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Respiratory > Therapeutics for airflow obstruction > Flashcards

Therapeutics for airflow obstruction Flashcards

1
Q

What are preventors and relievers?

A 
Preventor = anti-inflammatory 
Reliver = bronchodilator
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2
Q

What are anti-inflammatories?

A

Corticosteroids
Cromones
Theophylline

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3
Q

What stops mediators and TH2 cytokines

A

Antileukotrines or antihistamines

Monoclonal antibodies - Anti-IgE, Anti-interlukin 5

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4
Q

What can calm twitchy smooth muscles - hyper-reactivity?

A

Beta2 agonists

Musarinic antagonists

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5
Q

What is the asthma treatment pyramid?

A

Reliever - beta2 agonist as needed
Preventor (1st line) - inhaled steroid such as beclomethasone
Controller (2nd line additive to ICS) - theyophylline, LTRA, LABA/LAMA, Anti-IgE/Anti-IL5
Oral steroid

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6
Q

When are coricosteroids used?

A

In asthma and COPD but may cause pneumonia in COPD due to local immune suppression and impaired mucociliary clearance especially with fluticasone due to prolonged lung retention

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7
Q

What is an example of an oral steroid?

A

Prednisolone has a low theraputic ratio and is only used for acute exacerbations not maintenance

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8
Q

What is an example of an inhaled steroid?

A

Beclomethasone has a high theraputic ratio which is used for maintenance monotherapy in asthma

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9
Q

How are corticosteroids used in COPD?

A

In a combo of ICS and LABA not as a monotherapy. This helps to reduce exacerbations in esoinohpilic COPD and optimises lung delivery

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10
Q

What are the actions of a spacer device?

A

Avoids the coordination problems with pMDI
Reduces oropharyngeal and laryngeal side effects
Reduces systemic absorption from swallowed fraction
Acts as a holding chamber for aerosol
Reduces particle size and velocity
Improves lung deposition

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11
Q

When are cromones used?

A

Only used in asthma - cromoglycate
Mast cell stabiliser - weak anti-inflammatory when compared to steroids
Cromoglycate effective in atopic children
Inhaled route only
Not used much due to poor efficacy

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12
Q

What is the role of leukotrines in asthma?

A

Increased mucus secretion
Eosinophil influx
Edema
Contraction and proliferation of airway smooth muscles

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13
Q

When are leukotrine receptor agonists used?

A

Only used in asthma as an anti-inflammatory
Montelukast - oral route, once daily, high theraputic ratio
Less potent anti-inflammatory than inhaled steroid
Used as a second line as a compltemntary drug to non steroidal anti-inflammatory additive inhaled steroid
Effective in allergic rhinitis

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14
Q

When are anti-IgE’s used?`

A

Omalizumab which prevents the binding of high-affinity IgE receptors and inhibits TH2 response and associated meditator release from basophils/mast cells
Injection every 2/4 weeks for asthma only
Only used in patients with severe persistent allergic asthma - a raised IgE
Very expensive

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15
Q

When is anti-IL5 used?

A

Mepolizumab
Blocks the effects of TH2 cytokine IL-5 which is responsible for eosinophilic inflammation in asthma
Injection every 4 weeks for patients with severe refractory eosinophilic asthma
Very expensive
Little effect on pulmonary function or symptoms but reduces exacerbations and oral steroid sparing effect

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16
Q

What do beta agonists do?

A

They stimulate bronchial smooth muscle B2-receptors by increasing cAMP

17
Q

What is an example of a short acting and long acting b2-agonist?

A

Salbutamol -SABA

Salmeterol/formoterol LABA

18
Q

How are B2 agonists prescribed in asthma and COPD?

A

Combo inhalers such as beclometasone and formeterol
ICS/LABA used in asthma
ICA/LABA/LAMA used in COPD

19
Q

Why is the inhaled route prefered?

A

High theraputic ratio. There is b2 down regulation and tachyphylaxis with chronic LABA use
High nebulised doses given in acute attacks

20
Q

When are muscarinic antagonists used?

A

To block post junctional end plate M3 receptors
Short acting - Ipratropium
Long acting - Tiotropium
Inhaled route only, high therapeutic ratio
Used mostly in COPD to reduce exacerbations on its own or as a LAMA/LABA/ICS
Beclometasone/formoterol/glycopyrronium
High doses of neb ipratropium used in acute COPD and asthma

21
Q

When are methylxanthines used?

