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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
what type of Th cells are part of the cell-mediated immune response involving IgG and macrophages in response to an allergen? (non-atopic)
low-level Th1 response
26
what do interleukins signal between?
white blood cells
27
what type of environment fo Th2 cells produce?
cytokine environment
28
what is the induction phase in the development of allergic asthma?
antigen presentation | cloncal expansion and maturation
29
what cell type differentiates and activates in response to IL 5 released from Th2 cells?
eosinophils
30
what type of cells express IgE receptors in response to IL 4 and IL 13 released from Th2 cells?
mast cells (in airway tissues)
31
when the specific allergen becomes present and links to the antibodies covering the mast cell, what is stimulated?
calcium entry into mast cells causing the release of calcium from intracellular stores
32
when calcium enters the mast cells and calcium is released from intracellular stores what 2 things occur?
1. release of substances that cause airway smooth muscle contraction (spasmogens) 2. release of substances that attract cells that cause inflammation
33
what substances released from the mast cell are spasmogens?
histamine | leukotriens (LTC4 LTD4)
34
what substances released from the mast cells are chemotaxins/ cytokines?
LTB4, PAF, PGD2 | leukotriene, platelet activating factor, prostaglandin
35
what type of leukocytes do chemotaxins/cytokines released from mast cells (in response to an allergen) attract?
Th2 cells monocytes eosinophils
36
which group of substances released from a mast cell is responsible for the immediate phase response of an asthma attack?
spasmogens
37
what group of substances released from a mast cell is responsible for the delayed phase response of an asthma attack?
chemotaxins and cytokines
38
what does the inflamamtion caused by the inflammatory cells induced by chemotaxins and cytokines released by mast cells cause in the airways?
airway inflammation epithelial damage airway hyper-reactivity bronchospasm, wheezing, cough
39
what are the 2 types of drugs used in the treatment of asthma?
relievers | controllers/preventors
40
what are the function of relievers?
bronchodilators
41
what are the function of controllers/preventors?
anti-inflammation
42
what is the mechanism of bronchodilators?
B2-adrenoceptor agonists
43
once a B2-adrenoceptor has been stimulated in the airway smooth muscle, what is the result of the chain of pathways?
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]
44
what happens to the G-coupled protein receptors in the case of persistent activation of B2-adrenoceptors?
receptor desensitisation and endocytosis | loss of function
45
what kinases are involved in the desensitisation process of B2-adrenoceptors?
PKA (protein kinase A) | GRK (G protein receptor kinase)- specifically B-adrenoceptor kinases
46
what molecule causes linking of the desensitized B-adrenoceptor to the endocytotic machinery?
B-arrestin
47
what happens to the B-adrenoceptor once inside the cell?
recycles in endosomes or degraded in lysosomes
48
what is salbutamol?
short acting B2-adrenoceptor agonist (SABA)
49
what type of asthma drug are SABAs (eg salbutamol)? (reliever or preventor)
reliever | bronchodilator
50
how is a SABA (eg salbutamol) generally administered? | and why?
inhalation | to lessen systemic effects
51
when are SABAs administered oral or IV?
emergency
52
when is the maximal effect of SABAs (eg salbutamol?
within 30 mins
53
by stimulation of the sympathetic system what 3 effects do SABAs (eg salbutamol) have?
dilation of airway smooth muscle increased mucus clearance decreased mediator release from mast cells
54
what are the adverse effects of SABAs eg salbutamol? (rare when administered by inhalation) + why do they occur?
fine tremor tachycardia due to unanted systemic absorption
55
what salmeterol?
long acting B2-adrenoceptor agonist (LABA)
56
why are LABAs (eg salmeterol) not recommened for acute relief of bronchospasm despite technically being relievers (bronchodilators)?
relatively slow to act
57
when are especially LABAs useful?
nocturnal asthma
58
can SABAs be used in monotherapy?
yes
59
can LABAs be used in monotherapy?
