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PMP 201 > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

what is asthma?

A

an obstructive disease, where there is resisitance to the flow of air through the airways during inspiration and expiration

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2
Q

what does the degree of resistance depend on?

A

airway diameter
laminar turbulent flow

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3
Q

what is FEV1?

A

amount breathed out in 1 second
forced expiratory volume

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4
Q

what does the FEV1/FVC ratio indicate?

A

under 70%= diagnose with asthma

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5
Q

what are the showing signs of asthma?

A

dyspnoea
wheezing
tight chest
cough

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6
Q

what are the 3 main factors of asthma?

A

airway constriction (narrowing)
airway hypersensitivity and responsivness
mucous hyper-secretion

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7
Q

what are the causes of asthma?

A

cytokine response profiles
allergens
pollutants
infection
stress
age

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8
Q

how do the host factors and environmental exposusres become asthma?

A

altered innate and adaptive immune responses
symptoms and chronic changes

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9
Q

what does inflammation due to asthma cause?

A

airway obstruction
AHR/ bronchospasm
Airway remodelling (long term changes in the airway

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10
Q

what are some trigger factors of asthma?

A

allergens
chemicals
drugs
foods
environmental chemicals
cold air
excersise
stress
workplace

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11
Q

how is the IgE antibody associated with asthma?

A

the propensity to develop IgE antibosies to common antigens
this is associaated to succeptability to develop asthma, allergic rhinitis, eczema

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12
Q

pin prick test for asthma?

A

early onset asthma will have more of a positive result
1/3 of pop have +ve results
about a 1/3 of them end up getting asthma

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13
Q

what causes extrinsic asthma?

A

specific triggers

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14
Q

what causes intrinsic asthma?

A

non-specific triggers

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15
Q

what ar specific triggers of asthma?

A

allergens, occupational agents (SO2, ciggarette smoke)

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16
Q

what is the process of sensitisation of genitically predisposed individuals to allergens?

A

allergen–> dendritic cell (antigen presenting cell)–> Th0 helper cell –> immune response –> Th2 lymphocyte –> cytokines–> call in immune cells (mast cells and eosinophils)

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17
Q

what are the 2 phases of an asthma attack?

A

early phase; increase in resistant airflow
immediate response to release of inflammatory mediators from mast cells
late phase: can occur a long time after allergen exposure
driven by continuation of inflammation chara terised by an influx of eosinophils into the lungs

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18
Q

what is the paradigm of asthma pathophysiology?

A

mast cell activation/ degranulation
immediate inflammatory responses
late inflammation responses
inflammation reduced airway remodelling

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19
Q

what happens when epithelium breaks down?

A

smooth muscle grows over–> narrowing the airway

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20
Q

what is the process of mast cell degranulation?

A

Cross linking IgE receptor by binding antigen results in mast cell to degranulate leading to the release of histamine and other inflammatory mediators.

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21
Q

what happens during mucus plugging?

A

during inspiration the air moving in can fold the mucus over blocking the bronchus, which mean that the air cannot escape during expiration

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22
Q

what are the theraputic goals of asthma?

A

Minimal symptoms day & night​

Minimal need for reliever medication​

No exacerbations​

No limitation of activity​

Normal lung function​

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23
Q

what are the therapeutic treatments given for asthma?

A

reliever (bronchodilators)
preventer (corticosteroids)`

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24
Q

why are drugs given through the respiratory route?

A

rapid onset of activity when given for a local affect
smaller dose required

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25
Q

what are the pulmonary drug delivery fundamentals?

A

patient
formulation
delivery systems
drug physiocochemucal properties

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26
Q

why is density important for aerodymic factors?

A

Density is important for the aerodynamic factor of the particle​

Small aerodynamic is what we want for drugs that are delivered to the lungs​

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27
Q

what size particles are going to reach the alveolar duct?

A

1-2 micron particles

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28
Q

what does every branch in the airways add?

A

a generation

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29
Q

what are the pulmonary drug delivery devices?

A

pressurised metered-dose inhalers
dry powder inhalers
nebulisers
electronic ciggarettes

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30
Q

how does the phase of drug change in PMDIS?

A

held under hih pressure in the canister= liquid
release= lower pressure= gas

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31
Q

what is the cold filling of pMDI canisters?

A

Drug + excipients + propellant chilled to -60°C and added to canister​
Further (chilled) propellant added and canister sealed (with the valve)​

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32
Q

what is the pressure filling of pMDIs?

A

Drug + excipients + propellant added to canister under pressure (through the valve)
Further propellant (under pressure) added​

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33
Q

how has the formulation of pMDIs changed over the years?

A

pMDIs originally contained chlorofluorocarbons (CFCs) but discovered in 1980s that these damaged the ozone layer ​

CFCs removed from pMDIs during the late 1990s/ early 2000s and replaced with hydrofluoroalkanes (HFAs)​

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34
Q

what are the advantages of pMDIs?

A

Portable (vs. nebulisers)​

Low cost​

Drug protected from environment in canister​

Multiple doses in one device​

Reproducible dose​

Efficient at drug delivery (cf. oral route)​

Disposable ​

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35
Q

what are the disadvantages of pMDIs?

A

Incorrect use by patients​
Greenhouse gases​
Inefficient at drug delivery!​
Disposable!​

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36
Q

what is COPD?

A

a disease state characterised by the presence of chronic bronchitis and/or emphysema associated with airflow obstruction: air flow obstruction is often accompanied by airway hyperreactivity and may be partially reversible

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37
Q

what is chronic bronchitis?

