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Year 1 HLB Respiratory > Asthma and COPD: Aetiologies, Symptoms and Aids to Diagnose > Flashcards

Asthma and COPD: Aetiologies, Symptoms and Aids to Diagnose Flashcards

1
Q

What is obstructive airway disease?

A
  • narrowing of the airways
  • large, medium and small airways affects
  • inhale but difficult to exhale
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2
Q

In obstructive lung disease we can see hyperinflammation and trapping of air, why is this?

A
  • air becomes trapped in <2cm sized airways
  • increased mucus causing mucus plugs
  • ⬇️ elastic recoil
  • forced vital capacity may appear normal
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3
Q

What type of hypersensitivity is asthma?

A
  • type I hypersensitivity
  • hyper responsive to stimuli
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4
Q

Is asthma reversible or permanent?

A
  • reversible
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5
Q

What is atopy?

A
  • genetic susceptibility
  • susceptible to allergic reactions
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6
Q

What as the 4 basic symptoms of asthma?

A

1 - wheezing

2 - breathlessness

3 - cough

4 - chest tightness

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7
Q

Do patients with asthma always have symptoms?

A
  • no
  • can have acute attacks or be normal
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8
Q

What does the British Thoracic Society (SIGN) say about the symptoms of asthma, to be diagnosed with asthma?

A
  • must have 1 or more of the common symptoms
  • wheezing, breathlessness, cough or chest tightness
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9
Q

What does the British Thoracic Society (SIGN) say about the reversibility of asthma?

A
  • diagnosis of asthma must show its reversible
  • variable air flow improves with treatment
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10
Q

Roughly how many people a year die due to asthma?

A
  • 3-5 people
  • poor asthma management and education
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11
Q

Is asthma more common in adults of children?

A
  • children
  • more likely to develop allergies
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12
Q

What is the prevalence of asthma in UK adults and children?

A
  • adults = 8%
  • children = 20%
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13
Q

In patients with atopy (genetic susceptibility) what antibody do they produce a lot of that triggers the hypersensitivity?

A
  • IgE
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14
Q

Is asthma caused by one thing?

A
  • no
  • multifactorial, but needs a stimulus
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15
Q

In patients with atopy, are they likely to have other allergies?

A
  • yes
  • hayfever, rhinitis, eczema and urticaria (hives)
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16
Q

In patients with atopy, why is it important to ask them about family history?

A
  • genetic
  • may run in family
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17
Q

What is skin prick testing?

A
  • patients will receive small prick on arm
  • then exposed to multiple common allergans
  • positive test = raised skin
  • IgE can then be measured in blood if positive
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18
Q

Patients with atopy and asthma have polygenic inheritance, what does that mean?

A
  • multiple genes cause traits - traits may be asthma or allergies
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19
Q

What is a common chromosome where atopy and asthma have been shown?

A
  • 11q13
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20
Q

What is Dermatophagoides pteronyssinus more commonly known as?

A
  • dust mite
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21
Q

Generally what are the 2 common things that need to occur for someone to have an asthma attack?

A

1 - sensitisation of atopic patient

2 - inhalation of allergen

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22
Q

Asthma can be divided into a 2 stage process, how long does each phase last?

A

1 - phase 1 = 20 minutes

  • IgE binds to mast cells and degranulate.

2 - phase 2 = 6-12 hours

  • T cells, mast, basoinophil and esionphils cells all migrate to lungs and induce bronchoconstriction and inflammation
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23
Q

Which lymphocytes regulate the inflammatory response in asthma?

A
  • T lymphocytes
  • specifically T helper cells
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24
Q

T1 and T2 are classes of T helper cells, which is inflammatory and which is anti-inflammatory?

A
  • T1 = anti-inflammatory
  • T2 = inflammatory
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25
Q

Once IgE has been produced by B cells, what does IgE generally bind with in an asthma attack?

A
  • mast cells
  • basophils and eosinophils also involved
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26
Q

What is the process mast cells undergo to release inflammatory stiumulus?

A
  • degranulation
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27
Q

What is the initial compound released from mast cells during an asthma attack?

