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Mpharm Y2S1 > Respiratory system > Flashcards

Respiratory system Flashcards

Exam 1

1
Q

What is the pathology of asthma?

A

A narrow lumen in people with asthma which means air restriction flow
An increase in goblet cells (hyperplasia) so more mucus is secreted
Smooth muscle is thicker and increase in blood vessels which have oedema and become leaky
An increase in collagen makes it thicker

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2
Q

What is the early phase of asthma?

A

– Hypersensitivity
– Spasm of airways smooth muscle
– Hyper secretion of mucus
– Bronchoconstriction

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3
Q

What is the late phase of asthma?

A

– Cellular infiltration – injury of airway epithelium – hypersensitivity – loss of ciliary function –bronchoconstriction

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4
Q

What are the symptoms of asthma?

A

– Wheezing (especially on expiration)
– Breathlessness (not enough O2)
– Coughing
– Chest tightness

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5
Q

What is bronchitis?

A

Inflammation of bronchioles

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6
Q

What is emphysema?

A

The membranes in the alveoli which hold them are broken down which leads to large holes in air spaces
Not efficient gas exchange

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7
Q

What are symptoms of chronic bronchitis?

A

– Excess mucus production – bronchospasm – wheezing dyspnea – hypoxia and hypercapnia – productive cough – overweight

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8
Q

What are the symptoms of emphysema?

A

– Increase dyspnoea even at rest – Minimal cough – hyperventilation – thin pursed lips to compensate for lack of elastic recoil

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9
Q

What does hyperplasia mean?

A

An enlargement due to the increase in production of cells

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10
Q

What does hyper trophy mean?

A

An enlargement due to the cell size increase

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11
Q

Why is there an increase in luminal mucus with asthma and COPD?

A

Goblet cells hyperplasia and metaplasia
Submucosal gland hyper trophy

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12
Q

What is the name given when cilia can’t clear mucus?

A

Abnormal mucociliary clearance

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13
Q

Is it common to have COPD if under 35?

A

No it is rare

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14
Q

Is a chronic productive cough present in asthma symptoms?

A

No more of a dry cough

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15
Q

Where are the guidelines for asthma treatment and diagnosis?

A

BTS/ SIGN 2019

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16
Q

Where are the guidelines for COPD treatment and diagnosis?

A

NICE NG115

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17
Q

What does atopic history mean?

A

Strong links with other allergies for example eczema

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18
Q

What can be some triggers of asthma?

A

Allergen exposure, infection, cold air, exercise, some medication (NSAID’s)

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19
Q

What is included in a high diagnosis probability of asthma?

A

Typical symptoms, wheeze, no suggestion of alternative
Record likely asthma, start treatment for six weeks with inhaled corticosteroid reassess symptoms

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20
Q

What is included in a medium diagnosis probability of asthma?

A

Some but not all typical features or do not respond to initial treatment
Carry out reversibility test with Bronco dilator repeat after ICS

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21
Q

What is peak expiratory flow and give the benefits?

A

Measurement of volume of air expelled from lungs
Cheap and easy to use
Can keep a diary
Useful diagnosis and monitoring

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22
Q

Give red flags in asthma diagnosis:

A

– Unexpected clinical features (crackles)
– Persistent breathlessness
– X-ray shows shadows
– Chronic sputum production

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23
Q

If over 35, what other symptoms are likely to be COPD?

A
  • Excertional breathlessness
  • Chronic cough
  • Regular sputum production
  • Freq winter bronchitis
  • Wheeze
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24
Q

What are two red flag symptoms of COPD?

A

Chest pain and haemoptysis- coughing up blood

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25
Q

What is a dyspnoea scale?

A

Scale from grade 1 to 5, one being the least and five being the most

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26
Q

What is spirometry?

A

Monitors lung function and diagnosis respiratory conditions
Measured expelled from lungs by mouth, not nose (sealed)

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27
Q

What is a normal forced expiratory volume compared to one of asthma?

