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Respiratory KC > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Stimulation of post-ganglionic cholinergic fibres in the parasympathetic pathway is mediated by ___ Muscarinic Ach Receptors on ASM

A

M3

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2
Q

What does post-ganglionic stimulation of cholinergic fibres cause?

A

bronchial smooth muscle contraction

increased mucous secretion

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3
Q

Stimulation of post-ganglionic non-cholinergic fibres causes bronchial smooth muscle contraction - true or false?

A

false - causes relaxation by Nitric Oxide and Vasoactive intestinal peptide

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4
Q

Peptides involved in parasympathetic non-cholinergic fibres?

A 
Nitric Oxide (NO)
Vasoactive Intestinal Peptide (VIP)
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5
Q

Which nerve provides parasympathetic stimulation to the airway smooth muscle?

A

Vagus - CN X

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6
Q

There is no sympathetic innervation of bronchial smooth muscle in humans - true or false?

A

true

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7
Q

Stimulation of sub-mucosal glands and smooth muscle of blood vessels by post-ganglionic sympathetic fibres causes…(4)

A
  • bronchial smooth relaxation via b2-adrenoceptors
  • decreased mucous secretion mediated by b2-adrenoceptors on goblet cells
  • increased mucociliary clearance mediated by b2-adrenoceptors on epithelial cells
  • vascular smooth muscle contraction mediated by a1-adrenoceptors
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8
Q

contraction stimulated by a1-adrenoceptors

A

vascular smooth muscle

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9
Q

relaxation stimulated by b2 adrenoceptors

A

bronchial smooth muscle

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10
Q

Activation of the M3 receptors leads to activation of which G protein?

A

Gq/11

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11
Q

Gq/11 activates ____ which converts PIP2 to ____ and ____

A

PLC, IP3, DAG

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12
Q

IP3 stimulates calcium release from the _______ _______ via the ____ receptor

A

sarcoplasmic reticulum, IP3

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13
Q

Calcium induced calcium release is mediated by which receptor in smooth muscle?

A

ryanodine receptor

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14
Q

Cellular depolarisation causes the closure of voltage gated calcium channels - true or false?

A

false

causes VGCC to open and allow calcium to influx allowing contraction of the smooth muscle

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15
Q

Calcium binds and activates _______, this allows the subsequent activation of _______. Active MLCK allows phosphorylated ______ cross bridge binding to ______ via the breakdown of ATP

A

Calmodulin, MLCK, myosin, actin

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16
Q

What is calmodulin?

A

calmodulin is a cytoplasmic Ca receptor which undergoes a conformational change when bound to Ca

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17
Q

In the presence of high IC Ca, the rate of phosphorylation exceeds the rate of dephosphorylation of MLCK by myosin phosphatase - true or false?

A

true

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18
Q

How is IC calcium removed from the cell for smooth muscle relaxation?

A

primary and secondary active transport

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19
Q

Primary Active Transport

A

utilises energy in the form of ATP to drive a process of moving the ion from a low concentration to a high concentration

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20
Q

Secondary Active Transport

A

utilises energy from another process where the energy is not required to move another ion i.e. a symporter

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21
Q

In order to counteract the action M3 causing contraction, _______ activates b2 adrenoceptors which activates the G-protein ___.

A

adrenaline, Gs

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22
Q

Activation of the Gs protein stimulates the enzyme…

A

adenylate cyclase

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23
Q

adenylate cyclase produces _____ which is broken down by _____

A

cAMP, PDE

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24
Q

What does cAMP activate?

A

PKA

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25
Q

PKA phosphorylates and stimulates MLCK - true or false?

A

false

PKA phosphorylates and thus inhibits MLCK

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26
Q

PKA phosphorylates and stimulates…

A

myosin phosphatase

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27
Q

Overall, activation of PKA causes what?

A

bronchial smooth muscle relaxation

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28
Q

cAMP is degraded to what by PDE?

A

5’AMP

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29
Q

What is the incidence of Asthma in industrialised countries?

A

5-10%

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30
Q

How can asthma be defined?

A

recurrent and reversible obstruction to airways in response to substance or stimuli that are not necessarily noxious and do not normally affect non-asthmatics

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31
Q

Examples of asthma attack causes

A 
Allergens
Exercise
Respiratory Infections
Smoke
Dust
Pollutants
Weather
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32
Q

Asthma is not just bronchospasm, it is….

A

intermittent attacks of bronchoconstriction; tight chest, wheezing, difficulty in breathing and coughs

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33
Q

Pathological changes that occur in the bronchioles of chronic asthmatics as a result of long standing inflammation (5)

A
  • increased mass of smooth muscle (hyperplasia/trophy)
  • accumulation of interstitial fluid
  • increased secretion of mucous
  • epithelial damage exposing sensory nerve fibres
  • sub-epithelial fibrosis
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34
Q

Airway narrowing due to inflammation and bronchoconstriction increases the ______ _______ and decrease the ____ and _____

A

airway resistance, FEV1, PEFR

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35
Q

Which fibres are exposed in chronic asthma?