A
  • histamine
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28
Q

In addition to histamine release, what else is released during an asthma attack that is able to stimulate inflammation further?

A
  • leukotrienes
  • prostaglandins
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29
Q

Why do anti-histamines not work in asthma?

A
  • other inflammatory mediators involved
  • such leukotrienes and prostoglandins
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30
Q

In an asthma attack what is the main problem histamines, leukotrienes and prostaglandins cause?

A
  • bronchospasm
  • bronchoconstriction
  • followed by inflammation
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31
Q

In asthma attacks, why do treatments target histamines, leukotrienes and prostaglandins?

A
  • target inflammation - target bronchospasm
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32
Q

In the late phase response of an asthma attack, vasodilation occurs in addition to bronchoconstriction. What does this encourage?

A
  • ⬆️ permeability
  • same as in acute inflammation
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33
Q

In an asthma attack increase permeability leads to infiltration of the smooth muscle by what immune cells?

A
  • neutrophils, basophils and eosinophils (granular)
  • monocytes and dendritic cells
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34
Q

In an asthma attack increase permeability leads to infiltration of the smooth muscle of immune cells, what can this do to the epithelial cells?

A
  • desquamation (shedding of cells)
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35
Q

In a late phase asthma attack what happens to goblet cells?

A
  • hyperplasia - ⬆️ mucus production - ⬆️ plugging and blocking of airways
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36
Q

In a late phase asthma attack what happens to smooth muscle cells?

A
  • hypertrophy and hyperplasia
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37
Q

What causes smooth muscles to contract during a late phase asthma attack?

A
  • cytokines
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38
Q

What is polyphonic wheezing?

A
  • lots of different whistling/wheezing sounds - caused by different size airways
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39
Q

Patients with asthma can experience dynamic hyperinflammation, how small do bronchi generally have to become for air to be trapped and for dynamic hyperinflammation to occur?

A
  • <2cm
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40
Q

Although asthma is generally reversible, what can happen if not managed and asthma becomes chronic?

A
  • remodelling of airways due to chronic inflammation
  • collagen deposition
  • fibrotic tissue replaces parenchymal tissue
  • fixed narrowing
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41
Q

Are eosinophils in asthma attacks generally associated with acute or chronic asthma?

A
  • acute - inflammation and airway obstruction
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42
Q

Are neutrophils in asthma attacks generally associated with acute or chronic asthma?

A
  • chronic
  • inflammation and steroid dependent asthma
  • just like in COPD, chronic marker in WBCs
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43
Q

What is the main cell in an asthma attack that causes bronchospams?

A
  • mast cells
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44
Q

What are a few environmental triggers for asthma?

A
  • animal hair, pollen, mould
  • infections (viral/bacterial)
  • pollution
  • perfumes and sprays
  • smoking
  • chlorine
  • temperature changes
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45
Q

What are some common drugs that may contribute to an asthma attack?

A
  • aspirin and NSAIDs (some anti-inflammatory pathways are ⬇️)
  • B-blockers (off target effects, B1 and 2 can be affected)
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46
Q

What are some basic physiological, non disease specific aspects that may cause asthma?

A
  • pregnancy
  • premenstrual (pre period)
  • exercise
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47
Q

Can peoples jobs contribute to asthma?

A
  • yes
  • occupational asthma is main occupational lung disease
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48
Q

What is diurnal variability?

A
  • variation in peak expiratory flow
  • measured over 24 hours
  • >20% variation is a diagnosis of diurnal variability
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49
Q

During an acute exacerbation of asthma, what may happen to respiratory rate?

A
  • ⬆️ respiratory rate
  • body attempts to ⬆️ O2
  • tachypnoea (abnormal rapid breathing)
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50
Q

During an acute exacerbation of asthma, what may happen to heart rate?

A
  • ⬆️ heart rate - tachycardia
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51
Q

In severe asthma, what can happen to the colour of finger tips and skin?

A
  • cyanosis - blue skin
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52
Q

What is normal respiratory rate and what might you expect in asthma?

A
  • normal = 12-16 breaths/min - asthma = >20 breathes/min
53
Q

What is a silent chest?

A
  • no sound heard from chest
  • RED FLAG
  • VERY dangerous
54
Q

What is also common in silent chests?

