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Pharmacology Flashcards

1
Q

what is the role of the parasympathetic system in the regulation of airways

A

stimulation of postglanglionic CHOLINERGIC fibres cause:

  1. ASM contraction
  2. increased mucus secretions

stimulation of postglanglionic NON-CHOLINERGIC fibres cause:
1. ASM relaxation

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2
Q

what is ASM contraction mediated by

A

M3 muscarininc ACh receptors

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3
Q

what is mucus secretion mediated by

A

M3 muscarininc ACh receptors

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4
Q

what is ASM relaxation (via NON-cholinergic fibres) mediated by

A

NO and vasoactive intestinal peptide

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5
Q

what is the role of the sympathetic system in the regulation of airways

A

THERE IS NO INNERVATION OF ASM

stimulation of submucosal glands and smooth muscle blood vessels causes:

  1. ASM relaxation
  2. decreased mucus secretions
  3. increased mucocilliary clearance
  4. vascular smooth muscle contraction
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6
Q

what is bronchial smooth muscle relaxation mediated by (in sympathetic stimulation)

A

cholinergic release of adrenal from the adrenal glands acting upon the B2-adrenoceptors

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7
Q

what is decreased mucus secretion mediated by

A

B2-adrenoceptors

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8
Q

what is increased mucocilliary clearance mediated by

A

B2-adrenoceptors

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9
Q

what is vascular smooth muscle contraction mediated by

A

A1-adrenoceptors

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10
Q

what is asthma

A

recurrent and reversible obstruction to the airways in response to substances

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11
Q

describe the pathological changes in the airways that occurs in chronic/poorly controlled asthma

A
  1. increased smooth muscle mass
  2. accumulation of interstitial fluid (oedema)
  3. increased secretion of mucus
  4. epithelial damage
  5. sub-epithelial fibrosis
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12
Q

what does epithelial damage result in

A

exposure of sensory nerve endings causing increased sensitivity to bronchocontstrictor influences

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13
Q

what is hyper-sensitivity

A

decreased tolerance to bronchoconstriction

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14
Q

what is hyper-activity

A

increased response to bronchoconstriction

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15
Q

what is the reaction of a non-atopic individual to an antigen (TH____ + what immune cells)

A

low level TH1 response

cell mediated immune response involving IgG and macrophages

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16
Q

what is the reaction of an atopic individual to an antigen (TH____ + what immune cells)

A

strong TH2 response

antibody mediated immune response involving IgE

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17
Q

what are the 2 phases of an asthma attack

A
  1. immediate

2. delayed

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18
Q

describe the immediate phase of an asthma attack

A

eliciting agent is recognised and processed

mast cells and mononuclear cells release histamine etc. causing bronchospasm and early inflammation

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19
Q

describe the delayed phase of an asthma attack

A

infiltration of cytokine releasing TH2 cleaned monocytes which activate inflammatory cells (especially eosinophils)
mediators and eosinophilic proteins are released causing epithelial damage, airway inflammation, hyper-responsiveness, bronchospasm, wheezing, mucus over secretion, cough

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20
Q

what do TH0 cells mature to

A

TH1 and TH2

prefer to mature to TH2

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21
Q

what do TH2 cells do

A

activate B cells in 2 ways:

