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Respiratory > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Transmission occurs between which fibres?

A

pre-ganglionic and post-ganglionic fibres

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2
Q

True/False:

Bronchial smooth muscle is innervated

A

False:

It isn’t

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3
Q

What 2 types of post-ganglionic fibres are there

A

cholinergic and non-cholinergic

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4
Q

what do cholinergic fibres do…

A

Mediated by Muscarinic Receptors

  • Bronchial SM contraction (M3 receptors on ASM)
  • Inc mucus secretion (M3 on gland cells)
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5
Q

What do non-cholinergic fibres do…

A

Mediated by B2 ADRs

  • Bronchial SM relaxation
  • Dec mucus secretion
  • Inc mucociliary escalator
  • Vascular SM contraction (A1 ADR)
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6
Q

How is SM contraction controlled?

A
  1. G protein converts Gg/11 to PLC
  2. PLC converts PIP2 to IP3
  3. IP3 binding to receptor triggers Ca2+ release
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7
Q

How does SM contract?

A
  1. Ca2+ > calmodulin Ca2+
  2. Calmodulin Ca2+ activated MLC Kinase
  3. MLC Kinase modulates binding of ATP to activate
  4. Myosin cross bridge
    - MLCK regulated by adrenaline
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8
Q

How does SM relax?

A

De-phosphorylation of MLCK by myosin phosphatase achieved by Ca2+ returning to basal levels.

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9
Q

What is Asthma?

A

Reversible obstruction of airways due to antigen (bronchoconstriction)

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10
Q

2 types of asthma are…

A

Intermittent: tight chest, wheeze, cough (can come on when cold or exercise)
Chronic: changes to bronchioles

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11
Q

What are some changes that can come about to bronchioles in chronic asthma?

A
  1. Inc in SM
  2. Inc in mucus secretion
  3. Epithelial damage
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12
Q

What’re the 2 phases of an asthma attack and what do they consist of?

A

Immediate Phase: bronchospasm

Delayed Phase: inflammatory reaction

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13
Q

What is allergic asthma?

A

Asthma caused by an antigen and immune response kicks in

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14
Q

True/False:

TH2 response occurs in severe asthma and forms IgG antibodies

A

False:
TH2= mild asthma, IgE
TH1= severe, IgG

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15
Q

Explain the pathogenesis of allergic asthma in terms of

  • Induction
  • Clonal Expansion & Maturation
  • Effector Phase
A
  1. Antigen binds to CD4+ T-Cells which cause the T cells to divide into TH0 helper T cells
    TH0 then mature into TH2 cells
  2. Some TH0 become TH1 cells, while most become TH2 which activate B-Cells which themselves become plasma cells
  3. Eosinophils activate (due to TH2 & IL-5)
    Mast cells degranulate (due to IgE binding to receptor)
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16
Q

How are IgE receptors expressed?

A

In response to IL-4 and IL-13 being released by TH2

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17
Q

*How is a memory reaction instigated?

A
  • Cross-linking of IgE receptors cause Ca2+ influx
  • This causes degranulation of pre-formed histamine and other inflammatory agents
  • These cause SM contraction
  • & Platelets and prostaglandins are released which attract inflammatory cells
18
Q

True/False:

Agonist mimics normal action

A

True

Antagonist blocks normal action

19
Q

What is the treatment for asthma

A

Bronchodilators: B2 ADR Agonists, CystLT1 Antagonist, xanthines
Anti-inflammatories: Glucocorticoids, Mineralocorticoids
Cromoglycate & Omalizumab

20
Q

Give a run down of SABA?

A 
SABA
e.g: Salbutamol 
Used for: mild asthma 
Admin: Inhaled
Why g: Rapid 
Adverse Effects: Tremors, Tachycardia
21
Q

Give a run down of LABA?

A 
e.g: Salmeterol 
Used for: chronic asthma 
Admin: Inhaled 
Why g: Nocturnal asthma 
Note: taken as dual therapy with glucocorticoids
22
Q

Give a run down of CysLT1 Antagonists

A 
Eg: Montelukast 
Used for: mild asthma, exercise induced bronchoconstriction 
Admin: Oral
Why g: infiltrates inflammatory cells 
SE: may cause oedema
23
Q

How does the mixed asthma treatment Xanthines work?

A

Inactivates cAMP and cGMP

24
Q

Give a run down on Glucocorticoids

A

Examples: Prednisolone
Used for: mild asthma
Admin: Inhaled
Why g: inflammatory and immunological responses decrease

25
Q

Why are mineralocorticoids contraindicated?

A

Have many side effects so usually Cortisol used as mixed treatment

26
Q

What are cromoglycate and omalizumab used for?

A

Allergic asthma- reduce immune response.

27
Q

How do glucocorticoids work cellularly?

A
  • inc transcription of anti-inflammatory proteins, dec transcription of inflammatory proteins
  • induce inflammatory cells to undergo apoptosis
28
Q

What is COPD?

A

chronic bronchitis and emphysema

inc resistance to airflow during expiration

29
Q

True/False:

COPD neurotransmission involves Ach binding to M3 muscarinic receptors causing bronchoconstriction

A

True

30
Q

Where are M1 receptors located and what do they do?

A

Ganglia; act on nicotine receptors

31
Q

Where are M2 receptors located and what do they do?

A

Post-ganglionic terminals; inhabit further release of Ach

32
Q

Where are M3 receptors located and what do they do?

A

ASM; airway SM contraction & inc in mucus secretion

33
Q

What is the overview for COPD treatment…

A

Muscarinic Receptor Antagonists, Glucocorticoids and phosphodiesterase inhibitors

34
Q

Give a run down of SAMA drugs…

A 
e.g: Ipratropium 
Used for: Bronchodilation 
Admin: Inhaled 
Why g: Reduces mucus secretion
- Palliative
35
Q

Give a run down of LAMA drugs…

A 
e.g: Tiotropium 
Used for: Bronchodilation 
Admin: Inhaled 
Why g: Reduces mucus secretion 
- Palliative
36
Q

Why is it good to have a selective muscarinic receptor antagonist?

A

Because ideally M3 receptor should be blocked but not M2 as if M2 is also blocked then more Ach is released (causing more constriction) contradicting the antagonists effect

37
Q

How is muscarinic antagonist selectivity achieved?

A

Through rate of association and dissociation of antagonist to receptor

38
Q

Why are combination drugs more desirable?

A

B2 ADR agonists cause more bronchodilation and M3 Muscarinic antagonists cause less bronchoconstriction. Best at inc FEV1 by promoting ASM relaxation

39
Q

How do glucocorticoids and phosphodiesterase inhibitors work as treatment for COPD?

A

inflammatory suppressors. Usually added onto SAMA/LAMA.

40
Q

Give 4 similarities between rhinitis and asthma…

A
  1. Allergen inc IgE levels
  2. IgE binds to basophils and mast cells
  3. Re-exposure causes rapid degranulation of inflammatory mediators by immune cells- sneezing etc
  4. Delayed recruitment of lymphocytes and eosinophils causes congestion

Respiratory (19 decks)

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