Case 3 Flashcards

1
Q

what are intrinsic risk factors for COPD?

A
  • anti-proteinase (alpha1-antitrypsin) deficiency

- airway hyper-reactivity - easily triggered bronchospasm

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2
Q

what are symptoms of COPD?

A
  • productive cough
  • white or clear sputum
  • wheeze
  • breathlessness
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3
Q

what investigations can be done for diagnosis of COPD?

A
Lung function tests:
- Evidence of airflow limitation.
- FEV1 less than 80%.
- FEV1:FVC ratio is less than 70%.
- PEFR is low.

Blood gases:
- In advanced cases: hypoxaemia and hypercapnia.

Sputum examination:
- Useful in patients with purulent coughs.
- Sputum colour can help identify infection.
- E.g. rust-coloured sputum = pneumococcal bacteria (pneumonia).
- α1-Antitrypsin levels and genotype.

Blood count:
- Useful to exclude anaemia or document polycythaemia.

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4
Q

what’s treatment for COPD?

A

Smoking cessation remains the only intervention proven to decelerate the decline in FEV1.

Bronchodilators:
 - Mild COPD: β-Adrenergic agonists (salbutamol)
 - In severe COPD: long-term β-Adrenergic agonists (salmeterol)
 - Antimuscarinic drugs (ipratropium):
- more prolonged and greater bronchodilation is achieved.
 - Theophyllines

Corticosteroids:
 - In some patients, there has been a reversible element to their disease and airway function may improve considerably.
 - The combination of inhaled corticosteroids with long-acting β2-agonists produces further improvement in breathlessness and reduces the frequency and severity of exacerbations.

Antibiotics:
 - Prompt antibiotic treatment shortens exacerbations and should always be given in acute episodes as it may prevent hospital admission and further lung damage.
 - Patients can be given a supply of antibiotics to keep at home to start as soon as their sputum turns yellow or green.

Oxygen Therapy:
 Long-term domiciliary oxygen therapy has been shown to:
o Improve survival
o Prevent progression of pulmonary hypertension
o Decrease the incidence of secondary polycythaemia
o Improve neuropsychological health

- The aim of therapy is to increase the PaO2 to at least 8 kPa (60 mmHg).
- 100% oxygen isn’t given to a COPD patient. In a COPD patient, there is less new oxygen going in and less old carbon dioxide coming out. Therefore, there is a higher carbon dioxide concentration in the alveoli. Over time the patient becomes sensitised to this hypercapnia and so relies on hypoxaemia to drive their ventilation. Administering oxygen will reduce the hypoxaemia, thus reducing the respiratory drive whilst the levels of CO2 remain high. The patient hypoventilates instead of hyperventilating, thus their respiratory drive ids reduced which is fatal (look at clinical features notes on the next page).
- Usually 24-28% oxygen is administered.
- If the respiratory rate increases above 30, then around 40% oxygen is administered.

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5
Q

what are the clinical features of COPD?

  • oxygen and carbon dioxide
  • V/Q
A

Va/Q mismatch occurs partly because of damage and mucus plugging of smaller airways from chronic inflammation, and partly because of the rapid expiratory closure of the smaller airways owing to loss of elastic recoil from emphysema.
 - This leads to a fall in PaO2 and an increase in the work of respiration.

CO2 excretion is not impaired to the same extent.
 - Many patients will show low normal PaCO2 values due to increasing their ventilation (hyperventilation) in an attempt to maintain normal blood gases by increasing their respiratory effort.
 - Other patients fail to maintain their respiratory effort and as a consequence their CO2 levels increase.
 - In the short term, this rise in CO2 leads to stimulation of respiration but in the long term, these patients often become insensitive to CO2 and come to depend on hypoxaemia to drive their ventilation.
o These patients appear less breathless and because of their reduced O2 saturation, they start to retain fluid and stimulate erythrocyte production (leading to polycythaemia).
o In consequence they become cyanosed.
o Attempts to abolish hypoxaemia by administering oxygen can make the situation much worse by decreasing respiratory drive in these patients who depend on hypoxia to drive their ventilation.

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6
Q

what are the three mechanisms for the limitation of airflow in the small airways?

A
  1. loss of elasticity and alveolar attachments of airways due to emphysema - this reduces the elastic recoil and the airways collapse during expiration
  2. inflammation and scarring cause the small airways to narrow
  3. mucus secretion which blocks the airways
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7
Q

each mechanism narrows the small airways and causes air trapping, what does this lead to?

A

hyperinflation of the lungs and breathlessness

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8
Q

what diseases is COPD composed of?

A
  • emphysema

- chronic bronchitis

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9
Q

what is emphysema?

