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342 > treatments for the respiratory system > Flashcards

treatments for the respiratory system Flashcards

1
Q

what is asthma characterised by

A

airway obstruction

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2
Q

in context to asthma, what is airway obstruction caused by (2)

A

hyper responsive airway smooth muscle - e.g. change in temp of air, PM, can be spontaneous - narrowing, wheezing, shortness of breath

airway inflammation - overproduction of proinflammatory proteins

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3
Q

what can airway hyper responsiveness be triggered by (4)

A

allergens
cold air
excercise
emotional stress

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4
Q

what does exposure to stimuli result in

A

release of pro-inflammatory proteins

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5
Q

what are symptoms of asthma (4)

A

difficulty breathing
shortness of breath
wheezing
coughing

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6
Q

what drugs are used to treat asthma (2)

A

anti inflammatory drugs
bronchodilators

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7
Q

what drugs can patients with asthma benefit from

A

corticosteroids (type of glucocorticoid)

ideal as asthma is inflammatory

reduces inflammation

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8
Q

how to minimise off target systemic effects from corticosteroids

A

inhaled corticosteroids (ICSs)

goes to lungs

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9
Q

examples of inhaled corticosteroids (3)

A

fluticasone
budesonide
beclomethasone

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10
Q

are inhaled corticosteroids useful for long or short term asthma attack prevention

A

long term

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11
Q

how are inhaled corticosteroids administered and why

A

spacer device e.g. AeroChamber

dec. amount of drug deposited from mouth and upper airways

facilitates delivery of ICSs to bronchioles

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12
Q

what occurs when corticosteroids are inhaled

A

diffuse across cell membrane, bind to glucocortioid receptors in cell cytoplasm

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13
Q

what are glucocorticoid receptors (GRs)

A

type of nuclear receptor

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14
Q

what are nuclear receptors

A

sense steroid and thyroid hormones

bind directly to DNA in nucleus and regulate expression genes

are thus classified as transcription factors

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15
Q

what occurs once glucocorticoid receptors (GRs) are activated

A

in cell cytoplasm form homodimer

translocate into nucleus and produce effect

the glucocorticoid receptors interact with the glucocorticoid response element (GRE) in the promoter region of steroid responsive genes

this switches on (sometimes off) gene transciption

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16
Q

examples of genes activated by inhaled corticosteroids (ICSs) (2)

A

β2-adrenergic receptors

Anti-inflammatory proteins

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17
Q

2 examples of anti inflammatory proteins

A

secretory leukoprotease inhibitor

mitogen activated protein kinase phosphatase-1 (MKP-1)

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18
Q

what does mitogen activated protein kinase phosphatase-1 (MKP-1) do

A

inhibit MAP kinase pathways which thus promotes mucus production to obstruct airways

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19
Q

what occurs when glucocorticoid receptors (GRs) interact with negative glucocorticoid response element (GRE)

A

may suppress gene transcription

may be important in mediating side effects associated with ICS use

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20
Q

when glucocorticoid receptors (GRs) interact with negative glucocorticoid response element (GRE) gene transcription may be suppressed. this may be important in mediating side effects associated with ICS use. what is an example of this?

A

corticosteroids inhibit the expression of osteocalcin that is involved in bone synthesis

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21
Q

what is the major action of corticosteroids

A

to switch off multiple activated inflammatory genes that encode for pro-inflammatory mediators e.g. cytokines

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22
Q

corticosteroids switch off multiple activated inflammatory genes that encode for pro-inflammatory mediators e.g. cytokines. how are these genes switched on in airways?

A

by proinflammatory transcription factors e.g. nuclear factor-κB (NF-κB)

interact with coactivator molecules like CREB-binding protein (CBP)

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23
Q

what is an example of a proinflammatory transcription factor

A

nuclear factor-κB (NF-κB)

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24
Q

Corticosteroid-activated glucocorticoid receptors (GR) interact with coactivator molecules such as CREB-binding protein (CBP) and this inhibits the action of ____ with coactivators

A

NF-κB

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25
Q

Corticosteroid-activated glucocorticoid receptors (GR) interact with coactivator molecules such as ____ and this inhibits the action of NF-κB with coactivators

A

CREB-binding protein (CBP)

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26
Q

ICSs only inhibit inflammation when____

A

it is activated through proteins such as NF-κB

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27
Q

what are bronchodilators

A

treatment of asthma

dilates bronchi and bronchioles to decrease airway resistance in and increase airflow to lungs

relaxes smooth muscle

28
Q

what are the three main drug classes of bronchodilators

A

Short-Acting β2-agonists (SABA) aka ‘Reliever inhalers’

Long-Acting β2-agonists (LABA) aka ‘Preventer inhalers’, taken once daily

Muscarinic acetylcholine receptor antagonists, also called short - acting muscarinic antagonists (SAMA)
29
Q

what is an example of a Short-Acting β2-agonist (SABA)

A

salbutamol

30
Q

mechanism of action of Short-Acting β2-agonists (SABA)

A

SABAs bind to β2-adrenergic receptors (β2-AR) in the lower respiratory tract

activates Gas

β2-AR stimulates cyclic adenosine monophosphate (cAMP) production

cAMP activates protein kinase A (PKA)

myosin light chain kinase (MLCK) promotes airway muscle contraction via sliding filament theory - two filaments contract and slide together

cAMP and PKA inhibit MLCK, promotes bronchodilation

cAMP and PKA activate myosin light chain phosphatase (MLCP), promotes smooth muscle relaxation

31
Q

how much does asthma cost the NHS

A

1.1 billion annually

32
Q

what are β2-adrenergic receptors (β2-AR) an example of

A

GPCRs

33
Q

what are β2-adrenergic receptors (β2-AR) GPCRs coupled to

A

Gas/ G alpha stimulatory pathway

activates adenylate cyclase

34
Q

myosin light chain phosphatase (MLCP)