A

lung damage and inflammation in the airways (bronchi)

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38
Q

what are the symptoms of chronic bronchitis?

A

chronic cough
sputum production
haemoptysis
initially mild dyspnea
cyanosis
peripheral oedema

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39
Q

what is emphysema?

A

lung damage and inflammation of alveoli

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40
Q

what are the symptoms of emphysema?

A

enlargement of the air spaces distal, further away to the terminal bronchioles
dyspnea
minimal cough
pink flush in the face
hyperinflation
tachypnea

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41
Q

what are the COPD functional changes?

A

Airway obstruction​

Air trapping​

Hyperinflation​

Mucus hypersecretion​

Ciliary dysfunction​

Gas exchange impairment​

Pulmonary hypertension​

Cardinal triad of COPD​

Dyspnoea​

Chronic cough​

Sputum production​

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42
Q

what is the epidemiology of COPD (smokers)?

A

Approximately 90% of COPD patients are smokers ​

although only 15% of smokers develop COPD​

In the 10% of non-smokers who suffer from COPD, causative factors include environmental factors (passive smoking, pollutants, inhalation of other toxins) and developmental lung changes​

COPD increase with age and are higher in men​

Inflammation dominated by neutrophil invasion of the lung tissue​

The most important identified genetic risk factor for the evolution of COPD is deficiency of α1-protease (α1-antitrypsin) inhibitor​

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43
Q

when should a diagnosis of COPD be considered?

A

over the age of 35 ​

who have a risk factor (generally smoking) ​

and who present with: ​

exertional breathlessness​

chronic cough​

regular sputum production​

frequent winter ‘bronchitis’ ​

or wheeze. ​

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44
Q

what is the pathophysiology of COPD?

A

Inflammatory response –’> amplified –> macrophages–> attract immune cells–>increase of neutrophils–>proteases–> alveolar wall destruction and mucus hypersecretion​

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45
Q

what is the treatment of COPD?

A

corticosteroids
long acting beta-agonists
anticholinergics
oxygen
avoid respiratory infections
smoking cessation

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46
Q

what are the tests used to make an asthma diagnosis?

A

Spirometry​

Peak Expiratory Flow​

Asthma Control Questionnaire (ACQ)​

Asthma Control Test​

FeNO​

Eosinophil differential count

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47
Q

what are the classifications of uncontrolled asthma?

A

Uncontrolled asthma describes asthma that has an impact on a person’s quality of life​

3 or more days a week with symptoms or​

3 or more days a week with required use of a SABA for symptomatic relief or​

1 or more nights a week with awakening due to asthma.​

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48
Q

what is maintenance and reliver therapy (MART)?

A

MART is a type of asthma treatment plan. ​

If a patient is on a MART plan, they have just one inhaler to use as a preventer and a reliever.​

A MART inhaler is a combination inhaler that contains:​

An inhaled steroid + A long-acting bronchodilator with a fast onset of action (Formoterol)​

Not all combination inhalers are licensed for MART​

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49
Q

when is it appropriate to use MART?

A

patients on step 2 or 3 or 4 with a personalised action plan, able to self manage and who are compliant with their own treatment, uncontrolled symptoms

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50
Q

what are the high risk drugs for use in asthma?

A

selective B2-agonists
inhaled corticosteroids
theophylline
leukotriene receptor antagonists

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51
Q

what is the treatment guidline for COPD?

A

spirometrically confirmed diagnosis –> assesment of airflow limitation –> assessment of symptoms/ risk of exacerbations –> post-bronchodilator

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52
Q

what are the pharmocological management of COPD?

A

LAMA (leads to hospitalisation)
a bronchodilator (not leading to hospital admission)

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53
Q

what is the follow up pharmocological treatent for dyspnea?

A

LABA–> LAMA
–> switching inhaler devices or molecules –> investigate other causes of dyspnea

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54
Q

what is the follow up pharmocological treatment of exacerbation?

A

LABA–> LAMA–> ICS –> azithromycin –> roflumilast

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55
Q

what are the step of treatment of COPD?

A

assessment
diagnosis
refer
prescribe
review

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56
Q

what are some of the inhaled antimuscarinics?

A

sama
lama

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57
Q

what is exacerbtion in COPD?

A

increased dyspnea, increased sputum volume, increased sputum purulence

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58
Q

what is the management of exacerbation of COPD?

A

short acting (sama, saba) usually at higher doses through nebuliser
withold lama if sama is given
short course of oral perdnisolone
antibiotics for sings of infection

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59
Q

what are the prevention of exacerbations of copd?

A

pulmonary rehabilitation
education and self management
integrated care programs

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60
Q

what is custic fibrosis?

A

It is a genetic disorder affecting the lungs, pancreas, liver, intestine, and reproductive organs. ​

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61
Q

what are the main clinical signs of cystic fibrosis?

A

pulmonary disease, with recurrent infections and the production of copious viscous sputum, and malabsorption due to pancreatic insufficiency.

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62
Q

what are the complications of cystic fibrosis?

A

include hepatobiliary disease, osteoporosis, cystic fibrosis-related diabetes, and distal intestinal obstruction syndrome.​

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63
Q

what are the aims of treatment of cystic fibrosis?

A

Preventing and managing lung infections​

Loosening and removing thick, sticky mucus from the lungs​

Preventing or treating intestinal obstruction​

Providing sufficient nutrition and hydration​

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64
Q

what is a key predictor of life expectancy in prople with cystic fibrosis?

