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General > Respiratory Pharmacology 1 > Flashcards

Respiratory Pharmacology 1 Flashcards

1
Q

where are cell bodies of the preganglionic fibres located?

A

Cell bodies of the preganglionic fibres are located in the brainstem.

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2
Q

Where are cell bodies of the postganglionic fibres located?

A

Cell bodies of postganglionic fibres are embedded in the walls of the bronchi and bronchioles.

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3
Q

what does stimulation of postganglionic cholinergic fibres cause?

A

Bronchial smooth muscle contraction mediated by M3 muscarinic ACh receptors on airway smooth muscle cells. It also causes increased mucus secretion mediated by M3 muscarinic ACh receptors on goblet cells.

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4
Q

What does stimulation of postganglionic noncholinergic fibres cause?

A

Stimulation of postganglionic noncholinergic fibres causes bronchial smooth muscle relaxation mediated by nitric oxide and vasoactive intestinal peptide (VIP).

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5
Q

Stimulation of the sympathetic division of the nervous system has what effect on bronchial smooth muscle? What is the transmitter?

A

Sympathetic stimulation causes bronchial smooth muscle relaxation via β2-adrenoceptors of airway smooth muscle cells. Transmitter is adrenaline released by the adrenal gland.

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6
Q

Stimulation of the sympathetic division of the nervous system has what effect on mucus secretion? What are its mediators?

A

Sympathetic stimulation by adrenaline decreases mucus secretion. Its mediators are β2-adrenoceptors of goblet cells.

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7
Q

Stimulation of the sympathetic division of the nervous system has what effect on mucociliary clearance? What are its mediators?

A

Sympathetic stimulation increases mucociliary clearance. Its mediators are β2-adrenoceptors of epithelial cells.

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8
Q

Stimulation of the sympathetic division of the nervous system has what effect on vascular smooth muscle? What are its mediators?

A

Sympathetic stimulation causes vascular smooth muscle contraction. Its mediators are α1-adrenoceptors of vascular smooth muscle cells.

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9
Q

How do actin and myosin filaments generate contraction of smooth muscle?

A

Actin and myosin filaments of muscle slide across each other to generate force- contraction.

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10
Q

What does MLCK stand for? What is its function?

A

MLCK is myosin light chain kinase. It phosphorylates dephosphorylated MLC.

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11
Q

How does smooth muscle contract?

A

Phosphorylation of MLC in the presence of elevated intracellular Ca2+ and ATP enables contraction of smooth muscle.

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12
Q

How does smooth muscle relax?

A

Dephosphorylation of MLC by myosin phosphatase causes smooth muscle relaxation.

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13
Q

What is the function of myosin phosphatase?

A

Myosin phosphatase dephosphorylates MLC to produce dephosphorylated MLC and enable smooth muscle relaxation.

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14
Q

Compare the rates of phosphorylation and dephosphorylation in the presence of elevated intracellular Ca2+.

A

In the presence of elevated intracellular Ca2+, the rate of phosphorylation exceeds the rate of dephosphorylation, resulting in increased contraction of smooth muscle.

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15
Q

How is the return of intracellular Ca2+ concentration to basal level achieved?

A

Primary and secondary transport.

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16
Q

Chronic asthma involves pathological changes to the bronchioles from long-standing inflammation, name them.

A
  1. Increased smooth muscle mass (hyperplasia and hypertrophy).
  2. Accumulation of interstitial fluid (oedema).
  3. Increased secretion of mucus.
  4. Epithelial damage (exposing sensory nerve endings).
  5. Sub-epithelial fibrosis.
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17
Q

What effect does airway narrowing by inflammation and bronchoconstriction have on airway resistance, FEV1 and PEFR?

A

Airway narrowing increases airway resistance, decreases FEV1 and decreases PEFR.

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18
Q

Bronchial hyper-responsiveness in asthma is due to what?

A

Epithelial damage, exposed sensory nerve endings, and increased airway sensitivity.

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19
Q

What do provocation tests involve and reveal?

A

Patient inhales bronchoconstrictors e.g. histamine or methacholine. The test reveals hyper-responsiveness.

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20
Q

What type of hypersensitivity reaction is the immediate phase of an asthma attack?

A

A type 1 hypersensitivity, consisting of early phase bronchospasm and acute inflammation. Involves mast cells and mononuclear cells, which release spasmogens, chemotaxins and chemokines.

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21
Q

What type of hypersensitivity reaction is the delayed phase of an asthma attack?

A

A type 4 hypersensitivity reaction, consisting of late phase bronchospasm and delayed inflammation. Also causes epithelial damage, airway hyper-responsiveness, wheeze, mucus hypersecretion and cough. Involves TH2 cells, monocytes, eosinophils.

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22
Q

What type of cells contribute to asthma in a nonatopic individual?

