PBL 3 - smoking, COPD etc Flashcards
1
Q
what does COPD stand for?
A
chronic obstructive pulmonary disease
2
Q
what does COPD consist of?
A
chronic bronchitis + emphysema
3
Q
what is the definition of COPD?
A
a disease state characterised by airflow limitation that is not fully reversible
4
Q
what is chronic bronchitis?
A
long-term inflammation of the mucous membranes of the bronchi
5
Q
what are causes of chronic bronchitis?
A
- caused almost entirely by smoking
- infection — viral, bacterial
- air pollution — smog
- occupational exposure
6
Q
bronchitis effects on bronchi and mucus
A
- immobilisation and damage to cilia (due to cigarette smoke)
- enlargement of mucus secreting glands in the trachea and bronchi, leading to hypersecretion of mucus
- bronchial mucosal inflammation
- progressive airflow limitation
7
Q
what is the effect of paralysed cilia on mucus?
A
mucus gets stuck
8
Q
name 4 structural histological changes in chronic bronchitis
A
- much more mucus glands in smoker = more mucus
- fibrous tissue
- inflammation
- smooth muscle cell hypertrophy
9
Q
how does mucus build up cause inflammation?
A
mucus that airway hasn’t been able to shift collects bacteria — more inflammation
10
Q
how does fibrous tissue affect the airways?
A
makes the airway rigid — failure to get rid of mucus by coughing — remodelling of airway — airways less able to contract and expand
11
Q
pathogenesis of chronic bronchitis
A
- primary or initiating factor is the long-standing irritation by inhaled substances (eg. tobacco smoke)
- initially, proteases released from neutrophils stimulate mucus hypersecretion in the large airways
- results in hypertrophy of the submucosal glands in the trachea and bronchi
- increase in goblet cells of small airways leads to excess mucus production — contributes to airway obstruction
- it is thought that both the submucosal gland hypertrophy and the increase in goblet cells are protective meta plastic reactions against tobacco smoke or other pollutants
12
Q
what is emphysema?
A
long term, progressive disease of the lungs in which there is loss of alveolar walls, reducing SA for exchange of gases
13
Q
what are alveolar walls and their elasticity critical for?
A
the retention or potency of small airways
14
Q
why is emphysema an obstructive lung disease?
A
because airflow on exhalation is slowed or stopped
15
Q
what is responsible for opening up air spaces in inhalation?
A
elasticity of the alveolar walls
16
Q
how does emphysema affect the opening and closing of air spaces?
A
it is reduced because emphysema destroys the alveolar walls so the airway opening by pull of elasticity is reduced
17
Q
what are the 2 main types of emphysema?
A
centriacinar (centrilobular) and panacinar (panlobular)
18
Q
what is the main difference between the 2 types of emphysema?
A
- centrilobular is associated with smoking (more common)
- panlobular is inherited
19
Q
what do tobacco products release from white cells and what is the effect?
A
- release inflammatory products from white cells, mainly neutrophil polymorphs
- these inflammatory products break down elastic tissue
20
Q
what does tobacco products inhibit?
A
a-1-antitrypsin therefore more elastase activity breaking down air space walls
21
Q
what does circulating a-1-antitrypsin usually do?
A
has anti-elastase activity (elastase breaks down alveolar walls)
22
Q
what happens to the size of airspaces in emphysema compared to a normal lung?
A
airspaces on average are 2x the diameter of a normal lung
23
Q
if the diameter of air spaces 2x normal, what is the effect on oxygen transfer?
A
decreases area of wall available for oxygen transfer = 16x less (2^3)
24
Q
what is pulmonary fibrosis?
A
excess deposition of collagen and other extracellular matrix components in the lungs = “scarring of the lung”
25
what is the most common form of smoking-related interstitial lung disease?
idiopathic pulmonary fibrosis
26
what happens to type 1 and 2 pneumocytes in pulmonary fibrosis?
