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4TH YEAR - CPTP > Week 6 - Asthma & COPD > Flashcards

Week 6 - Asthma & COPD Flashcards

1
Q

What is the pathophysiology of asthma?

A

Inflammation precipitated by an allergen → leads to mast cell degranulation through the formation of IgE.
Leads an allergic response by releasing inflammatory cytokines → plasma leakage and oedema of the bronchiole wall → causes obstruction and an increase in mucus hypersecretion leading to a mucus plug

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2
Q

Why does asthma cause bronchoconstriction?

A

Cholinergic reflex from muscarinic receptors

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3
Q

What is the inflammatory changes that happen in asthma?

What 2 effects does this have?

A

Phospholipids in plasma membrane (phospholipase A2) → Arachidonic acid

  1. Cyclooxygenase → release of the inflammatory mediators prostaglandins, which cause bronchoconstriction
  2. 5-lipoxygenase → release of the inflammatory mediators leukotriene’s, which cause bronchoconstriction, promote mucus secretion and recruit immune cells which enhance airway inflammation.
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4
Q

What are the 2 classes of Beta 2 adrenergic receptor agonists?

A

SABA (short acting)

LABA (long acting)

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5
Q

What type of drug is salbutamol?

A

Short acting Beta 2 adrenergic receptor agonists

SABA

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6
Q

What type of drug is salmeterol?

A

Long acting Beta 2 adrenergic receptor agonists

LABA

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7
Q

What are the actions of Salbutamol?

A

Acute bronchodilator effect, onset 5-30min, relief for 4-6h

Protects against various challenges e.g. cold air, exercise

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8
Q

What is the nickname for salbutamol?

A

Reliever

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9
Q

What are the routes of administration for salbutamol?

A

o Aerosol inhalation - metered-dose inhaler (MDI)
o Inhalation of powder
o Inhalation of nebulised solution
o Oral (tablet or solution) administration
o Parenteral → IV, SC or IM injection

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10
Q

How do we minimise the systemic side effects of SABAs?

A

Side effects minimised with delivery via inhalation versus systemic route

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11
Q

How do we prolong the actions of Salmeterol?

A

Chemical analogues of salbutamol with a long lipophilic side chain anchors the drug in the lipid membrane,
o Allows the active portion of the molecule to remain at the receptor site

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12
Q

What is the mechanism of action of Beta 2 agonists?

A
  • Act on beta2 adrenergic receptor

* Cause smooth muscle relaxation

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13
Q

When do we use SABA vs LABA?

A

Salbutamol - reliever (acute exacerbation)

Salmeterol - Slow onset- NOT for relief of an acute asthma attack – good as prophylactic i.e. used before a known trigger (exercise)

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14
Q

What are the side effects of beta 2 agonists and what causes the side effects?

A

From binding to other B2 receptors around the body, like invoking a fight/flight response

  • Fine tremor
  • Anxiety
  • Headache
  • Muscle cramps
  • Palpitation
  • Hypokalaemia
  • Others: tachycardia, arrhythmias, peripheral vasodilation, myocardial ischaemia, disturbances of sleep and behaviour
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15
Q

What is the drug class of tiotropium and ipratropium?

A

Muscarinic antagonist

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16
Q

When are muscarinic antagonists used?

A

Useful in patients who are unable to tolerate adrenergic agonists (patients with ischaemic heart disease or tachycardia)

Generally reserved as adjunct in the management of acute severe asthma

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17
Q

How do tiotropium and ipratrodium work?

A
  • Competitively antagonise the effects of endogenous acetylcholine at M3 receptors
  • Relaxes bronchial smooth muscle and decreases mucus secretion
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18
Q

What receptor does muscarinic antagonists work at?

A

M3 receptors

Competitively antagonise the effects of endogenous acetylcholine at M3 receptors

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19
Q

What are the 2 types of muscarinic antagonists (+ example)?

A

Short-acting muscarinic antagonists (SAMA) e.g ipratropium

Long-acting muscarinic antagonists (LAMA) e.g tiotropium (better)

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20
Q

Name a phosphodiesterase inhibitor….

A

Theophylline

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21
Q

How does theophylline work?

A

Inhibits phosphodiesterase to cause an increase in cAMP in smooth muscle cells → activates protokinases (PKA) –> inhibits TNF-alpha and Inhibits leukotriene synthesis –> therefore reduces inflammation + innate immunity
Also reverses steroid insensitivity

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22
Q

How are phosphodiesterase inhibitors usually administered?

A

PO

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23
Q

What type of drug is theophylline?

A

phosphodiesterase inhibitor

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24
Q

Name a leukotriene receptor antagonist…

A

Montelukast

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25
Q

How do leukotriene receptor antagonists like montelukast work?

A

Leukotriene antagonists inhibit the cysteinyl L1 receptor

Approved for the prophylaxis of asthma (preventer not reliever)

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26
Q

How are leukotriene receptor antagonists excreted?

A

Metabolised in liver and undergo biliary excretion

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27
Q

What type of drug is Montelukast?