A

Phagocytes phagocytose the antigen presented by dendritic cells. There is a cell-mediation immune response involving IgG and macrophages. There is also a low-level TH1 response.

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23
Q

What type of cells contribute to asthma in an atopic individual?

A

In an atopic individual, in mild/moderate asthma, it is predominantly a TH2, antibody-mediated immune response involving IgE. In severe atopic asthma, TH1 also contributes.

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24
Q

How are eosinophils involved in the development of allergic asthma?

A

Eosinophils differentiate and activate in response to IL-5 released from TH2 cells.

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25
Q

How mast cells involved in the development of allergic asthma?

A

Mast cells in airway tissue express IgE receptors in response to IL-4 and IL-13 released from TH2 cells.

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26
Q

In the development of allergic asthma, crosslinking of IgE receptors stimulates what?

A

Calcium entry into mast cells and release of Ca2+ from intracellular stores causing the release of spasmogens, e.g. histamine and leukotrienes that cause airway smooth muscle contraction. They also cause release of prostaglandins, chemokines and chemotaxins attracting inflammation causing cells, e.g. monocytes and eosinophils.

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27
Q

What are the two broad categories of drugs used in the treatment of asthma?

A

Relievers and controllers/preventors.

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28
Q

What do relievers do in asthma? Name them.

A

Act as bronchodilators.

  1. Short acting β2-adrenoceptor agonists.
  2. Long acting β2-adrenoceptor agonists.
  3. CysLT1 receptor antagonists.
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29
Q

What do controllers/preventers do in asthma? Name them.

A

Controllers/preventors act as anti-inflammatory agents that reduce airway inflammation.

  1. Glucocorticoids.
  2. Cromoglicate.
  3. Humanised monoclonal IgE antibodies.
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30
Q

Explain mechanism of action of β2-adrenoceptor agonists.

A

Act as antagonists of smasmogens. They cause airway smooth muscle relaxation.

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31
Q

Explain mechanism of action of short acting β2-adrenoceptor agonists, their indication and an example.

A

SABAs, e.g. Salbutamol. First line in mild, intermittent asthma. Relievers. Act rapidly to relax bronchial smooth muscle, maximal effect within 30 minutes, and persists for 3-5 hours. They increase mucous clearance, and decrease mediator release from mast cells and monocytes.

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32
Q

Explain the mechanism of long acting β2-adrenoceptor agonists, their indication and an example.

A

E.g. salmeterol and formeterol, or combination inhalers (symbicort and seratide). They should be used in nocturnal asthma. Should never be used alone, but in combination with a glucocorticoid.

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33
Q

explain the mechanism of action of cysteinyl leukotriene (CysLT1)receptor antagonists.

A

CysLT1 receptor antagonists act as competitors at the CysLT1 receptor. CysLTs are derived from mast cells (inflammatory cells), and cause smooth muscle contraction, mucus secretion and oedema. CysLT1 receptor antagonists block these, relaxing bronchial smooth muscle.

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34
Q

Give an example of, and an indication for CysLT1 receptor antagonists.

A

E.g. montelukast, zafirlukast. Given orally.
They are used as an add-on therapy in bronchospasm of mild, persistent asthma.
They are also used in combination with e.g. ICS in more severe asthma. May cause headaches and GI upset.

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35
Q

Give an example of methylxanthines, and their indications.

A

E.g. theophylline and aminophylline (oral).
Have both bronchodilator and anti-inflammatory properties. They are used second-line in combinations with β2-adrenoceptor agonists and glucocorticoids.

36
Q

Describe the mechanism of action of methylxanthines.

A

Methylxanthines inhibit mediator release from mast cells, increase mucus clearance, increase diaphragmatic contractility and reduce fatigue. They are thought to potentiate the anti-inflammatory action of glucocorticoids.

37
Q

Describe the side effects of methylxanthines.

A

Methylxanthines have a very narrow therapeutic index and may cause dysrhythmias, seizures, hypotension, nausea, vomiting, abdo. discomfort and headaches. They have numerous drug interactions, particularly with antibiotics inhibiting CYP450s.

38
Q

What is the role of glucocorticoids in the body?

A

Glucocorticoids are steroid hormones produced by the adrenal cortex. Main glucocorticoid is cortisol, which reduces inflammatory and immunological responses.

39
Q

Give examples of synthetic derivatives of cortisol.

A

E.g. include beclometasone, budesonide, fluticasone. Used as anti-inflammatory drugs in asthma.

40
Q

Why are synthetic derivatives of cortisol, rather than cortisol itself used in the treatment of asthma?

A

Cortisol has no direct bronchodilator action and are thus ineffective at relieving acute bronchospasm.

41
Q

Why is inhaled glucocorticoid administration preferred in mild/moderate asthma?