A

lung function

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65
Q

what are the non-drug treatments of cystic fibrosis?

A

Provide advice on airway clearance, nebuliser use, musculoskeletal disorders, physical activity, and urinary incontinence (by specialist physiotherapists). ​

Regular exercise improves both lung function and overall fitness.​

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66
Q

whaat are the drug treatments of cystic fibrosis?

A

Treatment is based on the prevention of lung infection and the maintenance of lung function. ​

Patients, who have clinical evidence of lung disease, the frequency of routine review should be based on their clinical condition.​

Adults should be reviewed at least every 3 months. ​

More frequent review is required immediately after diagnosis.​

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67
Q

what should patients with cystic fibrosis who have evidence of lung disease be offered?

A

mucolytic

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68
Q

what is mucolytics?

A

Dornase alfa is the first choice mucolytic. ​

If there is an inadequate response, dornase alfa and hypertonic sodium chloride, or hypertonic sodium chloride alone should be considered.​

Mannitol dry powder for inhalation is recommended as an option when dornase alfa is unsuitable, when lung function is rapidly declining, and if other osmotic drugs are not considered appropriate.​

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69
Q

what should be offered to patient with cytsic fibrosis with a pulmonary infection?

A

Staphylococcus aureus: Offer an antibacterial oral or IV​

Pseudomonas aeruginosa: Offer an oral antibacterial in combination with an inhaled antibacterial.​

Aspergillus fumigatus complex: Offer an antifungal drug only to suppress chronic complex respiratory infection in patients with declining pulmonary status.​

​

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70
Q

what are the innervation of the lungs?

A

Parasympathetic nervous system activation triggers bronchoconstriction​

Predominantly VAGAL nerve​

Sympathetic nervous system activation triggers bronchodilation​

Increased lung capacity​

Preparation for exercise

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71
Q

what are the steps to smooth muscle contraction?

A

Ca2+ ions increase​

Extracellular​

Sarcoplasmic reticulum​

Ca2+ Bind to calmodulin​

Ca2+ / calmodulin complex then activates myosin (light chain) kinase (MLCK)​

MLCK phosphorylates myosin ​

Allows myosin heads to bind to actin ​

Fibres contract (power stroke)​

Background level of tone​

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72
Q

what is the process of parasympathetic innervation?

A

Parasympathetic dominant​

VAGAL Nerve (cranial nerve X)​

M1, M2, M3 present, M3 most important​

M3:​

Produce mostly stimulatory effects​

Glands (secretion)​

Smooth muscles of airways (contraction)​

(NB Relaxation of vascular smooth muscle - vasodilatation)​

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73
Q

what is the processof sympathetic NS innervation?

A

Sympathetic nerves innervate blood vessels and glands in trachea and bronchus​

NOT airway smooth muscle​

Many Beta-adrenoreceptors human smooth airway muscle and alveoli​

Beta 2 ​

Respond to circulating agonists​

Relax bronchial smooth muscle​

Mast cells: Inhibit mediator release​

Epithelium: enhance muco-cilliary clearance​

Reduced calcium​

​

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74
Q

what receptors are contained in brochial smooth muscle?

A

histamine-bronchoconstriction
leukotrienes -bronchoconstriction

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75
Q

what are the therapeutic aims of asthma and COPD?

A

relief- rescue patient from bronchospasm
prophylaxis - reduce frequency and severity of attacks, limit structural remodelling

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76
Q

what are the classes of bronchodilaters?

A

β-adrenoceptor agonists​

Xanthines​

Muscarinic receptor antagonists​

Leukotriene receptor antagonists​

Histamine receptor antagonists​

​

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77
Q

what are the classes of anti-inflammatory drugs?

A

Glucocorticoids​

Cromoglicate and nedocromil (Cromones)​

Anti-IgE (immunotherapy)​

Phosphodiesterase (PDE) inhibitors (also bronchodilator effect) – cover in COPD​

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78
Q

what are the mechanisms of beta adrenoceptor agonists?

A

β2 receptor stimulation ​

via Gs activates adenylyl cyclase that increases intracellular levels of cAMP - cAMP activates protein kinase A (PKA)​

PKA phosphorylates numerous targets leading to bronchodilation (reduction of intracellular Ca2+)​

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79
Q

why use inhaled therapy?

A

lower doses leading to fewer side effects
faster onset of action with inhaled bronchodilators than systemic

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80
Q

what are the different types of beta-adrenoreceptor antagonists?

A

short acting
long acting

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81
Q

what are the characteristics of short acting beta-adrenoreceptor agonists?

A

Hydrophilic in nature​

Short duration of action (4-6 hours)​

As needed, PRN

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82
Q

what are the characteristics of long acting beta-adrenoreceptor agonists?

A

Lipophilic in nature​

Leech out of membrane prolonging duration of action (gen 8-12 hours)​

NOT given as needed​

Adjunctive therapy ​

MUST NOT be given in the absence of a corticosteroid​

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83
Q

what are the unwanted effects of beta-adrenoreceptor agonists?

A

Result from Systemic absorption​

Commonest​-

Tremor​

Other​-

Nervous tension​

Headache ​

Muscle cramps​

Peripheral vasodilatation​

High doses​-

Hypokalemia after high doses​

Tachycardia​

Cardiac dysrhythmias​

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84
Q

what are the classes of drugs for respiratory system?

