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  1. Progression of shock
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  2. What are the compensation mechanisms for shock?
    • decrease BP
    • Stimulate SNS- thirst, anxiety, restlessness, tachycardia, vasoconstriction
    • Renin- angiotensin- aldosterone- vasoconstriction, retention of Na and water, oliguria
    • Increase ADH secretion- retain water
  3. What are the effects of shock?
    • - direct effects of decreased BP- leathargy, weakness, anaerobic metabolism- acidosis which =
    • - vasodilation and decreased cell function- slow blood flow in microcirulation- thrombus forms, ischemia in organs- decreased function, necrosis
    • - decreasd venous return
    • - further decrease in CO- severe acidosis, CNS depression, organ damage eg renal failure
  4. What is the cellular response of shock?
    • -shock ultimately exerts its effect at the cellular level- hypotension- failure to supply oxygen and nutrients
    • - cll uses two pathways to convert nutrients to ATP- anerobic and aerobic
  5. When oxygen is lacking in the cellular res?onse
    • - build up of lactic acid- acidosis
    • - limited amounts of ATP
    • - dysfunction of cells- Na/ K ATPase pump
    • - Cell damage/ death
  6. Manifestations of shockImage Upload
  7. What are the complications of shock?
    • - acute renal failure
    • - shock lung, or adult respiratory distress syndrome
    • - hepatic failure
    • - Paralytic ileus, stress or hemorrhagic ulcers
    • - infection or septicemia
    • - disseminated intravascular coagulation
    • - depression of cardiac function
    • - multiorgan failure
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  8. What is the role of the respiratory system?
    • transport O2 in blood
    • remove CO2 out of blood
  9. What makes up the respiratory membrane?
    • Squamous epithelial cells ofthe alveolar wall
    • enodthelial cells of the capillary walls
    • (this is where gas exchange occurs)
  10. What makes up theupper respiratory tracts?
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  11. What is the function of the upper respiratory system?
    Filter, warm and moisten the air
  12. WHat does the upper respiratory system consist of?
    • Hair
    • Mucosa- pseudostratified columnar epithelium
    • Mucus secreting goblet cells and cilia
  13. What defence mechanisms does the upper respiratory tract consist of?
    • - traps and sweep particles out of the system'mucosal excretion- cough/ sneeze
    • - Gag reflex
    • Pharyngeal and palatime tonsils
  14. How is the upper respiratory system vulnerable?
    • mouth breathing- air not warmed or filtered
    • auditory (eustachain) tube and sinus infection
    • Oropharynx infection- sore throat
    • Laryngopharyx infections
    • Resident flora vs infection
  15. What makes up the lower respiratory system?
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  16. What is the difference between the bronchus in the lungs?
    Right is larger and straighter
  17. WHat are the bronchioles made up of and what nervous system innervates?
    • smooth muscle
    • sympathetic nerve activity (adrenaline release dilation)
  18. Decreibe what epithelial tissue are in the alveoli?
    single layer simple squamous epithelial tissue
  19. What is the respiratory membrane?
    alveolar and capillary walls
  20. Where does gas exchange occur?
    in the alveoli-they provide a very large wurface area for diffusion of gases?
  21. What is on the inside of the alveoli?
    surfactant leyer- lipoproteins, reduces surface tension
  22. What are teh alveolar macropahges?
    • Phagocytic cell
    • become active and mobile with inflammation
    • interact with lymphocytes to prodcue antibodies
  23. WHat is an example of an upper respiratory viral tract infection?
    • Common cold- rhinoviruses, adenovirusus, parainfluenca virus, coronavirus
    • Influenza- type A
    • Croup- para influenza and adenoviruses
  24. What factors affect type of virus ofthe common cold?
    • time of year, age, host defence, psychological stress.