A
  • bradycardia
  • body is shutting down
55
Q

In patients with suspected asthma, why would a full blood count be helpful?

A
  • measure eosinophils as part of WBCs
  • eosinophils associated with acute asthma
56
Q

In patients with suspected asthma, in addition to a full blood count, what other protein in blood can be useful to measure that may have contributed to the asthma attack?

A
  • IgE
  • identify atopy
57
Q

Why might PEF and a PEF diary be useful in patients with suspected asthma?

A
  • diurnal relates top variation in a day
  • non asthmatics have very small variability in PEF
  • asthmatics are likely to have variation throughout day
58
Q

What are the 2 main scans that will be performed on the chest if a patient is suspected with asthma?

A
  • chest X-ray - high sensitivity CT may be performed
59
Q

In a patient with suspected asthma why might a spirometry test and/or full lung function test be useful?

A
  • identify if symptoms are reversible - distinguish between obstructive and restrictive
60
Q

In asthma is FEV1 or FVC reduced more?

A
  • FEV1
61
Q

In asthma what would the FEV1/FVC ratio be expected to be?

A
  • <70%
  • due to reduction in FEV1
62
Q

To determine if the asthma is reversible what may patients be given, and how long would this take to take effect?

A
  • short acting B agonist (salbutamol) - over 20 minutes
63
Q

To determine if the asthma is reversible patients can be given a short acting B agonist (Salbutamol), what improvement in FEV1 is needed to determine if the asthma is reversible?

A
  • >15%
64
Q

In patients with asthma, why might the patients total lung capacity increase and their residual lung volumes increase?

A
  • due to hyperventilation and air trapping
65
Q

In patients with asthma, would DLCO/TLCO be low or normal?

A
  • normal as interstium and alveoli are not generally affected
  • if air reaches alveoli it will perfuse
  • ventilation is low though
66
Q

What can be seen in X-rays in some patients with asthma?

A
  • hyperinflammation
67
Q

In patients with hyperinflammation due to asthma, how may ribs will be evident posteriorly and anteriorly?

A
  • anterior = >6 ribs
  • posterior = 10 ribs in mid clavicular line
68
Q

What is COPD?

A
  • restrictive lung disease
  • progressive airflow obstruction
  • not fully reversible
  • symptoms always present
69
Q

The risk of COPD increases with age, at what age does the risk generally start to increase?

A
  • >35 years
70
Q

In addition to the natural progression of COPD, what is the main cause that accentuates COPD?

A
  • smoking
  • 90% of COPD is caused by smoking
71
Q

How much FEV1 generally decline each year in COPD patients?

A
  • 30ml/year
72
Q

What % of the UK is diagnosed with COPD?

A
  • 2%
73
Q

How many deaths in the UK are caused by COPD?

A
  • 30,000
74
Q

How many GP and hospital admissions are due to COPD?

A
  • 1.4 million GP appointments - 12.5% (1/8) of acute hospital admissions
75
Q

Are respiratory inhalers expensive for the NHS?

A
  • yes - top 5 costliest drug - 29% of respiratory disease costs
76
Q

What is the formula for calculating pack years in COPD?

A
  • (no. cigs per day x years) / 20
  • divide by 20 as packs contain 20 cigarettes
  • e.g 10 cigs for 10 years = (10x10)/20 = 5 pack years
77
Q

Why are pack years calculated in COPD?

A
  • ⬆️ pack years = ⬆️ risk of COPD
  • main risk factor for COPD
78
Q

Can pipes and cigars increase the risk of COPD?

A
  • yes - less than smoking though
79
Q

Can passive smoke increase risk of COPD?

A
  • yes
80
Q

In patients who smoke, what % go on to develop COPD?

A
  • aprox 15-25%
81
Q

Can occupational exposure (coal, dust etc.) and air pollution increase the risk of COPD?

A
  • yes
82
Q

Why is the inverse care law important in COPD?

A
  • ⬇️ socio-economic = ⬆️ risk of COPD
83
Q

What is trypsin?

A
  • enzyme that digests proteins
84
Q

What is alpha-1 antitrypsin?

