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Respiratory > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what is the dominant neuronal control of bronchial smooth muscle tone?

A

parasympathetic cholinergic innervation

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2
Q

what nerve carries the preganglionic fibres that will eventually supply the bronchial smooth muscle?

A

vagus nerve

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3
Q

where are the parasympathetic ganglia that will go onto supply the bronchial smooth muscle?

A

embedded in the walls of bronchi and bronchioles

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4
Q

post ganglionic parasympathetic fibres innervate what within the airways?

A

smooth muscle

submucosal glands

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5
Q

what 2 things does stimulation of parasympathetic division cause within the airways?
(and what is the combined result?)

A
  1. bronchial smooth muscle contraction
  2. increased mucous secretion
    (collectively increases airway resistance)
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6
Q

what types of receptors are the parasympathetic division acting upon in the airways?

A

M3 muscarinic ACh receptors

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7
Q

how does the sympathetic system achieve its effects on the airways if its has no real innervation of bronchial smooth muscle?

A

causes release of adrenaline into circulation which acts on B2-adrenoceptors on bronchial smooth muscle

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8
Q

what 3 things does the sympathetic division cause within the airways?
(and what is the combined result?)

A

bronchial smooth muscle relaxation
decreased mucus secretion
increased mucociliary clearance
(collectively reduces airway resistance)

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9
Q

what type of receptors is the adrenaline (stimulated by the sympathetic system) acting on in the airways?

A

B2-adenoceptors

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10
Q

what is mucociliary clearance mediated by?

A

ciliated epithelium layer of the airways which remove particles and bacteria from airways by propelling upwards

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11
Q

what is asthma?

A

a recurrent and reversible obstruction to the airflow (caused by bronchoconstriction due to bronchiole spasms) in response to certain stimuli

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12
Q

what are 4 main causes (stimuli) of an asthma attack?

A

allergens (in atopic individuals)
exercise (cold, dry air)
respiratory infections
smoke, dust, environmental pollutants

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13
Q

what is the name for the acute severe type of asthma which is a medical emergency and can be fatal?

A

status asthmaticus

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14
Q

what do intermittent asthma attacks cause?

A

cough
wheeze
difficulty in breathing

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15
Q

what is chronic asthma?

A

long standing inflammation causing pathological changes to the bronchioles

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16
Q

what 4 pathological changes can be caused by chronic asthma?

A
  1. increased mass of smooth muscle (hyperplasia + hypertrophy)
  2. accumulation of intestitial fluid
  3. increased secretion of mucus
  4. epithelial damage
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17
Q

why in chronic asthma is there the accumulation of interstitial fluid?

A

due to increased secretions

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18
Q

what is exposed in epithelial damage and what does this result in?

A

epithelial damage exposes sensory nerve endings and cause them to become more sensitive- hyper-responsiveness

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19
Q

what causes a decreased FEV1 and PEFR in asthma?

A

increased airway resistance

due to inflammation and bronchoconstriction which causes airway narrowing

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20
Q

what are the sensory nerve endings that can be exposed if there is epithelial damage in asthma?

A 
C-fibres
a class of irritant receptors
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21
Q

what type of substance works on C-fibre endings?

so will have an increased effect if there is epithelial damage- hyperesponsiveness

A

bronchoconstrictors (spasmogens)

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22
Q

what 2 phases make up an asthms attack usually?

A

immediate phase- bronchospasm

delayed phase- inflammatory reaction

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23
Q

what is the delayed inflammatory response triggered by?

A

acute bronchospasm

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24
Q

what type of Th cells are part of the antibody-mediate response involving IgE in response to an allergen? (atopic)

A

Strong Th2 response

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25
Q

what type of Th cells are part of the cell-mediated immune response involving IgG and macrophages in response to an allergen? (non-atopic)

A

low-level Th1 response

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26
Q

what do interleukins signal between?

A

white blood cells

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27
Q

what type of environment fo Th2 cells produce?

A

cytokine environment

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28
Q

what is the induction phase in the development of allergic asthma?

A

antigen presentation

cloncal expansion and maturation

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29
Q

what cell type differentiates and activates in response to IL 5 released from Th2 cells?

A

eosinophils

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30
Q

what type of cells express IgE receptors in response to IL 4 and IL 13 released from Th2 cells?

A

mast cells (in airway tissues)

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31
Q

when the specific allergen becomes present and links to the antibodies covering the mast cell, what is stimulated?

