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RESP > Airway pharmacology > Flashcards

Airway pharmacology Flashcards

1
Q

Define mechanism of action

A

process by which drug achieves its therapeutic

effects

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2
Q

What does increasing contractile tone involve?

A

Ca2+ mobilisation (Ca2+ entering cytosol from intracellular stores or ECF)
Increasing contractile machinery’s calcium sensitivity (the level of Ca2+ required to produce certain level of contraction)

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3
Q

How do bronchodilator drugs act?

A

binds to specific receptor or E expressed by ASM cell inducing intracellular change interrupting contractile process –> relax

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4
Q

How do β2 adrenergic receptor agonists act?

A
  • Agonism on β2 adrenergic receptors on ASM
  • stimulates Gs
  • ↑adenylate cyclase
  • ↑cAMP
  • ↑PKA inhibiting MLCK
  • ↓Ca2+ mobilisation
  • relax
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5
Q

eg of Short-acting β2 agonist (SABAs) + when’s it used?

A

salbutamol

first-line therapy in asthma, administered as reliever therapy by metered-dose inhaler

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6
Q

eg of Long-acting β2 agonist (LABAs) + when’s it used?

A

salmeterol, formoterol

add-on, preventer, used w inhaled corticosteroids in metered-dose inhalers, 2x daily, continual dosing

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7
Q

Why use LABA w corticosteroids?

A

decreases risk of sudden death

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8
Q

eg of long-acting muscarinic receptor antagonists (LAMAs) + when’s it used?

A

tiotropium

treat chronic bronchitis + add-on, preventer therapy in asthma. Daily dose continual basis via metered-dose inhalers

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9
Q

How do long-acting muscarinic receptor antagonists work?

A
  • blocks Ach receptors on ASM
  • Ach can’t bind to M3 on ASM + glands
  • less bronchoconstriction
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10
Q

Why are long-acting muscarinic receptor antagonists less effective for asthma therapy?

A

Ach plays minor role in ASM contraction

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11
Q

How do long-acting muscarinic receptor antagonists benefit patients w obstructive airway diseases?

A

reducing mucus secretion + inhibiting cough

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12
Q

Why will the anti-inflammatory efficacy of a certain pharmacological treatment vary depending on its individual mechanism of action?

A

inflammation has diff initiating factors (allergens vs. tobacco), immune cells, tissue environments (protease-anti protease balance, level of oxidative stress), cytokines,inflammatory mediators

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13
Q

eg of corticosteroids + when is it used?

A

fluticasone, beclometasone, budesonide
most effective at reducing allergic inflammation in asthma via metered-dose inhaler to maximise relative exposure of drug to respiratory tissue vs systemic circulation

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14
Q

How do corticosteroids work?

A
  • binds to glucocorticoid receptors in cytosol of immune + structural cells
  • drug-receptor migrates to nucleus
  • binds to DNA, modulating transcription, translation, protein expression
  • decrease pro-inflammatory mediator + increase anti-inflammatory mediator expression
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15
Q

What are leukotrienes?

A

group of pro-inflammatory lipid mediators that are implicated in asthmatic immune response, released by mast cells and eosinophils

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16
Q

eg of leukotriene receptor antagonists + when is it used?

A

montelukast

orally, add-on preventer therapy w continual dosing for asthma

17
Q

eg of biologics + when is it used?

A

omalizumab

asthma

18
Q

How do biologics work?

A

Drugs = mAb block/inhibit a specific pro- protein (IgE or IL-4, IL-5, IL-13) involved in inflammatory pathway

19
Q

eg of mast cell stabilisers + when is it used?

A

sodium cromoglicate

allergies, asthma

20
Q

How do mast cell stabilisers work?

A

Prevents degranulation of mast cells (not in asthma?) and/or sensory nerve activation

21
Q

eg of PDE4 inhibitors + when is it used?

A

roflumilast

COPD

22
Q

How do PDE4 inhibitors work?

A
  • Inhibits cAMP metabolism

- Intracellular signalling effects leads to changes in protein expression + neutrophil responses

23
Q

What are the ways drugs can cause adverse effects + eg?

A

-Interacting excessively w primary target:
opioids suppress cough by inhibiting neural function within brainstem but leads to respiratory depression
-Interacting w targets expressed in other tissues:
eg β2 agonists activate both β1+2 receptors in heart leading to cardiac side effects

24
Q

How to prevent adverse effects of drugs + why?

A

delivered by inhalation via metered-dose inhaler so applied directly to target tissue w highest dose

25
Q

Why doesn’t all dose via metered dose inhaler stay within respiratory system?

A

drug swallowed due to poor inhaler technique

26
Q

How can poor inhaler technique be improved?

A

use spacer devices + proper ‘training’

27
Q

Why are some drugs given orally + eg?

A

-systemic effect:
oral steroids to inhibit body inflammation
-drug has narrow therapeutic window so consistent dose must reach the systemic circulation:
theophylline avoids risk associated w multiple inhalations or varying amounts of drug being swallowed vs inhaled
-expensive to formulate inhaler due to physical/chemical properties of drug:
monoclonal antibodies - anti-IgE, mAb, omalizumab

28
Q

What are the adverse effects of Salbutamol?

A

SAN + myocardium has β1, some β2, β2 agonist interacts w β1 so tachycardia+ palpitations
β2 in skeletal muscle so tremor (not major issue as tolerance develops), hypertrophy+muscle growth
Sudden death if not used w corticosteroids

29
Q

Why’s clenbuterol used for doping in sports?

A

Activation of β2 skeletal muscle—> hypertrophy + muscle growth

30
Q

When do corticosteroids lead to adverse effects?

A

Used long-term, at high doses, in patients at risk of independently developing the complications (osteoporosis in post-menopause)

31
Q

What are the adverse effects of corticosteroids?

A

Growth retardation, skin ulcers, depression, candidiasis, hypercortisolism, osteoporosis

32
Q

What are the features of cost-benefit analysis when prescribing?

A

BENEFITS - drug efficacy
increase: quality of life, life expectancy
decrease: symptoms, severity
COST - adverse effects
increase: risk of developing other disease
decrease: quality of life
-economic costs

33
Q

What are the rules by NICE to produce recommended therapeutic strategies?

A
  • All patients w sig bronchospasm given SABA
  • Drugs w greater general efficacy (SABA before LAMA)
  • Drugs w ↓ adverse effects(SABA→ SABA + ICS → +PDEi)
  • Drugs w broad mechanisms of action(ICS before omalizumab)
  • Cheaper drugs before more expensive drugs (ICS before omalizumab)
  • Less drugs before more(SABA → SABA + ICS, SABA + ICS + X)
  • Combine drugs if decreases risk of adverse effects (LABA w ICS)
34
Q

What are the steps for asthma therapy?

A
  • SABA
  • ICS
  • LABA, ↑ ICS, LTRA, PDEi
  • max ICS, 4th drug
  • oral CS, specialist care, anti-IgE
35
Q

eg of Phosphodiesterase inhibitor?

A

theophylline

36
Q

eg of Inhaled corticosteroids?

A

Fluticasone, Budesonide, Beclometasone

37
Q

eg of Oral/systemic steroids?

A

Prednisone, Dexamethasone

38
Q

What are the steps for COPD therapy?

A
  • Smoking cessation, education,lifestyle/environment interventions
  • SABA for exacerbations
  • LAMA/LABA
  • Inhaled corticosteroids if frequent exacerbations
  • Long term oxygen therapy
  • Surgical interventions (LVRS, transplantation)

RESP (11 decks)

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