- loss of type 1 pneumocytes (thin and squamous, responsible for gas exchange)
- replaced by type 2 pneumocytes (make alveolar surfactant, failure of normal maturation)
27
symptoms of lung fibrosis
- dry cough on exertion
- progressive SOB with exercise
- crackles on auscultation (velcro-like)
- finger clubbing
- inexorable progression
28
what is pulmonary fibrosis associated with?
reduced FVC but normal FEV1/FVC ratio
29
where do most secondary lung cancers arise from?
breast, kidney and GIT
30
clinical features of lung cancer
- weight loss
- cough — tumours infiltrate nerves of the airways
- haemoptysis — tumours infiltrate the blood vessels and allow them to leak into the lumen
- dyspnoea
- finger clubbing
- voice change
- effects of metastasis in other organs
- non-metastatic distant effects
31
what are the 4 histological classifications of primary lung cancer?
1. squamous cell carcinoma (20-30%): arise in the areas where the mucosa has undergone metaplasia as a response to the irritation caused by tobacco smoke
2. small cell carcinoma (15-20%): arise from neuroendocrine components of the airways (bronchitis has lots of little neuroendocrine cells at the base of the respiratory epithelium — these can respond to persistent irritation by becoming neoplastic)
3. adenocarcinoma (30-40%)
4. large cell undifferentiated carcinoma (10-15%)
DONT LEARN %
32
what is the “therapeutic” classification of primary lung cancer?
- small cell lung cancer (SCLC) vs NSCLC
| - central vs peripheral
33
what is amelioration?
the act of making something; improvements
34
what is palliation?
making a disease (or symptoms) less severe without removing the cause
35
SCLC treatment
- generally incapable of being treated by resection at th time of 1st diagnosis
- treated with amelioration and palliation
- can be treated with chemotherapy — increases survival but doesn’t allow them to reach a tumour-free state
36
where are central lung cancers? treatment?
- occur in bronchi near the hilum
| - difficult to treat by surgery — can’t get a resection margin as it is so close to the trachea bifurcation
37
what are peripheral lung cancers usually? treatment?
- often adenocarcinomas
- typically less aggressive than other forms
- more capable of surgical curative resection — lobectomy
38
what are the 3 main pathological effects in COPD?
1. loss of elasticity of the alveoli
2. inflammation and scarring — reducing the size of the lumen, as well as reducing elasticity
3. mucus hypersecretion — reducing the size of the lumen and increases diffusion distance
39
what are proteases released from and what do they stimulate?
proteases released from neutrophils — stimulate mucus hypersecretion in the large airways
40
what does mucus hypersecretion result in?
hypertrophy of the submucosal glands in the trachea and bronchi (increase in goblet cells)
41
how does excess collagen deposition result in a loss in alveolar expansion?
scarring = rigid airway —> failure to get rid of mucus by coughing —> remodelling of airway —> airways less able to contract and expand
42
what is inherited a-1-antitrypisn deficiency associated with?
fewer and larger alveoli
43
describe genetic a1-antitrypsin inheritance. what % of COPD cases does it account for?
- autosomal dominant
- if this enzyme is deficient, several proteases including trypsin, elastase and collagenases aren’t destroyed — therefore continue to eat away at lung tissue
- 2%
44
why are more proteinases released in the lung in a smoker/someone with emphysema?
there are more inflammatory cells such as macrophages around which release proteinases
45
what are other causes of COPD?
