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Respiratory > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

in the parasympathetic division of the ANS, what types of fibers are stimulated to regulate airway function

A

postganglionic cholinergic/ noncholinergic

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2
Q

what does the stimulation of postganglionic cholinergic fibres cause

A

bronchial muscle contraction and increased mucous secretion

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3
Q

what is bronchial muscle contraction mediated by

A

M3 muscarinic Ach (acetylcholine) receptors on airway smooth muscle cells

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4
Q

what is increased mucous secretion mediated by

A

M3 muscarinic Ach receptors on gland (goblet) cells

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5
Q

what does stimulation of postganglionic nonchlorinergic fibers do

A

bronchial smooth muscle relaxation

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6
Q

what mediates bronchial smooth muscle relaxation?

A

nitric oxide, vasoactive intestinal peptide (VIP)

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7
Q

what does the sympathetic region of the ANS innervate to regulate airway fuction?

A

post-ganglionic fibers supply sub-mucosal glands and smooth muscle of blood supply

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8
Q

what does the sympathetic nervous system not innervate in humans

A

bronchial smooth muscle

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9
Q

what does stimulation of the sympathetic nervous system cause (4)

A

bronchial smooth muscle relaxation, decreased mucous secretion, increased mucociliary clearance, vascular smooth muscle contraction

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10
Q

what mediates bronchial smooth muscle relaxation

A

stimulation of the B(beta)2-adrenoceptors on ASM cells by adrenaline

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11
Q

what mediates decreased mucous secretion

A

B2-ADR on gland (goblet) cells

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12
Q

what mediates increased mucociliary clearance

A

B2-ADR on epithelial cells

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13
Q

what mediates the contraction of vascular sooth muscle

A

a(alpha)1-adrenoceptors on vascular smooth muscle cells

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14
Q

describe how transmitters/hormones cause contraction in ASM

A

activate GPCR which stimulates IP3 production and therefore IP3 receptors which move calcium secreted from calcium stores

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15
Q

describe how depolarisation causes contraction in ASM

A

activates voltage activated Ca2+ channel which then activates a second Ca2+ channel

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16
Q

how does calcium initiate contraction

A

binds to from calcium compounds which then activate myosin light chain kinase. MLCK then phosphorolates a myosin cross bridge which glides across actin to produce contraction

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17
Q

what does relaxation of ASM result form

A

dephosphorylation of myosin light chain by myosin phosphatase

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18
Q

what happens to the rates of de/phosphorylation in the presence of elevated intracellular calcium

A

phosphorylation exceeds dephos…

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19
Q

what does relaxtion require in terms of Ca+ concentration and how is this achieved

A

return to basal level via primary and secondary active transport

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20
Q

what is the activity of MLCK and myosin phophatase dependent on, give and example

A

extracellular signals e.g adrenoline and B(eta)2-adrenoceptor

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21
Q

define asthma

A

intermittent attacks of bronchoconstriction: recurrent and reversible (in the short term) obstruction to the airways in response to substances or stimuli

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22
Q

note asthma’s prevalence

A

5-10% of the population in industrialised countries

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23
Q

list common causes of asthma

A

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

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24
Q

what pathological changes occur in chronic, poorly controlled asthma as a result of long standing inflammation

A

increased mass of smooth muscle (hyperplasia and hypertrophy), accumulation of interstitial fluid (oedema), increased secretion of mucus, epithelial damage (exposing sensory nerve endings), sub epithelial fibrosis

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25
Q

what is bronchial hyper-responsiveness

A

hyper sensitivity and hyper reactivity as a result of epithelial damage that has exposed sensory nerve endings

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26
Q

when can an immune response cause asthma

A

when there is an imbalance between TH1 and TH2 lymphocyte-mediated responses

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27
Q

in the development of allergic asthma what does the initial presentation of the allergen result in

A

an adaptive immune response

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28
Q

describe the induction phase of the adaptive immune response that leads to allergic asthma (2 steps)

A

antigen presentation; antigen presented to T CD4 cell
colonial expansion and maturation; TH0 cells differentiate into TH1 and 2 cells (preferably TH2 which produce a cytokine environment). TH2 cells activate B cells that mature to IgE secreting P cells

