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OSCE - Respiratory Year 1 > respiratory > Flashcards

respiratory Flashcards

1
Q

The types of respiratory disorders are …..

A

Restrictive and obstructive

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2
Q

characteristics of restrictive lung conditions are…..

A

Main characteristic is decrease in lung volume & compliance and Increse in WOB
Shrinkage of lung tissue: i.e. lung fibrosis

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3
Q

charcteristics of obstructive repiratory disease are…

A

reduced airflow -
Reversible: e.g. inflammation, bronchospasm, mucus plugging
Irreversible: e.g. fibrotic airway wall, loss of elastic recoil (floppy airway walls)

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4
Q

COPD is…

A

COPD is a common, preventable and treatable disease that is characterised by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities

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5
Q

Chronic Bronchitis is defined by

A

Increased mucus secretion – ↑ size & number of Goblet cells & mucinous glands. Airway obstruction develops from repeated irritation of the airway inflammation causing fibrotic changes, bronchospasm

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6
Q

Emphysema is defined by

A

Emphysema is defined by structural changes – enlargement of alveoli - increase residual volume

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7
Q

How is COPD caused by smoking ?

A

Caused by irritants like tobacco smoke that triggers an inflammatory reaction in the alveoli, release inflammatory cells & mediators (e.g. macrophages, neutrophiles, cytokines, Neutrophils, destructive proteases & collagenases breaks down elastin & collagen causes loss of elastic recoil (floppy airway)

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8
Q

COPD is?

A

The defining feature of COPD is persistent expiratory airflow limitation (lungs don’t empty properly leaving air trapped inside) Additional pathophysiological features include gas trapping and gas exchange abnormalities secondary to parenchymal tissue destructions, mucus hypersecretion, pulmonary hypertension, exacerbations and systemic morbidity

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9
Q

COPD management

A
  • Stop smoking!•Pharmacological: bronchodilators, inhaled corticosteroids, antibiotics, Oxygen (LTOT)
  • Corticosteroids – normally combined with LABAo Inhaled: Budesonide, fluticasone, mometasone, ciclesonide•LTOT: for patients with severe resting arterial hypoxaemia. Clearly specify dosage L / day (hr)
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10
Q

Physiotherapy issues with COPD

A

Dyspnoea – signs of ↑ WOB – increased residual volume••Retained secretions•

•↓ Exercise Tolerance•

•Musculoskeletal dysfunction of the thoracic cage and limbs (i.e. peripheral muscle weakness

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11
Q

Bronchiectasis – Definition

A

•Abnormal and permanent dilation and distortion of the bronchi and bronchioles, resulting from chronic inflammation of the airways, and leading destruction of the bronchial walls/lungs

  • This permanent bronchial damage can lead to a vicious cycle of bacterial infections and impaired mucus clearance•
  • Main clinical features: cough with mucus hypersecretion and airflow limitation
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12
Q

Type 1 respiratory failure

A

•Type I respiratory failure - hypoxaemic RF•PaO2 < 8KPa (60mmHg) •PaCO2 = normal or low (termed normocapnic/hypocapnic)

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13
Q

Type 2 respirtory failure

A

•Type II respiratory failure - hypoxaemic & hypercapnicRF•PaO2 < 8KPa

AND

•PaCO2 >6.0KPa (some literature 6.5KPa - 40/45mmHg)

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14
Q

Causes of respiratory failure ?

A

lack of neural stimulation - phrenic nerve (C3,4,5 - keeps diaphragm alive), cardial failure, lack of 02 to the alveoli

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15
Q

tachypnea

A

Fast breating

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16
Q

Stridor

A

Loud nasal breathing

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17
Q

hypocemia ?

A

too much C02 in the blood

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18
Q

hypocapnia

A

hypocapnia, is a decrease in alveolar and blood carbon dioxide (CO2) levels below the normal reference range of 35 mmHg. CO2 is a metabolic product of the many cellular processes within the body involved in the processing of lipids, carbohydrates, and proteins.

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19
Q

normal breaths per minute ?

A

12 - 20

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20
Q

Normal 02 sats ?

A

96%

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21
Q

Normal pH value ?

A

7.35 - 7.45

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22
Q

PaC02 normal value

A

4.7- 6 kPa

35-45 mmHg

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23
Q

What is Bronchiectasis ?

