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The Respiratory System > Obstructive and Restrictive Lung Disease > Flashcards

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
Q

Name a SAMA

A

Ipratropium

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26
Q

Name two LAMAs

A
  1. Tiotropium
  2. Glycopyrronium
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27
Q

Methylxanthines act as ____________ and also ___________

A

Bronchodilators

Anti-inflammatory drugs

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28
Q

Name an example of a methylxanthine

A

Theophylline

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29
Q

What is the function of phosphodiesterase 4 enzymes?

A

Hydrolyse cAMP

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30
Q

What is the overall function of PDE4 inhibitors?

A

Prevent cAMP hydrolysis allowing high levels of cAMP in cells

Bronchial smooth muscle will become relaxed

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31
Q

PDE4 inhibitors are for use only in ____

A

COPD

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32
Q

Give an example of a PDE4 inhibitor

A

Roflumilast
works by increasing cyclic adenosine monophosphate (cAMP) levels in immune cells, inhibiting PDE4 and leading to reduced inflammation in the airways.

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33
Q

Why are PDE4 inhibitors used infrequently?

A

Side effects suh as nausea, diarrhoea and headaches

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34
Q

What are mucolytics?

A

Drugs which reduce the viscocity of mucous and reduce inflammation

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35
Q

Give two examples of mucolytics?

A
  1. Carbocisteine
  2. Erdosteine
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36
Q

In an acute astha attack what treatment is given?

A
  • Oral prednisolone (40mg)
  • At least 60% oxygen aim for 94-98% SpO2
  • Nebulised salbutamol
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37
Q

What are some treatment methods for COPD?

A
  • Smoking cessation
  • Immunisation
  • Pharmacotherapy
  • Oxygen
  • Increase exercise
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38
Q

Name two LAMAs

A
  1. Titropium
  2. Aclidinium
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39
Q

Name two LABAs

A
  • Olodaterol
  • Formeterol
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40
Q

Name an ICS for COPD use

A

Beclometasone

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41
Q

Which antibiotic may be used for COPD?

A

Azithromycin

(also amoxicillin and doxycycline)

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42
Q

How is acute COPD treated?

A
  • Nebulised high dose salbutamol and ipratropium
  • Oral prednisolone
  • Antibiotic (amoxicillin/doxycycline) if infection
  • 24-28% O2
  • Non-invasive ventilation
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43
Q

Which external factors can cause lung restriction?

A
  1. Skeletal causes (broken ribs, kyphoscoliosis)
  2. Muscle Weakness (intercostal/diaphragmatic)
  3. Obesity (due to compression)
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44
Q

What are the effects of lung compression from external sources?

A
  1. Reduced partial pressur eof oxygen
  2. Reduced partial pressure of carbon dioxide
  3. Reduced lung volumes
  4. Hypoxia
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45
Q

What is DPLD?

A

Diffuse Parenchymal Lung Disease

Interstitial lung disease

An umbrella term for lung diseases affecting the interstitium

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46
Q

What is the interstitium of the lungs?

A

The space and tissues surrounding the alveoli

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47
Q

What are the three main categories for DPLD (ILD)?

A
  1. Those with a known cause
  2. Those with an unknown cause (idopathic)
  3. Those associated with systemic disease
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48
Q

Why may hypoxia occur at a thickened alveolar/arteriolar barrier?

A

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

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49
Q

Give two different causes for DPLD

A
  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
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50
Q

What is consolidation in the lungs?

A

It occurs when the small air sacs in the lungs (alveoli) fill up with fluid, which can be caused by a variety of conditions, such as pneumonia, pulmonary edema, or lung cancer.

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51
Q

What can cause consolidation on a chest X-ray?

A
  1. Pneumonia
  2. PE
  3. Alveolitis
  4. Cryptogenic pneumonia (not infectious)
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52
Q

What is alveolitis?

A

This is the infiltration of inflammatory fluid into the alveolar walls

It can be caused by:

  • Drugs
  • Toxic gases
  • Fibrosing alveolitis
  • Autoimmune disease
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53
Q

What is pneumoconiosis?

A

Dust disease

Restrictive lung disease that can be either fibrogenic (asbestosis, silicosis) or non-fibrogenic (siderosis (due to iron), stenosis, baritosis (due to barium))

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54
Q

What is carcinomatosis?

A

Body-wide spread of cancer and can contribute to DPLD

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55
Q

How do eosinophils contribute to DPLD?

A

They occur alongside all sides of inflammation which is present in DPLD

56
Q

Symptoms of DPLD?

