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Respiratory (Annie) > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what does stimulation of post-ganglionic cholinergic fibres cause? (2)
(Parasympathetic)

A

1) bronchial smooth muscle contraction

2) increased mucus secretion

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2
Q

what is bronchial smooth muscle contraction mediated by?

Para

A
  • M3 muscarinic ACh receptors on airway smooth muscle cells
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3
Q

what is mucus secretion mediated by?

para

A
  • M3 muscarinic ACh receptors on gland (goblet) cells
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4
Q

what does stimulation of post-ganglionic non-cholinergic fibres cause?
(parasympathetic)

A

1) bronchial smooth muscle relaxation

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5
Q

what is bronchial smooth muscle relaxation mediated by?

A
  • nitric oxide & vasoactive intestinal peptide (VIP)
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6
Q

since there is no innervation of bronchial smooth muscle in the SYMPATHETIC division, what mechanism is used to alleviate asthma symptoms?

A
  • post-ganglionic fibres supply sub-mucosal glands and smooth muscle of blood vessels
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7
Q

In the sympathetic division, what brings about bronchial smooth muscle relaxation via B2-adrenoceptors on ASM cells?

A
  • activation by release of adrenaline from adrenal gland
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8
Q

In the sympathetic division, what is the result of stimulated B2-adrenoreceptors? (3)

A

1) Bronchial smooth muscle relaxation
2) Decreased mucous secretion (on gland (goblet) cells)
3) Increased mucociliary clearance (on epithelial cells)

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9
Q

In the sympathetic division, what is the result of stimulated Alpha-1 adrenoceptors?

A
  • vascular smooth muscle contraction
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10
Q

describe how contraction of Airway smooth muscle occurs due to transmitters (proteins or hormones)?

A

1) activation of G-protein coupled receptor via a transmitter (hormone or protein)

(transmitter is cholinergic transmitter = parasympathetic)
(G-protein is specific = GQ/11)
(activated GQ/11 activated phospholipase C = PLC)
(PLC generates this intracellular signals IP3)

2) generates an intracellular signal IP3
3) IP3 carries signal to an IP3 receptor
4) mediates calcium release

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11
Q

describe how contraction in airway smooth muscle when initiated by calcium.

A

1) Ca binds to calmodulin (calcum compound)
2) this compound then activates a kinase = Myosin light chain kinase (MLCK)

3) active MLCK phosphorylates a myosin cross bridge
(by hydrolysing an ATP, yielding an inorganic phosphate which is transferred to the inactivemyosin cross bridge)

4) the cross bridge glides across actin, causing contraction

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12
Q

since contraction of ASM results from phosphorylation of myosin light chain cross bridge due to presence of Ca, how does RELAXATION of ASM occur?

A

= DEPHOSPHORLYATION of MLC by myosin phosphatase

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13
Q

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

A

phosphorylation exceeds dephos…

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14
Q

what does relaxation require in terms of intracellular Ca2+ concentration to basal level and how is it achieved?

A

1) requires return of Ca2+ concentration to a basal level

2) achieved by active transport

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15
Q

what is the activity of myosin light chain kinase and myosin phosphatase dependent on?

A

= extracellular signals

  • e.g. adrenaline activating B2-adrenoceptors
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16
Q

what 5 pathological changes occur to the bronchioles in chronic asthma as a result of long standing inflammation.

A

1) increased mass of smooth muscle
- hyperplasia & hypertrophy

2) accumulation of interstitial fluid
- oedema

3) increased secretion of mucus

4) epithelial damage
- exposing sensory nerve endings

5) sub-epithelial fibrosis

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17
Q

what effect does airway narrowing by inflammation & broncho-constriction have on FEV1 & PEFR?

A
  • airway resistance causing deceased FEV1 & PEFR
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18
Q

what are the 2 components in bronchial hyper-responsiveness in asthma?

A

1) hypersensitivity

2) hypereactivity

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19
Q

what 2 factors cause hypersensitivity & hyperactivity in bronchial hyper-responsiveness in asthma.

A

1) epithelial damage
2) exposing sensory nerve endings
= contributing to increased sensitivity of the airways to broncho-constrictor influences

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20
Q

what type of hypersensitivity correlates to the early phase of an asthma attack?
- bronchospasm & acute inflammation

A

type I hypersensitivity

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21
Q

what type of hypersensitivity correlates to the late phase of an asthma attack?
- bronchospasm & delayed inflammation

A

type IV hypersensitivity

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22
Q

in non-atopic individuals, in response to an allergen & phagocytosis by antigen presenting cells, describe the response.

