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Pharmacology Flashcards

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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
when might an oral asthma drug be used?
In children or people unable to sufficiently use an inhaler
26
what are the advantages of using aerosol asthma drugs?
``` low dose required effective distribution effective for bronchodilators effective in mild/moderate disease little risk of adverse affects as drug rapidly clears systemic circulation ```
27
what are the advantages of using oral asthma drugs?
easy to administer, as unaffected by airway diseae easy to administer effective in severe disease
28
what is the mechanism of a B2- Adrenoceptor agonist?
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
29
which drug type act as physiological antagonists of all spasmogens?
B2- adrenoceptor agonists
30
what does SABA stand for?
short acting B2-ADR agonists
31
what does LABA stand for?
long acting B2-ADR agonists
32
salbutamol is an example of which type of B2-ADR agonist?
SABA
33
what is the usual route of administration for salbutamol?
inhaler
34
how might salbutamol be administered in more severe cases?
nebulised oral (in children) IV
35
How long does it take for salbutamol to act and how long for maximal effect?
5 mins | 30 mins
36
what is the effect of salbutamol?
Bronchodilation (ASM cell relaxaation) Increased mucus clearance decreased mediator release from mast cells and monocytes
37
what are some potential adverse effects of salbutamol?
fine tremor (can be observed in a general examination) tachycardia cardiac dysrythmia hypokalaemia (low blood potassium levels)
38
salmeterol and formoterol are examples of which type of B2-ADR agonist?
LABA
39
What should LABAs be used for?
Nocturnal asthma | Add on therapy in astma inadequately controlled by corticosteroids
40
what kind of drug is isoprenaline?
a non-selective B2-ADR agonist
41
what adverse side effect could using a non-selective B2-ADR agonist potentially cause?
stimulation of cardiac B1-ADR
42
propranolol is an example of which kind of drug?
non-selective B-ADR antagonist
43
why should using a B-ADR antagonist for asthma be carefully considered?
risk of causing bronchospasm
44
LTC4, LTD4 and LTE4 are examples of what? and where are they derived from?
CysLTs (cysteinly leukotrienes) | derived from mast cells & infiltrating inflammatory cells
45
what do CysLT1 receptor antagonists prevent?
ASM contraction mucus secretion oedema
46
montelukast and zafirlukst are example of what type of drug?
CysLT1 receptor antagonists
47
when should CysLT1 receptor antagonists be used?
As an add on therapyagainst early and late bronchospasm in mild persistent asthma Should be used with corticosteroids in more severe conditions
48
which bronchosmasms are CysLT1 receptor antagonists effective against?
antigen induced | exercise induced
49
how are CysLT1 receptor antagonists administered?
Oral route
50
Theophylline and aminophylline are example of which asthma drug?
Methylxanthines
51
what is the mechanism of action for methylxantines?
uncertain might inhibit isoforms of phosphodiesterases, which inactivate cAMP and cGMP
52
how are methylxanthines administered?
oral route
53
which asthma drug has a very narrow therapeutic window?
methylxanthines
54
which asthma drug combines bronchodilatory and anti-inflammatory responses?
methylxanthines
55
which major classes of steroids are synthesised in the adrenal cortex and released into the circulation?
glucocorticoids | mineralocorticoids
56
what are the main essential processes glucocorticoids regulate?
decrease inflammatory responses | decrease immunological responses
57
mineralocorticoids (eg. aldosteone) regulate what?
retention of salt and water by the kidney
58
what are the main synthetic derivatives of cortisol used in asthma?
Beclometasone Budesonide Fluticasone
59
What are glucocorticoids for?
for the prophylaxis of asthma (prevention)
60
How are glucocorticoids administered?
inhalational route
61
How do glucocorticoids signal?
via nuclear receptors- specifically GRa
62
What are glucocorticoid effects on gene transcription?
increase transcription of genes encoding anti-inflammatory proteins Decrease transcription of genes encoding inflammatory proteins
63
What do glucocorticoids do to inflammatory response?
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
what are cromones?
second line drug used prophylactically in childhood asthma (mast cell stabilizers) has no direct effect on ASM
65
what is omalizumab?
a monoclonal antibody directed against IgE
66
what is mepolizumab?
a monoclonal antibody directed against IL-5
67
What is chronic bronchitis?
``` Inflammation of bronchi and bronchioles Cough Clear mucoid sputum Infections with purulent sputum Increasing breathlessness ```
68
What is emphysema?
Distension and damage to alveoli Destruction of acinial pouching in alveolar sacs Loss of elastic recoil
69
What do muscarinic receptor antagonists do?
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
What receptor responds to ACh released from postganglionic parasympathetic fibres?
M3 receptors
71
where are M1 receptors located?
Ganglia
72
where are M2 receptors located?
postganglionic neurone terminals
73
where are M3 receptors located?
ASM
74
what is the function of M1 receptors?
facilitate fast neurotrasmission mediated by ACh acting on nicotinic receptors reducing ACh release
75
what is the function of M2 receptors?
act as inhibitory autoreceptors reducu
76
what is the function of M3 receptors?
Mediate contraction to ACh
77
which SAMAs are used for COPD treatment?
Ipratropium
78
which LAMAs are used for COPD treatment?
Tiotropium Glycopyrronium Aclidinium Umeclidinium
79
how are SAMA and LAMA COPD treatments administered?
By inhalation | Quaternary ammonium group reduces absorption and systematic exposure
80
what weak anti-inflammatory drug is used in allergic asthma? particularly in children/young people?
Inhaled sodium chroglycate

Respiratory (19 decks)

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