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ESA3 > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

What is Boyle’s law?

A

The pressure of gas is inversely proportional to volume at a constant temperature in a closed system, so if a given amount of gas is compressed into a smaller volume pressure will increase.

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2
Q

What is Charles’s law?

A

Increasing temperature increases the kinetic energy so pressure increases

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3
Q

Why is the partial pressure of oxygen in the alveolus less than the atmosphere?

A

Air becomes saturated as it passes through the nose and water molecules exert a gas vapour pressure, thus reducing the partial pressure of oxygen.

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4
Q

What is meant by tension?

A

Dissolved gases exert tension on liquid, at equilibrium the partial pressure is equal to the tension.

Amount of gas dissolved = solubility X tension

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5
Q

Why might a diver get ‘the bends’?

A

Pressure below the sea level is 1atm + the weight of the water so air inspired is at a higher level than on the ground.
N2 moves from high pressure in the lungs into the blood, when returning to the surface quickly N2 does not have time to completely leave the blood and forms gas bubbles.

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6
Q

Name the paranasal sinuses:

A

Frontal sinus, ethmoid sinus, maxillary sinus, sphenoid sinus

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7
Q

What are the functions of the nasal cavity?

A

Filters air, humidifies and warms air, contribute to sense of smell, receives local secretions.

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8
Q

What is the larynx?

A

Vocal cords act as a ‘valve’ guarding the entrance to the trachea.
Open in respiration, closed when swallowing, partially closed in speech.

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9
Q

What is the glottis?

A

2 vocal cords and the aperture between them, moved by the intrinsic muscles of the larynx.
Adduction closes, abduction opens glottis.

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10
Q

What can cause hoarseness of voice?

A

Damage to the left recurrent laryngeal nerve that supplies the intrinsic muscles of the larynx.

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11
Q

Describe the histology throughout the respiratory tract:

A

Nasal cavity to bronchioles- pseudostratified columnar ciliated epithelium with goblet cells
Terminal bronchioles- simple columnar with cilia and Clara cells
Respiratory bronchioles and alveolar ducts- simple cuboidal with Clara cells
Alveoli- simple squamous, type I and II cells

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12
Q

Describe the histology if the olfactory region:

A

Tall pseudostratified epithelium with microvilli and olfactory cells (bipolar neurones associated with non-motile cilia to increase surface area and respond to odours).

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13
Q

What is the function of Clara cells?

A

Secrete surfactant lipoproteins that prevent walls sticking on expiration and Clara cell protein which is a maker is bronchoalveolar lavage fluid and serum.

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14
Q

What is the structure of alveoli?

A

Have capillaries supported by basket work of elastic and reticular fibres, type I pneumocytes and type II cells that secrete surfactant.

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15
Q

What is a partial pressure?

A

Molecules of gas behave independently and each gas exerts a fraction of the total pressure in a mixture

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16
Q

What makes up the bony thorax?

A

12 thoracic vertebrae, 12 ribs and costal cartilages, sternum

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17
Q

Describe the differences between ribs:

A

Ribs 1-7 connected by costal cartilages
8-10 connected to costal cartilage above
11+12 ‘floating ribs’ end free in abdominal muscles

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18
Q

List the features of a typical rib and the differences in atypical ones:

A

Typical- 2 articulate facets, head, neck, tubercle, shaft, costal groove and transverse process.
Atypical ribs- first rib is the shortest with only a single head facet, second rib has a poorly marked costal groove, 11/12 have a single facet and a no tubercle

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19
Q

How do the intercostal muscles move the ribs?

A

External, internal and innermost muscles in the intercostal spaces.
External muscles elevate upper ribs to increase AP diameter and elevate lower ribs to increase lateral diameter.
Internal and innermost muscles depress ribs in forced expiration.

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20
Q

Why should a chest drain be inserted at the bottom of an intercostal space above the next rib?

A

The neurovascular bundle (VAN) runs in the costal groove on the inferior surface of each rib between the internal and innermost intercostal muscles.

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21
Q

What is the neurovascular supply to the intercostal muscles?

A

Nerves from anterior rami of T1-12 supply muscles skin and parietal pleura.
Anterior intercostal artery from internal thoracic and posterior from the thoracic aorta.
Venous drainage into the azygous system.

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22
Q

At what vertebral levels do various structures cross the diaphragm?

A

IVC T8, oesophagus T10, aorta T12

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23
Q

What is the nervous supply to the diaphragm?

