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Resp - mine > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what is the role of the parasympathetic system in the regulation of airways

A

stimulation of postglanglionic CHOLINERGIC fibres cause:

  1. ASM contraction
  2. increased mucus secretions

stimulation of postglanglionic NON-CHOLINERGIC fibres cause:
1. ASM relaxation

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2
Q

what is ASM contraction mediated by

A

M3 muscarininc ACh receptors

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3
Q

what is mucus secretion mediated by

A

M3 muscarininc ACh receptors

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4
Q

what is ASM relaxation (via NON-cholinergic fibres) mediated by

A

NO and vasoactive intestinal peptide

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5
Q

what is the role of the sympathetic system in the regulation of airways

A

THERE IS NO INNERVATION OF ASM

stimulation of submucosal glands and smooth muscle blood vessels causes:

  1. ASM relaxation
  2. decreased mucus secretions
  3. increased mucocilliary clearance
  4. vascular smooth muscle contraction
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6
Q

what is bronchial smooth muscle relaxation mediated by (in sympathetic stimulation)

A

cholinergic release of adrenal from the adrenal glands acting upon the B2-adrenoceptors

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7
Q

what is decreased mucus secretion mediated by

A

B2-adrenoceptors

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8
Q

what is increased mucocilliary clearance mediated by

A

B2-adrenoceptors

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9
Q

what is vascular smooth muscle contraction mediated by

A

A1-adrenoceptors

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10
Q

what is asthma

A

recurrent and reversible obstruction to the airways in response to substances

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11
Q

describe the pathological changes in the airways that occurs in chronic/poorly controlled asthma

A
  1. increased smooth muscle mass
  2. accumulation of interstitial fluid (oedema)
  3. increased secretion of mucus
  4. epithelial damage
  5. sub-epithelial fibrosis
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12
Q

what does epithelial damage result in

A

exposure of sensory nerve endings causing increased sensitivity to bronchocontstrictor influences

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13
Q

what is hyper-sensitivity

A

decreased tolerance to bronchoconstriction

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14
Q

what is hyper-activity

A

increased response to bronchoconstriction

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15
Q

what is the reaction of a non-atopic individual to an antigen (TH____ + what immune cells)

A

low level TH1 response

cell mediated immune response involving IgG and macrophages

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16
Q

what is the reaction of an atopic individual to an antigen (TH____ + what immune cells)

A

strong TH2 response

antibody mediated immune response involving IgE

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17
Q

what are the 2 phases of an asthma attack

A
  1. immediate

2. delayed

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18
Q

describe the immediate phase of an asthma attack

A

eliciting agent is recognised and processed

mast cells and mononuclear cells release histamine etc. causing bronchospasm and early inflammation

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19
Q

describe the delayed phase of an asthma attack

A

infiltration of cytokine releasing TH2 cleaned monocytes which activate inflammatory cells (especially eosinophils)
mediators and eosinophilic proteins are released causing epithelial damage, airway inflammation, hyper-responsiveness, bronchospasm, wheezing, mucus over secretion, cough

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20
Q

what do TH0 cells mature to

A

TH1 and TH2

prefer to mature to TH2

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21
Q

what do TH2 cells do

A

activate B cells in 2 ways:

  1. by binding
  2. via IL-4 production

activate Eosinophils in response to IL-5

release IL-4 and IL-13 which causes mast cells to express IgE receptors

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22
Q

what do B cells mature to

A

plasma cells

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23
Q

what do plasma cells secrete

A

IgE

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24
Q

what cytokines does TH2 release

A

IL-4
IL-5
IL-13

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25
Q

what does IL-4 do

A

activates B cells and causes mast cells to express IgE receptors

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26
Q

what does IL-5 do

A

activated eosinophils

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27
Q

what does IL-13 do

A

causes mast cells to express IgE receptors

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28
Q

what are the 2 pharmacological method of asthma

A

relievers (bronchodilators)

controllers/preventers

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29
Q

Give examples of relievers (bronchodilators)

A

SABA
LABA
CystLt 1 receptor antagonist
methylxanthines

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30
Q

what is a SAMA

A

short acting B2-adrenoceptor agonist

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31
Q

what is a LABA

A

long acting B2-adrenoceptor agonist

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32
Q

give examples of controllers/preventers

A

inhaled corticosteroids (ICS)
cromoglicate
humanised monoclonal IgE antibodies
methylxanthines

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33
Q

describe the mechanism of action of LABA and SABA

A

bind to B2-adrenoceptor causing smooth muscle relaxtion

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34
Q

give examples of SABA

A

salbutamol, albuterol

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35
Q

give examples of LABA

A

salmeterol, formeterol

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36
Q

describe the mechanism of action of CystLt 1 receptor antagonist

A

act COMPETITIVELY at the CystLt 1 receptor

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37
Q

give examples of CystLt 1 receptor antagonist

A

montelukast, zafirlukast

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38
Q

describe the mechanism of action of methylxanthines

A

no one knows

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39
Q

give examples of methylxanthines

A

theophylline, aminophylline

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40
Q

describe the mechanism of action of cromones

A

no one knows

may be mast cell stabilisers

41
Q

give an example of cromone

A

sodium cromoglicate

42
Q

describe the mechanism of action of monoclonal IgE antibodies

A

binds to IgE via Fc to prevent attachment to FC receptors to suppress mast cell response to allergens

