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EMS > Theme 3: Inflammation, Infection and Immunology: Part 3 > Flashcards

Theme 3: Inflammation, Infection and Immunology: Part 3 Flashcards

1
Q

What are the key features of the innate immune system?

A
  • pre-programmed
  • no memory
  • triggered within seconds
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2
Q

What are the key features of the adaptive immune system?

A
  • highly tailored to infection
  • memory
  • takes 4-6 weeks
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3
Q

Which cells of the innate immune system are APCs that recognise threat?

A
  • dendritic cells

- macrophages/monocytes

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4
Q

Which cells of the innate immune system engulf and destroy threat?

A
  • phagocytes (macrophages, neutrophils)

- granulocytes (neutrophils, eosinophils, mast cells, basophils)

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5
Q

What are cytokines?

A
  • proteins of the innate system

- chemical signals which modulate cell activity or attract cells (chemokine_

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6
Q

What are complement proteins?

A
  • proteins of innate system

- multiple functions: opsonisation, killing, activation, chemoattraction

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7
Q

What are the functions of lymphocytes?

A
  1. B lymphocytes - secrete antibodies: humoral immunity
  2. Cytotoxic T lymphocytes: kill / cellular immunity
  3. Helper T lymphocytes: secrete growth factors (cytokines) which control immune response
  4. Suppressor T lymphocytes - dampen down immune response
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8
Q

What is autoimmunity/ auto inflammation?

A

innappropriately increased response to danger signals

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9
Q

What is immunodeficiency?

A

inappropriately decreased response to danger signals

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10
Q

Which factors pre-dispose to autoimmune conditions?

A
  • sex (hormonal influence) - women more than men
  • age - more common in elderly
  • environmental triggers - infection, smoking
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11
Q

Which cells cause autoimmunity?

A
  1. autoreactive B cells and autoantibodies
    - directly cytotoxic, activation of complement
    - autoreactive T cells
    - directly cytotoxic, cytokine production
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12
Q

What is Hashimoto’s thyroiditis?

A
  • destruction of thyroid follicles by autoimmune processes
  • associated with autoantibodies to thyroglobulin and thyroid peroxidase
  • leads to hypothyroidism
  • symptoms: weight gain, fatigue, cold, hair loss, constipation
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13
Q

What is graves disease?

A
  • innappropriate stimulation of thyroid gland by anti-TSH-autoantibody
  • leads to hyperthyroidism
  • symptoms: weight loss, anxiety, diarrhoea, palpitations, hot, goitre
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14
Q

What are examples of systemic autoimmune diseases?

A
  • systemic lupus erythematosus (SLE)
  • scleroderma
  • polymyositis
  • vasculitis
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15
Q

What is urticaria?

A

skin rash

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16
Q

What is neutrophilic urticarial dermatosis?

A
  • neutrophillic dermal infiltrate with substantial interstitial spreading
  • absence of confluence of neutrophils
  • no oedema
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17
Q

What are 3 NLRP3-related autoinflammatory diseases?

A
  1. Familial cold urticaria
    - relatively mild
    - autosomal dominant
    - cold induced rash
    - arthralgia (pain at joints)
    - conjunctivitis
  2. Muckle Wells syndrome
    - autosomal dominant
    - moderate severity
    - urticarial rash
    - sensorineural deafness
    - AA amyloidosis (25%)
  3. NOMID/CINCA
    - sporadic
    - severe
    - progressive chronic meningitis
    - deafness, visual and intellectual damage
    - destructive arthritis
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18
Q

What are the differences between auto inflammation and autoimmunity in terms of:

  1. Immune response
  2. Main cellular involvement
  3. Antibody involvement
  4. Clinical features
  5. Therapy
  6. Example diseases
A
  1. autoinflammation - innate immunity
    autoimmunity - adaptive immunity
  2. autoinflammation - neutrophils, macrophages
    autoimmunity - B and T cells
  3. Autoinflammation - few or no autoantibodies
    autoimmunity - autoantibodies present
  4. autoinflammation - recurrent, unprovoked attacks
    autoimmunity - continuous progression
  5. autoinflammation - anti-cytokine (IL-1, TNF)
    autoimmunity - anti-B and T cell
  6. autoinflammation - chrons disease
    autoimmunity - monogeny ALPS and IPEX
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19
Q

What is immunosuppression?

A

a natural or artificial process which turns off the immune response, partially or fully, accidentally or on purpose

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20
Q

What are examples of secondary or acquired immunodeficiencies?

A
  • stress
  • surgery/burns
  • malnutrition
  • cancer
  • irridiation
  • AIDS
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21
Q

What is primary immunodeficiency?

A
  • very rare
  • often in childhood but can present in adult life
  • recurrent, unusual and opportunistic infection
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22
Q

Why are defects in T cells more severe than defects in B cells?

A

B cells also need T cell help

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23
Q

What would happen if you have defects in both B and T cells?

A
  • severe combined immunodeficiency syndromes (SCID)
  • bone marrow transplant is curative
  • gene therapy
24
Q

What is hypersensitivity?

A
  • a reaction produced by the normal immune system in a pre-sensitised (immune) host
  • undesirable, damaging, uncomfortable, sometimes fatal
25
Q

What did Coombs and Gell (1963) discover?

A

IV types of hypersensitivity - I, II, III, IV

26
Q

Describe type 1 hypersensitivity

A
  • IgE antibody binds to mast cell and causes degranulation of mast cell
  • fast onset, can be mild, moderate or severe
  • primary response: histamine, proteases, chemotactic factors
  • late phase response: eosinophils, central role for Th2 T cell
27
Q

What are the systemic effects of histamine?