A

Normal 4 litres
Asthma 2 litres

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28
Q

Before changing asthma treatment, what are three things to check?

A
  • Adherence
  • Inhaler techniques
  • Eliminate triggers
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29
Q

What is an SABA?

A

Short acting B2 agonist (salbutamol)
Releiver

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30
Q

What is an LABA?

A

Long acting B2 agonist (salmeterol)

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31
Q

What is an ICS?

A

Inhaled corticosteroids (beclomethasone) Preventer

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32
Q

What is an LTRA?

A

Leukotriene receptor antagonists (Montelukast)

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33
Q

What is MART?

A

Maintenance and reliever therapy (LABA+ ICS)

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34
Q

What is a SAMA?

A

Short acting muscarinic antagonists (Ipratropium)

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35
Q

What is a LAMA?

A

Long acting muscarinic antagonists (Tiotropium)

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36
Q

What is the basic first treatment of asthma?

A

ICS

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37
Q

What do you add to the first treatment of asthma if it doesn’t work?

A

Inhaled LABA

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38
Q

What are three nonpharmaceutical treatments for COPD?

A

– Treatment and support to stop smoking
– Pneumonnical and influenza vaccines
– Pulmonary rehabilitation (physiotherapist)

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39
Q

What pharmaceutical treatment should be used for COPD if the patient also has asthma symptoms?

A

LABA+ ICS

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40
Q

What pharmaceutical treatment should be used for COPD if the patient doesn’t have asthma symptoms?

A

LABA+ LAMA

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41
Q

What if there is no improvement on the second stage of treatment for COPD?

A

Use LABA, LAMA and ICS

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42
Q

Name the five inhaled corticosteroids:

A

Beclometasone
Budsonide
Fluticasone
Ciclesonide
Mometasone
Last two only licensed for asthma as they’re single ingredient inhalers

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43
Q

What are the other formulations of corticosteroids and their use?

A

Nasal spray- allergic rhinitis
Topical creams/ ointments- eczema

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44
Q

What are the two brands beclometasone is available in?

A

Qvar
Clenil

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45
Q

Are the two brands of beclometasone interchangeable and why?

A

No, must be prescribed by brand and not generic name
Qvar has extra fine particles and approx twice the potency of Clenil

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46
Q

Why are oral corticosteroids used for in asthma and COPD?

A

Usually a short term rescue therapy to bring symptoms under control e.g.
-asthma exacerbation
-COPD when patient gets URTI, usually with antibiotics

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47
Q

What are local adverse affects of corticosteroids?

A

Hoarseness
Throat irritation
Dysphonia- changes in voice
Candida- T cells important against fungal infections

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48
Q

What are practical considerations in corticosteroids?

A

Can be given in multiple routes but lead to more systemic SE
Effect can be slow so needs to make sure to take regularly
Don’t stop them abruptly
Children can take it, can leads to slow growth
COPD, only in combo with LABA or LAMA

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49
Q

Give the counselling points for corticosteroids:

A

Regular use as preventative
Morning and evening dose, usually fits in with routine
Oral dose first thing in morning with breakfast as decreases GI disturbances and better with natural steroid production

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50
Q

Which corticosteroid are less likely to contribute to adrenal suppression and why?

A

Fluticasone, Mometasone and Ciclesonide
Poorly absorbed from the GI tract and undergo almost complete pre-systemic metabolism

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51
Q

Which steroids are used at which point in the treatment of airway diseases?

A

Regular bronchodilator: low dose inhaled beclometasone
More severe: high dose inhaled fluticasone
Acute exacerbations: IV hydrocortisone and oral prednisolone

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52
Q

What are bronchi and trachea usually lined with and made up of?

A

Ciliated columnar epithelium
Have cartilage to prevent collapse, then goes to half rings and then to smooth muscle

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53
Q

What is the zone in the bronchi regions and then after this?

A

In the bronchi regions- air conducting
After bronchi regions- gas exchange zone

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54
Q

What are the types of cells lining the bronchial region and what do these do?