A

Beta-2 Agonists (SABA + LABA)​

Leukotriene Receptor Antagonists​

Methylxanthines ​

Muscarinic Agents (SAMA + LAMA)​

Corticosteroids​

Mucolytic Agents​

​

​

85
Q

what is a pharmacophore?

A

The section of the drug structure that is responsible for its biological activity (often the part that binds to a receptor)​
Pharmacophore modelling is often used to establish the essential criteria for the drug​

86
Q

hydrophobic meaning?

A

hydrophobicity measures the association of nonpolar groups or molecules in an aqueous environment which arises from the tendency of water to exclude nonpolar molecules.

87
Q

lipophilicity meaning?

A

Lipophilicity represents the affinity of a molecule or a moiety towards a lipophilic environment

88
Q

addition of methylene groups impact drug activity?

A

increase size, lipophilicity

89
Q

increase degree of saturation impact drug activity?

A

increase flexibility

90
Q

addition of ring system groups impact drug activity?

A

increase size, rigidity, hydrophobicity (pockets)

91
Q

addition of halogen groups impact drug activity?

A

increase lipophilicity, reactivity (electronegativity)

92
Q

addition of methyl groups impact drug activity?

A

increase lipophilicity, size (binding pockets)

93
Q

addition of hydroxy groups impact drug activity?

A

increase hydrophilicity, H-bonding (polar)

94
Q

addition of basic groups impact drug activity?

A

increase hydrophilicity, H-bonding , salt formation

95
Q

addition of carboxylic acid impact drug activity?

A

increase hydrophilicity, H-bonding, salt formation

96
Q

addition of thiols and sulphides impact drug activity?

A

metal chelation (rarely introduced otherwise)

97
Q

what are the sructural characteristics of leukotriene receptor antagonists?

A

Lipophilic tetraene (4 double bonds) tail of LTD4 can be imitated by several of more stable aromatic rings ​
Sulfide of the glycyl-cysteine dipeptide can be supplanted by an alkyl carboxylic acid​
C1 Carboxylate of LTD4 must be maintained. ​

98
Q

what is a positive result for FeNO?

A

40 ppb or more

99
Q

what is a positive result for obstructive spirometry?

A

FEV/FVC less than 60%

100
Q

what is a positive result for bronchodilator reversability?

A

improvemnet of 12% or more in FEV1 and increase in volume of 200ml or more

101
Q

what is a positive result for Peak flow variability?

A

variability of over 20%

102
Q

what is a positive result for direct bronchiol challenge test with histamine or methacholine?

A

proactive concentration of methacholine causing a 20% fall in FEV1 of 8mg/ml or less

103
Q

spacers cleaning

A

If you keep your spacer clean it will last longer and be more effective. Clean the spacer regularly. The instruction leaflet tells you how often to clean it. Use warm water and mild detergent, such as washing up liquid. Rinse and allow to air dry. Do not dry with a cloth or towel. ​

104
Q

spacer technique

A

Breathe in through your mouth, slowly and steadily over 4 to 5 seconds or, breathe in and out through your mouth, slowly and steadily.​

105
Q

scinitigraphy

A

Scintigraphy = radiation emitting substances are administered to a patient and the subsequent emissions are capture by a gamma camera and an image produced​

Lung scintigraphy can be used as a diagnostic tool and also to evaluate new respiratory formulations​

Diagnostic: patient inhales nebulized radionuclide-containing solution and/or has radiopharmaceutical injected iv​

Formulation: drug-carrier aggregates are radiolabelled (Tc99m) and loaded into the device. Participants would inhale from the device and deposition of drug would be imaged​

106
Q

what are the bronchodilator classes of drugs?

A

β2-adrenoceptor agonists​

Muscarinic receptor antagonists​

Xanthines​

Leukotriene receptor antagonists​

Histamine receptor antagonists​

107
Q

wht are the anti-inflammatory classes of drugs?

A

Glucocorticoids​

Cromoglicate and nedocromil (Cromones)​

Anti-IgE (immunotherapy)​

Phosphodiesterase (PDE) inhibitors (also bronchodilator effect)​

108
Q

what are the cholinergic receptors in the muscarinic system?

A

nicotinic (somatic and autonomic)
muscarinic (para)

109
Q

what is the main muscarinic receptor type that has the biggest effect on the bronchiole muscles?

A

M3

110
Q

what is the mechanism for muscarinic receptor antagonists?

A

block the m3 receptor on the smooth muscle cell to be activated by ACh to release ca2+ which leads to contraction of airway smooth muscle

111
Q

what is the characteristics of the m2 receptor?

A

m2 is an inhibitory as the ACh could bind to it, therefore lowering the amount of ACh that goes to the m3
it is non-specific

112
Q

what are the effects of muscarinic antagonists being non-specific?

A

limited effect on smooth muscle contraction
bronchodilatory effect
reduces mucus build up
may increase muc-cillary clearance
no effect on the late phase of asthma

113
Q

what are the different types of muscarinic receptor antagonists?

A

ipratropium
tiotropium

114
Q

what are the characteristics of ipratropium?

A

Derivative of N-isopropylatropine​

Onset of action 30 mins; lasts 3-5 hours​

Not selective for M receptor subtypes​

115
Q

what are the characteristics of tiotropium?

A

longer-acting​

once daily dosing​

More lipophilic​

116
Q

what are the adverse effects of muscarinic receptor antagonists?

