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Flashcards

Respiratory System

Dan Wiendl Medicine 2016 Semester 1 Alemão 148 flashcards

Flashcards do conjunto (148)

  1. 1Overview• Ventilation (V) – air movedin & out of lungs to facilitate exchange of
    O2/CO2betweenenvironmentand air sacs (alveoli);
    • Exchange takes place by process of diffusion across pulmonary capillaries;
    • rate is proportional to metabolic requirements.
  2. 2Perfusion(Q)• each air sac is covered in a coat if capillaries to allow blood gas exchange
  3. 3V without Q• Dead space
  4. 4Q without V• Shunt
  5. 5Respiratory dysfunction• Problem occurs with either
    ⇒ Oxygenation process
    ⇒ Ventilation process
  6. 6Repiratory failure typesType 1 or Type 2
  7. 7Type 1• Hypoxia with normal/lowCO2
    • Mainly due to V/Q mismatch
  8. 8Cause of type 1pneumonia,pulmonary oedema, asthma, emphysema, PE,
    congenital heart disease
  9. 9Type 2• Hypoxia with hypercapnia (high CO2)
    • Due to alveolar hypoventilation+/-V/Q mismatch
  10. 10Cause of type 2• Pulmonary – COPD, asthma, pulmonary fibrosis, obstructive sleep
    apnoea
    • Central – reduced respiratory drive(e.g., drugs)
    • Neuromuscular– GBS, polio, cord lesion
    • Chest wall abnormalities
  11. 11Features of respiratory failure• Thoseof causative illness (e.g.,asthma)
    • Hypoxia: short of breath, restlessness, confusion, agitation,
    Central cyanosis,“BLUE BLOATER”
    ⇒ Can develop:pulmonary hypertension,cor pulmonale,polycythemia
    • Hypercapnia: headache,bounding tachycardia,peripheral dilatation
    ” PINK PUFFER”
    ⇒ Can develop:drowsiness, coma
  12. 12Diagnose• Bloods (esp. ABGs), x-rays, cultures,spirometry
  13. 13Management• Treat cause
    • O2 therapy (with care in type 2 failure)
  14. 14Dyspnoea• Awareness of breathingdifficulty
    • +/- awareness of muscleeffort to expand chest
    • +/-awarenessof effort to exhale
    • +/- respiratorymusclefatique
  15. 15Physiologic• exertion
    • hypoxia (altitude)
    • high CO2
  16. 16Pulmonary• restriction,
    • obstruction
    • failure of V&/or Q
  17. 17Cardiacpulmonary congestion
  18. 18Haematological• anemia
  19. 19Biochemicalacidosis
  20. 20Pain• often inspiratory
    ⇒ pleuritis
    ⇒ tracheitis
  21. 21Wheeze• soft expiratory whistle, often musical, due to obstruction
  22. 22Stridor• coarse, inspiratory noise, upper airway obstruction
  23. 23Cough• sudden explosive expiratory manoeuvre that tends to clear material from the airways
  24. 24Haemoptysis• coughing up of blood/blood stained mucous
  25. 25Asthmafollowing
  26. 26Definition• Disease characterised by episodic, diffuse airway inflammation and hyperreactivity
  27. 27Results in• reversible airway obstruction
  28. 28Incidence• Affects 10% of population
    • Attacks triggeredby a variety of stimuli
  29. 29Symptoms• Dyspnoea
    • Cough
    • Wheeze
    • Sputum
  30. 30Pathophysiology• Airways are hyperresponsiveto various triggers, mast cells and
    Eosinophils activate
  31. 31Features• Three features combineto cause result and airways narrowing
    ⇒ Contraction of smooth muscle in bronchial walls
    ⇒ Oedema/inflammation of bronchial walls
    ⇒ Excess mucous production
  32. 32Mild/moderate symptoms• Wheeze
    • Cough
    • Increased respiratory rate
    • Tachycardia
    • Upright posture
  33. 33Moderate/severe symptoms•In addition to mild/mod symptoms
    ⇒Recession
    ⇒Use of accessory muscles
    ⇒inability to speak
    ⇒Cyanosis
    ⇒Decreased breath sounds (“silent chest”)
  34. 34Accompanied• V/Q mismatch causes arterial hypoxaemia & hyperventilation
    • As the attack progresses,the patient’s capacity to compensate by hyperventilating unobstructed areas of lung
    • is further impaired by more extensive airways narrowing &
    muscle fatigue
  35. 35Basics of management• Assessseverity
    • Education
    • Trigger avoidance
    • Monitoring(self, clinical)
    • Developmentof personalised AsthmaAction Plan
