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pharmacology Flashcards

1
Q

what happens when postganglionic cholinergic fibres are stimulated in the parasympathetic?

A
  • bronchial smooth muscle contraction mediated by M3 muscarinic ACh receptors on ASM cells
  • increased mucus secretion mediated by M3 muscarininc ACh receptors on gland cells
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2
Q

what happens when postganglionic non-cholinergenic fibres are stimulated in the parasympathetic?

A
  • bronchial smooth muscle relaxation medicated by nitric oxide (NO) and vasoactive intestinal peptide (VIP)
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3
Q

what does stimulation of sympathetic cause?

A
  • bronchial smooth muscle relaxation via B2-adrenoceptors on ASM cells activated by adrenaline released from the adrenal gland
  • decreased mucus secretion mediated by B2-adrenoceptors on gland/goblet cells
  • increased mucociliary clearance mediated by B2-adrenoceptors on epithelial cells
  • vascular smooth muscle contraction, mediated by a1-adrenoceptors on vascular smooth muscle cells
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4
Q

steps of inhibition of contraction of Ca 2+ in smooth muscle

A
  1. Ca2+ converts calmodulin to Ca2+- calmodulin
  2. Ca2+-calmodulin activates MLCK
  3. active MLCK dephosphorylates ATP and uses Pi to phospharlate and activated the myosin cross bridge
  4. this permits binding with actin
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5
Q

how do smooth muscles contract and relax?

A
  • contraction = phosphorylation of MLC by MLCK in the presence of elevated intracellular Ca2+ and ATP
  • relaxation = dephosphorylation of MLC by myosin phosphatase
  • in the presence of elevated intracellular CA2, the rate of phosphorylation exceeds the rate of dephosphorylation
  • relaxation thus requires return of intracellular Ca2+ concentration to basal level - achieved by primary and secondary active transport
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6
Q

definition of asthma

A

recurrent and reversible (short term) obstruction to the airways in response to substances that are

  • not noxious
  • do not affect non-asthmatic subjects
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7
Q

what are asthma attacks?

A

intermittent attacks of bronchoconstriction causing tight chest, wheezing, difficulty in breathing, cough

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8
Q

what is the pathology changes for poorly controlled chronic asthma?

A
  • pathological changes to the bronchioles result from long standing inflammation
    1. increased mass of smooth muscle (hyperplasia and hypertrophy)
    2. accumulation of interstitial fluid (oedema)
    3. increased secretion of mucus
    4. epithelial damage (exposing sensory nerve endings)
    5. sub-epithelial fibrosis
  • airway narrowing by inflammation and bronchoconstriction increase airway resistance decreasing FEV1 and PEFR
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9
Q

what causes bronchial hyper-responsiveness in asthma?

A
  • epithelial damage, exposing sensory nerve endings, contributes to increase sensitivity of the airways to bronchoconstrictor influences (and may cause neurogenic inflammation by the release of various peptides)
  • the two components are hypersensitivity and hyper-reactivity
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10
Q

what happens when IgE receptors are activated on mast cells?

A
  1. stimulates calcium entry

2. releases leukotrienes that cause airway smooth muscle contraction

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11
Q

what is a normal persons response to an allergen?

A
  1. phagocytosis by antigen presenting (dendritic) cell

2. low-level Th1 response, cell-mediated immune response involving IgG and macrophages

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12
Q

what is an atopic individuals response to an allergen?

A
  1. allergen through airway epithelium
  2. CD4+ express to THO cells that mature to TH2 cells
  3. these activate B cells that mature to IgE secreting P cells
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13
Q

what are the key events in immediate phase of asthma?

A
  • eliciting agent: allergen or non-specific stimulus plus mast cells, mononuclear cells
    1. spasmogens, CysLTs, Histamine = bronchospasm, early inflammation
    2. chemotaxins chemokines = late phase
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14
Q

what are the key events in late phase of asthma?

