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1st Year - Respiratory (Sophia White) > Pharmacology 3 - COPD and Rhinitis > Flashcards

Pharmacology 3 - COPD and Rhinitis Flashcards

1
Q

Is airflow obstruction reversible in COPD?

A

Little or no reversibility (compared to reversible airway obstruction in asthma)

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2
Q

What is the pathogenesis of COPD?

A

Cigarette smoke and other noxious chemicals stimulate resident alveolar macrophages (possibly also influenced by CD8+ lymphocytes)This causes the release of neutrophilic chemotactic factor, IL-8, LTB4 and O2 radicalsThese cause the activation of neutrophils, and more macrophages and CD8 T cells These release proteases (matrix metalloproteinases) and free radicalsThis leads to chronic bronchitis and emphysema

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3
Q

What do matrix metalloprotineases cause in terms of bronchitis? (symptoms of chronic bronchitis)

A

They causes inflammation of bronchi and bronchioles, cough, clear mucoid sputum, infections with purulent sputum

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4
Q

What do matrix metalloprotineases cause in terms of emphysema? (symptoms of emphysema)

A

Distension and damage to alveolarDestruction of acinial pouching in alveolar sacs

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5
Q

What 3 different types of muscarinic acetylcholine receptors do human airways contain?

A

M1, m2, m3

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6
Q

What nerve is the preganglionic neurone that supplies the bronchial smooth muscle?

A

Vagus nerve (No sympathetic innervation_

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7
Q

What receptors are located in the ganglia of the parasympathetic branch which is supplying the airways? (2)

A

nAChR (nicotinic receptors)M1 receptors (mediate a slow excitatory post synaptic potential that increases action potential frequency resulting from nicotinic receptor stimulation)

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8
Q

Where is M2 located and what does it do (in terms of parasympathetic supply to airways)?

A

Located on the postganglionic neurone terminals (acts as inhibitory auto receptors reaching release of ACh)

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9
Q

Where is M3 located and what does it do (in terms of parasympathetic supply to smooth muscle)?

A

Present on smooth muscle and mucus-secreting cellsmediates contraction and increased secretion

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10
Q

Apart from the drugs in the guidelines, what do drug do doctors sometimes prescribe patients who have difficult to control asthma?

A

Muscarinic antagonists

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11
Q

What happens when ACh activates M3 muscarinic receptors on airway smooth muscle cells?

A

Through Gq, PLC (phosopholipase C) is activated which converts PIP2 to IP3 IP3 binds to the IP3 receptor on the sacroplasmic reticulum (basically a ligand gated ion channel)This causes calcium to diffuse into the cytoplasm leading to contraction

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12
Q

How do muscarcinic acetylcholine receptor antagonists work?

A

They are block the M3 muscarinic receptor, meaning ACh cannot bind leading to contraction of the smooth muscle (bronchoconstriction)

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13
Q

Are muscarcinic acetylcholine receptor antagonists currently used competitive or non-competitive?

A

Competitive

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14
Q

What are the 2 categories of competitive muscarinic receptor antagonists current licensed?

A

Short acting muscarinic antagonists (SAMAs)Long active muscarinic antagonists (LAMAs)

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15
Q

What are the 2 SAMAs currently licensed?

A

IpratropiumOxitropium

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16
Q

What are the 2 LAMAs currently licensed?

A

TiotropiumAclidinium

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17
Q

How are all the muscarcinic receptor antagonists given?

A

Inhalation

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18
Q

What feature of muscarinic receptor antagonists reduces absorption and system exposure avoiding multiple potential adverse effects?

A

Quaternary ammonium group

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19
Q

How long is the onset of action of muscarinic ACh receptor antagonists roughly?

A

Delayed (grater than 30 mins)

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20
Q

What effect do using macaroni ACh receptor antagonists have? (3)

A

Relax bronchospasm caused by irritant stimuli (irritants initiate a vagal reflex that liberates ACh) Also block Ach-mediated basal toneDecrease mucus secretion

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21
Q

Do muscarinic ACh receptor antagonists have any effect on the development of COPD?

A

Only have a little effect - their effect is mainly palliative

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22
Q

Why do muscarinic ACh recepto antagonists have few adverse effects?

A

Due to the possession of a quaternary ammonium grou

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23
Q

What is the main disadvantage of ipratropium?

A

It is a non-selective blocker of M1, M2 and M3 receptors

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24
Q

Why is Tiotropium functionally selective for M2 muscarinic receptors?

