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Case 3 Sem 2 > COPD > Flashcards

COPD Flashcards

1
Q

What is COPD?

A

Disease of adults usually 45+ with airflow obstruction that is not fully reversible

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2
Q

How is COPD caused?

A

Long term exposure to toxic particles and gases (usually long term smoking)
Occupational coal miners (cadmium)
Air pollution
Cannabis

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3
Q

Intrinsic risk factors

A

Anti proteinase (a1-anti trypsin) deficiency
Airway hyperreactivity (easily triggered bronchospasm)

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4
Q

Symptoms of COPD

A

Productive cough
White/clear sputum
Wheeze
Breathlessness

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5
Q

Diagnosis of COPD

A

Evidence of airflow limitation
FEV1 less than 80%
FEV1:FVC ratio less than 70%
PEFR is low
a1 antitrypsin levels

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6
Q

Blood gases COPD

A

Hyoxaemia and hypercapnia

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7
Q

Rust coloured sputum indicates

A

Pneumococcal bacteria (pneumonia)

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8
Q

Smoking cessation

A

Only intervention proven to decelerate decline in FEV1

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9
Q

Bronchodilator treatment COPD

A

mild COPD: B adrenergic agonists (salbutamol)
severe COPD: long term B adrenergic agonists (salmeterol)
Antimuscarinic drugs (ipratropium) more prolonged and greater bronchodilation achieved
Theophyllines

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10
Q

Antimuscarinic drugs

A

Stops acetylcholine binding, calcium, stops lung contracting

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11
Q

Theophyllines

A

Prevents and treats wheezing, shortness of breath and chest tightness

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12
Q

Corticosteroids and COPD

A

Airway function may improve considerably
Combination of inhaled corticosteroids with long acting B2 agonists produces further improved eg in breathlessness, reduces frequency and severity of exacerbations

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13
Q

Antibiotics and COPD

A

Shortens exacerbations, should always be given in acute episodes, may prevent hospital admission and further lung damage
When sputum turns yellow/green

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14
Q

Oxygen therapy COPD

A

Improves survival, prevent progression of pulmonary hypertension, decrease incidence of secondary polycythameia

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15
Q

Polycythaemia

A

Higher amount of RBC, makes blood thicker, harder to flow through blood vessels

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16
Q

Why is 100% oxygen not given to patient?

A

In COPD, less new oxygen going in and less old CO2 coming out, therefore a higher C02 conc in alveoli, patient sensitised to this hypercapnia, relies on hypoxaemia to drive ventilation. Administering oxygen reduces hypoxaemia, reducing respiratory drive whilst CO2 remains high. Patient hypoventilates instead of hyperventilating, respiratory drive reduced = fatal

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17
Q

Aim of oxygen therapy

A

Increase Pa02 to at least 60mmHg

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18
Q

What % oxygen administered to COPD?

A

24-28%, increased to 40%

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19
Q

Prognosis COPD

A

Poor prognosis predictor: increasing age, worsening airflow limitation (fall in FEV1), Weight loss, pulmonary hypertension

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20
Q

Emphysema

A

Abnormal permanent enlargement of air spaces distal to terminal bronchiole, destruction of their walls without obvious fibrosis

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21
Q

Centriacinar (centrilobular) emphysema

A

Central or proximal parts of acini, formed by respiratory bronchioles are affected, distal alveoli spared, therefore emphysematous and normal airspace’s exist within the same acinus and lobule
Legions more common in upper lobe, particularly apical segments
Walls of emyphysematous spaces contain black pigment
Most common form

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22
Q

Panacinar (panlobular) emphysema

A

Less common
Distension and destruction involves the whole of the acinus, from respiratory bronchiole to terminal blind alveoli
Severe airflow limitation and V/Q mismatch occurs
Occurs in a1 antitrypsin deficiency
Occurs in lower lobes of lung

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23
Q

Distal acinar (paraseptal) emphysema

A

Proximal portion of acinus normal, distal part involved
Emphysema adjacent to pleura, along lobular connective tissue septa and margins of lobules
Multiple enlarged airspace’s forming cyst like structures with progressive enlargement (bullae)
Underlies many cases of spontaneous pneumothorax in young adults

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24
Q

Irregular emphysema (airspace enlargement with fibrosis)

A

Acinus irregularly involved, associated with scarring, eg resulting from healed inflammatory disease
Clinically asymptomatic

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25
Q

Pathogenesis of emphysema

A

COPD characterised by mild chronic inflammation throughout airways, parenchyma, pulmonary vasculature
Macrophages, CD8+ and CD4+ T lymphocytes, neutrophils increased in the lung
Activated inflammatory cells release mediators capable of damaging lung structures/ sustaining neutrophilic inflammation

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26
Q

Protease-antiprotease imbalance hypothesis

A

Genetic deficiency of antiprotease a1 antitrypsin, enhanced tendency to develop pulmonary emphysema
Neutrophils normally isolated in peripheral capillaries, few gain access to alveolar spaces
Any stimulus that increases number of leukocytes (neutrophils and macrophages) in the lung or the release of protease containing granules increases Proteolytic activity
Low levels of serum a1 antitrypsin, elastic tissue destruction unchecked, emphysema results
Emphysema results from destructive effect of high protease activity in subjects with low antiprotease activity