A

permanent dilation and distortion of the bronchi and bronchioles, resulting from chronic inflammation of the airways, and leading to progressive destruction of the bronchial walls and lung parenchyma. •This permanent bronchial damage can lead to a vicious cycle of bacterial infections and impaired mucus clearance​

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24
Q

treatment of Bronchiectasis

A

chest physio…..

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25
Q

Brochiectasis signs and symptoms

A

constant cough and infections, due to damaged cillia and unable to remove mucus. (can be as a result of other lung diseases)

causinf fatigue, weightloss and shortness of breath

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26
Q

(COPD) bronchitis is

A

defined by it’s symptoms - persistant cough* inflammation of the brochi

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27
Q

emphysema

A

structural changes to the alveoli where they are Overinflation of the air sacs is a result of a breakdown of the alveoli walls. It causes a decrease in respiratory function and breathlessness. Damage to the air sacs can’t be fixed. It causes permanent holes in the lower lung tissue.

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28
Q

Scenario 1:

•54 year old lorry driver•Admitted post road traffic accident•Emergency laparoscopic liver surgery•Now medically stable and extubated•Residual right basal atelectasis•Prescribe ACBT to reduce the atelectasis

A

Breathing technique - then thorasic expansions on affected side - with a hold… then out (patient can do their own BT after demonstartion). They hold then sniff in which allows alveolar expansion. as you run through the cycle.

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29
Q

Atelectasis is?

A

Atelectasis (at-uh-LEK-tuh-sis) is a complete or partial collapse of the entire lung or area (lobe) of the lung. It occurs when the tiny air sacs (alveoli) within the lung become deflated or possibly filled with alveolar fluid

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30
Q

factors that affect the oximeter ?

A
  • No nail varnish, acrylics or gel nails
  • Fingers should be clean
  • Fingers should be warm
  • Avoid bright overhead light
  • Make sure the battery is working
  • If monitoring continuously, change the finger used regularly to avoid pressure damage
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31
Q

Positioning with V/Q mismatch ?

A

Lie the patient on the good lung so that the bad lung is able to drain and you’re able to access it and the good lung can compensate and improve ventilation.

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32
Q

Cystic fibrosis is ?

A

Gentic condiion which causes excess sputum in the lungs and digesive system.

identifyied by the heel prick test. signs and coughing and regular chest infections.

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33
Q

Postural position for anterior lobe

A
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34
Q

posterior apex (apical segment) drainage

A
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35
Q

anterior lung drainage

A
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36
Q

right postrior lung drainage

A
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37
Q

left posterior segement

A
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38
Q

right middle lobe

A
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39
Q

left bottom (lingular)

A
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40
Q

anterior lower lobes

A
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41
Q

anterior right (lower) segmement

A
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42
Q

left lateral lower segement

A
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43
Q

Posterior lower segements

A
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44
Q

anterior/superior segments lung drainage

A
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45
Q

Cystic Fibrosis cause/aetiology ?

A

Aetiology: •CFTR: protein that transports chloride ions (Cl-) across cell membranes. Involved in production of sweat, digestive fluid and mucous (exocrine glandular system) → CF: dehydrated & thicken secretions due to imbalance between Cl- & water in/out of cell

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46
Q

A-E systematic approach: Look, Feel and Listen. Objective assessment

A

•Airway: patent? self-ventilating? able to communicate?•Breathing: spontaneous, non-invasive, invasive?, respiratory rate (RR), use of diaphragm, accessory muscles, purse-lip breathing, prolonged expiration? wounds?, Intercostal drains? Auscultate and percuss.••Circulation: patient’s colour, HR, BP, raised JVP, fluid charts•Disabilities: level of consciousness•Exposure: other considerations – trauma / fracture / fall risk – mobility

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47
Q

Breathing techniques for bronchiectasis

A

Forced Expiratory technique - FET - 1 level huff

  • Take a normal sized breath in. Open the mouth to an O shape or place breathing tube in the mouth•Breathe out with some force (not a lot of force) and good flow
  • The breath out is similar to fogging up a mirror – use a tissue in front of the mouth to check technique - 3 levels are Small, medium and large
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48
Q

ABCT is important becuase

https://bronchiectasis.com.au/resources/videos/the-active-cycle-of-breathing-technique

A

improves ventilation of the lungs and assist in the clearance of excess secretions.

use bronchoddilators before use and the technique is generally taught in sitting.