no
60
why should you use selective B2-adrenoceptor agonists and not general adrenoceptor agonists for asthma treatment?
to reduce the potentially harmful stimulation of cardiac B1-adrenoceptors
61
why should propanolol not be used in asthmatic patients?
propanolol is a non-selective b-adrenoceptor antagonist so will cause the constriction of airway smooth muscle
62
what type of asthma drugs are cysLT1 receptor antagonists? | cysteinyl leukotriene receptor antagonists
relievers | bronchodilators
63
how do cysLT1 receptor antagonists work in patients with asthma?
block cysLTs (LTC4, LTD4, LTE4) derived from mast cells and so cause smooth muscle relaxation, decreased mucus secretion and decreased oedema
64
what is montelukast or zafirlukast?
a cysLT1 receptor antagonist
65
what type of asthma drugs are cysLT1 receptor antagonists? | cysteinyl leukotriene receptor antagonists
relievers (bronchodilators) [but not recommeneded for relief of acute severe asthma]
66
how are cysLT1 receptor antagonists administered?
oral route
67
what are theophylline and aminophylline?
xanthines
68
what type of asthma drugs are xanthines?
relievers AND controllors/preventors
69
how are xanthines prepared and administered?
sustained release preparations by oral route
70
how do xanthines work?
relax bronchial smooth muscle inhibit mediator release from mast cells increase mucus clearance
71
what are the adverse effects of xanthines?
``` nausea vomiting abdominal discomfort headache (also numerous drug interactions) ```
72
where are steroid hormones synthesised in the body?
adrenal cortex
73
what 2 types of steroid hormone are synthesised and released on demand from the adrenal cortex?
glucocorticoids | mineralcorticoids
74
what is the main glucocorticoid in the body?
cortisol (hydrocortisone)
75
what are the 2 main functions of glucocorticoids that are important in immune regulation?
decreases inflammatory responses | decreases immunological responses
76
why are exogenous glucocorticoids not recommened for systemic use? (unless its an emergency)
multiple effects on metabolism
77
what is the main mineralcorticoid in the body?
aldosterone
78
what is the main function of mineralcorticoids?
regulate the retention of salt (and therefore water) by the kidney
79
what type of drug is beclometasone?
a corticosteroid
80
what type of asthma drug are corticosteroids?
preventers | anti-inflammatory NOT bronchodilation
81
what do glucocorticoids signal via within cells?
nuclear receptors | specifically GRalpha
82
how do glucocorticoids enter cells across the plasma membrane?
diffusion
83
within the nucleus what happens to the glucocorticoid-GRa monomer complex?
assemle into homodimers and then bind to glucocorticoid response elements (GRE) in the promotor region of specific genes
84
what is the end result of glucocorticoids entering into a cell?
transcription of specific genes are transactivated or transrepressed to increase expression of anti-inflamatory proteins and decrease expression of inflammatory proteins
85
what is the function of histones?
package the DNA double helix within the nucleus
86
what is chromatin?
DNA plus histones
87
in addition to its function with GRE (glucocorticoids response elements) what can glucorticoids do to chromatin?
deacetylation of histones to modify chromatin structure to become condensed and not able to be transcribed
88
what are the 4 main effects of glucocorticoids that are particularly relevant to inflammation in bronchial asthma?
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
what are the 4 smaller structural effects of glucocorticoids that are particularly relevant to inflammation in bronchial asthma?