A

Theophylline for maintenance therapy. SR formulation used for nocturnal drips. Used as an add on to inhaled steroids as a complementary non steroidal anti-inflammatory
Low theraputic ratio but used in asthma and COPD

22
Q

When are PDE4 inhibitors used?

A

Roflumilast as an oral tablet used in COPD only. Has minimal effect on FEV1 - anti-inflammatory action
Reduces exacerbations - additive to LABA or LAMA
Adverse effects - nausea, diarrhoea, headache, weight loss

23
Q

How is chronic asthma treated?

A

Abolish symptoms, mininum B2-use, normalise FEV1, reduce PEF variability, reduce exacerbations, prevent long term airway remodeling. Avoid triggers
Supress the inflammatory cascade with ICS
Non steroidal anti-inflamm therapy such as theophylline ,anti-leukotrine, cromoglycate
Stabilise smooth muscles with LABA/LAMA

24
Q

How is acute asthma treated?

A

Oral prednisolone or IV hydrocortisone
Nebulised high dose salbutamol, neb ipratropium, IV aminophylline/magnesium
At least 60% O2
ITU assisted mechanical intubated ventilation if falling PaO2 and rising PaCO2 but never use a resp stimulant

25
Q

How is COPD treated non-pharmacologically?

A 
To reduce exacerbations, improve pulmonary functino , improve QOL 
Prevent pulmonary heart disease 
Smoking cessation 
Immunisation 
Pharmacotherapy 
Pulmonary rehab 
Oxygen
26
Q

How is COPD treated pharmacologically?

A 
LAMA/LABA mono
LABA/LAMA combo 
ICS/LABA combo
ICS/LABA/LAMA combo
PDE4I - Roflumilast 
Mucolytic - carbocisteine 
Antibiotics - aithromycin
27
Q

How is acute COPD treated?

A

Nub high dose sabutamol + ipratropium
Oral prednsiolone
Antibiotic (amoxycillin/doxycycline) if infection
24-28% O2 titrated against PaO2/PaCO2
Physio to aide sputum expectoration
Non-invasive ventilation to allow a higher FiO2
ITU intibated assisted ventilation only if reversibel component

28
Q

What leads to patients retainig CO2?

A

V/Q mismatch
Haldane effect
Hypoxic drive

29
Q

What is V/Q mismatching?

A

Areas of poor ventilation have reactive vasoconstriction
Give excess oxygen and that reactive vasoconstrction reverses
Perfusion becomes good but the ventilation is still poor

30
Q

What is the haldane effect?

A

Chronically hypoxaemic pateints have a low Hb saturation
CO2 occupies the empty binding sites on the Hb
Giving a high FiO2 pushes the CO2 off the Hb into the system

31
Q

What is the hypoxic drive?

A

Normal respiration is driven by CO2 chemoreceptors
Chronic hypercarbia leads to the denstisation of these receptors
Oxygen chemoreceptors then become important

32
Q

What are the characteristics of hypoxaemia?

A

Altered mental status, cyanosis, dyspnoea, tachypnoea, arrhythmias
Hyperventilation increases dramatically when pO2 is less than 5.3 kPa
Loss of consciousness occurs at around 4.3 kPa

33
Q

What are the different types of hypoxia?

A

Circulatory
Anaemic
Toxic
Hypoxaemic

34
Q

What can cause the alveolar endothelial interfaces to fail?

A 
Interstitial thickening 
Pulmonary fibrosis 
Sarcoidosis 
Lymphangitis 
Vascular dysfunction 
Pulmonary vasculitis 
Endothelial malignancy
35
Q

What is shunting?

A

Perfusion without ventilaion

36
Q

What is dead space

A

Ventilation without perfusion

37
Q

What is type 1 resp failure?

A

Hypoxemic respiratory failure (type I) is characterized by an arterial oxygen tension (PaO2) lower than 60 mm Hg with a normal or low arterial carbon dioxide tension (PaCO2). This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.

38
Q

What is type 2 resp failure?

A

Hypercapnic respiratory failure (type II) is characterized by a PaCO2 higher than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma and chronic obstructive pulmonary disease [COPD]).

Respiratory (24 decks)

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