Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Respiratory: Immunology > Hypersensitivity Diseases 2 > Flashcards

Hypersensitivity Diseases 2 Flashcards

1
Q

What is the onset, infectious trigger, environmental trigger, adaptive immune mediators, and innate immune mediators for a Type 1 - Immediate hypersensitivity reaction?

A
  • Onset - seconds (if IgE pre-formed)
  • Infectious trigger - parasites e.g. schistosomiasis
  • Environmental trigger - Allergens
  • Adaptive immune mediators - TH2 cells, B cells, IgE
  • Innate Immune mediators - Mast cells, eosinophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is type II hypersensitivity reaction?

A

Direct cell killing - antibody binding to cell surface antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the pathophysiology of type II hypersensitivity reaction?

A
  • Antibody binds to cell surface antigen

* Results in: activation of complement system (cell lysis, opsonisation), opsonisation (antibody-mediated phagocytosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does activation of compliment system in type II hypersensitivity reaction result in?

A
  • Cell lysis

* Opsonisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does opsonisation of cell by antibodies in type II hypersensitivity reaction result in?

A

Antibody-mediated phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are functions of antibodies?

A

Look at post-lecture slides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the complement system?

A

20 tightly regulated, linked proteins that are produced by the liver and circulate in blood as inactive molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens when complement proteins are activated?

A

When activated, activate other proteins in a biological cascade - results in rapid, highly amplified response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which immune response is the complement system involved in?

A

Important role in both innate and antibody-mediated immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What response is triggered in the liver by the innate immune system?

A

Acute phase response (occurs in response to inflammatory signals released during innate immunity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the effects of complement activation? (4)

A
  • Chemotaxis: stimulates migration of macrophages and neutrophils to site of inflammation
  • Solubilisation of immune complexes
  • Direct killing of bacteria through formation of membrane attack complex (especially encapsulated bacteria)
  • Opsonisation: enhances phagocytosis by macrophages and neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are examples of proteins produced in the acute phase response?

A

CRP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the function of the membrane attack complex?

A

Punches holes in bacterial cell membranes, directly killing them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What complement proteins increase permeability of blood vessels once activated?

A

C3a and C5a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are C3a and C5a known as?

A

Anaphylotoxins - they increase the permeability of blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the purpose of C3a and C5a increasing the permeability of blood vessels?

A

Increases traffic of cells to sites of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the role of opsonins?

A

Act as a bridge between the pathogen and phagocyte receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What acute phase proteins, antibodies and complement proteins are examples of opsonins?

A

C3b, CRP, IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the effect of solubilisation of immune complexes by the complement system?

A

Switches off complement activation through allowing clearance of dissolved immune complexes by phagocytes - regulation of pathway through negative feedback

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the effects of antibody binding to cell surface antigen in type II hypersensitivity reaction? (3)

A
  • Complement activation and osmotic lysis of the cell
  • NK cell and eosinophil activation (ADCC)
  • Acts as an opsonin for phagocytes, leading to phagocytosis of infected cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What Ig classes are involved in type II hypersensitivity reactions?

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are clinical examples of type II hypersensitivity reactions? (2)

A

Immune haemolytic anaemias

  • acute haemolytic transfusion reaction
  • Drug-induced haemolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What type of hypersensitive reaction is ALLERGIC haemolytic anaemia?

A

Type I immediate hypersensitivity reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Explain the process of allergic haemolytic anaemia (4)

A
  • Recipient IgE binds to donor plasma proteins
  • Mast cell activation
  • Histamine release
  • Urticarial (within 1 hour)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is acute haemolytic transfusion reaction (AHTR)?

A

ABO incompatibility leading to lysis of donor erythrocytes by pre-formed recipient IgG antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are signs and symptoms of AHTR? (5)

A
  • Decreased SaO2
  • Increased RR
  • Tachycardia
  • Kidney problems
  • Deceased blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What should be done if you notice Decreased SaO2, increased RR, tachycardia, kidney problems or deceased blood pressure during a blood transfusion? (5)

A
  • Stop transfusion immediately
  • Regulate breathing
  • Regulate HR
  • Flush out kidneys
  • Take samples from both the patient and blood bag to check for clinical error
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Why is it important to catch AHTR early?

A

It can kill the patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are signs and symptoms of drug-induced haemolysis? (4)

A
  • Acute fatigue
  • Breathlessness
  • Pale
  • Mild jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is drug induced haemolysis caused by penicillin known as?

A

Penicillin-induced immune haemolytic anaemia

31
Q

How can a diagnosis of penicillin-induced immune haemolytic anaemia be confirmed? (2)

A
  • Tests showing evidence of RBC destruction

* Tests showing presence of antibodies specific to RBC/penicillin complexes

32
Q

How does penicillin induce immune haemolysis? (5)

A
  • Penicillin is too small to induce antibodies
  • Penicillin binds to a protein on the surface of RBCs
  • The penicillin now acts as a happen and induces antibody production
  • The antibody binds to an FcR on a splenic macrophage
  • The red cell will be destroyed
33
Q

How is type II hypersensitivity managed? (2)

A
  • Plasmapheresis

* Immunosuppression

34
Q

What is the aim of plasmapheresis?

