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Mucosal Surfaces > 24- Respiratory Medicines > Flashcards

24- Respiratory Medicines Flashcards

1
Q

What are the 5 main categories of bronchodilators

A

LA,SA anti cholinergic
LA,SA B2 agonists
Theophylline (derivatives of xanthine)

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2
Q

Why isn’t a large dose needed

A

Inhalation and not systemic meaning directly flows to the lungs

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3
Q

Which property are LA

A

Lipophilic

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4
Q

What 3 things happen in asthmatic airways

A

Sm contraction, inflammation and mucus secretion

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5
Q

What is the immediate phase

A

Where igE bind and present allergens to the fcr on mast cells which causes degranulation of arachidonic products causing permeability (leukotrienes also release mucus and bronchoconstrict)
And histamine also contraction = bronchospasm

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6
Q

How does the immediate phase relate to late phase

A

Th2 cytokines from mart cells eg il4 and il6 then allow th2 response and attraction of eosinophils etc which cause inflammation and hyper reactivity of airways

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7
Q

Which drugs target the late phase

A

Glucocorticoids

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8
Q

What are th2 responsible for

A

Ige release, eosinophilia attraction, mast cell stimulation = airway sensitivity

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9
Q

Which article discusses eosinophils in asthma

A

Mcbrien et al 2017

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10
Q

Which protein in eosinophils granules you increases histamine release from mast cells

A

Mbp major basic protein

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11
Q

Which th2 cytokines do eosinophils release

A

Il4 and il13

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12
Q

What apc do they attract for more T cell responses

A

Dc

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13
Q

How does mbp cause tissue/ epithelial damage

A

It’s toxic to them

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14
Q

How does ach from PNS cause smooth muscle contraction and mucus secretion from goblet cells/submucosal glands

A

Binds to M3 receptors on smooth muscle cells in airways and submucosal glands to cause secretion

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15
Q

What type of receptor is it

A

Gpcr

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16
Q

How does it cause sr calcium release for constriction

A

Activates Phospholipase c and then production of ip3 and dag. Ip3 binds ryr and allows ca release

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17
Q

How does calcium then cause contraction

A

Binds troponin releasing tropomyosin from myosin bs allowing cross bridging

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18
Q

How do anticholinergics work

A

Competitive antagonists of the muscarinic receptors stopping constriction and mucus release from vagal stimulation

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19
Q

What is the short acting one to relieve symptoms

A

Ipratropium bromide (lasts around 1-6 hours)

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20
Q

What is the LA one for prevention

A

Tiotropium bromide (up to 18 hours)

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21
Q

Why isn’t it first choice for asthma but good for copd

A

Doesn’t stop mast cell stimulated constriction eg via histamine

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22
Q

Why does copd need it

A

They have cholinergic hypersensitivity eg causing cb

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23
Q

What are some side effects of blocking PNS

A

Dry mouth, urinary retention, constipation (lack of bladder contraction)

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24
Q

Why do they have poor penetration and interaction

A

Only 1-2% of ipratropium is absorbed systemically. They are inhaled and stay in lungs mostly

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25
Q

Why isn’t it advised for pregnant yet

A

Not enough studies

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26
Q

Why is ipratropium not given with cromolyn sodium drugs

A

Because can form a precipitate which stops nast cell stabilisation

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27
Q

Which article discusses how cromolyn works and how

A

Puzzovio et Al 2022

Suggested by secreting il10 cromolyn reduces the stimulation of mast cells via igE and there’s a shift to igg4. Means no mast cell degranulation

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28
Q

B2 agonists bind to B2 gpcr and help it reduce ic calcium. What does gpcr activate and what does this do

A

Activates adenylyl cyclase which increases atp to cyclic amp transition. Camp then activates pka

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29
Q

Which 2 channels are activated by pka which help reduce ic calcium or help hyperpolarisation

A

Ca2 activated k channel activation

Na/k activation which helps ncx exchanger as sodium gradient

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30
Q

Hydrolysis of what is reduced in pka which stops ca release

A

Phosphoinositol which forms ip3

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31
Q

Which kinase needed for contraction is blocked by pka

A

Myosin light chain kinase MLCK

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32
Q

Which article says how this works and how

A

Schaub 2017

It is a ca/calmodulin dependant kinase which phosphorylates the regulatory light chain RLC on myosin 2 , This causes the contraction through cross linking

33
Q

What is the ca activated k channel called

A

Maxi K

34
Q

Give an example of SA and how it’s given how long it lasts

A

Salbutamol
Given as powder, aerosol or nebulised inhalation
Or iv
Lasts up to 4 hours