A

abnormal, permanent enlargement of the air spaces distal to the terminal bronchiole, accompanied by destruction of their walls and without obvious fibrosis

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10
Q

how is emphysema classified? and what are the different types of emphysema?

A

according to its autonomic distribution within the lobule

  1. centriacinar (centrilobular) emphysema
  2. panacinar (panlobular) emphysema
  3. distal acinar (paraseptal) emphysema
  4. irregular emphysema (airspace enlargement with fibrosis)
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11
Q

what is centriacinar emphysema? and when does it occur?

A
  • the central or proximal parts of the acini, formed by respiratory bronchioles are affected, while distal alveoli are spared
  • thus, both emphysematous and normal airspaces exist within the same acinus and lobule
  • the lesions are more common in the upper lobes, particular in the apical segments
  • the walls of the emphysematous spaces often contain large amounts of black pigment
  • centriacinar emphysema occurs predominantly in heavy smokers, often in association with chronic bronchitis
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12
Q

what is panacinar emphysema? and when does it occur?

A
  • this is less common
  • distension and destruction appear to involve the whole of the acinus, from the level of the respiratory bronchiole to the terminal blind alveoli
  • severe airflow limitation and V/Q mismatch occur
  • this type of emphysema occurs in alpha1-antitrypsin deficiency
  • panacinar emphysema tends to occur in the lower lobes of the lungs
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13
Q

what is distal acinar (paraseptal) emphyema? and when does it occur?

A
  • the proximal portion of the acinus is normal but the distal part is primarily involved
  • the emphysema is more striking adjacent to the pleura, along the lobular connective tissue septa and at the margins of the lobules
  • the characteristic findings are the presence of multiple, contiguous, enlarged airspaces that form cyst like structures that with progressive enlargement are referred to as bullae
  • this type of emphysema probably underlies many of the cases of spontaneous pneumothorax in young adults
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14
Q

what’s irregular emphysema?

A
  • airspace enlargement with fibrosis
  • the acinus is irregularly involved, is almost invariably associated with scarring, such as resulting from healed inflammatory diseases
  • although clinically asymptomatic, this may be the most common form of emphysema
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15
Q

what is the protease-antiprotease imbalance hypothesis?

A
  • Based on the observation that patients with a genetic deficiency of the antiprotease α1-antitrypsin have a markedly enhanced tendency to develop pulmonary emphysema, which is compounded by smoking.
  • (Normally) α1-Antitrypsin:
     - Found in serum, tissue fluids, and macrophages.
     - Is a proteinase inhibitor which is produced in the liver, secreted into the blood and diffuses into the lung.
     - Here it inhibits proteolytic enzymes (proteinases) such as neutrophil elastase, which are capable of destroying alveolar wall connective tissue.

The following sequence is postulated:
 - Neutrophils (the principal source of cellular proteases) are normally sequestered (isolated) in peripheral capillaries, including those in the lung, and a few gain access to the alveolar spaces.
 - Any stimulus that increases either the number of leukocytes (neutrophils and macrophages) in the lung or the release of their protease-containing granules increases proteolytic activity.
 - With low levels of serum α1-antitrypsin, elastic tissue destruction is unchecked and emphysema results.

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16
Q

how does the protease-antiprotease hypothesis help explain the effect of cigarette smoking on the development of emphysema?
and so what is the main factor leading to emphysema in smokers?

A

The protease-antiprotease imbalance hypothesis also helps explain the effect of cigarette smoking in the development of emphysema, particularly the centriacinar form in subjects with normal amounts of α1-antitrypsin:
In smokers, neutrophils and macrophages accumulate in alveoli:
 - The mechanism of inflammation is not entirely clear.
 - These activate the transcription factor NF-κB, which switches on genes that encode TNF and chemokines.
 - These, in turn, attract and activate neutrophils.
Accumulated neutrophils are activated and release their granules:
 - The granules are rich in a variety of cellular proteases resulting in tissue damage.
Smoking also enhances elastase activity in macrophages:
 - Macrophage elastase is not inhibited by the antiprotease α1-antitrypsin and, indeed, can proteolytically digest this antiprotease. Therefore the accumulation of macrophages is the main factor leading to emphysema in smokers.

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17
Q

what’s another way that smoking causes tissue damage?

A

Normally:
- The lung contains antioxidants (substances that inhibit oxidation).
- This prevents oxidative damage.
Tobacco smoke:
- Contains abundant reactive oxygen species (free radicals).
- These deplete the antioxidant mechanisms, thereby inciting tissue damage.

• Activated neutrophils increase the amount of reactive free radicals in the alveoli.
• A secondary consequence of oxidative injury is inactivation of native antiproteases:
 - This results in “functional” α1-antitrypsin deficiency even in patients without enzyme deficiency.

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18
Q

what does the loss of elastic tissue lead to?