    • Can survive outside body for hours- highly contagious
  25. What is the process of the common cold?
    • first 3 days: shredding- nasal mucosa- transmission through droplets
    • infects nasal mucosa, conjunctival surface of eyes incubation 3-5 days
    • infection process, cellular response to infection/ inflammation
    • Note- low O2 = good envt for organisms to growth thus compromising cell function. Often self limiting, complicated if unresolved or pre-existing compromise of defence systems- seconday infection
  26. What are factors that affect influenza?
    time of year, age, host defence, psychological stress, new subtypes and antigen shifts
  27. What is the process of influenza?
    • incubation 1-4 days
    • infectious at 1 day (6 days in kids) before symptoms and then for next 5 days (up to 10 days in kids)
    • immuno-compromised shredding virus for weeks to months
    • rapid onset of fatigue, fever, pain
  28. What are the three responses of influnza A?
    • uncomplicated rhinotracheitis (upper)
    • viral pneumpnia (lower)
    • Respiratory viral infection (upp and low) follwed by bacterial
  29. What age group does the upper respiratory viral tract infection CROUP occur in?
    Children between the ages of 1 and 2 years!
  30. What is expansion lung disorder?
    • Also know as disorders of lung inflation
    • Caused by:
    • - lung compression
    • - obstruction of airways
    • - Lung collapse

    • Lung inflation impairment:
    • - reduces lung function
  31. What is laryngotracheobronchitis?
    • Upper respiratory viral invasion
    • mucosal inflammation, nasal congestion, exudate, cough
    • Swelling and inflammation of larynx and trachea- results airway obstruction
  32. How can you tell if somone has an upper respiratory obstruction?
    • Brking cough
    • Hoarse voice
    • Inspiratory stridor (high pitched vibration/ whistle)
  33. What do viral infections cause?
    • Necrosis
    • shredding cells (serous and ciliated of respiratory tract)
    • Holes in basal cells - runny nose
  34. What the upper tract is recovering whatcells are replaced faster?
    • Serous cells faster than cillary cells
    • mucous is produced but not removed
  35. Upper respiratory viral infections?
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  36. WHat are some examples of upper respiratory bacterial infections?
    • Epiglottiis, tonsillitis, sinusitis, otitis meia
    • Streptococcus, pneumococci, haemophilus infuenza B
  37. What is the process of UTR bacterial infection?
    • Penertation- damaged cells, cross mucous membranes
    • Direct contact- inhalation, ingestion (invasive factors eg enzymes)

    Structured community, colony, abscess, space occupying, pain, airflow poblems
  38. What is an example of the lower respiratoy viral infection?
    • Bronchiolitis- RSV (respiratory syncitial virus)- myxovirus
    • Severe avute respiratory Syndrome (SARS)
  39. What are some examples lower respirtaory viral infections- pneumonia?
    • influenza A or B
    • Adenovirus
    • RSV
    • coronavirus (SARS)
  40. What are some of the lower respiratory bacterial infections- pneumonia?
    • Staphylococcus aureus
    • Legionella
    • Streptococcus pneumoniae
  41. What are some examples of lower respiratory fungi infections- pneumonia?
    Candida (in immune supressed individuals)
  42. What is the process of upper respiratory bacterial infections?
    • Penetration- damaged cells, cross mucous membrane
    • direct contact- inhalation, ingestion (invasion enzymes)
  43. What factors affect lower respiratory viral infection bronchiolitis?
    • Family histroy of asthma
    • exposure to cigarettes smoking
  44. What is the process of infection for lower respiratory viral infections?
    • Transmission by oral droplet
    • necrosis and inflammation in the small bronchi and bronchioles (bronchiolitis)
    • edema- increasedsecretions and reflex bronchospasm. Obstruction of the small airways, wheezing, rapid shallow breathing, cough, fever, malaise, hyper inflation in the alveolus- air trapping
    • atelectasis- non aeration- lack of gas exchange
  45. What are the stages of SARS?
    • stage 1- flulike symptoms for 2-7 days (fever, headache, myalgia, chills, anorexia, diarrhea)
    • stage 2- dry cough, dyspnea, patchy interstitial congestion (problem inbetween alveoli and blood vessel), hypoxia, lymphopenia, thromocytopenia (low platelets), increase CRP levels and liver enzymes
