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PBL SEM 2 > PBL 3 - smoking, COPD etc > Flashcards

PBL 3 - smoking, COPD etc Flashcards

1
Q

what does COPD stand for?

A

chronic obstructive pulmonary disease

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2
Q

what does COPD consist of?

A

chronic bronchitis + emphysema

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3
Q

what is the definition of COPD?

A

a disease state characterised by airflow limitation that is not fully reversible

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4
Q

what is chronic bronchitis?

A

long-term inflammation of the mucous membranes of the bronchi

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5
Q

what are causes of chronic bronchitis?

A
  • caused almost entirely by smoking
  • infection — viral, bacterial
  • air pollution — smog
  • occupational exposure
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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
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7
Q

what is the effect of paralysed cilia on mucus?

A

mucus gets stuck

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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
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9
Q

how does mucus build up cause inflammation?

A

mucus that airway hasn’t been able to shift collects bacteria — more inflammation

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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

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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
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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

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13
Q

what are alveolar walls and their elasticity critical for?

A

the retention or potency of small airways

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14
Q

why is emphysema an obstructive lung disease?

A

because airflow on exhalation is slowed or stopped

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15
Q

what is responsible for opening up air spaces in inhalation?

A

elasticity of the alveolar walls

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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

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17
Q

what are the 2 main types of emphysema?

A

centriacinar (centrilobular) and panacinar (panlobular)

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18
Q

what is the main difference between the 2 types of emphysema?

A
  • centrilobular is associated with smoking (more common)

- panlobular is inherited

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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
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20
Q

what does tobacco products inhibit?

A

a-1-antitrypsin therefore more elastase activity breaking down air space walls

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21
Q

what does circulating a-1-antitrypsin usually do?

A

has anti-elastase activity (elastase breaks down alveolar walls)

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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

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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)

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24
Q

what is pulmonary fibrosis?

A

excess deposition of collagen and other extracellular matrix components in the lungs = “scarring of the lung”

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25
Q

what is the most common form of smoking-related interstitial lung disease?

A

idiopathic pulmonary fibrosis

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26
Q

what happens to type 1 and 2 pneumocytes in pulmonary fibrosis?

A
  • loss of type 1 pneumocytes (thin and squamous, responsible for gas exchange)
  • replaced by type 2 pneumocytes (make alveolar surfactant, failure of normal maturation)
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27
Q

symptoms of lung fibrosis

A
  • dry cough on exertion
  • progressive SOB with exercise
  • crackles on auscultation (velcro-like)
  • finger clubbing
  • inexorable progression
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28
Q

what is pulmonary fibrosis associated with?

A

reduced FVC but normal FEV1/FVC ratio

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29
Q

where do most secondary lung cancers arise from?

A

breast, kidney and GIT

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30
Q

clinical features of lung cancer

A
  • 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
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31
Q

what are the 4 histological classifications of primary lung cancer?

A
  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 %

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32
Q

what is the “therapeutic” classification of primary lung cancer?

A
  • small cell lung cancer (SCLC) vs NSCLC

- central vs peripheral

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33
Q

what is amelioration?

A

the act of making something; improvements

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34
Q

what is palliation?

A

making a disease (or symptoms) less severe without removing the cause

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35
Q

SCLC treatment

A
  • 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
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36
Q

where are central lung cancers? treatment?

A
  • 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

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37
Q

what are peripheral lung cancers usually? treatment?

A
  • often adenocarcinomas
  • typically less aggressive than other forms
  • more capable of surgical curative resection — lobectomy
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38
Q

what are the 3 main pathological effects in COPD?

A
  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
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39
Q

what are proteases released from and what do they stimulate?

A

proteases released from neutrophils — stimulate mucus hypersecretion in the large airways

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40
Q

what does mucus hypersecretion result in?

A

hypertrophy of the submucosal glands in the trachea and bronchi (increase in goblet cells)

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41
Q

how does excess collagen deposition result in a loss in alveolar expansion?

A

scarring = rigid airway —> failure to get rid of mucus by coughing —> remodelling of airway —> airways less able to contract and expand

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42
Q

what is inherited a-1-antitrypisn deficiency associated with?

A

fewer and larger alveoli

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43
Q

describe genetic a1-antitrypsin inheritance. what % of COPD cases does it account for?