A

dry mouth (m3 effects on salivary glands)
GI tract effects
glaucoma
urinary retention
broncospasm in asthma

117
Q

what are phosphodiesterases (PDEs)?

A

enzymes that regulate intracellular levels cAMP
(digest cAMP)

118
Q

what do xanthines do?

A

maintain high cAMP levels

119
Q

what happens if there is a lot of cAMP?

A

relaxation of the bronchial smooth muscle NMJ

120
Q

what is the mechanism of xanthines?

A

Phosphodiesterase (PDE) metabolises cAMP​

Methylxanthines inhibit PDE, maintaining high cAMP levels​

MLCK inactivated​

Myosin not phosphorylated​

Achieves bronchial smooth muscle relaxation​

121
Q

what are the other possible mechanisms for xanthines?

A

adenosine receptor antagonisms
anti-inflammatory effect
CNS stimulation

122
Q

what are the different types of xanthines?

A

theophyline
aminophyline

123
Q

what rae the unwanted effects of xanthines?

A

stem from effects on other systems
narrow therapeutic window
serious CVS CNS
cardiac dysrhythmia
seizures
monitor
absorption from gut unpredictable
plasma concentration

124
Q

what are leukotriene receptor antagonists?

A

antagonise the CysLT1receptor in respiratory mucosa

125
Q

what do leukotrienes do?

A

synthezised from arachidonic acid and bind to receptors on target tissues
activated mast cells and eosinophils

126
Q

how are cysteinyl leukotriene receptor​ activated?

A

Leukocyte recruitment​

mucus secretion​

vascular permeability / airway oedema​

smooth muscle contraction​

127
Q

what is the mechanism of Leukotriene receptor antagonists?

A

Prevents bronchoconstriction mediated by LTs​

Inhibit early & late phase responses to irritants in asthma​

Generally taken orally with inhaled corticosteroid​

Not used widely

128
Q

what do anti-histamine drugs do?

A

Mast cell degranulation and release of histamine – important in early phase of allergic asthma in particular / some exercise induced asthma and other types​

Histamine binds to H1 receptor​

Mucus secretion / SOME (Bronchoconstriction)

129
Q

whata re antiinflammatory drugs?

A

Used to reduce severity and frequency of asthma attacks​

​

Limit progression of disease by inhibiting remodelling​

​

Reduce night-time asthma attacks by preventing late-phase

130
Q

what are the characteristics of glucocorticoids?

A

Main drugs used for their anti-inflammatory properties in asthma​

Not bronchodilators (don’t relieve early phase)​

Prevent progression of chronic asthma​

Effective in acute severe asthma​

Wide range of effects​

Add-on inhalational therapy in asthma when bronchodilator is used more than once daily​

131
Q

what is the mechanisms of glucocorticoids?

A

Glucort bind to gluco receptors, guc recept move into the nuc bind to dna to reduce pro-inflammatory gene products and increase anti-inflammatory gene products​

132
Q

what are the therapeutic effects of glucocorticoids?

A

immunosuppression
anti-inflammatory

133
Q

what are the names of inhaled glucocorticoids?

A

Beclometasone dipropionate (BDP)​

Budesonide​

Fluticasone propionate (2 x potent as BDP)​

Mometasone​

134
Q

what are the names of the oral glucocorticoids?

A

Prednisolone​

Given as a single dose in the morning to mimic the body’s cortisol secretion​

135
Q

what are the names of the IV glucocorticoids?

A

hydrocortisone

136
Q

what are the unwanted effects of glucocorticoids?

A

Uncommon with inhaled​
Systemic effects only in high doses​
Spacers minimise​

Oropharyngeal candidiasis (thrush)​
Suppress T-lymphocytes important against fungal infection​
Spacer devices reduce​

Regular high doses​
adrenal suppression esp in children​

Iatrogenic Cushings​
(moonface, increased abdominal fat, hypertentsion)​

Osteoporosis ​

Increased risk of pneumonia in elderly with COPD​

Poor absorption from GI tract​

137
Q

what are the charactristics of mast cell stabalsers?

A

Not in common use ​

Poor/variable efficacy shown in antigen-, exercise-, and irritant-induced asthma (especially in children)​

Not bronchodilator​

Weak anti-inflammatory effects​

Reduce immediate & late-phase responses​

Reduce bronchial hyper-reactivity​

Mechanism unclear​

Mast cell stabilisation plays no part cf. oral anti-histamines​

Depress signals from irritant receptors​

May inhibit cytokine release​

138
Q

what are the 2 roles of a cough?

A

the final pathway of mucocilinary clearance
part of the defence mechanisms against inhaled particles and noxious substances

139
Q

what are the causes of a cough?

A

Irritants-smokes, fumes, dusts, etc.​

Diseased conditions like COPD, tumors of thorax, etc.​

Pressure on respiratory tracts​

Infections​

140
Q

what are the components of cough reflex?

A

Cough receptors​

Afferent nerves​

Cough center (medulla)​

Efferent nerves​

Effector muscles​

141
Q

what are the phases of a cough?

A

irritation-A stimulus irritates the upper airways and results in a reflex action leading to cough​
inspiration- Occurs to achieve optimum thoracic gas volume - , thus allowing the most efficient use of the expiratory muscles​
compression-With the glottis closed, the abdominal muscles and the thoracic cage actively contracts, leading to high intrathoracic pressures​
expulsion-The glottis opens and a high airflow results. The force of expression is increased by collapsing the airways following the explosive decompression caused by glottic opening​
relaxation-At the end of the cough, the intrathoracic pressure decreases as the expiratory muscles relax and a transient bronchodilatation occurs​

142
Q

whats an acute cough?

