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Medicine Respiratory > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Where are the cell bodies of the preganglionic and postganglionic fibres located?

A

Preganglionic - brainstem

Postganglionic - walls in bronchi and bronchioles

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2
Q

Which receptor is involved in bronchial smooth muscle contraction stimulated by postganglionic cholinergic fibres?

A

M3 muscarinic ACh receptors on ASM cells

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3
Q

Which receptor is involved in increased mucus secretion stimulated by postganglionic cholinergic fibres?

A

M3 muscarinic ACh receptors on goblet cells

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4
Q

What does stimulation of postganglionic non-cholinergic fibres cause?

A

Bronchial smooth muscle relaxation mediated by nitric oxide and vasoactive intestinal peptide

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5
Q

What does contraction of smooth muscle result from?

A

Phosphorylation of the regulatory myosin light chain in the presence of elevated intracellular calcium

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6
Q

What does relaxation of smooth muscle result from?

A

Dephosphorylation of the myosin light chain by myosin phosphatase

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7
Q

Changes in bronchioles that lead to chronic asthma

A
  • Increased mass of smooth muscle
  • Acculumulation of interstitial fluid
  • Increased secretion of mucous
  • Epithelial damage
  • Sub-epithelial fibrosis
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8
Q

Bronchial hyper-responsiveness in asthma

A

Epithelial damage exposes sensory nerve endings that contributes to increased sensitivity of the airways to bronchoconstrictor influences.

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9
Q

Which tests reveal hyper-responsiveness in asthma

A

Provocation tests with inhaled bronchoconstrictors

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10
Q

2 components which result in bronchial hyper-responsiveness in asthma

A

Hypersensitivity and hyper-reactivity

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11
Q

What type of hypersensitivity reaction is the early phase of an asthma attack vs the late phase of an asthma attack

A 
Early = type I hypersensitivity
Late = type IV hypersensitivity
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12
Q

Immune imbalance in asthma - 2 pathways and what they are mediated by

A

Low level TH1 response - cell mediated immune response involving IgG and macrophages
High level TH2 response - anti-body mediated immune response involving IgE

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13
Q

Development of allergic asthma

A

Induction phase - initial presentation of an antigen imitates an adaptive immune response
Effector phase - eosinophils differentiate and activate in response to IL-5 released from TH2 cells, mast cells in airway tissues express IgE receptors in response to IL-4 and IL-13 released from TH2 cells
Subsequent presentation of antigen

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14
Q

In allergic asthma, what does the presentation of the antigen do?

A

Cross-links IgE receptors

Stimulates calcium entry into mast cells and releases calcium from intracellular stores

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15
Q

In allergic asthma, what does the increase in calcium evoke?

A

Release of secretory granules containing preformed histamine and production of other agents that cause smooth muscle contraction
Release of substances that attract cells causing inflammation into the area

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16
Q

2 types of drugs used in the treatment of asthma

A

Relievers (act as bronchodilators) and controllers/preventers (act as anti-inflammatory agents that reduce airway inflammation)

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17
Q

Which drugs are relievers in the treatment of asthma?

A

Short acting beta-2-adrenoreceptor agonists, long acting beta-2-adrenoreceptor agonists, CysLT1 receptor agonists

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18
Q

Which drugs are controllers/preventers in the treatment of asthma?

A

Glucocorticoids, cromoglicate, humanised monoclonal IgE antibodies

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19
Q

Which drug acts as a reliever and a controller/preventer in the treatment of asthma?

A

Methylxanthines

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20
Q

What do beta-2-adrenoreceptor agonists act as?

A

Physiological antagonists of all spasmogens

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21
Q

SABAs:

  • Example
  • When and how they are taken
  • How often after administration they react
  • What they do
  • Side effects
A
  • Salbutamol
  • First line treatment for mild, intermittent asthma, usually administered by inhalation as and when patient needs
  • Act rapidly (within 5 minutes), maximal effect in about 30 mins and last for about 3-5 hours
  • Relax bronchial smooth muscles, increase mucus clearance and decrease mediator release from mast cells and monocytes
  • Have few adverse effects, fine tremor (common), tachycardia, dysrhythmia and hypokalaemia (rarer)
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22
Q

LABAs:

  • Examples
  • When they are taken
  • How long they react for
  • What they should be co-administered with
A
  • Salmeterol, formoterol
  • At night - useful for nocturnal asthma
  • Around 8 hours
  • Glucocorticoid
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23
Q

Why is the use of non-selected beta-adrenoreceptor antagonists (non-selective beta blockers) contraindicated in patients with asthma?