A

Ciliated cuboidal cells
Secrete no mucous and serous glands

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55
Q

What are alveoli lined with and what do they not contain?

A

Lined with phospholipids
Don’t have smooth muscle/ cartilage

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56
Q

Which type of enzymes are found in the bronchi and alveoli region?

A

Drug metabolising enzymes:
- Cyp450
- Esterase
- Protease
- Peptidases

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57
Q

What type of drug can be deposited in the lung and how much is?

A

5% and polar macromolecule drugs
Less than 5micrometers

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58
Q

How much drug is swallowed rather than effectively used and why?

A

95%, trapped in cilia and wafted back up, mucociliary clearance
Abosrption from gut and liver metabolism

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59
Q

What size particles are rapidly and slowly absorbed?

A

Macromolecular, less or equal to 40kDa rapidly absorbed
Molecules higher or equal to 40kDa absorbed more slowly

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60
Q

What type of drug does the lung prefer?

A

Lipophilic over hydrophilic

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61
Q

Where are the receptors of histamine blockers?

A

Vascular endothelial cells, smooth muscle of bronchi

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62
Q

Where are the receptors of beta agonists found?

A

B2 receptors in trachea, bronchial smooth muscle, serous glands

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63
Q

Where are the receptors for anticholinergics found?

A

Tracheal, bronchial smooth muscle, serous glands

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64
Q

Where are the receptors for corticosteroids found?

A

Epithelial cells, fibroblasts, basophils, macrophages and lymphocytes
Conncective tissues at all levels of respiratory tree

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65
Q

How long should you wait between doses of inhalers?

A

30 seconds

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66
Q

Which system do muscarinic receptors work on?

A

Parasympathetic, apart form sympathetic for sweat glands

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67
Q

What happens in a parasympathetic reaction?

A

Decrease HR, dilation of BV, constriction of bronchi, increased GIT motility, bladder contraction, pupil contraction, gland secretion

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68
Q

What are muscarinic receptors?

A

GPCRs
Activated by acetylcholine
Classic 7 transmembrane domain
Muscarine, an alkaloid from the fungus an an agonist for these receptors

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69
Q

Name the types of muscarinic receptors and where are they found:

A

M1- neural, CNS
M2- cardiac, heart
M3- glandular, increasing secretion / smooth muscle
M4 and M5, mainly CNS, not well defined

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70
Q

Which muscarinic receptors signal via calcium?

A

M1, M3, M5- the odd numbers, Gq G protein

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71
Q

Which muscarinic receptors signal via decreasing cAMP?

A

M2, M4- even numbers, Gi G protein

72
Q

What are the terms given to drugs that have agonistic or antagonistic effects on muscarinic receptors?

A

Agonists- parasympathomimetics
Antagonists- parasympatholytics

73
Q

Name and describe three muscarinic agonists and their selectivity and degradation by AchE:

A
  • Acetylcholine, specific for both nicotinic and muscarininc, hydrolysed
  • Carbachol, specific for both, hydrolysed
  • Methacholine, more selective for muscarininc, hydrolysed
74
Q

Name two muscarinic agonists that have no degradation from AchE and their clinical use:

A

Bethanechol- specific for musc, for bladder
Pilocarpine- specific for musc, for glaucoma

75
Q

What are the main effects of muscarinic agonists?

A

Parasympathetic effects: rest and digest
Decrease cardiac output
Vasodilation
Decreased BP/ HR
Secretion in glands
Pupil constriction
Central effects, tremor

76
Q

What are the clinical uses of muscarinic agonists?

A

Not used a lot due to many SE
Main use for glaucoma, rarely, pilocarpine
Urinary retention, rarely, bethanechol

77
Q

Give six examples of muscarinic antagonists:

A

Atropine- no selective, crosses the BBB
Tiotropium
Hyoscine
Tropicamide
Pirenzepine- M1
Darifenacin- M3

78
Q

What are the effects of muscarinic antagonists?

