Respiratory Medicine Flashcards

1
Q

what is the pathophysiology of Asthma ?

A

Type 1 hypersensitivity reaction leads to TH2/ Eosinophilic inflammation via degranulation .
Leads to airway remodelling via -
Mucosal oedema , Bronchoconstriction and mucus plugging

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2
Q

what specially do B2 agonists target in Asthma ?

what about steroids ?

A

SM dysfunction

Inflammation

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3
Q

why is Asthma difficult to manage ?

A

heterogeneous disease
pathologically can vary (Eosinophils and neutrophils)
Symptom paterns and triggers vary
response to treatment vary

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4
Q

how do you define asthma control ?

A
Minimal symptoms during day + night 
Minimal need for reliever
No exacerbations 
no limitations of physical activity 
normal lung function
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5
Q

what should you check before starting therapy ?

A

Check compliance with existing therapy
inhaler technique
eliminate trigger factors

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6
Q

what is Step 1 on Management of Asthma ?
What drug ?
what do you need to be aware of ?

A

Short acting B2 agonists - Salbutamol, Terbutaline
Only for relief

if used regularly = reduce asthma control

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7
Q

what is site of action of B2 agonist if only for symptom relief ? what can happen on overuse?

A

Predominant action on SM in airway

also inhibit mast cell degranulation but if overuse happens this can reverse and sensitivity increases

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8
Q

how does B2 adrenorecpetor work in smooth muscle ?

A

Alpha s Subunit phosphorylates GDP to GTP and activates Adenyl cyclase to increase cAMP =
Inhibits Myosin light chain
activates PKA-
relaxation

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9
Q

name 1 fast onset long duration B2 agonist and its uses

A

Formoterol -
Reliever
reduce sever asthma Exacerbation

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10
Q

name 1 long onset long duration B2 agonist and its use

A

Salmeterol

prophylaxis

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11
Q

what are side effects of B2 Agonists ?

A

Tachy , palpitation and tremor

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12
Q

when should you use step 2 therapy ?

A
  1. using inhaler more than 3 times a wek
  2. symptoms 3 times a week
  3. waking up once a week
  4. Exacerbations requiring oral steroids in the last 2 yrs
    (symptoms more than x2 a mnth)
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13
Q

what is step 2 therapy?

A

regular preventer via inhaled corticosteroids

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14
Q

how do steroids work ?

A

Attaches to transcription factor (GCS receptor) and chaperones disassociate allows gene transactivation of Anti-inflammaotries and also increase B2 receptor production
also Transrepression of inflammatory mediators

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15
Q

name 2 inhaled steroids

A

Beclomethasone dipropionate, Budesonide, Fluticasone,

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16
Q

What chemical changes were done to previous steroids and what changes therefore happened to new ones ?

A

Lipophilic side chain added

a higher affinity for GCS receptor . increased uptake and dwell time in tissue
inactivates hepatic metabolism

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17
Q

how does inhaled steroids enter circulation ?

A

Lung depsostion and absorption

Swallowed fraction and gut absorption and phase 1 met in liver

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18
Q

what asthma do you have to be aware of when giving steroids ?

A

Non - eosinophlic patients do not respond as well to inhaled steroids than eosinophilic

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19
Q

what is step 3 therapy?
when is it indicated ?
what drugs ?

A

add-on
long acting B2 Agonists
Over 400 mcg/day of ICS
Formoterol and salmeterol

20
Q

which of the LABA is the most potent ?

A

Formoterol and then Salmeterol

21
Q

how do you measure potency ?

A

the dose at causing half the max response

22
Q

which of the LABA is the most efficacy ?

A
foametrol = 100% repsonse 
Salmeterol = 50%
23
Q

how do you measure efficacy ?

A

the dose at which the max response is occurring

24
Q

what are features of LABAs?

A

reduce asthma exacerbations , improve symptoms and lung functions
not anti-inflammatory

25
Q

what are good Steroid combinations ?

A

Budesonide/formoterol
• Beclomethasone/formoterol
• Fluticasone/formoterol
• Fluticasone/salmeterol

26
Q

what is a major benefit of LABA and ICS in single inhaler ?

A

increase compliance

reduce cost

27
Q

what does the evidence suggest LABA and SABA as as a reliever ?

A

LABA are better relievers when on step 3 management

28
Q

what are alternative in step 3 to LABA ?

A

Higher dose ICS (eosoniphilic)
luekotriene receptor antagonist
Theophylline- methylxanthines
tiotropium

29
Q

how do LRAs work ?

name 1

A

LTC4 released by mast cells and eosinophils = induce bronchoconstriction, mucus secretion and oedema
LRA block LTs by blovking CysLT1 receptor
Montelukast

30
Q

what are side effects of LRAs?

A

angioedema , dry mouth

insomnia , nightmares

31
Q

how does Theophylline work ?

A

methylxanthine that anatagonosies the adenosine receptor - inhibit PDesterase increase cAMP

32
Q

What disadvatages and side effects of theophylline ?

A

Poorly efficacious , narrow therapeutic window with freequnet side effects:
Nausea , headaches and reflux, Arrhythmias , fits
levels increase from CYP450 inhibitors

33
Q

name 2 long acting Anticholingerics

A

Ipratropium bromide, Tiotropium bromide

34
Q

what are indications for tritropium bromide ?

what does it work on?

A

COPD and sever step 4/5 asthma
Reduces exacerbations
M3 receptor

35
Q

side effects of LAMAs?

A

Dry mouth, urinary retention and glaucoma

36
Q

what is step 5 management ?

A

Oral steroids - prednisolone

biological therapies

37
Q

what biological therapies are used? how do they work ? what is the main advantage ?

A

Anti-IgE
attached to IgE receptor and tops cross linking of mast cells
Anti-IL 5 - must have high eosinophil number
Reduce esoniophil numbers
reduce exacerbations

38
Q

what could you implement to asthma patients to help with asthma control ? what do they include ?

A

self management plan

when and how to step up and step down treatment

39
Q

why should patients step down?

A

may be receive too high dose of steroid

40
Q

what is particle size of inhalers ? what is important of this ?

A

1-5 microns

the closer to this number the more is deposited in the lungs / small airways

41
Q

define acute severe asthma

A

any one of :

  1. unable to complete sentence
  2. pulse >= 110 bpm
  3. respiration rate >= 25 min
  4. peak flow 33-50%
42
Q

define life threatening asthma

A
any one of acute sever plus
PEF <33%
• sPO2 <92
• PaO2 <8 kPa
• PaCO2 >4.5 kPa
• Silent chest
• Cyanosis
• Feeble respiratory effort
• Hypotension, bradycardia, arrhythmia
• Exhaustion, confusion, coma
43
Q

define Near-fatal asthma

A

PaCO2 >6 kPa, mechanical

ventilation

44
Q

what is treatment of acute severe asthma ?

A
  1. oxygen 94-98%
  2. nebulised salbutamol
  3. oral prednisolone for 10-14 days
45
Q

what is treatment of life threatening asthma ?

A

same as sever but add nebulised Ipratropium bromide

IV aminophyline