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Respiratory System > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

How does the parasympathetic division causes changes in the respiratory system?

A

Stimulation of cholinergic and noncholinergic fibres

  • Stimulation of postganglionic cholinergic fibres causes:
    • bronchial smooth muscle contraction
      • mediated by M3 muscarinic ACh receptors on ASM cells
    • increased mucus secretion
      • mediated by M3 muscarinic ACh receptors on goblet cells
  • Stimulation of postganglionic noncholinergic fibres causes
    • bronchial smooth muscle relaxation mediated by nitric oxide and vasoactive intestinal peptide
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2
Q

Where cell bodies of preganglionic and postganglionic located in the parasympathetic division of the resp. system?

A
  • Cell bodies of the preganglionic fibres are located in the brainstem
  • Cell bodies of the postganglionic fibres are embedded in walls of the bronchi and bronchioles
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3
Q

Adrenaline kickstarts a chain of reactions to relax bronchial smooth muscle. What is the end result of these chain reactions?

A
  1. Inhibits myosin light chain kinase to inhibit contraction
  2. Stimulates myosin phophatase to facilitate relaxation
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4
Q

Is there sympathetic innervation of bronchial smooth muscle in humans?

A

NO

Post-ganglionic fibres supply:

  1. submucosal glands
  2. smooth muscle of blood vessels
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5
Q

What does stimulation of sympathetic division cause in the resp. system?

A
  • Bronchial smooth muscle relaxation via B2-adrenoreceptors on ASM cells activated by adrenaline released from the adrenal gland
  • Decreased mucus secretion mediated by B2-adrenoreceptors on goblet cells
  • Increased mucociliary clearance mediated by B2-adrenoreceptors on epithelial cells (mucociliary escalator)
  • vascular smooth muscle contraction by a1-adrenoreceptors on vascular smooth muscle cells
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6
Q

How does smooth muscle contraction occur?

A
  1. Increased intracellular Ca2+
  2. Calmodulin –> Ca2+-calmodulin
  3. Inactive MLCK –> Active MLCK
  4. ATP degrades to ADP and Phosphate
  5. Inactive myosin cross bridge becomes phosphorylated
  6. Phosphorylated myosin cross bridge binds with actin

Actin and myosin filaments of muscle ‘slide’ across each other to genrate force- contraction.

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7
Q

If contraction results from phosphorylation of the regulatory myosin light chain in the presence of elevated Ca2+ and ATP; what causes relaxation?

A

Relaxation results from dephosphorylation of myosin light chain by myosin phosphatase

In the presence of elevated intracellular Ca2+ the rate of phosphorylation exceeds the rate of dephosphorylation so relaxation requires return of intracellular Ca2+ concentration to basal level

This is achieved by primary and secondary active transport

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8
Q

Define asthma

A

Is a recurrent and reversible (in the short term) obstruction to the airways in response to substances (or stimuli) that: -are not necessarily noxious -normally do not affect non-asthmatic subjects

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9
Q

What are some of the common causes of asthma?

A

-allergens (in atopic individuals) e.g. dust mite faeces & pollen -exercise (cold, dry air) -respiratory infections (e.g. viral) -smoke, dust, environmental pollutants etc.

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10
Q

What is the incidence of asthma?

A

Affects 5-10% of the population in industrialized countries

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11
Q

List four symptoms of asthma

A
  1. Tight chest
  2. Wheezing
  3. Difficulty in Breathing
  4. Cough
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12
Q

What pathological changes to the bronchioles occur from long standing inflammation associated with chronic asthma?

A
  1. Increased mass of smooth muscle -hyperplasia & 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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13
Q

What effect does asthma have on PEFR and FEV1?

A
  • Decreases FEV1
  • Decreases PEFR

Airway narrowing by inflammation and bronchoconstriction increase airway resistance which decreases FEV1 and PEFR

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14
Q

What are the two wings of bronchial hyper-responsiveness?

A
  1. Hypersensitivity
  2. Hyper-reactivity
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15
Q

Explain what is meant by ‘bronchial hyper-responsiveness’.

A

Epithelial damage exposes sensory nerve endings which contributes to increased sensitivity of the airways to bronchoconstrictor influences and may cause neurogenic inflammation by the release of various peptides

Hyper-Responsiveness

As seen in the graph, this increases the extent of the response and so increases the % decrease in PEFR

Hyper-sensitivity

As seen in the graph, this means a lower concentration of the antigen is required for a response

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16
Q

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

A

Tyoe 1

17
Q

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

A

Type IV

18
Q

What is one major caues of asthma thought to be?