A
  • infiltration of cytokine releasing Th2 cells and monocytes, activation of inflammatory cells, particularly eosinophils
    1. mediatorys, CysLTs and others
    2. eosinophil major basic and catonic proteins = epithelial damage = airway hyper-responsiveness / airway inflammation = bronchospasm, wheezing, mucous oversecretion, cough
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15
Q

what drugs are used as relievers?

A
  • SABA
  • LABA
  • CysLT1 receptor antagonists
  • methylxanthines
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16
Q

what drugs are used as controllers / preventers?

A
  • glucocorticoids
  • cromogilcate
  • humanised monoclonal IgE antibodies
  • methylxanthines
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17
Q

pharmacokinetics of aerosol and oral

A 
aerosol = Slow absorption from lung surface and rapid systemic clearance
oral = Good oral absorption (with exceptions) and slow systemic clearance
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18
Q

dose of aerosol and oral

A 
aerosol = Low dose delivered rapidly to target
oral = High systemic dose necessary to achieve an appropriate concentration in the lung
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19
Q

systematic concentration of drug of aerosol and oral

A 
aerosol = low
oral = high
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20
Q

distribution of drugs of aerosol and oral

A 
aerosol = reduced in severe airway disease
oral = unaffected by airway disease
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21
Q

incidence of adverse effects of aerosol and oral

A 
aerosol = low
oral = high
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22
Q

compliance of aerosol and oral

A 
aerosol = Good with bronchodilators, less so with anti-inflammatory drugs
oral = good
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23
Q

ease of administration of aerosol and oral

A 
aerosol = difficult for small children and infirm people
oral = good
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24
Q

effectiveness of aerosol and oral

A 
aerosol = good to mild in moderate disease
oral = good even in severe disease
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25
Q

what drugs are used in treatment of asthma bronchodilators?

A
  • b2-adrenoceptor agonists - act as a physical antagonist of all spasmogens
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26
Q

b2-adrenoceptor agonists classification

A
  • short-acting (SABA)
  • long-acting (LABA)
  • ultra long-lasting (ultra-LABA)
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27
Q

what are SABAs? (short acting B2-adenoreceptors)

A

eg = salbutamol, albuterol, terbutaline

  • bronchodilator
  • rapid - 5 minutes
  • reliever
  • fine tremor
  • first line treatment
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28
Q

LABA (long acting B2-adenoreceptors)

A

eg = salmeterol, foroterol

  • nocturnal use - 8 hours
  • must be co-administered with a glucocorticoid
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29
Q

CysLT receptor agonists

A
  • monteleukast
  • blocks CysLT1 receptor for LTs from mast cells
  • bronchodilator
30
Q

what are methylxanthines?

A
  • eg therophylline and aminophylline
  • inhibits PDE3
  • bronchodilator and anti-inflammatory actions
31
Q

what are glucocorticoids?

A
  • decreases Th2 cytokines, mast cells, IgE antibodies
  • prevents inflammation and resolve established inflammation
  • synthesised from the adrenal cortex into the circulation
32
Q

what treatment is used for mild/moderate asthma?

A
  • beclometasone
  • budesonide
  • fluticasone - inhaled - hoarse voice
  • candidiasis

(glucocorticoids)

33
Q

what treatment is used for severe asthma?

A

oral predinisolone

glucocorticoids

34
Q

do glucocorticoids have a direct bronchodilator action?

A

no, they are ineffective when relieving bronchospasm when given acutely

35
Q

what is the molecular mechanism of action of glucocorticoids?

A
  • they signal via nuclear receptors (class 1)
    1. glucocorticoids are lipophilic - the enter cells by diffusion acoss the plasma membrane
    2. in the cytoplasm, they combine with GRa, producing dissociation of inhibitory heat shock proteins. the activated receptor translocates to the nucleus aided by importins
    3. within the nucleus activated receptor, monomers are assembled into homodimers and bind to gluccorticoid response elements (GRE) in the promoter region of specific genes
    4. the transcription of specific genes is either switched on or switched off to alter mENA levels and the rate of synthesis of mediator proteins
36
Q

what are the glucocorticoid effects on gene transcription?