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29
Q

describe the effector phase of the adaptive immune response that leads to allergic asthma (2 steps)

A

Eosinophils differentiate and activate in response to IL-5 released from TH2 cells.
Mast cells in airway tissues express IgE receptors in repsonse to IL-4 and IL-3 released from TH2 cells

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30
Q

how is calcium involved subsequent to TH2 lymphocyte activation

A

cross link IgE receptors stimulates calcium entry into mast cells and release of Ca2+ from intracellular stores

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31
Q

what does the entry and release of calcium evoke (2)

A

release of secretory granules containing histamine and the production and release of other agents (leukotrienes) that cause ASM contraction

release of substances that attract cells that cause inflammation into the area

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32
Q

describe the phases of an asthma attack

A

immediate (mainly bronchospasms) late/delayed (mainly inflammatory response)

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33
Q

what are the products of mast cells and mono nuclear cells that result in bronchospasms and early inflammation in the immediate phase of an asthma attack

A

spasmogens, CysLTs, histamine

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34
Q

what is produced by mast cells and mono nuclear cells in the immediate phase that evokes the late/delayed phase

A

cytokines, chemotaxis

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35
Q

what inflammatory cells in particular is activated in the late phase

A

eosinophils

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36
Q

what pathologically happens in the late phase (*)

A

airway inflammation, epithelial damage, airway hyper responsiveness, bronchospasm, wheezing, mucous oversecretion, cough

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37
Q

what are the two categories of drugs used to treat asthma and

A

relievers and controllers/preventors

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38
Q

how to relievers work and give 3 examples

A

act as bronchodilators; short acting Beta2-adrenoceptor agonist (SABAs), LABAs, CysLT1 receptor antagonist

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39
Q

how to controllers/ preventors work and give 3 examples

A

anti-inflammatory agents; glucocorticoids, cromoglicate, humanised monoclonal IgE antibodies

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40
Q

what are controllers/preventors NOT used to treat

A

acute asthma attacks- long term usage reduces frequency of them

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41
Q

what should be used to treat an acute asthma attack

A

B2- agonist (can be supplemented with relievers)

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42
Q

why is the oral route avoided

A

to avoid adverse affects

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43
Q

what are the advantages of administering drugs through the inhalation route

A

smaller dose needed to acquire appropriate concentration in lungs

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44
Q

Explain how B2-adr agonists treat asthma as bronchodilators

A

act as physiological antagonists of all spasmogens (substance that induces spasms). Cause ASM relaxation via formation of protein kinase A which phosphorylates MLCK and myosin phosphatase + reduce intracellular Ca conc + activate potassium channels

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45
Q

name two SABAs

A

salbutamol and turbutaline

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46
Q

what are SABAs used to treat

A

mild intermittent asthma

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47
Q

name two LABAs

A

salmeterol and formoterol

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48
Q

what are LABAs used to treat and what do they not treat

A

nocturnal asthma (last 8 hours) don’t treat acute attacks

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49
Q

describe how LABAs should be used

A

not as monotherapy, must always by co-administered with a glucocorticoid

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50
Q

how do Cysteinyl leukotriene (CysLT1) receptor antagonist work

A

act competitively at the CysLT1 receptor. Cyslts (e.g LTC4, LTD4 and LTE4) which are derived from mast cells and infiltrating inflammatory cells cause ASM contraction, mucous secretion and oedema

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51
Q

how are CYsLT1 receptor agonists administered

A

orally

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52
Q

how do Xanthines work

A

combine bronchodilator and anti-inflammatory actions, inhibit mediator release from mast cells, increase mucous clearance

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53
Q

describe the role of glucocorticoids in the body

A

class of hormone- main hormone cortisol (hydrocortisone)- regulate numerous essential process e.g. inflammatory and immunological responses

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54
Q

why are synthetic derivatives of cortisol, rather than cortisol itself are used in the treatment of asthma

A

as have little or no mineralcocorticoid activity (regulation of retention of salt and water by kidney)

