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MB1: Respiratory > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what does stimulation of cholinergic postganglionic fibres do to ASM

A

M3 muscarinic Ach receptors cause ASM to contract increased mucus secretion on goblet cells

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2
Q

what do non cholinergic postganglionic fibres do to ASM

A

muscle relaxation

mediated by Nitric oxide and VIP

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3
Q

What does the sympathetic division do to ASM

A

no direct effect, but causes release of adrenaline into system which binds to beta 2 adrenoceptors to relax ASM cells, decrease goblet cell secretion and increase activity of mucociliary escalator

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4
Q

smooth muscle contraction in heart is regulated by

A

alpha 1 adrenoceptor

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5
Q

Describe the chain of events which cause ASM contraction

A

IP3 allows calcium entry to cell to phosphorylate MLC to MLCK and allows sliding of actin and myosin for contraction

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6
Q

How is ASM relaxed

A

Adrenaline binds to B2 adrenoceptors to produce cAMP and inhibit MLCK. dephosphorylates MLC by myosin phosphatase

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7
Q

What is asthma

A

recurrent and reversible obstruction to airways in response to substances that are not necessarily noxious

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8
Q

what are causes of asthma

A

allergens

cold air, environmental pollutants, dust and smoke

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9
Q

What is asthma an onset of and what can it involve

A

Acute, intermittent attacks of bronchoconstriction

involves pathological changes to bronchioles form longstanding inflammation

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10
Q

What are the long term consequences of asthma

A

hyperplasia and hypertrophy of smooth muscle
Oedema
Sub epithelial fibrosis
epithelial damage that exposes sensory nerve endings
increased secretion of mucus

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11
Q

airway resistance is increases. how does this affect FEV1 and PEFR

A

Decreased FEV1 and peak expiratory flow rate (PEFR)

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12
Q

how is bronchial hyperresponsiveness caused

A

increased airway sensitivity due to exposure of sensory nerve endings
Inflammation induced by release of peptides by these endings

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13
Q

What is hyperreactivity

A

excessive response made due to presence of sensitive stimuli

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14
Q

What is hypersensitivity

A

more prone to abnormal respons in presence of particular antigen

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15
Q

how is hyperreactivity diagnosed

A

Administration of spasmogens to test spasm of bronchioles

Mannitol, histamine, methacholine

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16
Q

How many phases does an asthma attack have and what are they

A

2
Immediate bronchospasm
Delayed inflammatory response

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17
Q

what reaction does a nonatopic individual have to an allergen

A

TH1 response with Immunoglobulin G

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18
Q

what response does an atopic asthmatic individual have presented with an allergen

A

TH2 response with IgE

usually a poor prognosis

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19
Q

how does atopic allergic asthma develop

A

dendritic cell presents allergens antigens to CD4 T cell
proliferates to TH0 cell and then a TH2, producing a cytokine environment
TH2 promotes proliferation of B cells by IL-4, proliferating to plasma cells secreting IgE

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20
Q

What does IgE in an asthmatic do

A

IgE, IL-4, IL-13 cause calcium entry into mast cells which causes histamine and leukotrine release
Prostaglandins released which attract other inflammatory cells

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21
Q

what two part of asthma should be treated in consideration with drug prescription

A

drugs that treat the acute asthma phase as well as long term immune and inflammatory treatment

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22
Q

2 rough classes of drugs in asthma treatment

A

Relievers

Preventors

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23
Q

How do B2 adrenoceptor agonists work?

A

increases cAMP so phosphorylates myosin phosphatase to inhibit MLCK and relaxes smooth muscle

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24
Q

Names of 3 SABA drugs and their adverse effects

A

Salbutamol
Albuterol
Terbutaline
Few adverse effects noted, except fine tremor, tachycardia and cardiac dysrythmia due to presence of B2 adrenoceptors on cardiac muscle

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25
Q

how are SABA administered and what do they do

A

Usually inhaler to minimize systemic effect
rapid acting on bronchial smooth muscle, reduced constriction as well as decreasing mediator release from mast cells and increasing mucus clearance

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26
Q

Name of LABAs

A

formoterol

salmeterol

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27
Q

What are LABA most used for?

A

not great for acute bronchospasm but used in nocturnal treatment
Add on therapy, not monotherapy

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28
Q

What must a LABA always be administered with?

A

Glucocorticoid

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29
Q

true/false - beta blockers are safe for use with SABA/LABA

A

false - it is contraindicted due to risk of bronchospasm. beta blockers are B2 adrenoceptor antagonists

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30
Q

Why is isoprenaline redundant for use in asthma

A

it is non selective between B2-adrenoceptors and cardiac B1-adrenoceptors so can increase heart rate

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31
Q

What do cysteinyl leukotrine receptor antagonists act on

A

competitively on CysL1 receptor to inhibit it

32
Q

what are cysteinyl leukotrines derived from and what do they do

A

Derived from mast cells

Increase smooth muscle contraction, mucus secretion and oedema

33
Q

name of CysLT1 receptor antagonist and how they are used

A

monteleukast
zafirlukast
add on with other medications by oral route
not recommended for relief of acute phase asthma

34
Q

Name 2 Methylxanthines

A

theophylline

aminophylline

35
Q

What are xanthines believed mechanism of action?

A

inhibits PDE so prevents breakdown of cAMP and so cAMP continues to stimulate pathway that relaxes ASM

36
Q

Xanthines are used in combination with ____

A

B2-adrenoceptor agonists and glucocorticoids

37
Q

What do xanthines do?

