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Human Pharm, MTE > Respiratory Pharmacology Module > Flashcards

Respiratory Pharmacology Module Flashcards

1
Q

Name the main beta2-receptor agonists used in Asthma treatment

A

Salbutamol (SABA), terbutaline (SABA)
Salmeterol (LABA), eformoterol (LABA)
Indacaterol (Ultra-LABA)

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2
Q

What is the MOA of respiratory Beta2-agonists?

A

Binding of B2 agonist to beta2 adrenoceptor > activation of Gs protein (GPCR) > ATP is converted into cAMP > protein kinase (PK) conversion into protein kinase A (PKA) > relaxation of smooth muscle

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3
Q

Name and explain some issues with B2-adrenoceptor agonists

A
  • Chronic, high dose exposure = enhance Th2 inflammatory pathway through IL-12 and IFN-gamma inhibition. Also increase airway hyperresponsiveness
  • Pre-treatment with B2-adrenoceptor agonist = increased severity of late asthma
  • Continuous treatment without inhaled corticosteroids (ICS) = Increased sputum eosinophils
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4
Q

How long approximately do SABAs take to work?

A

<5 mins (salbutamol, terbutaline)

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5
Q

How long approximately is the half-life of the SABAs?

A

3-6 hrs (salbutamol)
4-6 (terbutaline)

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6
Q

What is the onset of action for LABAs?

A

Salmeterol = 15 mins
Formoterol= 7 mins
Olodaterol, Vilanterol = 5 mins

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7
Q

What is the duration of action/half life of the LABAs?

A

All 12 hours

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8
Q

What is the half life and onset of action for the Ultra-LABA?

A

Half life = 24 hours
Onset of Action = 5 mins

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9
Q

What are the indications for B2-agonists?

A

SABAs = Symptom relief of asthma and COPD, prevention of exercise induce bronchoconstriction

LABAs = Maintenance treatment of asthma with ICS, COPD

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10
Q

Name some B2-agonist ADR

A

Tremor (B1 activation), Palpitations (b2 activation), tachycardia, agitation, insomnia = beta1 activation

Hyperglycaemia (due to sympathetic response), hypokalaemia = as insulin exits cells into blood it will be exchanged for K+
- Hypokalaemia worsened by = xanthines, steroids, diuretics

Lactic acidosis (high IV dose), Urticaria, angioedema

Hyperactivity in children, headache, muscle cramps

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11
Q

Name the relevant inhaled corticosteroids (ICS)

A

Beclomethasone dipropionate, budesonide, ciclosonide, fluticasone

Prednisone (metabolised in the liver to prednisolone)

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12
Q

Based on oral bioavailability and lung delivery, what are the better ICS?

A

Ciclesonide = lung deliver (50%), F (<1/<1)
Fluticasone = lung delivery (20%), F (</=1)
Mometasone furoate = lung delivery (11%), F (<1)

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13
Q

Briefly explain the MOA of ICS

A

Corticosteroid acts on glucocorticoid receptor > transactivation (Anti-inflammatories), cis-repression (causes side effects), trans-repression (inflammatory signals/proteins = enzymes, receptors, proteins, cytokines, chemokines)

Basically, entering into the nucleus and causing a series of gene activations and repressions

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14
Q

In the context of asthma, what are some wanted outcomes/effects of ICS?

A

Increase b2 receptor expression, decrease Th2 cell counts, downregulate PGD2 (reducing bronchoconstriction)

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15
Q

Name some inhaled corticosteroid adverse reactions

A

Common= Dystonia (talk different/deeper voice), oropharyngeal candidiasis, bruising, facial skin irritations

Rare = allergic reactions (bronchospasm, rash, urticaria)

Potential for systemic effects = dose, duration, and drug interaction dependent

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16
Q

Name some of the systemic ADRs seen with corticosteroids

A

Psychological effects = headache, mental disturbances (euphoria/depression), altered mood, insomnia (cortisol is physiologically low at night, the drug will increase it at night causing insomnia)

Phenotypical effects = skin atrophy, fat redistribution, acne, hirsutism, cataracts (increased intraocular pressure)

Immune effects = masking of infection, increased risk of infection

Other = hypokalaemia, hyperglycaemia, sodium and water retention, adrenal suppression, osteoporosis

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17
Q

Which receptor is targeted by the Cysteinyl leukotrienes (CystLT)?