A

present for less than three weeks and can be divided into infectious and non-infectious causes. ​

143
Q

what is a subacute cough?

A

resolves over three to eight weeks

144
Q

what is a chronic cough?

A

present for more than eight weeks

145
Q

what are the characteristics of antitussives?

A

‘Cough suppressants’​

All in clinical use are opioid analgesics​

Suppress cough in doses below those required for pain relief​

Action is poorly defined​

Suppress cough centre​

Common examples​

pholcodine ​

increase bronchial secretion to facilitate removal by coughing

146
Q

what are the characteristics of short acting muscarinic antagonists?

A

Ipratropium Bromide​

Bronchodilator​

Onset around 30 mins​

Effects last 3-5 hours​

Quaternary nitrogen compound​

Does not discriminate between muscarinic receptor subtypes ​

147
Q

what are the types of inhibition?

A

competitive and non-competitive

148
Q

what is competitive inhibition?

A

A specific model of receptor antagonism whereby two molecules compete for a single binding site on the receptor, and the kinetics of binding of both the agonist and antagonist are rapid enough to allow mass action to control the relative proportions of receptor bound to agonist and antagonist.

149
Q

what is a non-competitive inhibition?

A

the antagonist, while still opposing the action of the agonist, does so without competing with it for the binding site.

150
Q

what are the characteristics of long acting muscarinic antagonists?

A

A few common drugs​

Bronchodilator (blocks bronchoconstriction)​

Onset varies – can be rapid​

Effects last 12-24 hours (depending on drug)​

Also quaternary nitrogen compounds​

Greater selectivity for M₃ receptor​

151
Q

what do mucolytic agents do?

A

mucolytic agents breaks down disulfide bonds in mucus gels to reduce viscosity

152
Q

what is the definition of chirality?

A

non-superimposable mirror images

153
Q

S and R chiral?

A

The molecule is viewed along the axis from the chiral centre to the lowest priority element​

If the remaining priorities define a right / clockwise circle, the structure is R, and S if the relationship is left / counter-clockwise​

154
Q

louis pasteur seperation?

A

The first to succeed at separating a pair of enantiomers (1848)​

Noticed that his crystals of sodium ammonium tartrate were not identical​

Right-handed and Left-handed crystals observed​

Separated the crystals using tweezers and then dissolved into solution​

The solution of the RH crystals rotated plane-polarised light clockwise and the LH crystals rotated the light counter-clockwise​

Tartaric acid is obtained from grapes – racemus is Latin for “a bunch of grapes” ​

Separation of enantiomers is called resolution of a racemic mixture​

155
Q

seperating enantiomers via chromatography?

A

Dissolve mixture in a solvent​

Pass solution through a packed column​

Use chiral material to absorb compound​

Two enantiomers have different affinities for chiral material​

One enantiomer emerges before the other ​

​

156
Q

what is cystic fibrosis?

A

inheritable autosomal recessive disease
mucus build up in the lungs
doesnt get any better
mutation of the cystic fibrosis transmembrane conductane regulator (CFTR) gene

157
Q

what is the CFTR gene?

A

involved in the production of sweat, digestive fluids and mucus

158
Q

what are the long term issues of cystic fibrosis?

A

Include difficulty breathing / coughing up sputum as a result of frequent lung infections. ​

Other symptoms include sinus infections, poor growth, fatty stool, clubbing of the finger and toes, and infertility in males among others. ​

Different people have different degrees of symptoms.​

159
Q

what does CFTR gene encode for?

A

protein ion channel in the transmembrane that leaves chlorine out
in cystic fibrosis the gene has mutated

160
Q

what are the main sugns and symptoms of cystic fibrosis?

A

salty-tasting skin​

poor growth and poor weight gain despite normal food intake​

accumulation of thick, sticky mucus​

frequent chest infections, and coughing or shortness of breath​

161
Q

why does cystic fibrosis affect the whole body?

A

because of the wide spread of the CFTR mutataed gene, systems are exacerbated

162
Q

what type of gene is CFTR?

A

chloride ion channel, known as an ABC gene
transmembrane protein, dependant on ATP

163
Q

what happens in the CFTR channel in cystic fibrosis?

A

chloride ions arent transported through chloride channels
affects consistency of mucus
Na+ and cl- on airway surfaces, coupled to reduced flow to the airway lumen, dehydrate mucuc

164
Q

what are the diagnosic tests for CF?

A

large number of CFTR mutations limit utility of DNA tests in diagnosis but can be done= the heel pricj test blood test newborns

sweat tet for chlorine levels (>60mM)
nasal transepithelial potential difference

165
Q

what is the management of CF?

A

Life-style and psychological support required​

Poly-pharmacy is common​

Stratification of treatment to disease severity:​

Am J Respir Crit Care Med 2007;176:957-69​

Maintenance to improve QoL and limit exacerbations​

Treat exacerbations aggressively

166
Q

what are the treatment objectives of CF?

A

Promote clearance of secretions​

Control lung infection​

Provide adequate nutrition​

Prevent intestinal obstruction

167
Q

what drugs promote mucous clearance?

A

inhaled dornase alfa
inhaled hypertonic saline
inhaled mannitol
bronchodilators

168
Q

what drugs are used for inflammation in CF?

