Obstructive and Restrictive Lung Disease Flashcards

1
Q

What are the two general categories for drugs that treat obstructve airway conditions?

A
  1. Relievers - bronchodilators
  2. Preventers - anti-inflammatory
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2
Q

What is step 1 in asthma treatment?

A

SABA

Salbutamol

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3
Q

What is step 2 in asthma treatment?

A

SABA + ICS (200-800micrograms)

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4
Q

What is step 3 in asthma treatment?

A

SABA + LABA + ICS

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5
Q

What is step 4 in asthma treatment?

A

Increase ICS dose from step 3

Add fourth drug e.g. theophylline or a leukotriene receptor antagonist

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6
Q

What is step 5 in asthma treatment?

A

Use daily steroid tablet (prednisolone)

Maintain high dose ICS (2000micrograms)

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7
Q

Which immune cells are corticosteroid effcetive aginst in the mucose?

A

Eosinophils

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8
Q

What is a downside to corticosteroid use in asthma or COPD?

A

It weakens the immune system, and impairs the mucociliary escalator.

This increases chance of infection

In COPD chances of pneumonia infection are boosted

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9
Q

ICS have a ____ therapeutic ratio and are _______ due to being delivered directly to the organ of interest

A

High

Topical

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10
Q

Oral corticosteroids have a ___ therapeutic ratio

A

Low

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11
Q

Why is a spacer useful for administering asthma medication?

A
  • Reduces oropharngeal and laryngeal side effects (gag reflex/nausea)
  • Reduces systemic absorption (no swallowing)
  • Acts as a holding chamber aiding inhalation
  • Reduces particle size and velocity allowing the particle to embed deeper in the lungs increasing effectivity
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12
Q

What are cromones and what is their function?

A

Cromones are used in asthma and are propsed mast cell stabilisers

This means they can prevent pro-inflammatory mediator release

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13
Q

How are leukotrienes formed during asthma?

A

They are produced due to processes involving the lipids in the cell membrane

The enzyme phospholipase A2 detaches fatty acids from the second carbon group of the glycerol molecule that makes up a lipid

One of these acids is arachidonic fatty acids

When arachidonic acid is acted on by 5-lipoxygenase leukotienes are formed

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14
Q

What happens when cyclo-oxygenase acts on arachidonic acid?

A

Prostaglandins and thromboxanes are produced aiding inflammation and amplification

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15
Q

Which leukotriene is over produced in asthma?

A

LTD4

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16
Q

What is the effect of overproduction of leukotrienes in asthma?

A
  • Trigger contraction and proliferation of smooth muscle
  • Cause eosinophil influx (which release cationic proteins damaging epithelial cells)
  • Increased mucus secretion, bu decreased transport
  • Oedema
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17
Q

Lekotriene receptor antagonists are used in asthma, name one that is use dto bind to LTD4?

A

Montelukast

(taken orally)

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18
Q

What is anti-IgE and what is the name of one key form in relation to asthma called?

A

Monoclonal antibody

Omalizumab

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19
Q

Omalizumab has what effects?

A

Binds stongly to IgE inactivating it

Prevents pro-inflammatory mediators being released from basophils and mast cells

Boosted every 2-4 weeks via injection

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20
Q

Name two anti-IL5 drugs

A
  1. Mepolizumab
  2. Reslizumab
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21
Q

How does anti-IL5 therapy work?

A

TH2 cells produce IL-5 in the immune response aiding eosinophilic inflammation in asthma

The use of anti-IL5 therapy is that eosinophilic inflammation is much reduced

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22
Q

Name 2 LABAs

A
  1. Formeterol
  2. Salmeterol
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23
Q

What are the three different types of muscarinic receptors?

A
  1. M1 - enhance cholinergic reflex
  2. M2 - inhibit acetylcholine release
  3. M3 - mediate bronchoconstriction and mucus release
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24
Q

Muscarinic antagonists inhibit which type of muscarinic receptor?