A

Inhaled administration minimizes unwanted systemic effects. They prevent inflammation and resolve any existing inflammation. Efficacy develops over several days.

42
Q

Common side effects of glucocorticoids?

A

Dysphonia and oropharyngeal candidiasis,

43
Q

What is the mechanism of action of glucocorticoids?

A

Glucocorticoids reduce production of TH2 cytokines, prevent IgE production and reduce mast cells and Fc expression. They also prevent allergen induced eosinophil influx into the lungs.

44
Q

What is the molecular mechanism of action of glucocorticoids?

A

Glucocorticoids are lipophilic and enter cells by diffusion. They are activated in the cytoplasm and translocate to the nucleus aided by importins. In the nucleus, they assemble into homodimers and bind to glucocorticoid response elements (GRE) in the promotor region of specific genes, causing their transcription to switch on or off, altering mRNA levels and rate of synthesis of mediator proteins.

45
Q

Account for the clinical use of glucocorticoids in asthma.

A

Glucocorticoids are effecting long-term treatment options (particularly when combined with LABA).
Used in mild/moderate asthma as preventers.

In chronic, severe or rapidly deteriorating asthma oral prednisolone may be used alongside ICS.

46
Q

When is cromoglycate used in the treatment of asthma?

A

e.g. sodium cromoglycate. Infrequently used prophylactically in the treatment of allergic asthma in children. They reduce both phases of an asthma attack, but efficacy can take weeks to develop and requires frequent dosing.

47
Q

When are monoclonal antibodies used in the treatment of asthma?

A

Monoclonal antibodies, e.g. omalizumab. They are used in asthma associated with severe eosinophilia. They suppress mast cell response to allergens, require IV administration and are very expensive.

48
Q

Outline the treatment of asthma.

A

Avoid triggers.

  1. Salbutamol (SABA).
    • Beclometasone (ICS).
    • Salmeterol or formeterol (LABA), if ineffective increase ICS dose.
    • montelukast or theophylline.
    • oral prednisolone (steroid) and refer to specialist care.
49
Q

Describe corticosteroid use in asthma and COPD.

A

They may cause pneumonia in COPD.
Oral, e.g. prednisolone has a low therapeutic ratio and should only be used in acute exacerbations.
Inhaled, e.g. beclomethasone, is used as maintenance monotherapy in asthma. Or in combo. with LABA in COPD to reduce eosinophilic COPD exacerbations.

50
Q

Actions of a spacer device.

A
  1. Overcomes coordination issues with pMDI.
  2. Reduces oropharyngeal and laryngeal side effects.
  3. Reduces systemic absorption from swallowed fraction.
  4. Holding chamber for aerosol.
  5. Reduces particle size and velocity.
  6. Improves lung deposition.
51
Q

What are cysteinyl leukotrienes generated by?

A

Inflammatory cells, e.g. mast cells and eosinophils.

52
Q

Overview of anti-inflammatory anti-IL5.

A

E.g. mepolizumab and reslizumab.
They inhibit IL-5 responsible for eosinophilic inflammation in asthma. Require injection every 4 weeks for severe refractory eosinophilic asthma despite max. therapy. Reduces exacerbations and are oral steroid sparing.

53
Q

Decribe muscarinic (cholinergic) receptors: M1, M2 and M3.

A

M1 receptors enhance cholinergic transmission.
M2: inhibit acetyl choline release.
M3: mediates bronchoconstriction and mucus secretion.

54
Q

Describe muscarinic antagonists mechanism of action.

A

Muscarinic antagonists block post-junctional end plate M3 receptors.

55
Q

Give an example of a short acting muscarinic antagonist.

A

Ipratropium is a SAMA. It is a non-selective muscarinic antagonist and should not be used in conjunction with LAMA.

56
Q

Give an example of a long acting muscarinic antagonist.

A

Tiotropium, glycopyrronium and aclidinium are all LAMA.

57
Q

Uses of muscarinic antagonists.

A

Asthma: tiotropium as triple therapy at step 4 (ICS+LABA+LAMA).
COPD: reduce exacerbations.
Acute COPD or acute asthma: high nebulized doses of ipratropium (SAMA).

58
Q

Give examples and uses of mucolytics.

A

Oral carbocisteine and erdosteine, reduce sputum viscosity and aide sputum expectoration. Also reduce exacerbations in COPD. Used rarely, and as an add-on to other treatments.

59
Q

Treatment of acute asthma.

A
  1. Oral prednisolone or IV hydrocortisone.
  2. Nebulised high dose salbutamol +/- neb. ipratropium +/- IV aminophylline/magnesium.
  3. min. of 60% O2.
  4. ITU assisted mechanical intubated ventilation if falling PaO2 and rising PaCO2.
60
Q

COPD treatment.