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
why are corticosteroids useful in the long term not short term?
they do not alleviate early stage bronchospasm but resolve established inflammation
91
when does efficacy of corticosteroids develop?
over several days
92
what are the most common adverse effects of corticosteroid inhalers? (and why?)
dysphonia (hoarse and weak voice) oropharyngeal thrush due to steroid deposit in the oropharynx
93
what is a good way to prevent dysphonia and oropharyngeal thrush when using corticosteroid inhalers?
drinking water after using inhaler
94
what form of oral corticosteroid is used in chronic, severe or rapidly deteriorating asthma?
oral prednisolone
95
how do cromolins work?
mast cell stabiliser: prevents degranulation weak anti-inflammatory effect decreased hypersensitivity of sensory C-fibres
96
what is sodium cromoglicate?
cromolin
97
how is sodium cromoglicate administered for asthma treatment?
inhalation
98
what type of drug is sodium cromoglicate?
reliever AND preventer | ie bronchodilation and anti-inflammatory but not recommended for use for relief during an acute attack
99
how long does efficacy of sodium cromoglicate take to develop?
several weeks
100
what is omalizumab?
monoclonal antibody against IgE
101
how do monoclonal antibodies work in the treatment of asthma?
Bind IgE via Fc to prevent attachment to FC receptors | -prevents mast cells becoming activated
102
how are monoclonal antibodies administered?
IV
103
what is COPD?
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
what can COPD be divided into?
chronic bronchitis | emphysema
105
what are 5 characteristics of chronic bronchitis?
1, inflammation of bronchi and bronchioles 2. cough 3. clear mucoid sputum 4. infections with purulent sputum 4. increasing breathlessness
106
what are the 2 characteristics of emphysema?
1. distension and damage to alveoli | 2. destruction of acinal pouching in alveolar sacs
107
where are M1 muscarinic ACh receptors int he airways located?
in galnglia
108
what is the function M1 muscarinic ACh receptors in the airways?
faciliate transmission mediated by ACh acting on nicotinic receptors
109
where are M2 muscarinic ACh receptors in the airways located?
postganglionic neurone terminals
110
what is the function of M2 muscarinic ACh receptors in the airways?
act as inhibitory autoreceptors reducing the release of ACh
111
where are M3 muscarinic ACh receptors in the airways located?
smooth muscle effector | submucosal glands
112
what is the function of M3 muscarinic ACh receptors in the airways?
contraction of airway smooth muscle | increased secretion of submucosal glands
113
what is ipratropium?
short acting muscarinic antagonists (SAMAs)
114
what is tiotropium?
long acting muscarnic antagonists (LAMAs)
115
how are muscarinic antagonists administered?
inhalation
116
atropine is also a muscarinic antagoinist, how is it different to the muscarinic antagonists used in COPD?
contains a tertiary amine instead of a quaternary ammonium like ipratropium and tiotropium
117
why is a quaternary ammonium more useful than a tertiary amine in the treatment of COPD?
reduces absorption and systemic exposure
118
what is the general onset of action for muscarinic antagonists used in the treatment of COPD? (SAMAs and LAMAs)
>30mins onest of action | delayed
119
what 3 effects do muscarinic antagonists have in the treatment of COPD do?
1. relaxes bronchospasm caused by irritant stimuli (which initiate a vagal reflex that liberates ACh) 2. blocks ACh-mediated basal tone 3. reduces mucus secretion
120
why do muscarinic ACh receptor antagonists have few adverse effects?
little systemic absorption due to quaternary ammonium group
121
why is tiotropium more effective than ipatropium? (apart from the fact it is longer acting)
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
what 4 -adrenoceptor agonists are also used in the treatment of COPD?
salbutamol (SABA) | salmeterol, formoterol and indacaterol (LABA)
123
why is indacaterol classed as an ultra-LABA?
rapid onset of action vs normal LABAs
124
what combination of drugs is especially effective in moderate COPD?
LABA/LAMA combo | eg salmeterol/tiotropium
125
what is the prominent PDE expressed in neutrophils, T cells and macrophages?
PDE4
126
what does PDE4 cause?
inflammation
127
what is rofumilast?
a selective PDE4 inhibitor
128
what does rofumilast do?
suppresses inflammation and emphysema
129
how is rofumilast administered?
oral
130
what type of adverse effects does rofumilast have?