A

It has a greatly longer half life at the M3 muscarinic receptor - Aclidinium works in the sam way

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25
Q

Why is block of M2 by muscarinic antagonists not desirable?

A

Release of ACh from parasympathetic post-ganglionic neurones is increased (M2 acts as a pre junctional inhibitory auto receptor - activaiton by ACh inhibits further ACh release)

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26
Q

Are b2-adrenoceptor agonists used to treat COPD?

A

Yes - they provide some bronchodilation although have no effect on underlying inflammation (both LABAs and SABAs)

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27
Q

What is indaceterol?

A

A recently licensed “ultra-LABA” that has rapid onset of action (unlike salmeterol)

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28
Q

What is superior to using either a LABA or a LAMA along?

A

A combination of a LABA and a LAMA (e.g. salmeterol/ tiotropium) - superior to either drug separately in increasing FEV1 - recommended for moderate COPD

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29
Q

What are MABAs?Advantage of these?

A

Muscarinic antagonist B2-agonistsLABA/ LAMA combinations are likely to be most effective when both drugs are deposited in the same location in the airways - MABAs are a novel approach that are attempting to develop ligands that possess both LABA and LAMA activity within the same molecule

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30
Q

What is the prominent phosphodiesterase found in neutrophils, T cells and macrophages?What does this do?

A

PDE4cAMP degenerating enzyme that therefore reduces the amount if PKA activation and therefore bronchodilation(therefore by inhibiting it, we can inhibit inflammatory and immune cells

31
Q

What is the name of a selective PDE4 inhibitor?What does this do?What is it approved for treatment of?Adverse effects?

A

RofumilastSuppresses inflammation and emphysema in animal models of COPDApproved as an oral treatment for severe COPD accompanied by chronic bronchitisHas limiting adverse effects on GI system

32
Q

What are B2-adrenoceptor agonists co-administered with?

A

Glucocorticoids in combination inhalers - benefit of the routine inclusion of a glucocorticoid in most COPD patients has been debated, since even high dose glucocorticoids alone do not suppress inflammation

33
Q

What is glucocorticoid unresponsiveness in COPD patients thought to be due to possibly?

A

Oxidative/ nitrative stress (associated with chronic inhalation of tobacco smoke)

34
Q

What is in the “triple inhaler”?

A

Formoterol (LABA)Tiotropium (LAMA)Ciclesonide (glucocorticoid)

35
Q

What types of medications are used to treat COPD?

A

Muscarinic ACh receptor antagonists (SABAs and LABAs)B2-adrenoceptor agonists (LAMA works better when given along with a LABA - B2-agonists are routinely given along with glucocorticoids but with a questionable benefit)Glucocorticoids are beneficial in patients with frequent and severe exacerbationsPDE4 inhibitor (Rofumilast) is used in patients with severe COPD*triple inhaler is available with LABA, LAMA and glucocorticoid

36
Q

What is rhinitis?

A

A common and often debilitating disease involving acute, or chronic, inflammation of the nasal mucosa which is characterised by rhinorrhoea, sneezing, itching, nasal congestion and obstruction

37
Q

What is the scientific name for runny nose?

A

Rhinorrhoea

38
Q

What is swelling of nasal mucosa largely due to?

A

Dilated blood vessels - particularly in cavernous sinusoids

39
Q

What are the 3 different types of rhinitis?

A

AllergicNon-allergicMixed

40
Q

What are the 3 different types of allergic rhinitis?

A

SeasonalPerennial (present all year)Episodic

41
Q

In allergic rhinitis, what does inhalation of the allergen cause?

A

Increases specific IgE levelsThis causes IgE to bind to receptors on mast cells and basophilsRe-exposure to allergen causes mast cell and basophil degranulationThis causes the release of mediators inclusion histamine, cysts, tryptasae, prostaglandins, causing acute itching, sneezing, rhonorrhoea and nasal congestionDelayed response caused by recruitment of lymphocytes and eosinophils to nasal mucosa contributes to congestion and obstruction(very similar to asthma)

42
Q

What is non-allergic rhinitis?

A

Any rhinitis, acute or chronic, that does not involve IgE dependent events

43
Q

What are some examples of causes of non-allergic asthma? (5)

A

Infectious rhinitis (largely viral)Hormonal rhinitisVasomotor rhinitis (cause unknown)Non-allergic rhinitis with eosinophilia syndrome (NARES)Drug induced rhinitis

44
Q

Is occupational rhinitis allergic or non-allergic?