A
  • this causes the respiratory bronchioles to collapse during expiration
  • this leads to functional airflow obstruction despite the absence of mechanical obstruction
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19
Q

apart from loss of elastic tissue, what else leads to airway obstruction in emphysema?

A
  1. goblet cell metaplasia with mucus plugging of the lumen
  2. inflammatory infiltration of the walls with neutrophils, macrophages, B cells, CD4 and CD8+ T cells
  3. thickening of the bronchiolar wall due to smooth muscle hypertrophy and peribronchial fibrosis
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20
Q

what stage of emphysema are the lungs voluminous?

A

advanced

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21
Q

which type of emphysema are large apical blebs or bullae more characteristic of?

A

irregular emphysema secondary to scarring and of distal acinar emphysema

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22
Q

what is bullous emphysema?

A
  • Large subpleural blebs or bullae (spaces more than 1 cm in diameter in the distended state) that can occur in any form of emphysema.
  • They represent localized accentuations of emphysema and occur near the apex.
  • On occasion, rupture of the bullae may give rise to pneumothorax.
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23
Q

why is the FEV1:FVC ratio reduced?

A

because FEV1 is reduced but FVC is normal

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24
Q

what is death in most patients with emphysema due to?

A
  • respiratory acidosis
  • right-sided heart failure
  • massive collapse of the lungs secondary to pneumothorax
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25
Q

what is chronic bronchitis?

A

long-term inflammation of the mucous membranes of the bronchi

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26
Q

how is chronic bronchitis diagnosed?

A

by the presence of a persistent productive cough that lasts for more than three consecutive months or more per year for at least two consecutive years

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27
Q

when chronic bronchitis persists for years, what may it lead to?

A
  • progress to COPD
  • lead to cor pulmonale and heart failure
  • cause atypical metaplasia and dysplasia of the respiratory epithelium providing a rich soil for cancerous transformation
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28
Q

describe the pathogenesis of chronic bronchitis

A
  • The primary or initiating factor in the genesis of chronic bronchitis seems to be long-standing irritation by inhaled substances such as tobacco smoke, & dust from grain/cotton.
  • Initially, proteases released from neutrophils stimulate mucus hypersecretion in the large airways.
  • This results in hypertrophy of the submucosal glands in the trachea and bronchi.
  • As chronic bronchitis persists, there is also a marked increase in goblet cells of small airways—small bronchi and bronchioles—leading to excessive mucus production that contributes to airway obstruction.
  • It is thought that both the submucosal gland hypertrophy and the increase in goblet cells are protective metaplastic reactions against tobacco smoke or other pollutants.
  • Although mucus hypersecretion in large airways is the cause of sputum overproduction, it is now thought that accompanying alterations in the small airways of the lung can result in physiologically important and early manifestations of chronic airway obstruction. This feature is similar to that described earlier in emphysema and seems to be a common denominator in COPD.
  • The role of infection seems to be secondary. It is not responsible for the initiation of chronic bronchitis but is probably significant in maintaining it and may be critical in producing acute exacerbations.
  • Cigarette smoke predisposes to infection.
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29
Q

what happens to the mucous membranes in chronic bronchitis?

A

• There is hyperemia (excess of blood in vessels), swelling, and edema of the mucous membranes, frequently accompanied by excessive mucinous or mucopurulent secretions.
• The characteristic histologic features are chronic inflammation of the airways and enlargement of the mucus-secreting glands of the trachea and bronchi.
 - Although the numbers of goblet cells increase slightly, the major change is in the size of the mucous gland (hyperplasia).

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30
Q

what is cor pulmonale?

A
  • Is enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance or high blood pressure in the lungs (pulmonary hypertension).
  • Pulmonary vascular resistance is increased because of loss of pulmonary vascular tissue and because of pulmonary vasoconstriction caused by hypoxia and acidosis.
  • The increased pulmonary vascular resistance leads to pulmonary hypertension, which initially occurs only during an acute respiratory infection.
  • Eventually, the pulmonary hypertension becomes persistent and progressively more severe.
  • The pulmonary vascular bed is gradually obliterated by muscular hypertrophy of the arterioles and thrombus formation.
  • Right ventricular function is progressively compromised because of the increased pressure load.
  • Hypoxia further impairs right ventricular function and, as it develops, left ventricular function is also depressed.
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31
Q

what are some acute and chronic lung infections?

A

acute:

  • mainly lower respiratory tract infections
  • acute bronchitis
  • pneumonia

chronic:
- bronchiectasis

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32
Q

what is pneumonia?

A

infection of the lung interstitium, alveoli and airways, resulting in inflammation of the lungs; usually caused by bacteria

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33
Q

what are symptoms of pneumonia?