A

c-fibres

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36
Q

What are the components of hyper-responsiveness in asthma?

A

hypersensitivity and hyperreactivity

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37
Q

Which substance can be used to provoke asthma via H1 receptors?

A

histamine

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38
Q

Which substance can be used to provoke asthma via M3 receptors?

A

methacholine

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39
Q

What type of reaction is the early phase asthma attack?

A

type I hypersensitivity (bronchospasm)

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40
Q

What type of reaction is the late phase asthma attack?

A

type IV hypersensitivity (bronchospasm and inflammatory)

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41
Q

What response is normal following exposure to an allergen?

A

low levels of Th1 involving IgG and macrophages

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42
Q

Cell-mediated response following exposure to an allergen

A

low levels Th1
IgG
Macrophages

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43
Q

Preferred allergen response pathway in asthmatics

A

Th2 anti-body mediated response

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44
Q

Antigen presenting cell presents allergen to ____ T cells which differentiate into ___ cells.

A

CD4+, Th0

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45
Q

In asthmatics, Th2 cells activate ____ cells which mature into ______ cells which secrete ____.

A

B, Plasma, IgE

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46
Q

What do Th2 cells secrete that enhances the B cell response?

A

IL-4

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47
Q

What interleukin do Th2 cells secrete to activate eosinophils?

A

IL-5

48
Q

IL-13

A

activates mast cells which express IgE receptors in response to ILs

49
Q

IL4

A

activates B cells and also mast cells to express IgE receptors

50
Q

Cells which have IgE receptors to help activate them

A

eosinophils and mast cells

51
Q

During activation, IgE receptors dimerise and allow Ca entry into the mast cells - true or false?

A

true

52
Q

Mast cells release…

A

preformed histamine and other agents including leukotrienes LTC4 and LTD4.
Substances (PAF and LTB4, PGDs) that attract pro-inflammatory mediators and cells

53
Q

Leukotrienes cause…

A

airway smooth muscle contraction

54
Q

Cells that cause inflammation in asthma

A

mononuclear cells

eosinophils

55
Q

Key cells in the immediate phase of an asthma attack

A

mast cells and mononuclear cells

56
Q

mast cells and mononuclear cells produce

A
  • spasmogens, CysLTs, Histamine -> bronchospasm

- chemotaxins and chemokines -> late phase

57
Q

Late phase asthma attack involves…

A

infiltration of cytokine releasing Th2 and monocytes, activation of inflammatory cells in particular eosinophils

58
Q

During the late phase, mediators and CysLTs cause ______ _______, hyper-responsiveness, bronchospasm, ________, cough and ________.

A

airway inflammation, wheezing, mucous

59
Q

During the late phase, eosinophils and major basic and cationic proteins cause epithelial damage, ______ _______, hyper-responsiveness, bronchospams, wheezing, ______ and mucous

A

airway inflammation, cough

60
Q

Step 1 Asthma treatment

A

SABA

61
Q

Step 2 Asthma treatment is given when…

A

SABA use is more than once daily

62
Q

Step 2 asthma treatment

A

regular ICS

63
Q

Step 3 Asthma treatment

A

Add LABA with ICS
If LABA is not effective increase ICS dose, discontinue LABA
If still not adequate consider other therapies i.e. monteleukast or theophylline

64
Q

Step 4 asthma treatment

A

persistent poorly controlled, increase ICS and add 4th drug i.e. Monteleukast, theophylline, oral b2-agonist

65
Q

Step 5 asthma treatment

A

introduce oral glucocorticoid and refer to specialist

66
Q

B2-adrenoceptor agonists act as phsyiological ______ of all spasmogens.

A

antagonist

67
Q

b2 agonists activate Gs –> AC which converts ATP to _____ which activates _____

A

cAMP

PKA

68
Q

Types of b2-agonist

A

SABA, LABA, ultra long acting

69
Q

Examples of SABA

A

salbutamol
tertabutaline
albuterol

70
Q

SABAs are the _____ line treatment in ______, _________ asthma and are used as relievers when ______

A

first, mild, intermediate, required

71
Q

SABAs are usually administered orally or nebulised - true or false?

A

false

usually in MDI, oral and IV or nebulised is used in severe and life-threatening asthma

72
Q

Overall effects of SABAs (3)

A

bronchial smooth muscle relaxation
increased mucus clearance
decreased mediator release from mast cells and monocytes

73
Q

Adverse effects of SABAs

A

fine tremor
tachycardia
cardiac dysrhytmia
hypokalaemia

74
Q

Examples of LABAs

A

Salmeterol

Formoterol

75
Q

What are LABAs not recommended for?