A

There is a risk of bronchospasm

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24
Q

CysLT1 receptor antagonists:

  • Where do they act?
  • What are they derived from?
  • What do they do?
A
  • They competitively at CysLT1 receptor
  • Mast cells and infiltrating inflammatory cells
  • Cause smooth muscle contraction, mucous secretion and oedema
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25
Q

CysLT1 receptor antagonists:

  • Examples
  • At which stage are they added to therapy?
  • What are they effective against?
  • Administration
  • Side effects
A
  • Montelukast, zafirlukast
  • Add on therapy against early and late bronchospasm in mild persistent asthma and in combination with other medications in more severe conditions
  • Antigen induced and exercise induced bronchospasmm
  • Administered orally
  • Generally well tolerated, headache and GI upset
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26
Q

Methylxanthines:

  • Examples
  • Beverages which contain them
  • When are they introduced?
  • Administration
  • Side effects
A
  • Theophylline, aminophylline
  • Present in tea, coffee and chocolate containing beverages
  • Second-line drugs used in combination with beta-2-adrenoreceptor agonists and glucocorticoids
  • Administered orally
  • Very narrow therapeutic window. Above window causes dysrhythmia, seizures, hypotension. At therapeutic range cause nausea, vomiting, abdominal discomfort, headache
27
Q

What do methylxanthines do?

A

Inhibit mediator release from mast cells, increase mucus clearance
Increase diaphragmatic contractility and reduce fatigue - may improve lung ventilation

28
Q

What does cortisol (made by the body) do?

A

Regulates numerous processes e.g. decrease inflammatory responses, decrease immunological responses, increase liver glycogen deposition, increase gluconeogenesis

29
Q

What do mineralocorticoids do?

A

Regulate the retention of salt and water by the kidney

30
Q

How do glucocorticoids enter the cell?

A

They are lipophilic molecules that enter the cell by diffusion across the plasma membrane

31
Q

Glucocorticoid role in inflammation in asthma

A

They increase transcription of genes encoding anti-inflammatory proteins and decrease transcription of genes encoding inflammatory proteins

32
Q

Glucocorticoids:

  • Examples
  • At what stage are they given?
  • Administration
  • How long does it take to reach maximum efficiency?
  • Side effects
A
  • Beclometasone, budenoside, fluticasone
  • Mild/moderate asthma
  • Given by inhalation from a metered dose inhaler
  • Efficacy develops over several days
  • Dysphonia (weak and hoarse voice) and oropharyngeal candidiasis (thrush)
33
Q

What is COPD characterised by?

A

Airflow reduction that is in some patients partially reversible (with bronchodilators) but which progressively worsens as assessed by FEV1 and exacerbations of symptoms including cough and mucus production
Increased resistance to air flow during expiration

34
Q

M1, M2 and M3 muscarinic receptors:

- Where are they located and what are their functions?

A

M1 - ganglia - facilitates the fast neurotransmission mediated by ACh acting on nicotinic receptors
M2 - postganglionic neurone terminals - act as inhibitory auto receptors reducing release of ACh
M3 - ASM - mediate contraction to ACh

35
Q

Drugs used in the treatment of COPD and how they are administered

A

Short-acting muscarinic antagonists and long-acting muscarinic antagonists. All administered by inhalation

36
Q

Short-acting muscarinic antagonist example

A

Ipratropium

37
Q

Long-acting muscarinic antagonist examples

A

Tiotropium, Glycopyrronium, Aclidinium, Umeclidinium

38
Q

What do muscarinic receptor antagonists do?

A

Reduce bronchospasm caused by irritant stimuli and also block ACh mediated basal tone, decrease mucus secretion

39
Q

Why are M3 receptor blockers superior to ipratropium?

A

Ipratropium is non-selective and blocks M1, M2 and M3 receptors. Block of M2 is not desirable because release of ACh from parasympathetic post-ganglionic neurones is increased by autoreceptor antagonism

40
Q

Why can it be effective to prescribe a combination of muscarinic antagonist and beta-2 agonist in the treatment of COPD?

A

B-2 agonists provide bronchodilatation but have no effect on the underlying inflammation. A combination of both drugs is superior to either drug alone in increasing FEV1

41
Q

When are LABA/LAMA combinations most likely to be effective in treating COPD?

A

When both drugs are deposited in the same location in the airways

42
Q

What suffix is associated with muscarinic antagonists?

A

-ium

43
Q

What suffix is associated with beta-2 agonists?

A

-ol

44
Q

When are glucocorticoids of benefit in the treatment of COPD?

A

In patients who develop frequent and severe exacerbations. They are given with a LABA

45
Q

What may glucocorticoid unresponsiveness be due to in patients with COPD?