A
- Cough
- Sputum (purulent) - rust-coloured 
- Breathlessness
- Fever
- Pleuritic chest pain
- Signs of consolidation (filling with fluid)
	  -Proteinaceous fluid and inflammatory cells congest the airspaces.
- Chest x-ray changes
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34
Q

why causes rust-coloured sputum?

A

Streptococcus pneumonia

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35
Q

how is pneumonia classified?

A

By site/localization:
- Bronchopneumonia – refers to more patchy alveolar consolidation associated with bronchial and bronchiolar inflammation often affecting both lower lobes.
- Lobar pneumonia - is a radiological and pathological term referring to homogeneous consolidation of one or more lung lobes, often with associated pleural inflammation.

By mechanism/ pathogen:
- Bacterial pneumonia
- Viral pneumonia
- Aspiration pneumonia:
           - Contents of the stomach travel up the oesophagus and down the trachea, causing infection in the alveoli and making the conditions acidic. 

By locality:
 CAP: community acquired pneumonia
 HAP: hospital acquired pneumonia
 VAP: ventilator acquired pneumonia

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36
Q

what are our defence mechanisms?

A

Nose
- Filters
- Warms
- Humidifies

Larynx
- Coughing

Lungs and Tract
- Mucociliary clearance

Cellular/ humoral immunity

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37
Q

what are risk factors for pneumonia?

A
  • age
  • impaired cough (problem with larynx)
  • impaired mucociliary clearance - smoking, congenital
  • immunosuppression
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38
Q

community-acquired pneumonia

  • pathogen
  • most common cause
  • pathogenesis
A

• Bacterial or viral.
• Bacterial infection follows an upper respiratory tract viral infection.
• Usually caused as a result of infection by Streptococcus pneumonia.
• Pathogenesis:
1. Attachment of bacteria to the upper respiratory tract epithelium.
2. Necrosis of the cells.
3. Inflammatory response.
4. This extends to the alveoli.
 - Interstitial inflammation .
 - Inhibition of mucociliary clearance.

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39
Q

what type of bacteria is streptococcus pneumonia?

A

gram-positive bacteria (positive to be in the community rather than hospital)

40
Q

hospital-acquired pneumonia

  • most common cause
  • what is it
  • how common
  • leads to
  • who particularly at risk
A
  • Usually as a result of infection by Staphylococcus aureus or gram-negative rods (Enterobacterium).
  • HAP refers to a new episode of pneumonia occurring at least 2 days after admission to hospital.
  • It is the second most common hospital-acquired infection (HAI).
  • It is the leading cause of HAI-associated death.
  • These are common in patients with severe underlying disease and immunosuppression.
  • The elderly and patients on mechanical ventilation are particularly at risk.
41
Q

aspiration pneumonia

  • who most common in
  • what is it
  • what does it cause
  • what type of bacteria predominates
A

• Occurs mainly in:
 Markedly debilitated patients.
 Patients that aspirate gastric contents:
 These patients have abnormal gag and swallowing reflexes that facilitate aspiration.
• The resultant pneumonia is partly chemical, resulting from the extremely irritating effects of the gastric acid, and partly bacterial.
• Anaerobic bacteria predominate.
• This type of pneumonia is often:
 - Necrotizing.
 - Pursues a fulminant (severe and sudden onset) clinical course.
 - A frequent cause of death in persons predisposed to aspiration.

42
Q

what are complications of pneumonia?

A

Lung abscess (swollen area containing pus) – Caused by tissue destruction and necrosis
 - Severe localized suppuration (formation of disease causing matter and discharge of pus)
 - Cavity formation on the chest X-ray, often with the presence of a fluid level.
 - There are many causes of lung abscess, but the most common cause is aspiration.
 Clinical features:
 - Persisting and worsening pneumonia associated with the production of large quantities of sputum, which is often foul-smelling owing to the growth of anaerobic organisms.
 - There is usually a swinging fever; malaise (discomfort) and weight loss occur.

Empyema – Spread of infection to the pleural cavity
- Empyema means the presence of pus within the pleural cavity.
This usually arises from:
 - Bacterial spread from a severe pneumonia.
 - Or after the rupture of a lung abscess into the pleural space.
- An empyema cavity becomes infected with anaerobic organisms and the patient is severely ill with a high fever and a neutrophil granulocytosis.

43
Q

what are the different colours of sputum? and what are their causes?

A
  • Yellow/green sputum indicates sputum neutrophils and suggests bacterial colonization or infection. This colour of sputum indicates that antibiotics will be effective.
  • The presence of blood suggests neoplasm or pulmonary infarct.
  • Serous/frothy/pink suggests blood present.
  • Foamy white - may come from obstruction or even oedema. This is ineffective against antibiotics as it may be viral.
  • Rusty coloured - usually caused by pneumococcal bacteria.
44
Q

what is erythromycin?