A

Removal of pathogenic antibody

35
Q

Explain the process of plasmapheresis (4)

A
  • Patient blood removed via cell separator
  • Cellular constituents replaced
  • Plasma replaced by donated fresh frozen plasma (FFP) or pooled immunoglobulin
  • Approx 50% of plasma removed each time
36
Q

When is immunosuppression given as treatment for type II hypersensitivity reactions?

A

When rebound antibody production limits the efficacy of plasmapheresis

37
Q

Explain the process of immunosuppression

A

Given potent immunosuppressive agent to switch off B cell production of antibody

38
Q

What is the onset, infectious trigger, environmental trigger, adaptive immune mediators, and innate immune mediators for a Type II hypersensitivity reaction?

A
  • Onset - Immediate (depends if pre-formed antibody) or minutes, hours, days
  • Infectious trigger - almost any pathogen as simply an over-exaggeration of normal immune response
  • Environmental trigger - AB antigens, drugs like penicillin
  • Adaptive immune mediators - IgG, B cells
  • Innate immune mediators - macrophages, complement system
39
Q

What are type III hypersensitivity reactions?

A

Immune complex mediated - antibody binds to soluble antigens

40
Q

What is the pathophysiology of type III hypersensitivity reactions? (2)

A
  • In presence of excess antigen, antibody binds forming small immune complexes
  • These complexes can get too large and are trapped in small blood vessels, joints and glomeruli
41
Q

What are the types of tissues affected by type III hypersensitivity reactions? (4)

A
  • Joints (arthritis)
  • Skin (rashes)
  • Kidney (nephritis)
  • Respiratory tract
42
Q

What is the effect of immune complexes becoming stuck in small blood vessels? (3)

A
  • Immune complexes deposited in wall of blood vessel
  • Fc region sticks out, allowing activation of inflammatory cells like neutrophils and activation of the complement system
  • Enzymes are released from neutrophils causing damage to the endothelial cells of the basement membrane
43
Q

Why do neutrophils release enzymes (degranulate) rather than phagocytose in hypersensitivity type III reactions?

A

Cannot phagocytose as immune complexes are too big, so will degranulate leading to tissue damage

44
Q

What is a clinical example of type III hypersensitivity reaction?

A

Farmer’s lung

  • Inhaled fungal particles form hay etc deposited in lung
  • Stimulate antibody formation
  • Antibodies form immune complex with antigen
  • Results in complement activation, inflammation, recruitment of leukocytes
45
Q

What are examples of causes of hypersensitive pneumonitis?

A
  • Farmer’s lung - mouldy hay, straw, grain
  • Bird fancier’s lung - avian excreta, feathers
  • Malt worker’s lung - mouldy maltings
  • Cheese worker’s lung - mouldy cheese
  • Maple bark stripper’s lung - bark from stored maple
46
Q

What organisms cause Farmer’s lung, Bird fancier’s lung, Malt worker’s lung, Cheese workers lung and Maple bark stripper’s lung?

A
  • Farmer’s lung - aspergillus fumigatus or micropolyspora faeni
  • Bird fancier’s lung - avian serum proteins
  • Malt worker’s lung - aspergillus clavatus
  • Cheese worker’s lung - aspergillus clavatus or penicillum casei
  • Maple bark stripper’s lung - cryptostroma corticale
47
Q

What causes acute hypersensitivity pneumonitis?

A

Immune complexes deposited in the walls of alveoli and bronchioles

48
Q

What causes the symptoms of acute hypersensitivity pneumonitis?

A

Leukocyte accumulation and inflammation within alveoli

49
Q

What are the symptoms of acute hypersensitivity pneumonitis?

A
  • Causes wheezing and malaise after 4-8 hours exposure to antigen
  • Dry cough
  • Pyrexia
  • Breathlessness
  • Examination often normal
50
Q

What is the difference between acute hypersensitivity pneumonitis and chronic hypersensitivity pneumonitis?

A
  • Acute - mediated by type III hypersensitivity response

* Chronic - is not mediated by type III hypersensitivity response (type IV?)

51
Q

Explain the clinical features of acute hypersensitivity pneumonitis

A

Post-leture slides :(

Wheeze…
Breathlesssness….
Malaise, pyrexia….

52
Q

How are type III hypersensitivity reactions managed?

A
  • Avoidance of antigen
  • Corticosteroids used to reduce inflammation
  • Immunosuppression used to decrease production of antibody
53
Q

What are corticosteroids important in treating?

A
  • Allergic disorders
  • Autoimmune disease
  • Inflammatory diseases
  • Transplantation
  • Malignant disease
54
Q

What are the drawbacks of immunosuppressant drugs?

A

Leave patient open to infection

55
Q

What is the onset, infectious trigger, environmental trigger, adaptive immune mediators, and innate immune mediators for a Type III hypersensitivity reaction?