A
  • low level TH1 response

- cell mediated immune repose involved IgG & macrophages

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23
Q

in atopic individuals, in response to an allergen & phagocytosis by antigen presenting cells, describe the response.

A
  • strong TH2 response
  • antibody mediated immune response
  • involving IgE
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24
Q

in the development of asthma, what does the initial presentation of an antigen innate?

A
  • an ADAPTIVE immune response
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25
Q

describe the induction phase of the adaptive immune response that leads to allergic asthma.

A

1) antigen presentation
2) CD4+ T cells colonise into THO cells
3) THO cells differentiate into TH1 or TH2 cells
4) TH2 cells activate B cells with the help of IL-4
5) activated B cells mature plasma cells which secrete IgE

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26
Q

what do eosinophils differentiate & activate in response to?

A

in response to IL5, released from TH2 cells

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27
Q

what do the mast cells in airway tissue express IgE receptors in response to?

A

in response to IL4 and IL13, released from TH2 cells

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28
Q

after the TH2 lymphocyte activation, what does the cross link IgE receptors stimulate?

A

stimulate;

  • calcium entry into mast cells
  • release of Ca2+ from intracellular stores
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29
Q

what does entry and release of Ca2+ evoke?

2

A

1) release of secretary granules containing performed histamine & production & release of other agents
- e.g. leukotrienes, LTC4 & LTD4) causing ASM contraction

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

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30
Q

what are the 2 phases of an asthma attack?

A

1) immediate

2) late phase

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31
Q

what are the products of mast cell and mononuclear cells that result in broncho-spasms & early inflammation in the IMMEDIATE PHASE ASTHMA ATTACK.

A

1) spasmogens
2) CysLTs
3) histamine

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32
Q

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

A

1) cytokines

2) chemotaxis

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33
Q

what inflammatory cells in particular is activated in the LATE PHASE ASTHMA ATTACK

A

eosinophils

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34
Q

What 4 pathological things happen in the late phase of an asthma attack?

A

1) epithelial damage
2) airway inflammation
3) airway hyper responsiveness
4) bronchospasm, wheezing, mucus over-secretion & cough

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35
Q

what are the 2 categories of drugs used to treat asthma?

A

1) relievers

2) controllers

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36
Q
  • what do delivers do?

- give 3 examples of relievers

A

= bronchodilators

1) short acting B2 adrenoceptors agonists (SABAs)
2) long acting B2 adrenoceptors agonists
(LABAs)
3) CysLT1 receptor antagonists

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37
Q
  • what do controllers do?

- give 3 examples of controllers?

A

= inflammatory agents that reduce airway inflammation

1) glucocorticoids
2) cromoglicate
3) humanised monoclonal IgE antibodies

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38
Q

explain how B2 adrenoceptor agonists treat asthma as bronchodilators.

A
  • act as physiological antagonists of all spasmogens
    (substances that induce spasms)
  • causes ASM reaction via formation of protein kinase A
  • this phosphorylates MLCK & myosin phosphatase
  • reduces intracellular Ca conc & activates potassium channels
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39
Q

what should be used to treat an acute asthma attack?

A

= relievers

= B2 adrenoceptor agonists

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40
Q

give 2 examples of a SABA

A

1) salbutamol

2) terbutaline

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41
Q

what are SABAs used to treat?

A

mild intermittent asthma

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42
Q

how are SABAs usually administered?

A

via inhalation

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43
Q

describe SABAs acting time?

A
  • they act rapidly to relax bronchial smooth muscle
  • maximum effect within 30minutes
  • relaxation persists fo 3-5hours
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44
Q

what are the few adverse effects of SABAs when administered by the inhalation route?

A
  • unwanted systemic absorption
  • few adverse effects;
    e. g. finne tremors, tachycardia, cardiac dysrhythmia
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45
Q

give 2 examples of LABAs

A

1) salmeterol

2) formoterol

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46
Q

what are LABAs not recommended for and what are they useful for?

A

NOT RECOMMENDED FOR;
- acute relief bronchospasm

USEFUL FOR;
- nocturnal asthma (last 8 hours)

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47
Q

describe how LABAs should be used?