A

calcium entry into mast cells causing the release of calcium from intracellular stores

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32
Q

when calcium enters the mast cells and calcium is released from intracellular stores what 2 things occur?

A
  1. release of substances that cause airway smooth muscle contraction (spasmogens)
  2. release of substances that attract cells that cause inflammation
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33
Q

what substances released from the mast cell are spasmogens?

A

histamine

leukotriens (LTC4 LTD4)

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34
Q

what substances released from the mast cells are chemotaxins/ cytokines?

A

LTB4, PAF, PGD2

leukotriene, platelet activating factor, prostaglandin

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35
Q

what type of leukocytes do chemotaxins/cytokines released from mast cells (in response to an allergen) attract?

A

Th2 cells
monocytes
eosinophils

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36
Q

which group of substances released from a mast cell is responsible for the immediate phase response of an asthma attack?

A

spasmogens

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37
Q

what group of substances released from a mast cell is responsible for the delayed phase response of an asthma attack?

A

chemotaxins and cytokines

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38
Q

what does the inflamamtion caused by the inflammatory cells induced by chemotaxins and cytokines released by mast cells cause in the airways?

A

airway inflammation
epithelial damage
airway hyper-reactivity
bronchospasm, wheezing, cough

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39
Q

what are the 2 types of drugs used in the treatment of asthma?

A

relievers

controllers/preventors

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40
Q

what are the function of relievers?

A

bronchodilators

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41
Q

what are the function of controllers/preventors?

A

anti-inflammation

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42
Q

what is the mechanism of bronchodilators?

A

B2-adrenoceptor agonists

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43
Q

once a B2-adrenoceptor has been stimulated in the airway smooth muscle, what is the result of the chain of pathways?

A

phosphorylation of MLCK
(myosin light chain kinase)
reduction in intracellular Ca2+

[MLCK cause contraction of smooth muscle, phosphorylation of MLCK inhibits this process and causes relaxation]

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44
Q

what happens to the G-coupled protein receptors in the case of persistent activation of B2-adrenoceptors?

A

receptor desensitisation and endocytosis

loss of function

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45
Q

what kinases are involved in the desensitisation process of B2-adrenoceptors?

A

PKA (protein kinase A)

GRK (G protein receptor kinase)- specifically B-adrenoceptor kinases

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46
Q

what molecule causes linking of the desensitized B-adrenoceptor to the endocytotic machinery?

A

B-arrestin

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47
Q

what happens to the B-adrenoceptor once inside the cell?

A

recycles in endosomes or degraded in lysosomes

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48
Q

what is salbutamol?

A

short acting B2-adrenoceptor agonist (SABA)

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49
Q

what type of asthma drug are SABAs (eg salbutamol)? (reliever or preventor)

A

reliever

bronchodilator

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50
Q

how is a SABA (eg salbutamol) generally administered?

and why?

A

inhalation

to lessen systemic effects

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51
Q

when are SABAs administered oral or IV?

A

emergency

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52
Q

when is the maximal effect of SABAs (eg salbutamol?

A

within 30 mins

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53
Q

by stimulation of the sympathetic system what 3 effects do SABAs (eg salbutamol) have?

A

dilation of airway smooth muscle
increased mucus clearance
decreased mediator release from mast cells

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54
Q

what are the adverse effects of SABAs eg salbutamol? (rare when administered by inhalation)
+ why do they occur?

A

fine tremor
tachycardia
due to unanted systemic absorption

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55
Q

what salmeterol?

A

long acting B2-adrenoceptor agonist (LABA)

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56
Q

why are LABAs (eg salmeterol) not recommened for acute relief of bronchospasm despite technically being relievers (bronchodilators)?

A

relatively slow to act

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57
Q

when are especially LABAs useful?

A

nocturnal asthma

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58
Q

can SABAs be used in monotherapy?

A

yes

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59
Q

can LABAs be used in monotherapy?

A

no

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60
Q

why should you use selective B2-adrenoceptor agonists and not general adrenoceptor agonists for asthma treatment?

A

to reduce the potentially harmful stimulation of cardiac B1-adrenoceptors

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61
Q

why should propanolol not be used in asthmatic patients?

A

propanolol is a non-selective b-adrenoceptor antagonist so will cause the constriction of airway smooth muscle

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62
Q

what type of asthma drugs are cysLT1 receptor antagonists?

cysteinyl leukotriene receptor antagonists

A

relievers

bronchodilators

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63
Q

how do cysLT1 receptor antagonists work in patients with asthma?