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49
Q

ABCT teaching the tecnhique

A

The ACBT is taught in 3 stages. Breathing control (hand on diaphragm x5). Thoracic expansion exercises (holding ribcage x5 with a 2-3 second hold). Forced expiratory huff - small, medium and large (fogging up a mirror with an open glottis)

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50
Q

What is V/Q mismatch ?

A
51
Q

Bronchiectasis causes/Aetiology

A

The cause is unknown for 50% of cases, but it has been linked to inflammatory bowel disease, rheumatoid arthritis, and in 29-50% of patients, COPD

52
Q

treatment for bronchiestasis

A

due to 15% reduction in mucus clearance - physiotherapy and education are effective in the removal of consolidated secretions.

53
Q

Management for bronchiestasis

A

bronchodilators - steriods to help with an anti inflammatory response. check sputum isn’t green otherwise it could be infection.

Breathing techniques - Breathing exercise - TTE - hold and huff - helps clearence of secretions - percussions/shaking - through cycle

54
Q

Bronchiestasis treatment

A

Positive Expiratory Pressure (PEP) Devices

flutter and acapella - exhale agiast a fixed resistance - air gets behind the mucus, mucas moves from the lungs to the airway wall and holds the airways open for longer

55
Q

what is asthma?

A

Asthma is a relatively common condition that is characterised by at least partially reversible inflammation of the airways and reversible airway obstruction due to airway hyperreactivity. It can be acute, subacute or chronic[ and/or exercise induced or by allergens (inflammatory response)

56
Q

Treatment for asthma

A

Short/long-acting beta 2-agonists

bronchodilators - relaxing diphragmatic breathing, deeper breathing, decreasing respiratory rate.

Education - using spacers and medication correctly

57
Q

Asthma pathophysiology is?

A

Asthma is characterised by narrowing of the airway and is usually reversable and is an OBSTRUCTIVE lung condistion. The narrowing is caused by bronchconsstriction of the bronchial smooth muscle. Asthma attacks can be caused by pollen, allergens smoke and a rapid change if temperature. The inflammation in the airway can result in yellow mucus and mucus plugging

58
Q

Causes of Asthma

A

Onset in childhood, allergens, pollen, smoke respiratory tract infections and other inhaled irritants

59
Q

Symptoms of asthma include

A

Expiratiory wheeze is a sign of worsening airway obstruction, Accessory muscel use, breathlessness and chest tightness

60
Q

Managment of asthma

A

Inhaled bronchodialators (long and short acting), corticosteriods, PEP therpy, ACBT and manual therapy.

61
Q

Bronchiestasis aetiology

A

Bronchiestasis is caused by lower respiratory tract infections, pneumonia, aspergillosis and can co-exist with other diseases such as COPD

62
Q

Pathophysiology of Bronchiestasis

A

Permanent dialation and distortion of the bronchioloes and damage to the cillia, this causes fibosis and reduces the elastic properties of the bronchial walls. Inflammatory process leads to chronic mucus production and infection (can affect lobes of whole lungs)

63
Q

Symptoms of bronchiectasis

A

A productive cough with sputum, wheeze on auscultation. Exacerbations and crackles on auscultation are associated with SOB, clubbing is common and reduced exercises tolerance

64
Q

Bronchiectasis treatment

A

pulmonary rehab, smoking cessation, antibiotics, clearence techniques in line with timing of nebuliser (techniques that increase hyperinflation to be avoided). ACBT +- PEP, manual therapy and postural drainage

65
Q

COPD Aetiology

A

The leading cause of COPD is smoking in the first world. Biomass fuel exposure (burning biofuels)

66
Q

COPD pathophysiology

A

(Emphysema and bronchitis) The airway becomes inflamed, narrow and floppy which causes airtrapping, hyperinflation and airflow limitation.

67
Q

COPD symptoms

A

SOB, fatigue, wheeze and sputum, use of accessory muscles, hypoxia and reduced exercise tolerance (Barrel shaped chest)

68
Q

COPD management

A

Smoking cessasstion, 02 therapy, pulmonary rehab, airway clearance techniques *avoid any hyperinflation due to already barrel chest/air trapped.

69
Q

Cystic fibrosis aetiology/cause

A

Genetic gene mutation diagnosed by the heel prick at brith that affects the lungs, pancreas and digestive tract. CF reduces the secreetion of chloride and water by the airway cells which increases respiratory secretions and consolidated mucus.