A

C3,4,5 phrenic nerve

Also is sensory to the pericardium and mediastinal pleura.

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24
Q

What is the ‘pleural seal’?

A

Pleural fluid resists the parietal and visceral pleura from pulling apart.

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25
Q

What passes through the hilum of the lung?

A

Pulmonary vessels, bronchus, nerves and lymphatics

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26
Q

What is meant by a bronchopulmonary segment?

A

An area of lung supplied by its own segmental bronchus and segmental branches of the pulmonary artery and vein.

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27
Q

What are the boundaries of the mediastinum?

A

Superior boundary- thoracic inlet and plane through sternal angle
Anterior- body of sternum and fibrous pericardium
Posterior- between pericardium and vertebral bodies

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28
Q

How do we bring about inspiration?

A

Contraction of diaphragm and external intercostals to increase volume and decrease intrathoracic pressure so air moves in

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29
Q

Explain expiration:

A

Passive elastic recoil decreases volume and increases the intrathoracic pressure so air flows out.

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30
Q

Explain what happens in forced expiration:

A

Requires force exerted by abdominal muscles (external and internal oblique, rectus abdominis) and rest of the intercostals

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31
Q

What are the accessory muscles required for forced inspiration?

A

Sternocleidomastoid, scalene, serratus anterior, pectoralis major

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32
Q

What is meant by lung compliance?

A

Stretchiness, volume change per unit pressure change. So compliance means easier to stretch. Elastic recoil is inversely proportional to compliance.

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33
Q

What is the purpose of surfactant?

A

Reduces surface tension and therefore compliance.

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34
Q

Why do smaller alveoli not collapse?

A

Alveoli get bigger surface tension increases and surfactant is not as effective so pressure is higher and therefore equalised to the smaller alveoli.

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35
Q

What causes infant respiratory distress syndrome?

A

Premature babies have too little surfactant so there are a few large alveoli and lungs are very stiff so breathing and gas exchange is compromised.

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36
Q

What is Poiselle’s Law?

A

Small tubes have high flow resistance but branching increases parallel airways thus reducing overall resistance. Therefore highest resistance is in the trachea and larger bronchii, and lowest in the small airways.

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37
Q

How would you calculate pressure?

A

Number of moles X gas constant X absolute temp / volume

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38
Q

What is Fick’s law?

A

Diffusion rate = pressure difference X cross-sectional area X solubility / distance X sqrt(molecular weight)

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39
Q

Does O2 or CO2 diffuse faster- explain why:

A

Oxygen is smaller so diffuses faster through gases.

Carbon dioxide is much more soluble than oxygen so diffuses faster through liquid e.g. in tissues.

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40
Q

How can you calculate permeability?

A

Diffusion coefficient X solubility / thickness of membrane

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41
Q

What makes up the diffusion barrier?

A

5 cell membranes, 3 layers of cytoplasm and 2 layers of tissue fluid

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42
Q

What factors can affect the rate of gas diffusion across a membrane?

A 
Thickness (increased by oedema)
Surface area (reduced by emphysema)
- diffusion coefficients and pressure differences shouldn't change
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43
Q

Why is exercise not limiting on oxygen diffusion?

A

Equilibrium is reached a third of the way along the capillary so when the partial pressure of carbon dioxide goes up and blood spends less time in the capillary exchange of oxygen is not affected.

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44
Q

What is the advantage of several breaths being required to totally exchange alveolar air?

A

Guards against sudden changes in blood gas levels so of respiration is temporarily interrupted blood gas levels and pH are unaffected

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45
Q

How could you calculate the alveolar ventilation rate?

A

Pulmonary ventilation rate (TV X RR) - dead space ventilation rate (DSV X RR)

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46
Q

What is meant by physiological dead space?

A

Anatomical dead space (volume of airways measured by nitrogen washout) and distributive dead space (parts of lungs not functioning e.g. damaged alveoli)

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47
Q

What are the advantages of lung function tests?

A

Non-invasive, cheap, technically simple

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48
Q

Explain the principles of spirometry:

A

Subject breathes from a closed chamber over water attached to a pen which creates a Spirograph trace.

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49
Q

What affects vital capacity?

A

Compliance on inspiration, force of inspiration muscles, airway resistance on expiration

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50
Q

What is meant by FEV1.0?

A

Volume expired in the first second

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51
Q

How would you recognise an obstructive pattern on a flow volume plot?