- pet dander (trigger)
- smoking
- coal mining
- air pollution
- low socioeconomic status
- low birth weight
- asthma
46
signs of COPD
- tachypnoea
- use of accessory muscles of respiration
- reduced chest expansion
- resonant chest sounds — suggestive of hyperinflation
- wheeze — due to narrowed airways
- cyanosis
- cor pulmonale
- prolonged expiration
- pursed lip breathing
47
what is cor pulmonale and what is it often due to?
failure of RHS of heart, often due to pulmonary hypertension
48
why do COPD patients have prolonged expiration?
because FEV1 is low, they have a prolonged expiratory phase to allow for adequate respiration
49
why is FEV1 reduced in COPD?
airways are narrowed or inflamed — hinders how fast air can leave the lungs
50
why does pursed lip breathing improve gas exchange?
creates smaller opening through which air can exit the respiratory system, thus keeping the pressure in the airways high — helps prevent smaller airways from collapsing, maintaining a larger SA for gas exchange
51
what is required to confirm a diagnosis of COPD?
spirometry
52
in patients with loss of pulmonary elastic tissue, what exceeds the elastic recoil of the lung tissue?
the recoil of the chest wall
53
what would a CXR of a patient with emphysema show?
areas with reduced lung markings
54
restricted vs. obstructive disease FEV1/FVC
restricted disease: FEV1/FVC over 75%
obstructive disease: FEV1/FVC less than 75%
55
what is vital to managing COPD?
smoking cessation
56
what does nicotine stimulate?
the release of dopamine
57
what does nicotine imitate?
- Ach
| - binds to nicotinic receptors
58
what is the effect of nicotine binding to nicotinic receptors?
- nicotine, unlike Ach, is not regulated by the body
- therefore body increases levels of Ach dye to all the unregulated stimulation
- heightened activity in cholinergic pathways in the brain — feel re-energised and also increases the amount of dopamine released — activates reward pathways
- also stimulates release of glutamate
59
what is glutamate involved in?
learning and memory — enhances connections between the sets of neurons — these stronger connections create a memory loop of the good feelings you get and further drive the desire to use nicotine
60
what is the effect of nicotine on blood vessels?
causes blood vessels to constrict or narrow, which limits the amount of blood that flows to organs
61
what is the result of constant constriction of vessels?
blood vessels become stiff and less elastic — cells receive less oxygen and nutrients
62
what is the effect of constricted vessels on the heart?
HR and BP increase to compensate for reduced delivery of oxygen — can contribute to clots forming in arteries
63
effect of carbon monoxide on oxygen?
CO binds Hb which decreases the amount of O2 that’s can bind to form HbO — cells therefore receive less O2
64
effect of smoking on cilia?
smoking paralyses and eventually destroys the cilia in our airways
65
effect of smoking on lungs in general?
- airways become irritated and inflamed, making them narrow — harder for air to get in and out of the lungs
- lungs become stiffer as the sacs lose their elasticity and deflate — harder for them to expand and take the O2 in and then recoil to remove the waste gas (CO2)
66
what does tobacco inhibit?
a1-antitrypsin
67
what is the inflammatory response from neutrophils to tobacco smoke?
mucus hypersecretion
68
what is tar?
sticky brown substance in cigarettes that collects in the lungs — contains cancer-causing chemicals
69
who and where is COPD most common?
- most common in Scotland and NE/NW of England
- more common in men
- most common in people over 40
- highest prevelance in white population, lowest in black
70
what is pneumonia?
a common lower respiratory tract infection, characterised by inflammation of the lung tissue. it is almost always an acute infection and almost always characterised by bacteria. diagnosis is typically confirmed by a CXR
71
what do the alveoli contain in pneumonia?
fluid and blood cells
72
what happens to the alveolar walls in pneumonia?
they become thickened by oedema
73
what is the most common cause of pneumonia?
Streptococcus pneumoniae
74
what does pneumonia infection begin with?
infection in the alveoli — pulmonary membrane becomes inflamed and highly porous so that fluid and even red and white blood cells can leak out of the blood into the alveoli — infection spreads from alveolus to alveolus
75
what happens due to the decreased total SA for gas exchange and decreased ventilation-perfusion ratio in pneumonia?
hypoxia and hypercapnia
76
what oxygen saturation is worrying?