70
Q

Symptoms of Cystic Fibrosis

A

Chronic and productive cough, reduced pancreatic function (poor nutritional status), breathlessness, reduced exercises tolerance and common respiratory infection and heamopysis, weight loss, change of sputum production

71
Q

CF physio treatment

A

Airway cleatance techniques (OBSTRUCTIVE LUNG DISEASE), antibiotics, hypertonic saline ABCT, PEP, manual techniques and postural drainage

72
Q

CF management

A

Avoid hyperinflation * time nebulisors with physio treatement, antibiotics for infection and analgesia, manage breathlessness with breathless managment techniques.

73
Q

Interstitial lung disease Cause/aetiology

A

Group of lung diseases that cause fibrosis of the lungs interstitium (space around the alveoli). It is irreversable and it can be idopathic or secondary to connective tissue disorder, inhaled substances, infection, drug or malignancy.

74
Q

Pathophysiology of interstitial lung disease

A

Repetitive injury to the alveoli epithelium, capillary endothelium and basal membrane causes an overreacted tissue repair cascade. This lays down fibrotic scar tissue which leads to restricted and impaired gas diffussion, over time the interstituim thickens leading to lung infection.

75
Q

Interstitial lung disease symptoms

A

Dyspnoea (), non productive cough, and end expiratory crackles, you may alos see weight loss and fatigue, clubbing and cyanosis.

76
Q

Managment of interstitial lung disease

A

02 therapy, corticosteriods (prednisilone), reduce exertion, improve lung mechnics, pulmonary rehab, smoking cessation

77
Q

ACBT contraindications?

A

Subject tolerance

78
Q

ACBT precautions ?

A

Cardiovascular instability, wheeze, SOB, symptoms of hyperventilation, Coughing in rapid succession with increasing intensity,

79
Q

Contraindications to Percussion, shakes and vibration ?

A

Prolonged use of high dose steroids (bone weakness), unstable bone fractures, osteoporosis, osteopenia, wheezing, bronchial hypersensitivity, burns, Frank heamoptysis, low platelet count (clotting disorder), pulmonary embolus

80
Q

Precautions to Percussion, shakes and vibration

A

Rigid thorax, increased bronchial construction, breathlessness, cardiovascular instability, pulmonary carcinoma paroxysm coughing

81
Q

Underpinning principles of ACBT technique?

A

BC helps dyspnoea, TEE improves collateral ventilation to Improve aeration of alveoli to improve lung volume/compliance. FET- aid with expectation @ different lung volumes- percussion to help expel/ aid secretion removal

82
Q

Underlying pathology of COPD on respiratory function

A

Bronchitis- increases goblet cells and mucus secretions and mucus glands. Air obstruction develops from repeated irritation of the airway, inflammation and fibrotic changes, bronchospasm

83
Q

COPD- emphysema pathology

A

Parenchyma tissue destruction- permanent enlargement and loss of elasticity of the alveolar wall - neutrophils- destructive proteases & Collagenases break down elastin & collagen - causes loss of elastic recoil (floppy airway)

84
Q

Position to reduce WOB ?

A

Sitting, Learning forward on a table or standing with their bum against a wall

85
Q

Teach a patient in a reduced WOK breathing control to reduce dyspnoea ?

A

Hand over diaphragm and focuses on thy rather than the accessory muscles (shortened position), reduces bronchospasm during the forced element of the FET - normal tidal volume breaths with upper chest and relaxed shoulders

86
Q

Assess efficacy of treatment when managing SOB

A

Contraindications: patient tolerance/comfort: RR, HR, improve P02 & reduced use of accessory muscles

87
Q

Asthma pathology

A

Chronic inflammation of the airway - airway obstruction and hypersensitivity of bronchial smooth muscle. Mast cells, neutrophils and macrophages cause inflammation- vasoconstriction/obstruction REVERSIBLE after treatment

88
Q

Postural drainage contact-indications

A

Patient intolerance, ENT surgery, eye surgery, cardiac surgery, unstable spinal cord injury, central insult, anything that will increase intracranial pressure pnumonectomy

89
Q

Postural drainage precautions

A

Hypertension, headache, recent seizure, gastric reflux, full stomach

90
Q

Pneumonia definition

A

LRTI- as inhal breach of lung defences muccocillary escalator, macrophages, inflammation responses of bronchioles, the alveoli fill and consolidate with bacteria blood and puss, may impair V/Q ratio

91
Q

Bronchitis is …..