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27
Q

a1-antitrypsin

A

Found in serum, tissue fluids, macrophages
A proteinase inhibitor produced in liver, secreted into blood, diffuses into the lung
Inhibits Proteolytic enzymes (proteinases) eg neutrophil elastase (capable of destroying alveolar wall connective tissue)

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28
Q

Protease-antiprotease imbalance hypothesis and cigarette smoking

A

Centriacinar form
In smokers, neutrophils and macrophages accumulate in alveoli, activate transcription of factor NF-kB switching on genes that encode TNF and chemokines, attract and activate neutrophils
Accumulated neutrophils activated and release their granules rich in cellular proteases resulting in tissue damage
Smoking enhances elastase activity in macrophages, macrophage elastase can Proteolytically digest antiprotease a1 antitrypsin

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29
Q

Oxidant-antioxidant imbalance (smoking)

A

Normally the lung contains antioxidants (inhibit oxidation) preventing oxidative damage
Tobacco smoke contains reactive oxygen species (free radicals), deplete antioxidant mechanisms, inciting tissue damage

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30
Q

What increases amount of reactive free radicals in alveoli

A

Activated neutrophils

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31
Q

Secondary consequence of oxidative injury

A

Inactivation of native proteases, resulting in functional a1 antitrypsin deficiency

32
Q

Elastic tissue in alveolar walls contribute to

A

Elastic recoil of lung parenchyma

33
Q

Loss of elastic tissue

A

Causes respiratory bronchioles to collapse in expiration, functional airflow obstruction

34
Q

Inflammation of small airways

A

Goblet cell Metaplasia with mucus plugging of lumen
Inflammatory infiltration of walls with neutrophils, macrophages, B cells , CD4 and CD8 T cells
Thickening of bronchioles wall, due to smooth muscle hypertrophy and peribronchial fibrosis
These changes narrow bronchioles lumen, airway obstruction

35
Q

Morphology of emphysema

A

Advanced emphysema produces voluminous lungs
Large apical blebs/bullae characteristic of irregular emphysema secondary to scarring/distal acinar emphysema

36
Q

Bullous emphysema

A

Large subpleural blebs/bullae (spaces more than 1cm diameter in distended state) occur
Represent localised accentuations of emphysema and occur near apex
Rupture of bullae may give rise to pneumothorax

37
Q

Clinical course emphysema

A

Clinical symptoms Do not appear until at least 1/3 of functioning pulmonary parenchyma damaged
Dyspnoea (first symptom, progressive), cough and wheezing, reduced FEV1, normal FVC (FEV1:FVC ratio reduced), weight loss
Barrel chested, dyspneic, prolonged expiration, sits forward hunched over, breathes through pursed lips

38
Q

Dyspnoea (dyspneic)

A

Shortness of breath

39
Q

Death in emphysema due to

A

Respiratory acidosis, right sided heart failure, massive collapse in lungs secondary to pneumothorax

40
Q

What is pneumonia?

A

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

41
Q

Pneumonia symptoms

A

Cough, purulent sputum (rust coloured: streptococcus pneumonia), breathlessness, fever, pleuritic chest pain, consolidation (filling with fluid - proteinaceous fluid/ inflammatory cells cogent airspaces, chest x ray changes

42
Q

Classification of pneumonia

A

By site/localisation:
bronchopneumonia - more patchy alveolar consolidation associated with bronchial and bronchiole inflammation affecting both lower lobes
Lobar pneumonia - homogenous consolidation of one or more lung lobes, associated with pleural inflammation
By mechanism/pathogen:
Bacterial pneumonia, viral pneumonia, aspiration pneumonia (contents of stomach travel up oesophagus and down trachea causing infection in alveoli, making conditions acidic)
By locality:
CAP (community acquired pneumonia)
HAP (hospital acquired pneumonia)
VAP (ventilator acquired pneumonia)

43
Q

Defence mechanisms (pneumonia)

A

Nose (filters, warms, humidifies)
Larynx (coughing)
Lungs and tract (mucociliary clearance)
Cellular/humoral immunity

44
Q

Risk factors for pneumonia

A

Age, impaired cough (larynx problem), impaired mucociliary clearance (smoking/congenital), immunosupression

45
Q

Clinical examination of pneumonia

A

Tachypnea, tachycardia, fever, hypotension (due to fluid loss in inflammation)

46
Q

Tachypnea

A

Fast breathing

47
Q

Pneumonia treatment

A

Antibiotics -must cover streptococcus pneumonia, cephalosporin (cefuroxime), macrolide (clarithromycin), oral glucocorticoids, oxygen, IV fluids, nutrition

48
Q

Community Acquired Pneumonia (CAP)

A

Bacterial/viral
Bacterial infection follows an upper respiratory tract viral infection
Usually caused as a result of infection by streptococcus pneumonia