43
Q

give an example of humanised monoclonal IgE antibodies

A

omalizumab

44
Q

how are cromones used

A

infrequently used PROPHYLACTICALLY in kids

45
Q

describe the mechanism of action of Glucocorticoids

A

suppress inflammation:

prevent it and resolve established inflammation

46
Q

give examples of ICS

A

beclometasone, budesonide

47
Q

give example of ORAL steroids

A

prednisolone

48
Q

common side effects of ICS

A

dysphonia (hoarse/weak voice)

thrush (candidiasis)

49
Q

common side effects of LABAs/SABAs

A 
fine tremor (common)
tachycardia, cardiac dysrhymia, hypokalaemia
50
Q

how should a LABA be administered

A

CO-ADMINISTERED with a Glucocorticoid

or as an add on therapy

51
Q

can LABA be prescribed on its own

52
Q

can SABA be prescribed on its own

53
Q

how are CystLt 1 receptor antagonist administered

54
Q

how are methlyxamines administered

55
Q

side effects of methlyxamines

A

MANY, very narrow therapeutic window

nausea, vomiting, abdominal discomfort, headache (common)

dysrhymia, seizures, hypotension (rarer)

56
Q

describe the MOLECULAR mechanism of action of Glucocorticoids

A

enters cells via diffusion
series of interactions results in the transcription of specific genes to activate OR repress mRNA levels and the rate of synthesis of mediator proteins

57
Q

what causes the anti-inflammatory actions of Glucocorticoids

A

increases the transcription of genes encoding anti-inflammatory proteins
decreases the ranscription of genes encoding inflammatory proteins
decrease formation of TH2 cytokine
prevents production of IgE antibodies
prevents allergen-induced influx of eosinophils into lungs
reduce the number of cells and decrease Fc expression

58
Q

how is omalizumab administered

59
Q

why is synthetic derivates of cortisol used instead of the real thing

A

they contain NO traces of unwanted mineralocorticoids

60
Q

what 2 conditions make up COPD

A

chronic bronchitis

emphysema

61
Q

what is chronic bronchitis

A

inflammation of bronchi/bronchioles

62
Q

what does emphysema result in

A

distension + damage to alveoli

63
Q

what receptor causes contraction of the airways in COPD

A

muscarinic acetylchloline (M3) receptor

64
Q

how does muscarinic acetylchloline (M3) receptor causes contraction of airway smooth muscle

A

stimulation of M3 leads to release of Ca2+ from Sarcoplasmic reticulum which causes contraction

65
Q

what does stimulation of muscarinic acetylchloline (M1) receptor result in

A

fast neurotransmission

66
Q

what is stimulation of muscarinic acetylchloline (M1) receptor mediated by

A

ACh acting on nicotinic receptors

67
Q

what does stimulation of muscarinic acetylchloline (M2) receptor result in

A

inhibition of ACh release

68
Q

what does stimulation of muscarinic acetylchloline (M3) receptor result in

A

airway smooth muscle contraction

69
Q

treatment of COPD

A 
SAMA
LAMA
SABA
LABA
ICS
70
Q

can you mix SAMA and LAMA

71
Q

give an example of a SAMA

A

ipratropium

72
Q

give an example of LAMA

A

tiotropium

73
Q

what is the mechanism of action for ipratropium

A

it is an non-selective, anti-cholinergic bronchodilator

74
Q

why is it not useful to block M2 receptors in COPD

A

active M2 receptors will inhibit further ACh release

75
Q

what are LABA/SABA used for

A

bronchodilation

76
Q

what drugs are used in the treatment of allergic and non-allergic rhinitis (4)

A
  1. steroids = anti-inflammatory
  2. antihistiamines
  3. cysLT’s
  4. sodium cromoglicate
77
Q

what is the mechanism of action of antihistiamines

A

competitive antagonists of H1 receptors = reduces effects of mast cells

78
Q

what muscarinic acetylchloline receptors does ipratropium block

A

M1, M2, M3

79
Q

what muscarinic acetylchloline receptors does tiotropium block

80
Q

describe the selectivity of tiotropium

A

M3 selective

81
Q

describe the selectivity of ipratropium

A

NON-selective

82
Q

give an example of PDE4 inhibitor

A

Romfumilast

83
Q

what does the drug “Romfumilast” do?

A

suppresses inflmaation and emphysema in COPD

84
Q

what is Phosphodiesterase-4 (PDE4)

A

the main PDE expressed in neutrophils, T cells and macrophages

85
Q

what cells express PDE

A

neutrophils
T cells
macrophages

86
Q

how are cromones administered

87
Q

when would “Romfumilast” be used

A

as an add on to ICS + LABA+ LAMA

fairly last line

88
Q

what do mucolytics do

A

reduce sputum viscosity and aid sputum expectoration

rarely used

89
Q

where are M1 receptors located

90
Q

where are M2 receptors located

A

postganglionic neurone terminals

91
Q

where are M3 receptors located

92
Q

how are SAMAs administered

A

via inhalation

93
Q

how are LAMAs administered

A

via inhalation

94
Q

how do LAMA and SAMA drug names end

A

“-ium”

95
Q

what type pf ammonium group is found on SAMAs and LAMAs, what charge does it have

A

quaternary

postive charge

96
Q

LAMA/SAMA blocks which reflex

A

cough reflex

97
Q

how do SABA drug names end

A

“-mol”

98
Q

how do LABA drug names end

A

“-rol”

99
Q

explain the logic behind combining SABA/SAMA or LABA/LAMA

A

SABA = causes relaxation
SAMA = prevents contraction
SYNERGISTIC ACTIONS

Resp - mine (18 decks)

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