A
  • protease inhibitor
  • inhibits elastase in lungs following pathogen death
  • elastin cannot be broken down
85
Q

Why does alpha-1 antitrypsin deficiency cause COPD?

A
  • elastaste destroy pathogens, but also degrade elastin
  • alpha-1 antitrypsin inhibits elastate following pathogen death
  • in pathients with deficiency, such as in COPD, lungs elastin ⬇️
  • lungs lose elastic properties and cannot exhale
  • can cause emphysema
86
Q

What forms of COPD can alpha-1 antitrypsin deficiency cause?

A
  • causes emphysema (damaged alveoli)
  • chronic bronchitis (damaged bronchi, main airways)
  • bronchieltasis (smaller airways)
87
Q

What is chronic bronchitis as a form of COPD?

A
  • affects upper airways
  • hyperplasia of goblet cells
  • ⬆️ mucus production blocking airways
  • ⬆️ risk of infection
88
Q

What is the diagnosis of chronic bronchitis as a form of COPD?

A
  • sputum production >3 months/year - 2 consecutive years
89
Q

Chronic bronchitis is a form of COPD, what symptoms can patients present with?

A
  • breathlessness, mainly on exertion - gets worse over time - thick creamy sputum
90
Q

What is emphysema as a form of COPD?

A
  • destruction of alveoli distal to terminal bronchiole
  • ⬇️ in elastic properties
  • ⬇️ surface area
  • interstitium becomes fibrotic and ⬇️ perfusion
91
Q

If the interstium is damaged or blocked in COPD, what happens to the TLCO/DLCO?

A
  • reduced - CO cannot diffuse
92
Q

How can smoking increase risk of COPD?

A
  • smoke activates neutrophils in lungs
  • neutrophils release elastase to clear damaged tissue
  • chronic smoking = chronic neutrophils and inflammation
93
Q

What is a large bullae?

A
  • damaged alveolar sacs - small alveoli form one large sac called a bullae
94
Q

In emphysema what happens to surface area and perfusion?

A
  • ⬇️ surface area - ⬇️ perfusion
95
Q

In COPD there is hyperplasia of goblet cells, which increases mucus production. What can this lead to in the lung of a patient with chronic bronchitis?

A
  • ⬆️ viscous mucus - ⬆️ infection as mucus acts as a medium - damaged cilia - fixed airway obstructions
96
Q

In COPD there is a reduction in elastic properties, how does this cause an increase in air trapping?

A
  • following inspiration airways collapse
  • elastic recoil of lungs forces air out, but not possible in COPD
  • air becomes trapped
97
Q

Why can trapped air and reduced elastic properties of the lungs increase work of breathing?

A
  • expiration is generally passive due to elastic recoil
  • accessory muscles need to be used to exhale causing fatigue
  • pursed lip breathing helps
  • both require more energy
98
Q

When trying to diagnosis a patient with suspected COPD, what are the 2 most important risk factors to consider?

A
  • age (>35 years)
  • smoking duration
99
Q

What are the most common symptoms in COPD?

A
  • breathlessness on exertion (important distinction with asthma)
  • chronic cough
  • chronic sputum production
  • winter bronchitis
  • wheeze
  • frequent infections
  • peripheral oedema (end stage COPD)
100
Q

When performing a spirometry test on a patient with COPD, would there be a >15% improvement in FEV1, and what would the FEV1/FVC ratio be?

A
  • no improvement in FEV1 - FEV1/FVC ratio is <70%
101
Q

In patients with suspected COPD due to their symptoms, but also present with significant weight loss is a red flag for what?

A
  • lung cancer
102
Q

What is haemoptysis?

A
  • coughing up blood - red flag for lung cancer
103
Q

What is the respiratory rate of a patient with COPD expected to be?

A
  • tachypnoea - >20 breaths/min
104
Q

Why might patients with COPD experience flapping or muscle tremors?

A
  • due to CO2 build up
  • chronic use of B2 agonist activate B2 receptors in skeletal muscle
105
Q

Why might we see an increase in jugular venous pressure in patients with COPD?