A

Persisting cough 3 months of the year, with increase in mucus secretion. Increase in goblet cells, sub-mucus glands, decrease number and length of cilia

92
Q

Emphysema definition…

A

Permanent dilation of the air space distal to the terminal bronchioles and destruction to the walls of these airways.

93
Q

Asthma definition

A

All ages but often starts in children, attacks of breathlessness and wheezing. Due to inflammation and irritation of the airway. Reducing airflow in/expiration (WHO 2004)

94
Q

Aetiology of asthma

A

More common in children and boys 10% of children under 10! Most common cause of missing school. Remits after puberty but will come back later in life

95
Q

Definition of lobar pneumonia ?

A

Inflammatory exudate (pus) that leaks from blood vessels due to infection (inflammation, odema) into intra-alveolar space resulting in consolidation of the lobe parenchyma.

96
Q

Stages of lobar pneumonia

A

Congestion: neutrophils & bacteria intra-alveolar space, leaking of fluid (white blood cells/leukocytes) 24 hours. Vascular engorgement Red hepitization/ consolidation: 48-72 hours. Alveoli in the lobes dry, granular and cellular debris consolidates in the alveolar parenchyma. Neutrophil and fibrin break down creating more exudate fluid and macrophages form. Grey hepitization: 4-8 days - neutrophils, fibrin and red cells break down leading to more exudate - macrophages form. Recovery/resolution: 8-10 days: exudate (pus) is cleared by the macrophages cough will be used to clear sputum and lymphatic drainage.

97
Q

Diagnosis of pneumonia

A

Test Sputum/culture. CT scan or X-ray of lungs for light areas of consolidation. Streptococcus bacteria or fungal aspergillosis

98
Q

Complications of pneumonia

A

Respiratory failure, Acute respiratory disease syndrome (ARDS), sepsis.

99
Q

Prevention of pneumonia ?

A

Regular vaccinations for flu etc, anything that will be boost the immune system. Good diet nutrition, not smoking, regular exercise.

100
Q

Risk factor for pneumonia

A

Anything that will suppress the immune system. Smoking, diabetes, heart disease, long term steroid use, flu, HIV, heart failure.

101
Q

Underlying physiological principles of ACBT - Thoracic expansion and Forced Expiratory techniques

A

-ACBT: BC - help with dyspnoea, Thoracic expiratory exercises - collateral ventilation channels to improve aeration of alveoli / improve lung compliance and volume; Forced Expiratory Techniques – aid with expectoration / @ different lung volume.-Percussions: aid secretion expectoration

102
Q

How does COPD affect respiratory function?

A

Airflow limitation = increases mucus secretion, loss of elastic recoil in the lungs, airway collapse and trapping gas, airway inflammation and impair gaseous exchange V/Q mismatch.

chronic inflammation, oxidative stress, protease/antiprotease imbalance

103
Q

Pathology of Chronic Bronchitis

A

repeated irritation of the airway (smoking) causes increase in goblet cells, mucinous glands, chronic inflammation causes fibrotic changes and brochospasm (bronchoconstriction)

hypercapnia and hypocemia and V/P ratio mismatch

104
Q

Emphysema pathology

A

parenchyma tissue destruction permanent enlargement and loss of elasticity of the alveolar walls (increased compliance = negative). Inflammatory mediators and response of cytokines, neutrophils and macrophages. neutrophils release destructive proteases that break down elastin and collagen causing a floppy airway (loss of elastic recoil)

105
Q

Positions for work of breathing

A
106
Q

Underlying pathophysiology of breathing control

A

reduces the risk of bronchospasm during the huff element during the forced expiratory technique, normal tidal volume in the upper chest with relaxed shoulders and the patient. Emphasis use of the diaphragm rather than accessory inspiratory muscles

107
Q

Discuss the underpinning anatomical/physiological principles of the techniques for Breathing techniques for ASTHMA

A

To reduce energy requirements so patient can focus on manage their SOB, provide mechanical advantage for the work of accessory muscles and diaphragm, to control their breathing and try to relax.

108
Q

Any contra-indications to the breathing technique and how you would assess the efficacy of your treatment?

