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Infection and immunity > Malcom Watson Semester 2 > Flashcards

Malcom Watson Semester 2 Flashcards

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
Q

What are the actions of IL-13 and IL-4 in intrinsic asthma?

A 
Increased eosinophil adhesion and migration
Increased VCAM-1 expression 
Mucus secretion 
Tissue remodelling 
airway SM contraction
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26
Q

Montelukast

A

Leukotriene receptor antagonist specifically inhibits LTC4 and LTD4

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27
Q

Zileuton

A

Inhibits 5-lipoxygenase so inhibits leukotrien synthesis inhibitors

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28
Q

Sodium cromoglycate

A

Mast cell stabilisers - inhibit mediator release from lung mast cells

Also inhibit sensory nerve fibre excitation and neural reflex

Inhibit eosinophil chemotaxis

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29
Q

Olmalizumab

A

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
Q

What is COPD?

A

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
Q

Chronic bronchitis is characterised by….

A

Productive cough and excessive sputum production.

Overweight, and cyanotic, elevated haemoglobin, peripheral oedema and wheezing.

32
Q

Emphysema is characterised by….

A

Alveolar wall destruction, irreversible enlargement of the terminal air spaces

Older
Thin, severe dyspnea, quiet chest, x-ray shows hyperinflation with flattened diaphragms

33
Q

The following symptoms are associated with what….. Overweight and cyanotic (blue), elevated haemoglobin, peripheral oedema and wheezing

A

Chronic bronchitis

34
Q

The following symptoms are associated with what? Underweight, severe dyspnea, quiet chest

A

Emphysema

35
Q

What are risk factors for COPD?

A 
Smoking
Urban pollution - smog
industrial pollution 
textile dust
biomass fuels
36
Q

COPD risk factors all have what in common?

A

All contain ROS, toxins and particulate matter

37
Q

Outline the four stages of COPD

A

Stage 1 - asymptomatic
Stage 2 - progressive dyspnoea
Stage 3 - systemic disease, co-morbidies
Stage 4 - respiratory failure and death

38
Q

The sputum in COPD is rich in what cell?

A

Neutrophil rich sputum

39
Q

The sputum in asthma is rich in what type of cell?

A

Eosinophilic sputum

40
Q

What T cells are involved in COPD?

A

TH1 and TC

41
Q

What kind of fibrosis is present in COPD?

A

Peribronchiolar fibrosis

42
Q

What kind of fibrosis is present in Asthma

A

Subepithelial fibrosis

43
Q

What are the three mechanisms of airflow reduction in COPD?

A

Occulusion of airway by mucus
Thickened airway fall
Loss of elasticity

44
Q

How does increased mucus arise in COPD?

A

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
Q

What are the consequences of inflammation in COPD?

A

Epithelial damage

  • decreased cililary cell function
  • increased mucus secretion from globlet cells
  • increased bronchial permeability

stimulation of sensory nerves

  • neurogenic inflammation
  • cough
46
Q

Outline the mechanism of cough in COPD

A

Increased inflammatory mediators leads to increased stimulation of the vagus nerve stimulating the brain stem

47
Q

What is the proteinase-antiproteinase hypothesis?

A

Association of decreased serum alpha1 antitrypsin proteins with emphysema in some patients. This is an inherited deficiency.

48
Q

Lung elastases are derived from what?

A

Neutrophils and macrophages

49
Q

What inhibits the production of elastases from neutrophils and macrophages?

A

Alpha1 trypsin

50
Q

Alpha1 trypsin is produced where?

A

Liver

51
Q

Metalloproteinases are produced by what?

A

Monocytes and neutrophils

52
Q

What are the key cytokines involved in COPD?

A

TNF and IL-8

53
Q

What are TGFB and EGF?

A

Fibroblast growth inhibitors implicated in fibrosis and mucus secretion

54
Q

Why are bronchodilators not used to treat COPD?

A

Bronchoconstriction is not the major cause of airway obstruction so would have a limited effect.

55
Q

Ipratropium

A

Muscarinic antagonist

56
Q

Tiotropium

A

Muscarinic antagonist M

M3 selective

57
Q

What is the problem with non-specific muscarinic antagonists

A

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
Q

Rofulimast

A

PDE IV selective inhibitor

59
Q

What are common causes of bacteria infections in COPD patients?

A

Haemophilus influenza

Strep. pneumonia

60
Q

N-acetylcysteine

A

Mucolytic. Breaks down disulphide bonds in mucin

61
Q

Why don’t glucocorticoids work well in COPD?

A

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
Q

Histone acetylation on DNA leads to what?

A

Increased binding of transcription factors such as NFKB, AP-1 as DNA is no longer constrained by the histone

63
Q

what does histone acetyltransferase (HAT) do?

A

HAT acetylates histones, unpacks chromatin and allows RNA polymerase binding to DNA. Amplifies NFKB action

64
Q

What does deacetylase (HDAC) do?

A

HDAC represses inflammatory gene expression

65
Q

What is the affect of inflammatory stimuli on HAT and HDAC activity?

A

Increased HAT

decreased HDAC

66
Q

What is the most common gene mutation in cystic fibrosis?

A

F508

67
Q

Discuss CF screening

A

Immunoreactive trysinogen test (IRT) carried out in all newborns in the UK

if IRT positive (or siblings) screened for common mutations.

68
Q

What is the rationale behind the IRT test?

A

Trypsinogen is made by the pancreas and secretion into the gut is impaired in CF so levls will be elevated in the blood

69
Q

Class I cystic fibrosis mutations are what?

A

G542X non-sense mutations

70
Q

Class II cystic fibrosis mutations are what?

A

F508 deletion

71
Q

How does Ataluran work?

A

Forces read through of a premature stop codon in Class II CF mutations

72
Q

How does Amiloride work?

A

Blocks sodium resportion which repairs ASL.

Risk of hyperkalaemia

Infection and immunity (13 decks)

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