A

oral corticosteroids
inhaled corticosteroids

169
Q

what needs to be on a repeat prescription (private)?

A

Written/printed statement on prescription. E.g. Repeat x 3​

In this example, the item may be supplied a total of four times ​

the one original dispensing, followed by three repeats ​

The first dispensing must take place within 6 months of the date on the prescription.​

If a number is not stated, they can only be repeated once (dispensed twice) unless the prescription is for an oral contraceptive in which case it can be repeated five times (dispensed six times in total)​

No time limit for remaining repeats, use professional judgement​

170
Q

what are the characteristics of military prescriptions?

A

Some military medical centres have outsourced the dispensing process to designated community pharmacies under a Ministry of Defence (MOD) contract​

Community pharmacies not covered by the contract will not routinely handle military prescriptions​

Military prescriptions are written on a military form FMed 296​

Pharmacies with a dispensing contract with the MOD will usually invoice the MOD directly​

For a non-contracted pharmacy, the prescription should be treated as a private prescription​

Therefore, charge the patient the appropriate fee​

​

171
Q

what are the chracteristics of optometrist and podiatrist signed order?

A

Certain POMs can be given directly to patients in accordance with a signed patient order from any registered optometrist or podiatrist.​

Must be medicine which can be legally sold or supplied by the practitioner​

Rather than one which they can only administer. ​

Additional Supply Optometrists can issue signed patient orders for an extended range of medicines.​

The practitioner must provide sufficient advice to enable the patient to use the medicine safely and effectively.​

Pharmacist should ensure that the medicine is labelled accordingly as a dispensed medicinal product​

Appropriate record must be made in the POM register. ​

Any additional counselling​

172
Q

what should a signed oreder for school supply contained?

A

Name of the school​

Product details (including spacer if relevant)​

Strength (if relevant)​

Purpose for which the product is required​

Total quantity required​

Signature of the principal or head teacher ​

​

173
Q

whaat is a patient group direction?

A

written direction that allows the supply and/or administration of a specified medicine or medicines, by named authorised health professionals, to a well-defined group of patients requiring treatment for a specific condition.​

It is important that pharmacists involved with PGDs understand the scope and limitations of PGDs as well as the wider context into which they fit to ensure safe, effective services for patients.​

The supply and administration of medicines under a PGD should only be reserved for those limited situations where this offers an advantage for patient care, without compromising patient safety​

A PGD should only be developed after careful consideration of all the potential methods of supply and/or administration of medicines, including prescribing, by medical or nonmedical prescribers.​

174
Q

supply of naloxone

A

Deaths in the UK involving heroin and/or morphine have significantly increased in recent years. Naloxone is an opioid /opiate antagonist which can completely or partially reverse the central nervous system depression, especially respiratory depression, caused by natural or synthetic opioids and is licensed for the treatment of suspected acute opioid overdose.​
Anyone can administer naloxone for the purpose of saving a life (Schedule 19 of the Human Medicines Regulations 2012) and there is evidence for the effectiveness of training family members or peers in how to administer the drug​

175
Q

anyone trading medicines, othe than to a patient is required to …

A

Hold a wholesaler licence – wholesale distribution authorisation (WDA)​

Comply with the Good Distribution Practice (GDP) standards​

Responsible Person​

176
Q

what are the exemptions of wholesale distribution authorisation?

A

Pharmacies supplying stock to another pharmacy within the same legal entity are not required to have a WDA.​

Where however, a legal entity does hold a WDA, the pharmacy supplying the medicines for the purposes of wholesaling must be named on the WDA. ​

Medicines Act 1968​

177
Q

what are serious shortage protocols?

A

Serious Shortage Protocols (SSPs) in England, Wales and Northern Ireland enable pharmacists to make amendments to prescriptions and supply an alternative medicine to those in short supply. SSPs are specific to each home country.​

178
Q

what are written requisitions?

A

These are where practitioners or other authorised individuals require a medicinal product for use during the course of their practice or business. This may not, at this stage, be for a named patient. This would include, for example, where a GP requests something for use during home visits or an optician requests a medicinal item for use during eye examinations.​

179
Q

where are written requisitions not considered wholesale distribution?

A

The transaction takes place on an occasional basis​

The quantity of medicines supplied is small​

The supply is made on a not for profit basis​

The supply is not for onward wholesale distribution.​

180
Q

what does the degree of resistance depend on?

A

airway diameter and laminar or tubular flow

181
Q

what causes the high pressure in asthma?

A

lining of airway becomes irregular in asthma therefore there is resistance from airway diamter, therefore need higher pressure to achieve the same level of airflow

182
Q

what is the process of sensitisarion?

A

allergen goes on the Th0 helper lymphocyte in the lymph node that stimulates immune response, then differntiation happens to Th) helper cells to form Th2 lymphocytes that activates into cytokines and B-cell that form IgE and eosinophils

183
Q

what do B cells do?

A

B cells are plasma cells that secrete antibodies (IgE)
B cells also produce memory b and t cells

184
Q

what happens to IgE in early onset asthma?

A

ige immediately binds to their fc receptor on mast cells which then release histamine and eosinophils attractant factors
IgE are on the surface of mast cells in the lungs

185
Q

what happens to IgE in re-exposure to the allergen in asthma?

A

mast cell degradation (re-exposure to allergen) is when allergen binds to IgE on mast cell, cross links with IgE recepor, causes mast cells to degrnulate, release histamine and other inflammatory responses, which can vasodilate and attract eosinophils (Type 1 hypersensitivity)

186
Q

what does histamine cause?