A 
Smoking cessation
Immunisation
Pharmacotherapy
Pulmonary rehab
Oxygen
61
Q

COPD treatment.

A

A: SAMA/ SABA prn.
B: LAMA
C: LABA/LAMA or ICS/LABA
D: ICS/LAMA/LABA

62
Q

Acute COPD treatment.

A
  1. Neb. high dose salbutamol + ipratropium.
  2. Oral prednisolone
  3. Antibiotic (amoxicillin/doxycycline) if infection
  4. 24-28% O2 titrated against PaO2/PaCO2.
  5. Physio for sputum expectoration.
  6. Non-invasive ventilation to raise FiO2.
  7. ITU intubated assisted ventilation - only if reversible component, e.g. pneumonia.
63
Q

What is the effect of blocking M3 cholinergic receptors?

A

Stops contraction of airway smooth muscle.

64
Q

Pathology of allergic rhinitis.

A

Acute/chronic inflammation of nasal mucosa. Allergen inhalation increases IgE, which binds to mast cells and basophils. Allergen re-exposure causes mast cell and basophil degranulation. Mediator release, e.g. histamine, cause acute sneezing, itching, rhinorrhea and nasal congestion. Delayed lymphocyte and eosinophil recruitment to nasal mucosa increases congestion.

65
Q

Pathology of non-allergic rhinitis.

A

Refers to acute/chronic rhinitis in which IgE is not involved. May result from infection, hormonal imbalance, vasomotor disturbances and medications. May be: non-allergic rhinitis with eosinophilia syndrome.

66
Q

treatment of rhinitis.

A

glucocorticoids- inflammation.
H1 and CysLT1 receptor antagonists- block mediator receptors.
Vasoconstrictors - reduce nasal blood flow.
Sodium cromoglycate - anti-allergic.
Muscarinic receptor antagonists.

67
Q

Mechanism of anti-histamines (H1-receptor antagonists).

A

Reduce effects of mast cell derived histamine. Administered orally or as an intranasal spray. Examples include loratidine, cetirizine and fexofenadine.

68
Q

Mechanism of action of muscarinic receptor antagonists in treatment of rhinitis.

A

Blocks muscarinic receptors from producing secretions. Administered nasally. May dry out nasal membranes. E.g. ipratropium.

69
Q

Mechanism of action of cysteinyl leukotriene receptor antagonists in treatment of rhinitis.

A

reduce cysLTs effects on nasal mucosa. oral administration. E.g. montelukast.

70
Q

Mechanism of action of vasoconstrictors in treatment of rhinitis.

A

Vasoconstrictors mimic the effects of noradrenaline. To decrease swelling and congestion of vascular mucosa. E.g. oxymetazoline (alpha-1-selective). Should be used short-term.

71
Q

Oxygen travels in blood:

A
  1. bound to haemoglobin

2. dissolved in plasma.

72
Q

Define SaO2.

A

SaO2 is oxygen saturation of arterial blood.

73
Q

Define SpO2.

A

SpO2 is oxygen saturation detected by a pulse oximeter.

74
Q

Define PaO2.

A

PaO2 is the amount of oxygen dissolved in arterial blood plasma.

75
Q

Define FiO2.

A

FiO2 is the fraction of inspired oxygen. It is a fraction of the amount of oxygen a patient is inhaling produced by an oxygen device e.g. nasal cannula or mask.

76
Q

Note when giving COPD patients oxygen:

A

They are patients with chronic type 2 respiratory failure, and are thus sensitive to high concentrations of inspired oxygen. They develop hypercapnia (CO2 retention) and quickly become acidotic.

77
Q

symptoms of hypoxaemia?

A

Altered mental state, cyanosis, dyspnea, tachypnea, arrhythmias.

78
Q

oxygen targets for a COPD patient?

A

SpO2 of 88-92%.

79
Q

Oxygen targets in a normal individual?

A

94-98%.

80
Q

advantages and disadvantages of nasal cannulae?

A

Nasal cannulae are well tolerated, but capable of low flow only. FiO2 cannot be controlled and they are dependent on nasal breathing.

81
Q

Variable performance mask advantages and disadvantages?

A

Cheap, simple to use, flow rate of 5-15L/min. FiO2 cannot be controlled, and they are unable to cope with high flow.

82
Q

Venturi mask pros and cons?

A

Fixed performance, with flow rates of up to 25L/min.

83
Q

Non-rebreather mask pros and cons?

A

Up to 85% FiO2, uncontrolled FiO2. Flow is limited to the outflow of the wall.

84
Q

side effects of rifampicin.

A

Colours all bodily fluids orange, potent inducer of cytochrome enzymes including hormonal contraception.

85
Q

Side effects of ethambutol.

A

Optic neuritis.

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