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Respiratory > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

where are cell bodies of preganglionic fibres located?

A

The brainstem

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2
Q

Where are cell bodies of postganglionic fibres located?

A

The walls of the bronchi and bronchioles

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3
Q

What is the result of parasympathetic stimulation of postganglionic CHOLINERGIC fibres?

A

Bronchial smooth muscle contraction

Mediated by M3 muscarinic ACh receptors on ASM cells

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4
Q

What is the result of parasympathetic stimulation of postganglionic NONCHOLINERGIC fibres?

A

Bronchial smooth muscle relaxation

Mediated by NO and VIP

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5
Q

What is the result of sympathetic stimulation?

A

Bronchial smooth muscle relaxation via B2-ADRon ASM cells (activated by adrenaline released from the adrenal gland)

Decreased mucus secretion mediated by B2-ADR on goblet cells

Increased mucociliary clearance mediated by B2-ADR on epithelial cells

Vascular smooth muscle contraction mesiated by a1 adrenoceptors on vascular smooth muscle cells

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6
Q

what is the General mechanism of contraction in smooth muscle cells mediated by M3 ACh receptors activated by parasympathetic stimulation?

A

Contraction caused by Ca2+ exiting the SARCOPLASMIC RETICULUM
(via Ca2+ activated Ca2+ channel/ IP3 receptor)

*Voltage activated Ca2+ channels bring calcium ions into ASM cell

*GCPRs produce IP3 via
Gq -> PLC -> IP3

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7
Q

How does calcium initiate contraction?

A
  1. binds to calmodulin (makes Ca2+ - calmodulin)
  2. this activates MLCK
  3. active MLCK Dephosphorylises ATP and the Pi goes on to phosphorylate MYOSIN CROSS BRIDGE
  4. This permits binding of myosin with actin- causing contraction
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8
Q

What causes reaxation in ASM cells?

A

Dephosphorylation of MLCK by myosin phosphatase

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9
Q

Increase of intracellular calcium leads to…

A

constriction

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10
Q

Decrease of intracellular calcium leads to…

A

Relaxation

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11
Q

How does adrenaline promote ASM relaxation?

A
  1. activates B2-ADR
  2. activates Gs
  3. actvates AC
  4. activates cAMP (If converted to 5’AMP then pathway switched off)
  5. activates PKA
  6. Phosphortlates & stimulates myosin phosphatase- which dephosphorylates MLCK- which promotes relaxation
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12
Q

Causes of asthma attacks?

A

allergens, exercise, respiratory infections, smoke, dust, environmental pollutants

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13
Q

What are the airway problems associated with asthma?

A
  1. increase in SM mass
  2. Accumulation of fluid in tissue (oedema)
  3. increased mucus secretion
  4. epithelium damage (exposed sensory & parasymp. nerves- causes contraction)
  5. sub-epithelial fibrosis
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14
Q

What are the two “Hyper”s associated with asthma?

A

Hypersensitivity- decrease in conc. inhaled from bronchoconstrictor

Hyper-reactivity- larger fall in FEV1

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15
Q

What are the two main types of hypersensitivity?

A

I: Immediate bronchospasm
IV: delayed bronchospasm

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16
Q

What TH response is associated with a nonatopic individual?

A

TH1

  • low level response
  • IgG and macrophages
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17
Q

What TH response is associated with atopic individuals?

A

TH2

  • strong response
  • IgE
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18
Q

What makes up the induction phase of allergic asthma?

A 
APCs 
CD4+
TH cells
TH2 (IL-4 production)
B cells
plasma cells
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19
Q

what makes up the effector phase of allergic asthma?

A

plasma cells
antibodies (IgE)
IL-5 / IL-4 and IL-13
eosinophils / mast cells

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20
Q

What are the two categories of asthma treating drugs?

A

Relievers & controllers/preventers

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21
Q

What are three types of asthma relieving drugs?

A

Short acting B2 agonists
long acting B2 agonists
CysLT1 receptor antagonists

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22
Q

what are some examples of asthma controllers/ preventors?

A

Corticosteroids
chromoglicate
humanised monoclonal IgE antibodies

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23
Q

what do methylxanthine drugs do?

A

can be used to relieve and control/ prevent asthma symptoms

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24
Q

what is the preferred route of administration for asthma drugs?

A

aerosol or nebulised

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25
Q

when might an oral asthma drug be used?

A

In children or people unable to sufficiently use an inhaler

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26
Q

what are the advantages of using aerosol asthma drugs?

A 
low dose required
effective distribution
effective for bronchodilators
effective in mild/moderate disease
little risk of adverse affects as drug rapidly clears systemic circulation
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27
Q

what are the advantages of using oral asthma drugs?

A

easy to administer, as unaffected by airway diseae
easy to administer
effective in severe disease

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28
Q

what is the mechanism of a B2- Adrenoceptor agonist?

A

B2-ADR activated
Gs protein activates AC
AC is phosphorylised by ATP to produce cAMP
(If converted to 5’AMP then pathway stopped)
cAMP activates PKA
phosphorylation of MLCK and myosin phosphatase
ASM Relaxation

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29
Q

which drug type act as physiological antagonists of all spasmogens?

A

B2- adrenoceptor agonists

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30
Q

what does SABA stand for?

A

short acting B2-ADR agonists

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31
Q

what does LABA stand for?

A

long acting B2-ADR agonists

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32
Q

salbutamol is an example of which type of B2-ADR agonist?

A

SABA

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33
Q

what is the usual route of administration for salbutamol?

A

inhaler

34
Q

how might salbutamol be administered in more severe cases?