A

vasodilation meaning that blood and plasma will fill the wall of the bronchus leading it to swell therefore narrowing the diameter of the lumen.

187
Q

what causes inflammation in COPD?

A

neutrophile invasion of lung tissue

188
Q

what is the genetic risk factor for COPD?

A

deficiency of a1-protease (a1-antitripsin) inhibitor
AATD is a genetic condition wherby there is a deficiency of the protease inhibitor, therefore carriers are less able to inhibit these enzymes if damage occurs from smoke

189
Q

how does smoke have an influence for the development of COPD?

A

toxins from cigarette smoke stimulate macrophages and epithelial cells to secrete cytokines that attract immune cells to the lung, neutrophils and macrophages release protease which breakdown elastin in the alveolar walls, and mucus hypersecretion

190
Q

what gives the elastic recoil in the alveolar wall?

A

elastin

191
Q

what stimulates fibrosis in smooth muscle cells?

A

epithelial cells also stimulate fibrosis where fibroblasts grow in amongst smooth muscle cells leading to thickening

192
Q

what causes emphysema?

A

loss of elastic recoil andd increased lung compliance leads to floppy airways where airway resistance is increased and fev1/fvc ratio is reduced

193
Q

what causes chronic bronchitis?

A

neutrophil elastase (protease) causes mucous hypersecretion, prolonged inflammation leads to permanent changes within the airway (hypertrophy of mucous glands), hyperplasia of goblet cells

194
Q

which nerve is activated by the nervous system for bronchodilation/constriction?

A

vagal nerve
CNS control is in the respiratory centre in the medulla modulated by vagal afferents, theyre affected by conc of co2 and o2 in the blood

195
Q

smooth muscle contraction?

A

Ca2+ ions increase and bind to calmodulin–> activate myosin kinase–> phosphorylate myosin –> myosin heads bind to actin–> fibrates contract (power stroke)
smooth muscle contraction has a backround level of tone which is when there is always a small set amount of calcium to allow for contraction

196
Q

what receptor is activated in parasympathetic activation?

A

M3 receptor is activated causing the calcium to be released to end up with a contraction due to myosin-P
nicotinic and muscarinic

197
Q

what receptor is activated in sympathetic activation?

A

beta 2 receptor is activated to release cAMP and PKA to cause relaxataion due to myosin (myosin light chain kinase)
nicotinic only

198
Q

muscarinic receptors?

A

muscarinic receptors are found between the neurone and the effector on the bronchiol smooth muscle wall
M3 is on the smooth muscle cell wall which releases calcium to contract, when ACh lands on the M3
M2 is on the postganglionic nerve, it inhibits ACh to bind to M3 as it attaches to M2 as wel as M3.

199
Q

muscarinic drugs?

A

muscarinic drugs are not selective for M3 therefore they have a limited effect on smooth muscle contraction and bronchodilatory effect, howeveer reduces mucus build up (m3 increases gland secretion) and may increase muco-cillary clearance

200
Q

beta agonists?

A

beta adrenoceptor agonists cause bronchodilation, inhibit release from mast cells, enhanced mucocillarily clearance and has little effect on bronchial hypereactivity in asthma

201
Q

methylxanthines?

A

phosphodiesterases regulate intracellular level of cAMP,phosphodiesterases metabolise cAMP, methylxanthines inhibit phosphodiesterases, maintaining high cAMP levels
cAMP increases inactive MLCK which leads to myosin not phosphorylated which leads to relaxation of bronchioles

202
Q

leukotrine receptor antaonists? (lukast)

A

antagonise the CysLT1 receptor
cysteinyl leukotrienes act on CysLT1 receptor in respiratory mucosa leading to airway inflammation and hyper-reactivity

203
Q

glucocorticoids effect?

A

glucocorticostseroids will eventually reduce number of mast cells which may have an effect on early phase
the responses are increase in anti inflammatory, and decrease in pro-inflammatory by recruiting eosinophils and suppress COX 2

204
Q

immunotheraapies for COPD (omalizumab)?

A

bind to IgE to be removed which reduces mediators released from mast cells which gradually reduces inflamation

205
Q

what is cystic fibrosis caused by?

A

mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene
CFTR gene is responsible for mucus, sweat and digestive fluids production
is a chloride ion channel important in creating sweat, digestive juices and mucus
ion transport abnormalities dehydrates mucous
CFTR are in endothelial cell membranes, aloows chloride ions to leave the cell in active transport
in CF chloride ions are not transported through= reduced extracellularly chloride= thicker mucus= Na+ and Cl- on airway surface= dehydrate mucus= reduced HCO3- to the airway surface= acidifying layer

206
Q

why are LABAs long acting?

A

longer hydrophobic tail increase affinity to receptor, hydrophobicity allow the drug to remain near the receptor longer
hydrophobicity is The tendency of non-polar groups of a molecule to aggregate in order to minimise the unfavourable exposition to the surrounding polar solvent (water)

207
Q

when cant eneantiomers be sepeerated?

A

cannot seperate enantiomers using fractional distilation (same boiling point) or crytalisation (same solubility)

208
Q

when can enantiomers be seperated?

A

seperate enantiomers via chromatography is to dissolve in a solvent, pass through a packed column, use chiral material to absorb compound, two enantiomers have differemt affinities for chiral material, one enentiomer emerges before the other

209
Q
A

PMP 201 (4 decks)

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