A

a macrolide antibiotic

45
Q

how do macrolides work?

- bacteriostatic or bactericidal

A

the macrolides inhibit bacterial protein synthesis by an inhibitory effect on translocation (process of tRNA shifting from site A to site P on ribosome)

  • the A remains occupied and, thus, the addition of an incoming tRNA and its attachment amino acid to the polypeptide chain is inhibited
  • this interferes with the production of functionally useful proteins
  • macrolide antibiotics bind reversibly to the P site on the subunit 50S of the bacterial ribosome - this action is considered to be bacteriostatic but may be bactericidal at high concentrations
46
Q

how does the antimicrobial spectrum of erythromycin compare to that of penicillin?

A

very similar - it has proven to be a safe and effective alternative for penicillin-sensitive patients

47
Q

what is and isn’t erythromycin effective against?

A

gram-positive bacteria and spirochaetes (gram-negative) but not against most gram-negative organisms

48
Q

what are the side effects of erythromycin?

A

Gastrointestinal disturbances:
- Common and unpleasant but not serious.
Hypersensitivity reactions:
- Such as skin rashes and fever.

49
Q

what is cefuroxime?

A

a cephalosporin antibiotic

50
Q

what’s cefuroxime used to treat?

A

pneumonia

51
Q

what type of antibiotics are cephalosporins? and what does this mean?

A

B-lactam antibiotics

β-lactam antibiotics (beta-lactam antibiotics) are a class of broad-spectrum antibiotics, consisting of all antibiotic agents that contain a beta-lactam ring in their molecular structures. This includes penicillin derivatives (penams), cephalosporins (cephems), monobactams, and carbapenems.

52
Q

how do B-lactam antibiotics work?

A
  1. This will attack the cell wall.
  2. Attaches via its β-lactam ring (which opens up) to the target in the cell wall (Penicillin Binding Protein (PBP)).
  3. This changes the functional group of the protein on the cell wall and causes inhibition of the transpeptidation enzyme that cross-links the peptide chains attached to the backbone of the peptidoglycan.
  4. As the cell wall grows in coordination with bacterial growth, the cell wall is weakened and crumbles. Extracellular fluid enters the bacteria, leading to the death of the bacteria.
  5. The bacteria can responds by producing the enzyme β-lactamase
53
Q

is cefuroxime affected B-lactamase?

A

nope it is resistant to B-lactamase

54
Q

what are side effects of cefuroxime?

A

hypersensitivity reactions

55
Q

what is lung fibrosis?

A

excessive deposition of collagen and other extracellular matrix components in the lungs - scarring of the lungs

56
Q

what is the pathogenesis of lung fibrosis?

A

As a result of chronic injury.

Chronic injury leads to chronic inflammation, which is associated with:
- The proliferation and activation of macrophages and lymphocytes.
- The production of inflammatory and fibrogenetic growth factors.
- The production of cytokines.

57
Q

what are examples of walk tests?

A

Walk tests include the self-paced 6-minute walk and the externally paced incremental ‘shuttle’ test, where patients walk at increasing pace between two cones 10 m apart.

58
Q

what is a common reason for performing an exercise test? explain this.

A

A common reason for performing an exercise test is to evaluate the main cause of breathlessness and, in particular, to determine whether this is due predominantly to cardiac or ventilatory abnormalities.

- If a patient achieves the predicted maximum heart rate during a progressive test (as is seen in normal subjects), it is reasonable to conclude that the limit to further exercise is set by the cardiovascular system.
- In most respiratory diseases, patients cease exercise with a lower heart rate as more often the limit is set by the maximum ventilation achievable.

59
Q

what are the measurements taken during an exercise test?

A
  • The subject exercises at increasing loads until no longer able to continue because of discomfort, or until stopped by the investigator.
  • The maximum oxygen consumption is a useful indicator of overall exercise capacity.
  • Comparison of the maximum ventilation and heart rate at the end of progressive exercise with those predicted from spirometric measurements and age, respectively, gives some indication of the likely factor(s) limiting performance.
60
Q

has the decline in smoking been faster in men or women?

A

men

61
Q

what are the three theories of addiction?

