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My Respiratory > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Where are cell bodies of the parasympathetic preganglionic fibres located?

A

brainstem

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2
Q

Where are cell bodies of parasympathetic postganglionic fibres located?

A

Walls of the bronchi and bronchioles

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3
Q

What nerves carries preganglionic fibres to the bronchial and bronchi walls?

A

Vagus nerve (CN X)

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4
Q

Stimulation of postganglionic cholinergic fibres cause what?

A

Bronchial smooth muscle contraction (ASM airway smooth muscle cells)

Mucus secretion from goblet cells

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5
Q

Which neurotransmitter is used in stimulation of postganglionic cholinergic fibres?

A

ACh (acetylocholine)

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6
Q

What are the receptors which the ACh binds to on the smooth muscle cells and goblet cells?

A

M3 muscarinic ACh receptors

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7
Q

what does Stimulation of postganglionic noncholinergic fibres cause?

A

Relaxation of smooth muscle cells (ASM)

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8
Q

What neurotransmitters are involved in the noncholinergic pathway?

A

Nitric oxide (NO)

Vasoactive intestinal peptide (VIP)

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9
Q

There is sympathetic innervation of bronchial smooth muscle in humans true or false?

A

false

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10
Q

How does the sympathetic system act on bronchial smooth muscle cells?

A

Nicotinic acetylcholine receptor (nAChR) which are located on the adrenal grand, chromaffin cells when stimulated release adrenaline into circulation which act on smooth muscles

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11
Q

Which receptors does the adrenaline act on in both goblet and smooth muscle cells?

A

beta2 adrenoceptors

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12
Q

What does sympathetic stimulation cause on the airways?

A
  1. ASM cells relaxation
  2. decreased mucus secretion on goblet cells
  3. increased mucociliary clearance on epithelial cells
  4. vascular smooth muscle contraction- alpha 1 adrenoceptors
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13
Q

How does the release of Ca2+ cause contraction of smooth muscles?

A
  1. Ca2+ activates calmodulin to Ca2+ calmodulin
  2. Inactive MLCK is activated by Ca2+ calmodulin to form active MLCK
  3. Active MLCK and phosphate group (formed from hydrolysis of ATP) Cause inactive myosin cross bridge to phopshyrlated cross bridge (binds to actin)
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14
Q

What enzyme is responsible for phosphorylation of Myosin light chain (MLC) (contraction)?

A

Myosin light chain kinase (MLCK)

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15
Q

What enzyme is responsible for dephosphorylation of myosin Light chain (relaxation)?

A

Myosin phosphatase

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16
Q

What is asthma?

A

recurrent and episodic condition of the obstruction to the airways in response to substances or stimuli

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17
Q

What are the main causes of asthma?

A
  1. Allergens
  2. Exercise (cold,dry air)
  3. Resouratiry infections
  4. smoke, dust and environmental pollutants
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18
Q

What effects does chronic asthma have on the airways?

A
  1. increased mass of smooth muscle (hyperplasia + hypertrophy)
  2. accumulation of intestitial fluid (oedema)
  3. increased secretion of mucus
  4. epithelial damage (exposes sensory nerve endings)
  5. Sub-epithelial fibrosis
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19
Q

What is acute severe asthma called?

A

status asthmaticus

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20
Q

What effect does air narrowing have on airway resistance?

ii. what does this cause

A

Increases it

ii. FEV1 and PEFR values decrease

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21
Q

Epithelial damage from chronic asthma exposes what type of sensory nerve endings?

A

C fibres- irritant receptors

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22
Q

What does epithelial damage lead to in the airways?

A

Hypersensitivity (X axis)

Hyper-reactivity (Y axis)

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23
Q

What is inhaled with provocation tests which real hyper-responsiveness?

A

Broncho constrictors (spasmogens)

e.g. histamine (activates ASM H1 receptors)

Methacholine (activates ASM M3 receptors)

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24
Q

What does an asthma attack consist of ?

A
  1. immediate phase- Bronchospasm Type 1 hypersensitivity reaction
  2. Delayed phase ( inflammatory reaction) Type IV hypersensitivity reaction
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25
Q

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

A

TH2 cell- strong response

T helper cell

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26
Q

What type of Th cells are part of cell-mediated immune response involving IgG and macrophages (nonatopic)?

A

TH1 cell- low level response

T helper Cell

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27
Q

What cell matures in TH2?

ii. what environment needs to be present for to occur?

A

TH0

ii. cytokine environment

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28
Q

How do TH2 cells activate B lymphocytes?

A
  1. directly binds to B cells

2. releases Interleukins which bind to B cells (IL 4)

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29
Q

What do B lymphocytes mature to?