    • Stage 3- severe respiratory distress
    • Can bea rapid progression
  46. Process of infection for pneumonia?
    • Inhalation, mucosal spread, aspiration (sucking) fluid, blood born organism
    • underlying cardiovascular or respiratory disease predispose individuals
  47. What are the lesions for pneumonia?
    • may be diffused and patchy throughout lungs or involve a single (whole) lobe
    • predominately in the interstitial tissue and alvolar septae- more tupical with viral
    • Inflamed alveoli filled with exudate (protein and cellular elements)- more typical of bacterial
  48. What is congestion in bacterial pneumonia?
    • Inflammation and vascular congestion develop in alveolar walls, exudate forms in alvoli- low O2 diffusion
    • 1. hypoxia
    • 2. metabolic acidosis
  49. What is consolidation of pneumonia (bacteria)?
    • Neutrophils
    • RBC
    • fibrin
    • accumulate into solid mass
  50. What is resolution of pneumonia (bacteria)
    • lobar pneumonia
    • 1. RBC breakdown (rusty sputum)
    • 2. Macrophagesbreakdown exudate
    • 3 Pleural involvement (pleurisy or pleuritis) & empyema (pleural cavity)
  51. Pneumonia Bacteria
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  52. Lower respiratory infections- bacterial examples?
  53. What is tb?
    Mycobacterium tb- lower respiratory bacterial infection
  54. What features does bacterial TB have?
    • resistant to drying and many disinfectants
    • wall resist neutrophils (PMNs)- no purulent exudate
  55. What is the process of infection of TB?
    • transmission- oral droplets
    • stage 1- primary infection- TB microorganism is engulfed by macrophages in lungs- local inflammation
    • Asymptomatic (showing no evidence of disease)
    • Stage 2- secondary infection (re-infection)
    • insidious onset (dont no why it hapens)
  56. What usually develops first with TB?
    systemic signs and symptoms before lung signs and symptoms- malaise, anorexia, fatigue before cough, sputum becomes purulent (pus)
  57. What is the development of TB?
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  58. primary Tb, ghon complex, cavitationImage Upload
  59. What is an example of lower respiratory fungal infection?
    Histoplasmosis- histoplasma capsulatum
  60. What is the process of infection for a lower respiratory fungal infection?
    • Spores inhaled
    • opportunistic infection spread in (parasite- like) macrophages
    • Stage 1- primary infections
    • - asymptomatic
    • Stage 2- secondary infection
    • - granuloma formation, necrosis and consolidation in lungs
    • spread to other organs
  61. What is aspiration?
    • involves the passage of food, fluid, vomitus, drugs,foreign material into trachea and lungs
    • Often cough, vocal cords or epiglottis prevent entry to lower respiratory tract.
    • Destiation is usually the right lung
    • effects depend on location and content
  62. What occurs with aspiration and solids?
    • Physical size- total or partial obstruction
    • In the bronchus- non aeration (no air or circulating of air)- collapse of area distal to obstruction
    • Ball- valve effect- obstruction caused by a free r partially attached foreign body in tubular or cavitary structure
    • inflammation- trauma, fatty solids ie peanut- bronchoconstriction
  63. Aspiration- liquid
    • inflammation
    • narrow airways- increase secretions, decrease lung expansion which results in decrease gas diffusion
  64. What is obstructive sleep apnea?
    • Pharyngeal tissue collapse during sleep
    • repeated or momentary apnea- osa is defined as cessation of airflow for greater than 10 sec occuring 5 times hour of sleep.
    • Loud snoring with intermittent gasps of air
  65. What are some complications to obstructive sleep apnea?
    • chronic hypoxia
    • fatigue
    • Pulmonary hypertension
    • Right sided congestive heart failure
  66. What is cyctic fibrosis?
    • Mucoviscidosis
    • inherited disorders causing obstruction
  67. What is the cause ofo cystic fibrosis?
    • Gene mutation protein (CFTR) involved in chloride ion in the cell membrane
    • Defect in exocrine glands causes thick secretion 'tenacious or sticky mucus'
    • Effects many tissue including lungs- muscou obstructsair flow in bronchos- air traps and atelectasis- perm damage. Stagnant mucus is a good medium for bacteria- leads to destruction of lung tissue.