A

block cysLTs (LTC4, LTD4, LTE4) derived from mast cells and so cause smooth muscle relaxation, decreased mucus secretion and decreased oedema

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64
Q

what is montelukast or zafirlukast?

A

a cysLT1 receptor antagonist

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65
Q

what type of asthma drugs are cysLT1 receptor antagonists?

cysteinyl leukotriene receptor antagonists

A

relievers
(bronchodilators)
[but not recommeneded for relief of acute severe asthma]

66
Q

how are cysLT1 receptor antagonists administered?

A

oral route

67
Q

what are theophylline and aminophylline?

A

xanthines

68
Q

what type of asthma drugs are xanthines?

A

relievers AND controllors/preventors

69
Q

how are xanthines prepared and administered?

A

sustained release preparations by oral route

70
Q

how do xanthines work?

A

relax bronchial smooth muscle
inhibit mediator release from mast cells
increase mucus clearance

71
Q

what are the adverse effects of xanthines?

A 
nausea
vomiting
abdominal discomfort
headache
(also numerous drug interactions)
72
Q

where are steroid hormones synthesised in the body?

A

adrenal cortex

73
Q

what 2 types of steroid hormone are synthesised and released on demand from the adrenal cortex?

A

glucocorticoids

mineralcorticoids

74
Q

what is the main glucocorticoid in the body?

A

cortisol (hydrocortisone)

75
Q

what are the 2 main functions of glucocorticoids that are important in immune regulation?

A

decreases inflammatory responses

decreases immunological responses

76
Q

why are exogenous glucocorticoids not recommened for systemic use? (unless its an emergency)

A

multiple effects on metabolism

77
Q

what is the main mineralcorticoid in the body?

A

aldosterone

78
Q

what is the main function of mineralcorticoids?

A

regulate the retention of salt (and therefore water) by the kidney

79
Q

what type of drug is beclometasone?

A

a corticosteroid

80
Q

what type of asthma drug are corticosteroids?

A

preventers

anti-inflammatory NOT bronchodilation

81
Q

what do glucocorticoids signal via within cells?

A

nuclear receptors

specifically GRalpha

82
Q

how do glucocorticoids enter cells across the plasma membrane?

A

diffusion

83
Q

within the nucleus what happens to the glucocorticoid-GRa monomer complex?

A

assemle into homodimers and then bind to glucocorticoid response elements (GRE) in the promotor region of specific genes

84
Q

what is the end result of glucocorticoids entering into a cell?

A

transcription of specific genes are transactivated or transrepressed to increase expression of anti-inflamatory proteins and decrease expression of inflammatory proteins

85
Q

what is the function of histones?

A

package the DNA double helix within the nucleus

86
Q

what is chromatin?

A

DNA plus histones

87
Q

in addition to its function with GRE (glucocorticoids response elements) what can glucorticoids do to chromatin?

A

deacetylation of histones to modify chromatin structure to become condensed and not able to be transcribed

88
Q

what are the 4 main effects of glucocorticoids that are particularly relevant to inflammation in bronchial asthma?

A
  1. decrease formation of Th2 cytokines and cause apoptosis
  2. prevent production of IgE
  3. reduce number of mast cells and decrease Fc receptor expression
  4. prevent allergen-induced eosinophil influx into lungs and cause apoptosis
89
Q

what are the 4 smaller structural effects of glucocorticoids that are particularly relevant to inflammation in bronchial asthma?

A
  1. decrease production of cytokine mediators from epithelial cells
  2. reduces leaking from endothelial cells
  3. increase B2-receptor expression in airway and smooth muscle
  4. reduced mucus secretion
90
Q

why are corticosteroids useful in the long term not short term?

A

they do not alleviate early stage bronchospasm but resolve established inflammation

91
Q

when does efficacy of corticosteroids develop?

A

over several days

92
Q

what are the most common adverse effects of corticosteroid inhalers?
(and why?)

A

dysphonia (hoarse and weak voice)
oropharyngeal thrush
due to steroid deposit in the oropharynx

93
Q

what is a good way to prevent dysphonia and oropharyngeal thrush when using corticosteroid inhalers?

A

drinking water after using inhaler

94
Q

what form of oral corticosteroid is used in chronic, severe or rapidly deteriorating asthma?

A

oral prednisolone

95
Q

how do cromolins work?

A

mast cell stabiliser: prevents degranulation
weak anti-inflammatory effect
decreased hypersensitivity of sensory C-fibres

96
Q

what is sodium cromoglicate?