A

M3

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25
Name a SAMA
Ipratropium
26
Name two LAMAs
1. Tiotropium 2. Glycopyrronium
27
Methylxanthines act as ____________ and also \_\_\_\_\_\_\_\_\_\_\_
Bronchodilators Anti-inflammatory drugs
28
Name an example of a methylxanthine
Theophylline
29
What is the function of phosphodiesterase 4 enzymes?
Hydrolyse cAMP
30
What is the overall function of PDE4 inhibitors?
Prevent cAMP hydrolysis allowing high levels of cAMP in cells Bronchial smooth muscle will become relaxed
31
PDE4 inhibitors are for use only in \_\_\_\_
COPD
32
Give an example of a PDE4 inhibitor
Roflumilast
33
Why are PDE4 inhibitors used infrequently?
Side effects suh as nausea, diarrhoea and headaches
34
What are mucolytics?
Drugs which reduce the viscocity of mucous and reduce inflammation
35
Give two examples of mucolytics?
1. Carbocisteine 2. Erdosteine
36
In an acute astha attack what treatment is given?
* Oral prednisolone (40mg) * At least 60% oxygen aim for 94-98% SpO2 * Nebulised salbutamol
37
What are some treatment methods for COPD?
* Smoking cessation * Immunisation * Pharmacotherapy * Oxygen * Increase exercise
38
Name two LAMAs
1. Titropium 2. Aclidinium
39
Name two LABAs
* Olodaterol * Formeterol
40
Name an ICS for COPD use
Beclometasone
41
Which antibiotic may be used for COPD?
Azithromycin | (also amoxicillin and doxycycline)
42
How is acute COPD treated?
* Nebulised high dose salbutamol and ipratropium * Oral prednisolone * Antibiotic (amoxicillin/doxycycline) if infection * 24-28% O2 * Non-invasive ventilation
43
Which external factors can cause lung restriction?
1. Skeletal causes (broken ribs, kyphoscoliosis) 2. Muscle Weakness (intercostal/diaphragmatic) 3. Obesity (due to compression)
44
What are the effects of lung compression from external sources?
1. Reduced partial pressur eof oxygen 2. Reduced partial pressure of carbon dioxide 3. Reduced lung volumes 4. Hypoxia
45
What is DPLD?
Diffuse Parenchymal Lung Disease Interstitial lung disease An umbrella term for lung diseases affecting the interstitium
46
What is the interstitium of the lungs?
The space and tissues surrounding the alveoli
47
What are the three main categories for DPLD (ILD)?
1. Those with a known cause 2. Those with an unknown cause (idopathic) 3. Those associated with systemic disease
48
Why may hypoxia occur at a thickened alveolar/arteriolar barrier?
Carbon dioxide is very soluble and easily diffuses across to can be blown off Oxygen will not be able to pass the barrier into the blood as easily potentially leading to hypoxia
49
Give two different causes for DPLD
1. LVF - fluid in alveolar lumen due to a raised pulmonary venous pressure 2. Sepsis, adult respiratory distress syndrome damage, altitude sickness - Non-cardiac pulmonary oedema
50
What is consolidation in the lungs?
Fluid within areas which there normally is not any fluid
51
What can cause consolidation on a chest X-ray?
1. Pneumonia 2. PE 3. Alveolitis 4. Cryptogenic pneumonia (not infectious)
52
What is alveolitis?
This is the infiltration of inflammatory fluid into the alveolar walls It can be caused by: * Drugs * Toxic gases * Fibrosing alveolitis * Autoimmune disease
53
What is pneumoconiosis?
Dust disease Restrictive lung disease that can be either fibrogenic (asbestosis, silicosis) or non-fibrogenic (siderosis (due to iron), stenosis, baritosis (due to barium))
54
What is carcinomatosis?
Body-wide spread of cancer and can contribute to DPLD
55
How do eosinophils contribute to DPLD?
They occur alongside all sides of inflammation which is present in DPLD
56
Symptoms of DPLD?
* Breathlessness * Cough (without wheeze - no obstruction) * Finger clubbing * Lung crackles (inspiration) * Central cyanosis * Pulmonary fibrosis (chronic inflammation)
57
How is FEV1 affected in DPLD?
It is reduced
58
How is FVC affected in DPLD?
It is reduced
59
What happen to the FEV1/FVC ratio in DPLD?
It remains normal as both variables decrease in proportion
60