A

nebulised
oral (in children)
IV

35
Q

How long does it take for salbutamol to act and how long for maximal effect?

A

5 mins

30 mins

36
Q

what is the effect of salbutamol?

A

Bronchodilation (ASM cell relaxaation)
Increased mucus clearance
decreased mediator release from mast cells and monocytes

37
Q

what are some potential adverse effects of salbutamol?

A

fine tremor (can be observed in a general examination)
tachycardia
cardiac dysrythmia
hypokalaemia (low blood potassium levels)

38
Q

salmeterol and formoterol are examples of which type of B2-ADR agonist?

A

LABA

39
Q

What should LABAs be used for?

A

Nocturnal asthma

Add on therapy in astma inadequately controlled by corticosteroids

40
Q

what kind of drug is isoprenaline?

A

a non-selective B2-ADR agonist

41
Q

what adverse side effect could using a non-selective B2-ADR agonist potentially cause?

A

stimulation of cardiac B1-ADR

42
Q

propranolol is an example of which kind of drug?

A

non-selective B-ADR antagonist

43
Q

why should using a B-ADR antagonist for asthma be carefully considered?

A

risk of causing bronchospasm

44
Q

LTC4, LTD4 and LTE4 are examples of what? and where are they derived from?

A

CysLTs (cysteinly leukotrienes)

derived from mast cells & infiltrating inflammatory cells

45
Q

what do CysLT1 receptor antagonists prevent?

A

ASM contraction
mucus secretion
oedema

46
Q

montelukast and zafirlukst are example of what type of drug?

A

CysLT1 receptor antagonists

47
Q

when should CysLT1 receptor antagonists be used?

A

As an add on therapyagainst early and late bronchospasm in mild persistent asthma
Should be used with corticosteroids in more severe conditions

48
Q

which bronchosmasms are CysLT1 receptor antagonists effective against?

A

antigen induced

exercise induced

49
Q

how are CysLT1 receptor antagonists administered?

A

Oral route

50
Q

Theophylline and aminophylline are example of which asthma drug?

A

Methylxanthines

51
Q

what is the mechanism of action for methylxantines?

A

uncertain

might inhibit isoforms of phosphodiesterases, which inactivate cAMP and cGMP

52
Q

how are methylxanthines administered?

A

oral route

53
Q

which asthma drug has a very narrow therapeutic window?

A

methylxanthines

54
Q

which asthma drug combines bronchodilatory and anti-inflammatory responses?

A

methylxanthines

55
Q

which major classes of steroids are synthesised in the adrenal cortex and released into the circulation?

A

glucocorticoids

mineralocorticoids

56
Q

what are the main essential processes glucocorticoids regulate?

A

decrease inflammatory responses

decrease immunological responses

57
Q

mineralocorticoids (eg. aldosteone) regulate what?

A

retention of salt and water by the kidney

58
Q

what are the main synthetic derivatives of cortisol used in asthma?

A

Beclometasone
Budesonide
Fluticasone

59
Q

What are glucocorticoids for?

A

for the prophylaxis of asthma (prevention)

60
Q

How are glucocorticoids administered?

A

inhalational route

61
Q

How do glucocorticoids signal?

A

via nuclear receptors- specifically GRa

62
Q

What are glucocorticoid effects on gene transcription?

A

increase transcription of genes encoding anti-inflammatory proteins
Decrease transcription of genes encoding inflammatory proteins

63
Q

What do glucocorticoids do to inflammatory response?

A

decrease Th2 formation
cause apoptosis

prevent antibody production

prevent allergen-induced influx into lung

reduced number of mast cells, eosinophils, macrophages and dendritic cells

64
Q

what are cromones?

A

second line drug used prophylactically in childhood asthma (mast cell stabilizers)

has no direct effect on ASM

65
Q

what is omalizumab?

A

a monoclonal antibody directed against IgE

66
Q

what is mepolizumab?

A

a monoclonal antibody directed against IL-5

67
Q

What is chronic bronchitis?

A 
Inflammation of bronchi and bronchioles
Cough
Clear mucoid sputum
Infections with purulent sputum
Increasing breathlessness
68
Q

What is emphysema?

A

Distension and damage to alveoli
Destruction of acinial pouching in alveolar sacs
Loss of elastic recoil

69
Q

What do muscarinic receptor antagonists do?

A

Reduce parasympathetic neuroeffector transmission

Act as pharmacological antagonists of bronchocontriction caused by ASM M3 receptor activation in response to ACh released from postganglionic parasympathetic fibres

70
Q

What receptor responds to ACh released from postganglionic parasympathetic fibres?

A

M3 receptors

71
Q

where are M1 receptors located?

A

Ganglia

72
Q

where are M2 receptors located?

A

postganglionic neurone terminals

73
Q

where are M3 receptors located?

A

ASM

74
Q

what is the function of M1 receptors?

A

facilitate fast neurotrasmission mediated by ACh acting on nicotinic receptors reducing ACh release

75
Q

what is the function of M2 receptors?

A

act as inhibitory autoreceptors reducu

76
Q

what is the function of M3 receptors?

A

Mediate contraction to ACh

77
Q

which SAMAs are used for COPD treatment?

A

Ipratropium

78
Q

which LAMAs are used for COPD treatment?

A

Tiotropium
Glycopyrronium
Aclidinium
Umeclidinium

79
Q

how are SAMA and LAMA COPD treatments administered?

A

By inhalation

Quaternary ammonium group reduces absorption and systematic exposure

80
Q

what weak anti-inflammatory drug is used in allergic asthma? particularly in children/young people?

A

Inhaled sodium chroglycate

Respiratory (19 decks)

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