A
  • increased pressure in lungs moves back through pulmonary artery and into right side of the heart
  • pressure in right side of heart increases
  • right heart failure increases pressure
106
Q

Would patients with COPD be more likely to develop type 1 or 2 respiratory failure?

A
  • type 2 respirator failure - ⬇️ PaO2 and ⬆️ PaCO2
107
Q

Breathing difficulty is associated with severity of COPD, what is the method for classifying breathlessness?

A
  • mMRC - modified Medical Research Council Scale
108
Q

When defining the severity of COPD, what method defines the severity of COPD and in spirometry values, what would we expect the FEV1/FVC to be lower than?

A
  • GOLD initiative
  • in patients with FEV1/FVC <70%
109
Q

In COPD will pulse oximetry always be low?

A
  • no - but can <92% during exertion
110
Q

Why would polycythaemia, which is high RBCs, be common in patients with COPD?

A
  • patients with COPD have low PaO2
  • bone marrow increases RBCs to increase haemoglobin and increase O2 saturation
  • attempt to increase PO2
111
Q

If cor pulmonale is suspected in patients with COPD, what are the 2 most common cardiac assessments?

A
  • ECG - electrocardiogram - right ventricle failure and hypertrophy
112
Q

What are 2 common assessments of quality of life in patients with COPD?

A
  • COPD Assessment Test (CAT) - St. Georges Respiratory Questionnaire (SGRQ)
113
Q

What are predominant cells in asthma and COPD?

A
  • asthma = eosinophils
  • COPD = neutrophils (N is closer to C than A in COPD and Asthma)
114
Q

In asthma and COPD what is the major difference in FEV1/FVC ratio?

A
  • both have a FEV1/FVC <70% - asthma = reversible - COPD = non reversible
115
Q

In asthma and COPD what is the major difference in DLCO/TLCO?

A
  • asthma = normal TLCO/DLCO
  • COPD = ⬇️ TLCO/DLCO
116
Q

In asthma and COPD what is the major difference in lung structure?

A
  • asthma = normal structure - COPD = remodelled structure
117
Q

What is sleep apnea?

A
  • cessation of breathing when asleep
118
Q

What is obstructive sleep apnea?

A
  • cessation of breathing due to obstructive lung problem
119
Q

What is hyponea?

A
  • slow breathing
120
Q

How common is obstructive sleep apnea in men and women?

A
  • male = 3-7% - female = 2-5%
121
Q

Which part of the airway is most commonly affected in obstructive sleep apnea?

A
  • upper airways collapsing
122
Q

What are common symptoms for patients with obstructive sleep apnea/hyponea?

A
  • snoring
  • apnoeic (means without breath) episodes (>10 secs)
  • excessive daytime sleepiness (Epworth Sleepiness Scale)
  • nocturnal choking
  • morning headaches
  • unrefreshed upon waking
  • nocturia (urinating at night)
  • ⬇️ concentration, libido, memory
123
Q

What is the Epworth Sleepiness Score?

A
  • diagnostic test for obstructive sleep apnea
124
Q

What can obstructive sleep apnea/hyponea cause?

A
  • hypoxia as not breathing - sleep fragmentation
125
Q

What are some common risk factors for obstructive sleep apnea/hyponea?

A
  • obesity
  • ⬆️ collar size
  • enlarged tongue/tonsils
  • long uvular
  • nasal pathology
  • down syndrome
126
Q

What are the 3 most common methods for diagnosing obstructive sleep apnea/hyponea?

A

1 - overnight oximetry 2 - full polysomnography 3 - Epworth Sleepiness Score

127
Q

What are the common treatment options for obstructive sleep apnea/hyponea?

A
  • weight loss - surgery - mouth guards - continuous airway pressure (CPAP)
128
Q

What are some red flags in lung disease that may suggest serious lung disease such as cancer?

A
  • haemoptysis (coughing up blood)
  • persistent unexplained fever
  • persistent unexplained night sweats
  • weight loss
  • stridor (high pitched wheezing)
129
Q

Which is the main myeloid lineage cell that is associated with COPD and asthma?

A
  • asthma = esinophils
  • COPD = nurtrophils

Year 1 HLB Respiratory (25 decks)

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