A

leukotriene receptor antagonist

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28
Q

When are these commonly used, why?

A

leukotriene pathway is just one of several process responsible for the inflammatory response in asthma therefore they are less effective than ICS

However they have very few side effects compared to inhaled corticosteroids.

Therefore commonly prescribed to KIDS as step 1 treatment

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29
Q

Name an Anti-IgE monoclonal Ab (Biologic)

A

Omalizumab

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30
Q

How does omalizumab work?

A

Monoclonal Ab binds to IgE and reduces effects

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31
Q

When are inhaled corticoid steroids used?

A

Low dose = step 1 of asthma treatment ladder.

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32
Q

What type of drug is omalizumab?

A

Anti-IgE monoclonal Ab (Biologic)

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33
Q

What is the MoA od ICS?

A

Reduce inflammation and mucus production

34
Q

What are 2 common side effects that we give patients direct advise on how to prevent?

A

Oral candida & Hoarseness

Brush teeth after use

35
Q

What are the common side effects of corticoid steroids?

A 
o	Oral candida & Hoarseness
•	Bruising
•	Increased appetite/Weight gain
•	Gastritis / GI Bleeds
•	Osteoporosis
•	Cataracts
•	Mood changes
•	Difficulty sleeping
•	Glucose intolerance/Diabetes
•	Adrenal Supression
36
Q

Are corticoid steroids preventers or relievers?

A

preventers - continuous use

37
Q

What is the order of stepwise treatment?

A
  1. β2 agonist (short acting) - Salbutamol
    short-acting, occasional use, for symptom relief
    If more than once daily or at night? à go to step 2
  2. Corticosteroid (INH) - Beclametasone or Fluticasone
  3. β2 agonist (long acting) - Salmeterol
    Some benefit but not enough? –> increase steroid dose.
    No benefit? –> stop.
  4. Corticosteroid (ORAL?) or Theophylline or Leukotrine receptor agonist
    ALL = in conjunction with previous therapy
  5. Corticosteroid (ORAL) - Prednisalone
    Oral & Regular
38
Q

Give 2 examples of ICS?

A

Beclametasone or Fluticasone

39
Q

What is step 0 in asthma treatment?

A

SABA only

40
Q

What is step 1 in asthma treatment?

A

SABA + ICS

41
Q

What is step 2 in asthma treatment?

A

SABA + ICS + LABA

42
Q

What is step 3 in asthma treatment?

A

SABA + ICS (increase to med dose) + LABA (discontinue if little use and try alternative - LAMA? Leuk? theo?)

43
Q

How do we manage exercise induced asthma?

A

Generally the same - SABA

i. inhaled corticosteroids
ii. leukotriene receptor antagonists
iii. B2 agonists (long acting)
iv. Chromones
v. B2 agonists (oral)
vi. Theophyllines + B2 agonists (short-acting) = immediately prior to exercise

44
Q

What is step 4 in asthma treatment?

A

SABA + ICS (high dose)+ LABA + 4th drug

45
Q

Which drugs may exacerbate asthma?

A

B-blockers
o Can cause bronchoconstriction and bronchospasm (especially non-cardioselective e.g propranolol, timolol)
• Give prostaglandin analogue instead e.g. bimatoprost, travoprost

NSAIDS
o Can cause bronchospasm in those sensitive
o Aspirin sensitivity affects 5-20% of asthma patients
• Use clopidogrel instead

46
Q

How can we increase amount of drug inhaled?

A

Spacer

47
Q

What are the goals of COPD treatment?

A

Smoking cessation

Short-term goals – immediate benefits
• Relief of symptoms (breathlessness)

Long-term goals
•	Prevent disease progression
•	Reduce exacerbations
•	Improve quality of life
•	Improve exercise tolerance
•	Reduce mortality
48
Q

What drives treatment choice in COPD?

A

FEV1 (lung function)

also patients decisions, cos you know, ICE

49
Q

What is the most basic treatment in COPD?

A

All patients should have a SABA or SAMA for acute breathlessness

50
Q

What is the optimum treatment of COPD?

A

LAMA + LABA + ICS

+ SABA for acute

51
Q

What treatment do we offer in COPD exacerbations?

A 
Oxygen
Oral steroids (short course)
Antibiotics (short and simple)
Nebulised bronchodilators
NIV in sever cases
52
Q

How do we deliver uncontrolled O2 to patients?

A

Nasal cannula, face mask and reservoir mask

53
Q

How do we deliver controlled O2 to patients?

A

Venturi mask.

54
Q

What sats should we aim for in patients?

A

88-92%

55
Q

What are the advantages of nebulised bronchodilators?

A
  • Little skill/ co-ordination/ inspiratory effort required

* Nebuliser can be prepared /administered

56
Q

What are the disadvantages of nebulised bronchodilators?

A
  • High doses bronchodilator may cause systemic effects, e.g. angina in this patient (prev MI)
  • Expensive
  • Regular maintenance needed
  • May delay seeking medical advice in a severe attack
  • Takes a long time to administer drug to patient.
  • Not portable (c.f. MDI)
57
Q

What are the signs/symptoms/definition of a moderate acute asthma attack?