A
  • Breathlessness
  • Cough (without wheeze - no obstruction)
  • Finger clubbing
  • Lung crackles (inspiration)
  • Central cyanosis
  • Pulmonary fibrosis (chronic inflammation)
57
Q

How is FEV1 affected in DPLD?

A

It is reduced

58
Q

How is FVC affected in DPLD?

A

It is reduced

59
Q

What happen to the FEV1/FVC ratio in DPLD?

A

It remains normal as both variables decrease in proportion

60
Q

Aside from FEV1 and FVC what are the thee main checks which must be covered for diagnosing DPLD?

A
  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
Q

How is DPLD treated?

A
  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
Q

In asthma, FVC is ______ but FEV1 is _________

A

Normal

Reduced

63
Q

What type of graph can help diagnose lung conditions?

A

Flow volume curve

64
Q

How does peak expiratory flow rate differ between obstructive and restrictive when compared to a normal result?

A

Obstructive - reduced

Restrictive - normal

65
Q

How does FEV1 differ between obstructive and restrictive when compared to a normal result?

A

Both are reduced

66
Q

How does FVC differ between obstructive and restrictive when compared to a normal result?

A

Obstructive - asthma (normal), COPD (reduced)

Restrictive - reduced

67
Q

How does FEV1/FVC ratio differ between obstructive and restrictive when compared to a normal result?

A

Obstructive - Decreased (<75%)

Restrictive - The same, if not slightly increased (>75%)

68
Q

What is bronchial challenge testing?

A

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
Q

How will FEV1 and PEF be affected after asthma if the patient has asthma?

A

Both will decrease

70
Q

What is DLCO?

A

Diffusing capacity of the lung for CO

Partial pressure of CO is measure before and after inspiration and the difference indicates the ease at which oxygen can cross the barrier.
* DLCO decreased in emphysema -> this because decrease in the surface area for gas exchange. This is because the walls of the air sacs (alveoli) become weakened and lose their ability to expand and contract properly. As a result, the walls of the alveoli can break down, creating larger air spaces (like plastic bags) that are less efficient in exchanging gases with the bloodstream.

71
Q

What is impulse oscillometry?

A

Non invasive technique using passive breathing to detrmine airway resistance

Pressure is measured at the mouth at different resonant frequencies

72
Q

Name 3 obstructive airway diseases

A
  1. Asthma
  2. Emphysema
  3. Chronic Bronchitis
73
Q

What is atopic asthma?

A

Asthma brought on by allergy

74
Q

What is extrinsic asthma?

A

Asthma that has triggers out with the body

75
Q

What is the asthma triad?

A

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
Q

How can asthma “evolve” and become worse over time?

A
  • Bronchoconstriction - causes brief symptoms
  • Chronic aiway inflammation - can cause scarring
  • Airway remodelling - airways are permanently changed by scarring
77
Q

Describe the process of airway remodelling

A

The basement membrane thickens, collagen is deposited in the submucosa and hypertrophy of smooth muscle occurs

This will constrict airways reducing their efficiency

78
Q

Asthma triggers will initiate ________ which causes release of inflammatory mediators and TH2 _________

A

Mast cells

Cytokines

79
Q

What are TH2 cytokines responsible for and why are they important?

A

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
Q

How can airways become blocked in asthma?

A

Inflammation can lead to desquamation - shedding of epithelium into airways

Mucus plugging
In other words
Mucous build up and smooth muscle of bronchial contract

81
Q

How is athma diagnosed?

A
  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
Q

What is COPD?

A

An umbrella term

It encompasses chronic bronchitis and emphysema

83
Q

How does COPD develop?

A

The inhaltion of naxious particles over an extended timeframe

84
Q

What does inhaltion of noxious chemicals do over time?

A

Causes:

  • Mucociliary dysfunction
  • Inflammation
  • Tissue damage
85
Q

Noxious chemicals will stimulate the recruitment of what into the alveoli?

A

Macrophages

Potentially also CD8+ T cells

Alveolar macrophages also activate neutrophils by releasing IL-8, LTB4 and oxygen radicals

86
Q

How do neutrophils and macrophages damage lung tissue?

A

Both cells will release proteases which breaks down connective tissue in the lung parenchyma which causes mucus hyper secretion

87
Q

Of the two, which is more reversible, chronic bronchitis ot emphysema?

A

Chronic bronchitis is partially reversible

Emphysema is not reversible at all

88
Q

What happens when alveoli are destroyed in emphysema (COPD)?

A

Dead spaces are created - these areas are not availble for gas exchange and increase residual lung volume

89
Q

Emphysema is due to an imbalance of _________ to ____-__________

A

Proteases

Anti-proteases

90
Q

What is different about a cough in asthma and a cough in COPD?