    • Bronchiectasis and emphysematour changges may result as fibrosis worsens. Ultimately respiratory failure- right side.
  68. Lung tumors
    • Are a form of obstruction
    • begnin tumors are rare
    • primary and secondary cancers are more common
    • secondary metastatic cancer develops due to spread of cells from distal in the body by the blood and lymphatics
  69. what factors contribute to lung tumors?
    • smoking
    • genetics
    • carcinogen (asbestos)
  70. Bronchogenic carcinoma and bronchial epithelium
    • squamous cell- bronchus near hilum, obstruction
    • adenocarcinoma- from glands- secret mucin
    • Bronchoalveolar cell carcinoma on periphery of lung- initially limited impat and difficult to detect.
  71. What is the process of a lung tumor?
    • - irritants lead to chronic inflammation and infections- metaplasia in epithelial tissue- reversible if irritant removed
    • Loss of ciliated and pseudostratified epitheliu- vulnerable to irritant and further inflammation
    • - Dysplasia in situ develops- limited symptoms
    • Staged based on size, location (metastases) stage 1- localised, stage 3- disseminated
  72. What effects does a lung tumor have?
    • obstruction of airway (bronchus)
    • Sounds cahnge and dyspnea
    • inflammation causes cough, secretion pool distal to tumor- secondary and frequent infection risk
    • Tumors on the lung periphery may lead to inflammation or erosion of pleural membrane- pleural effusion, hemothorax, pneumothorax
    • Tumor cells release hormones or ADB, ACTH- get paraneoplactic syndrome
  73. What is asthma?
    hypersensitive or hyper responsive airways
  74. What are the two types of asthma?
    • Extrinsic
    • Intrinsic
  75. What is extrinsic asthma?
    • acute episodes of type 1 hypersensitivity reaction to inhaled antigen
    • predisposition- familyhistory
  76. What is intrinsic asthma?
    asthma where other stimuli (respiratory infection, exposure to cold, exercise, irritant, inhalation, stress) target hyper- responsive tissues of airs ways- initiates an attack
  77. What is the pathophysiology of acute asthma?
    • In the bronchi and bronchioles:
    • 3 changes to stimuli
    • inflammation of mucosa with edema
    • increase secretion of thick mucuc
    • bronchoconstriciton
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  78. What is the first phase of extrinsic asthma?
    • antigen reacts with immunoglobulin E on previously sensitised mast cells in respiratory mucosa
    • - release of histamine, kininsm prostaglandins and other chemical mediators
    • -these cause inflammation, bronchospasm, edema and increased mucus secretion
    • - vagus nerve stimulation results in reflex bronchoconstrictions
  79. What is phase 2 of extrinsic asthma?
    • Few hr later
    • - increase in leukocytes- releases leukotrienes and other chemical mediators resulting in proonged inflammation, bronchoconstriction and epithelial damage
    • Chemotactic factors and cytokines are released by mast cells attractring more WBCs
  80. What is the causation of intrinsic asthma?
    • mechanism not well understood
    • - chronic t lymphocyte activation- ? internal antigen
    • - Hyper- responsive tissue- chronic inflammation an ? autonomic innervation altered
  81. Partial obstruction in asthma efffects?
    • - air trapping and hyperinflation- air pass into area distal to obstruction but air is only partly expired
    • - expiration usually passive so less force is availabel and forced expiration causes collapse of bronchial wall, further resistance to expiratory flow, residual volume increases, more difficulat to inspire and cough
  82. Total obsruction in asthma effects?
    • - mucus plugs which leads to atelectasis and collapse
    • - hypoxia exacerbated by increased metabolic activity associated with increased muscle activity and stress
    • - respiratory and metabilic acidosis results- blood and body fluids more acidic- neural and cardiovascular system effects
    • - hypoxemia cause vasoconstriction in pulmonary blood flow causing increased workload on right side of heart
  83. what is atelectasis?
