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Infection and immunity > Malcom Watson Semester 2 > Flashcards

Malcom Watson Semester 2 Flashcards

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1
Q

What is asthma?

A

Chronic inflammatory disorder of the airways usually associated with:

  • variable airflow obstruction
  • increased in airway response to a variety of stimuli
  • obstruction is often reversible either spontaneously or with treatment
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2
Q

What are the four mechanisms of hyperresponsiveness in asthma?

A
  1. Increased smooth muscle contractility
  2. Increased excitatory nerve activity
  3. Decreased bronchodilator activity
  4. Inflammation
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3
Q

Mitogens (promote cell division) involved in smooth muscle growth in asthma include what?

A

Platlet dervied growth factor
Endothelian
Cytokines
Histamine

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4
Q

How does increased excitatory nerve activity come about in asthma?

A

Autonomic NS in the airways cause bronchoconstriction. Excitatory non-adrenergic non-cholinergic transmitters (eNANC) include neurokinin A, neurokinin B, substance P.

All stimulate GPCR Gq coupled

  • raised intracellular CA
  • increases activity of myosin light chain kinase (MLCK)
  • phosphorylation of myosin light chain leads to contraction
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5
Q

Why are muscarinic antagonists not commonly used in asthma?

A

May lead to loss of negative feedback mechanism (on M2) and cause more enhanced airway contraction.

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6
Q

How does circulating adrenaline cause bronchodilation?

A

Acts on the B adrenoreceptors of autonomic nervous system.

B2 receptor leads to increased cAMP levels and increased PKA activity, this leads to:

  • opening of K+ channels
  • inactivates MLCK
  • calcium sequestration

OVERAL LESS CONSTRICTION

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7
Q

Salbutamol

A

Short acting B2 adrenoreceptor agonist

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8
Q

Formeterol

A

Long acting B2 adrenoreceptor agonist

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9
Q

Salmeterol

A

Long acting B2 adrenoreceptor agonist

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10
Q

How do B2 receptor agonists work?

A

Binding to B2 receptor leads to increased cAMP levels and increased activity of PKA. This results in:

  • opening of K+ channels
  • inactivation of MLCK
  • calcium sequestration

Overall get less constriction

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11
Q

Theophylline

A

Phosphodiesterase inhibitor (PDE III and IV in airway smooth muscle)

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12
Q

What does phosphodiesterase do?

A

Breaks down cAMP

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13
Q

How does theophylline cause bronchdilation?

A

Inhibits PDE. This leads to increased cAMP

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14
Q

What T cell phenotype is associated with allergic disease/asthma?

A

TH2

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15
Q

What is the role of TH2 cells in asthma?

A

TH2 cell releases IL-13 AND IL-1 which activates B ells

B cells produce IgE antibody which interacts with FCR1 receptors on mast cells –> degranulation

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16
Q

Outline the mast cell degranulation products?

A

Histamine
TNF and other cytokines
Proteases
Heparins

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17
Q

What is found in mast cells located in the lungs?

A

Tryptase
Chondriotin sulfate E
LOW histamine

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18
Q

What is found in mast cells located in the skin

A

Tryptase
Chymotrypase
Heparin
HIGH histamine

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19
Q

Which leukotrienes are responsible for constriction of airway muscle in asthma?

A

LTC4 and LTD4

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20
Q

what affect does PGD2 have on airway smooth muscle

A

Bronchoconstrictor

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21
Q

what affect does PGE2 have on airway smooth muscle

A

Relaxes airway smooth muscle

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22
Q

What cytokine is involved in non-allergic asthma?

A

IL-13

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23
Q

what is meant by intrinsic asthma?

A

non-allergic asthma

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24
Q

what is meant by extrinsic asthma?