  36. 36Treatment• Determined by severity& frequency of attacks
    • Medications divided into preventers& relievers
  37. 37Preventers• Inhaled corticosteroids
    • Leukotriene antagonists
    • Mast cell stabilisers
  38. 38Relievers (bronchodilators)• B-agonists (SABA & LABA)
    • Anticholinergics
    • Methylxanthines no longer in widespread use,but may still have rolein treatment of status asthmaticusin some patients
  39. 39Chronic obstructive pulmonary diseaseCOPD as following
  40. 40Definition• Chronic, progressiveairways obstruction with little or no reversibility
    • Fourth main cause of mortality in Australia
  41. 412 types• Frequently co-exist
    • Chronicbronchitis(clinicaldiagnosis)
    • Emphysema(histologicaldiagnosis)
  42. 42Causes• SMOKING
    • Genetic (alpha-1-AT deficiency)
    • Occupational
  43. 43Development• Presents as a slow progression of exertional dyspnoea &
    disability,
    • punctuated by acute symptomatic exacerbations
    • (either infective or non infective)
  44. 44Diagnosis• clinical
    • x-ray
    • spirometry
  45. 45Clinically• Typically middle aged
    • Hyperinflated chest
    • +/- wheeze
    • Pursed lips (pink puffer)
    • Cyanosed(blue bloater)
  46. 46X-ray• Normal
    • Hyperflation
    • Infection
    • Bullae
  47. 47Spirometry• Obstructive pattern
    • Little reversibility
  48. 48Emphysema•Enlargement of terminal air spaces ( distal to terminal bronchioles)
    • Accompanied by destructive change in alveolar walls
  49. 49Chronic bronchitisas following
  50. 50dEfinition• chronic cough & sputum production most days for 3/12 in 2
    consecutive years
  51. 51Cause• chronic mucous hypersecretion
    • and hypertrophy of mucous membranes of airways
  52. 52Management• Confirm diagnosis
    • Optimise function
    • Prevent deterioration
    • Develop support
    • Manage exacerbations
  53. 53Optimise function by• Stop smoking
    • Exercise
    • SABA, anticholinergics,ICS
    • Chest physio
  54. 54Obstructive sleep apnoeaas following
  55. 55Definition• Intermittent closure of pharyngeal airways that cause
    • episodes of apnoea during sleep
    • (note that not all sleep apnoea is obstructive)
  56. 56Presentation• Snoring
    • Day-time somnolence
    • Waking unrefreshed
    • +/- decrease in cognitive functioning libido& mood
  57. 57Complications• Increased risk stroke, hypertension, vascularevents
    • Pulmonary hypertension
    • Type 2 respiratory failure
  58. 58Diagnosis• Sleep studies
    • Measure RR, O2 saturation, airflow at nose and mouth, chest wall
    • movement, limb movements etc.
    • Severeif AHI >30 (apnoeas or hypopnoeas/hour)
  59. 59Treatment• Weight loss
    • Splint (e.g.,mandibular advancement)
    • CPAP
    • Surgery
  60. 60Lower respiratory tract infectionas following
  61. 61Definition• Acute infection of lung parenchyma (alveolar & interstitial tissue)
    • Generally associated with fever and often CXR signs
  62. 62Classification• Lobar
    • Segmental
    • Bronchopneumonia
    • Interstitial
  63. 63Clinical features• Fever,
    • cough,
    • sputrum,
    • haemoptysis,
    • dyspnoea,
    • pleuritic pain
  64. 64Diagnosis• clinical
    • cultures
    • x-ray
    • serology
  65. 65Pneumoniaas following
  66. 66Aetiologybacterial
    viral (primarily kids)
    fungal
  67. 67BActerial typical• Strep (Pneumococcus)
    • Staph
    • Haemophilus
  68. 68Bacterial AtypicalMycoplasma
    • Legionella
    • Mycobacterial(TB)
  69. 69Viral (especially kids)• Influenza
    • RSV
    • Adenovirus
  70. 70Risk factors• URTI/agent exposure
    • Institutionalisation (HAP)
    • Debility
    • Smoking
    • Decreased level of consciousness
    • Immunosuppression
    • Swallowing difficulties(aspiration)
  71. 71Ayptical pneumonia: Legionnaire’s diseaseas following
  72. 72Definition• Legionella pneumophilia identified in 1976 with outbreak of acute
    respiratory illness in American army veterans.