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55
Q

name an example of a CystLT receptor agonist

A

montelukast

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56
Q

name an example of a Xanthine

A

theophylline

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57
Q

why is the inhalation route of glucocorticoid administration favoured in the treatment of mild or moderate asthma

A

minimise adverse effect

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58
Q

how do glucocorticoids signal

A

via nuclear receptors specifically GRalpha

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59
Q

how do glucocorticoids enter cells

A

are lipophillic so enter through diffusion across cellular membrane

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60
Q

describe the molecular mechanism of glucocorticoid action within the cytoplasm

A

in cytoplasm bind with GRalpha which dissociates heat shock proteins. ctivated nucleus then translocates to nucleus via importins.

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61
Q

describe the molecular mechanism of glucocorticoid action within the nucleus

A

activated receptor monomers assemble into homodimers and bind to GLUCOCORTORICOID RESPONSE ELEMENTS (GRE) in the promoter region of specific genes

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62
Q

what does the transcription or inhibition of specific genes result in

A

alter mRNA levels, rate of synthesis of mediator proteins

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63
Q

what does the transcription or inhibition of specific genes result in that is specific to treating asthma

A

increase transcription of anti-inflammatory proteins and decrease transcription of inflammatory proteins

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64
Q

what are the four effects of glucocorticoids that are relevant to bronchial inflammation in asthma

A

prevent IgE production, decrease number of mast cells, prevent allergens, decrease formation of TH2 cytokines,

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65
Q

how and what inflammatory cells do corticosteroids affect

A

decrease in number; eosinophils, mast and dendritic

decrease cytokines from; T-lymphocytes and macrophages

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66
Q

how do corticosteriods affect epithelial cells

A

decrease cytokine mediators

67
Q

how do corticosteriods affect endothelial cells

A

makes them less leaky

68
Q

how do corticosteriods affect ASM cells

A

increases beta 2 receptors

decreases cytokines

69
Q

how do corticosteriods affect mucous gland cells

A

decreases secretion

70
Q

summarise what glucocorticiodes do and dont do

A

suppress the inflammatory component of asthma, do not alleviate early stage bronchospasms caused by allergens or exercise

71
Q

describe cromoglicate

A

second line drug now infrequently used for the treatment of of allergic asthma particularly in children. no direct effect on bronchial smooth muscle. delivered by inhalation. can reduce both phases of an asthma attack but could take weeks to develop efficiency.

72
Q

describe omalizumab

A

monoclonal antibodies directed against IgE. Prevents binding of IgE (by binding to IgE) to receptors which suppresses mast cell response to allergens. requires IV administration. expensive

73
Q

what components of the inflammation cascade can be blocked by monoclonal antibodies

A

TSLP, IL-4, IL-5, IL-13 and IgE

74
Q

what does PRN mean

A

as required

75
Q

what is a LAMA

A

long acting muscarinic antagonist

76
Q

why are inhaled steroids used throughout treatment

A

as they act on eosinophils

77
Q

when are LAMAs and LABAs used

A

in the 3rd step- moderate persistent

78
Q

what may corticoidsteroids cause in COPD

A

pneumonia

79
Q

what has a higher therapeutic ratio oral/inhaler drugs for lungs

A

inhaler

80
Q

when can inhaled steroids be used alone

A

in asthma (not COPD)

81
Q

what does ICS stand for

A

inhaled cortical steroids

82
Q

what is the carina

A

the bifurcation of the trachea

83
Q

how small must particles be to get past the carina

A

5 microns

84
Q

how small must particles be to get past the 7th generation splitting of the bronchioles

A

2 microns

85
Q

what is the role of spacers

A

reduce velocity and size of particles, stops need to coordination, improves lung deposition