A

IgE secreting plasma cells

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30
Q

Interleukin 5 (IL 5) which are released from TH2 cells cause what?

A

Activation of eosinophils

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31
Q

Mast cells express what in response to to IL 4 and IL 13 from TH 2 cells?

A

IgE receptors

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32
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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33
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 chemotaxins and chemokines that attract cells that cause inflammation (eosinophils)
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34
Q

What are the spasmogens released from mast cells?

A

Histamine

Leukotrienes ( LTC4,LTD4)

both also released by eosinophils.

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35
Q

What chemotaxins and chemokines are released?

A

LTB4

Platelet -activating factor (PAF)

Prostaglandins (PGD2)

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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

How do relievers treat asthma?

A

act as bronchodilators

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39
Q

How do controllers treat asthma?

A

Act as anti-inflammatory agents

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40
Q

Give examples of relievers?

A

Short acting beta 2 adrenoceptor agonists (SABAs)

Long acting Beta 2 adrenoceptor agonists (LABAs)

CysLT1 receptor antagonists-block cysLTs (LTC4, LTD4, LTE4) derived from mast cells and so cause smooth muscle relaxation, decreased mucus secretion and decreased oedema

Methylxanthines

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41
Q

Give examples of controllers?

A

Glucorticoids

Cromoglicate

Humanised monoclonal IgE antibodies

methylxanthines

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42
Q

Describe the differences between aerosol and oral therapy for asthma?

A

Pharmacokinetics:
Aerosol- slow absorption from lung surface and rapid systemic clearance
Oral- Good absorption and slow

systemic clearance
Dose: Aerosol: Low
Oral: High

systemic concentration of drugs:
aerosol - Low
Oral- high

Incidence of adverse effects:
Aerosol- Low
Oral- high

distribution of drug:
aerosol- reduced in severe airway disease oral- unaffected by any airway disease

Compliance:
aerosol: good with bronchodilators not good with anti-inflammatory.
Oral: Good with both

Ease of administration:
aerosol- difficult for small children and infirm people.
Oral: Easy

Effectiveness:
aerosol- only effective in mild to moderate diseases.
Oral: very effective

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43
Q

When are SABAs used?

A

first line treatment for mild/intermittent asthma

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44
Q

How are SABAs administered?

A

inhalation via metered dose/dry powder device

can be administered:

Oral(children)

IV (emergency)

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45
Q

How long does it take SABAs to act on bronchial smooth muscle?

A

Very rapid ( maximal effect within 30 mins) feel effect in 5 mins

lasts for 3-5 hours

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46
Q

What is the main effect of SABAs?

ii. what are the adverse effects?

A

Increase mucus clearance and decrease mediator release from mast cells

ii. Very few- fine tremor most common. Can have tachycardia, cardiac dysrhythmia and hypokalaemia

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47
Q

What is the main type of SABA?

A

salbutamol

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48
Q

When are LABAs used?

A

Useful for noctural asthma (lasts for 8 hours)

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49
Q

Should you use LABAs for acute relief of bronchospasm??

A

NO- slow to act especially salmeterol

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50
Q

Can LABAs be used as a monotherapy for asthma?

ii. if not then what should it be co-administered with?

A

No- can worsen asthma increase risk of death

ii. Always a glucocorticoid

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51
Q

Give examples of LABAs.

A

Salmeterol

Formoterol

52
Q

What should you use to reduce potentially harmful stimulation of Cardiac B1 adrenocopetors?

A

Selective Beta 2 adrenoceptor agonists

53
Q

What happens if you use non selective beta adrenoceptor agonists?

A

increase risk of bronchospasm

54
Q

When are CysLT1 receptor antagonists used?

A

Add on therapy (inhaled corticosteroids

used for early and late bronchospasm in mild persistent asthma

Effective against antigen and exercised induced bronchospasm

55
Q

What are the effects of cysLts?

ii. what are the adverse effects?

A

relax bronchial smooth muscle

ii. well tolerated can have headaches and GI upset

56
Q

How do you administer CysLts?

ii. when shouldn’t you administer them?

A

Orally

Acute severe asthma

57
Q

Give examples of CysLt1 receptor antagonist.

A

montelukast

zafirlukast

58
Q

Give examples of Methylxanthines

A

Theophylline

Aminophylline

59
Q

What effects do methylxanthines have?

A

Inhibit mediator release from mast cells

increase mucus clearance

increase diaphragmatic contractility

reduce fatigue- increases lung ventilation

60
Q

When are methylxanthines used?

ii. what are they co-administered with?

A

second line therapy

ii. B2 adrenoceptor agonist
and
glucorticoids

61
Q

How are methylxanthines administered?

A

orally

62
Q

What are the adverse effects of methylxanthines?