A

can be bronchodilators at high dose
anti inflammatory mediation by mast cell inhibition
increased mucus clearance

38
Q

true/false - xanthines have a large window of therapeutic treatment with little contraindication

A

False- narrow range

severe contraindication in use with antibiotics like CYP450s

39
Q

How do xanthines improve lung ventilation

A

increase diaphragmatic contractility and reduce fatigue

40
Q

What are the two types of steroid hormones synthesised by the adrenal cortex

A

glucocorticoids

mineralocorticoids

41
Q

What are glucocorticoids and what is the main one in man

A

corticosteroids which regulate decrease of inflammatory and immunological responses
Hydrocortisone

42
Q

what are mineralocorticoids and what is the main one

A

Corticosteroids which regulate the retention of salt and water by the kidney
aldosterone

43
Q

true/false - inhaled glucocorticoids are given for acute bronchoconstriction

A

fasle - they do not have any bronchodilator effect and are given as a prophylaxis by inhalation

44
Q

3 types of glucocorticoids and how are they administered

A

beclometasone
budesonide
fluticasone
administered by inhaler in metered dose

45
Q

glucocorticoids signal by _____ receptors

A

nuclear

46
Q

glucocorticoids combine with what receptor in the cytoplasm to translocate to the nucleus

A

GRa

47
Q

what happens to glucocorticoids in the nucleus

A

monomers assemble into homodimers and bind to glucocorticoid response elements in promoter region

48
Q

transcription of genes can be …

A

transactivated or transrepresed

49
Q

How do glucocorticoids affect transcription of inflammatory genes besides transrepression

A

deacylation of histones, condensing them and preventing them from being transcribed

50
Q

Name a chromone and its frequency and means of use

A

sodium chromoglicate

used infrequently, and in prophylaxis by inhalation

51
Q

what phase of asthma can chromones treat and who is it effective in

A

both phases, but can take weeks to work

more effective in children and young adults

52
Q

what is omalizumab?

A

a monoclonal antibody treatment of asthma, binds IgE with Fc to prevent attachment to mast cell receptors

53
Q

How do muscarinic ACh receptor antagonists work

A

antagonists of M3 receptor activation - prevents binding of ACh which causes bronchoconstriction

54
Q

What does M1 do

A

facilitates fast neurotransmission mediated by ACh

55
Q

what does M2 do

A

inhibitory autoreceptor - reduce ACh release

56
Q

What does M3 do

A

Present on ASM and mediates contraction in response to ACh binding

57
Q

Why are broad spectrum muscarinic antagonists not useful and name one

A

they inhibit all muscarinic receptors in the body. Atropine

58
Q

Name SAMA

A

ipratropium

non selectively blocks M1,2,3

59
Q

name 4 LAMAs

A

Tiotropium
Glycopyrronium
Aclidinium
Umeclidinium

60
Q

describe how SAMA/LAMAs are administered, adverse effects and their action mechanism

A 
Inhalation
Little adverse effect due to quaternary ammonium group
delayed onset bronchodilator 
decrease mucus secretion
they do little to stop COPD progression
61
Q

Why are selective muscarinic antagonists that bind selectively to M3 better than iprotropium

A

they prevent the unwanted block of M2, which helps to block the release of ACh

62
Q

true/false - a beta agonist and muscarinic antagonist are better in combination than either drug alone

A

true

63
Q

why are LABA/LAMA combinations logical

A

they work in opposite yet complementary ways to relax smooth muscle

64
Q

Name a PDE4 inhibitor and how they work

A

Rofumilast

Inhibits PDE4 to suppress inflammatory and immune cells to suppress inflammation and emphysema

65
Q

when would a glucocorticoid be administered with a beta agonist and LAMA/LABA and how could they be administered

A

eosinophilic COPD

Potentially administered separately or in triple inhaler

66
Q

when might a glucocorticoid not work in a patient with eosinophilic COPD

A

Oxidative/nitrative stress - chronic inhalation of cigarette smoke

67
Q

What is rhinitis and how could it be caused

A

Acute or chronic inflammation of nasal mucosa

Can be allergic, non allergic or mixed

68
Q

How can allergic rhinitis be classified and what does it strongly resemble in terms of similarity

A

Seasonal
Perennial
Episodic
Linked to asthma

69
Q

What type of rhinitis involves allergic and non allergic compounds

A

occupational

70
Q

How is non allergic rhinitis classed as such and what are its causes

A

it isnt involved with IgE dependent events

Infectious, hormonal, vasomotor, NARES, drug induced

71
Q

What rhinitis can corticosteroids be used and which ones are used

A

SAR and PAR

Prednisolone (oral), beclometasone, fluticasone

72
Q

How do antihistamines treat allergic rhinitis and which are used

A

competitive agonists to H1 receptor, reduce effects of mast cell derived histamine
Cetirizine, Loratidine, fexofenadine

73
Q

What muscarinic antagonist can be used and how does it stop rhinorrhoea

A

Iprotropium

Prevents binding of ACh which causes watery secretion from glands

74
Q

what drug used in rhinitis treatment stabilises mast cells and is not as effective as a corticosteroid

A

Sodium cromoglicate

75
Q

CysLTR antagonists

A

reduce effect of CysLTs
Oral route for asthma and allergic rhinitis
montelukast

76
Q

Vasoconstrictors

A

Mimic effect of noradrenaline to vasoconstrict vessels

Oxymetazoline

MB1: Respiratory (15 decks)

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