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ASTHMA

ASTHMA

Anatomical structures: Small and large airways

Physiology: Transfer of air in and out of lungs. Efficient gas exchange.

Structural abnormalities: Reversible airflow obstruction and bronchospasm.

Physiological abnormalities: 

  • Inflammatory disorder of the airways
  • Reduces rate of flow to and from alveoli
  • Limits effectiveness
  • Reduction in airflow (worst during expiration) - pressure causes compression rather than expansion.
  • Dynamic hyperinflation: air from previous breath remains in lungs during next breath --> increase in volume of air in the lungs.
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ASTHMA 2

Prior events: 

  • Exposure to allergens and irritants. 
  • Exercise or cold induced.
  • Prior eczma or hay fever.
  • Family history of asthma

Experienced:

  • Wheezing
  • Coughing
  • Chest tightness
  • Shortness of breath

Clinical signs:

  • Wheeze heard with stethoscope on chest
  • Use of accesory respiratory muscles in respiration
  • Paradoxical pulse (weaker during inhalation, stronger during exhalation)
  • Over-inflation of the chest
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ASTHMA 3

Abnormal test results:

  • Reduced FEV1 that is reversible
  • Chest X-Ray shows hyperexpanation of the chest

Medical/ surgical intervention:

  • Inhaled short-acting beta-2-agonist (e.g salbutamol)
  • Long acting beta-2-agonist (e.g salmeterol)
  • Inhaled corticosteroid (e.g. beclometasone)
  • Oral corticosteroid (e.g prednisolone)

Primary and secondary prevention:

  • Avoiding triggers - i.e. allergens, irritants and medications i.e. aspirin.
  • Leukotriene antogonists.
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BRONCHIECTASIS

BRONCHIECTASIS

Anatomical structures: Small and large airways

Physiology: Transfer of air in and out of lungs. Efficient gas exchange. Projection if lungs from infection.

Structural abnormalities: Localised, irreversible dilation of part of the bronchial tree. Associated with wide range of disorders.

Physiological abnormalities: 

  • Bronchi are dilated, inflamed, and easily collapsable resulting in airflow obstruction and impaired clearance of secretion.
  • Obstructive lung disease (same category COPD)
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BRONCHIECTASIS 2

Prior events: 

  • Usually results from prior infections (i.e. Bordetella pertussis), measles and bacterial pneumonia.
  • Immunodefiences
  • Aquired causes: e.g. TB, conncective tissue diseases, allergic bronchopulmonary aspergillosis, and foreign body aspiration. 
  • Congential causes: e.g. cillary dyskinesis inc. Kartagener syndrome, Alpha-1 antitrypsin def. 

Experienced:

  • Dysponea (breathlessness)
  • Repeated chest infections. Chronic sputum production which is often green/yellow in colour
  • Halitosis (bad breath)

Clinical signs:

  • Course crepitatoins heard with stethoscope over affeced area of lung
  • Hypoxaemia (low blood pressure)
  • Hypercapnia (high blood CO2)
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BRONCHIECTASIS 3

Abnormal test results:

  • CT scan (high res): "signet ring sign" (dilated airways with ring shadows). Obstructive pattern in spirometry.
  • Abnormal blood gases (Low O2, high CO2)

Medical/ surgical intervention:

  • Controlling infections and bronchial secretions
  • Relieving airway obstruction
  • Prompt antibiotic therapy for pulmonary exacerbations
  • Rare: localised surgery of affected area. Removal of airway secretions with chest physiotherapy such as postulal drainage. 
  • Use of nebulised antibiotics (colomycin, tobramycin and Aztreonam) to reduce pulmonary exacerbations in patients colonised with Pseudomonas aeruginosa.
  • Maintain body weight

Prevention: Child immunisation (measles, pertussis and other acute respiratory infections), adult vaccination (pneumonia and influenza). Patients should avoid smoking. 

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Chronic obstructive pulmonary disease (COPD)

COPD

Anatomical structures: Small and large airways. Alveoli. Inserstital lung tissue.