A

Patient’s comfort – RR & HR – Improve SPO2 – reduced use of accessory muscle

109
Q

Pathology of Asthma

A

Chronic inflammatory, reversible airway obstruction due to hypersensitive smooth muscle. Insult cold air, pollen etc, inflammatory response - t cells, mast cells, neutrophils, macrophages, causes bronchospasm (bronchoconstriction). causes wheezing, chest tightness, coughing and is reversible with bronchodilators

110
Q

Postural drainage contraindications

A

subject tolerance, cerebral oedema, cardiovascular instability, undrained pneumothorax, hiatus hernia, ENT surgery, eye surgery, anything that increases intercranial pressure, unstable spinal cord injury, cardiac/gastric surgery, bronchial plural fistula

111
Q

postural drainage precautions

A

hypertension, headache, recent seizure. gastro-reflux, full stomach (eaten with 1.5 hours), abdominal distension

112
Q

Pneumonia Definition

A

LRTI - bacteria/fungi/virus breach the body’s defences and reach the lung parenchyma in alveloi/brocnhi. The inflammatory response of the macrophages fill the alveoli with exudate, consolidating the alveoli with pus.

Congestion -neutrophils, vascular engorgement bacteria/virus/fungi

consolidation ‘red hepatization’ red cells, neutrophils and fibrin, filling the consolidation of the alveolar parenchyma.

Grey hepatization: red cells disintegrate due to neutrophils and fibrin and turn grey.

Resolution: the exudate (pus) is digested by enzyme activity (macrophages) sputum is released by cough or lymph drainage.

113
Q

CONTRAINDICATIONS to percussions, vibrations, shaking

A

subject tolerance, prolonged steroid use, osteoporosis/osteopenia, unstable spine fractures, rib fractures, coughing up blood, thoracic burns and loss of skin integrity, wheeze or bronchial sensitivity, pulmonary embolus

114
Q

precautions to percussion, vibs, shaking

A

breathlessness, bronchial constriction, non compliant rigid thorax, coughing , cardiovascular instability,

115
Q

how to use the Oscillatory PEP (flutter device)

A

used in sitting - inspiration through the nose, slow deep breath, hold for 3-5 seconds, breath out at twice the normal speed until max oscillations is achieved, 4-8 reps. can be used with a cough or FET and BC in a cycle.

116
Q

Pathology of PEP

A

Positive Expiratory Pressure increases resistance to airflow (increase positive pressure). promotes mucus clearance and prevents airway closure by increasing collateral ventilation. A flutter device combines high frequency airflow with positive expiratory pressure. vibration helps move mucus from the surface of the airway.

117
Q

percussion, expiratory vibrations and shaking to assist expectoration of sputum, into the Active Cycle of Breathing Technique (ACBT) what is the pathology of the technique ?

A

•ACBT: BC - reduce WOB, TEE - collateral ventilation channels to improve aeration of alveoli / improve lung compliance and volume; FET – aid with expectoration / @ different lung volume

•Manual Techniques: Aid to mobilise tenacious sputum from airway

118
Q

How to measure efficacy of treatment of percussions, vibrations and ACBT with patients with pneumonia

A

Amount of sputum expectorated – reduced signs respiratory distress – improve SpO2

119
Q

position to increase lung volume

A
120
Q

Teach your patient how to use the Active Cycle of Breathing Techniques (ACBT) to aid secretion removal and reduce breathlessness

A
121
Q

Pathophysiology of ACBT - BC

A

-ACBT: BC – helps with dyspnoeic patients, breathing using least effort; FET – aid with expectoration / @ different lung volume. (1-2 huffs at different pressures)

122
Q

why is pursed lip breathing good for COPD (emphysema) patients ?

A

-Pursed-lip breathing: helps to keep airway open longer during expiration in an attempt to avoid collapsing with the consequent air trapping inside the lungs. Helps to slow down the breathing.

Assess on patients with hyperinflation – remember that in people with emphysema the elastic recoil of the lung is affected (they do not need more air in!)

123
Q

Bronchiectasis affect how many people in the UK?

A

1in 100 people in the UK

124
Q

What is the bronchiectasis cycle

A

Infection -inflammation- impaired mucocillary clearance - bacterial consolidation - destruction of airway - infection

OSCE - Respiratory Year 1 (1 decks)

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