phagocytes express C3b receptors, so they normally remove the immune complex from the tissues and circulation
43
Q

Where are the immune complexes phagocytosed?

A

In the spleen and liver

44
Q

What happens when immune complexes bind erythrocytes?

A

They are carried to the spleen and liver

45
Q

What happens to immune complexes when someone has type III hypersensitivity?

A

The immune complexes are not cleared, and instead persist in the circulation and tissues

46
Q

Describe the features of immune complexes that persist in the circulation (3)

A

They tend to be small and form in antigen excess. They may be associated with low affinity antibody, or antibodies which don’t activate complement

47
Q

Where do immune complexes that persist in the circulation tend to deposit?

A

tend to deposit in blood vessel walls where, when aggregated, they trigger the complement cascade

48
Q

What kinds of inflammatory processes are triggered by deposited immune complexes? (4)

A
  • generate anaphylotoxins, neutrophils, mast cell degranulation
  • induce macrophage cytokine release
  • directly activate platelets (aggregation) and basophils (vasoactive amines)
  • Vasoactive amines – increased vascular permeability and cellular infiltrates

(all this leads to cell damage and tissue injury)

49
Q

What are anaphylotoxins?

A

Anaphylatoxins, or complement peptides, are fragments (C3a, C5a) that are produced as part of the activation of the complement system.

50
Q

List 7 autoimmune diseases for which type III hypersensitivity is a component

A
  1. cicatricial pemphigold
  2. stevens johnoson syndrome
  3. behcet’s syndrome (form of uveitis)
  4. sympathetic ophthalmia (form of uveitis)
  5. sarcoidosis
  6. retinal vasculitis
  7. scleritis
51
Q

What type of cells is type IV hypersensitivity due to?

A

Due to persisting antigen specific T cells (CD4 or CD8)

52
Q

What does it mean for antigen specific T cells to persist? How does this happen?

A

Normally, macrophages which have engulfed microorganisms are stimulated to kill them by helper T cells

When the organism, or stimulating agent persists, macrophages and T cells accumulate at the antigen site in large numbers and result in pathology

53
Q

Describe the steps in the sensitisation phase of type IV hypersensitivity (4)

A
  1. APC needs to reuptake the antigen (endocytose it) and process it within the cytoplasm of the cell and present it to an MHC class II molecule
  2. APC needs to then migrate from the tissues into the draining lymph nodes, where it will encounter T cells
  3. It will present those antigens to the T cells in the lymph node – this activates the T cells
  4. Normally, the antigen is removed, however if antigens continue to persist, then activated macrophages and T cells can accumulate in the tissue
54
Q

Describe the steps in the response phase of type IV hypersensitivity (6)

A
  1. Activated Th1 cells and macrophages accumulate
  2. persistently activated Th1 cells continue to secrete IFNy and TNF
  3. this causes the macrophages to recruit more mononuclear cells
  4. macrophages also start to secrete oxygen radicals and nitric oxides, which are damaging to tissue
  5. excessive Th1 activation can also induce fusion of the macrophages to themselves as well as to epithelial cells
  6. activated CD8 T cells may also accumulate – leading to cytotoxicity of the resident host cell tissues
55
Q

What is another name for type IV hypersensitivity?

A

Delayed type hypersensitivity (DTH)

56
Q

What type of stimuli can result in the occurrence of contact dermatitis and conjunctivitis? (3)

A

Direct irritants - e.g. cosmetics, detergents
Metals, resins, topical antibiotics, anti-histamines
Infectious agents - bacterial or viral

57
Q

What is ACAID and what does it do?

A

Anterior chamber associated immune deviation. this suppresses DTH responses

58
Q

Name a scenario where ACAID can be overcome by DTH?

A

Graft rejection

OD2 Semester 1 - Applied Clinical Training (47 decks)

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