A
  • NOT as mono therapy

- but as an add-on therapy, always co-administered with a glucocorticoid

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48
Q

give 2 examples of CysLT1 receptor antagonists.

A

1) montelukast

2) zafirlukast

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49
Q

what are CysLTs derived from and what do they cause?

A
  • derived from mast cells & infiltrating inflammatory cells
  • they cause smooth muscle contraction, mucus secretion & oedema
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50
Q

how do CysLT1s receptor antagonists work?

A
  • act competitively at the CysLT1 receptor

- therefore, relaxing bronchial smooth muscle

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51
Q

how are CysLT1 receptor antagonists administered?

A

ORALLY

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52
Q

should CysLT1 receptor antagonists be used as a mono therapy or as an add-on therapy.

A
  • are effective as add on therapy against early & late bronchospasm in mild persistent asthma & in combination with other medication, including inhaled corticosteroids
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53
Q

what are 2 possible side effects of CysLT1 receptor antagonists?

A

1) headache
2) GI upset
- but are generally well tolerated

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54
Q

what are CysLT1 receptor antagonists not recommended for?

A

not recommended for acute severe asthma

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55
Q

give 2 examples of Xanthinens.

A

1) theophylline

2) aminophylline

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56
Q

How do xanthines work?

A
  • combine bronchodilator (at high dose) & anti-inflammatory actions
  • inhibit mediator release from mast cells
  • increase mucus clearance
57
Q

how should xanthines be administered?

A

orally

58
Q

at what concentration do xanthines exert adverse effects involving CNS, CVS, GI tract & kidney?
give examples of these adverse effects.

A

at Supra-therapeutic concentrations they exert adverse effects

Examples;

  • seizures
  • hypotension
  • dysrhythmia
59
Q

what adverse effects are caused at therapeutic concentrations of xanthins?

A
  • nausea
  • vomiting
  • abdominal discomfort
  • headache
60
Q

why are xanthines problematic?

A

because of numerous drug interactions, involving CYP450s as an example.

61
Q

describe the therapeutic window of xanthines?

A

narrow therapeutic window.

62
Q

what are the 2 classes of corticosteroids used?

A

1) glucocorticoids

2) mineralocorticoids

63
Q

what is the main hormone in glucocorticoids?

what do glucocorticoids do?

A

= cortisol (hydrocortisone)

  • regulates numerous essential processes e.g. inflammatory & immunological
64
Q

what sort of steroids may contain both glucocorticoid & mineralocorticoid action?

A

endogenous steroids

65
Q

give 3 examples of synthetic derivatives of cortisol.

A

1) beclometasone
2) budesonide
3) fluticasone

66
Q

why are synthetic derivatives of cortisol used in the treatment of asthma more so than cortisol itself?

A

because synthetic derivatives have little or no mineralocorticoid activity

67
Q

do glucocorticoids have bronchodilator activity?

A

no

- they are ineffective in receiving broncho-spasms

68
Q

what type of asthma are glucocorticoids the mainstay treatment?

A

prophylaxis of asthma

used to PREVENT THE DISEASE

69
Q

why is the inhalation route the preferred option for delivering glucocorticoids?

what are the most common side effects? - think about how they are delivered.

A

to minimise systemic effects

  • hoarse voice
  • thrush
70
Q

how do glucocorticoids signal?

A

via nuclear receptors, specifically GRalpha

71
Q

how do glucocorticoids enter cells?

A
  • they are lyophilic molecules so enter by diffusion

lipophilic = dissolve in lipids or fat

72
Q

what happens when glucocorticoids are within the cytoplasm?

A
  • glucocorticoids combine with GRalpha
  • this causes dissociation of heat shock proteins (HSP)
  • the activated receptor translocates (moves from one place to another) to the nucleus aided by importins
73
Q

what happens when glucocorticoids are within the nucleus?

A
  • activated receptor monomers assemble into homodimers & bind to GLUCOCORTICOID RESPONSE ELEMENTS (GRE) in the promoter region of specific genes
74
Q

when the transcription of specific genes is either switched on or off, what happens?

A
  • alters mRNA levels & the rate of synthesis of mediate proteins
75
Q

what do glucocorticoids do to the coding genes of inflammatory proteins in terms of transcription?

A
  • they INCREASE TRANSCRIPTION of genes encoding anti-inflammatory proteins
  • they decrease transcription of genes encoding inflammatory proteins
76
Q

what are the 4 effects of glucocorticoids that are relevant to brachial inflammation in asthma?