Physiology: Transfer of air in and out of lungs. Efficient gas exchange.

Structural abnormalities: Narrowing of the airways. Enlargement of the spaces distal to the terminal bronchioles with destruction of their walls (Emphysema) and expansion of the chest.

Physiological abnormalities: 

  • Reduces rate of flow, of air, to and from the air spaces.
  • Limits the effectiveness of the lungs.
  • Reduction in airflow (worst during expiration) - pressure causes compression rather than expansion.
  • Dynamic hyperinflation: air from previous breath remains in lungs during next breath --> increase in volume of air in the lungs.

Same as Asthma

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Chronic obstructive pulmonary disease 2 (COPD)

Prior events: 

  • Smoking
  • Repeated chest infections
  • Family history
  • Exposure to dust in workplace or air pollution.

Experienced:

  • Dypsnoea
  • Wheeze
  • Phlegm
  • Cough

Clinical signs:

  • Tachypnea (rapid breathing). Breath sounds decreased.
  • Prolonged expiration. 
  • Hyper-inflated chest
  • Wheeze
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Chronic obstructive pulmonary disease 3 (COPD)

Abnormal test results:

  • Reduced FEV1 (not reversible and often progressive)
  • Chest X-Ray: hyperinflated lungs
  • Hypoxia (low blood O2 levels)
  • Hypercapnoea (raised blood CO2 levels)

Medical/ surgical intervention:

  • Antiobiotics (for episodes of infective bronchitis)
  • Beta-2 receptor agonsts (bronchdilator therapy) and long acting agonists (e.g. salmeterol)
  • Anticholinergic broncodilator therapy
  • Inhaled steroids (e.g. budesonide)
  • Oral steroids (e.g. prednisolene) anti-inflammatory therapy (bad episodes of wheezing)
  • Oxygen therapy (low flow)

Primary and secondary prevention:

  • Not smoking
  • Oxygen supplement
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Chronic obstructive pulmonary disease 3 (COPD)

Abnormal test results:

  • Reduced FEV1 (not reversible and often progressive)
  • Chest X-Ray: hyperinflated lungs
  • Hypoxia (low blood O2 levels)
  • Hypercapnoea (raised blood CO2 levels)

Medical/ surgical intervention:

  • Antiobiotics (for episodes of infective bronchitis)
  • Beta-2 receptor agonsts (bronchdilator therapy) and long acting agonists (e.g. salmeterol)
  • Anticholinergic broncodilator therapy
  • Inhaled steroids (e.g. budesonide)
  • Oral steroids (e.g. prednisolene) anti-inflammatory therapy (bad episodes of wheezing)
  • Oxygen therapy (low flow)

Primary and secondary prevention:

  • Not smoking
  • Oxygen supplement
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CYSTIC FIBROSIS

CYSTIC FIBROSIS

Anatomical structures: Airway epithelial cells that line the respiratory tract. Multi-system disorder e.g. lungs, sweat glands, pancreas and bowel.

Physiology: Transfer of air in and out of lungs. Efficient gas exchange. Protection of lungs from infection. 

Structural abnormalities: 

  • Due to congenital abnormalities of the vas deferens males usually infertile.
  • Mutation in apical membrane CFTR Cl- channel protein.
  • Gene is required to regulate the hydration of sweat, digestive juices, and mucous
  • Development of bronchiectasis
  • Loss of Islets of Langerhans cells in the pancreas (which produce insulin) 

which leads to specific CF related diabetes. 