A
  • glucocorticoids increase transcription of genes encoding anti inflammatory proteins and decrease the transcription of genes encoding inflammatory proteins
37
Q

what are the glucocorticoid effects on inflammation in bronchial asthma?

A
  • they decrease formatoin of Th2 cytokines eg IL-4 and IL-5 and causes apoptosis
  • they prevent allergen-inducedinflux into lung and cause apoptosis
  • they prevent production
  • they reduce the number of cells and decrease FCe expression
38
Q

what are the cellular effects of glucocorticoids in relation to asthma?

A
  • reduced number of eosinophils, mast cells and T cells
39
Q

what are the clinical uses of glucocortiocids in asthma?

A
  • surpress the inflammatory component of asthma by 1. preventing inflammation and 2. resolves established inflammation
40
Q

what are the short term clinical uses of glucocorticoids?

A

short term: they dont aliviate early stage bronchospasm caused by allergens, or exercise

  • in mild asthma: they are given by inhalation from a metered dose inhalerand efficacy develops after several days
  • common side effects are dysphonia and oropharyngeal candidiasis
41
Q

what are the long term clinical uses of glucocorticoids?

A
  • oral prednisolone may be used in combination eith an inhaled steroid to reduce oral dose required and minimise unwanted systemic effects - bronchodilators are co-administered
  • patietns are stronly encouraged to take sufficient inhaled glucocortioids to control symptomsand avoid disease progression which may be irreversible
42
Q

what are the components of COPD?

A

emphysema and chronic bronchitis

43
Q

what is emphysema?

A
  • distention and damage to alveoli

- loss of elastic recoil

44
Q

what is chronic bronchitis?

A
  • inflammation of bronchi and bronchioles
  • cough
  • clear mucoid sputum
  • increasing breathlessness
45
Q

what is COPD characterised by?

A
  • increased resistance to air flow during expiration eg easy to breath in but hard to breath out
46
Q

what does a blockage of M3 do?

A
  • prevents contraction of airway smooth muscle
47
Q

what is M1?

A
  • ganglia

- facilitate fast neurontransmission mediated by ACh acting on nicotinic receptors (nAChR)

48
Q

what is M2?

A
  • postganglionic neurone tterminals

- act as inhibitory autoreceptors reducing release of ACh

49
Q

what is M3?

A
  • ASM

- mediate contraction to ACh

50
Q

what drugs are used in the treatment of COPD?

A
  • short acting muscarinic antagonist (SAMA) = iptratropium
  • LAMA = tiotropium, glycopyrronium, aclidnium, umeclidinium
  • these are all administered by inhalation
51
Q

what does the quartenary ammonium group on drugs in the treatment of COPD do?

A

it reduces absorption and systemic exposure avoiding multiple potential adverse effects of a generalised parasympathetic block

52
Q

what do muscarinic receptor antagonists do?

A
  • delayed onset of bronchodilator action relative to a SAMA
  • reduce bronchospasm caused by iriitant stimuli and also block ACH-mediated basal tone
  • decrease mucus secretion
  • have little effect on the progression of COPd, their effect is mainly palliative
  • hae few adverse effects
53
Q

give an example of SAMA

A
  • ipratropium = inhalation
  • 15 mins onset
  • non selective blocker of M1,2,3
54
Q

give an example of LAMA

A

tiotropium = inhaled

  • > 30 mins onset
  • selective for M3 (greater half life for M3), so beter than ipratropium (also blockage of M2 not desireable since release of Ach from parasympathetic post ganglionic neurons is decreased)
55
Q

what do relievers do?

A

causes bronchodilation

56
Q

what do controllers / preventers do?

A

act as anti-inflammatory agents that reduce airway inflammation

57
Q

give an example of an ultra LABA

A
  • indacaterol

- rapid onset of action

58
Q

what is a PDE4 inhibitor?

A
  • rofumilast

- suppress inflammation and emphysema

59
Q

what is rhinitis and what is it characterised by?