A

Same volume expired, curve falls more rapidly.

FVC normal, FEV1 reduced

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52
Q

How would you recognise a restrictive pattern on a flow volume plot?

A

Less volume expired, curve narrowed. Decreased FVC, FVC:FEV1 ratio the same.

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53
Q

What are the features of myoglobin?

A

Binds one oxygen molecule. Stored in muscles.

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54
Q

What are the features of haemoglobin?

A

Binds four oxygen molecules in tetramer.
Has 2 alpha chains and 2 beta chains.
Low affinity T state, high affinity R state with cooperative binding.

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55
Q

What is the Bohr shift and what is its physiological significance?

A

pH is lower in metabolically active tissues so extra oxygen is given up (curve is shifted to the right).
Increased temperature also shifts curve to the right.

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56
Q

How does carbon monoxide affect blood?

A

Reacts to form CoHb and increases the affinity of subunits for oxygen but don’t give up to tissues.

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57
Q

What is pulse oximetry?

A

Detects level of haemoglobin saturation by differences in light absorption (only arterial).

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58
Q

What is the Henderson-Hasselbach equation?

A

pH=pK + Log10(HCO3/pCO2 x solubility factor 0.23)

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59
Q

What reactions take place in red blood cells?

A

Conversion of CO2 to bicarbonate ions using carbonic anhydrase which are extruded by the chloride bicarbonate exchanger. Hydrogen ions bind to haemoglobin.

60
Q

How does haemoglobin act as a buffer?

A

If more oxygen binds there is more R-state so less hydrogen binds to haemoglobin and buffering capacity is reduced.
If more H+ binds then there is less oxygen so more cells in T-state.

61
Q

What reactions allow very little pH change in venous blood?

A

More oxygen is lost so more hydrogen is bound to haemoglobin allowing the formation of more bicarbonate to form and be exported into plasma but increases dissolved carbon dioxide so little pH change.
Extra hydrogen ions from tissues combine with bicarbonate to produce carbon dioxide that is breathed out.

62
Q

How is carbon dioxide transported in the blood?

A

As hydrogen carbonate, carbamino compounds (bound to amine groups of Hb) and dissolved in plasma.

63
Q

What is hypoventilation and hyperventilation?

A

Hyperventilation- increased ventilation without change in metabolism, leading to hypocapnia and respiratory alkalosis.
Hypoventilation- decreased ventilation without change in metabolism, leading to hypercapnia and respiratory acidosis.

64
Q

What determines plasma pH?

A

Ratio of bicarbonate ions to pCO2.

65
Q

What do peripheral chemoreceptors do and where are they located?

A

Located in carotid and aortic bodies.
Triggered when metabolic demands are not met e.g. large falls in pO2 stimulates hyperventilation, changes in HR and blood flow distribution.

66
Q

How do central chemoreceptors operate and where are they located?

A

Found in the medulla of the brain.
BBB is impermeable to bicarbonate and hydrogen ions, only CO2 passes, hydrogen ions are then produced using carbonic anhydrase and released into the CSF.
Bicarbonate ions in CSF are controlled by choroid plexus cells, these cells may change the concentration of bicarbonate and “reset” then system.

67
Q

What causes persisting hypoxia?

A

Hyperventilation decreases pCO2 so choroid plexus cells alter bicarbonate and hydrogen ion composition to “accept” the lower pCO2 as normal.

68
Q

What is hypoxia?

A

Oxygen deficiency at tissue level, measured by SaO2

69
Q

What types of hypoxia are there?

A

Respiratory, anaemic, circulatory, cytotoxic (e.g. Cyanide poisoning)

70
Q

What is respiratory failure?

A

Not enough oxygen enters the blood and not enough carbon dioxide leaves the blood, caused by ventilatory failure, poor diffusion, V/Q mismatch.

71
Q

How can you classify type 1 and type 2 respiratory failure?

A

Type 1- pO26.1kPa

72
Q

What causes ventilatory failure?

A

Stiff lungs, high airway resistance, respiratory centre depression.
Causes type II respiratory failure with hypoventilation and high pCO2

73
Q

What can cause poor diffusion?

A

Fibrotic lung disease, pulmonary oedema, emphysema.

Causes type I respiratory failure with hyperventilation due to decreased SA/increased diffusion distance.

74
Q

What causes ventilation/perfusion mismatch?