    partial or completely collapsed lung
  84. What is chronic obstructive disease (COPD)?
    involves progressive and irreversible damage to lungs
  85. What does COPD induce?
    • respiratory failure
    • - severe hypoxia or hypercapnia (high amount of CO2 in blood)
    • - right sided heart failure due to cor-pulmonale (enlargement of the right ventricle due to increase blood pressure in the lungs)
  86. What conditions does COPD invlude?
    • emphysema
    • chronic bronchitis
    • chronic asthma
    • may be a mix
  87. What is emphysema?
    • the destruction of alveolar walls and septae
    • Results in large permanently inflated alveolar air space
    • Loss of elastin function
    • Note there are many types of emphysema
  88. WHat is dyspnea?
    hard to breath or labored breathing
  89. What is a pink puffer?
    • a pt with COPD and severe emphysema who have a pink complexion and dyspnea
    • Hyperinflation/dyspnea in order to maintain oxygen levels.
  90. What are the different types of emphysema?
    • Centrilobular (centriacinar)
    • Panlobular (panacinar)
    • Paraseptal
    • irregular
  91. What is centrilobular emphysema
    • Centricinar
    • - airspaces in centre of lobules
    • - common in smokers
  92. What is panlobular emphysema?
    • panacinar
    • - all airspaces distal to terminal bronchioles
  93. What is paraseptal emphysema?
    Affects periphery of lobules
  94. What is irregular emphysema?
    where different areas of the lungs are affected.
  95. What are the contributing factors to emphysema?
    • Genetic
    • Smoking
  96. What are the genetic contributing factors to emphysema?
    • deficinecy of the enzyme- alpha,- antitrypsin
    • normally inhibits the activity of prooteases (such as elastase) relaeased form neutrophils during inflammation
    • breakdown of elastin- decreased recoil
  97. What are the contributing factors to emphysema does smoking have?
    • Increases neutrophil number in the alveoli
    • Decreases the effect of alpha1 antitrypsin
    • increases elastase release and activity
    • Bacteria presentwith infection produce proteases
  98. What does alpha1- antitrypsin do?
    inhibits the digestive action of elastase on the tissues of the lungs
  99. Empysema contributing factorsImage Upload
  100. What are the progressive effects of emphysema?
    • Breakdown of the alveolar wall
    • Fibrosis and thickening of bronchial wall
    • Prosressive difficulty with expansion
  101. What happens with emphysema and the breakdown of the alveolar wal?
    • loss of SA for gas exchange
    • Loss of pulmonary capillaries
    • Loss of elastic fibres
    • Altered ventilation-perfusion ratio
    • Loss of support for other structures resulting in collapse
  102. What happens with emphysema and the fibrosis and thickening of bronchial wall?
    • Narrowed airways
    • Weakened walls
    • Interference with passive air flow
  103. What occurs with emphysema and the progressive difficulty with expanison?
    • Air trapping
    • Overinflation
  104. What is chronic bronchitis?
    Significant changes in the bronchi associated with irritation. uch as smoking and air pollution
  105. What occurs with thosewith chronic bronchitis?
    • Hyper- secretion of mucus
    • frequent infections
    • chronic productive cough
    • Obstruction and inflammation
  106. What is a blue bloater?
    • Those with chornic bronchitis
    • - hypoxia, cyanosis (bluish colour of the skin) and edema
    • Clinical manifestations of low O2 levels
  107. What are the progressive effects of chronic bronchitis?
    • irritant causes mucosa to become inflamed and swollen
    • hypertrophy and hyperplasia (The enlargement of an organ or tissue caused by an increase in the reproduction rate of its cells) of musous glands and goblet cells. Increase secretions and decrease ciliated cells.
    • Further inflammation- fibrosis and thickening of bronchial wall, narrowing of airways- obstruction. Increase secretions which may pool = obstruction
    • Increased risk of infection- purulent exudate- bacteria become embedded in secretions
    • Low O2- cyanosis with coughing
    • Severe dyspnea and fatigue
    • Pulmonary hypertension
  108. COPD summary
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  109. What is pulmonary ventilation?
