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treatments for the respiratory system Flashcards

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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
Corticosteroid-activated glucocorticoid receptors (GR) interact with coactivator molecules such as ____ and this inhibits the action of NF-κB with coactivators
CREB-binding protein (CBP)
26
ICSs only inhibit inflammation when____
it is activated through proteins such as NF-κB
27
what are bronchodilators
treatment of asthma dilates bronchi and bronchioles to decrease airway resistance in and increase airflow to lungs relaxes smooth muscle
28
what are the three main drug classes of bronchodilators
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
what is an example of a Short-Acting β2-agonist (SABA)
salbutamol
30
mechanism of action of Short-Acting β2-agonists (SABA)
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
how much does asthma cost the NHS
1.1 billion annually
32
what are β2-adrenergic receptors (β2-AR) an example of
GPCRs
33
what are β2-adrenergic receptors (β2-AR) GPCRs coupled to
Gas/ G alpha stimulatory pathway activates adenylate cyclase
34
myosin light chain phosphatase (MLCP)
promotes smooth muscle relaxation
35
myosin light chain kinase (MLCK)
promotes airway muscle contraction
36
what is an example of a Long-Acting β2-agonist (LABA)
salmeterol with ICS fluticasone
37
mechanism of action of Long-Acting β2-agonist (LABA)
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
how are Long-Acting β2-agonist (LABAs) administered
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
synergistic drug action example
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
what is a synergistic effect
two drugs used together and result is greater than what you would expect if you add together the effect of each drug independently
41
what is an additive effect
two drugs used together and result is what you would expect if you add together the effect of each drug independently
42
β2-adrenergic receptor mutations
can cause inc in downregulation
43
what are nebulisers
mist of drug to breathe in, easier to enter lung tissue
44
nebulisation and COVID-19
may cause dispersion of COVID-19 into surrounding environment, potentially putting surrounding people at risk
45
Viable SARS-CoV-2 is reported in aerosols generated by nebulisers for up to __ hours
3
46
other than LABAs and SABAs, ___ ___ ___ are also used bronchodilators
muscarinic receptor antagonists or anticholinergic bronchodilators
47
muscarinic receptor antagonists or anticholinergic bronchodilators exert their function through
muscarinic acetylcholine receptors (mAChRs)
48
muscarinic acetylcholine receptors (mAChRs) are
Gq - coupled GPCRs that raise intracellular calcium levels
49
muscarinic acetylcholine receptors (mAChRs) pathway
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
examples of muscarinic acetylcholine receptor (mAChR) antagonists (2)
ipratropium tiotropium
51
muscarinic acetylcholine receptor (mAChR) antagonist mechanism of action
inhibit activation of mAChRs no inc in intracellular calcium no MLCK activation prevent contraction of smooth muscle in airways
52
chronic obstructive pulmonary disease (COPD) treatment focus
no cure, therapies slow progression
53
chronic obstructive pulmonary disease (COPD) treatments
ICSs SABAs LABAs mAChR antagonists smoking prevention nicotine cessation therapy
54
what is nicotine
major psychoactive compound in cigarette smoke binds to nicotine acetylcholine receptors (nAchRs)
55
what contributes most to nicotine-dependence
rate of metabolism (varies by person) nmr
56
how is nicotine metabolised
phase 1 metabolism via cyp2a6 (90%) and cyp2b6 (10%) into cotenine via cyp2a6 into 3' hydroxycotinine
57
how does nicotine absorption occur
oral cavity mostly skin lung urinary bladder gastrointestinal tract
58
respiratory absorption of nicotine is __ to __ %
60 to 80 large value when smoked due to high surface area of alveoli in lungs
59
absorption of nicotine when ingested
poorly absorbed as gastric fluid is acidic causing ionisation in stomach well absorbed in small intestine
60
three types of nicotine cessation therapy
nicotine replacement therapy e.g. nicotine patches varenicline bupropion
61
varenicline
competitive partial agonist for nAChR competes with nicotine, get lesser effect when exposed to nicotine