A

Caused by pulmonary embolism, pneumonia, COPD.

Causes type I respiratory failure with hypoxic vasoconstriction and hyperventilation.

75
Q

What are the clinical features of respiratory failure?

A

Tachypnoea, cerebral hypoxia, cyanosis

76
Q

Why is it dangerous to deliver high flow oxygen to patients with COPD?

A

COPD leads to hypercapnia which is then adjusted for in the brain so the central chemoreceptors can no longer react to increasing pCO2, thus respiratory drive is now driven by hypoxia, if this oxygen is delivered then the patient may lose respiratory drive.

77
Q

What is asthma?

A

Chronic disorder characterised by reversible airflow obstruction, airway wall inflammation and an increase in airway responsiveness.

78
Q

What can trigger airway smooth muscle contraction?

A

Muscarinic agonists, histamine, cold air, arachadonic acid metabolites e.g. Prostaglandins

79
Q

What causes asthma?

A

Family risk, sensitivity to allergens, hygiene hypothesis

80
Q

What are the symptoms of asthma?

A

Expiratory wheeze, breathlessness, chest tightness, dry cough (worse at night)

81
Q

What investigations might you carry out for asthma?

A

Diurnal variation to PEFR, reversibility of restriction patterns on spirometry, hyperesonant lung fields and allergy testing e.g. skin prick

82
Q

How would you manage asthma?

A

Education, personal asthma action plan, primary prevention e.g. stop smoking.
Beta-2 agonists or muscarinic antagonists, anti-infammatories and corticosteroids

83
Q

What are the signs of life-threatening asthma?

A

Cyanosis, SaO2

84
Q

What is COPD?

A

Condition characterised by airflow obstruction that is progressive and not fully reversible, predominantly caused by smoking.

85
Q

How does emphysema affect ventilation?

A

Destruction of terminal bronchioles and distal air spaces leading to loss of alveolar airspace surface area and development of bullae. Small airways close on expiration due to loss of supporting tissue causing hyperinflation (inability to recoil).

86
Q

What are the effects of chronic bronchitis?

A

Chronic mucus hypersecretion following inflammation in large airways leading to proliferation of mucus secreting cells, remodelling and narrowing of the airways.

87
Q

What can cause COPD?

A

Smoking, alpha-antitrypsin deficiency, occupation exposure

88
Q

What are the symptoms of COPD?

A

Productive cough, progressive breathlessness, infective exacerbations

89
Q

What signs might a patient with COPD have?

A 
Purse lip breathing 
Tachypnoea
Use of accessory muscles 
Barrel chest 
Wheeze
Cyanosis and CO2 retention flap
Cor pulmonale with oedema
90
Q

How would you diagnose COPD?

A

Spirometry, FEV1

91
Q

How do beta2 agonists work?

A

Activates adenylyl cyclase which increases cAMP that activates PKA leading to phosphorylation of MLCKs and relaxation of bronchial smooth muscle.

92
Q

What are the benefits of methylxanthines?

A

Cause bronchodilation and increased respiratory drive with anti-inflammatory action

93
Q

How would you manage an acute exacerbation of COPD?

A

Controlled oxygen therapy (only if patient does not retain CO2)
Nebulised bronchodilators
Steroids
Antibiotics

94
Q

What compromises to respiratory defences may cause a patient to be susceptible to infection?

A

Viridans streptococci, Neisseria spp, streptococcus pneumoniae, strep. pyogenes and Haemophilus influenzae

95
Q

What is acute bronchitis?

A

Inflammation of medium sized airways causing cough, shortness of breath, fever

96
Q

What is pneumonia?

A

Inflammation of the lung alveoli leading to exudation of fibrin-rich fluid and infiltration of neutrophils and macrophages.

97
Q

What organisms cause community acquired pneumonia?

A

Strep. Pneumoniae
H. Influenzae
Kleibsella pneumoniae
M. Cattharlis

98
Q

What are the symptoms of CAP?

A

Shortness of breath, productive cough with yellow/green sputum, fever, rigors, pleuritic chest pain, malaise, nausea, vomiting.

99
Q

What might you find on examination of a patient with pneumonia?

A

Pyrexia, tachycardia, tachypnoea, cyanosis, dullness to percussion, tactile vocal fremitus, bronchial breathing and crackles

100
Q

What is the CURB65 score?

A

Confusion, urea>7mmol/L, respiration rate>30, BP

101
Q

What empiric antibiotic therapy would you prescribe for CAP?