A

Oxidative/nitrative stress

46
Q

Rofumilast:

  • What type of drug is it?
  • What is it used in the treatment of?
  • What does it do?
  • When is it given?
  • Side effects
A
  • PDE4 inhibitor
  • COPD
  • Suppresses inflammation and emphysema
  • Given as oral treatment in patients with severe COPD accompanied by chronic bronchitis
  • Limiting adverse gastrointestinal effects
47
Q

Rhinitis

A

Common and often debilitating disease involving acute or chronic inflammation of the nasal mucosa which is characterised by rhinorrhea, sneezing, itching and nasal congestion and obstruction

48
Q

3 classifications of allergic rhinitis

A

Seasonal, perennial, episodic

49
Q

Pathology of allergic rhinitis

A
  • Inhalation of allergen increases specific IgE levels
  • IgE binds to receptors on mast cells and basophils
  • Re-exposure to antigen causes mast cell and basophil degranulation
  • Release of mediators incl. histamine, cysLTs, tryptase, prostaglandins causes acute itching, sneezing etc
  • Delayed response caused by recruitment of lymphocytes and eosinophils to nasal mucosa contributing to nasal congestion and obstruction
50
Q

Non-allergic rhinitis

A

Any rhinitis that does not involve IgE dependent events

51
Q

Causes of non-allergic rhinitis

A
  • Infection (infectious rhinitis)
  • Hormonal imbalance (hormonal rhinitis - pregnancy)
  • Vasomotor disturbances (vasomotor rhinitis)
  • Non-allergic rhinitis with eosinophilia syndrome
  • Medications - drug induced rhinitis
52
Q

Anti-inflammatory treatment in rhinitis and rhinorrhoea

A

Glucocorticoids

53
Q

Mediator receptor blockade treatment in rhinitis and rhinorrhoea

A

H1 receptor antagonists, CysLT1 receptor antagonists

54
Q

Nasal blood flow treatment in rhinitis and rhinorrhoea

A

Vasoconstrictors

55
Q

Anti-allergic treatment in rhinitis and rhinorrhoea

A

Sodium cromoglicate

56
Q

Mechanism of glucocorticoids in rhinitis and rhinorrhoea

A

Reduce vascular permeability, recruitment and activity of anti-inflammatory cells and the release of cytokines and mediators

57
Q

Glucocorticoids - rhinitis:

  • Administration
  • What types of rhinitis are they used in?
  • How long does it take to work?
  • Examples
A
  • Most frequently applied topically as a spray to nasal mucosa
  • SAR, PAR, and sometimes NARES and vasomotor rhinitis
  • Over several weeks reduces all symptoms of rhinitis
  • Beclometasone, fluticasone, prednisolone (oral. Used in very severe intractable cases)
58
Q

Mechanism of antihistamines (H1 receptor antagonists) in rhinitis

A

Competitive antagonists that reduce effects of mast cell derived histamine including vasodilation and increased capillary permeability, activation of sensory nerves, mucus secretion from submucosal glands

59
Q

Antihistamines (H1 receptor antagonists) - rhinitis:

  • Administration
  • What type of rhinitis are they used in?
  • Examples
A
  • Orally or as an intranasal spray
  • SAR, PAR, EAR
  • Loratidine, fexofenadine, cetirizine, azelastine (intranasal)
60
Q

Mechanism of anti-cholinergic drugs (muscarinic receptors) in rhinitis

A

Block ACh released from post-ganglionic parasympathetic fibres activates muscarinic receptors on nasal glands causing a watery secretion that contributes to rhinorrhoea

61
Q

Anti-cholinergic drugs - rhinitis:

  • Administration
  • What types of rhinitis are they used in?
  • Adverse effects
  • Example
A
  • Administered intranasally
  • PAR and SAR but have no influence upon itching, sneezing and congestion
  • Dryness of nasal membranes
  • Ipratropium
62
Q

Sodium cromoglicate - rhinitis:

  • Potential mechanism
  • What type of rhinitis is it used in?
  • How long does it take to work?
  • Administration
A
  • Purportedly mast cell stabilisation
  • Allergic
  • Onset action of 4-7 days but weeks may be required for full effect
  • Nasal administration - but less effective than nasal corticosteroids
63
Q

Leukotriene receptor antagonists - rhinitis:

  • Mechanism
  • What types of rhinitis are they used in?
  • Administration
  • In which patients should this therapy be considered?
  • Example
A
  • Reduce the effects of CysLTs upon the nasal mucosa
  • PAR and SAR
  • Orally
  • Patients with allergic rhinitis and asthma
  • Montelukast
64
Q

Vasoconstrictors - rhinitis:

  • Mechanism
  • Example
  • Administration
A
  • Mimic the affect of noradrenaline. Produce vasoconstriction via activation of alpha-1 adrenoceptors to decrease swelling in vascular mucosa
  • Oxymetazoline - effective short-term in treating congestion in allergic rhinitis
  • Intranasally

Medicine Respiratory (12 decks)

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