A

Sympathetic effects: fight or flight
Tachycardia, increases HR
BP unchanged
GIT motility inhibited
Urinary retention
Dilation of pupil

79
Q

What are the clinical uses of antimuscarinics and some examples:

A

Asthma and COPD:
tiotropium, ipratropium
Antispasmatics:
hyoscine, dicycloverine
Motion sickness
hyoscine hydrobromide
Urinary incontinence:
darifenacin
Ophthalmology:
mydriasis

80
Q

What are the side effects of muscarinic antagonists?

A

Relate to sympathetic action:
Dry mouth, dry skin, reduced bronchial secretions, tachycardia, constipation, urinary retention, blurred vision, drowsiness

81
Q

Name and describe the short acting muscarinic antagonist (SAMA) for COPD:

A

Ipatropium
Lisenced for airway obstruction, bronchospasm and acute life threatening asthma
Max effect within 30 mins, effects last 3-6 hours
3-4 times daily

82
Q

Name four long acting muscarninc antagonists:

A

-Tiotropium, Handihaler for COPD only, Respimat for asthma also
- Glycopyrronium- Seebri breezhaler
- Umeclidinium- Ellipta
Aclidinium- Elikra Genuair

83
Q

What are cautions for prescribing antimuscarinics:

A

Prostatic hyperplasia
Glaucoma
Bladder outflow obstruction

84
Q

What are practical considerations when prescribing a LAMA?

A

Discontinue SAMA if going to use LAMA
Duration of action is usually long so OD use is fine

85
Q

What are counselling points for SAMA/ LAMA’s?

A

SAMA as reliever
LAMA take regularly
Nebulised ipatropium, risk with glaucoma so cover eyes or use a mouth piece nebuliser rather than a face mask

86
Q

What are the main principles of Leukotriene Receptor Antagonists (LTRAs)?

A

Block effects of cysteinyl leukotrienes in airways
Effective against allergic and non allergic asthma
Relaxes airways
Additive effects with corticosteroids

87
Q

How do LTRAs work?

A

Receptors for leukotrienes are found on airway smooth muscle and immune cells
They block CysLt1 receptor (LTC4, LTD4, LTE3) which can decrease both early and late responses to allergens in asthma
They relax airways and reduce eosinophils
Bronchodilator and anti-inflammatory effects

88
Q

How are LTRAs used?

A

Not for COPD
Popular in children, 6 months upwards
Additive effect with corticosteroids
Are in the additional controller therapy after LABA and low dose ICS

89
Q

Give an example of an LTRA and it’s info:

A

Montelukast, OD evenings
Oral (tabs, chewable, granules)
Used at earlier stage for children to reduce steroid burden
SE: GI disturbances

90
Q

What are two major considerations when using LTRAs?

A

Neuropsychiatric reactions:
- depression, speech impairment,
stuttering
Churg- strauss syndrome:
Inflammation of BV, associated with patients who have been on oral steroids

91
Q

Name the two xanthines used for the treatment in asthma/ COPD:

A

Theophylline
Aminophylline

92
Q

Describe the MOA for xanthines:

A

Not fully understood
Inhibits phosphodiesterase
Antagonise adenosine induced bronchospasm
Direct effects on intracellular calcium levels
Effect on late phase inflammatory response
Activates histone deacetylase (HDAC), which controls gene expression and may thereby reverse resistance to the anti-inflammatory effects of corticosteroids

93
Q

What are the directions for taking xanthines:

A

BD dose using M/R preps
Prescribed as brand as not interchangeable
Additive effect when used with B2 agonist but can increase SE

94
Q

How does theophylline work?

A

Decrease:
- eosinophil
- T cells
- Mast cells
- Cytokines
- Macrophages
Causes bronchodilator, less leaky endothelial cell, increase the strength of respiratory muscles

95
Q

What are the side effects of xanthines?