  1. by binding
  2. via IL-4 production

activate Eosinophils in response to IL-5

release IL-4 and IL-13 which causes mast cells to express IgE receptors

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22
Q

what do B cells mature to

A

plasma cells

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23
Q

what do plasma cells secrete

A

IgE

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24
Q

what cytokines does TH2 release

A

IL-4
IL-5
IL-13

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25
what does IL-4 do
activates B cells and causes mast cells to express IgE receptors
26
what does IL-5 do
activated eosinophils
27
what does IL-13 do
causes mast cells to express IgE receptors
28
what are the 2 pharmacological method of asthma
relievers (bronchodilators) | controllers/preventers
29
Give examples of relievers (bronchodilators)
SABA LABA CystLt 1 receptor antagonist methylxanthines
30
what is a SAMA
short acting B2-adrenoceptor agonist
31
what is a LABA
long acting B2-adrenoceptor agonist
32
give examples of controllers/preventers
inhaled corticosteroids (ICS) cromoglicate humanised monoclonal IgE antibodies methylxanthines
33
describe the mechanism of action of LABA and SABA
bind to B2-adrenoceptor causing smooth muscle relaxtion
34
give examples of SABA
salbutamol, albuterol
35
give examples of LABA
salmeterol, formeterol
36
describe the mechanism of action of CystLt 1 receptor antagonist
act COMPETITIVELY at the CystLt 1 receptor
37
give examples of CystLt 1 receptor antagonist
montelukast, zafirlukast
38
describe the mechanism of action of methylxanthines
no one knows
39
give examples of methylxanthines
theophylline, aminophylline
40
describe the mechanism of action of cromones
no one knows | may be mast cell stabilisers
41
give an example of cromone
sodium cromoglicate
42
describe the mechanism of action of monoclonal IgE antibodies
binds to IgE via Fc to prevent attachment to FC receptors to suppress mast cell response to allergens
43
give an example of humanised monoclonal IgE antibodies
omalizumab
44
how are cromones used
infrequently used PROPHYLACTICALLY in kids
45
describe the mechanism of action of Glucocorticoids
suppress inflammation: prevent it and resolve established inflammation
46
give examples of ICS
beclometasone, budesonide
47
give example of ORAL steroids
prednisolone
48
common side effects of ICS
dysphonia (hoarse/weak voice) | thrush (candidiasis)
49
common side effects of LABAs/SABAs
``` fine tremor (common) tachycardia, cardiac dysrhymia, hypokalaemia ```
50
how should a LABA be administered
CO-ADMINISTERED with a Glucocorticoid or as an add on therapy
51
can LABA be prescribed on its own
NO
52
can SABA be prescribed on its own
yes
53
how are CystLt 1 receptor antagonist administered
orally
54
how are methlyxamines administered
orally
55
side effects of methlyxamines
MANY, very narrow therapeutic window nausea, vomiting, abdominal discomfort, headache (common) dysrhymia, seizures, hypotension (rarer)
56
describe the MOLECULAR mechanism of action of Glucocorticoids
enters cells via diffusion series of interactions results in the transcription of specific genes to activate OR repress mRNA levels and the rate of synthesis of mediator proteins
57
what causes the anti-inflammatory actions of Glucocorticoids
increases the transcription of genes encoding anti-inflammatory proteins decreases the ranscription of genes encoding inflammatory proteins decrease formation of TH2 cytokine prevents production of IgE antibodies prevents allergen-induced influx of eosinophils into lungs reduce the number of cells and decrease Fc expression
58
how is omalizumab administered
IV
59
why is synthetic derivates of cortisol used instead of the real thing
they contain NO traces of unwanted mineralocorticoids
60
what 2 conditions make up COPD
chronic bronchitis | emphysema
61
what is chronic bronchitis
inflammation of bronchi/bronchioles
62
what does emphysema result in
distension + damage to alveoli
63
what receptor causes contraction of the airways in COPD
muscarinic acetylchloline (M3) receptor
64
how does muscarinic acetylchloline (M3) receptor causes contraction of airway smooth muscle
stimulation of M3 leads to release of Ca2+ from Sarcoplasmic reticulum which causes contraction
65
what does stimulation of muscarinic acetylchloline (M1) receptor result in
fast neurotransmission
66
what is stimulation of muscarinic acetylchloline (M1) receptor mediated by
ACh acting on nicotinic receptors
67
what does stimulation of muscarinic acetylchloline (M2) receptor result in
inhibition of ACh release
68
what does stimulation of muscarinic acetylchloline (M3) receptor result in
airway smooth muscle contraction
69
treatment of COPD
``` SAMA LAMA SABA LABA ICS ```
70
can you mix SAMA and LAMA
No
71
give an example of a SAMA
ipratropium
72
give an example of LAMA
tiotropium
73
what is the mechanism of action for ipratropium
it is an non-selective, anti-cholinergic bronchodilator
74
why is it not useful to block M2 receptors in COPD
active M2 receptors will inhibit further ACh release
75
what are LABA/SABA used for
bronchodilation
76
what drugs are used in the treatment of allergic and non-allergic rhinitis (4)
1. steroids = anti-inflammatory 2. antihistiamines 3. cysLT's 4. sodium cromoglicate
77
what is the mechanism of action of antihistiamines
competitive antagonists of H1 receptors = reduces effects of mast cells
78
what muscarinic acetylchloline receptors does ipratropium block
M1, M2, M3
79
what muscarinic acetylchloline receptors does tiotropium block
M3
80
describe the selectivity of tiotropium
M3 selective
81
describe the selectivity of ipratropium
NON-selective
82
give an example of PDE4 inhibitor
Romfumilast
83
what does the drug "Romfumilast" do?
suppresses inflmaation and emphysema in COPD
84
what is Phosphodiesterase-4 (PDE4)
the main PDE expressed in neutrophils, T cells and macrophages
85
what cells express PDE
neutrophils T cells macrophages
86
how are cromones administered
inhaled
87
when would "Romfumilast" be used
as an add on to ICS + LABA+ LAMA | fairly last line
88
what do mucolytics do
reduce sputum viscosity and aid sputum expectoration | rarely used
89
where are M1 receptors located
ganglia
90
where are M2 receptors located
postganglionic neurone terminals
91
where are M3 receptors located
ASM
92
how are SAMAs administered
via inhalation
93
how are LAMAs administered
via inhalation
94
how do LAMA and SAMA drug names end
"-ium"
95
what type pf ammonium group is found on SAMAs and LAMAs, what charge does it have
quaternary | postive charge
96
LAMA/SAMA blocks which reflex
cough reflex
97
how do SABA drug names end
"-mol"
98
how do LABA drug names end
"-rol"
99
explain the logic behind combining SABA/SAMA or LABA/LAMA
SABA = causes relaxation SAMA = prevents contraction SYNERGISTIC ACTIONS

Resp - mine (18 decks)

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