    • the physical movement of air in and out of lungs
    • Uses contraction/ relaxation of intercostal mm and diaphragm
    • Designed to maintainair flow to alveoli
    • ensures O2 is delivered and CO2 is removed.
  110. What is boyle's law and what to do with?
    • pulmonary ventilation
    • P1V1 = P2V2
    • Changes of the intrapleural pressure in the lungs to encourage the air to move in and out of the lung.Low pressure air goes in high pressure air goes out
  111. What is maximal inspiration?
    The amount of air a person can inhale abou 6000ml
  112. What is inspiratory reserve volume?
    Maimum amount of air that can be inspired over normal breathing.
  113. What is vital capcity?
    Volume of maximal inspiration and expiration
  114. What is inspiratory capacity?
    Volume of maximal inspiration
  115. What is total lung capacity?
    Maximum volume the which the lungs can be expanded with a great deal of effort.
  116. What is maximal expiration?
    All the way breathing out
  117. What is tidal volume?
    Volume inspired and expired with each normal breath
  118. What is expiratory reserve volume?
    Maximum volume that can be expired after the expiration of a normal breath
  119. What is residule volume?
    Volume that remains in the lungs after a maximal expiration
  120. What is functional residual capacity?
    Volume of gas reamingin in lung after normal expiration
  121. Pulmonary volumes/ capacities
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  122. What occurs due to restrictive lung disorders?
    • Lung expansion is imapired- reduced lung capacity
    • Loss of Compliance
    • Two groups:
    • -chest wall restriction
    • Lung tissue restriction
  123. Describe restrictive lung disorders- chest wall restriction?
    • Skeletal- kyphosis, scoliosis
    • MM dysfunction - poliomyelitis, amyotrophic lateral sclerosis, botulism, mm dystrophy.
  124. What is interstitial lung disease?
    • lung tissue restriction (restrictive lung disorder)
    • disease affection support tissue such as interalveolar septa/ interstitium
  125. What does lung tissue disease involve?
    • - idiopathic pulmonary fibrosis
    • - pneumoconiosis- occupation lung disease- asbestosis, silicosis, anthracosis, farmer's lung
    • - sarcoidosis- granulona formation
    • Acute forms- pulmonary edema, ARDS
  126. What is the pathophysiology of restirctive lung disorders?
    • - chronic inflammation
    • - fibrosis
    • - loss of elasticity
    • - lungs beome stiff and hard to inflate
    • Loss of compliance
    • * reduced diffusion, hypoxemia- dyspnea (no wheesing), tachypnea (small more frequent breaths)
    • * Later stages- hypercapnia, respiratory acidosis
  127. What is a vascular lung disorders- pulmonary edema?
    • - excessive fluid in the lung- interstitial areaand alveoli
    • - caused by many conditions
    • - reduces lung compliance and gas exchange
  128. What is the pulmonary edema- vascular lung disorders induced by?
    • - pulmonary hypertension- increases vascular resistance- this increases hydrostatic pressure
    • - decrease plasma protein levels- decrease plasma osmotic pressure
    • - lymphatic obstruction
    • - lung inflammation- increase capillary permeability
  129. What are the consequences of pulmonary edema?
    • - excessive fluid
    • - decrease diffusion of gases
    • - hypoxemia
    • - decrease surfactant action
    • - decrease lung inflation
    • - capillary rupture
  130. Pulmonary edema pathogenesis:
    • - excessive fluid
    • - decrease diffusion of gases
    • - hypoxemia
    • - decrease surfactant action
    • - decrease lung inflation
    • - capillary rupture
  131. What is the vascular lung disorder pulmonary embolus?
    Mass that blocks ulmonary artery or a branch
  132. What are the masses that blocks the pulmonary artery or a branch with pulmonary embolus?
    • Thrombi (blood clot)
    • Emboli (fator other)