A

COPD involves a productive cough

91
Q

How does emphysema affect breath sounds?

A

It reduces them - dead spaces do not make sounds

92
Q

What is the condition involving both asthma and COPD?

A

Asthma COPD Overlap Syndrome

Hard to diagnose

93
Q

What is stridor?

A

An inspiratory wheeze due to obstruction

94
Q

What may cause stridor in children?

A

Croup, epiglotitis, diphtheria, retropharngeal abscess, foreign bodies, anaphylaxis

95
Q

What may cause stridor in adults?

A

Neoplasms, anaphylaxis, goitre (enlargement of thyroid gland), trauma

96
Q

What is tracheomalacia?

A

The loss of cartilage rings in the trachea

This leads to negative pressure in inspiration causing the collapse of the trachea

97
Q

How can stridor be investigated?

A
  • Laryngoscopy - caution with acute epiglottitis
  • Bronchoscopy
  • Flow volume loop via spirometry
  • CXR
  • CT/thyroid scan
98
Q

How can a laryngeal obstruction be treated?

A
  • 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
Q

What may cause anaphylaxis?

A
  • Food - nuts, shellfish
  • Insect venom - bees, wasps
  • Drugs - penicillin, aspirin
100
Q

How can anaphylaxis be treated?

A
  • IM adrenaline (EpiPen)
  • IV antihistamine
  • IV corticosteroid
  • Nebulized bronchodilators
  • Endotracheal intubation (if needed)
101
Q

What causes snoring?

A

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
Q

What is sleep apnoea?

A

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
Q

What does recurrent (more than 5 per hour) instances of sleep apnoae cause?

A
  • Recurrent hypoxia
  • Recurrent arousals and sleep fragmentation causing chronic fatigue
104
Q

What are the risk factors for sleep apnoea?

A
  • 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
Q

What are the three main consequences of sleep apnoea?

A
  1. Chronic fatigue
  2. Personality and mood changes
  3. Cognitive impairment
106
Q

What are some indirect consequences of sleep apnoea?

A
  • 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
Q

How can sleep apnoea be diagnosed?

A
  • Snoring
  • Raised Epworth (sleepiness) score
  • Overnight sleep studies - oximetry, domiciliary recording
  • Full polysomnography - full sleep study (gold standard)
108
Q

How can sleep apnoea be treated?

A
  • Remove underlying cause
  • Continuous postive airway pressure (CPAP) - 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
109
Q

The atopic triad refers to genetic predisposition to
anomaly react against specific types of allergens,
and it is formed by the following conditions:N.N

A

Allergic rhinitis, atopic dermatitis & asthma.

110
Q

On the etiopathology of ASA sensitivity, which enzyme activity of the AA
pathway results inhibited and which one results increased?N.n

A

Allergic rhinitis, atopic dermatitis & asthma.

111
Q

Name of the cytokine responsible of promoting the production of IgE: N.N

A

b) IL-4

112
Q

**cell that is responsible of releasing histamines and leukotrienes N.N

A

Mast cell

113
Q

what are reversible airway changes during an onset attack of asthma, N.N

A

a) Inflamed mucosa
b) Increased vascular permeability
c) Bronchoconstriction
HOWEVER
FIBROSIS is not REVERSIBLE

114
Q

What are the three most common symptoms on
asthma?

A

a) Dry cough, shortness of breath & tightness of breath.

115
Q

following finding during physical examination is a
sign that indicates hyperinflation of lungs(Hyper inflation of the lungs air stuck in ) :N.N

A

d) Hyper-resonance to percussion.

116
Q

3) An 8-year-old boy is presented in the emergency room
with productive cough and sever shortness of breath.
Physical examination reveals wheezing upon
expiration and use of accessory muscles.
Knowing the diagnostic test of choice to this case
according to the diagnostic protocol of asthma, what
parameter will reveal the obstructive pattern of this
condition?
What parameter reveals the reversibility of this
condition? N.N

A

b) Relation FEV1/FVC <75%

  • e) FEV1 >12% after taking a SABA.
117
Q

1) The mechanism of action of beta 2 receptor agonist in the bronchial
asthma include N.N

A

a) Relaxation of airway smooth muscle
b) Inhibition of plasma exudation and airway edema
c) Increased mucociliary clearance

118
Q

2) The most common side effects of beta- 2 agonists are; N.N

A

a) Dry mouth, urinary retention, and glaucoma

119
Q

3) Cromolyn sodium and nedocromil sodium are asthma controller drugs that
appear to: N.N

A

Inhibit mast cell and sensory nerve
activation

120
Q

Acute management of bronchial asthma include

A

b) Short-acting inhaled beta-2-agonists
c) A slow infusion of aminophylline with monitoring blood values.
d) A rapid infusion of dopamine

121
Q

1) In severe asthmatic attack, what medication will
address underlying airway hyperresponsiveness?

A

b) Hydrocortisone
In cases of severe acute exacerbations, systemic
corticosteroids are necessitated. Hydrocortisone or
methylprednisolone are the choices.
Formoterol is a LABA and is predominantly used for
prevention, not for emergency cases. Salbutamol is a
SABA used for relief of bronchoconstriction.

122
Q

2) You know you are dealing with an asthmatic with a
higher risk of dying when:

A

c) Corticosteroids are not included in the treatment
regimen
Risk factors for deaths in bronchial asthma:
It should be increased frequency of bronchodilator inhalers.
This means that ↑frequency and persistence of symptoms
despite use bronchodilators. If they are underutilized, it
means there risk can still be decreased by corrective
usage.
Corticosteroid therapy is the cornerstone of asthma
treatment mainly because asthma is an inflammatory
disease. If your asthma is solely treated by bronchodilators
and was not stepped up to include corticosteroids, then you
don’t have the right medicine.

123
Q

2) You know you are dealing with an asthmatic with a
higher risk of dying when:

A

c) Corticosteroids are not included in the treatment
regimen
Risk factors for deaths in bronchial asthma:
It should be increased frequency of bronchodilator inhalers.
This means that ↑frequency and persistence of symptoms
despite use bronchodilators. If they are underutilized, it
means there risk can still be decreased by corrective
usage.
Corticosteroid therapy is the cornerstone of asthma
treatment mainly because asthma is an inflammatory
disease. If your asthma is solely treated by bronchodilators
and was not stepped up to include corticosteroids, then you
don’t have the right medicine.

124
Q

3) What is the next line of drug for a patient with severe
exacerbations, non-response to corticosteroids, and
needing rest from prolonged administration of
corticosteroids?

A

Theophylline
This is a PDE-i which can provide diaphragmatic rest.
Ipratropium is a SAMA which should be included in the first
line of drug choices for mild/ intermittent symptoms of
COPD exacerbation. Hence, this should be removed from
the answers you are thinking of.
Azithromycin is an antibiotic which is for long-term treatment
and do not address the need for diaphragmatic rest.
High flow oxygen SHOULD NOT be given because it
removes the hypoxemic drive and hypoxemic
vasoconstriction

125
Q

The mechanism of action of beta 2 receptor agonist in the bronchial

A

a) Relaxation of airway smooth muscle
b) Inhibition of plasma exudation and airway edema
c) Increased mucociliary clearance

126
Q

The most common side effects of beta- 2 agonists are;

A

a) Dry mouth, urinary retention, and glaucoma

127
Q

3) Cromolyn sodium and nedocromil sodium are asthma controller drugs that
appear to:

A

Inhibit mast cell and sensory nerve
activation

128
Q

4) Acute management of bronchial asthma include all the following,

A

a) A high concentration of oxygen to achieve oxygen saturation of >90%
b) Short-acting inhaled beta-2-agonists
c) A slow infusion of aminophylline with monitoring blood values.

129
Q

5) Which of the following drug is NOT available as metered-dose inhaler
(MDI?
a) Salbutamol
b) Terbutaline
c) Albuterol
d) Aminophylline

A

d) Aminophylline

130
Q

Beclomethasone dipropionate is commonly administered as:

A

Aerosolized steroids

131
Q

Which of the following drugs is leukotriene-modifying drug indicated in the management of bronchial asthma?

A

Zafirlukast

132
Q

9) Which of the following is the primary long-term controller medication for a
5-year-old girl with moderate persistent asthma?

A

Fluticasone propionate twice daily

133
Q

. She is normally fit and well, but has been finding running increasingly difficult, particularly when it is cold.
She complains of feeling short of breath and wheezing.
There are no abnormal findings on examination and no significant past medical history.

A

Intrinsic asthma

134
Q

He says he feels like he sometimes can’t get air in, and his mother is worried he has hayfever as it seems to be worse in the summer.
He has a past history of eczema and his father has asthma and says he has allergies.
On auscultation he has a generalised wheeze.

A

Atopic asthma

135
Q

marker of mast cell degranulation
determine if a severe allergic reaction has occurred.

A

Serum tryptase

The Respiratory System (19 decks)

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