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CYSTIC FIBROSIS 2

Physiological abnormalities: 

  • Autosommal recessive genetic condition
  • Ciliated airway epithelial cells in patient have mutated protein
  • Leads to airway dehydrations and abnormally viscous mucous production
  • Affects entire body, and causes progressive disability, leading in death

Prior events: 

  • Family history of cystic fibrosis
  • Symptoms often appear in infancy
  • Bowel obstruction: meconium ilius in newborn
  • Thick, sticky mucous and frequent chest infections

Experienced symptoms:

  • Coughing/ sputum production/ pyrexia (fever, raised temp.)
  • Shortness of breath
  • Chronic lung infection, and repeated chest exacerbations
  • Abnormal bowel movements
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CYSTIC FIBROSIS 3

Clincal signs:

  • Salty skin/ poor growth/ poor weight gain
  • Poor absorption of nutrients through GI tract - fat-soluble vitamins
  • Coughing up blood (haemoptysis)
  • Finger clubbing/ cyanosis

Abnormal test results:

  • Before or at birth through genetic screening
  • Sweat test during early childhood
  • Obstuctive lung function
  • Sputum cultures +ve Staph. Haemophilus and Pseudomonas aeruginonas
  • Abnormal pancreatic functions
  • Azoospermia (no sperm)
  • Difficulties getting enough oxygen to the body (hypoxia)
  • High BP in the lung (pulmonary hyoertension)
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CYSTIC FIBROSIS 4

Medical/Surgical Intervention

  • Specialist multidisciplinary centres
  • Physiotherapy/ Nutrition
  • Treat chronic and acute infections
  • Ultimately, lung transplantation is often necessary

Primary & Secondary Prevention

  • Antenatal genetic counselling of parents
  • There is no cure  for cystic fibrosis
  • Proactive treatment of airway infection
  • Encouragement of good nutrition and an active lifestyle
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LUNG CANCER

LUNG CANCER

Anatomical structures: All lung tissue: particularly bronchi

Physiology: Transfer of air in and out of lungs. Efficient gas exchange. Protection against infection

Structural abnormalities: Blockage of bronchi due to intra-luminal growth or extra-luminal compression. Accumulation of pleural fluid compressing lung.

Physiological abnormalities: 

  • Limits effectiveness of the lung
  • Wide range of paraneoplastic (beside the cancer) syndromes e.g.
  •         i) Lambert-Eaton myasthenic syndrome (muscle weakness due to autoantibodies)
  •         ii) hypercalacaemia
  •         iii) syndrome of inappropriate ADH production (SIADH)
  •         iv) tumours in the top (apex) of the lung, known as Pancoast tumours, may invade the local part of the SNS, leading to changed sweating patterns and eye muscle problems (a combination known as Horner's syndrome) as well as muscle weakness in the hands due to invasion of the brachial plexus.
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LUNG CANCER 2

Prior events: 

  • Smoking
  • Asbestos exposure

Experienced:

  • Dyspnoea (shortness of breath)
  • Haemoptysis (coughing up blood)
  • Chronic coughing (or change in regular pattern)
  • Wheezing 
  • Chest pain
  • Weight loss

Clinical signs:

  • Cachexia (weight loss, fatigue and loss of appetite
  • CT scan (masses, enlarged lymph nodes or metastis with other organs)
  • Clubbing of the finger nails
  • Dysphagia (difficulty swallowing)
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LUNG CANCER 3

Medical/ surgical intervention:

  • Lobectomy, pneumonectomy (surgical removal of the tumour)
  • Chemotherapy 
  • Radiotherapy

Primary and secondary prevention:

  • Often spreads and metastasises before they have symptoms and seek medical attention. Common sites inc. brain, bone, adrenal glands, contra-lateral (opposite) lung, liver, pericardium, and kidneys.
  • 10% of patients do not have symptoms at diagnosis; usually found on routine chest X-ray
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PNEUMONIA

PNEUMONIA

Anatomical structures: Paranchyma of the lung (alveoli). Bronchil tree often involved.

Physiology: Alveoli responsible for gas exchange. 

Structural abnormalities: Alveoli filling with fluid (consolidation and exudation). Bronchial obstruction due to tumour or plugging by secretions. 

