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resp failure (3)
1) hypoventilation -> leads to...
2) impaired diffusion -> leads to...
3) pleural disorders
- 1) hypoventilation -> leads to hypercapnia (high CO2 in blood) and hypoxia
- 2) impaired diffusion -> leads to hypoxemia (low O2 in blood) but not hypercapnia
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Hypoventilation causes (3)
- depression of respiratory center
- disease of resp nerves or muscles
- thoracic cage disorders
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Impaired diffusion can occur as a result of... (4)
- interstitial lung disease
- ARDS (acute resp distress syndrome)
- pulmonary edema
- pnemonia
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hypoxemia
PO2 < ?; leads to... (5)
- PO2 <60 mm Hg
- cyanosis results
- leads to impaired function of vital centers
- symptoms include agitated or combative behaviour, euphoria, impaired judgment, convulsions, delirium, stupor, coma
- hypotension and bradycardia (decrease HR and CO -> decrease BP)
- results in activation of sympatehtic system
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hypercapnia
PCO2 > ?
Respiratory acidosis leads to...
- increase resp
- decrease nerve firing (disorientation, coma)
- decrease muscle contraction
- vasodilation in the head region - headache, warm flushed skin
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plural space disorders (2)
- 1) pleural effusions (fluid in the pleural cavity)
- 2) pneumothorax
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pleural effusion (flluid in the pleural cavity) (4)
- hydrothorax: serous fluid
- empyema: pus
- chylothorax: lymph
- hemothorax or fibrothorax: blood
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pneumothorax
a) ?
b) ?; i) ? ii) ?
- air enters the pleural cavity
- air takes up space, restrictin glung expansion
- partial or complete collapse of the affected lung
- a) spontaneous: an air-filled blister on the lung ruptures
- b) traumatic: air enters through chest injuries (intense pain on injured side)
- i) tension: air enters pleural cavity through the wound on inhalation but cannot leave on exhalation (compression of the inferior ven cava + obstruction of blood flow thru) (clinical man >intense pressure preventing inhalation >can be fatal if intervention is delayed)
- ii) open: air enters pleural cavity through the wound on inhalation and leaves on exhalation
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spontaenous pneumothorax
an air-filled blister on the lung ruptures
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traumatic pneumothorax
i) tension pneumothorax
ii) open pneumothorax
air enters through chest injuries (intense pain on injured side)
i) tension: air enters pleural cavity through the wound on inhalation but cannot leave on exhalation (compression of the inferior ven cava + obstruction of blood flow thru) (clinical man >intense pressure preventing inhalation >can be fatal if intervention is delayed)
ii) open: air enters pleural cavity through the wound on inhalation and leaves on exhalation
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features of pneumothorax (3)
- tracheal shift
- cardiac compression
- lung deflation
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obstructive diseases (5)
- (bronchial) asthma
- COPD i) emphysema; ii) chronic bronchitis
- bronchiectasis
- cystic fibrosis
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restrictive diseases
- chest wall - kyphosis
- pleural - effusion, pneumothorax
- parenchymal - occupational, ARDS-IRDS, atelectasis
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resp obstruction in children
1) extrathoracic airways (upper)
2) intrathoracic airways (lower)
Describe the above.
increased airway resistance = decreased airway conductance
(upper): - > prolonged inspirationl inspirational stridor (labored)
- > inspiratory retraction as ribs are moved outward and body wall does not expand with rib cage (= insuf expansion)
- intrathoracic airways (lower)> prolonged expiration with wheezing> rib cage retraction as ribs are pulled inward but air does not leave lungs
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Upper airway obstructive disorders (2)
- epiglottitis
- croup:
- age range 3 months - 3 years
- brought by variety of viral infection (e.g. flu)
- characterized by hoarseness, a brassy cough
- fever
- inspirational stridor
- cough is lessened by inlhation of cold air
- can lead to cyanosis, pallor in severe cases (restriction of blood flow; Hg decr.)