<92%
77
what may XR show in pneumonia?
show infiltrate in the form of consolidation — can also show the spread of any infection by distribution of the infiltrate
78
what is CURB-65 score?
- confusion
- urea
- respiratory rate
- blood pressure
- >65 years
79
describe streptococcus pneumoniae
- lancet-shaped
- gram positive
- facultative anaerobic bacteria
- more than 90 different strains
- present in lots of people
80
describe covid pneumonia
- viral pneumonia
- tends to be in both lungs
- air sacs in the lungs fill with fluid, limiting their ability to take in oxygen and causing SOB, cough and other symptoms
- can be very severe, causing low levels of oxygen in the blood and lead to respiratory failure and in many cases a condition called acute respiratory distress syndrome (ARDS)
81
what type of cancer causes the most number of deaths?
lung cancer
82
what does green or yellow phlegm indicate?
- sign of infection
- colour comes from WBCs
- may start yellow then progress to green
- change occurs with the severity and length of potential sickness
- commonly caused by bronchitis, pneumonia, sinusitis, CF
83
what does brown phlegm indicate?
- old blood gives brown colour
| - commonly caused by bacterial pneumonia, bacterial bronchitis, CF, pneumoconiosis, lung abscess
84
what causes white phlegm?
- viral bronchitis
| - COPD
85
what does clear phlegm indicate?
- phlegm is mostly filled with water, protein, antibodies, and some dissolved salts to help lubricate and moisturise the resp system
- an increase in clear phlegm may mean body is trying to flush out an irritant such as pollen, or some type of virus
- commonly caused by allergic rhinitis (hay fever), viral bronchitis, viral pneumonia
86
what does red or pink phlegm indicate?
- blood in phlegm
| - commonly caused by pneumonia, TB, congestive heart failure (CHF), pulmonary embolism, lung cancer
87
what are the different layers of the very thin respiratory membrane?
1. a layer of fluid (surfactant) lining the alveolus
2. the alveolar epithelium of thin epithelial cells
3. an epithelial basement membrane
4. a thin interstitial space between the alveolar epithelium and capillary membrane
5. the capillary endothelial membrane
88
what are type 1 alveolar cells?
form wall of alveoli — simple squamous epithelium
89
what are type 2 alveolar cells?
produce surfactant — reduce surface tension
90
what is NRT?
= nicotine replacement therapy
- all forms of NRT increase the likelihood that attempt to quit smoking will succeed (by 50-60%)
- gum, transdermal patch, nasal spray, inhaler, sublingual tablets/lozenges
91
what is Varenicline (Champix)?
reduces cravings for nicotine but also blocks reward centres
92
what is Bupropion (Zyban)?
- affects reward centres
93
did more people stop smoking with NRT, Champix or Zyban?
Champix
- standard dose of champix more than doubled chances of quitting compared to placebo
94
what is operant conditioning?
about rewards and punishment — when we reward a behaviour, the behaviour increases. when we punish, behaviour decreases.
can relate to smoking cessation
95
positive vs negative punishment?
```
+ve = giving a punishment
-ve = taking away a punishment you were going to give
```
96
what is a normal FEV1/FCV ratio?
approx 70-85% (declines with age)
97
name 4 obstructive diseases
- asthma
- COPD
- chronic bronchitis
- emphysema
98
what happens to FEV1 in obstructive diseases and why?
it decreases because of increased airway resistance to expiratory flow
99
what happens to FVC in obstructive diseases?
may be decreased too, but not as much as FEV1, due to the premature closure of airway in expiration
100
what receptors does SARS-CoV2 attach to?
ACE2
101
what are the benefits of exercise in managing COPD?
- exercise helps the blood to circulate and helps the heart send oxygen to the body
- strengthens respiratory muscles — easier to breathe
- increases strength and energy levels and reduces fatigue
- can decrease risk of infection
- may help stop smoking — can reduce nicotine withdrawal symptoms
- makes you feel happier
102
what is bronchiectasis?