35
Q

Give an example of a long acting

A

Salmeterol
Inhaled or iv
Lasts up to 12 hours

36
Q

What cardiac effects can they have

A

Tachycardia

37
Q

Why are selective B2 preferred

A

No tachycardia, tremors, headaches which are common in non specific

38
Q

Interaction with what with sabutamol causes hypokalemia as non specific

A

Corticoids, diuretics, theophylline

39
Q

Which antidepressants induce salmeterol action and risk of hypokalenia and tachy

A

Maoi/ tricyclic

Monoamine oxidase inhibit

40
Q

Which article discusses side effects of non specific B2 agonists

A

Abosamak et al 2021

41
Q

What do they do to ensure ac activation

A

Stabilise the gs-gtp complex

42
Q

What does systemic exposure to B2 agonists cause

A

Systemic dilation causing headaches

43
Q

Hypokalemia presents as what with non specific

A

Tachycardia, tremors, hallucinations, hypotension, hallucinations

44
Q

How does theophylline work

A

Blocks pde which increases camp and therefore pka effects occur

45
Q

They are last resorts if B2 agonists don’t work. Why

A

Very small therapeutic window. Can have adverse effects

46
Q

Where are they metabolised and what reduces this

A

Liver. Reduced eg in hepatic failure, taking drugs which block enzymes eg cimetidine

47
Q

What can increase clearance from liver

A

Drugs inducing metabolism eg alcohol or smoking

48
Q

Which drug is most important anti asthmatic and taken at each step of severity (all 6)

A

Glucocorticosteroids/ anti inflammatory/antimucosal

49
Q

What is step 1 of the asthma treatment (for intermittent asthma

A

Saba and gc

50
Q

What is the last for severe asthma

A

Both oral and inhaled gc and also laba

51
Q

Which receptor do they bind which then translocates to the nucleus for gene modulation

A

A glucocorticoid ic receptor

52
Q

What sorts of genes are downreg

A

Pro inflam cytokines and modulators

53
Q

Why isn’t it taken for symptom relief

A

Takes days to work

54
Q

Why are oral avoided where possible

A

Bad side effects like reducing bone density causing osteoporosis ,

Also diabetes, weight gain

55
Q

What minor side effects do inhaled have

A

Hoarseness and oral candidiasis as inhaled and so immunosuppressive

56
Q

Which type are used as preventative inhalers

A

Inhaled gc eg beclomethasone

57
Q

Which article discusses gc effects

A

Van der velden 1998

58
Q

Which tf can gr bind to after nucleus translocation

A

Ap-1

59
Q

What does ap1 binding stop

A

Reg genes of cytokines and chemokines

60
Q

How does gr also block nfkb and therefore inflammation

A

Binds to the p65 subunit

61
Q

Which enzyme do glucocorticoids directly block

A

Cox2 and Phospholipase a2

62
Q

What does H1 histamine binding do

A

Increase calcium

Increase bronchoconstriction, vasodilation, mucus secretion, sensory pain nerve endings stimuated, increased permeability eg nasal secretions

63
Q

Why are first generation not ideal

A

Lipophulkuc so cross the bbb and cause cns detession like drowsiness, loss of cognition, psychomotor ability and hallucinations

64
Q

What other receptor can it bind to and block causing things like dry mouth and blurred vision

A

It is anticholinergic

65
Q

Second generation can’t cross bbb so better. Give example

A

Terfenadine

66
Q

What are mucoactice medications

A

Ones which increase ability to expel sputum with mucus

or reduce mucus

67
Q

What type of muco actives increase salinity of mucus making it easier to expel

A

Expectorants

68
Q

What do mucoregulstors do

A

Type of anticholinergics which blocks mucus release

69
Q

What do mucolytics do

A

They break ss bonds in mucins so easy to clear

70
Q

Which type of mucoactives are bronchodilators whcih increase cough peak flow

A

Mucokinetics

71
Q

How does a cough work after vagal stimulation

A

Glottis closes first then abdominals and intercostals contract to increase positive pressure

The air expelled out when vocal cords/larynx opens again and loud as tight airway

72
Q

What are the meds called which suppress cough (not efficient)

A

Anti tussives

73
Q

Give an example of a non narcotic which is anti tussive but was approved 60 years ago

A

Dextromethorphan

74
Q

Codeine can be used as an anti tussive but why not

A

Sedative effects and affects gi too

75
Q

Which drugs can be used to treat infection which can excacerbste asthma

A

Antibiotics/antivirals

76
Q

How does pirfenidone work for ipf but not good enough so need transplant

A

Tgf b inhibitors which blocks profibrotic effects

77
Q

Which 2 therapies excacerbsted ipf

A

Triple therapy and the mab simtuzimab

78
Q

What does simtuzimab block

A

Lysyl oxidase like 2.

Enzyme which cross links collagen

Mucosal Surfaces (33 decks)

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