    • Bacteria colonises water tanks <60ºC (such as hotel air conditioners and hot-water systems)
  73. 73Outbreak• Sporadic
  74. 74Presentation• with fever, malaise, myalgia & headache, dry cough
  75. 75Risk• Can progress to pneumonia, GIT symptoms, renal failure,hepatitis and coma and death
    • 10% mortality, even with treatment
  76. 76Diagnosis• serology, antigen in urine, CXR – bibasal consolidation
  77. 77Treatment• Azithromycin or doxycycline
  78. 78Atypical: mycoplasma pneumonia•Mycoplasma pneumoniae common cause in 5-35yo
    • Epidemics common(e.g., schools,military – close contact spread)
  79. 79Symptoms• Presents with flu-like illness of dry cough, myalgia, arthralgia and headache
    • Can develop rash, severe pneumonia, haemolytic anaemia,
    • Guillain-Barre Syndrome & meningo encephalitis
  80. 80Diagnosis• serology,x-ray – bilateral patchy consolidation
    • out of keeping with clinical presentation
  81. 81Treatment• macrolides, tetracyclines
  82. 82Tuberculosisas following
  83. 83Definition• Leading cause of death due to infectious disease world wide
    (includingHIV TB)
  84. 84Cause of infection• atypical Acid Fast Bacillus (AFB), Mycobacterium tuberculosis,
    • can affect any part of the body,
    • but usually the lungs is the primary site (othercommonsites are gut and lymph nodes)
  85. 85Pulmonary tuberculosis• primary infection is not usually very severe
  86. 86Presentation• Fever
    • Nightsweats
    • Persistentcough
    • Hoarseness
    • Haemoptysis
    • Chest pain – pleuritic
    • Weightloss
    • Anorexia
    • Fatigue
  87. 87Pimrary TB• Generally mild inflammatory reaction at infectionsite (e.g.,subpleural,pharynx or ileum)
    • May get spread to regional nodes(e.g., hilar,cervical or mesenteric)
    • Characteristics eating granuloma appears at thesesites with the
    Development of “tuberculin”sensitivity
    • “Primary complex”often heals with fibrosis and calcification with
    out any treatment leaving the bacterium encapsulated in tubercles
  88. 88Secondary TB• Occursin previouslysensitisedindividuals
    • Reactivation/reinfection results in immediate granulomatous
    Response with localisation –
    • lymph node involvement uncommon
  89. 89Granuloma may then• Heal
    • Rupture into bronchi– TB pneumonia
    • Rupture into blood vessel– miliary spread
  90. 90Diagnosis• Suspect in high risk groups (immigrants,ATSI)
    • CXR (may be incidential)
    • Sputum culture AFBs
    • Skin testing – does NOT indicate activity
  91. 91Treatment• Failure rate if drug sensitive<1%
    • 1% multi-drug resistant
    • 5 year relapse rate<5%
  92. 92Multiple drug regimen• Isoniazid
    • Rifampicin
    • Pyrazinamide
    • Ethambutol
  93. 93Treatment• Treat6-12/12
    • Monitor weight, renal function, liver function, vision
  94. 94Bronchiectasisas following
  95. 95Definition• Irreversible focal bronchial dilatation caused by
    • inflammation & chronic infection
    • can be diffuse or focal
  96. 96Diffuse tends to occur in• Immunocompromise
    • Genetic defects (e.g.,cystic fibrosis)
  97. 97Aetiologyevere pneumonia(e.g., Staph)
    • Measles/pertussis
    • Foreign body
    • Tumours
    • CF
  98. 98Presentation• Chronic cough
    • Purulent sputum
    • +/- SOB , fever & haemoptysis
    • Bronchial wall shows extensive destruction,
    • inflammation,
    • increased mucous and loss of cilia
  99. 99Diagnosis• clinical features and RFs
    • x-ray
    • CT
  100. 100Treatment• Anitbiotics (culturs important )
    • Physiotherapy
    • Surgery
  101. 101Cor pulmonaleas following
  102. 102Definition• Right ventricular enlargement & right heart failure due to
    • Chronic pulmonary hypertension
  103. 103Pumonary hypertension can be• Idiopathic (primary)
    Secondary
    • COPD
    • ILD
    • OSA
    • Obesity
    • Vascular disorders
    • Tumours
  104. 104Treatment• Diuretics
    • Vasodilators
    • Surgery
  105. 105Interstitial lung diseaseas following
  106. 106Aetiology• Idiopathic
    • Infective–TB
    • Connective tissue diseases– SLE, RA, AS
    • Industrial dust diseases- silicosis
    • Radiation
    • Medications
  107. 107Presentation• Shortness of breath
    • Chestpain
    • Clubbing
    • Crackleson chest
  108. 108Diagosis• Restrictive pattern on spirometry
    • CXR
    • CT