A

1 . moral model: addiction as a result of weakness and a lack of moral fibre

  1. biomedical model: addiction as a disease
  2. social learning theories: behaviours as behaviours that are learned according to the rules of learning theory
62
Q

describe the moral model (Criminal Justice model) of addiction

A
  • Addicts are “weak” and can overcome a compulsion to use with willpower.
  • Drug abusers choose to use drugs.
  • Drug abusers are anti‐social and should be punished.
  • Drugs are evil.
63
Q

describe the biomedical model of addiction

A
•	Addiction as a “brain disease”.
•	Neurotransmitter imbalance.
•	Disease Model:
	Agent: drug
	Vector: dealers
	Host: addict
•	Need to “stamp out” the disease by eliminating drugs.
•	Drug antagonist medications: Welbutrin; naltrexone; antabuse
64
Q

describe the social model of addiction

A

• Drug use is a learned behaviour:

  • classical conditioning
  • operant conditioning
  • observational learning
  • cognitive factors
  • People use drugs because drug use is modelled by others.
  • Peer pressure.
  • Environmental effects lead to drug use (advertising, etc).
  • Drug use is a maladaptive relationship negotiation strategy.
65
Q

what are the 4 types of learned behaviours?

A

Classical conditioning: associative behaviour (e.g. associating smoking with feeling relaxed)

Operant conditioning: probability of behaviour occurring is increased if it is either positively reinforced by the presence of a positive event, or negatively reinforced by the absence or removal of a negative event (e.g. probability of smoking increased by feelings of social acceptance, confidence and control and removal of withdrawal symptoms).

Observational learning/ modelling: behaviours are learnt by observing significant others carrying them out (e.g. parents smoking).

Cognitive factors: factors such as self-image, problem-solving behaviour, coping mechanisms.

Classical conditioning:
Learning theory – a given response is made more or less likely when it is followed by particular types of stimulus termed positive and negative reinforcers
- Habit theory with smoking – associate a certain place to smoking

Operant conditioning:
About the rewards and punishment we get
- Punishment = decreasing behaviour
- Reinforcement = increasing behaviour

Role modelling:
Learning from other people

Social learning:
Learning from our environment

66
Q

what are flaws with the registrar general’s occupational measure of class?

A
  • It does not have an option for the unemployed.

- It does not deal adequately with women’s occupations.

67
Q

what are the 4 major theoretical explanations for the increasing disparity in morality rates between social classes presented in the black report?
and which hypothesis is favoured?

A
  1. Cultural/behavioural explanation
    • This stresses individual or lifestyle differences rooted in personal characteristics and levels of education, which influence behaviour and are, therefore, open to alteration through health-education inputs leading to changes in health behaviour.
  2. Materialist of structuralist explanation
    • These emphasize the role of economic and associated socio-structural factors, for example, the labour and housing markets, in the distribution of health and well-being.
    • Supporters of this explanation believe that social structure is characterized by permanent social and economic inequality, which exposes individuals to different probabilities of ill health and injury:
     Poor-quality and damp housing has been associated with worse health.
     Low socio-economic status, low pay, and insecurity produce inadequacies in diet.
  3. Social selection
    • These argue that the occupational class structure is seen to act as a filter or sorter of human beings, and one of the major bases of selection is health: physical, strength, vigour, or agility. In this hypothesis, health determines social class (social mobility).
  4. Artefact explanation
    • This suggests that both health and class are artificial variables produced by attempts to measure social phenomena and that; therefore, the relationship between them may itself be an artefact – an accidental effect – of little significance.
  • Artefact (of measurement) – might be an artefact of the way its measured – as size of population with lower status declines, there may be more people left with higher risk of death – however, other ways of looking at economic status also show same link between status and health inequality
  • Social selection (class) – pre-existing health status determines someone socioeconomic position in society – actually most evidence shows that link is the other way around – It’s disadvantage that causes health problems
  • Behavioural (individual) – individual choices that we make and how that affects health
  • Materialist (living standards) – people with lower living standards are more exposed to risks that will affect their health

The materialist/structural hypothesis is favoured.

68
Q

what is the Drift Hypothesis?

A

Drift Hypothesis, concerning the relationship between mental illness and social class, is the argument that illness causes one to have a downward shift in social class.

69
Q

what is the Social Causation Theory?

A

The Social Causation theory argues that low social status causes stress and leads to mental illness.

70
Q

cessation involves a shift across five basic stages - what are these stages?

A
  1. Pre-contemplation: defined as not seriously considering quitting
  2. Contemplation: having some thoughts about quitting
  3. Preparation: seriously considering quitting
  4. Action: initial behaviour change
  5. Maintenance: maintaining behaviour change for a period of time.
71
Q

what is varenicline? how’s it taken? what are the side effects?