86
Q

what type of inhaler must always be used with a spacer

A

meter dose

87
Q

how are dry powder inhalers administered

A

breath actuated

88
Q

name a pro and con of dry powder inhalers

A

pro- dont need coordination

con- bug particles

89
Q

when in asthma is cromoglycate most effective

A

raised IgE/ exercise

90
Q

what does LTD4 do in the inflammatory cascade

A

amplify it

91
Q

how is montelukast administered

A

never on its own, always with inhaled steriods, orally

92
Q

how are corticoid steroids administered in COPD

A

never as monotherapy- as ICS/LABA combo

93
Q

what is the action of cromones

A

anti inflammatory, mast cell stabilizer

94
Q

when are cromones used

A

to treat asthma (cromoglycate)

95
Q

how are cromones administered

A

inhalation only

96
Q

when are leukotriene receptor antagonists used

A

only for asthma

97
Q

what does the binding of omalizumab to IgE receptor cause

A

inhibits TH2 response and associated mediator release from basophils/mast cells

98
Q

what does mepolizumab do

A

blocks the effect of the TH2 cytokine LT-5

99
Q

what does LT-5 do

A

is responsible for eosinophilic inflammation in asthma

100
Q

what does smart stand for

A

single maintenance and reliever therapy (combined inhalers

101
Q

what is tachyphylaxis

A

when body adapts during use of B2 agonists to have less B2 receptors

102
Q

what do B2 agonists do

A

stimulate bronchial smooth muscle- bronchodilators

103
Q

what do you not treat with LABA

A

an acute attack, only use high doses of salbutamol for that

104
Q

name a LAMA

A

tiotropium

105
Q

what are the two bronchodilators

A

B2 antagonists, muscarinic antagonists

106
Q

how is methylxanthine administered

A

orally with inhaled steroid

107
Q

what is methylxanthine used for

A

maintenance therapy in asthma and COPD. useful for nocturnal dips

108
Q

describe methylxanthine

A

non steroid, non specific, anti inflammatory + bronchodilator

109
Q

what do mucolytics do

A

thin the mucous

110
Q

what type of steroids should and shouldn’t be used to treat acute asthma

A 
should= systemic 
shouldn't= inhaled
111
Q

when should a respiratory stimulant be used in asthma

A

NEVER

112
Q

what is more effective than the ICS/LABA combo used to treat COPD

A

ICS/LABA/LAMA combo

113
Q

when should the LABA/LAMA combo be used

A

when the inflammation is non eosinophilic

114
Q

what type of steroids should and shouldn’t be used to treat acute COPD

A 
should= systemic 
shouldn't= inhaled
115
Q

what does smoking activate

A

macrophages

116
Q

how is bronchoconstriction by smooth muscle initiated

A

M3 receptor activation by ACh

117
Q

what releases ACh

A

postganglionic parasympathetic fibres

118
Q

what do M1 muscarinic receptors do

A

facilitate fast neurotransmission mediated by ACh

119
Q

what do M2 muscarinic receptors do

A

act as inhibitory autoreceptors reducing release of ACh

120
Q

what do M3 muscarinic receptors do

A

mediate contraction of ASM to ACh

121
Q

what do muscarinic receptor facilitate

A

ganglionic transmission- nicotinic stimulation

122
Q

what does blockage of nicotonic stimulation stop

A

stops ACh ptoduction

123
Q

what muscarnic receptor adds to the blockage of M3 by reducing release of ACH

A

M1

124
Q

via what mechanism do M2 receptors work and their role in COPD management

A

negative feedback, stimulated by ACh and then triggers M1 and M3, so blockage counterproductive in COPD treatment

125
Q

which muscarinic receptor is targeted (blocked) first in the management of COPD

A

M3

126
Q

what do drugs ending in ium usually do (e.g. ipatropium (sama), and other LAMAs)

A

act on a ACh receptor- are competitive muscarinic receptor antagonists

127
Q

why are Quaternary structures beneficial in MAs

A

as positively charged and cant cross biological membranes to enter into blood stream and cause adverse effects (stop effects of parasympathetic system)