Aside from FEV1 and FVC what are the thee main checks which must be covered for diagnosing DPLD?
1. Arterial oxygen saturation (should be lowered in DPLD) 2. Chest X-ray (bilateral consolidation is common) 3. Presence of antibodies (caused by infection)
61
How is DPLD treated?
1. Cause is removed 2. Inflammation is treated 3. Oral prednisolone (systemic corticosteroids) 4. ICS - if oral fails 5. Oral azathioprine (immunosuppressor) 6. Anti-fibrotic drugs (pirfenidone, nintedanib) 7. Oxygen (if hypoxic) 8. Lung transplant - end stage disease
62
In asthma, FVC is ______ but FEV1 is \_\_\_\_\_\_\_\_\_
Normal Reduced
63
What type of graph can help diagnose lung conditions?
Flow volume curve
64
How does peak expiratory flow rate differ between obstructive and restrictive when compared to a normal result?
Obstructive - reduced Restrictive - normal
65
How does FEV1 differ between obstructive and restrictive when compared to a normal result?
Both are reduced
66
How does FVC differ between obstructive and restrictive when compared to a normal result?
Obstructive - asthma (normal), COPD (reduced) Restrictive - reduced
67
How does FEV1/FVC ratio differ between obstructive and restrictive when compared to a normal result?
Obstructive - Decreased (\<75%) Restrictive - The same, if not slightly increased (\>75%)
68
What is bronchial challenge testing?
This involves putting strain on the airways and monitoring the response. Tis can be done by exercise or by provoking a response through the introduction of allergens or chemicals
69
How will FEV1 and PEF be affected after asthma if the patient has asthma?
Both will decrease
70
What is DLCO?
Diffusing capacity of the lung for CO Partial pressure of CO is measure ebfore and after inspiration and the difference indicates the ease at which oxygen can cross the barrier.
71
What is impulse oscillometry?
Non invasive technique using passive breathing to detrmine airway resistance Pressure is measured at the mouth at different resonant frequencies
72
Name 3 obstructive airway diseases
1. Asthma 2. Emphysema 3. Chronic Bronchitis
73
What is atopic asthma?
Asthma brought on by allergy
74
What is extrinsic asthma?
Asthma that has triggers out with the body
75
What is the asthma triad?
The three symptoms required for asthma 1. Airway inflammation - usually eosinophilic 2. Airway hyper-responsiveness - any stimulus can cause abnormal airway reactions 3. Reversible airflow obstruction - the airway can dilate again
76
How can asthma "evolve" and become worse over time?
* Bronchoconstriction - causes brief symptoms * Chronic aiway inflammation - can cause scarring * Airway remodelling - airways are permanently changed by scarring
77
Describe the process of airway remodelling
The basement membrane thickens, collagen is deposited in the submucosa and hypertrophy of smooth muscle occurs This will constrict airways reducing their efficiency
78
Asthma triggers will initiate _________ inflammation which causes release of inflammatory mediators and TH2 \_\_\_\_\_\_\_\_\_
Eosinophilic Cytokines
79
What are TH2 cytokines responsible for and why are they important?
They produce IL 4, 5 and 13 These aid production of IgE antibodies This promotes further eosinophilic activation and amplification This can cause twitchy smooth muscle (hyper-reactivity)
80
How can airways become blocked in asthma?
Inflammation can lead to desquamation - shedding of epithelium into airways Mucus plugging
81
How is athma diagnosed?
1. History/examination 2. Daily variation in peak flow rate 3. Reduced FER 4. Reversal of symptoms when inhling salbutamol 5. Provocative tests to induce bronchospasms
82
What is COPD?
An umbrella term It encompasses chronic bronchitis and emphysema
83
How does COPD develop?
The inhaltion of naxious particles over an extended timeframe
84
What does inhaltion of noxious chemicals do over time?
Causes: * Mucociliary dysfunction * Inflammation * Tissue damage
85
Noxious chemicals will stimulate the recruitment of what into the alveoli?