A

• Partial agonist of the α4β2 subtype of the nicotinic acetylcholine receptor.
• It stimulates the nicotine receptors more weakly than nicotine itself does.
• Varenicline does not greatly increase the downstream release of dopamine.
• It is given as a means of smoking cessation.
• Oral medication.
• Side Effects:
 - Nausea
 - Headaches
 - Difficulty sleeping

72
Q

interstitial lung disease

  • what is it
  • what types are there
  • examples
  • causes
A

Interstitial lung disease is a general category that includes many different lung conditions

  • The interstitium is a lace-like network of tissue that extends throughout both lungs
  • It provides support to the lungs’ microscopic air sacs
  • Tiny blood vessels travel through the interstitium, allowing gas exchange
  • It’s so thin in can’t be seen on chest x-rays or CT scans

Types of interstitial lung disease:
- All forms of interstitial lung disease cause thickening of the interstitium
- The thickening can be due to inflammation, scarring or oedema
- Some forms of interstitial lung disease are short-lived; others are chronic and irreversible
Examples
- Interstitial pneumonia
- Idiopathic pulmonary fibrosis
- Nonspecific interstitial pneumonitis
- Hypersensitivity pneumonitis
- Acute interstitial pneumonitis
- Asbestosis

Causes:

  • Bacteria, viruses, and fungi are known to cause interstitial pneumonias
  • Regular exposures to inhaled irritants at work or during hobbies can also cause some interstitial lung disease – these irritants include:
  • asbestos
  • silica dust
  • talc
  • coal dust
73
Q

how should oxygen be administered to patients with COPD? what are you aiming for?

A
  • For most COPD patients, you should be aiming for an SaO2 of 88-92% (compared with 94-98% for most acutely ill patients NOT at risk of hypercapnic respiratory failure)
  • Mark the target saturation clearly on the drug chart
  • The aim of oxygen therapy is to raise the PaO2 without worsening acidosis (increasing acidity in the blood)
  • Therefore, give oxygen at no more than 28% (via venture mask, 4 L/minute) or no more than 2 L/minute (via nasal prongs) and aim for oxygen saturation 88-92% for patients with a history of COPD until arterial blood gases (ABGs) have been checked
  • Measure ABGs within 60 minutes of starting supplemental oxygen or changing its concentration
  • If PaO2 improves with an associated drop in PaCO2 and the pH is relatively unaffected then the concentration of the supplemental oxygen may be increased to maintain PaO2 > 7.5 kPa
74
Q

what about oxygen administration with type I and type II respiratory failure?

A
  • High concentrations safe in Type I respiratory failure
  • In Type II, brain stem sensitivity to CO2 is reduced
  • Patients depend on hypoxic drive
  • High oxygen concentration leads to hypercapnoea and apnoea (suspension of breathing)
  • Controlled oxygen titrated to blood gas should be used
75
Q

what is the most common cause of type II respiratory failure?

A

COPD

76
Q

what can tobacco do to blood vessels?

A

cause atherosclerosis

77
Q

how does the FEV1/FVC ratio help diagnose COPD rather than lung fibrosis?

A

Lung fibrosis is restrictive so both FEV1 and FVC lower equally, where as with COPD FEV1 lowers more than FVC

78
Q

what type of pulmonary disease is lung fibrosis?

A

restrictive

79
Q

what’s clarithromycin (Biaxin)? what’s it used for?

A
  • a macrolide antibiotic

- used to treat many different types of bacterial infections affecting the skin and respiratory system

80
Q

what’s amoxicillin? what’s it used for?

A
  • A penicillin antibiotic (B-lactam antibiotic)
  • Amoxicillin is used to treat many different types of infection caused by bacteria, such as tonsillitis, bronchitis, pneumonia, gonorrhoea, and infections of the ear, nose, throat, skin, or urinary tract
  • Amoxicillin is also sometimes used together with another antibiotic called clarithromycin (Biaxin) to treat stomach ulcers
81
Q

what is the proportion of adults that smoke in the UK?

A

15.8%

82
Q

what percentage of smokers try to stop smoking each year? and how many succeed? and how many attempts does it take?

A

50% try to stop smoking each year

2-3% succeed, on average, takes 4 quit attempts

83
Q

explain the psychopharmacology of smoking?

A
  • Puff on cigarette
  • Nicotine absorbed through large surface area of the lungs
  • Rapid transport to the brain’s ventral tegmental area where nicotine attaches to acetylcholine receptors
  • This activates neural pathway leading to dopamine release in nucleus accumbens
84
Q

what models are used for influences on smoking?

A
  1. The COM-B framework
  • Capability – physical & psychological
  • Opportunity – where can you smoke, social environment
  • Motivation – emotion
     Behaviour
  1. PRIME theory of motivation
  • Plans (intentions)
  • Evaluations (beliefs)
  • Motives (wants)
  • Impulses (urges)
  • Responses
    Our plans and beliefs are balanced by motives and impulses -> which lead to our responses
    Huge gap between intention and behaviour
    Prime – think about how primates think – impulses and wants?
85
Q

how does tobacco lead to emphysema?

A
  • Tobacco products release inflammatory products from white cells, predominantly neutrophil polymorphs
  • These inflammatory products break down elastic tissue
  • Circulating alpha-1-antitrypsin (alpha-1-antiprotease) has anti-elastase activity
  • Tobacco products inhibit alpha-1-antitrypsin
86
Q

what is the histological classification of primary lung cancer?