128
Q

what is first used to treat an acute constriction

A

B2 agonists

129
Q

why are muscarinic antagonists more effective for COPD

A

more effective but slower, decrease mucous secretion

130
Q

what reflex do MAs also repress

A

the cough (vago-vagal) reflex stimulated by the vagus nerve

131
Q

why are M3 selective blockers superior to ipratropium

A

functionally selective, Ip blocks all

132
Q

give an example of an M3 blocker and explain how they are selective

A

tiotropium, glycopyrronium, due to kinetics of drugs stay in M3 receptor longer

133
Q

what is salbutamol

A

a SABA

134
Q

what do B-adrenoceptor agonists do and dont do

A

bronchodilators but dont act on underlying inflammation

135
Q

what combination of drugs is best at increasing FEV1

A

B2 agonist and muscarinc antagonist

136
Q

when are LABA/LAMA combinations most effective

A

when deposited in same location in the airways (inhaled)

137
Q

what in LABA/LAMA treats underlying inflammation and immunosuppresses

A

neither of them

138
Q

what do muscarinic antagonist do when in combo with a LABA

A

block activation by ACh preventing contraction

139
Q

what do B2 agonists do when in combination with a LAMA

A

cause relaxation by binding to B2-adrenoreceptor

140
Q

what can be administered with LABA/LAMA combos to treat COPD

A

glucocorticoids- in moderately severe conditions

141
Q

what is rhinitis

A

acute or chronic inflammation of the nasal mucosa

142
Q

what are the three types of rhinitis

A

allergic (clear trigger), non-allergic, mixed (both allergic and non allergic features)

143
Q

what are the symptoms of rhinitis

A

rhinorrohea (runny nose), sneezing, itching, nasal congestion and obstruction

144
Q

what causes nasal congestion

A

dilated blood vessels in nasal mucosa

145
Q

what are the classifications of allergic rhinitis

A

seasonal, perennial, episodic

146
Q

what condition is allergic rhinitis very strongly linked to

A

asthma

147
Q

what are the similarities between allergic rhinitis and asthma

A

inhalation of allergen increases IgE levels which binds to receptors on mast cells and eosinophils. re-exposure causes granulation. calcium flood into cell releasing inflammatory mediators

148
Q

what does non allergic rhinitis NOT involve

A

IgE dependent event

149
Q

what can cause non allergic rhinitis

A

infection, hormones, vasomotor, drug induced, eosinophilia syndrome

150
Q

what may occupational rhinitis involve

A

both allergic and non allergic components

151
Q

what do rhinitis and rhinorrhoea both involve

A

increased mucosal blood flow, increased blood vessel permeability = increased volume of nasal mucosa and difficulty breathing in

152
Q

what are the 4 targets of treatments for rhinitis and rhinorrhoea

A

anti-inflammatory, mediator receptor blockade, nasal blood flow, anti-allergic

153
Q

what is used as anti-inflammatory treatment in rhinitis and rhinorrhoea

A

glucocorticoids (rhinitis with immunological basis)

154
Q

what is used as mediator receptor blockade treatment in rhinitis and rhinorrhoea

A

H1 receptor antagonists, CysLT1 receptor antagonists

155
Q

what is used as nasal blood flow treatment in rhinitis and rhinorrhoea

A

vasoconstrictors- decongestant, doesn’t remove mucous just reduces blood flow

156
Q

what is used as anti-allergic treatment in rhinitis and rhinorrhoea

A

sodium cromoglicate- immunosuppressant

157
Q

what is the mechanisms of glucocorticoids

A

reduce vascular permeability, recruitment and activity of inflammatory cells and release of cytokines and mediators, suppress recruitment of inflammatory cells in nasal mucosa

158
Q

how are glucocorticoids administered in rhinitis and rhinnorhoea

A

nasal spray for several weeks

159
Q

what is the mechanism for anti histamines

A

competitive antagonists that reduce effects of mast cell derived histamine

160
Q

what are the effects of the mast cell derived histamine

A

vasodilatation and increased capillary permeability, activation of sensory nerves, mucous secretion

161
Q

what is the mechanism of anti-cholinergic drugs

A

muscarinic receptor antagonists

162
Q

what is the mechanism of CysLT1 receptor antagonists

A

reduce the effect of CysLTs upon the nasal mucosa

163
Q

what is the mechanism of a vasoconstrictor

A

mimic the affect noradrenaline

Respiratory (26 decks)

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