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My Respiratory > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the role of the parasympathetic division of the autonomic nervous system in the regulation of airway function and how does it do this?

A

causes bronchial smooth muscle contraction by M3 muscarinic ACh on ASM cells, increased mucus secretion by M3 ACh receptors on goblet cells

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2
Q

What is the role of the sympathetic division of the ANS in the regulation of airway function and how does it do this?

A

causes bronchial smooth muscle relaxation via beta 2 adrenoceptors on ASM activated by adrenaline, decreased mucus secretion by beta 2 adrenoceptoes on goblet cells and increased mucociliary clearance and vascular smooth muscle contraction by alpha 1 adrenoceptors

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3
Q

What is the principle transduction pathway that regulates airway smooth muscle tone?

A

a GPCR being activated to activate PLC which converts PIP2 to IP3 so Ca2+ ions are made, these bind to calmodulin and activate MLCK which causes myosin cross bridges to be phosphorylated so there is contraction

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4
Q

Under what conditions does contraction of airway smooth muscle occur?

A

after phosphorylation of the regulatory MLC in the presence of elevated Ca2+ and ATP

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5
Q

Under what conditions does relaxation of airway smooth muscle occur?

A

dephosphorylation of MLC by myosin phosphatase

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6
Q

What is the definition of asthma?

A

Asthma is a recurrent and reversible obstruction to the airways in response to substances that are not necessarily noxious

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7
Q

What is the incidence of asthma in the population?

A

5-10% in industrialised countries

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8
Q

What are the pathological changes in chronic asthma?

A
  • increased smooth muscle so hypertrophy and hyperplasia
  • accumulation of interstitial fluid
  • increased mucus
  • epithelial damage
  • sub epithelial fibrosis
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9
Q

What is bronchial hyper-responsiveness?

A

bronchial hyper-responsiveness is when the airways have increased sensitivity to bronchoconstrictor due to epithelial damage and the exposing of sensory nerve endings

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10
Q

What changes will be seen with hypersensitivity and hyper-reactivity on a graph?

A

hyper-reactivity causes a vertical increase on a graph

hypersensitivity causes a left shift

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11
Q

What is the major cause of asthma? (immunologically)

A

in asthma, there is a strong Th2 repose involving IgE in response to an allergen instead of the normal mild Th1 response with IgG and macrophages

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12
Q

Describe in detail the events that occur after Th2 cell activation in asthma…

A
  • Th2 cells activate B cells by binding and by IL4 production
  • B cells then mature to P cells which secrete IgE
  • mast cells then express IgE receptors in response to IL4 and IL13
  • eosinophils differentiate and activate in response to IL5 from Th2
  • calcium ions into mast cells and release of ions so histamine and leukotrienes
  • platelet-activating factor and prostaglandins released causing inflammation
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13
Q

What events occur in the immediate phase of an asthma attack?

A

allergen stimulating mast cells to produce spasmogens for bronchospasm and chemotaxis which then stimulate the late phase

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14
Q

What events occur in the late phase of an asthma attack?

A
  • infiltration of cytokine releasing Th2 cells and monocytes
  • activation of inflammatory cells particularly eosinophils so epithelial damage
  • airway hyper-responsiveness and inflammation so bronchospasm
  • patient will present with wheezing and cough
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15
Q

What are the main pathological features of COPD?

A
  • mucous gland hyperplasia leading to chronic bronchitis and small airway narrowing and obstruction
  • bronchial thickening and fibrosis leading to small airway narrowing and obstruction
  • alveolar destruction leading to emphysema, loss of elastic recoil and dynamic airway collapse
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16
Q

How does activation of M3 receptors cause contraction of airway smooth muscle?

A

M3 muscarinic receptors activate Gq11 which activates PLC to convert PIP2 to IP3 which causes Ca2+ to be released from the sarcoplasmic reticulum leading to contraction of the smooth muscle

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17
Q

What is the role of M3 muscarinic receptors?

A

they mediate contraction to ACh and evoke increased secretion on mucus-containing cells

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18
Q

What does Ipratropium do?

A

it is a non-selective blocker of M1-3 receptors

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19
Q

What do muscarinic antagonists do?

A

block activation by ACh so contraction is prevented

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20
Q

What do beta 2 agonists do?