A

May involve both allergic and non-allergic componenets

45
Q

What types of targets are used in the drug treatment of rhinitis and rhinorrhoea?

A

Anti-inflammatoryMediator receptor blockadeNasal blood flowAnti-allergic

46
Q

What anti-inflammatory drugs are used for rhinitis?

A

Glucocorticoids

47
Q

What mediator receptor blockade drugs are used for rhinitis? (2)

A

H1 receptor antagonistsCysLT1 receptor antaonists

48
Q

What rhinitis medications affecting nasal blood flow is used for rhinitis?

A

Vasoconstrictors

49
Q

What anti-allergic drugs are used for rhinitis?

A

Sodium cromoglicate

50
Q

What is the mainstay therapy for seasonal allergic rhinitis and perennial allergic rhinitis and of value in NARES and vasomotor rhinitis?

A

Glucocorticoids

51
Q

How are glucocorticoids for rhinitis applied?

A

Topically as a spray to the nasal mucosa (usually once daily)Given orally (short term) in very severe intractable cases

52
Q

What can glucocorticoids be combined with in moderate-to-severe rhinitis?

A

Anti-histamines

53
Q

Specific examples of glucocorticoids for rhinitis?

A

BeclometasoneFluticasonePrednisolone (oral)

54
Q

What is the more common name of H1 receptor antagonists?

A

Anti-histamines

55
Q

How do anti-histamines (H1 receptor antagonists) work?

A

Competitive antagonists of H1 receptors reduce effects of mass cell derived histamine that include vasodilation and increased capillary permeability, activation of sensory nerves, mucus secretion from submucosal glands

56
Q

What types of rhinitis are anti-histamines effective in?

A

Allergic rhinitis (less so for non-allergic rhinitis)

57
Q

How are anti-histamines administered?

A

Orally or as an intranasal spray (azelastine)

58
Q

Why are second generation anti-histamines preferred over first generation anti-histamines?

A

Reduced sedation as they do not cross the blood brain barrier and lack of anti-cholinergic effects

59
Q

Examples of anti-histamines for allergic rhinitis?

A

LoratidineFecofenadineCetrizine (also has mild anti-inflammatory action)

60
Q

What causes the watery secretions that contribute to rhinorrhoea?

A

ACh released from post-ganglionic parasympathetic fibres which activates muscarinic receptors on nasal glands - blocked by muscarinic antagonists

61
Q

What symptom are anti-cholinergic drugs (muscarinic receptor antagonists) effective in treating?

A

Reducing rhinnorhoea in PAR and SAR - have no influence upon itching, sneezing and congestion

62
Q

How are muscarinic receptor antagonists for rhinnorhoea always administered?

A

Via the nasal route

63
Q

What is the adverse effect of muscarinic receptor antagonists?

A

Dryness of nasal membranes

64
Q

What is the only muscarinic receptor antagonist used for rhinitis?

A

Ipratropium

65
Q

what is sodium cromoglicate thought to do?

A

Stabilise mast cells

66
Q

What is sodium cromoglicate used for in terms of rhinitis?Onset of action?

A

Maintenance treatment of allergic rhinitis4 to 7 days

67
Q

How is sodium cromoglicate for allergic rhinitis administered?

A

Nasal administraiton - less effective than nasal corticosteroids

68
Q

What are cysteinyl leukotriene receptor antagonists used to treat in terms of rhinitis?

A

PAR and SAR (are equi-effecitve with H1 receptor antagonists in treating these, with which their effect may be additive)*should be considered in patients with asthma also

69
Q

How are Cysteinyl leukotriene receptor antagonists administered?

A

Orally

70
Q

What is the only cysteinyl leukotriene receptor antagonist used to treat Rhinitis?

A

Montelukast

71
Q

How do vasoconstrictors produce vasoconstriction (rhinitis)?

A

Act as direct, or indirect, sympathomimetics to mimic the effect of noradrenaline (produce vasoconstriction via activation of alpha 1 adrenoceptors to decrease swelling in vascular mucosa)

72
Q

What is a selective alpha1-adrenoceptor agonist which is effective, short term, in reducing congestion in allergic rhinitis?How is this given?

A

OxymetazolineNasally

73
Q

Why is nasal administration of oxymetazxoline for more than a few days not recommended for the treatment of allergic rhinitis?

A

Due to the development of a revue increase in nasal congestion upon discontinuation (rhinitis medicamentosa) - occurs due to receptor desensitisation and down regulation

1st Year - Respiratory (Sophia White) (31 decks)

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