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1ST YR RESP > Respiratory Pharmacology > Flashcards

Respiratory Pharmacology Flashcards

1
Q

Where are cell bodies of the preganglionic fibres located?

A

Located in the brainstem

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2
Q

What is a sympathetic response triggered by?

A

External stimuli

Causes smooth muscle relaxation

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3
Q

What does a parasympathetic response do?

A

Resets everything

Act through cholingeric neurones to stimulate muscle contraction

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4
Q

Where are the cell bodies of postganglionic fibres located?

A

Embedded in the walls of the bronchi and bronchioles

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5
Q

What does stimulation of postganglionic cholingeric fibres cause?

A
  • bronchial smooth muscle contraction (mediated by M3 muscarinic ACh receptors on ASM cells
  • Increased mucus secretion mediated by M3 muscarinic ACh receptors on gland (goblet) cells
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6
Q

What does stimulation of postganglionic noncholingeric fibres cause?

A
  • bronchial sooth muscle relaxation mediated by nitric oxide (NO) and vasoactive intestinal peptide (VIP)
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7
Q

Post ganglionic fibres supply what glands and muscle blood vessels?

A
  • Submucosal glands

- Smooth muscle

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8
Q

What does stimulation of autonomic transmitters (sympathetic) cause?

A
  • BRONCHIAL SMOOTH MUSCLE RELAXATION via Beta2-adrenoceptors on ASM cells activated by adrenaline released from adrenal gland
  • DECREASED MUCUS SECRETION mediated by beta2-ADR on gland (goblet) cells
  • INCREASED MUCOCILIARY SECRETION mediated by beta2-ADR on epithelial cells
  • VASCULAR SMOOTH MUSCLE CONTRACTION, mediated by alpha1-ADR on vascular smooth muscle cells
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9
Q

Contraction of smooth muscle results from what?

A

Phosphorylation

of the regulatory mysoin light chain (MLC) in the presence of elevated intracellular Ca2+ (and ATP)

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10
Q

Relaxation of smooth muscle results from what?

A

Dephosphorylation

of MLC by myosin phosphatase which has constitutive activity

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11
Q

What do activities of myosin light chain kinase (MLCK) and myosin phosphatase do to each other?

A

Oppose each other

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12
Q

What happens to the rate of phosphorylation in the presence of elevated intracellular Ca2+?

A

The rate of phosphorylation exceeds the rate of dephosphorylation

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13
Q

If the rate of phophorylation exceeds the rate of dephosphoryltion in the presence of elevated intraceullar Ca2+ what does relaxation of smooth muscle require?

A

The return of intracellular Ca2+ concentration to basal level - achieved by primary and secondary active transport

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14
Q

What is asthma (in the short term)?

A

A recurrent and reversible obstruction to the airways in response to substances that…

  • are not necessarily noxious
  • normally do not affect non-asthmatic subjects
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15
Q

What are the causes of asthma attacks?

A
  • Allergens (in atopic individuals)
  • Exercise (cold, dry air)
  • Respiratory Infections (e.g. viral)
  • Smoke, dust, environmental pollutants etc.
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16
Q

What are the symptoms of asthma? (intermittent attacks of bronchoconstriction)

A
  • tight chest
  • wheezing
  • difficulty in breathing
  • cough
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17
Q

Chronic asthma involves pathological changes such as…

A
  • increased mass of smooth muscle (hyperplasia and hypertrophy)
  • accumulation of interstitial fluid (oedema)
  • increased secretion of mucus
  • epithelial damage (exposing sensory nerve endings)
  • sub-epithelial fibrosis
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18
Q

Airway narrowing by inflammation and bronchoconstriction increase ______ decreasing ______ and ________

A
  • airway resistance
  • FEV1
  • Peak expiratory flow rate (PEFR)
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19
Q

Epithelial damage, exposing sensory nerve endings (C-fibres, inrritant receptors) contributes to what?

A

Increased sensitivity of the airways to bronchoconstrictor influences (and may cause) neurogenic inflammation by the release of various peptides

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20
Q

What are the two components of neurogenic inflammation?

A
  • Hypersensitivity

- Hyper-reactivity

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21
Q

Provocation tests for hypersensitivity and hyper-reactivity with inhaled bronchoconstrictors e.g. histamine or methacholine reveal what?

A
  • hyper-responsiveness
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22
Q

In many individuals, an asthma attack comprises what phases?

A
  • immediate (mainly bronchospasm)

- delayed (inflammatory reaction) phases

23
Q

What is IgE associated with?

A

Severe asthma

24
Q

What two general categories do drugs for treating asthma fall into?