49
Q

Pathogenesis of CAP

A

1.Attachment of bacteria to upper respiratory tract epithelium
2. Necrosis of cells
3.inflammatory response
4. This extends to alveoli (interstitial inflammation, inhibition of mucociliary clearance)

50
Q

Streptococcus pneumonia

A

Gram positive bacteria
False positives may be obtained (S. pneumoniae 20% of flora in adults)
Presence of numerous neutrophils containing gram positive, lancet shaped diplococci supports diagnosis of pneumococcal pneumonia

51
Q

Streptococcus pneumonia effects

A

Rapidly ill with high temp (up to 39.5)
Pleuritic pain
Dry cough
Hyperventilation and shallow breathing (affected side of chest moves less, signs of consolidation together with a pleural rub - where inflamed visceral pleura rubs against non inflamed parietal pleura)

52
Q

Hospital acquired pneumonia (HAP)

A

Result of infection by staphylococcus aureus/ gram negative rods (enterobacterium)
New episode of pneumonia at least 2 days after admission to hospital
Common in patients with severe underlying disease and immunosuppressive
Elderly/mechanical ventilation at risk

53
Q

Aspiration pneumonia

A

Occurs mainly in debilitated patients, patients that aspirate gastric contents (gag and swallowing reflexes that facilitate aspiration)
Resultant pneumonia partly chemical, resulting from irritating effects of gastric acid, partly bacterial
Anaerobic bacteria predominate
Necrotising, severe and sudden onset, frequent cause of death

54
Q

Fulminant

A

Severe and sudden

55
Q

Lung abscess (pneumonia)

A

Swollen and containing pus caused by tissue destruction and necrosis
Cavity formation on chest x ray, presence of a fluid level
Common cause is aspiration

56
Q

Suppuration

A

Formation of disease causing matter and discharge of pus

57
Q

Clinical features of lung abscess

A

Persisting and worsening pneumonia, large quantities of sputum (foul smelling due to growth of anaerobic organisms)
Swinging fever, malaise and weight loss

58
Q

Malaise

A

Discomfort

59
Q

Empyema (pneumonia)

A

Spread of infection to pleural cavity
Presence of pus in pleural cavity
Arises from bacterial spread from pneumonia, after a rupture of lung abscess in pleural space
Empyema cavity becomes infected with anaerobic organisms, patient severely ill with high fever and neutrophil granulocytosis

60
Q

Yellow/green sputum

A

Sputum neutrophils, bacterial colonisation/infection. Antibiotics will be effective

61
Q

Blood in sputum

A

Neoplasm/pulmonary infarct

62
Q

Serous/frothy/pink sputum

A

Blood present

63
Q

Foamy white sputum

A

Obstruction
Odema
Ineffective against antibiotics, may be viral

64
Q

Rusty coloured sputum

A

Pneumococcal bacteria

65
Q

Erythromycin (macrolides)

A

Macrolides inhibit bacterial protein synthesis by inhibitory effect on translocation (tRNA shifting from A to P site)
A remains occupied, therefore addition of incoming tRNA and its attached amino acid to the polypeptide chain is inhibited, interfering with production of functional proteins
Macrolide antibiotics bind reversibly to P site on subunit 50S of bacterial ribosome (bacteriostatic, may be bactericidal at high conc.)

66
Q

Antimicrobial spectrum of erythromycin

A

Similar to penicillin, safe and effective alternative for penicillin sensitive patients

67
Q

Erythromycin effective against

A

Gram positive bacteria and spirochaetes, not against gram negative organisms

68
Q

Can resistance against erythromycin occur

A

Yes

69
Q

Side effects of erythromycin

A

Gastrointestinal disturbances
Hypersensitivity reactions (skin rashes and fever)

70
Q

Cefuroxime (cephalosporin)

A

Treats pneumonia
All B lactam antibiotiss interfere with synthesis of bacterial cell wall peptidoglycan

71
Q

Action of Cefuroxime (cephalosporin)

A
  1. Attacks cell wall
  2. Attaches via B lactam ring to the target cell wall (Penicillin binding protein PBP)
  3. Changes functional group of protein on cell wall, causes inhibition of transpeptidition enzyme that cross links the peptide chains attached to backbone of peptidoglycan
  4. Cell wall weakened and crumbles. Extracellular fluid enters bacteria, leading to death of bacteria
  5. Bacteria can respond by producing B lactamase, however cefuroxime is B lactamase resistant
72
Q

Side effects of cefuroxime (cephalosporin)

A

Hypersensitivity reactions

73
Q

What is Lung fibrosis?

A

Excessive deposition of collagen and other Extracellular matrix components in lungs
“Scarring of the lung”

74
Q

Lung fibrosis symptom

A

Shortness of breath

75
Q

Pathogenesis of lung fibrosis

A

Result of chronic injury leading to chronic inflammation associated with: proliferation and activation of macrophages and lymphocytes, production of inflammatory and fibrogenetic growth factors, production of cytokines

Case 3 Sem 2 (1 decks)

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