A
  • 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%
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44
Q

why are more proteinases released in the lung in a smoker/someone with emphysema?

A

there are more inflammatory cells such as macrophages around which release proteinases

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45
Q

what are other causes of COPD?

A
  • pet dander (trigger)
  • smoking
  • coal mining
  • air pollution
  • low socioeconomic status
  • low birth weight
  • asthma
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46
Q

signs of COPD

A
  • 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
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47
Q

what is cor pulmonale and what is it often due to?

A

failure of RHS of heart, often due to pulmonary hypertension

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48
Q

why do COPD patients have prolonged expiration?

A

because FEV1 is low, they have a prolonged expiratory phase to allow for adequate respiration

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49
Q

why is FEV1 reduced in COPD?

A

airways are narrowed or inflamed — hinders how fast air can leave the lungs

50
Q

why does pursed lip breathing improve gas exchange?

A

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
Q

what is required to confirm a diagnosis of COPD?

A

spirometry

52
Q

in patients with loss of pulmonary elastic tissue, what exceeds the elastic recoil of the lung tissue?

A

the recoil of the chest wall

53
Q

what would a CXR of a patient with emphysema show?

A

areas with reduced lung markings

54
Q

restricted vs. obstructive disease FEV1/FVC

A

restricted disease: FEV1/FVC over 75%

obstructive disease: FEV1/FVC less than 75%

55
Q

what is vital to managing COPD?

A

smoking cessation

56
Q

what does nicotine stimulate?

A

the release of dopamine

57
Q

what does nicotine imitate?

A
  • Ach

- binds to nicotinic receptors

58
Q

what is the effect of nicotine binding to nicotinic receptors?

A
  • 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
Q

what is glutamate involved in?

A

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
Q

what is the effect of nicotine on blood vessels?

A

causes blood vessels to constrict or narrow, which limits the amount of blood that flows to organs

61
Q

what is the result of constant constriction of vessels?

A

blood vessels become stiff and less elastic — cells receive less oxygen and nutrients

62
Q

what is the effect of constricted vessels on the heart?

A

HR and BP increase to compensate for reduced delivery of oxygen — can contribute to clots forming in arteries

63
Q

effect of carbon monoxide on oxygen?

A

CO binds Hb which decreases the amount of O2 that’s can bind to form HbO — cells therefore receive less O2

64
Q

effect of smoking on cilia?

A

smoking paralyses and eventually destroys the cilia in our airways

65
Q

effect of smoking on lungs in general?

A
  • 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
Q

what does tobacco inhibit?

A

a1-antitrypsin

67
Q

what is the inflammatory response from neutrophils to tobacco smoke?

A

mucus hypersecretion

68
Q

what is tar?

A

sticky brown substance in cigarettes that collects in the lungs — contains cancer-causing chemicals

69
Q

who and where is COPD most common?

A
  • 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
Q

what is pneumonia?

A

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
Q

what do the alveoli contain in pneumonia?

A

fluid and blood cells

72
Q

what happens to the alveolar walls in pneumonia?

A

they become thickened by oedema

73
Q

what is the most common cause of pneumonia?

A

Streptococcus pneumoniae

74
Q

what does pneumonia infection begin with?

A

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
Q

what happens due to the decreased total SA for gas exchange and decreased ventilation-perfusion ratio in pneumonia?

A

hypoxia and hypercapnia

76
Q

what oxygen saturation is worrying?

A

<92%

77
Q

what may XR show in pneumonia?

A

show infiltrate in the form of consolidation — can also show the spread of any infection by distribution of the infiltrate

78
Q

what is CURB-65 score?

A
  • confusion
  • urea
  • respiratory rate
  • blood pressure
  • > 65 years
79
Q

describe streptococcus pneumoniae

A
  • lancet-shaped
  • gram positive
  • facultative anaerobic bacteria
  • more than 90 different strains
  • present in lots of people
80
Q

describe covid pneumonia

A
  • 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
Q

what type of cancer causes the most number of deaths?

A

lung cancer

82
Q

what does green or yellow phlegm indicate?

A
  • 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
Q

what does brown phlegm indicate?