A

CysLT1 receptor

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18
Q

Names the CystLT receptor antagonists used in asthma

A

Montelukast (once daily), Zafirlukast (twice daily)

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19
Q

What is the MOA of CysLT receptor antagonists?

A

competitive antagonising of CysLT1 receptor > inhibiting cysteinyl leukotrienes

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20
Q

What are the indication/s or uses for CysLT receptor antagonists in asthma?

A

Exercise-induced asthma

Decreases early and late responses to inhaled allergens

Can be used as add-on therapy with B2-agonists (have an additive effect) and ICS

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21
Q

What are CysLT not indicated for?

A

Reversal of bronchospasms

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22
Q

Name some ADRs seen with CysLT receptor antagonist use

A

Headaches, dizziness

Neuropsychiatric effects (potential suicidality = issue in kids)
- Mood or behavioural effects (anxiety, depression, aggression, irritability)
- Insomnia, nightmares, sleepwalking, tremor, hallucinations

Nausea, abdominal pain, Diarrhoea

Hypersensitivity reaction (rash, anaphylaxis, angioedema)

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23
Q

Name the mast cell stabilisers used in asthma treatment

A

Cromoglicate, nedrocromil

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24
Q

Describe the MOA of mast cell stabilisers

A

Prevent histamine release from mast cells through stabilising the mast cell’s membrane, making it stronger and less likely to break.