A

Supratherapeutic concentrations: Dysrhythmia, seizures and hypotension

therapeutic concentrations: Nausea, vomiting, abdominal discomfort and headache

63
Q

What are the two main steroid hormones synthesised by the adrenal cortex?

A
  1. Glucorticoids (zona fasiciculata)

2. Mineralocorticoids (zona glomerulosa)

64
Q

What are the effects of glucocorticoids?

A

Decreases inflammatory and immunological responses

increases Liver glycogen deposition, gluconeogenesis and glucose output from liver

Increases protein and bone catabolism

65
Q

what is the main glucocorticoid in the body?

A

cortisol

66
Q

What is the main mineralocorticoid which regulates salt retention via the kidney?

A

aldosterone

67
Q

Which type of steroid hormone is not wanted to treat inflammatory conditions?

A

mineralocorticoid

68
Q

When are glucocorticoids ineffective against bronchospasm?

ii. when is it mainly used?

A

When given acutely- no direct bronchodilator effect

ii. treatment in prophylaxis of asthma

69
Q

How are glucocorticoids administered?

A

inhalation- minimises adverse systemic effects

70
Q

What do glucorticoids bind to?

ii. specifically which receptor?

A

Nuclear receptors (class 1)

ii. GR alpha- bind to glucorticoid response elements

71
Q

What are the two main effects of clinically administered glucocorticoids in asthma treatment?

A
  1. prevent inflammation

2. resolve established inflammation

72
Q

How should glucocorticoids be administered?

A

Long term treatment- especially in combination with LABA

mild moderate asthma- inhalation from a metered dose inhaler

chronic/severe asthma- oral prednisolone with an inhaled steroid to reduce the oral dose required

73
Q

What are the main glucocorticoids used in an inhaler?

A

Beclometasone

budesonide

fluticasone

74
Q

What are the adverse effects of glucocorticoids in asthma?

A

Dysphonia

thrush

both caused by deposition of steroid in oropharynx

75
Q

When are cromones administered?

A

second line drug used prhophylactically in allergic asthma

used infrequently- used to be used a lot for children due to lack of adverse effects

76
Q

What is an example of a cromone?

A

sodium cromoglicate

77
Q

Give an example of a monoclonal antibody directed against IgE

A

omalizumab

given IV

78
Q

Give an example of a monoclonal antibody directed against IL 5?

A

Mepolizumab

very expensive- started being used against asthma associated with severe eosinophilia

79
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
80
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
81
Q

What are the two subtypes of COPD?

A
  1. chronic bronchitis

2. emphysema

82
Q

What are the symptoms of chronic bronchitis?

A
  1. Inflammation of bronchi and bronchioles
  2. cough
  3. Clear mucoid sputum
  4. Infections with purulent sputum
  5. Increasing breathlessness
83
Q

What are the symptoms of emphysema?

A

Distention and damage to alveoli

Destruction of acinal pouching in alveolal sacs

loss of elastic recoil

84
Q

What is the build up which leads to COPD?

A
  1. smoking (air pollution)
  2. Stimulation of resident alveolar macrophages
  3. Cytokine production
  4. Activation of neutrophils, CD8+, Increased macrophage numbers
  5. release of free radicals
85
Q

What is the main characteristic of COPD?

A

increased resistance to airflow during expiration

86
Q

Muscaranic receptor antagonists act against bronchoconstriction caused by which smooth muscle receptor?

A

M3 receptor

87
Q

Where are M1 muscarinic receptors found?

ii. what is their role?

A

Ganglia

Facilitate fast neurotransmission mediated by ACh acting on nictonic receptors

88
Q

Where are M2 muscarinic receptors found?

ii. what is their role

A

Postganglionic neurone terminals

act as inhibitory autoreceptors reducing release of ACh

89
Q

Where are M3 muscarinic receptors found?

ii. what is their role?

A

post junctional muscarinic end plate receptors found on smooth muscle effector submucosal glands

contraction of airway smooth muscle
increased secretion of submucosal glands

90
Q

What are the two types of competitive Muscarinic receptor antagonists used to treat COPD?

ii. how are they administered?

A
  1. SAMA
  2. LAMA
    ii. Inhalation
91
Q

Give an example of SAMA?

A

Ipratropium (non selective)

92
Q

Given examples of LAMA

A

Tiotropium (selective M3)

Glycopyrronium (selective M3)

aclidinum (selective M3)

93
Q

contraction of airway smooth muscle

increased secretion of submucosal glands

A

reduces absorption and systemic exposure

94
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
  3. reduces mucus secretion
95
Q

Why are selective M3 blockers superior to ipratropium?

