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CVR Lectures > Hypersensitivity and the lung > Flashcards

Hypersensitivity and the lung Flashcards

1
Q

What is innate immunity?

A

E.g. sputum and cilia in lungs
- It is the first line in defence and has an immediate response.
- It is composed of phagocytes, mast cells

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1
Q

What is innate immunity?

A

E.g. sputum and cilia in lungs
- It is the first line in defence and has an immediate response.
- It is composed of phagocytes, mast cells

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2
Q

What is adaptive immunity?

A

E.g. Pus, swelling, granuloma
- Often the second line
- Delayed response time, often > 4 days
- B and T -lymphocytes

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3
Q

What are the cellular components of the immune system?

A
  • Phagocytes e.g. monocytes and neutrophils
  • Lymphocytes: make and release antibodies and kill diseased cells
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4
Q

What are the humoral components of the immune system?

A
  • Immunoglobulins
  • Complement (form membrane attack complex)
  • Cytokines (allow communication between WBC and tissue cells)
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5
Q

What are antibodies produced by?

A

B-lymphocytes (plasma cells)

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6
Q

What do antibodies do?

A
  • Neutralise or eliminate pathogens
  • Can also cause disease
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7
Q

What are the 5 classifications of antibodies?

A

IgM, IgG, IgE, IgA, IgD

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8
Q

What are IgM antibodies?

A

they are circulating tetramers (a molecule (as an enzyme or a polymer) that consists of four structural subunits) made at the beginning of infection

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9
Q

What are IgG antibodies?

A

Monomer highly specific antibodies targeting single epitopes (pathogenic site)

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10
Q

What are IgE antibodies?

A

Likely to have developed in response to parasitic threats. Implicated in allergy, particularly alongside eosinophils

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11
Q

What are IgA antibodies?

A

Expressed in mucosal tissue. Forms dimers (a pair or them stuck together). Protects the neonatal gut

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12
Q

What are IgD antibodies?

A

Monomers, induction of antibodies in B cells, activates basophils and mast cells

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13
Q

What is Type I hypersensitivity?

A
  • Mediated by IgE antibodies (+ eosinophils)
  • Immediate (within an hour)
    E.g. anaphylaxis and hay fever
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14
Q

What is Type II hypersensitivity?

A
  • Mediated by cytotoxic antibodies bind to the cell antigen
  • Comes on in hours to days
    E.g. Transfusion reactions and Goodpastures (Anti GBM disease) - antibodies attack the basement membrane in lungs and kidneys
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15
Q

What is Type III hypersensitivity?

A
  • Mediated by deposition of immune complexes
  • Comes on typically 7-21 days
    E.g. Hypersensitivity pneumonitis; post streptococcal glomerulonephritis
16
Q

What is Type IV hypersensitivity?

A
  • Mediated by T-Cells (lymphocytes)
  • Takes days to weeks or months to come on
    E.g. Tuberculosis; Stevens-Johnson syndrome
17
Q

How does Type I hypersensitivity cause a reaction?

A
  • Antigen interacts with IgE bound to mast cells or basophils
  • Degranulation of mediators lead to local effects
  • Histamine is the predominant mediator
18
Q

What is anaphylaxis?

A
  • Sudden onset
  • Systemic degranulation of mast cells and histamine release
  • Skin, eyes, lips swelling, hypotension
  • Bronchospasm can result in airway occlusion and death if not managed
    (Type I Hypersensitivity)
19
Q

How to manage anaphlyaxis?

A
  • Adrenaline 0.5mg or auto injector
  • Steroids
  • Antihistamines
  • Second peak may occur after 12 hours
  • Measure tryptase
20
Q

How does Type II hypersensitivity cause a reaction?

A
  • Antibodies reacting with antigenic determinants on the host cell membrane
  • Usually IgG or IgM
  • Outcome depends on whether complement is activated and if metabolism of cell is affected
21
Q

What is Anti-Glomerular Basement Membrane Disease

A
  • Rare but deadly Type II HS disease
  • Alveolar involvement
  • GBM made of type IV collagen present in alveoli
  • The Alpha 3 subunit of this collagen becomes antigenic
    Very rare
22
Q

How do we treat AGBMD?

A
  • With plasmapheresis (remove plasma to extract offending Abs)
  • Immune suppression (Steroids)
  • Supportive lung treatment (ventilation) and kidneys (filtration)
23
Q

What is Mycoplasma Pneumonia?

A
  • Type II HS
  • Antibodies also attack red blood cells causing agglutination and haemolysis (rupture and destruction of RBC)
24
Q

How does Type III hypersensitivity cause a reaction?

A
  • Antigen-immunoglobulin complexes formed on exposure of allergen
  • Then deposited in tissues
  • Causes local activation of complement and neutrophil attraction (inflammation)
25
Q

What is Hypersensitivity pneumonitis

A

-Formerly “extrinsic allergic alveolitis” (EAA)
- Immune complexes formed with a range of different antigens
- Deposited in the acinar airways leading to inflammation acutely and scarring chronically
- Treatment by removal of antigen +/- immunosuppression

26
Q

How does Type IV hypersensitivity cause a reaction?

A
  • T-cell mediated, releasing IL2, IFᵧ and other cytokines
  • Requires primary sensitisation (doesn’t happen first time you are exposed)
  • Secondary reaction takes 2-3 days to develop
  • May result from normal immune reaction – if macrophages cannot destroy pathogen, they become giant cells and form granuloma
27
Q

How can we check for type IV HS?

A

Patch testing:
- Control test
- Other test
- Positive test
Or tuberculin skin test (only positive if been exposed before or had the vaccine)
- Takes several days for it to come up

28
Q

What is Sarcoidosis?

A
  • Possibly reaction to mycobacteria
  • Multisystem disease causing granuloma
    Eyes, skin, lungs, heart, nervous system…
  • 80% regress spontaneously
  • Some require systemic treatment – steroids, methotrexate, others
29
Q

What are some common drugs that are implicated in lung disease?

A
  • Amiodarone
  • ACE-inhibitors
  • Bleomycin
  • Methotrexate
  • Nitrofurantoin
  • Checkpoint inhibitors
30
Q

How do checkpoint inhibitors work?

A
  • Cancer cell presents PD-L1 allowing it to disguise as not foreign
  • Checkpoint inhibitors block the PD-L1 and PD-1 system
  • Allows T-Cell to recognise cancer as foreign so can be destroyed normally
31
Q

What are three consequences of T-cell hypersensitivity?

A
  • Diabetes
  • Thyroid disease
  • Hepatitis
    Any –itis!
  • Pneumonitis (life-threatening)
32
Q

What may those with eosinophilic asthma have?

A
  • Atopic or non-atopic
    Each different type can be treated based on the phenotype. Target the specific type of hypersensitivity causing the problem.

CVR Lectures (28 decks)

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