62
bupropion
non competitive antagonist of nAChR allosteric binding
63
what is the nicotine metabolite ratio (NMR)
ratio of '3 hydroxycotinine to cotinine indicates cyp2a6 ability in smokers
64
faster metabolisers of nicotine have a ____ NMR
greater
65
slower metabolisers of nicotine have a ____ NMR
smaller
66
faster metabolisers of nicotine are likely to benefit from ___
varenicline as not metabolised as quick as nicotine in nicotine patches would
67
slower metabolisers of nicotine are likely to benefit from ___
varenicline or nicotine replacement therapy equally
68
ICSs switch off activated inflammatory genes through recruitment of _____ _____ _____
histone deacetylase 2 HDAC2
69
COPD patients are _____ resistant
corticosteroid thus, admin. with LABAs
70
asthma patients who smoke are more _____ resistant. why
corticosteroid as reduction in HDAC2 expression, less target for ICSs to switch off
71
ICSs activate ______ which decreases inflammatory peptides like ______ and other inflammatory cells like ____ and ____
lipocortin-1 endothelin-1 mast cells and dendritic cells
72
ICS budenoside
greater first pass metabolism, less likely to produce systemic effects at high doses, inc local effect on airway mucosa
73
spacer chambers
reduce oropharyngeal deposition and reduces systemic absorption
74
in COPD, it was found that adding _____ to ICS is more effective than increasing ICS dose alone
salmeterol
75
ICS local side effects
dysphonia - common pneumonia - esp in COPD
76
ICSs systemic side effects
bruising as inhibits dermal fibrolasts that produce collagen, which is needed for resilience and skin structure
77
spacer device e.g. AeroChamber are attachments for ____ and (general indo)
pressurized metered-dose inhalers (pMDIs) ensures more med reaches lungs vs depositing in the oropharynx inc drug efficacy dec local side effects e.g. oral candidiasis
78
compare asthma treatments - 4 main points
ICS more effective as switch off inflammatory genes bronchodilators provide rapid symptom relief (or long term if LABA) better used synergystically - LABA and ICSs for moderate to severe cases ICS side effects dec by using spacer device/improved drug delivery - esp found in children dec side effects
79
Myosin light chain kinase (MLCK) and myosin light chain phosphatase (MLCP) control the activity of
myosin II - which is a motor protein involved in sliding filament mechanism
80
activated MLCK phosphorylates the regulatory light chain of myosin, inducing a
conformational change in myosin inc ATPase activity causing muscle contraction
81
Myosin light chain Phosphatase (MLCP) dephosphorylates the regulatory light chain of myosin, causing
red in myosin ATPase activity causing muscle relaxation
82
sliding filament theory in smooth muscle - 6 steps
calcium influx intracellularly calcium binds to calmodulin MLCK activation phosphorylation by MLCK of myosin light chain enables cross bridge cycling with actin myosin binds to actin, hydrolises ATP, produce sliding of actin filaments over myosin , causing contraction when MLCP dephosphorylates myosin, ATPase activity red and muscle relaxation
83
combination therapy in COPD case study
muscarinic receptor antag/ SAMA ipratroprium combined with albuterol SABA sig additive effects albuterol binds to B2 adrenergic receptors activates cAMP, inc PKA, MLCK function - bronchodilation ipratropium blocks M3 muscarinic receptors which normally activated by ACH, thus inhibits PLC IP3 pathway, dec intracellular calcium levels, bronchodilation separate mechanisms so additive - better symptom relief, improved lung function when used together
84
what clinicals we gaf - 2
asthma copd
85
types of drugs used to treat clinicals - 6
asthma and copd: anti inflammatory drugs (ICS bronchodilators (SABA, LABA, Muscarinic acetylcholine receptor antagonists, also called short - acting muscarinic antagonists (SAMA) copd only: smoking prevention nicotine cessation therapy
86
examples of each drug type - 10
asthma and copd: ICS: fluticasone, budesonide, beclomethasone (with nebulisers oops covid maybe) (copd dont do well so add laba) SABA: salbutamol LABA: salmeterol with ICS fluticasone - synergistic SAMA: ipratropium, tiotropium copd only: nicotine replacement therapy e.g. nicotine patches varenicline bupropion

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