Macrophages Potentially also CD8+ T cells Alveolar macrophages also activate neutrophils by releasing IL-8, LTB4 and oxygen radicals
86
How do neutrophils and macrophages damage lung tissue?
Both cells will release proteases which breaks down connective tissue in the lung parenchyma which causes mucus hyper secretion
87
Of the two, which is more reversible, chronic bronchitis ot emphysema?
Chronic bronchitis is partially reversible Emphysema is not reversible at all
88
What happens when alveoli are destroyed in emphysema (COPD)?
Dead spaces are created - these areas are not availble for gas exchange and increase residual lung volume
89
Emphysema is due to an imbalance of _________ to \_\_\_\_-\_\_\_\_\_\_\_\_\_\_
Proteases Anti-proteases
90
What is different about a cough in asthma and a cough in COPD?
COPD involves a productive cough
91
How does emphysema affect breath sounds?
It reduces them - dead spaces do not make sounds
92
What is the condition involving both asthma and COPD?
Asthma COPD Overlap Syndrome Hard to diagnose
93
What is stridor?
An inspiratory wheeze due to obstruction
94
What may cause stridor in children?
Croup, epiglotitis, diphtheria, retropharngeal abscess, foreign bodies, anaphylaxis
95
What may cause stridor in adults?
Neoplasms, anaphylaxis, goitre (enlargement of thyroid gland), trauma
96
What is tracheomalacia?
The loss of cartilage rings in the trachea This leads to negative pressure in inspiration causing the collapse of the trachea
97
How can stridor be investigated?
* Laryngoscopy - caution with acute epiglottitis * Bronchoscopy * Flow volume loop via spirometry * CXR * CT/thyroid scan
98
How can a laryngeal obstruction be treated?
* Underlying cause * Reservoir mask with high flow oxygen * Cricothyridotomy - incision through skin and cricoid membrane in life threatening situations due to obstruction * Tracheostomy - incision into trachea
99
What may cause anaphylaxis?
* Food - nuts, shellfish * Insect venom - bees, wasps * Drugs - penicillin, aspirin
100
How can anaphylaxis be treated?
* IM adrenaline (EpiPen) * IV antihistamine * IV corticosteroid * Nebulized bronchodilators * Endotracheal intubation (if needed)
101
What causes snoring?
Relaxation of pharngeal dilator muscles during sleep This causes upper airway narrowingleading to turbulent airflow and vibration of the soft palate and tongue base
102
What is sleep apnoea?
Complete upper airway collapse due to muscle relaxation during sleep This prevents breathing Microarousal is a process by which the body can awake itself to resolve this and awake the person
103
What does recurrent (more than 5 per hour) instances of sleep apnoae cause?
* Recurrent hypoxia * Recurrent arousals and sleep fragmentation causing chronic fatigue
104
What are the risk factors for sleep apnoea?
* Post-operative period after anaesthesia * Acromegaly, hypothyroidism * Neurological - stroke, MS, mytonic dystrophy * Drugs - benzodiazepines, opiates, alcohol * Oropharngeal deformity * Obesity * Retrognathia - lower jaw set back so tongue is also set back lessening space in oropharynx * Enlarged tonsils, adenoids
105
What are the three main consequences of sleep apnoea?
1. Chronic fatigue 2. Personality and mood changes 3. Cognitive impairment
106
What are some indirect consequences of sleep apnoea?
* Risk of hypertension * Activates sympathetic system and cortisol release * Raised CRP * Impaired endothelial function * Impaired glucose breakdown * Increased risk of strokes and cardiovascular events
107
How can sleep apnoea be diagnosed?
* Snoring * Raised Epworth (sleepiness) score * Overnight sleep studies - oximetry, domiciliary recording * Full polysomnography - full sleep study
108
How can sleep apnoea be treated?
* Remove underlying cause * Continuous postive airway pressure - airway mask can keep airway open * Mandibular advancement device - moves jaw forward * Surgery - removes soft palate meaning area becomes scarred and stiffens up reducing relaxation and collapsing * Jaw broken and moved forward