- an obstructive lung disease
- causes local irreversible dilation of the bronchial tree
- almost always a result of bronchial obstruction leading to infection with inflammation (distal to the obstruction)
- likely result of CF
- more of a complication of other conditions
103
what is the pathophysiology of bronchiectasis?
- an initial insult to the bronchi (eg. infection) results in immune cells being recruited to the bronchi
- these immune cells secrete cytokines and proteases, leading to inflammation
- this inflammation damages the muscle and elastin in the bronchial walls, leading to bronchial dilation
- in most people, this bronchial dilation is reversible however in patients with bronchiectasis, several factors prevent the bronchial dilation from reversing (eg. impaired mucociliary clearance)
- dilated bronchi are predisposed to persistent microbial colonisation, as mucus traps in the dilated bronchi
- vicious cycle — airways are colonised by micro-organisms — increases inflammation — worsening on bronchiectasis — increased susceptibility to airway colonisation
104
what is the pathophysiology of interstitial lung disease?
- there is inflammation and fibrosis in the lung interstitium
- fibrosis is triggered by repeated injury to the lung tissue (eg. from inhaled toxins)
- usually, fibroblasts respond to this lung injury by secreting extracellular matrix, which repairs the injuries
- in ILD, genetic mutations lead to excess secretion of extracellular matrix — accumulates in the lung interstitium, leading to fibrosis
- the lung interstitium becomes thicker, increasing the diffusion distance for oxygen to travel from the air to the alveoli to the blood in surrounding capillaries
- hence gas exchange in the lungs is compromised
105
what are the typical symptoms of interstitial lung disease?
- progressive exertional dyspnoea
- dry cough
- connective tissue disease symptoms (eg. arthralgia (joint stiffness), difficulty swallowing and dry eyes), general malaise and fatigue (due to underlying connective tissue disease or vasculitis (inflammation of blood vessels) )
106
what is fibrosis triggered by?
repeated injury to lung tissue from eg. inhaled toxins
107
what is the maximum volume in lungs?
tidal volume + inspiratory reserve volume + expiratory reserve volume + residual volume
108
what is the most common risk factor for mesothelioma?
past exposure to asbestos
109
what is 2,3-BPG?
a molecule which binds to Hb and decreases its affinity for O2
110
what role does the Herig-Breuer reflex play in breathing?
terminates inspiration to prevent hyperinflation of the lugs
111
what are symptoms of pink puffer (emphysema)? what is not a symptom?
- pursed lip breathing
- hyper inflated lungs
- barrel chest
- tachypnoea
NOT cyanosed skin
112
what is an example of a mucolytic drug?
carbocysteine
113
what is the moa of clarithromycin?
binds to the 50s subunit of bacterial ribosome and inhibits translation of peptides
114
what is the most common form of emphysema?
centriacinar
115
how does the social learning perspective differ from the disease model of addiction?
1. addictive behaviours are seen as acquired habits, which are learned according to the rules of social learning theory
2. addictive behaviours can be unlearned; they are not irreversible
3. addictive behaviours lie along a continuum; they are not discrete entities
4. addictive behaviours are no different from other behaviours
116
what is contingency contracting?
a procedure aimed to punish smoking and drinking and reward abstinence
117
approx ow many children per year are born with homozygous a1-anti trypsin deficiency?
1 in 500
118
what buffer system plays a supporting role in the ECF?
phosphate buffer system
119
what does COPD cause in terms of FEV1/FVC and PEFR?
reduced fev1/fvc and reduced pefr
120
what disease is defined as an anatomically abnormal enlargement of the alveolar spaces?
emphysema
121
what factors predict compliance under the Ley cognitive hypothesis model of patient compliance?
understanding, satisfaction and memory
122
central chemoreceptors in the medulla are stimulated mainly in response to changes in what?
PCO2