A

cromolin

97
Q

how is sodium cromoglicate administered for asthma treatment?

A

inhalation

98
Q

what type of drug is sodium cromoglicate?

A

reliever AND preventer

ie bronchodilation and anti-inflammatory but not recommended for use for relief during an acute attack

99
Q

how long does efficacy of sodium cromoglicate take to develop?

A

several weeks

100
Q

what is omalizumab?

A

monoclonal antibody against IgE

101
Q

how do monoclonal antibodies work in the treatment of asthma?

A

Bind IgE via Fc to prevent attachment to FC receptors

-prevents mast cells becoming activated

102
Q

how are monoclonal antibodies administered?

A

IV

103
Q

what is COPD?

A

airflow reduction that is in some patients partially reversible (with bronchodilators) but which progressively worsens and gets exacerbations of symptoms including cough and mucus production

104
Q

what can COPD be divided into?

A

chronic bronchitis

emphysema

105
Q

what are 5 characteristics of chronic bronchitis?

A

1, inflammation of bronchi and bronchioles

  1. cough
  2. clear mucoid sputum
  3. infections with purulent sputum
  4. increasing breathlessness
106
Q

what are the 2 characteristics of emphysema?

A
  1. distension and damage to alveoli

2. destruction of acinal pouching in alveolar sacs

107
Q

where are M1 muscarinic ACh receptors int he airways located?

A

in galnglia

108
Q

what is the function M1 muscarinic ACh receptors in the airways?

A

faciliate transmission mediated by ACh acting on nicotinic receptors

109
Q

where are M2 muscarinic ACh receptors in the airways located?

A

postganglionic neurone terminals

110
Q

what is the function of M2 muscarinic ACh receptors in the airways?

A

act as inhibitory autoreceptors reducing the release of ACh

111
Q

where are M3 muscarinic ACh receptors in the airways located?

A

smooth muscle effector

submucosal glands

112
Q

what is the function of M3 muscarinic ACh receptors in the airways?

A

contraction of airway smooth muscle

increased secretion of submucosal glands

113
Q

what is ipratropium?

A

short acting muscarinic antagonists (SAMAs)

114
Q

what is tiotropium?

A

long acting muscarnic antagonists (LAMAs)

115
Q

how are muscarinic antagonists administered?

A

inhalation

116
Q

atropine is also a muscarinic antagoinist, how is it different to the muscarinic antagonists used in COPD?

A

contains a tertiary amine instead of a quaternary ammonium like ipratropium and tiotropium

117
Q

why is a quaternary ammonium more useful than a tertiary amine in the treatment of COPD?

A

reduces absorption and systemic exposure

118
Q

what is the general onset of action for muscarinic antagonists used in the treatment of COPD? (SAMAs and LAMAs)

A

> 30mins onest of action

delayed

119
Q

what 3 effects do muscarinic antagonists have in the treatment of COPD do?

A
  1. relaxes bronchospasm caused by irritant stimuli (which initiate a vagal reflex that liberates ACh) 2. blocks ACh-mediated basal tone
  2. reduces mucus secretion
120
Q

why do muscarinic ACh receptor antagonists have few adverse effects?

A

little systemic absorption due to quaternary ammonium group

121
Q

why is tiotropium more effective than ipatropium? (apart from the fact it is longer acting)

A

tiotropium is selective for M3
ipratropium is non-selective for M1, M2 and M3
(block of M2 is not desirable + actually increases ACh release from parasymp post-ganglionic neurones)

122
Q

what 4 -adrenoceptor agonists are also used in the treatment of COPD?

A

salbutamol (SABA)

salmeterol, formoterol and indacaterol (LABA)

123
Q

why is indacaterol classed as an ultra-LABA?

A

rapid onset of action vs normal LABAs

124
Q

what combination of drugs is especially effective in moderate COPD?

A

LABA/LAMA combo

eg salmeterol/tiotropium

125
Q

what is the prominent PDE expressed in neutrophils, T cells and macrophages?

A

PDE4

126
Q

what does PDE4 cause?

A

inflammation

127
Q

what is rofumilast?

A

a selective PDE4 inhibitor

128
Q

what does rofumilast do?

A

suppresses inflammation and emphysema

129
Q

how is rofumilast administered?

A

oral

130
Q

what type of adverse effects does rofumilast have?