A
  • Onset - hours (if IgG is pre-formed)
  • Infectious trigger - post-streptococcal glomerulonephritis, etc
  • Environmental trigger - Farmer’s lung, etc
  • Adaptive immune mediators - B cells, IgG
  • Innate immune mediators - complement system, neutrophils
56
Q

What are type IV hypersensitivity reactions?

A

Delayed type hypersensitivity

57
Q

What is the difference between type I, II and II hypersensitivity reactions vs type IV hypersensitivity reactions?

A
  • Type I, II, III driven by antibodies

* Type IV driven by T cells (mainly CD4+T cells)

58
Q

What are diseases associated with delayed type IV hypersensitivity reactions?

A

Autoimmune

  • Type 1 diabetes
  • Psoriasis
  • Rheumatoid arthritis

Non-autoimmune

  • Contact dermatitis
  • Tuberculosis
  • Leprosy
  • Sarcoidosis
  • Cellular rejection of solid organ transplant
59
Q

What is a type IV hypersensitivity reaction?

A

Delayed type hypersensitivity - T cell mediated hypersensitivity

60
Q

What is the pathophysiology of type IV hypersensitivity reaction?

A

Initial sensitisation to antigen
* generation of “primed” effector TH1 cells and memory T cells (not much happens)

Subsequent exposure

  • Activation of previously primed T cells
  • Recruitment of macrophages, other lymphocytes, neutrophils
  • Release of proteolytic enzymes, persistent inflammation
61
Q

What is a clinical example of type IV hypersensitivity?

A

Posison ivy (contact dermatitis)

  • Chemical antigens in leaves initiate activation, proliferation and differentiation of antigen-specific T cells, leading to production of effector TH1 cells and memory T cells
  • There is no skin reaction on first encounter
  • Subsequent encounter after this initial sensitization step results in the activation of skin-resident TH1 cells that initiate an inflammatory response, resulting in dermatitis (rash) on the affected area
62
Q

Explain process by which type IV hypersensitivity reactions cause tissue damage

A
  • In delayed type IV hypersensitivity reactions, secondary presentation of the initiating antigen by APCs to TH1 cells results in secretion of cytokines that stimulate inflammation and activate macrophages and other leukocytes, leading to tissue damage
  • In some type IV diseases, CD8+ effector cells (CTLs) are also involved, directly kill antigen positive host cells
63
Q

What cytokines are released by TH1 cells in type IV hypersensitivity reaction?

A
  • IFN-y: activates macrophages increasing the release of inflammatory mediators
  • IL-3/GM-CSF - monocyte production by bone marrow stem cells
64
Q

What is the function of chemokines released by TH1 cells in type IV hypersensitivity reaction?

A

Macrophage recruitment to site of antigen

65
Q

What molecules are released by TH1 cells in type IV hypersensitivity reaction?

A
  • Cytokines
  • Chemokines
  • Cytotoxins
66
Q

What cytotoxins are released by TH1 cells in type IV hypersensitivity reaction?

A
  • TNF-a and Leukotrienes - local tissue destruction, increased expression of adhesion molecules on local blood vessels
67
Q

What is a clinical example of type IV hypersensitivity other than poison ivy?

A

Sarcoidosis

68
Q

What is the underlying pathophysiology of sarcoidosis?

A

Unknown aetiology

* Underlying pathophysiology is type IV delayed type hypersensitivity response to unknown antigen

69
Q

What is sarcoidosis?

A

Multisystem disorder characterised by granulomas

70
Q

Explain the disease process of sarcoidosis (6)

A
  • Unknown antigen
  • Stimulates alveolar macrophages, CD4, CD8 T cells, and B cells
  • TH1 cells release IFN-y to stimulate alveolar macrophages
  • Alveolar macrophages release TNF-a and free radicals
  • Failure to clear antigen causes persistent stimulation and granuloma formation
  • Persistent immune activation leads to tissue damage and fibrosis
71
Q

What are diseases characterised by type IV hypersensitive and granuloma formation?

A
  • Sarcoidosis
  • Tuberculosis
  • Leprosy (some forms)
  • Berylliosis, silicosis and other dust diseases
  • Chronic stage of hypersensitivity pneumonitis
72
Q

How is sarcoidosis managed?

A
  • Watchful waiting - many patients undergo spontaneous remission
  • Non-steroidal anti-inflammatory drugs (NSAIDs) - for acute onset of disease
  • Systemic corticosteroids - block T cell activation, block macrophage activation
73
Q

What is the onset, infectious trigger, environmental trigger, adaptive immune mediators, and innate immune mediators for a Type IV hypersensitivity reaction?

A
  • Onset - 2-3 days
  • Infectious trigger - Hepatitis B virus
  • Environmental trigger - contact dermatitis, sarcoidosis
  • Adaptive immune mediators - TH1 cells
  • Innate immune mediators - macrophages
74
Q

What is the A, B, C, D of hypersensitivity reactions?

A

I - *Allergic *Anaphylaxis and Atopy
II - antiBody
III - immune *Complex
IV - *Delayed

Respiratory: Immunology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions