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BMS3052 > WEEK 4 LUNGS: ASTHMA, COPD, IPF + SILICOSIS > Flashcards

WEEK 4 LUNGS: ASTHMA, COPD, IPF + SILICOSIS Flashcards

1
Q

What are the 5 main respiratory conditions worldwide?

A
  • COPD, Asthma, Acute LRI, TB, and lung cancer
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2
Q

What are the current respiratory health concerns?

A
  • Climate change, and biological or chemical terrorism
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3
Q

What % of respiratory conditions makes up the burden of disease in AUS?

A
  • 8%

- 6th leading contributer to global burden

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4
Q

Is asthma a long-term lung condition?

A
  • YES
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5
Q

What are the symptoms for asthma?

A

Shortness of breath, tightness of chest, cough, difficulty breathing.

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6
Q

What is an example of a preventive medicine for asthma?

A

Flixotide

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7
Q

How many people in 10 in Aus have asthma?

A
  • 1/10 (1 in 10)
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8
Q

When does thunderstorm asthma usually occur?

A
  • During or immediately after a storm and generally with the hotter temperatures (e.g. 35 degrees)
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9
Q

What is thunderstorm asthma and why is it different to normal asthma?

A
  • The moisture from the air goes into the rye grass pollen, these then ‘explode’ into the air
  • These pollens are MUCH smaller than normal pollen and can get into the lungs easily
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10
Q

Who is at risk for thunderstorm asthma?

A
  • Hayfever sufferers
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11
Q

is asthma triggered from only pollen?

A
  • NO, from many other potential triggers e.g. air pollution
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12
Q

What are some potential preventive measures that the state government has taken to respond better to these thunderstorm asthma events in the future (especially since there were 10 deaths)?

A
  • More money into predicting and responding to these events (forecasting system)
  • Public health education campaign
  • Clinical guidelines
  • Revised state health emergency plan
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13
Q

Are brown coal mines used overseas?

A
  • no, just domestically
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14
Q

How long did the Hazlewood mine fire burn for?

A
  • 45 days
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15
Q

What are the two types of emergencies that could be considered for the Hazlewood mine fire?

A
  • A fire emergency

- Public health emergency

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16
Q

From the Hazlewood fires, was there any significant relationships between the exposure to smoke and self reproted doctor diagnoses high BP, high LDL, CVD, diabetes or cancer?

A
  • NO
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17
Q

What are potential reasons for an increase in medical symptoms in those exposed to smoke from the Hazlewood fires and no diagnosis?

A
  • symptoms may have been sub-clinical
  • participants may not have reported symptoms to GPs
  • Symptom onset to diagnosis may be a long period of time (delayed)
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18
Q

Was there increased psychological stress in those in the hazlewood mine and if so, was it primarily children, adults, or both?

A
  • YES and both
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19
Q

What is an explanation for the 2019 report that there was no effect on the hazlewood fires on asthma related symptoms, lung function or airway inflammation in adults?

A
  • This means that people could be taking preventive medication properly (e.g. for asthma) so they are not showing those symptoms
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20
Q

What was the outcome of the Hazlewood fires investiagation on the miners?

A
  • They were fined for not having proper procedures in place, not cutting back vegetation, not wetting the ground properly etc. (fined 2 million) `
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21
Q

What are the health effects of bushfire smoke in relation to the social determinants of health?

A
  • Homelessness
  • Povertty (loss of business/job)
  • Social disruption/social isolation–> mental health
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22
Q

What can increased hospital presentations form bushfire smoke be due to?

A
  • Asthma
  • COPD
  • Other respiratory infections
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23
Q

What are the effects of bushfire smoke on the body a part from the lungs?

A
  • CV morbidity
  • Psychological disorders
  • Adverse birth outcomes
  • Eye irritation
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24
Q

What was the controversy with the Fiskville training centre firefighters?

A
  • b/w 1971 and 1999 firefighters training at this centre hd a SIR (obs/exp) =1.85 for all cancers
  • Due to toxic chemical build up at the site (used the same site for a long time)
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25
Q

In the 2014 health study report for firefighters, what was the health of firefighters?

A
  • Overall mortality lower
  • No increase in CV or resp. mortality -
  • Stat significant increase in prostate cancer for FT firefighters
  • Significant increase in melanoma
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26
Q

Why , in the 2014 fire fighter health report, was the overall mortality lower?

A
  • because these fire fighters are VERY fit

- When they are not working, they are training all the time - they don’t smoke

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27
Q

Is silicosis an occupational lung disease?

A
  • YES
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28
Q

What are the symptoms of silicosis?

A
  • breathing difficulties, cough, weight loss, tiredness
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29
Q

What does silicosis do to the lungs in broad terms?

A
  • Damages the lung air sacs, causes scarring and fibrosis
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30
Q

Who is at risk for developing silicosis?

A
  • Stonecutters cutting artificial stone (engineered stone) for benchtops -crystalline silica or silica dust
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31
Q

What are the three forms of silicosis?

A
  1. Acute silicosis
  2. Accelerated silicosis
  3. Chronic silicosis
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32
Q

In what time frame does acute silicosis develop and what damage occurs?

A

Develops after a short exposure (a few weeks to years. to very high levels of silica dust.
- Causes severe inflammation and an outpouring of protein into the lung.

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33
Q

In what time frame does accelerated silicosis develop and what damage occurs?

A
  • Develops after exposure 3 to 10 years to moderate to high levels of silica dust
  • causes inflammation, protein in the lung and scarring of the lung (fibrotic nodules)
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34
Q

In what time frame does chronic silicosis develop and watch type of damage occurs?

A
  • Develops after long-term exposure to lower levels of silica dust for example after 10 + years of exposure.
  • Is known as the ‘classic silicosis’
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35
Q

Which two factors are key in preventing silicosis?

A
  • Education

- OHS controls

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36
Q

Does silicosis generally occur in younger or older people?

A
  • Young people
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37
Q

In terms of spirometry, what does the FEV1 mean?

A
  • Forced expiratory volume in one second
  • Measures how quickly the lungs can be emptied
  • Volume expired in the first second of maximal expiration initiated at full inspiration (so you take your biggest breath in and exhale to your full capacity-measurement is within the first SECOND though)
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38
Q

In terms of spirometry, what is the FVC?

A
  • Volume expired from full inspiration to full expiration

- this is compared to reference values (so compare normal lung function with the same age, sex, and height)

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39
Q

What are examples of obstructive diseases?

A
  • Asthma and COPD
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40
Q

What are examples of restrictive diseases?

A
  • IPF and Silicosis
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41
Q

If the FEV1/FVC ratio is less than the predicted lower limit of normal, then what does that mean?

A
  • There is an airflow obstruction and they assess the severity of the obstruction by using the % predicted FEV1
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42
Q

What is teh FEV1 and FEV1/FVC ratio like in people with increased airway resistance?

A
  • It is decreased
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43
Q

If a patient has a decreased FEV1 and FEV1/FVC, and measurements are taken again with the addition of a bronchodilator, then if they have asthma will the values improve or not?

A
  • If they have asthma, then the values should improve BUT if they have COPD or fibrosis (e.g. IPF) then they won’t
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44
Q

What type of at home testing for lung function is available and what does it indicate?

A
  • Peak Expiratory flow rate (L/min)

- Can be used to rule out clinically significant COPD if given before a bronchodilator

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45
Q

What are the normal adult values for males and females respectively for the PEF (peak expiratory flow rate)?

A
  • Males: 450-700

- Females: 300-500

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46
Q

Does the PEF depend on age and time of day?

A
  • YES it depends on age, height, weight and the reading is generally lower in the morning
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47
Q

How are most drugs delivered for lung diseases?

A
  • Via the inhaled route because they are designed for deposit in lung
48
Q

In terms of drugs for lung diseases, what feature of the body aids in systemic absorption for these drugs?

A
  • The highly vascular pulmonary system
49
Q

What 4 main things is the delivery and absorption of drugs for lung diseases dependent on?

A
  • Inhaler technique
  • Particle/droplet size
  • Lipid solubility of the drug determining its duration of action
  • Some of the drug may be swallowed which can cause systemic effects
50
Q

A particle that is 5-10um in size is deposited on the ____ airways

A
  • Deposited on the UPPER airways
51
Q

A particle that is 0.5-5um in size is deposited in the ___ airways?

A

-Deposited in the SMALL airways

52
Q

Any particle that is <2um in size will reach the ____ in lungs

A
  • Will reach the alveoli in lungs
53
Q

Which type of women are most at risk of dying form asthma?

A
  • Baby boomer women
54
Q

Why might the risk of dying from asthma be the greatest in the elderly?

A
  • Because they may not be complying with their medication
55
Q

What is a formal definition of asthma?

A
  • “chronic inflammatory lung disease that leads to reversible narrowing of the airways, associated with increased airway hyperresponsiveness (AHR)”
  • Imbalance between airway contraction and relaxation
56
Q

What is a definition of asthma in terms of the symptoms experienced with it?

A
  • Shortness of breath
  • Wheezing, chest tightness
  • Night-time or early morning coughing
57
Q

What is the ‘extrinsic’ and more common form of asthma characterised by?

A
  • ‘allergic’ (Th2 response immune system)
  • Involving IgE antibodies/mast cell degranulation
  • Triggered by re-exposure to an allergen e.g. pollen, house dust mite, pets
58
Q

What is the ‘intrinsic’ and more severe form of asthma characterised by and what can it be caused by?

A
  • Hyperresponsive airways
  • ‘non specific bronchial hyperactivity’
  • Triggered by the cold and infection
  • Triggered by exercise (but exercise can reduce the frequency of attacks)
59
Q

What is the diagnosis of asthma (two main options)?

A
  • Compatible respiratory symptoms including response to triggers AND evidence of reversible airway obstruction even (spirometry)
    OR:
  • Variable airflow obstruction (peak expiratory flow monitoring)
60
Q

If the main criteria for diagnosis of asthma are not met but asthma is still suspected, then what should be done?

A
  • Bronchoprovocation with methacholine (but some contraindications)
  • Newer research going into testing based on the sputum (white= healthy and yellow or green= not good)
61
Q

In asthma, which part of the membrane undergoes fibrosis?

A
  • But is that like reversible or not.
62
Q

In asthma, what are the three main things occurring in its pathogenesis?

A
  • Excessive mucus (obstruction and barrier to inhaler therapy)
  • Basement membrane thickening (fibrosis)
  • More smooth muscle contraction (increased contraction)
63
Q

In the more severe form of asthma, what occurs with the ‘airway hyperresponsiveness’?

A
  • Influence of inflammatory mediators and increased bulk of “sensitised” muscle leads to airways contracting “too easily and too much”
64
Q

What type of T cell response occurs in healthy airways in response to aeroallergens?

A
  • Th1 immune response (macrophage, low level th1, IFN-7, IL-2, TNF-a)
  • Low level IgG
  • Normal airway maintained
65
Q

What type of T cell response occurs in asthmatic airways (allergic asthma) in response to aeroallergens?

A
  • Th2 response
  • IL-4, 5, 13
  • Eosinophil activation, mast cells, and IgE
  • Subepithelial fibrosis
  • Goblet cell hyperplasia
  • Airway edema
  • Smooth muscle hyperplasia and/or hypertrophy
66
Q

What are the 4 main phases in asthma pathogenesis?

A
  1. Induction phase
  2. Inflammation
  3. Airway remodelling
  4. Smooth muscle cell shortening
67
Q

What occurs in the induction phase of asthma in general and is this hard to prevent ?

A
  • This is poorly understood, often (not always) related to the acquisition of allergy.
  • YES hard to prevent
68
Q

What occurs in the inflammation phase of asthma?

A
  • not completely understood, some mediators known

- e.g. IgE in allergic asthma, IL-5 in eosinophilic asthma

69
Q

What occurs in the airway remodelling phase of asthma and is this phase difficult to reverse?

A
  • Not completely understood, changes well characterised
  • This is why we can’t cure it
  • YES it is difficult to reverse
70
Q

What occurs in the smooth muscle shortening of asthma pathogenesis?

A
  • Well understood, most important mediators identified. e.g. Histamine, Cys-LTs
71
Q

Which stage of the asthma pathogenesis can be targeted by preventing medication?

A
  • The inflammation stage
72
Q

Which stage of the asthma pathogenesis can be targeted by reliever or controller medication?

A

The smooth muscle shortening phase.

73
Q

What are the 5 layers of asthma treatments today?

A
  1. SABA reliever only (e.g. short acting b receptor agonist - salbutamol)
  2. Add ICS preventer (inhaled corticosteroid)
  3. Change to ICS/LABA preventer (LABA= long acting b2 agonist)
  4. Increase dose of ICS/LABA preventer
  5. Specialised inc biologics (e.g. mAbs)
74
Q

What is the point of using releivers for asthma?

A
  • They target the immediate (acute) phase of asthma

- They relieve airway smooth muscle spasm

75
Q

What is the point of using preventers (controllers) for asthma?

A
  • They target the late (chronic) phase of asthma

- They REDUCE inflammation

76
Q

What occurs in the late phase of asthma in terms of the immune system and what is it inhibited by?

A
  • Infiltration of cytokine releasing Th2 cells and monocytes
  • Activation of eosinophils
  • Leads to epithelial damage which can increase the airway hyperactivity amd lead to bronchospasm, wheexing and coughing
  • INHIBITED BY GLUCOCORTICOIDS
77
Q

What occurs in the early (immediate) phase of asthma and what can reverse it?

A
  • An allergen or non specific stimulus
  • This leads to mast cells and mononuclear cells that cause bronchospasm
  • B2 receptor agonists can reverse this or CysLT receptor antagonists, or theophylline
78
Q

In general terms, what are the relievers targeting in terms of asthma?

A
  • The airway contraction leading to relaxation via the sympathetic efferents to adrenal medulla / synthetic b2 adrenoceptor agonists (e.g. salbutamol, short acting)
79
Q

In terms of asthma, what is innervating the contraction of the bronchioles?

A
  • Parasymp vagal efferents (Ach via M3 receptors)
80
Q

What is an example of receptor antagonists that oppose the actions of HA (histamine), Cys-LTs (leukotreines) and Ach on the GPCR in terms of asthma and bronchoconstriction?

A
  • M receptor antagonists e.g. Ipratropium

- This is known as competitive antagonism

81
Q

What are examples of dilators that allow for functional antagonism?

A
  • B2 adrenoceptor agonists–> adrenaline (endogenous), salbutamol, PDE inhibitor (theophylline)
82
Q

Are reliever medications good at preventing against attacks?

A
  • no
83
Q

Via which pathway do beta agonists work to allow for muscular contraction?

A
  • Via a GPCR
  • ATP –> cAMP –> PKA (protein kinase A)
  • PKA inhibits calcium release from sarc reticulum
  • Due to this decrease, Ca2+ is then reduced which leads to reduced contraction
  • MLC is de P’d (via phosphatase)
84
Q

What is the mechanism of action of contraction in the smooth muscle bronchioles?

A
  • Ach, histamine and Cys-LTs
  • Phospholipase signalling (IP3)
  • Increased release of intracellular Ca2+ release from SR
  • P of MLC (Myosin light chain)
85
Q

What are two positives that come from SABA?

A
  • decrease the release of inflammatory mediators from mast cells
  • stimulate mucociliary clearance
86
Q

What are the adverse effects/limitations of SABA?

A
  • Tachycardia (B1- mediated)
  • Muscle tremor (B2 mediated)
  • Potential for tolerance with overuse or infection (receptor downregulation/desensitization)
  • No effect on remodelling
  • Reduced efficacy with smoking/infection
87
Q

What is another name for the asthma controllers?

A
  • LABA

- Long acting B2 adrenoceptor agonists

88
Q

What are examples of controllers (LABAs) ?

A
  • Salmeterol (12 hour duration and rapid onset)
  • Eformoterol (12 hour duration and rapid onset)
  • clenbuterol /bambuterol
  • Masks symptoms of inflammation and linked to increased mortality.
89
Q

What are the indications for the use of LABAs?

A
  • to only be used for prophylaxis!
  • Also only with inhaled steroids (Step 3)
  • Can be an alternative to an increased steroid dose
90
Q

What can LABAs protect against?

A
  • Exercise-induced/nocturnal asthma
91
Q

What is an example of a medicaton that is contra-indicated in asthma?

A
  • B adrenoceptor antagonists (Beta blockers-hypertension)
  • b1 selective antagonists still can’t be used because of potential non specificity
  • Could also cause bronchoconstriction
92
Q

What are examples of other bronchodilators?

A
  • Ipratropium (short acting M3 antagonist)

- Theophylline (Active component of aminophylline)

93
Q

How do the short and long acting M3 antagonists work? (e.g. Ipratropium and Tropropium)

A
  • Blocking vagal tone (bronchodilation and decreases mucous secretions)
94
Q

How does Theophylline (brondecon, Neulin) work?

A
  • Has variable pharmacokinetics/ narrow TI
  • PDE inhibitor INHIBITING cAMP breakdown (leading to bronchodilation)
  • Increases the effectiveness of the beta agonist
95
Q

What type of drug is theophylline?

A

PDE inhibiting drug

96
Q

What are two things that ICS (inhaled glucocorticoids) can do?

A
  • Reduce mucus and swelling
  • Prevent muscle spasm
  • These can both reduce the severity of an asthma attack
97
Q

What is the mechanism of action of ICS (Inhaled corticosteorids) ?

A
  • Glucocorticoids enter cell via glucocortocoid receptor (GR)
  • Enter nucleus and binds to TFs to transactivate - increase the anti-inflammatory proteins (e.g. annexin A1)
  • ALso binds to TFs that repress that NFkB TF thus decreasing pro-inflammatory proteins such as COX-2, PLA2, IL-1, TNFa
98
Q

What are 5 things that occur with the preventer/controller mechanism?

A
  1. reduced cytokine synthesis (thus decreased eosinophil activation)
  2. Reduced activity of PLA2 (vias increased annexin A1)
  3. Reduced COX-2 synthesis (decreased generation of prostaglandins/leukotrienes)
  4. Reduced IgE synthesis by B cells (decreased mast cell activation, less histamine release)
  5. Decreased symptoms of secretions; swelling; inflammation
    NO ACUTE EFFECT ON BRONCHOSPASM
99
Q

Can ICS (inhaled corticosteroids) have an acute effect on bronchospasms?

A
  • NO
100
Q

When are ICS used/reserved for?

A
  • As a rescue medication
  • Has dose limiting adverse effects
  • need to wean patients off chronic use to avoid withdrawal
101
Q

What are some of the adverse events related to corticosteroid use?

A
  • Suppressing endogenous glucocorticoid synthesis
  • cushings
  • suppressing response to infection or injury
  • behavioral symptoms
  • cataracts
  • metabolic effects (increased abdominal fat, easy bruising)
  • growth suppression
102
Q

What are LTRAs?

A
  • Leukotriene receptor antagonists

- e.g. Montelukast, Zafirlukast

103
Q

What do LTRAs do?

A
  • Orally active
  • PROPHYLACTIC USE ONLY (preventers)
  • Modest bronchodilation (1/2 compared to B2 agonists)
  • Has efficacy in asthma in combined therapy with ICS/LABA
104
Q

What are LTRAs indicated for?

A
  • Asprin and exercise induced asthma
105
Q

What is Omalizumab?

A
  • It is a mAb (monoclonal antibody) against IgE
  • Inhibits IgE induced release of mast cell mediators- histamine, cys LTs
  • ## Needs to be administered subcutaneously every 2-4 weeks by health provider.
106
Q

In which situations is Omalizumab rezerved for in asthma?

A
  • Severe, persistent allergic asthma that is uncontrolled even with high doses of coroicosteroids
  • There is a low potential for anaphylaxis
107
Q

What is the mAb Mepolizumab targeting in severe asthma treatment?

A
  • IL-5
  • Inhibits eosinophilia
  • Subcutaneous administration every 4 weeks by health provider
  • So only to be used for severe eosinophilic asthma!
108
Q

If a patient is undergoing life-threatening acute asthma and can’t inhale salbutamol, then what should be done?

A
  • Adrenaline should be administered and can administer salbutamol by continuous nebulisation
  • could also require ventilation, i.v. magnesium sulfate, nebulised SABA/SAMA
109
Q

What is COPD characterised by?

A
  • Progressive decline in lung function
  • Chronic bronchitis (excessive phlegm/sputum, cough) - emphysema –> breakdown of alveolar walls, riven by elastase-induced damage
  • most patients have both (bc of smoking as well)
110
Q

What is the reason why there is gas trapping in emphosema?

A
  • Tethering forces are destroyed (what the alveoli are attached by)
111
Q

What do I mean when I sat ‘blue bloater’?

A
  • This is to do with chronic bronchitis in COPD
  • Daily cough
  • Overweight and person is also cyanotic due to lack of O2. They have higher hemoglobin, peripheral edema and bronchi and wheezing
112
Q

What do I mean when I say ‘pink puffer’?

A
  • This is to do with emphysema with COPD
  • People are generally older and thin
  • Have severe shortness of breath
  • quiet chest
  • Have hyperinflation on X-ray with flattened diaphragms
113
Q

What type of remodelling occurs in COPD?

A
  • Increased muscle
  • Fibrosis
  • Emphysema
114
Q

What type of inflammation occurs in COPD?

A
  • Macrophage and neut based inflamm (neutrophil elastase), IL-8 (neut recruiter), Fibroblasts
  • mucus
115
Q

What are the 3 classifications of COPD?

A
  • Mild ( few symptoms, moderate exertion breathlessness, chest inflections, no effect on daily activities- FEV1 60-80%)
  • Moderate ( exacerbations that need coticosteroids and/or antibiotics etc FEV1 40-59%)
  • Severe ( minimal exertion breathlessness, chronic cough, regular sputum production- FEV1 <40%)
116
Q

What is a characteristic COPD PEF and FEV1?

A
  • They will both bee decreased
  • FEV1 will be lower due to decreased rate of expiration
  • PEF (peak expiratory flow rate) and extreme coving (someone can’t breathe out) = OBSTRUCTION
117
Q

What are some non-pharmacological treatments for COPD?

A
  • Assess the severity
  • Identify/avoid risk factors
  • cease smoking
  • flu vaccine
  • treat comorbidities
  • Assess exercise capacity

BMS3052 (14 decks)

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