A

1) prevent IgE production
2) decrease number of mast cells
3) prevent allergens
4) decrease formation of TH2 cytokines

77
Q

name the 5 inflammatory cells that glucocorticoids decrease the number of.

A

1) eosinophils
2) T lymphocytes
3) mast cells
4) macrophages
5) dendritic cells

78
Q

what effect does glucocorticoids have on airway smooth muscle cells?

A
  • increase B2 receptors
79
Q

what effect does glucocorticoids have on mucus glands?

A
  • decrease mucus secretion
80
Q

what effect does glucocorticoids have on endothelial cells?

A
  • decreased leakiness
81
Q

what effect does glucocorticoids have on epithelial cells?

A
  • cytokine mediators decrease
82
Q

since glucocorticoid suppress the inflammatory component in asthma, what does that resolve inn?

A
  • precent inflammation

- resolves existing inflammation

83
Q

should glucocorticoids be give as a mono-therapy or as an add-on in LONG TERM TREATMENT?

A

In long term treatment they should be used in COMBINATION WITH LABAs

84
Q

what type of drug is cromoglicate?

A

a SECOND LINE DRUG

85
Q

when should cromoglicate be used?

A

used prophylactically in treatment of allergic asthma (particularly children)

86
Q

what is cromoglicate often described as?

A

a MAST CELL STABILISER.

- agent that surpasses histamine release from mast cells

87
Q

does cromoglicate affect bronchial smooth muscle?

A

no - it has no effect on brachial smooth muscle

88
Q

how is sodium cromoglicate most commonly administered and why?

A

inhalation

- due to little systemic absorption

89
Q

what stages of an asthma attack does sodium cromoglicate target and how long will it take to develop?

A
  • it can target both phases of an asthma attack

- but efficacy may take several weeks to develop to block late phase reaction

90
Q

in what age category is sodium cromoligcate more effective in treating?

A

children & young adults rathe than older patients.

91
Q

give an example of a monoclonal antibody directed against IgE.

A

= omalizumab

92
Q

how dos omalizumab work?

A
  • binds to IgE via Fc
  • does to to prevent attachment of Fc receptors
  • this suppresses mast cell response to allergens
93
Q

how is omalizumab administered?

A

via IV

94
Q

give an example of a drug that is a monoclonal antibody directed against IL-5.

A

= mepolizumab

95
Q

muscarinic receptor antagonists are an important treatment of COPD, how do they work?

A

= reduce the parasympathetic neuro-effector transmission

96
Q

what do muscarinic receptor antagonists act as?

A

they act as antagonists of broncho-constriction

97
Q

how is broncho-constriction by smooth muscle initiated?

A

= M3 receptor activation in response to each release from post-ganglionic parasympathetic fibres

98
Q

what do M1 muscarinic receptors do?

A

facilitate fast neurotransmission mediated by ACh acting on nicotinic receptors

99
Q

what do M2 muscarinic receptors do?

A

= act as inhibitory auto-receptors reducing release of ACh

post ganglionic neurone terminals

100
Q

what do M3 muscarinic receptors do?

A

mediate ASM CONTRACTIONN to ACh

101
Q

which muscarinic receptor is the most useful to target in order to treat COPD?

A

M3 msucarinic receptor

102
Q

give 5 examples of competitive muscarinic receptor antagonists.

A

1) ipratropium (SAMA)
2) tiotropium (LAMA)
3) glycopyronium (LAMA)
4) aclidinium (LAMA)
5) Umeclidinium (LAMA)

103
Q

how are muscarinic receptor antagonists administered?

A

via inhalation

104
Q

what part of the muscarinic receptor antagonists reduces absorption & systemic exposure, thus avoiding potential adverse effects.

A

= QUATERNARY AMMONIUM group

105
Q

relative to a SAMA, describe the onset of bronchodilator action of muscarinic receptor antagonists.

A
  • they have a delayed onset of bronchodilator action relative to a SAMA
106
Q

what 2 things do muscarinic receptor antagonists reduce?

A

1) reduce broncho-spasms

2) decrease mucus secretions

107
Q

what do muscarinic receptor antagonists block?

A

they block ACh-mediated basal

108
Q

why are M3 selective blockers superior to ipratropium?