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25
What role do mast cell stabilisers play in asthma treatment?
Given as prophylactic to reduce both immediate and late phase asthmatic response; also reduces bronchial hyper-reactivity Weakly anti-inflammatory with a short duration of action Not bronchodilators and have no direct effect of smooth muscle
26
What are the ADRs for mast cell stabilisers?
- GI irritation (mild throat irritation, dyspepsia, abdominal pain, bitter taste) - Cough Tightening airways if inhaled (transient bronchospasms
27
What are the indications for Omalizumab?
Moderate to severe persistent asthma 6 years of age or older Chronic idiopathic urticaria
28
What is the MOA of omalizumab?
inhibits binding of IgE to the high affinity IgE receptor on surface of mast cells and basophils, reducing the inflammatory response
29
In relation to muscarinic receptors, what does the M2 receptor regulate?
The postganglionic parasympathetic M2 receptor limits ACh release, acting as an autoinhibitory receptor in a negative feedback loop. It does this by inhibiting ACh release from the postganglionic neuron, preventing M3 receptor stimulation
30
When would you see reduced M2 receptor function?
respiratory infections (viral), antigen challenge, and exposure to organophosphates Asthma <3
31
What role do the M3 receptors play in the lungs?
Increases serous secretion (mucus), increases mucociliary beat frequency
32
What is the mechanism of action for the muscarinic receptor antagonists used in COPD treatment?
Competitive inhibition of muscarinic receptors (ideally M3), preventing the binding of ACh to the muscarinic receptors --> decreasing smooth muscle contraction due to increased cAMP and decreased Ca2+.
33
Name the antimuscarinics used in COPD treatment
Ipratropium Tiotropium
34
Describe the selectivity/or lack there of for Ipratropium
Ipratropium blocks all muscarinic receptors with equal affinity, non selective Blocking of M2 = potential for vagally induced bronchoconstriction (fast), asthma patients already have reduced M2 function so this is not good
35
True or False Ipratropium is a more effective bronchodilator compared to B2 adrenoceptor agonists
FALSE It is a less effective bronchodilator and demonstrates no evidence in slowing rate of lung function decline in COPD
36
Which is a better drug for the treatment of COPD, ipratropium or tiotropium?
Tiotropium <3
37
Name the ADRs for tiotropium
Dry mouth, occasional cough
38
Describe the selectivity/or lack there of for Tiotropium
Higher affinity for the muscarinic receptors and is functionally selective for the M3 receptors. Able to dissociate from the M2 receptor 10x faster than from M3 receptor
39
Other than for COPD treatment, what else can tiotropium be used for?
Treatment of poorly controlled asthma
40
Why is tiotropium a better drug compared to ipratropium?
Tiotropium produces greater improvement in airflow limitations in comparison to ipratropium with only once a day dosing. It does not exacerbate ACh release from parasympathetic nerves like other anticholinergics Able to delay and reduce COPD exacerbations (including hospitalisations of exacerbation)
41
What's another class name for theophylline drugs
Methylxanthine
42
Name the relevant theophylline drugs, mentioning differences in water solubility
Theophylline = not very water soluble Aminophylline = more water soluble due to ethylenediamine
43
What functions are adenosine receptors responsible for?
Arousal, locomotion Regulating cardiac contractility, vascular tone Diuresis Immune response
44
True or False Theophylline is a narrow therapeutic index drug with a dose-dependent target affinity?
TRUE
45
True or False Theophylline is a first line drug
FALSE
46
What enzyme does theophylline effect at high doses? What effect does it have on it?
At high doses theophylline inhibits phosphodiesterase type III, increasing cAMP and cGMP concentrations Increased cGMP = decreased HR, inotropic response, reduced inflammatory response Increased cAMP = decreased Ca2+ availability, vasodilation, anti-inflammatory
47
Name the drug/s that are adenosine receptor antagonists
Theophylline Aminophylline (?)
48
What factors reduce theophylline clearance?
Co-morbidities = heart failure (dec hepatic blood flow --> dec metabolism ---> dec CL --> inc T1/2), liver disease (dec hepatic function ---> dec metabolism ---> dec CL --> inc T1/2) Medications = erythromycin, allopurinol, cimetadine, ciprloxacin
49
What factors increase theophylline clearance?
Smoking (inc hepatic protein/enzyme production ---> inc metabolism ---> dec t1/2 ---> dec drug effect) Not recommended for patient to stop smoking because it could have toxic effects. Patient will also need higher doses if they are a smoker due to increase metabolism and clearance
50
What enzyme is theophylline metabolised by?
Metabolised in phase I metabolism by CYP1A2 CYP1A2 = many genetic polymorphisms which means the effect and metabolism of the drug can vary greatly between people
51
What are the therapeutic doses for theophylline in children and adults?
Adults = 10-20 mg/L Children = 6-12 mg/L
52
What is the toxic concentration for theophylline?
>20 mg/L
53
True or False Theophylline is not a narrow therapeutic index drug
FALSE
54
When should theophylline serum trough levels be monitored?
Commencement of therapy, dose changes, prolonged fever, signs of toxicity, high doses, stop/starting smoking
55
What drugs decrease theophylline plasma concentrations?
Rifampicin, phenytoin, carbamazepine phenobarbital, CYP inducers
56
What drugs increase theophylline plasma concentrations?
Erythromycin, clarithromycin, ciprofloxacin, diltiazem, fluconazole, CYP inhibitors
57
Name some ADRs associated with theophylline use
Nausea/Vomiting, dyspepsia, loss of appetite, headache, tremor, insomnia Diarrhoea, palpitations = due to increased cAMP levels as a result of PDEIII inhibition Tachycardia, CNS stimulation, flushing, rash, hyperglycaemia, hypokalaemia, alopecia
58
What are some signs of theophylline toxicity?
CNS overdrive = agitation, anxiety, irritability, seizures, delirium, confusion Arrhythmias, nausea/vomiting, anorexia, hyperthermia, extreme thirst
59
Why would you combine inhaled antimuscarinics with beta2-adrenoceptor agonists?
Allows targeting of bronchoconstriction through two mechanism = sympathomimetic and anticholinergic beta2-agonist = dec ACh release through modulation of cholinergic neutrotransmission by pre-junctional b2-adrenoceptors muscarinic antagonists = reduce bronchoconstrictor effect of ACh
60
When comparing antimuscarinics and beta-2 agonists, what can antimuscarinics do that b2-agonists can’t?
Antimuscarinics can independently supress mucus/fluid secretions

Human Pharm, MTE (2 decks)

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