A

CNS stimulation
CV effects
-palpitations -tachycardia -vasodilation
GI effects
-nausea/ vomiting -GI irritation -Diarrhoea
Hyperkalemia

96
Q

What could side effects of GI disturbances when using xanthines indicate?

A

The patient is taking too high dose

97
Q

How do xanthines interact with macrolides?

A

Xanthines have a very small therapeutic window
The antibiotic inhibits the P450 enzyme which breaks down the xanthine
So an increase in P450 means an increase in xanthine and due to small therapeutic window it becomes toxic

98
Q

What can the conc of xanthines be increase by?

A

Heart failure
Hepatic impairment
Viral infections
Elderly

99
Q

What can the conc of xanthines be decreases by?

A

Smoking
Heavy alcohol consumption

100
Q

What are the therapeutic levels of xanthines?

A

10-12 mg/L optimal range
10-20 mg/L therapeutic range

101
Q

What are the measures put in place to ensure the correct dose of xanthines are being used?

A

Blood conc measured after 5 days of oral treatment
Sample 4-6 hours after IV aminophylline

102
Q

When are xanthines used in treatment for asthma and COPD?

A

Asthma- reserved for those with severe conditions- specialist
COPD- when can’t use inhaler therapies
Aminophylline used as IV in both when severe exacerbations

103
Q

When are mast cell stablisers used in asthma and COPD?

A

Asthma- specialist as prophylaxis, rarely used
COPD- not used

104
Q

Give two examples of mast cell stabilisers:

A

Nedocromil sodium
Sodium cromoglycate

105
Q

What can some patients experience with mast cell stabilisers and how is this fixed?

A

Cause paradoxical bronchospasm
Withdraw treatment slowly with SABA

106
Q

What three things can be used to manage asthma triggers:

A

Antihistamines
Avoidance
Nasal corticosteroids

107
Q

Name 2 biological drugs for asthma and how they work:

A

Interfering with the IL-5 receptors by decreasing eosinophils
Used for severe eosinophilic asthma via specialist prescribing by injection
-benzralizumab
-omalizumab
others ending in mab

108
Q

Name and describe a mucolytic agent for COPD:

A

Carbocisteine
Pts with chronic productive cough to reduce sputum viscosity
Only in patients with stable COPD and more bronchitis symptoms
Stop if no benefit after 4 week trial

109
Q

Name and describe a specialist COPD drug:

A

Human alpha-1 proteinase inhibitor
Inhibits neutrophil elastase in lungs
Used in emphysema patients with severe a-1 protease inhibitor deficiency
Limited use on NHS

110
Q

How is oxygen used for COPD:

A

Prescribed to hypoxaemic patients to increase alveolar oxygen tension and decrease work of breathing
Inappropriate use is harmful as CO2 levels drop decreasing respiration
Low conc for COPD, high conc for pneumonia
Fire risk

111
Q

What is oxygen therapy?

A

Prolongs survival in some patients with COPD
Use for a min of 15 hours per day
Ambulatory oxygen

112
Q

How to treat acute asthma?

A
  • Use O2 to maintain SpO2 level at 94-98%
  • High dose B2 agonist - nebulised, often with ipatropium aswell
  • Steroids, IV and continue for min of 5 days
113
Q

How to treat acute COPD?

A
  • Increase dose of short acting bronchodilators, often nebulised
  • Rescue pack
  • Theophylline if poor response to bronchodilator
  • Oxygen
  • In severe cases pt may require ventilation
    -Physiotherapy
114
Q

What are the gender trends in asthma?

A

More in boys but as age more in females

115
Q

What are three key cells in asthma?

A

Mast cells, CD4+ T cells, Eosinophil

116
Q

What are three key cell mediators in asthma?

A

Histamine, leukotriene, inflammatory cytokines (IL-4, IL-5)

117
Q

What are four key cells in COPD?

A

Macrophages, CD8+ T cells, Th1 cells, Neutrophils

118
Q

What is asthma COPD overlap syndrome?