A

they activate beta 2 adrenoceptors which causes relaxation

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21
Q

Who should you prescribe glucocovrticosteroids to?

A

patients with COPD that have frequent and severe exacerbations when given a LABA

22
Q

What are phosphodiesterase inhibitors used for?

A

they prevent inflammation responses and immune cells

23
Q

Why should you combine beta 2 adrenoceptors (LABAs) with LAMAs?

A

LAMAs prevent contraction and LABAs cause relaxation so FEV1 is increased

24
Q

What are the three type of rhinitis?

A

allergic, non-allergic and mixed

25
Q

What are the three types of allergic rhinitis?

A

seasonal, perennial or episodic

26
Q

What is the pathology of allergic rhinitis?

A
  • inhalation of allergen increases IgE levels
  • IgE binds to receptors on mast cells and basophils
  • re-exposure to allergen causes mast cell and basophil degranulation
  • release of mediators including histamine, cysLT, tryptase and prostaglandins
  • delayed response causes lymphocytes and eosinophils to be recruited to nasal mucosa
27
Q

What are the results of the mediator release in allergic rhinitis?

A

acute itching, sneezing, rhinorrhoea and nasal congestion

28
Q

What is non-allergic rhinitis?

A

any rhinitis that is acute or chronic but doesn’t involve IgE events

29
Q

What are causes of non-allergic rhinitis?

A

infection, hormone imbalance, vasomotor disturbance, medication or cystic fibrosis

30
Q

What is mixed rhinitis?

A

occupational rhinitis involving both allergic and non-allergic components

31
Q

What are the similarities between allergic asthma and allergic rhinitis?

A

pathway is similar

32
Q

What are the four treatments of rhinitis and examples of the drugs used?

A
  • anti-inflammatory = glucocorticoids
  • mediator receptos blockade = h1 receptor antagonist, cysLT receptor antagonists
  • nasal blood flow = vasoconstrictors
  • anti-allergic = sodium cromoglicate
33
Q

What do glucocorticoids do?

A

hormone receptors that cross the cell membrane readily and bind to extracellular receptors that doubles as nuclear transmitter

34
Q

What do glucocorticoids up-regulate and down-regulate?

A
  • up-regulate the expression of anti-inflammatory mediators

- down-regulate pro-inflammatory mediators so less swelling

35
Q

What is the effect of glucocorticoids?

A
  • reduce vascular permeability

- increase expression of proteins that hold endothelial cells together so reduced leakiness

36
Q

Which types are glucocorticoids used for?

A

SAR and PAR and in NARES

37
Q

In what form do glucocorticoids come?

A

a nasal spray that works over several weeks

38
Q

What are anti-histamines?

A

competitive antagonists that reduce effects of mast cell derived histamine

39
Q

What are the effects of anti-histamines?

A
  • reduce vasodilation and increase capillary permeability
  • reduce activation and increase capillary permeability
  • reduce mucus secretion from submucosal glands
40
Q

What types are anti-histamines used for?

A

SAR, PAR and EAR but not used in non-allergic rhinitis

41
Q

What do anti-cholinergic drugs do?

A

block the release of ACh from postganglionic parasympathetic fibres

42
Q

What do anti-cholinergic drugs reduce?

A

rhinorrhoea

43
Q

What types are anti-cholinergic drugs used for?

A

PAR and SAR

44
Q

What is the main anti-cholinergic drug that is used?

A

ipratropium

45
Q

What is sodium cromoglicate?

A

mast cell stabiliser and used for allergic rhinitis

46
Q

What do cysteinyl leukotriene receptor antagonists do?

A

reduce the effects of cysts upon the nasal mucosa

47
Q

What types are cysteinyl leukotriene receptor antagonists used to treat?

A

PAR and SAR so allergic rhinitis and asthma

48
Q

What is the common cysteinyl leukotriene receptor antagonists that is used?

A

oral montelukast

49
Q

What do vasoconstrictors do?

A

directly or indirectly act to mimic the effects of noradrenalin to produce vasoconstriction

50
Q

What is the main vasoconstrictor used?

A

oxymetazoline which is a selective alpha 1 adrenoceptor agonist which reduces congestion in allergic rhinitis

My Respiratory (15 decks)

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