GI effects | due to PO administration
131
even though glucocorticoids are of benefit in COPD patients who develop frequent and severe exacerbations, why might there be glucocorticoid unresponsiveness in some patients?
due to oxidative/nitrative stress associated with chronic inhalation of tobacco and smoke HDAC2 is reduced in COPD
132
what is a triple inhaler?
LABA/LAMA/glucocortidoic (eg formoterol/tiotropium/ciclesonide) not lisenced for use
133
what is rhinitis?
a common disease involving acute or chronic inflammation of the nasal mucosa
134
what 4 features is rhinitis charactersed by?
1. rhinorrhoea (runny nose) 2. sneezing 3. itching 4. nasal congestion and obstruction
135
why does rhinorrohea occur in rhinitis?
watery mucus accumulation in nasal cavity
136
why does nasal congestion and obstruction occur in rhinitis?
swelling of the nasal mucosa due to dilated blood vessels
137
what are the 3 types of rhinitis?
allergic non-allergic mixed
138
what are the 3 types of allergic rhinitis?
seasonal (SAR) perennial (PAR) episodic
139
what are some non-allergic causes of rhinitis?
``` infection hormonal imbalance (eg preg) vasomotor disturbances medications nonallergic rhinitis with eosiophilia syndrome (NARES) ```
140
what are the 5 types of rhinitis/rhinorrhoea treatment?
``` glucocorticoids H1 receptor antagonists CysLT1 receptor antagonists vasoconstrictors sodium chromoglicate ```
141
what is the function of glucocorticoids in the treatment of rhinitis/rhinorrhoea?
anti-inflammatory
142
what is the function of H1 receptor antagonists in the treatment of rhinitis/rhinorrhoea?
reduce effects of mast cell derived histamine eg prevent vasodilation, prevent activation of sensory nerves, decrease mucous secretion)
143
what is the function of sodium chromoglicate in the treatment of rhinitis/rhinorrhoea?
anti-allergic
144
what is the mainstay treatment of SAR and PAR?
glucocorticoids
145
in the treatment of rhinitis/rhinorrhoea how are glucocorticoids administered?
topical nasal spray | OD
146
what 3 glucocorticoids can be used in the treatment of rhinitis/rhinorrhoea?
beclometasone fluticasone prednisolone
147
which types of rhinitis ar H1 receptor antagonists more effective in?
SAR, PAR and episodic AR | not too good at non-allergic
148
how are H1 receptor antagonists administered?
orally or topical nasal spray
149
what are loratidine, fexofenadine and cetirizine?
second generation H1 receptor antagonists
150
what is the function of cysLT1 receptor antagonists in the treatment of rhinitis/rhinorrhoea?
reduces the effects of CysLTs upon the nasal mucosa
151
what is the function of vasoconstrictors in the treatment of rhinitis/rhinorrhoea?
decrease nasal blood flow via a1 adrenoceptors
152
what is the function of sodium chromoglicate in the treatment of rhinitis/rhinorrhoea?
mast cell stabilisers- prevent degranulation
153
what is the sole muscarinic receptor antagonist agent used for rhinorrhoea?
ipatropium
154
how is ipatropium administered for rhinorrhoea?
topical nasal spray
155
how is sodium cromoglicate administered for rhinitis/rhinorrhoea?
topical nasal spray
156
what type of rhinitis are CysLT1 receptor antagonists effective at treating?
PAR and SAR
157
how are CysLT1s administered for treatment of rhinitis/rhinorrhoea?
oral
158
what is the sole CysLT1s receptor antagonist used for the treatment of rhinitis/rhinorrhoea?
montelukast
159
what is oxymetazoline?
a selective a1-adrenoceptor (Vasoconstrictor) used for allergic rhinitis
160
how is oxymetazoline administered?
topical nasal spray
161
why does rebound increase in nasal congestion occur after use of oxymetaxoline for a few days?
receptor desensitisation and down regulation
162
what is the name for the rebound increase in nasal congestion which occurs after use of oxymetaxoline for a few days?
rhinitis medicamentosa

Respiratory (10 decks)

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