Physiological abnormalities: 

  • Inflammatory condition of the lung - bronchi and alveoli
  • Most commonly bacterial bronchopneumonia
  • Chemical or physical injury (e.g. heat) to the lungs
  • Pneumonia fills the alveoli with fluid
  • Stops O2 from reaching the bloodstream.
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PNEUMONIA 2

Prior events: 

  • Vomiting when semi-conscious and with unprotected airway --> aspiration pneumonia
  • Priory episode of viral flu

Experienced:

  • Productive cough
  • Fever/ shaking/ chills
  • Unilateral chest pain aggravated by breathing (pleuretic) - "sharp stabbing"
  • Difficulty breathing (dyspnoea)
  • Headache/ confusion/ unsteadiness

Clinical signs:

  • High temp, high HR (tachycardia), fast rate of breathing (tachypnoea)
  • Low BP (hypotension), low O2 (hypoxia) and cyanosis if severe
  • Bronchial breathing and crackles heard with a stethoscope
  • Green or brown sputum
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PNEUMONIA 3

Abnormal test results:

  • Chest X-Ray shows consolidation
  • Blood/ sputum production (Strep. pneumoniae)
  • Atypical pneumonias (e.g Mycoplasma pneumoniae, Haemophilus influenza & Chlamydia pneumoniae)

Medical/ surgical intervention:

  • Oxygen
  • Fluids (IV if low BP)
  • Bacterial pneumonia is treated with antibiotics (e.g. penicillin)
  • If severe - assissted ventilation may be required

Primary and secondary prevention:

  • Leading cause of death among the young. the old and the chronically ill
  • Vaccination is available for pneumococcal pneumonia and flu.
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PNEUMOTHORAX

PNEUMOTHORAX

Anatomical structures: The anatomical space between the lungs and the chest wall (pleural cavity). Boundaries are the visceral (lung) and parietal (chest wall) pleura.

Physiology: Normally contains thin film of serous fluid only to allow lubrication of lung against the chest wall - preventing fritction. Contains a vacuum (-ve pressure) to assist the process of inspiration/ lung expansion. 

Structural abnormalities: A collection of air or has in the pleural cavity of the chest between the lung and the chest wall. Causes collapse of the lung. 

Physiological abnormalities: 

  • Impaired mechanics of ventilatoin/ movement of air in and out of lungs. Reductin of blood oxygen if severe.
  • Reduction of blood oxygen if severe
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PNEUMOTHORAX 2

Prior events: 

  • "Primary" (without prior known lung disease)
  • "Secondary" - e.g. COPD or physical trauma to the chest (inc. iatrogenic - caused by doctor e.g. surgery or complication of central venous access)

Experienced:

  • Determined by size of air leak and the speed by which it occurs
  • Chest pain in most cases (same side as pneumothorax)
  • Shortness of breath

Clinical signs:

  • Diagnosis made by physical examination in severe cases
  • Deviated trachea (away from side of pneumothorax)
  • Stethoscope reduced breath sounds
  • Severe oxygen shortage (hypoxia)
  • Tension pneumothorax is related to hypotension (low BP) and progresses to cardiac arrest if not treated.
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PNEUMOTHORAX 3

Abnormal test results:

  • In milder forms: Diagnosed by tests and CT scans
  • Chest X-ray - shows air between lung and chest wall at the apex of the lung

Medical/ surgical intervention:

  • Small spontaneous pneumothoraces typically resolve themselves and require no treatment.
  • Larger pneumothoraces or with severe symptoms - air aspirated with a syringe, ot a one-way chest tube/ drain is inserted to allow the air to escape - inserted between T4-T5

Primary and secondary prevention:

  • Pleurodesis (sticking the lung to the chest wall) may be used if there is a significant risk of repeated eposides of pneumothorax
  • Avoid significant changes in atmospheric pressue (e.g. aeroplanes)
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TYPE-1 RESPIRATORY FAILURE

TYPE-1 RESPIRATORY FAILURE

Anatomical structures: Upper airway/ trachea/ bronchial tree/ alveoli/ pleural space/ chest wall/ diaphragm. Brain and central respiratory control.

Physiology: Normal reference: 

          PaO2: 10.0 - 13.3 kPa.          PaCO2: 4.7-6.0 kPa.