A

An immune inbalance between TH1 and TH2 lymphocyte-mediated responses

19
Q

Describe the events that occur subsequent to TH2 lymphocyte activation.

A
  1. Activated TH2 cells activate B cells by binding to them and by IL-4 production
  2. B Cells mature to IgE secreting Plasma cells

Meanwhile

  1. Activated TH2 cells also release IL-5
  2. Which causes eosinophils to differentiate and activate in response to IL-5 released from TH2 cells

Meanwhile

  1. Activated TH2 cells also release IL-4 and IL-13
  2. Causes mast cells in airway tissue to express IgE receptors
  3. This stimulates calcium entry into mast cells and release of Ca2+ from intracellular stores evoking:
    • release of secretory granules which release histamine and LTC4 and LTD4
      • ^they cause airway smooth muscle contraction
    • release of substances (e.g. prostaglandin 2) that attract cells causing inflammation such as mononuclear cells & eosinophils
20
Q

What are the indications for a SABA? Also name one.

A

SABAs are first line treatment for someone suspected to have asthma

  • They have asthma symptoms
  • FEV1/FEV <70%

Salbutamol

21
Q

What is the mechanism of action of a SABA?

A

They act as physiological antagonists of all spasmogens

  • Inhibits muscle contraction by increasing intracellular cAMP which activates protein kinase
  • this inhibits muscle contraction by phosphorylating and inhibiting myosin-light-chain kinase

NB: reduction in intracellular Ca2+ conc. and activation of large conductance potassium channels are also involved

22
Q

When is a LABA indicated? Name one.

A

Used in asthma that is poorly controlled in people who are already on SABA and ICS. Must always be co-administered with ICS. Combination inhalers are preferable.

Useful for nocturnal asthma

Salmeterol

23
Q

What is the mechanism of action for a LABA?

A

Act as physiological anatagonists of all spasmogens

  • Activation of B2-adrenoreceptors relaxes smooth muscle by increasing intracellular cAMP which activates protein kinase
  • This inhibits muscle contraction by phosphorylating and inhibiting myosin-light-chain kinase

NB: reduction in intracellular Ca2+ concentration and activation of large conductance potassium channels are also involved

24
Q

When would an LTRA be indicated? Name one.

A

If a person is on SABA, ICS and LABA and there is benefit from LABA but control is still inadequate continue LABA and ICS and consider trail of LTRA

Montelukast

25
Q

What is the mechanism of action of LTRA?

A

LTRAs act competitively at CysLT1 receptor

CysLT1s are derived from mast cells and inflammatory cells causing:

  • smooth muscle contraction
  • mucus secretion
  • oedema
26
Q

Describe the role of glucocorticoids in the body.

A

The main glucocorticoid hormone is cortisol (hydrocortisone) which regulates numerous essential process:

  • inflammatory responses decrease
  • immunological responses decrease
  • gluconeogenesis increase
  • glucose output from liver increases
  • glucose utilization decreases
  • protein catabolism increases
  • bone catabolism increases
  • gastric acid and pepsin secretion increases
27
Q

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

A

Synthetic derivaties of cortisol such as beclometasone have little or no mineralocorticoid activity.

28
Q

Why is is the inhalational route of glucocorticoid administration favoured in the treatment of mild and moderate asthma?

A

To avoid systemic effects.

29
Q

Outline the molecular mechanism of action of the glucocorticoids

A
  1. Glucocorticoids enter cells by diffusion
  2. Combine with GRalpha
  3. Dissociation of inhibitory heat shock proteins
  4. Activated receptor translocate to nucleus
  5. Within nucleus activated receptor monomoers assemble into homodimers
  6. Bind to glucocorticoid response elements in promoter region of specific genes
  7. Transcription of specific genes is either ‘switched on’ or ‘switched off’ to:
    • alter mRNA levels
    • alter rate of synthesis of mediator proteins
30
Q

Give examples of the cellular effects that underlie the anti-inflammatory action of glucocorticoids

A

INFLAMMATORY CELLS

Eosinophil numbers decrease due to apoptosis

T-Lymphocytes produce less cytokines

Mast cells decrease in numbers

31
Q

Provide a brief account of the clinical use of glucocorticoids in asthma.

A

Indications/Place in Step-Up Therapy

No use in acute

Long term treatment effective

Administration

Inhalation to avoid systemic effects

Efficacy develops over several days

Adverse Effects

Dysphonia (hoarse and weak voice)

Oropharyngeal candidiasis (thrush)

32
Q
A

Respiratory System (12 decks)

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