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respiratory block > Pharmacology - Asthma > Flashcards

Pharmacology - Asthma Flashcards

1
Q

where are cell bodies of preganglionic fibres located

A

brain-stem

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2
Q

parasympathetic stimulation of postganglionic cholinergic fibres causes…
(2)

A

bronchial smooth muscle contraction (mediated by ACh receptors)
increased mucus secretion

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3
Q

parasympathetic stimulation of postganglionic nonchilinergic fibres causes…

A

bronchial smooth muscle relaxation (mediated by NO vasoactive intestinal peptide)

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4
Q

sympathetic stimulation causes…

4

A

bronchial smooth muscle contraction (activated via adrenaline)
decreased mucus secretion
increased mucocilary clearance
vascular smooth muscle contraction

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5
Q

increase in concentration of calcium in smooth muscle causes…

A

depolarisation to occur

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6
Q

how calcium initiates contraction in smooth muscles

A

calcium bound calmodulin > activates Myosin light chain kinase > phosphorylates and activates myosin cross bridge > binds to actin > smooth muscle contraction occurs

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7
Q

how contraction of smooth muscle occurs

A

dephosphorylation of myosin light chain (on myosin cross bridge) by myosin phosphatase

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8
Q

examples of causes of asthma attacks

4

A

allergens
exercise
respiratory
smoke/dust/environmental pollutants

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9
Q

asthma is…

A

intermittent attacks of bronchoconstriction

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10
Q

symptoms of asthma

4

A

tight chest
wheezing
difficulty in breathing
coughing

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11
Q

chronic asthma

A

involves pathological changes to bronchioles from long standing inflammation

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12
Q

pathological changes which occur in relation to chronic asthma
(5)

A

increased smooth muscle mass (hypertrophy/hyperplasia)
accumulation of interstitial fluid (oedema)
increased mucus secretion
epithelial damage (sensory nerve ending exposure)
sub-epithelial fibrosis

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13
Q

2 types of asthma responses

A

low level TH1 reponse - initial (nonatopic individual)
strong TH1 repsonse - overtime (atopic individual)
[atopic = hyperallergic]

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14
Q

low level TH1 response involves…

A

cell-mediated immune response (IgG and macrophages)

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15
Q

strong TH2 response involves…

A

antibody mediated immune response (IgE)

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16
Q

types of drugs used in asthma

2

A

relievers - act as bronchodilators

controllers/preventors - act as anti-inflammatory agents (reduce airway inflammation)

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17
Q

examples of reliever drugs

4

A

short acting beta2-adrenoceptor agonists (SABAs)
long acting beta2-adrenoceptor agonists (LABAs)
cysLT1 receptor antagonists
methylxanthines

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18
Q

examples of controllers/preventor drugs

4

A

gluccorticoids
cromoglicate
humanised monoclonal IgE antibodies
methylxanthines

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19
Q

mechanism of action for beta2-adrenoceptor agonsits

A

act as physiological antagonists of all spasmogens

20
Q

short acting agents SABA

2

A

salbutamol

terbutaline

21
Q

short-acting agents result in…

A

increased mucus clearance

decreased mediator release from mast cells and monocytes

22
Q

long-acting beta2-adrenoceptor agonists

2

A

salmeterol

formoterol

23
Q

salmeratol
(LABA) is fast to act
(true/false)

A

false

saleterol is slow to act, however, formorterol is fast

24
Q

LABAs should always be coadministered with what drug?

A

glucocorticoid - steroid hormones

LABAs alone may worsen asthma by several mechanisms

25
Q

CystLT1 (cysteinyl leukotriene) receptors antagonists

2

A

monotelukast

zafirlukast

26
Q

mechanism of action for CysLT1 receptor antagonists

A

acts competitively at CysLT1 receptor

27
Q

CysLT1 receptor antagonists prevent…

3

A

smooth muscle contraction
mucus secretion
oedema

28
Q

oedema

A

swelling caused by buildup of fluid

29
Q

emphysema

A

lung disease - causes shortness of breath due to damaged alveoli

30
Q

via which route are CysLT1 receptor antagonists administered?

A

oral route

31
Q

xanthines

A

methylanthines

  • theophylline
  • aminophylline
32
Q

mechanism of action of xanthines

A

uncertain - might involve inhibition of isoforms of phosphodiesterases, inactivate cAMP and cGMP

33
Q

which drug has both anti-inflammatory and bronchodilator actions?

A

methylxanthines/xanthines

very narrow therapeutic window

34
Q

methylxanthines cause…

A

mediator release from mast cells
increased mucus clearance
may improved lung ventilation

35
Q

anti-inflammatory agents

A

corticosteroids

  • glucocortoids
  • mineralcocorticoids
36
Q

role of glucocorticoids

2

A

resolves established inflammatory

prevents inflammation

37
Q

why are synthetic derivatives of cortisol, rather than cortisol itself, used in treatment of asthma

A 
because cortisol (an endogenous steroid) possesses both glucocorticoid and minerlocorticoid actions - latter is unwanted in treatment for inflammatory conditions. 
[the derivatives have no mineralcorticoid activity]
38
Q

why is inhalational route of glucocorticoids administration is favoured in mild or moderate asthma?

A

despite not having no direct bronchodilator action glucocorticoids are delivered via inhalation to minimise adverse systemic effects

39
Q

molecular mechanism of action of glucocorticoids

4

A

signal via nuclear receptors (GRalpha) -
1/ bind to GR alpha in cytoplasm
2/ produce dissociation of inhibitory heat shock proteins
3/ activated receptors moves to nucleus and assemble into homodimers
4/ bind to DNA altering transcription of specific genes

40
Q

cellular effects underlying the anti-inflammatory action of glucocorticoids in inflammatory cells
(5)

A

eosinophil decrease (apoptosis)
decreased cytokine production in Th cells
mast cell decrease
decreased cytokine production from macrophages
dendritic cell decrease

41
Q

glucocorticoids decrease transcription of anti-inflammatory proteins and increase transcription of inflammatory proteins
(true/false)

A

false

they increase anti-inflammatory protein transcription and decrease inflammatory protein transcription

42
Q

role of HDAC (histone deacetylases) and
HATs
(histone acetyltransferases) - produced by glucocorticoids

A

HDAC - condenses chromatin to prevent transcription

HATs - unwinds DNA, allowing transcription

43
Q

cellular effects underlying the anti-inflammatory action of glucocorticoids in inflammatory cells

A

decreased cytokines mediators in epithelial cells
decreased leak in endothelial cells
increased beta-2-receptors and decreased cytokines in airway smooth muscles
decreased mucus secretion in mucus glands

44
Q

clinical use of glucocorticoids in asthma

A

short term use - do not alleviate early stage bronchospasms

long term use - more effective (combined with LABA)

45
Q

most common adverse effects of glucocorticoids

A 
dysphonia -hoarse and weak voice
oropharyngeal candidiasis (thrush)
46
Q

cromoglicate

A

delivered via inhalation (little systemic absorption)
can reduce both phases of an asthma attack
requires frequent dosing

47
Q

omalizumab

A

monoclonal antibodies against IgE
blocks IgE
expensive treatment
intravenous administration

respiratory block (6 decks)

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