A

Amoxicillin or in severe cases co-amoxiclav and clarithromycin

102
Q

What antibiotic therapy would you prescribe for an atypical pneumonia and why?

A

They are caused by organisms without a cell wall so protein synthesis agents are required e.g. erythromycin, doxycycline

103
Q

How does viral pneumonia affect the host?

A

Damages linings of the airways by viral replication and the immune response. If severe it can cause necrosis/haemorrhage into lung parenchyma leading to ARDS

104
Q

What organisms are likely to cause hospital acquired pneumonia?

A

Occurs after 48 hours in hospital

Staphylococcus aureus, pseudomonas spp, h. Influenzae

105
Q

How would you treat hospital acquired pneumonia?

A

Treat with co-amoxiclav then meropenem

106
Q

What are the features of mycobacterium tuberculosis?

A 
Non-motile rod-shaped bacteria 
Obligate anaerobes
Transmitted by respiratory droplets
Fatty acid complex waxes and glycolipids in cell walls
Survives and multiplies in macrophages
107
Q

Explain the pathogenesis of TB infection?

A

Inhaled aerosols are engulfed by alveolar macrophages and travel to local lymph nodes where they form a primary complex made up of Ghon’s focus and draining LN.
May progress to a primary TB infection, or be initially contained and then lead to a latent infection that can later be reactivated to produce post-primary TB.

108
Q

What are the symptoms of primary TB?

A

Fever, night sweats, weight loss, cough, haemoptysis, breathlessness (if effusion)

109
Q

How can you confirm a diagnosis of TB?

A

Microscopy- Ziehl-Nielsen stain

Culture takes 6 weeks

110
Q

How can you test for TB?

A

Intradermal tuberculin sensitivity test (may have false positives due to BCG and false negatives in immunocompromised patients)
Interferon gamma releasing assays (IGRAs) are antigen specific, there is no cross reaction to BCG but cannot distinguish between latent and active TB.

111
Q

What drugs are used to treat TB?

A

Rifampicin (may cause reduced efficacy of the contraceptive pill, orange secretions)
Isoniazid
Pyrazinamide
Ethamburol

112
Q

What are MDR and XDR strains of TB resistant to?

A

MDR- resistant to Rifampicin and isoniazid

XDR- also resistant to fluoroquinolones and one injectable

113
Q

What is miliary TB?

A

Lungs involved but few respiratory symptoms, often multiple organs involved e.g. pericardial/pleural effusion

114
Q

Give examples of extra pulmonary TB:

A 
GI
Peritoneal
Genitourinary
Bone and joint 
Meningitis
115
Q

What is a BCG vaccine?

A

Live attenuated strain of M. Bovis strain, but protection wanes

116
Q

What are the risk factors for lung cancer?

A

Smoking, asbestos, radon, occupational carcinogens, genetic risk

117
Q

How is lung cancer staged?

A

TNM staging, I-IV

Ia to IIb can offer radical treatment

118
Q

What can be symptoms of lung cancer?

A

Cough, dyspnoea, wheezing, haemoptysis, Lin infection, chest/shoulder pain, weight loss/malaise

119
Q

Give examples of paraneoplastic syndromes:

A

Endocrine- hypercalcaemia, Cushing’s syndrome, SIADH
Neurological- encephalopathy, peripheral neuropathy
Haematological- anaemia, thrombocytosis
Cutaneous- dermatomyositis
Skeletal- finger clubbing

120
Q

What types of lung cancer are there?

A

Non small cell- squamous cell carcinoma, adenocarcinoma, large cell carcinoma
Small cell carcinoma
Rare carcinoid tumours

121
Q

How can you treat lung cancer?

A

Surgery, radiotherapy, combination chemotherapy, biologically targeted therapy, palliative care

122
Q

What types of biopsy can be used to diagnose lung cancer?

A

Bronchoscopy, cervical lymph node fine needle aspiration, thoracocentesis, organ biopsies

123
Q

What are the symptoms of interstitial lung disease?

A

Shortness of breath, dry cough, cyanosis, tachypnoea and clubbing

124
Q

Give examples of some causes of interstitial lung disease:

A

Occupational e.g. Asbestosis, coal worker’s pneumoconiosis
Treatment e.g. Radiation/chemotherapy and methotrexate
Connective tissue disease e.g. Scleroderma, rheumatoid arthritis
Immunological e.g. Sarcoidosis
Idiopathic pulmonary fibrosis

125
Q

How does asbestos damage the lungs?