A

promotes smooth muscle relaxation

35
Q

myosin light chain kinase (MLCK)

A

promotes airway muscle contraction

36
Q

what is an example of a Long-Acting β2-agonist (LABA)

A

salmeterol with ICS fluticasone

37
Q

mechanism of action of Long-Acting β2-agonist (LABA)

A

LABAs bind to β2-adrenergic receptors (β2-AR) in the lower respiratory tract

activates Gas

β2-AR stimulates cyclic adenosine monophosphate (cAMP) production

cAMP activates protein kinase A (PKA)

myosin light chain kinase (MLCK) promotes airway muscle contraction via sliding filament theory - two filaments contract and slide together

cAMP and PKA inhibit MLCK, promotes bronchodilation

cAMP and PKA activate myosin light chain phosphatase (MLCP), promotes smooth muscle relaxation

same as SABA

38
Q

how are Long-Acting β2-agonist (LABAs) administered

A

with inhaled corticosteroids ICSs

as ICS suppresses chronic inflammation, activate genes to increase β2-adrenergic receptor production, reduce airway hyper responsiveness

synergistic drug action

39
Q

synergistic drug action example

A

Long-Acting β2-agonist (LABAs) with inhaled corticosteroids ICSs

as ICS suppresses chronic inflammation, activate genes to increase β2-adrenergic receptor production, reduce airway hyper responsiveness

thus, ICS increases drug targets for LABA

and protects against downregulation of β2-receptors after long term administration as ICSs switch on pathways

Long-Acting β2-agonist (LABAs) affect glucocorticoid receptors (GRs) and enhances anti inflammatory effects of ICSs by inc translocation into nucleus

40
Q

what is a synergistic effect

A

two drugs used together and result is greater than what you would expect if you add together the effect of each drug independently

41
Q

what is an additive effect

A

two drugs used together and result is what you would expect if you add together the effect of each drug independently

42
Q

β2-adrenergic receptor mutations

A

can cause inc in downregulation

43
Q

what are nebulisers

A

mist of drug to breathe in, easier to enter lung tissue

44
Q

nebulisation and COVID-19

A

may cause dispersion of COVID-19 into surrounding environment, potentially putting surrounding people at risk

45
Q

Viable SARS-CoV-2 is reported in aerosols generated by nebulisers for up to __ hours

A

3

46
Q

other than LABAs and SABAs, ___ ___ ___ are also used bronchodilators

A

muscarinic receptor antagonists

or anticholinergic bronchodilators

47
Q

muscarinic receptor antagonists or anticholinergic bronchodilators exert their function through

A

muscarinic acetylcholine receptors (mAChRs)

48
Q

muscarinic acetylcholine receptors (mAChRs) are

A

Gq - coupled GPCRs that raise intracellular calcium levels

49
Q

muscarinic acetylcholine receptors (mAChRs) pathway

A

Gq activation

some shit abt pip2 idk

inc intracellular calcium inc PKC activation

calcium ions interact with calmodulin forming calcium-calmodulin complex

complex activates MLCK

MLCK phosphorylates myosin, promotes smooth muscle contraction

50
Q

examples of muscarinic acetylcholine receptor (mAChR) antagonists (2)

A

ipratropium

tiotropium

51
Q

muscarinic acetylcholine receptor (mAChR) antagonist mechanism of action

A

inhibit activation of mAChRs

no inc in intracellular calcium

no MLCK activation

prevent contraction of smooth muscle in airways

52
Q

chronic obstructive pulmonary disease (COPD) treatment focus

A

no cure, therapies slow progression

53
Q

chronic obstructive pulmonary disease (COPD) treatments

A

ICSs
SABAs
LABAs
mAChR antagonists

smoking prevention
nicotine cessation therapy

54
Q

what is nicotine

A

major psychoactive compound in cigarette smoke

binds to nicotine acetylcholine receptors (nAchRs)

55
Q

what contributes most to nicotine-dependence

A

rate of metabolism (varies by person)

nmr

56
Q

how is nicotine metabolised

A

phase 1 metabolism via cyp2a6 (90%) and cyp2b6 (10%)

into cotenine

via cyp2a6

into 3’ hydroxycotinine

57
Q

how does nicotine absorption occur

A

oral cavity mostly
skin
lung
urinary bladder
gastrointestinal tract

58
Q

respiratory absorption of nicotine is __ to __ %

A

60 to 80

large value when smoked due to high surface area of alveoli in lungs

59
Q

absorption of nicotine when ingested

A

poorly absorbed as gastric fluid is acidic causing ionisation in stomach

well absorbed in small intestine

60
Q

three types of nicotine cessation therapy

A

nicotine replacement therapy e.g. nicotine patches

varenicline

bupropion

61
Q

varenicline

A

competitive partial agonist for nAChR

competes with nicotine, get lesser effect when exposed to nicotine

62
Q

bupropion

A

non competitive antagonist of nAChR

allosteric binding

63
Q

what is the nicotine metabolite ratio (NMR)

A

ratio of ‘3 hydroxycotinine to cotinine

indicates cyp2a6 ability in smokers

64
Q

faster metabolisers of nicotine have a ____ NMR

A

greater

65
Q

slower metabolisers of nicotine have a ____ NMR

A

smaller

66
Q

faster metabolisers of nicotine are likely to benefit from ___

A

varenicline

as not metabolised as quick as nicotine in nicotine patches would

67
Q

slower metabolisers of nicotine are likely to benefit from ___

A

varenicline or nicotine replacement therapy equally

342 (9 decks)

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