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Lower airway obstructive disorders
- acute bronchiolitis:
- incr. expiratory effects = wheezing
- brough by viral infection
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Asthma (2)
- Extrinsic (atopic): allergic reaction
- Intrinsic (nonatopic): attacks precipitated by:
- physical factors
- exercise
- psychological stress
- chemical irritants and air pollution
- bronchial infection
- aspirin
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extrinsic (atopic) asthma
- type 1 hypersensitivity
- mast cells' inflammatory mediators cause acute response within 10-20 min
- airway inflammation causes late phase response in 408 hours
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pathogenesis of asthma
- IgE interacts w/ mast cells and acts as receptors for allegens
- hisamine release triggers the change in airway walls (thicken) (from granules)
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histopathology of asthma
- mucus in lumen
- inflmmation and basment membrane thickening
- enlarged mucous glands
- smooth muscle hyperplasia
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clinical manifestations of asthma (3)
- 1) bronchial smooth muscle constriction
- 2) mucosal edema
- 3) hypersecretion of mucus
- others: epithelial injury, bronchospasm, edema
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intrinsic (nonatopic) asthma
- causes
- treatment
- 1) resp infection: epithelial damage, IgE produced
- 2) exercise, hyperventilation, cold air: lost of heat and water may cause bronchospasm
- 3) inhaled irritants: inflmmation, vagal reflex
- 4) aspirin and other NSAIDs: abnormal arachidonic acid metabolism
- treatment: anticholinergic (preventing contraction of smooth muscles)
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COPD disorders (3)
- emphysema: enlargment of air spaces and destruction of lung tissue
- chronic obstructive bronchitis: obstruction of small airways
- bronchiectasis: infection and inflammation destroy smooth muscle in airways, causing permament dilation
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mechanism of COPD (4)
- 1) inflmmation and fibrosis of bronchial wall
- 2) hypertrophied mucus glands -> excess mucus; obstructed airflow
- 3) loss of alveolar tissue: decr. surface area for gas xchange
- 4) loss of elastic lung fibers (emphysema): airway collapse, obstructed exhlation, air trapping, decr. air delivery
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treatment of asthma (4)
- 1) manage enviro
- 2) bronchodilators (Ventolin)
- 3) antihistamine
- 4) antiinflammatory (corticosteroid - Flovent) - synthesis of beta receptors therefore boost the effects of beta agonist
- beta agonist: related to CV system, mimics SNS; decr. receptors locally on smooth muscle; receptor down regulation
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treatment of COPD
- 1) bronchodilator
- 2) steroid (antiinflam)
- 3) antibiotics (decr. bacteria growth in the thickened mucus)
- 4) flu shot
- 5) O2 therapy
- 6) others - quit smoking, DB & C, exercise, reposition
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emphysema
- trypsin & neutrophil
- types
- emphysema: enlargment of air spaces and destruction of lung tissue
- neutrophils in alveoli secrete trypsin (digestive protein) - incr. neutrophil = incr. trpysin
- aplha-antitrypsin inactivates the trypsin before it can damage the alveoli
- trpysin damages protein, fibers, elastin in alv. wall
- alv loses radial fraction
- types: centrilobular (distended resp bronchiole) and pancinar (one lumped alv)
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pink puffer
(ephysema - COPD)
- breathe in deep
- chest muscle incr.
- barrel chest (narrow); lean forward when breathing
- pursed lip breathing
- dont suffer hypoxia by incr. drawing volume of air
- increase resps
- dyspnea (incr. ventilatory effot)
- use of accessory mucscles
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chronic bronchitis (4 char)
- chronic irritation fo airways
- increased number of mucus cells
- mucus hypersecretion
- productive cough
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chronic bronchitis
- needs to sit upright
- tachypnea (incr. resps)
- incr. temp due to incr. metabolic demand of muscles
- cannot increase resp enough to maintain oxygen level
- cyanosis and polycythemia (incr. RBC)
- cor pulmonale from think blood, incr. work for RS of heart, RS HF
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