A
  • old blood gives brown colour

- commonly caused by bacterial pneumonia, bacterial bronchitis, CF, pneumoconiosis, lung abscess

84
Q

what causes white phlegm?

A
  • viral bronchitis

- COPD

85
Q

what does clear phlegm indicate?

A
  • 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
Q

what does red or pink phlegm indicate?

A
  • blood in phlegm

- commonly caused by pneumonia, TB, congestive heart failure (CHF), pulmonary embolism, lung cancer

87
Q

what are the different layers of the very thin respiratory membrane?

A
  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
Q

what are type 1 alveolar cells?

A

form wall of alveoli — simple squamous epithelium

89
Q

what are type 2 alveolar cells?

A

produce surfactant — reduce surface tension

90
Q

what is NRT?

A

= 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
Q

what is Varenicline (Champix)?

A

reduces cravings for nicotine but also blocks reward centres

92
Q

what is Bupropion (Zyban)?

A
  • affects reward centres
93
Q

did more people stop smoking with NRT, Champix or Zyban?

A

Champix

  • standard dose of champix more than doubled chances of quitting compared to placebo
94
Q

what is operant conditioning?

A

about rewards and punishment — when we reward a behaviour, the behaviour increases. when we punish, behaviour decreases.

can relate to smoking cessation

95
Q

positive vs negative punishment?

A 
\+ve = giving a punishment 
-ve = taking away a punishment you were going to give
96
Q

what is a normal FEV1/FCV ratio?

A

approx 70-85% (declines with age)

97
Q

name 4 obstructive diseases

A
  • asthma
  • COPD
  • chronic bronchitis
  • emphysema
98
Q

what happens to FEV1 in obstructive diseases and why?

A

it decreases because of increased airway resistance to expiratory flow

99
Q

what happens to FVC in obstructive diseases?

A

may be decreased too, but not as much as FEV1, due to the premature closure of airway in expiration

100
Q

what receptors does SARS-CoV2 attach to?

A

ACE2

101
Q

what are the benefits of exercise in managing COPD?

A
  • 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
Q

what is bronchiectasis?

A
  • 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
Q

what is the pathophysiology of bronchiectasis?

A
  • 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
Q

what is the pathophysiology of interstitial lung disease?

A
  • 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
Q

what are the typical symptoms of interstitial lung disease?

A
  • 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
Q

what is fibrosis triggered by?

A

repeated injury to lung tissue from eg. inhaled toxins

107
Q

what is the maximum volume in lungs?

A

tidal volume + inspiratory reserve volume + expiratory reserve volume + residual volume

108
Q

what is the most common risk factor for mesothelioma?

A

past exposure to asbestos

109
Q

what is 2,3-BPG?

A

a molecule which binds to Hb and decreases its affinity for O2

110
Q

what role does the Herig-Breuer reflex play in breathing?

A

terminates inspiration to prevent hyperinflation of the lugs

111
Q

what are symptoms of pink puffer (emphysema)? what is not a symptom?

A
  • pursed lip breathing
  • hyper inflated lungs
  • barrel chest
  • tachypnoea

NOT cyanosed skin

112
Q

what is an example of a mucolytic drug?

A

carbocysteine

113
Q

what is the moa of clarithromycin?

A

binds to the 50s subunit of bacterial ribosome and inhibits translation of peptides

114
Q

what is the most common form of emphysema?

A

centriacinar

115
Q

how does the social learning perspective differ from the disease model of addiction?

A
  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
Q

what is contingency contracting?

A

a procedure aimed to punish smoking and drinking and reward abstinence

117
Q

approx ow many children per year are born with homozygous a1-anti trypsin deficiency?

A

1 in 500

118
Q

what buffer system plays a supporting role in the ECF?

A

phosphate buffer system

119
Q

what does COPD cause in terms of FEV1/FVC and PEFR?

A

reduced fev1/fvc and reduced pefr

120
Q

what disease is defined as an anatomically abnormal enlargement of the alveolar spaces?

A

emphysema

121
Q

what factors predict compliance under the Ley cognitive hypothesis model of patient compliance?

A

understanding, satisfaction and memory

122
Q

central chemoreceptors in the medulla are stimulated mainly in response to changes in what?

A

PCO2

PBL SEM 2 (44 decks)

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