A

Some symptoms of asthma can be present in COPD, they overlap
e.g. in asthma, some have neutrophil ridden diseases rather than eosinophils

119
Q

Describe the early phase of asthma in terms of cells and mediators involved:

A

Initial mast cell activation with IgE on surface responding to an allergen
Leads to mast cell degranulation; release of histamine, leukotrienes, prostaglandins
Leads to production of mucus, vasodilation, bronchoconstriction effect

120
Q

Describe the late phase of asthma in terms of cells and mediators involved:

A

Recruitment of inflammatory response, stickiness of endothelial cells, slowing immune cells down (bad)
Migration of leucocytes, eosinophils, causing injury to epithelial layer exposing nerves so become more hypersensitive next time

121
Q

What is the absolute first thing that needs to happen in order for a hypersensitivity reaction to occur?

A

The dendritic cells in epithelial layer are extending the dendrites and sampling antigens
Present to T cells which create antibodies
Second time, then the early and late phase happen

122
Q

Which drugs are used for the early phase of asthma?

A

Beta agonists – to dilate and open airways (SABA’s and LABA’s)
Leukotr

123
Q

Which drugs are used for the early phase of asthma?

A

Beta agonists – to dilate and open airways (SABA’s and LABA’s)
Leukotriene antagonists

124
Q

Which drugs are used in the late phase of asthma?

A

Steroids to block inflammatory effects, need long-acting medication as there is bronchoconstriction there too

125
Q

How are macrophages involved in COPD?

A

An increase in macrophages leads to an increase in bronchoalveolar lavage fluid (BAL)
Number in alveolar wall correlates with destruction, and in airways with obstruction

126
Q

How are neutrophils involved in COPD?

A

Increase levels in lung induced by cigarette smoke, stuck in lung capillaries
Found in BAL and sputum
Genetic cause, alpha- antitrypsin deficiency (lack inhibitor of neutrophil elastase, which breaks down alveolar attachments)

127
Q

How are airway epithelial cells involved in COPD?

A

First barrier defence, secrete cytokines and chemokines which recruit inflammatory response

128
Q

How are CD8+ cells involved in COPD?

A

Most abundant T-cell in COPD
Increase in epithelium which correlates with reduced lung function

129
Q

What are three imbalances in COPD?

A

Pro/anti-inflammatory
Pro/anti-proteases
Pro/antioxidants

130
Q

How are inflammatory responses involved in COPD?

A

Leukotrienes – neutrophil and T-cell chemoattractant
IL – 8 and monocyte chemotactic protein one (MCP1) attract cells from circulation
Pro inflammatory cytokines TH1
Increase in growth factors (TGF which leads to fibrosis)
Increase in IL-6 and TNF systemically

131
Q

How are proteases involved in COPD?

A

Protease= neutrophil elastase, with this neutrophils aren’t digested
Anti- protease= alpha antitrypsin, good to lack inhibitor of neutrophil
These proteases are degrading the extra cellular matrix and remodelling lung, not being inhibited by anti-proteases as they’re being reduced

132
Q

How are oxidants involved in COPD?

A

Reactive oxygen and nitrogen species from cigarette smoke cause damage to epithelial cells causing inflammatory response
Oxidative and nitrative stress activate macrophages
Smokers and COPD patients have increased H2O2 in inhaled breath
Oxidants inhibit protease inhibitors

133
Q

How is H2O2 involved in COPD?

A

H2O2 conc in exhaled air is a marker for oxidative stress and used to monitor COPD exacerbations
H2O2 increases with disease and decreases with treatment

134
Q

Name two Short Acting Beta Agonists (SABA’s):

A

Salbutamol (Ventolin)
Terbutaline

135
Q

How do SABAs work?

A

Have a direct action on B2 agonists active site on airways, causes bronchodilation

136
Q

What is the timescale on when SABAs work?

A

Max effect within 30 minutes
Bronchodilatory effects 4-6 hours

137
Q

When should a SABA be used and what are the counselling points?