    • DVT
  133. What do the effects of pulmonary embolus depend on?
    • Size
    • Location
  134. What are the consequences of pulmonary embolus?
    • fluid and blood fill alveoli
    • vasoconstriction in the area
    • decrease respiratory function
  135. What are the consequences of large emboli?
    • increase resistance in pulmonary arteries
    • increase chemical mediators
    • vasoconstriction
    • right sided CHF
    • derease cardiac output
    • shock
    • death
    • Image Upload
  136. What are expanison lung disorders caused by?
    • Lung compression
    • Obstruction of airways
    • Lung collapse

    Lung inflation impairment- reduced lung function
  137. What is the expansion lung disorders?
    • Pleural effusion
    • Atelectasis
    • Pneumothorax
  138. What is the expansion lung disorder Pleural effusion?
    • - excessive fluid in the pleural cavity- usually one lung is affected- pleurisy (inflamed, swollen pleura)
    • - normally lymphatic drain small amounts of fluid- increase fluid, increase pressure, separation of pleural membrane- transudate, exduate, purulent, chyle, sanguineous = decrease lung expansion- atelectasis.
  139. What are the consequences/ symptoms of pleural effusion?
    • - tracheal shift- deviation
    • - impaired venous return to vena cava, hypotension
    • - dyspnea, chest pain, tachcardia, tachypnea
    • Image Upload
  140. What is atelectasis?
    • - non- aeration or collapse of part of lung- decrease gas diffusion = hypoxia
    • - complication of many conditions- obstructive, compression, contaction, postoperative
  141. What is the pathophysiology of atelectasis?
    • -alveoli becomes airless
    • - elastic force dominates- shrivel up
    • - alters perusion and ventilation affecting O2 diffusion
  142. What is the compensation of the body with atelectasis?
    • increase respiratory rate which controls CO2 levels
    • Ifnot reinflated quickly get necrosis and infection developing= permanent lung damage
  143. What is the etiology of atelectasis?
    • - obstructive or reabsorption due to distal air trap
    • - compression due to mass/fluid/ air in intrapleural space which increase pressure on lung thys decrease expansion
    • - increased surface tension in alveoli with edema, or in respiratory distress syndrome
    • - fibrotic tissue in lung or pleura (contraction)
    • - postoperative- decrease ventilation due to pain, slow and shallow respiration (anaesthetic), secretion build up (supine position)
  144. What is the pneumothorax?
    • - air in the pleural cavity
    • - separation of the pleura
    • - decrease lung expansion = atelectasis
  145. What are the types of pneumpthorax?
    • - closed (spontaneous)
    • - open
    • - tension
  146. What is a spontaneous/ closed pneumothorax?
    • - tear in lung surface
    • - can be secondary due to underlying respiratory disease
  147. What is an open pneumothorax?
    • - atmospheric air enters cavity
    • - large opening- sucking wound
    • - mediastinum flutter
  148. What is a tension pneumothorax?
    • mixture- one way valve effect
    • open- parietal pleura and chest wall
    • closed- visceral pleura- mediastinum shift
  149. Pneumothorax:
    Image Upload
  150. What is the expansionlung disorder flail chest?
    • When the a rib breaks and becomes detached from the rest of the cage.
    • Image Upload
  151. What is the consequences of flail chest?
    • Mediastinum flutter
    • - kinking of the inferior vena cave
    • - decrease venous return
    • - decrease CO- hypoxia

    • Limited expansion
    • - decrease inspiratory volume
    • - shunting of stale air- decrease of O2 content- hypoxia
  152. What is acute respiratory distress syndrome (ARDS)?
    is a serious reaction to various forms of injuries or acute infection to the lung
  153. When is the onset of the of ARDS?
    • 1-2 days after precipitating event
    • Results from acute injury and inflammation to alveoli wall and capillary membrane.
  154. What happened when the injury occurs that causes ARDS?
    • Chemical mediator release- increase cap permeability
    • Increased fluid and protein in interstitial area and alveoli
    • Damage to surfactant producing cells- results in hypoxemia, decrease blood flow in lungs, difficult to expand lungs
    • = diffuse atelectasis, decrease tidal volume, progressive lung damage- fibrosis, hyaline membrane
    • Acute respiratory failure
  155. ARDSImage Upload
Card Set:
2012-04-30 11:49:22
Patho Heart Respiratory cards

Lecture 14- 20
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