  109. 109Environmental & occupational lung diseaseas following
  110. 110Cause• dust, chemicals, gases, allergens & pollutants
  111. 111Can involve• various parts of the lung
    • Pleura
    • Interstitium
    • Airways
  112. 112Aetiology• Particles small enough to pass into lung
    • May depend on mucociliary clearance
  113. 113Response depende on• Particle nature
    • Organic particles (e.g., bird fanciers lung)
    • Inorganic
    • Inert particles (e.g., fibrosis)
    • Gas (e.g., acute pulmonary oedema)
  114. 114Asbestosisas following
  115. 115Definition• Asbestos was commonly used in building trade (e.g., roofing,
    fire proofing, wire insulation)
  116. 116Fibre inhalation results in• pulmonary fibrosis,
    • pleural plaques
  117. 117Asbestos exposure associated with• increased incidence of mesothelioma & acenocarcinoma
  118. 118Coal workers pneumonconiosis• Inhalation of coal dust particles causing fibrosis and chronic bronchitis
  119. 119Silicosis• Inhalation of silica particles causing fibrosis;
    • Seen in metal mining,stone quarrying, ceramic manufacture
  120. 120Presentation with• Severe dyspnea
    • Nodules in upper lung fields
    • Predisposed to TB
    • Lymph node calcification
  121. 121Pleural disorderspleuritis
    pleural effusion
  122. 122Pleuritis definition• Inflammation of pleura secondary to infection
    • Inflammation of infarction
  123. 123Characteristics• Pain worse with inspiration
    • Often felt over the site
    • But may be referred to
  124. 124Signs• Localized oedema
    • Congestion
    • Infiltrate +/- adhesions
    • May have audible pleural rub
    • May be associated with pleural effusion
  125. 125Pleural effusion• Accumulation of fluid in pleural space
  126. 126Transudate produced by• pressure, low protein content, e.g., CCF, nephrotic syndrome)
    • or exudate (high protein content, due to inflammation, e.g., pneumonia, PE)
    •  Reduced BSI, dullness to percussion
  127. 127Pneumothorax• Free air in the pleural cavity between the layers of pleura
    • Normally thereis negative pressure in the pleural space that helps to keep the lungs inflated
    •  When there is communication with the atmosphere this
    pressure equalises
    •  The elasticity of the lung causes it to deflate
  128. 128Aetiology• Trauma (inc. barotrauma)
    • Spontaneous (e.g.,ruptured bullae)
    • Iatrogenic(e.g., needle)
  129. 129Clinical features• Dependent on size
    • Dyspnoea
    • Pleuritic pain
    • Mediastinal shift
    • Death– tension pneumothorax
  130. 130Diagnosis• CXR – may need insp/exp views if sma
  131. 131Treatment• Observation
    • Drain
    • Surgery for recurrences
  132. 132Atelectasis• Shrunken , airless part of lung
  133. 133Aetiology• Bronchial obstruction (internal – mucous, external – tumour)
    • Hypoventilation (post op, # rib)
    • Hypoperfusion (PE)
    • Intrinsic factors (e.g., reduced surfactant)
  134. 134Presentation• Depends on cause and extent
    • Dyspnea +/- pain, cough
  135. 135Treatment• Rx cause & physiotherapy
  136. 136Complications• Infection,
    • Bronchiectasiss
    • Fibrosis
  137. 137Lung tumoursas following
  138. 138classification• Benign
    • Malignant
    • Secondary (metastatic)
  139. 139Most common• Primary bronchogenic carcinoma
    • 85% smoking related
    • Main cause of cancer related death worldwide
  140. 1402 main types• •Small cell 15%
    • Non small cell
    ⇒ Largecell 15%
    ⇒ Adenocarcinoma 35%
    ⇒ Squamous cell 35%
  141. 141Primary lung tumours• Carcinoma obstruction lef main bronchus
  142. 142SCLC• 60% have metastasisedon diagnosis
    • Tend to be central in large airways – submucosal/perihilarmass
  143. 143NSCLC• 40% have metastasisedon diagnosis
    • May be peripheral (e.g.,adenocarcinoma)
  144. 144Prognosis• 15% 5 year survival with treatment
  145. 145Symptoms• cough
    • wheeze (monophonic)
    • haemoptysis
    • infection
  146. 146Signs• effusion
    • atelectasis
    • metastatic complications
  147. 147Secondary lung tumours• Malignant tumours may metastasise to the lungs from multiple primary sites
  148. 148Sites

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2016 Semester 1 Medicine (Week 4) FlashCards sobre Respiratory System, criado por Dan Wiendl em 23-03-2016.
Criado por
Dan Wiendl
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