A

allergic asthma

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25
What are the actions of IL-13 and IL-4 in intrinsic asthma?
``` Increased eosinophil adhesion and migration Increased VCAM-1 expression Mucus secretion Tissue remodelling airway SM contraction ```
26
Montelukast
Leukotriene receptor antagonist specifically inhibits LTC4 and LTD4
27
Zileuton
Inhibits 5-lipoxygenase so inhibits leukotrien synthesis inhibitors
28
Sodium cromoglycate
Mast cell stabilisers - inhibit mediator release from lung mast cells Also inhibit sensory nerve fibre excitation and neural reflex Inhibit eosinophil chemotaxis
29
Olmalizumab
Binds to Fc portion of IgE thus prevents IgE bind to mast cells. Approved for IgE mediated severe allergic asthma and is not responsive to glucocorticoids.
30
What is COPD?
Progressive airflow limitation that is not fully reversible. Associated with an abnormal inflammatory response of the lung to noxious particles or gases, primary cigarette smoke.
31
Chronic bronchitis is characterised by....
Productive cough and excessive sputum production. Overweight, and cyanotic, elevated haemoglobin, peripheral oedema and wheezing.
32
Emphysema is characterised by....
Alveolar wall destruction, irreversible enlargement of the terminal air spaces Older Thin, severe dyspnea, quiet chest, x-ray shows hyperinflation with flattened diaphragms
33
The following symptoms are associated with what..... Overweight and cyanotic (blue), elevated haemoglobin, peripheral oedema and wheezing
Chronic bronchitis
34
The following symptoms are associated with what? Underweight, severe dyspnea, quiet chest
Emphysema
35
What are risk factors for COPD?
``` Smoking Urban pollution - smog industrial pollution textile dust biomass fuels ```
36
COPD risk factors all have what in common?
All contain ROS, toxins and particulate matter
37
Outline the four stages of COPD
Stage 1 - asymptomatic Stage 2 - progressive dyspnoea Stage 3 - systemic disease, co-morbidies Stage 4 - respiratory failure and death
38
The sputum in COPD is rich in what cell?
Neutrophil rich sputum
39
The sputum in asthma is rich in what type of cell?
Eosinophilic sputum
40
What T cells are involved in COPD?
TH1 and TC
41
What kind of fibrosis is present in COPD?
Peribronchiolar fibrosis
42
What kind of fibrosis is present in Asthma
Subepithelial fibrosis
43
What are the three mechanisms of airflow reduction in COPD?
Occulusion of airway by mucus Thickened airway fall Loss of elasticity
44
How does increased mucus arise in COPD?
Mucus is formed by mucous glands and goblet cells. In COPD there in enlargement of mucus gland and goblet cell hyperplasia/metaplasia Mucus production is controlled by neuronal input and inflammatory mediators
45
What are the consequences of inflammation in COPD?
Epithelial damage - decreased cililary cell function - increased mucus secretion from globlet cells - increased bronchial permeability stimulation of sensory nerves - neurogenic inflammation - cough
46
Outline the mechanism of cough in COPD
Increased inflammatory mediators leads to increased stimulation of the vagus nerve stimulating the brain stem
47
What is the proteinase-antiproteinase hypothesis?
Association of decreased serum alpha1 antitrypsin proteins with emphysema in some patients. This is an inherited deficiency.
48
Lung elastases are derived from what?
Neutrophils and macrophages
49
What inhibits the production of elastases from neutrophils and macrophages?
Alpha1 trypsin
50
Alpha1 trypsin is produced where?
Liver
51
Metalloproteinases are produced by what?
Monocytes and neutrophils
52
What are the key cytokines involved in COPD?
TNF and IL-8
53
What are TGFB and EGF?
Fibroblast growth inhibitors implicated in fibrosis and mucus secretion
54
Why are bronchodilators not used to treat COPD?
Bronchoconstriction is not the major cause of airway obstruction so would have a limited effect.
55
Ipratropium
Muscarinic antagonist
56
Tiotropium
Muscarinic antagonist M | M3 selective
57
What is the problem with non-specific muscarinic antagonists
block both the M2 and M3 receptor so there is removal of the negative feedback pathway This leads to more ACh release which may be able to overcome the M3 block and activate the receptor (leading to constriction)
58
Rofulimast
PDE IV selective inhibitor
59
What are common causes of bacteria infections in COPD patients?
Haemophilus influenza | Strep. pneumonia
60
N-acetylcysteine
Mucolytic. Breaks down disulphide bonds in mucin
61
Why don't glucocorticoids work well in COPD?
Occlusion of airway is not due to bronchoconstriction, instead it is due to tissues remodelling and secretion. Oxidative stress results in decreased steroid sensitivity and neutrophil apoptosis inhibited by GC.
62
Histone acetylation on DNA leads to what?
Increased binding of transcription factors such as NFKB, AP-1 as DNA is no longer constrained by the histone
63
what does histone acetyltransferase (HAT) do?
HAT acetylates histones, unpacks chromatin and allows RNA polymerase binding to DNA. Amplifies NFKB action
64
What does deacetylase (HDAC) do?
HDAC represses inflammatory gene expression
65
What is the affect of inflammatory stimuli on HAT and HDAC activity?
Increased HAT | decreased HDAC
66
What is the most common gene mutation in cystic fibrosis?
F508
67
Discuss CF screening
Immunoreactive trysinogen test (IRT) carried out in all newborns in the UK if IRT positive (or siblings) screened for common mutations.
68
What is the rationale behind the IRT test?
Trypsinogen is made by the pancreas and secretion into the gut is impaired in CF so levls will be elevated in the blood
69
Class I cystic fibrosis mutations are what?
G542X non-sense mutations
70
Class II cystic fibrosis mutations are what?
F508 deletion
71
How does Ataluran work?
Forces read through of a premature stop codon in Class II CF mutations
72
How does Amiloride work?
Blocks sodium resportion which repairs ASL. Risk of hyperkalaemia

Infection and immunity (13 decks)

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