A
  • the functionally selectively of M3 blockers

- wherereas, ipratropium blocks all

109
Q

what do and don’t B-adrenoceptors do?

A

DO - bronchodilate

DON’T - act on underlying inflammation

110
Q

give 2 drugs that act as ultra LABAs.

A

1) indacaterol

2) olodaterol

111
Q

what combination of drugs is best an increasing FEV1.

A

combination of;

1) B2 agonists
2) muscarinic antagonist

112
Q

when are LABA/LAMA combinations most effective ?

A

when both drugs are deposited in the same location in thee airway

113
Q

what do muscarinic receptors do when in combo with a LABA?

A
  • block activation by ACh preventing contraction
114
Q

what do B2 agonists do when in combination with a LAMA?

A

cause relocation by brining to B2 adreenoceptorr

115
Q

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

A
  • glucocorticoids
116
Q

an example of a selective Phosphodiesterase 4 (PDE4) that suppresses inflammation & emphysema inn COPD.

A

roflumilast

117
Q

drawbacks of roflumilast?

A
  • adverse GI effects
118
Q

benefits of administering glucocorticoids in combination with LABAs in COPD.

A

Benefit;

- in patients who develop frequent & severe exacerbations when given with a LABA

119
Q

why are glucocorticoids unresponsive in patients with COPD?

A
  • due to oxidative/nitrative stress

- HDAC2 is reduced also

120
Q

3 examples of drugs used in triple inhalers as one daily treatment for COPD.

A

1) fluticasone
2) umeclidinium
3) vilantereol

121
Q

3 types of rhinitis

A

1) allergic
2) non-allergic
3) mixed

122
Q

what the classifications of allergic rhinitis?

A

1) seasonal
2) perennial
3) episodic

123
Q

what is the condition that allergic rhinitis is strongly linked to?

A

asthma

124
Q

what are the similarities between asthma & allergic rhinitis.

A

1) inhalation of allergens increase specific IgE levels
2) IgE binds to receptors on mast cells & basophils
3) re-exposure to allergen causes mast cell & basophil
de-granulation
4) release of mediators, e.g. histamine, cysLTs, tryptase, prostaglandins cause the symptoms

125
Q

what does non-allergic rhinitis NOT involve?

A

IgE dependant events

126
Q

what 5 things can cause non-allergic rhinitis?

A

1) infection
2) hormonal imbalance
3) vasomotor disturbances
4) non-allergic rhinitis with eosinophils syndrome
5) medication

127
Q

what may occupation rhinitis involve?

A

both allergic & non-allergic rhinitis

128
Q

what do both rhinitis & rhinorrhoea both involve?

A

1) increased mucosal blood flow
2) increased blood vessel permeability
= both increase the volume of nasal mucosa causing difficulty breathing in

129
Q

what is used as anti-inflammatory treatment in rhinitis & rhinnorrhoea?

A

glucocorticoids

130
Q

give 3 examples of glucocorticoids?

A
  • beclametasone
  • fluticasone
  • prednisolone
131
Q

what is the mechanism of glucocorticoids?

A
  • reduces vasucular permeability
  • recruitment & activity of inflammatory cells
  • release of cytokines & mediators
132
Q

give 3 examples of antihistamines (H1 receptor antagonists).

A

1) cetirizine
2) loratadine
3) fexofenadine

133
Q

what is the mechanism for anti-histamines

A

competitive antagonists that reduces the effects of mast cell derived histamine

134
Q

what are the 3 effects of mast cell derived histamine?

A

1) vasodilation & increased capillary permeability
2) activation of sensory nerves
3) mucus secretion from sub-mucosal glands

135
Q

what is the mechanism for anti-cholinergic drugs?

A

muscarinic receptor antagonists

136
Q

how do muscarinic receptors antagonists work?

A
  • ACh released from post-ganglionic parasympathetic fibres activates msucarinnci receptors on nasal glands causing a watery secretion contnributing to rhinorrhoea
137
Q

what is the mechanism of CysLT1 receptor antagonists.

A

= reduces the effects of CysLTs upon the nasal mucosa

138
Q

what is the mechanism of a vasoconstrictor?

A

mimics the effect of noradrenaline.

- produces vasoconstriction via activation of alpha 1 - andreoceptor to decrease swelling in vascular mucosa.

139
Q

what is the mechanism for sodium cromoglicate?

A

mast cell stabilisation

Respiratory (Annie) (47 decks)

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