A

GI effects

due to PO administration

131
Q

even though glucocorticoids are of benefit in COPD patients who develop frequent and severe exacerbations, why might there be glucocorticoid unresponsiveness in some patients?

A

due to oxidative/nitrative stress associated with chronic inhalation of tobacco and smoke
HDAC2 is reduced in COPD

132
Q

what is a triple inhaler?

A

LABA/LAMA/glucocortidoic
(eg formoterol/tiotropium/ciclesonide)
not lisenced for use

133
Q

what is rhinitis?

A

a common disease involving acute or chronic inflammation of the nasal mucosa

134
Q

what 4 features is rhinitis charactersed by?

A
  1. rhinorrhoea (runny nose)
  2. sneezing
  3. itching
  4. nasal congestion and obstruction
135
Q

why does rhinorrohea occur in rhinitis?

A

watery mucus accumulation in nasal cavity

136
Q

why does nasal congestion and obstruction occur in rhinitis?

A

swelling of the nasal mucosa due to dilated blood vessels

137
Q

what are the 3 types of rhinitis?

A

allergic
non-allergic
mixed

138
Q

what are the 3 types of allergic rhinitis?

A

seasonal (SAR)
perennial (PAR)
episodic

139
Q

what are some non-allergic causes of rhinitis?

A 
infection
hormonal imbalance (eg preg)
vasomotor disturbances
medications
nonallergic rhinitis with eosiophilia syndrome (NARES)
140
Q

what are the 5 types of rhinitis/rhinorrhoea treatment?

A 
glucocorticoids
H1 receptor antagonists
CysLT1 receptor antagonists
vasoconstrictors
sodium chromoglicate
141
Q

what is the function of glucocorticoids in the treatment of rhinitis/rhinorrhoea?

A

anti-inflammatory

142
Q

what is the function of H1 receptor antagonists in the treatment of rhinitis/rhinorrhoea?

A

reduce effects of mast cell derived histamine eg prevent vasodilation, prevent activation of sensory nerves, decrease mucous secretion)

143
Q

what is the function of sodium chromoglicate in the treatment of rhinitis/rhinorrhoea?

A

anti-allergic

144
Q

what is the mainstay treatment of SAR and PAR?

A

glucocorticoids

145
Q

in the treatment of rhinitis/rhinorrhoea how are glucocorticoids administered?

A

topical nasal spray

OD

146
Q

what 3 glucocorticoids can be used in the treatment of rhinitis/rhinorrhoea?

A

beclometasone
fluticasone
prednisolone

147
Q

which types of rhinitis ar H1 receptor antagonists more effective in?

A

SAR, PAR and episodic AR

not too good at non-allergic

148
Q

how are H1 receptor antagonists administered?

A

orally or topical nasal spray

149
Q

what are loratidine, fexofenadine and cetirizine?

A

second generation H1 receptor antagonists

150
Q

what is the function of cysLT1 receptor antagonists in the treatment of rhinitis/rhinorrhoea?

A

reduces the effects of CysLTs upon the nasal mucosa

151
Q

what is the function of vasoconstrictors in the treatment of rhinitis/rhinorrhoea?

A

decrease nasal blood flow via a1 adrenoceptors

152
Q

what is the function of sodium chromoglicate in the treatment of rhinitis/rhinorrhoea?

A

mast cell stabilisers- prevent degranulation

153
Q

what is the sole muscarinic receptor antagonist agent used for rhinorrhoea?

A

ipatropium

154
Q

how is ipatropium administered for rhinorrhoea?

A

topical nasal spray

155
Q

how is sodium cromoglicate administered for rhinitis/rhinorrhoea?

A

topical nasal spray

156
Q

what type of rhinitis are CysLT1 receptor antagonists effective at treating?

A

PAR and SAR

157
Q

how are CysLT1s administered for treatment of rhinitis/rhinorrhoea?

A

oral

158
Q

what is the sole CysLT1s receptor antagonist used for the treatment of rhinitis/rhinorrhoea?

A

montelukast

159
Q

what is oxymetazoline?

A

a selective a1-adrenoceptor (Vasoconstrictor) used for allergic rhinitis

160
Q

how is oxymetazoline administered?

A

topical nasal spray

161
Q

why does rebound increase in nasal congestion occur after use of oxymetaxoline for a few days?

A

receptor desensitisation and down regulation

162
Q

what is the name for the rebound increase in nasal congestion which occurs after use of oxymetaxoline for a few days?

A

rhinitis medicamentosa

Respiratory (10 decks)

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