A

As a rescue/reliever therapy (blue inhaler)
Carry with you at all times
Use ahead of exercise
Max eight doses a day, but in an acute situation can take as needed
If using more than three times a week, patient should be reviewed

138
Q

Name 3 LABA’s for asthma:

A

Salmeterol, formoterol, bambuterol

139
Q

Name 3 LABAs for COPD only:

A

Indacaterol
Olodaterol
Vilanterol

140
Q

How do LABAs work?

A

Find within the active site but also on the exosite
Binds in and out of active site

141
Q

What is the timescale on when LABAs work?

A

Work over 12-24 hours, so taken once or twice a day
Cant be used for patients experiencing acute symptoms as not an immediate bronchodilator

142
Q

Which LABA is used as MART and how does this work?

A

Maintenance And Reliever Therapy
Formoterol
Dual action as has both long and short acting components

143
Q

How is Bambuterol administered?

A

Only available as an oral tablet
Is a prodrug of terbutaline

144
Q

What are adverse effects of SABAs and LABAs?

A

Due to systemic adsorption:
Tremor, nervous tension, headache, tachycardia/ palpitations, hypokalaemia

145
Q

Why do some people experience a tremor due to SABAs and LABAs?

A

Direct stimulation of B2 agonists in skeletal muscle

146
Q

Why do some people experience tachycardia due to SABAs and LABAs?

A

Agonistic effects of B1 receptors in the heart

147
Q

Why do some people experience hyperkalemia due to SABAs and LABAs?

A

Increase K+ uptake
Be wary of people taking these: Xanthines, diuretics, steroids

148
Q

When should a LABA be used and what are the counselling points?

A

For preventer therapy (brown inhaler)
Take regularly, usually BD but for COPD sometimes OD

149
Q

What is MART therapy?

A

Famoterol + steroid combination
Has both long and short acting components
Usually taken BD as a preventer but also be used for rescue
When used as a rescue therapy, can increase steroid exposure, which can control exacerbations

150
Q

What is the advice for taking SABAs and LABAs during pregnancy?

A

The benefits outweigh the risks
SABA can also be used to delay premature labour as it causes relaxation of smooth muscle in the uterus

151
Q

Describe the B2 adrenergic receptor signalling pathway:

A

GPCR:
B2 receptor couples with Gas subunit
It dissociates to form beta- gamma and activates adenyl cyclase (enzyme found within the membrane)
It catalyses the conversion of ATP to cyclic AMP
cAMP inhibits Ca2+ ions release which is important for muscle contraction
It reduces Ca2+ entry and induces Ca2+ entering SER, so no Ca2+ for smooth muscle contraction
Gas interacting with K+ channels with are present in the airway smooth muscles

152
Q

How can tolerance occur with beta receptors?

A

Desensitisation occurs in response to the association of the receptor with the agonist molecule
Once a B2 receptor is repeatedly stimulated they become tolerant

153
Q

Give six overall functions of a B2 agonist:

A

-Bronchodilation
-Decrease in mast cell release
-Decrease in plasma execution
-Decrease in cholinergic neurotransmission
-Increase in mucociliary clearance
-Rapid desensitisation, no prolonged anti inflammatory effects

154
Q

Can a SABA/LABA be used as a mono therapy, explain why/ why not:

A

No, use like this has frequently been associated with hospital admissions and death
Discouraged for use for initial treatment, instead use low does of ICS

155
Q

Describe how corticosteroids can enter the body for response:

A

They are easily able to cross the plasma membrane
Enter the cytoplasm, then bind to the glucocorticoid receptor which causes homodimerization
This translocates to the nucleus and binds to hormone response elements

156
Q

Describe what happens to cells involved in asthma and COPD when corticosteroids are involved:

A

Decrease in:
Eosinophils, dendritic cells, mast cells
Decrease cytokine production from:
Macrophages, T cells, epithelial cells, smooth muscle cells
Goblet cells decrease mucous secretion
Smooth muscle cells increase B2 receptors
Endothelial cells decrease leakage
Corticosteroids first target is epithelial cells:
-decrease inflammation and adhesion molecules

157
Q

When can steroids become ineffective?