A

acute relief of bronchospasm

monotherapy

76
Q

Why are LABAs not recommended for monotherapy?

A

desensitisation to b-agonist by reducing the number of receptors

77
Q

Examples of CysLT1 Receptor Antagonists

A

Monteleukast

Zafirlukast

78
Q

LTC4, LTD4 and LTE4 are derived from ______ cells and infiltrate inflammatory cells causing smooth muscle ______, mucous _______ and _______.

A

mast, contraction, secretion, oedema

79
Q

Examples of xanthines

A

theophylline and aminophylline

80
Q

Suggested mechanism of action of methylxanthines

A

inhibition of PDE III and IV

81
Q

What sort of mechanisms are exhibited by methylxanthines?

A

bronchodilator and anti-inflammatory

82
Q

Theophylline activates HDAC which may ______ the activity of glucocorticoids

A

potentiate

83
Q

Adverse effects of methylxanthines

A 
dysrhythmias
seizures
hypotension
nausea
vomiting
GI upset
Headache
84
Q

Reason for methylxanthines being problematic

A

drug interactions involving CYP450s, particularly antibiotics that inhibit CYP450

85
Q

Glucocorticoids are produced in the ______ ________ of the adrenal cortex

A

zona fasiculata

86
Q

Glucocorticoids are essential in regulating: (5)

A 
decreased inflammatory responses
decreased immunological responses
increased liver glycogen deposits
increased gluconeogenesis
increased glucose output from the liver
87
Q

Main mineralocorticoid

A

aldosterone

88
Q

Site of production of mineralocorticoids

A

zona glomerulosa

89
Q

Action of glucocorticoids

A

anti-inflammatory

90
Q

In particular glucocorticoids decrease the formation of….

A

Th2 cytokines

91
Q

Glucocorticoids prevent the production of IgE and influx of…

A

eosinophils and mast cells

92
Q

common side affects of inhaled glucocorticoids

A

hoarse and weak voice, thrush

93
Q

When might oral prednisolone be given?

A

when there is an exacerbation or severe asthma

94
Q

Cromones are often described as _____ ____ ______ even though this is not their mechanism of action. An example is _______ _______

A

mast cell stabilisers

sodium cromoglicate

95
Q

cromones are more effective in…

A

children and young adults

96
Q

sodium cromoglicate is used to reduce _____ phases of an attack but efficacy may take several weeks to develop a block to _____ ______ attack

A

both.

late phase

97
Q

Monoclonal antibodies used in asthma

A

IgE - Omalizumab

IL-5 - Mepolizumab

98
Q

Preferred pharmacological target in the treatment of COPD?

A

M1 and M3 muscarinic receptors

99
Q

Why is it preferable to avoid M2 receptors in the treatment of COPD?

A

the M2 receptor is a auto-regulatory receptor which provides negative feedback when stimulated.

100
Q

Which immune cells are activated in COPD?

A

neutrophils, CD8 T cells and macrophages

101
Q

SAMA examples

A

ipratropium & oxitropium

102
Q

LAMA examples

A

tiotropium & aclidinium

103
Q

Route of administration for SAMA and LAMA and why?

A

inhalational to avoid blocking systemic parasympathetic nervous system

104
Q

B-adrenoceptor agonists used in COPD?

A

salbutamol, salmeterol, formoterol

105
Q

Rofumilast

A

PDE4 selective inhibitor which suppresses inflammation and emphysema

106
Q

Rhinitis or Rhinorrhoea may be allergic or non-allergic - TRUE or FALSE?

A

true

107
Q

in allergic rhinitis, what mediators may be released that contribute to the inflammatory response?

A

IgE, cysLTs, histamine, tryptase, prostaglandins,

108
Q

non-allergic causes of rhinitis

A

infection, hormonal, vasomotor, non-allergic rhinitis with eosinophilia syndrome, medications

109
Q

treatment targeting inflammation in rhinitis?

A

glucocorticoids

110
Q

glucocorticoids used in rhinitis?

A

beclometasone

fluticasone

111
Q

treatments targeting receptors in rhinitis?

A

H1 receptor antagonists, CysLT1 receptor antagonists

112
Q

H1 receptor antagonists used in rhinitis

A

fexafenadine
citerizine
loratidine

113
Q

CysLT1 receptor antagonists used in rhinitis?

A

montelukast

114
Q

oxymetazoline is used as…

A

a selective a1 adrenoceptor agonist for vasomotor rhinitis

115
Q

indications of using oxymetazoline

A

can only be used for a short time because of rebound increase in congestion upon discontinuation

Respiratory KC (20 decks)

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