A
  • a common disease involving acute or chronic inflammation of the nasal mucosa
  • rhinorrohea (runny nose)
  • sneezing
  • itching
  • nasal congestion and obstruction
  • it may be allergic, non allergic or mixed
60
Q

what can allergic rhinitis be classified by?

A
  • seasonal (SAR)
  • perennial (PAR)
  • episodic (EAR)
61
Q

what are the steps of allergic rhinitis?

A
  1. inhalation of allergen increases specific IgE levels
  2. IgE binds to receptors on mast cells and basophils
  3. re-exposure to allergen causes mast cell and basophil degranulation
  4. release of mediators including histamine, cysLTs, tryptase, prostaglandins, causing acute itching, sneezing rhinorrhoea and nasal congestion
  5. delayed response caused by recruitment of lymphocytes and eosinophils to nasal mucosa contributes to congestion and obstruction
62
Q

what is non-allergic rhinitis?

A
  • any rhinitis that doesnt involes IgE dependent events
  • causes include:
  • infection
  • hormonal imbalance
  • vasomotor disturbances
  • nonallergic rhinitis with eosinophilia syndrome
  • medication
63
Q

what is occupational rhinitis?

A

involve both allergic and non allergic components

64
Q

how do rhinitis and rhinorrhoea cause difficulty breathing?

A
  1. increased mucosal blood flow
  2. increased blood vessel permeability
  3. these increase the volume of the nasal mucosa and cause difficulty breathing in
65
Q

what treatments are used in rhinitis and rhinorrhoea?

A
  • glucocorticoids for anti-inflammatory
  • H1 receptor antagonists (anti-histamines) and CysLT1 receptor antagonists for mediator receptor blockade
  • vasoconstrictors for nasal blood flow
  • sodium cromoglicate for anti-allergen
66
Q

how to glucocorticoids work for rhinitis and rhinorrhoea?

A
  • they reduce vascular permeability, recruitment and activity of inflammatory cells and the release of cytokines and mediators
  • main therapy for SAR, PAR and NARES
  • applied as a spray to the nasal mucosa
  • effective as monotherapy
  • used over several weeks
  • in severe-moderate rhinitis = combine with anti-histamines
  • eg beclometasone, fluticasone, prednisolone
67
Q

how to anti-histamines work for rhinitis and rhinorrhoea??

A
  • they are a competitive antagonist that reduces effects of mast cell derived histamine including:
    vasoconstriction and increased capillary permeability
    activation of sensory nerves
    mucus secretion from submucosal glands
  • work in SAR, PAR, EAR
  • small effect on congestion
  • orally or intranasal spray
  • effective as monotherapy
  • second generation preferred due to reduced sedation
  • eg loratidine, fexofenadine, cetrizine
68
Q

how do anti-cholinergic drugs (muscarinic receptors) work for rhinitis and rhinorrhoea?

A
  • ACh is released from post ganglionic parasympathetic fibres and activates muscarinic receptors on nasal glands causing a watery secretion that contributes to rhinorrhoea - blocked by muscarinic antagonsits
  • they reduce rhinorrhoea in PAR and SAR but have no influence upon sneezing, itching and congestion
  • intranasally
  • side effects: dryness or nasal membranes
  • eg ipratopium
69
Q

how does sodium cromoglicate work on rhinitis and rhinorrhoea?

A
  • maybe mast cell stabilisation
  • used for maintenance treatment of allergic rhinitis with an onset action of 4-7 days
  • nasal administration - less effective than nasal corticosteroids
70
Q

how do cysteinyl leukotriene receptor antagonists work for rhinitis and rhinorrhoea?

A
  • CysLT1 receptor antagonists reduce the effect of CysLTs upon the nasal mucosa
  • equi-effective with H1 receptor antagonists in treating PAR and SAR
  • orally
  • should be considered in patients with allergic rhinitis and asthma
  • eg montelukast
71
Q

how do vasoconstrictors work in rhinitis and rhinorrhoea?

A
  • act as directly or indirectly to mimic the effect of noradrenaline. produce vasocontriction via activation of a1-adenoreceptors to decrease sweling in vascular mucosa
  • eg oxymetazoline

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