A
  • Relievers

- Controllers/ Preventors

25
Q

What do relievers act as?

A

Relievers act as bronchodilators

26
Q

What are the three types of relievers?

A
  • Short acting beta2_ADR agonists (SABAs)
  • Long acting beta 2 adrenoreceptor agonists (LABAs)
  • CysLT1 receprots antagonists
27
Q

What do controllers/ preventors act as?

A

Act as anti-inflammatory agents that reduce airway inflammation

28
Q

What are the three types of controllers/ preventors?

A
  • Glucocorticoids
  • Cromoglicate
  • Humanised monoclonal IgE antibodies
29
Q

What are the bronchodilator drugs used in the treatment of asthma?

A
  • beta2-adrenoceptor agonists
  • CysLT1 Receptor antagonists
  • Xanthines
30
Q

Beta2-ADR agonists act as what?

A

Physiological antagonists of all spasmogens

31
Q

What are the three classifications of beta2-adrenoceptor agonists

A
  • Short-acting (SABA)
  • Long-acting (LABA)
  • Ultra long-acting (ultra-LABA)
32
Q

What drugs in the treatment of asthma are anti-inflammatory agents?

A

Corticosteroids

33
Q

What are the two different types of corticosteroids

A
  • Glucocorticoids

- Mineralcorticoids

34
Q

What do glucocorticoids regulate?

A

They regulate…

  • Inflammatory responses
  • Immunological responses
35
Q

What do mineralocorticoids regulate?

A

They regulate…

- The retention of salt (and water) by the kidneys

36
Q

Endogenous steroids may possess which kind of actions between glucocorticoids? and mineralocorticoids?

A

Possess both actions

37
Q

Which corticosteroid action is unwanted in the treatment of inflammatory conditions?

A

Mineralocorticoid actions

38
Q

What are synthetic divisions of cortisol with little or no mineralocorticoid activity frequently used for?

A

Used for their anti-inflammatory effect in the treatment of asthma

39
Q

Glucocorticoids are ineffective in relieving what?

A
  • Ineffective in relieving bronchospasm when giving acutely

- Have no direct bronchodilator action

40
Q

Muscarinic Acetylcholine receptors work where?

A

In the airways

41
Q

What can you do to the parasympathetic neuroeffector transmission to treat COPD?

A

Reducing parasympathetic neuroeffector transmission with muscarinic receptor antagonists

42
Q

Muscarinic receptor antagonists act as _________ antagonists of bronchoconstriction caused by what?

A
  • Pharmacological

- caused by smooth muscle M3 receptor activation in response to ACh released from postganglionic parasympathetic fibres

43
Q

What blocks muscarinic receptor antagonists?

A

Activation by ACh of the M3 muscarinic receptor

44
Q

What is the M1 muscarinic receptor expressed for?

A

M1 Ganglia

- facilitate fast neurotransmission mediated by ACh acting on nicotinic receptors (nAChR)

45
Q

What is the M2 muscarinic receptor expressed for?

A

M2 Postganglionic Neurone Terminals

- Act as inhibitory autoreceptors reducing release of ACh

46
Q

What is the M3 muscarinic receptor expressed for?

A

M3 ASM

- Mediate contraction to ACh (also present on mucus-secreting cells evoking increased secretion)

47
Q

What are the five drugs used in the treatment of COPD (Muscarinic Receptor antagonists)

A
  • Ipratropium
  • Tiotropium
  • Glycopyrronium
  • Aclidinium
  • Umeclidinium
48
Q

Name the short acting muscarinic antagonist(s) (SAMAs)

A

Ipratropium

49
Q

Name the Long Acting Muscarinic Antagonist(S) (LAMAs)

A
  • Tiotropium
  • Glycopyrronium
  • Aclidinium
  • Umeclidinium
50
Q

How are the drugs used to treat COPD (SAMAs and LAMAs) administered?

A

Administered by inhalation

51
Q

What does the quaternary ammonium group on the muscarinic anatgonists do?

A

Reduces absorption and systemic exposure avoiding mutliple potential adverse effects of a generalized parasympathetic block

52
Q

What do muscarinic receptor antagonits do?

A
  • Reduce bronchospasm caused by irritant stimuli
  • Block ACh-mediated basal tone
  • Decrease mucus secretion
  • Little effect on progression of COPD, effect is mainly palliative
53
Q

What is ipratropium?

A
  • non-selective blocker of M1, M2 and M3 receptors

- preferred agents with some selectivity for M3 are available

54
Q

Why are M3 selective blockers superior to Ipratropium?

A
  • Difference in rates of association and dissociation from the M3 receptor

1ST YR RESP (8 decks)

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