A
  • blood clots
  • gastric acid secretion
  • vasodilation
  • bronchoconstriction
  • increases the permeability of the capillaries
  • adrenaline is released
  • swelling and inflammation
  • infrequent heart beat - tachycardia, bradycardia
28
Q

What is anaphylaxis?

A

an acute, potentially life-threatening IgE mediated systemic hypersensitivity reaction

29
Q

What are the symptoms of mild type 1 hypersensitivity?

A
  • itchy eyes or nose
  • cutaneous pruritus - itching of the skin
  • urticaria - red rash
  • oral tingling
  • abdo pain/ nausea/ vomiting
  • runny nose, sneezing
30
Q

What are the symptoms of moderate-severe type 1 hypersensitivity?

A
  • diffuse urticaria and angioedema
  • severe abdominal pain, vomiting diarrhoea
  • SOB
  • cough, wheezing and cyanosis
  • hypotension
  • dizziness, loss of consciousness, respiratory arrest
31
Q

What is the dual allergen exposure hypothesis?

A
  • early cutaneous exposure to food protein through a disrupted skin barrier lead to allergic sensitisation
    e. g excsma disrupts the skin barrier so can lead to allergies
  • whereas early oral exposure to food allergens induces tolerance
32
Q

Can allergies have a genetic influence?

A
  • allergies caused by a combination of genetic and environmental factors
  • however, genetic influences are not sufficient for disease, only susceptibility
33
Q

What is the atopic triad

A
  • eczma
  • asthma
  • rhinitis
34
Q

How do we diagnose allergies?

A
  • history
  • specific IgE
  • skin prick test
  • intra-dermal test
  • oral challenge test (gold standard)
35
Q

What is a positive test for a skin prick test?

A

where there is a hive that is >2mm bigger than negative control

36
Q

What is asthma?

A
  • disease of inflammation and hyperactivity of the small airway
  • immediate symptoms are IgE-mediated
  • damage to airways due to late phase response
37
Q

What is type II hypersensitivity?

A
  • cytotoxic
  • IgG/ IgM Ab response against combined self/foreign antigen at cell surface
  • complement activation/phagocytosis/ ADCC
  • onset minutes to hours
  • cell lysis/ necrosis
38
Q

what is a common antigen associated to type II hypersensitivity?

A

penicillin

39
Q

give 2 diseases resulting in type II hypersensitivity

A
  • goodpasture’s nephritis

- blood transfusion reaction

40
Q

What is a blood transfusion reaction?

A
  • example of type II hypersensitivity
  • if incorrectly matched blood
  • patients APC’s detect the foreign antigen, present it to B cells which makes antibodies which activates complement and has cytotoxic action
  • takes hours to a day
41
Q

What is the MAC Protein complex?

A
  • C1 binds IgG/M and the complement cascade follows
  • C3 activation generating C3a + C3b
  • focused target cell lysis
42
Q

What is type III hypersensitivity?

A
  • immune complex deposition

- IgG/ IgM Ab against soluble antigen

43
Q

What are the clinical features of type III hypersensitivity?

A
  • onset 3-8hrs
  • vasculitis
  • traditional cause: serum sickness
  • associated diseases - SLE
44
Q

What is the difference between type II and type III hypersensitivity?

A
  • same antibodies but bind to different things
  • type II sensitivity - IgG binds to cell
  • type III sensitivity - antibody binds to soluble antigen
45
Q

What is an example of Type III hypersensitivity condition?

A

Systemic lupus erythematosus (SLE)

-B cells recognises self as foreign so autoimmunity results

46
Q

Explain the complement cascade in Type III hypersensitivity ?

A
  • C1 from the complement system binds the antibody and C1-9 follow with increased permeability of vessels - triggers complement pathway
  • C3/4 used in large amounts - key blood test - as complement is used up
47
Q

What is type IV hypersensitivity?

A
  • delayed onset: 48-72hrs
  • antigen specific T-cell mediated cytotoxicity
  • erythema (redness of skin)
  • common antigens: metals e.g nickel, poison ivy
  • associated diseases: contact dermatitis
48
Q

Name 3 chemical mediators produced by a mast cell?

A

leukotrienes, histamine, prostaglandins

49
Q

What is anaphylaxis?

A

Massive degranulation of mast cells causing the release of chemical mediators

50
Q

What is perioperative anaphylaxis?

A

occurs during the period of anaesthesia and surgery

51
Q

How do we treat anaphylaxis?

A
  • first, adrenaline and fluids
  • fluids are needed because with increased vascular permeability that histamine causes you get a leakage of fluid from the intravascular compartments
  • if this doesn’t work, consider vasopressin and glucagon
  • steroids, antihistamines
52
Q

What are the two functions of adrenaline?

A
  1. treats symptoms - increase systemic vascular tone

2. stops anaphylaxis - stops mast cell degranulation

53
Q

Why do we collect tryptase samples instead of histamine in a allergic reaction?

A
  • tryptase is one of the chemical mediators released from mast cells when they degranulate
  • histamine has a very short half life so we cannot capture the histamine peak during anaphylaxis
54
Q

What are the main causal agents for preoperative anaphylaxis?

A
  • antibiotics
  • neuromuscular blocking agents
  • chlorhexidine
  • teicoplanin is most allergenic anaesthetic drug
55
Q

What is a challenge test?

A

give allergenic e.g penicillin in controlled environment and watch closely for symptoms

EMS (16 decks)

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