A

Block of M3 and M1 is good

Block of M2 is not as release of ACh from post-ganglionic neuronse is increased by autoreceptor antagonism

96
Q

Which LABAs should not be used in acute bronchospasm?

A

Indacterol

olodaterol

97
Q

What is the best way to treating COPD?

A

Combination of B2 agonist and muscarinic antagonist

(Muscarinic antagonist- prevent contraction of airways)

(Beta 2 agonists cause relaxation of airways)

98
Q

When are LABA and LAMAs combinations at the most effective?

A

Deposited in the same location in the airways

99
Q

What is administered in combination inhalers for COPD?

A

Glucocorticoids and Beta agonist or muscarinic antagonist

100
Q

What is Rofumilast?

A

a selective PDE4 inhibitor - suppresses inflammation and emphysema in animals

oral treatment for severe COPD with chronic bronchitis

101
Q

What is rhinitis

A

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

102
Q

What are the main symptoms of rhinitis?

A

rhinorrohea- runny nose

sneezing

itching

nasal congestion and obstruction ( swelling o nasal mucosa largely due to dilated blood vessels- mainly cavernous sinusoids

103
Q

What types of rhinitis are there?

A
  1. allergic- involved IgE dependent events
  2. non-allergic- not involve IgE dependent events
  3. mixed
104
Q

What are the subtypes of allergic rhinitis?

A
  1. seasonal
  2. perennial
  3. episodic
105
Q

what is a triple inhaler? (for COPD)

A

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

106
Q

What are the causes of Non allergic rhinitis?

A
  1. infection
  2. hormonal imbalance
  3. Vasomotor disturbances
  4. Non allergeic rhinitis with eosinophilila syndrome (NARES)
  5. Drug induced (aspirin)
107
Q

What does occupational rhinitis involve?

A

allergic and non allergic components

108
Q

What do both rhinitis and rhinorrhoea involve?

A

Increased mucosal blood flow

increased blood vessel permeability

or both

this causes increases volume of nasal mucosa- difficulty breathing

109
Q

What is the mechanism of Glucocorticoids for rhinitis treatment?

A

reduces vascular permeability

recruitment and activity of inflammatory cells

110
Q

What type of rhinitis are Glucocorticoids mainly used to treat?

A

seasonal allergic rhinitis

perennial allergic rhinitis

can be also used for NARES and vasomotor rhinitis

111
Q

How are Glucocorticoids administered for rhinitis?

A

Topically as a spray - effective as a monotherapy takes several weeks to reduce all symptoms

can be given orally in short term

112
Q

What can Glucocorticoids be combined with to treat severe-moderate rhinitis

A

Anti-histamines

113
Q

What is the mechanism for anti-histamine (H1 receptor antagonists) for treatment of rhinitis?

A

Competitive antagonist- reduces effect of histamine from mast cells

114
Q

What are the effects of histamine?

A
  1. vasodilatation and increased capillary permeability
  2. Activation of sensory nerves
  3. mucus secretion from submucosal glands
115
Q

What type of rhinitis do anti-histamines treat?

A

Mainly allergic

116
Q

How are Antihistamines adminsitered?

ii. when are they administered?

A

orally or intranasal spray

effective as monotherapy

ii. first or second - primarily second due to reduced sedation

117
Q

Give examples of second generation anti-histamines

A

Loratidine

fexofenadine

118
Q

What is the mechanism for anti-cholinergic drugs for treating rhinitis?

A

Blocks ACh released from post-ganglionic parasympathetic fibres activates M receptors on nasal glands causing a watery secretion that contributes to rhinnorhoea

119
Q

What type of rhinitis do anti-cholinergic drugs treat?

A

Reduces rhinorrhoea in PAR and SAR - has no effect on other symptoms though

120
Q

How are anti-cholinergics administered?

A

intranasally

121
Q

Give an example of an anticholinergic drug.

A

ipratropium

122
Q

When do you use sodium cromoglicate?

A

maintenance treatment of allergic rhinitis

via nasal administration- less effective than nasal corticosteroids

123
Q

When should you use CysLt1 for rhinitis?

A

PAR and SAR

124
Q

Give an example of CysLT1

A

Montelukast

125
Q

What is the mechanism of vasoconstrictors?

A

Directly/indirectly mimic noradrenaline- cause vasoconstriction via activation of alpha 1 adrenoceptor

126
Q

What is oxymetazoline?

A

selective alpha 1 adrenoceptor agonist- intranasally administered- only short term too long and nasal congestion can occur

127
Q

what does Chronic agonist induced stimulation of airway beta-2 receptors results in?

A

Beta-2 receptor up regulation and enhanced receptor coupling to G protein -adenylyl cyclase

My Respiratory (5 decks)

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