A

Causes plaques, diffuse pleural thickening, asbestosis and mesothelioma

126
Q

What are the features of idiopathic pulmonary fibrosis?

A

Usually occurs in 60-80 year olds

Diagnosed by CT

127
Q

What are the functions of the pleural space?

A

Allows movements of lung and chest wall, couples the chest wall to the lungs and allows pleural fluid circulation

128
Q

How is the pleura innervated?

A

Parietal pleura has somatic, sympathetic and parasympathetic innervation by the phrenic and intercostal nerves.
Visceral pleura is devoid of somatic innervation.
Pleuritic chest pain is described as a severe knife-like pain worse on inspiration.

129
Q

What is the daily production of pleural fluid and how is it turned over?

A

15ml per day produced by capillary filtration and absorbed by lymphatic drainage.

130
Q

How would you treat a pleural effusion?

A

Fluid obtained by thoracocentesis and is analysed for appearance, cell count, protein, LDH, glucose and amylase

131
Q

What types of pleural effusion are there?

A

Haemothorax caused by trauma
Chylothorax with milky appearance usually caused by lymphoma
Empyema caused by pus
Exudate caused by infection, TB, malignancy, PE
Translate caused by heart failure, cirrhosis, nephrotic syndrome

132
Q

What are the symptoms of pneumothorax?

A

Pleuritic chest pain, dyspnoea, hyperresonant to percussion

In tension pneumothoraces- mediastinal shift, cardiovascular compromise

133
Q

What causes a pneumothorax and how can you treat it?

A

May be spontaneous, iatrogenic or due to underlying lung disease
Treated by aspiration, thoracotomy/pleurectomy or thorascopy

134
Q

Give examples of chest wall disease?

A

Congenital pectus deformities, scoliosis/kyphosis, muscular dystrophy
Acquired trauma, ankylosing spondylitis, MND

135
Q

What are the symptoms of interstitial lung disease?

A

Shortness of breath, dry cough, cyanosis, tachypnoea and clubbing

136
Q

Give examples of some causes of interstitial lung disease:

A

Occupational e.g. Asbestosis, coal worker’s pneumoconiosis
Treatment e.g. Radiation/chemotherapy and methotrexate
Connective tissue disease e.g. Scleroderma, rheumatoid arthritis
Immunological e.g. Sarcoidosis
Idiopathic pulmonary fibrosis

137
Q

How does asbestos damage the lungs?

A

Causes plaques, diffuse pleural thickening, asbestosis and mesothelioma

138
Q

What are the features of idiopathic pulmonary fibrosis?

A

Usually occurs in 60-80 year olds

Diagnosed by CT

139
Q

What are the functions of the pleural space?

A

Allows movements of lung and chest wall, couples the chest wall to the lungs and allows pleural fluid circulation

140
Q

How is the pleura innervated?

A

Parietal pleura has somatic, sympathetic and parasympathetic innervation by the phrenic and intercostal nerves.
Visceral pleura is devoid of somatic innervation.
Pleuritic chest pain is described as a severe knife-like pain worse on inspiration.

141
Q

What is the daily production of pleural fluid and how is it turned over?

A

15ml per day produced by capillary filtration and absorbed by lymphatic drainage.

142
Q

How would you treat a pleural effusion?

A

Fluid obtained by thoracocentesis and is analysed for appearance, cell count, protein, LDH, glucose and amylase

143
Q

What types of pleural effusion are there?

A

Haemothorax caused by trauma
Chylothorax with milky appearance usually caused by lymphoma
Empyema caused by pus
Exudate caused by infection, TB, malignancy, PE
Translate caused by heart failure, cirrhosis, nephrotic syndrome

144
Q

What are the symptoms of pneumothorax?

A

Pleuritic chest pain, dyspnoea, hyperresonant to percussion

In tension pneumothoraces- mediastinal shift, cardiovascular compromise

145
Q

What causes a pneumothorax and how can you treat it?

A

May be spontaneous, iatrogenic or due to underlying lung disease
Treated by aspiration, thoracotomy/pleurectomy or thorascopy

146
Q

Give examples of chest wall disease?

A

Congenital pectus deformities, scoliosis/kyphosis, muscular dystrophy
Acquired trauma, ankylosing spondylitis, MND

ESA3 (5 decks)

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