Structural abnormalities: 

  • Significant obstruction of the upper airway/ trachea/ bronchial tree/ alveoli
  • Fluid, blood or air in plueural space
  • Weakness from damage to chest wall/ diaphragm
  • Damage to brain or central respiratory control by trauma or sedation by drugs

SAME AS TYPE-2 RESPIRATORY FAILURE

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TYPE-1 RESPIRATORY FAILURE 2

Physiological abnormalities: 

  • Type-1 Respiratory failure there is an absence of hypercapnia (High PaCO2)
  • Inadequate gas exchange by respiratory system
  • Arterial oxygen levels cannot be maintained within their normal ranges
  • Drop in blood oxygenation is known as hypoxaemia

Prior events: 

  • Typically causes by a ventilation/ perfusion (V/Q) mismatch
  • The volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs. 
  • e.g. pulmonary embolus: blocking pulmonary artery (also shunting of blood from right hand side of heart to the left hand side through a hole in the heart)
  • e.g. rheumatoid arthritis fibrotic lung disease resulting in poor gas transfer to and from the blood (also pneumonia and emphysema)

Experienced:

  • Dyspnoea (shortness of breath)
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TYPE-1 RESPIRATORY FAILURE 3

Clinical signs:

  • Hypoxia
  • Tachypnoea

Abnormal test results:

  • PaO2: Markedly decreased (<8.0 kPa)
  • PaCO2: Normal or low (<6.0 kPa)
  • pH: Normal or increased

Medical/ surgical intervention:

  • Identify and treat underlying causes
  • Oxygen

Primary & Secondary Prevention:

  • Flu vaccination
  • Prevent causes: pulmonary oedema (XS IV/ diuretic therapy), pulmonary embolus (prevent anticogulants if bedbound)
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TYPE-2 RESPIRATORY FAILURE

TYPE-2 RESPIRATORY FAILURE

Anatomical structures: Upper airway/ trachea/ bronchial tree/ alveoli/ pleural space/ chest wall/ diaphragm. Brain and central respiratory control.

Physiology: Normal reference: 

          PaO2: 10.0 - 13.3 kPa.          PaCO2: 4.7-6.0 kPa.

Structural abnormalities: 

  • Significant obstruction of the upper airway/ trachea/ bronchial tree/ alveoli
  • Fluid, blood or air in plueural space
  • Weakness from damage to chest wall/ diaphragm
  • Damage to brain or central respiratory control by trauma or sedation by drugs

SAME AS TYPE-1 RESPIRATORY FAILURE

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TYPE-2 RESPIRAORY FAILURE 2

Physiological abnormalities: 

  • Type-1 Respiratory failure there IS hypercapnia (High PaCO2)
  • Inadequate ventilation by respiratory system
  • Arterial oxygen and/ or carbon dioxide levels cannot be maintained within their normal ranges
  • Drop in blood oxygenation is known as hypoxaemia

Prior events: 

  • Reduced breathing effort (in a fatigued patient)
  • A decrease in the area of the lung available for gas exchange (i.e. emphysema in COPD)

Experienced:

  • Dyspnoea (shortness of breath)

Clinical signs:

  • Hypoxia (low O2 saturation)
  • Tachypnoea (fast respiration) or low rate of respiration (if drug sedation or brain injury)
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TYPE-2 RESPIRATORY FAILURE 3

Abnormal test results:

  • PaO2: Markedly decreased (<10.0 kPa)
  • PaCO2: Normal or low (>6.0 kPa)
  • pH: Decreased (respiratory acidosis)

Medical/ surgical intervention:

  • Identify and treat underlying cause
  • Low flow Oxygen (high flow may reduce the respiratory drive of the brain and cause reduced ventilation with CO2 increase.

Primary & Secondary Prevention:

  • If the respiratory failure resulted from an overdose of sedative drugs such as morphine/ heroin or benzodioates, then the appropriate antidote such as naloxene or flumazenil should be given. 
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