A

Histological classification of primary lung cancer:

  • Squamous cell carcinoma (20-30%) – radiotherapy maybe
  • Small cell carcinoma (15-20%) – the worst – very aggressive – beyond cure
  • Adenocarcinoma (30-40%) – doesn’t respond to chemotherapy
  • Large cell undifferentiated carcinoma (10-15%) – very aggressive

Small cell lung cancer: (20%) (originate from small, immature neuroendocrine cells)
• Small cell carcinoma (20%)
- Almost always in smokers
- Metastasises early & grow fast
- Worst prognosis
- Usually develop centrally in the lung, near a main bronchus
- By the time it’s found they are often large and found in multiple sites both inside and outside of the lung
- Can secrete hormones – paraneoplastic syndrome

Non-small cell lung cancer: (80%)
• Adenocarcinoma (35%)
- Most common cell type overall
- Most common in women
- Most common cell type in non-smokers but still most patient are smokers
- Peripheral – in bronchiole or alveolar wall

• Squamous cell carcinoma (30%)

  • Strongly associated with smoking
  • Most common carcinoma to cavitate
  • Poor prognosis
  • Central – main bronchi to the bronchioles, but less alveoli?

• Large-cell carcinoma (15%)

  • Peripheral (and centrally)
  • Very large, usually more than 4cm
87
Q

what is carcinoma?

A

type of cancer that develops from epithelial cells

88
Q

what’s Registrar General’s Social Class?

A
I = professional 
II = managerial and technical 
III = skilled non-manual 
IV = partly skilled manual 
V = unskilled manual
89
Q

what’s the National Statistics Socio-economic classification?

A
  1. 1.Large employers and higher managerial and administrative occupations
    2. higher professional occupations (doctors, lawyers)
  2. Lower managerial, administrative and professional occupations (nurses, teachers)
  3. Intermediate occupations (airline cabin crew, secretaries, photographers)
  4. Small employers and own account workers (hair dressers, builders)
  5. Lower supervisory and technical occupations (train drivers, plumbers)
  6. Semi-routine occupations (security guards, postal workers)
  7. Routine occupations (bus drivers, cleaners)
  8. Never worked and long-term unemployment
90
Q

what can spirometry be used for?

A
  • The spirometry test is performed using a device called a spirometer
  • A volume-time curve, showing volume (litres) along the Y-axis and time (seconds) along the X-axis
  • A flow-volume loop, which graphically depicts the rate of airflow on the Y-axis and the total volume inspired or expired on the X-axis
  • You can do a lot more than just a FEV1 and FVC
  • You can look at things like total lung capacity, transfer factors to see how well the lung parenchyma are working
91
Q

what is bronchiectasis?

A
  • An abnormal widening of the airways due to recurrent inflammation and infection
  • When the airways become dilated, extra mucus begins to pool in the enlarged areas
  • The pooling of mucus becomes a breeding ground for bacteria which leads to lung infections
  • This is further complicated by damage to the cilia – when the cilia are unable to clear the airways of debris and extra mucus, airway obstruction occurs
92
Q

describe obstruction and restriction in terms of FEV1, FVC and FEV1/FVC?

A
FEV1:
obstruction = decreased a lot 
restriction = decrease
FVC:
obstruction = decrease 
restriction = decrease
FEV1/FVC:
obstruction = <70% 
restriction = >_ 70%
93
Q

describe residual volume and RV/TLC in obstruction and restriction

A
RV:
obstruction = increase 
restriction = decrease 
RV/TLC:
obstruction = increase 
restriction = decrease
94
Q

what does COPD look like on a chest radiograph?

A
  • Often normal
  • Hyper-expansion (ribs 7-9 look greater?)
  • Low, flat diaphragms
95
Q

what are the normal values for pH, PaCO2, PaCO2, HCO3-?

A
pH = 7.35 - 7.45
PaO2 = 11 - 13 kPa 
PaCO2 = 4.5 - 6 kPa
HCO3- = 20 - 28 mMol/L
96
Q

describe cor pulmonale in simple steps

A

Hypoxia -> pulmonary arterial vasoconstriction -> increased pulmonary artery pressure -> right ventricular hypertrophy -> right ventricular failure

97
Q

what different types of antibiotics are there?

A
  • Penicillins (such as penicillin and amoxicillin)
  • Cephalosporins (such as cephalexcin)
  • Aminoglycosides (such as gentamicin and tobramycin)
  • Tetracyclines (such as tetracycline and doxycycline)
  • Macroslides (such as erythromycin and clarithromycin)
  • Fluoroquinolones (such as ciprofloxacin and levofloxacin)