A

PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm

58
Q

What are the signs/symptoms/definition of a severe acute asthma attack?

A

PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm

59
Q

What are the signs/symptoms/definition of a life-threatening acute asthma attack?

A 
PEFR < 33% best or predicted
Oxygen sats < 92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
60
Q

What is the aim of asthma treatment? How can we quantify this?

A

Complete control of disease - defined as:
• no daytime symptoms
• no night time awakening due to asthma
• no need for rescue medication
• no asthma attacks
• no limitations on activity including exercise
• normal lung function (in practical terms FEV1 and/or PEF >80% predicted or best)
• minimal side effects from medication.

61
Q

In normal asthma attacks (no purulent sputum) do you prescribe Abx?

A

No - usually viral

62
Q

In severe acute asthma, what is the treatment?

A 
Admit patient
Intravenous hydrocortisone
Nebulised salbutamol
Nebulised ipratropium bromide
High-flow oxygen
63
Q

In moderate asthma attacks what is the treatment?

A

Don’t admit
Give 02
Give B2 agonist
Give prednisolone

64
Q

When do you transfer a patient to ICU that has acute severe asthma?

A
  • Deteriorating PEFR, worsening or persisting hypoxia, or hypercapnea
  • Exhaustion, altered consciousness
  • Poor respiratory effort or respiratory arrest
65
Q

What are the issues with theophlline?

A

Loading dose needed (unless already on treatment)
Interactions with Abx (ciprofloxacin and macrolides)
Narrow therapeutic index

66
Q

What are the adverse effects of theophylline?

A
  • Nausea
  • Diarrhoea
  • Tachycardia
  • Headaches
  • Insomnia
  • Irritability
  • Dizziness
  • Arrhythmias
67
Q

After an acute severe asthma attack, when being discharged patients should have…

A
  • Been on discharge medication for 12-24 hours and have had inhaler technique checked and recorded
  • PEFR >75% of best or predicted and PEFR diurnal variability<25% unless discharge is agreed with respiratory physician
  • Treatment with oral and inhaled steroids in addition to bronchodilators
  • Own PEFR meter and written asthma action plan
  • GP follow up arranged within 2 working days
  • Follow up appointment in respiratory clinic within 4 weeks
68
Q

What is COPD?

A
  • “Airflow obstruction that is usually progressive, not fully reversible and does not change markedly over several months.’’
  • Chronic bronchitis and emphysema
69
Q

What is the most common cause of COPD?

A

smoking

70
Q

What are the symptoms of COPD?

A

Cough, sputum, dyspnoea, wheeze

71
Q

What are the Signs of COPD?

A

Tachypnea, use of accessory muscles, hyperinflation, cricosternal distance, expansion, resonant/hyperresonant percussion note, cyanosis, wheeze

72
Q

What FEV1/FVC ratio suggests airway obstruction?

A

<70%

73
Q

What are the different categories of severity in airway obstruction?

A 
FEV1 in obstructive disease
•	Mild >80% predicted
•	Moderate  50-80%
•	Severe 30-50%
•	Very severe <30%
74
Q

What is the most appropriate management in COPD if patient has a FEV1 < 60% OR exacerbation Hx?

A

Prognostic as well as symptomatic imperative
LABA + ICS + LAMA + SABA for acute
(Inhaled salmeterol, fluticasone, tiotropium and salbutamol)

75
Q

What is the most appropriate management in COPD if patient has a FEV1 > 60% and NO exacerbation Hx?

A
  1. SABA
  2. LAMA
  3. LABA
76
Q

What are the types of respiratory failure?

A 
•	Type I – ‘VQ mismatch’
                  -PaO2 low 
                  -PaCO2 normal or low
•	Type II – ‘Ventilatory failure’
                  -PaO2 low
                  -PaCO2 high
77
Q

What are the ABG hallmarks of chronic respiratory failure?

A

High CO2 + high bicarb (trying to correct acidosis)

78
Q

What is the pathophysiology of cor pulmonale? How does this help us treat it?

A

Cor pulmonale = Right sided heart failure due to pulmonary hypertension.
o Caused by bronchoconstriction → caused by sats of 86% when well, pulmonary arteries automatically constrict when there is deoxygenated blood in them.
o This increases pressure on Right side of the heart → Right ventricular dilatation. If you correct the oxygen saturation the right pulmonary vasoconstriction will reverse.

79
Q

What is the effect of correcting oxygen saturation in pts with cor pulmonale?

A

This can shrink the RV and improve the peripheral oedema

80
Q

What are the Sx of cor pulmonale?

A

Sx - combination of fatigue, tachypnea, exertional dyspnea, peripheral oedema and cough

81
Q

What are the treatments of cor pulmonale?

A

O2 therapy
+/- Diuretics
Patient education – smoking!
Pulmonary rehabilitation

4TH YEAR - CPTP (19 decks)

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