A

In steroid resistance, particularly seen in COPD with smokers

158
Q

What is Claisen condensation?

A

Carbon carbon bond forming reaction between two esters or one ester and another carbonyl in the presence of a strong base resulting in formation of Beta- dicarbonyl

159
Q

What does regiospecific mean and how does this relate to markovnikovs rule?

A

The addition is added to a specific side of a double bond
In addition of HX, the H attaches to the carbon with the fewer alkyl substituents
The X attaches to the carbon with the highest number of alkyl substituents

160
Q

Are steroids easily able to cross the plasma membrane and how does it do this?

A

Yes
They enter the cytoplasm and bind to the glucocorticoid receptor which causes homodimerisation
This translocates to nucleus which binds to hormone response elements

161
Q

What effect do corticosteroids have on asthma?

A

Decrease cells;
- dendritic cells
- mast cells
- eosinophils
- cytokines (T cells and macrophages)
- goblet cells
Smooth muscle cells, they increase B2 receptors and decrease receptor desensitisation (good for co therapy)
Endothelial cells decrease leakage
Inhibit IL-2 transcription so no Th2 synthesis

162
Q

What is the first main target for corticosteroids and how does it affect it?

A

Epithelial cells:
Decrease adhesion molecules
Decrease inflammation
Decrease cytokines, decrease mediators

163
Q

Describe the BTS SIGN asthma guidelines:

A

SABA as required at any stage
Regular preventer: low dose ICS
Initial add on therapy: LABA +low dose ICS
Additional controller therapies: Medium dose ICS or LTRA, remove LABA if not working
Specialist therapies

164
Q

Describe the NICE COPD guidelines:

A

Offer SABA or SAMA as needed
Asthmatic features: LABA+ ICS
Non asthmatic features: LABA+LAMA
Then add LAMA+LABA+ICS (remove ICS if no) improvement
Specialist therapies

165
Q

Why can’t Ach be administered as a drug?

A

Not orally as easily hydrolysed in stomach through acid catalysis
Not IV as hydrolysed in blood by esterases
Non selective so fire all receptors in body

166
Q

Which muscles do nicotinic and muscarinic receptors work on?

A

Nicotinic = skeletal
Muscarine= Smooth and cardiac

167
Q

Why is the ammonium group needed in muscarinic agonists?

A

Needed to form an ionic bond with Asp-311
Inactive without it
CH3 groups only on it to fit into small hydrophobic pocket

168
Q

Why is hydrogen bonding needed in muscarinic agonists?

A

Can be ester or ether as a HBA
Hydrogen bonding with Asn-617

169
Q

What ester substituents can be added for muscarinic agonists?

A

None
Can add NH2 on the end to make a bioisostere so stops hydrolysis

170
Q

What selectivity occurs when substitution occurs on alpha and beta chains in musarinic agonists?

A

Alpha- methyl selective for nicotinic
Beta- methyl selective for muscarinic

171
Q

Why is histamine tautomeric?

A

Has two isomeric stuctural forms

172
Q

Where do 2nd generation antihistamines work and what does this mean for them?

A

Must work in periphery, so has to be amphoteric (zwitterion)

173
Q

What is the function of the a, B1,B2 and B3 agonists?

A

a: contracts smooth muscle
B1: contracts cardiac muscle
B2: relaxes airway smooth muscle
B3: fat metabolism, relaxes bladder smooth muscle

174
Q

What changes can be made to adrenergic receptors to slow down the metabolism of COMT?

A

Change the meta OH to an extend OH chain, CO2H etc
Anything with hydrogen donating activity

175
Q

Which muscarininc receptor is most significant in airway diseases and how?

A

M3
They are found on bronchial smooth muscle and gland cells, and mediate bronchoconstriction and mucus secretion

Mpharm Y2S1 (12 decks)

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