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Respiratory > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

How do ‘relievers’ work?

A

act as bronchodilators

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2
Q

what drugs are classed as ‘relievers’?

A
  • short acting Beta2-adrenoceptor agonists (SABAs)
  • long acting beta2-adrenoceptor agonists (LABAs)
  • cysLT1 (leukotrine) receptor antagonist
  • methylxanthines
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3
Q

how do ‘controllers/prevents’ work?

A

act as anti- inflammatory agents that reduce airway inflammation

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4
Q

what drugs are classed as ‘preventers/relievers’?

A

glucocorticoids
cromoglicate
humanised monoclonal IgE antibodies
methylxanthines

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5
Q

How do beta2-adrenoceptor agonists work?

A

relax airway smooth muscle by inhibition of beta2 adrenoceptors and reduce intracellular Ca2+ concentration and activate large conductance potassium channels

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6
Q

what are examples of SABAs?

A

salbutamol aka albuterol

terbutaline

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7
Q

what is the first line treatment for mild, intermittent asthma?

A

SABAs

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8
Q

when are SABAs taken?

A

when needed

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9
Q

how are SABAs administered?

A

usually by inhalation, oral in children and IV in emergency

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10
Q

How long does it take for SABAs to start working?

A

often within 5 minutes, maximal effect within 30 minutes

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11
Q

how long does relaxation persist after using a SABA?

A

3-5 hours

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12
Q

what do SABAs do?

A

increase mucus clearance, decrease mediator release from mast cells and monocytes

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13
Q

what adverse effects may SABAs have?

A

fine tremor
tachycardia
cardiac dysrhythmia
hypokalaemia

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14
Q

what are examples of LABAs?

A

salmeterol and formoterol

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15
Q

How long do LABAs act for?

A

approx 8 hours

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16
Q

what must LABAs always be co-administered with?

A

glucocorticoids

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17
Q

what are examples of leukotriene receptor antagonists?

A

montelukast, zafirlukast

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18
Q

how do leukotriene receptor antagonists work?

A

act competitively at the cysLT1 receptor derived from mast cells and infiltrating inflammatory cells which cause smooth muscle contraction, mucus secretion and oedema

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19
Q

when are leukotriene receptor antagonists effective?

A

as add on therapy against early and late bronchospasm in mild persistent asthma and in combination with other medications, including inhaled corticosteroids in more severe conditions

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20
Q

what kind of bronchospams are leukotriene receptor antagonists effective against?

A

antigen-induced

exercise-induced

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21
Q

how are leukotriene receptor antagonists administered?

A

orally

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22
Q

what adverse effects have been reported for leukotriene receptor antagonists?

A

headache and GI upset

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23
Q

when are leukotriene receptor antagonists not recommended?

A

relief of acute severe asthma

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24
Q

what are methylxanthines present in?

A

coffee, tea and chocolate-containing beverages

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25
Q

what are examples of methylxanthines?

A

theophylline and aminophylline

26
Q

what does theophylline do at high doses?

A

inhibits PDE3 potentiating the action of cAMP in ASM

27
Q

what do methylxanthines do?

A

involve inhibition of isoforms of phosphodiesterases that inactivate cAMP and CGMP

28
Q

what effects fo methylxanthines have?

A

combine bronchodilator and anti-inflammatory actions, inhibit mediator release from mast cells, increase mucus clearance, increase diaphragmatic contractility and reduce fatigue

29
Q

when are methylxanthines used?

A

second line drugs used in combination with beta2-adrenoceptor agonists and glucocorticoids

30
Q

what are some adverse effects of methylxanthines if administered at supra-therapeutic concentrations?

A

dysrhythmia
seizures
hypotension

31
Q

what are some adverse effects of methylxanthines if administered at therapeutic concentrations?

A

nausea
vomiting
abdominal discomfort
headache

32
Q

what are the two major classes of steroid hormone that are released into circulation?

A

glucocorticoids

mineralcorticoids

33
Q

what does cortisol regulate?

A 
decreases inflammatory responses
decrease immunological responses
increase liver glycogen deposition
increase gluconeogenesis
increase glucose output from liver
decrease glucose utilisation
increase protein catabolism
increase bone catabolism
increase gastric acid and pepsin secretion
34
Q

what do mineralocorticoids (mainly aldosterone) do?

A

regulate the retention of salt (and water) by the kidney

35
Q

what are examples of synthetic derivatives of cortisol?

A

beclometasone
budesonide
fluticasone

36
Q

what are synthetic derivatives with little, or no mineralcorticoid activity, often used for?

A

their anti-inflammatory effect in the treatment of asthma

37
Q

what are glucocorticoids ineffective in?

A

relieving bronchospasm as they have no direct bronchodilator action.

38
Q

how are glucocorticoids administered?

A

preferably by the inhalation route to minimise adverse systemic effects

39
Q

why are glucocorticoids given in asthma?

A

for prophylaxis, they prevent inflammation

40
Q

what are the adverse effects of glucocorticoids?

A 
dysphonia (weak/hoarse voice)
oropharyngeal candiadias (thrush)
41
Q

what may be given in severe, rapidly deteriorating asthma?

A

oral prednisolone in combination with an inhaled steroid to reduce oral dose required and minimise unwanted systemic effects. bronchodilator drugs are co-administered

42
Q

when are cromones used?

A

second line drugs infrequently used in the prophylaxis of allergic asthma (particularly in children)

43
Q

what is an example of a cromone?

A

sodium cromoglicate

44
Q

how is sodium cromoglicate administered?

A

inhalation

45
Q

who is sodium cromoglicate more effective in?

A

children and young adults

46
Q

what does SAMA stand for?

A

short acting muscarinic antagonist

47
Q

what does LAMA stand for?

A

long acting muscarinic antagonist

48
Q

what are examples of SAMAs?

A

ipratropium

49
Q

what are examples of LAMAs?

A

tiotropium
glycopyrronium
aclidinium
umeclidinium

50
Q

how are SAMAs and LAMAs administered?

A

by inhalation

51
Q

how do SAMA/LAMA work?

A

reduce bronchospasm caused by irritant stimuli and also block ACh-mediated basal tone, decrease mucus secretion

52
Q

what is ipratropium a non-selective blocker for?

A

M1,M2,M3 receptors

53
Q

what will glucocorticoids do over several weeks in the treatment of rhinits?

A

reduce all symptoms, including nasal congestion

54
Q

what might glucocorticoids be combined with in moderate-to-severe rhinitis?

A

anti-histamines

55
Q

what are examples of glucocorticoids given for rhinitis?

A

beclometasone
fluticasone
prednisolone

56
Q

what do anti-histamines do?

A

competitive antagonists that reduce effects of mast cells derived histamine including vasodilatation and increased capillary permeability, activation of sensory nerves and mucus secretion from submucosal glands

57
Q

how are anti-histamines administered?

A

orally or an intranasal spray (azelastine)

58
Q

what are examples of anti-histamines?

A

loratidine
fexofenadine
cetirizine

59
Q

what drugs can be used in treatment of rhinitis?

A 
glucocorticoids 
anti-histamines
leukotriene receptor antagonists
muscarinic receptor antagonists 
sodium cromoglicate
vasoconstrictors
60
Q

what is the mechanism of action of vasoconstrictors?

A

act as directly, or indirectly, to mimic the effect of noradrenaline. produce vasoconstricton via activation of alpha1-adrenoceptors to decrease swelling in vascular mucosa

61
Q

what is an example of a vasoconstrictor?

A

oxymetazoline

Respiratory (12 decks)

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