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80 Cards in this Set
- Front
- Back
- 3rd side (hint)
Alveolar Gas Equation
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Gas Equation
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Causes of Hypoxemia
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-Alveolar hypoventilation
-Reduced partial pressure 02 (PiO2) -Ventilation perfusion (V/Q) mismatch -Shunt -Diffusion abnormality |
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Draw algorithm for determining cause of hypoxemia
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See Pathophysiology for the Boards and Wards p. 90
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Causes of PCO2 change
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-Hypoventilation
-V/Q mismatch -? |
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Restrictive diseases (hint available)
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Pleural disease
Alveolar filling disease Interstitial disease Neuromuscular disease Thoracic cage abnormality |
PAINT
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Difference between restriction and obstruction
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Restriction: Can't fully inhale
Obstruction: Can't fully exhale |
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Factors that affect DLCO
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-Ability to get CO to alveolus (ventilation)
-Ability of blood stream to pick up CO (perfusion) -Ability of RBC to pick up CO (hemoglobin) |
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Obstructive lung disease with normal DLCO
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-Asthma
-Bronchitis -Upper airway obstruction |
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Why might a TLC (total lung capacity) measured by plethmysography be higher than one measured by helium
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"Helium may not reach all areas of the lung. It will thus be diluted in a smaller volume of lung than actually exists."
(from syllabus p. 73 by J. Unterborn) |
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Causes of obstructive lung disease (Hint available)
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-Foreign body/upper airway problem
-Asthma -Chronic bronchitis/bronchiectasis -Emphysema -Small airways (ie bronchiolitis) |
FACES
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Obstructive lung disease with reduced DLCO
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Emphysema
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Restrictive lung disease with normal DLCO
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-Pleural disease
-Neuromuscular disease -Thoracic cage abnormality (Chest wall disease) |
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Restrictive lung disease with reduced DLCO
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-Alveolar filling disease
-Intersticial disease |
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Respiratory muscles: Two major physiologic principles governing function: Explanation
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1. Length-tension (the longer the muscle prior to contraction, the stronger the contraction)
2. Force-velocity (the faster a muscle contracts, the smaller the force) |
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Respiratory muscles: Two major physiologic principles governing function: Examples of dysfunction
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1. Length-tension. (In COPD, the diaphragm, scaleni, and sternomastoids are shortened already. Little tension can be generated.)
2. Force-velocity (High activity/severe obstruction --> increased velocity --> less force) |
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Definitions of muscle fatigue and weakness
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Fatigue: Decline of ability to generate force
Weakness: Inability to exert force to the degree expected given general physical fitness |
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What is the progression of ARDS (acute respiratory distress syndrome)
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1. Acute Lung Injury
2. Increased Permeability 3. Increased Lung Water (Interstitial/Alveolar) 4. Reduced Compliance AND/OR 4. Increased shunt leading to hypoxemia |
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What are the parameters measured in mechanical ventilation and why?
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1. PEEP (positive end-expiratory pressure - to maintain maximal recruitment of alveolar units)
2. mean airway pressure (to promote recruitment and predictor of hemodynamic effects) 3. plateau pressure (best predictor of alveolar overdistention) |
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Why are low tidal volumes preferred over high tidal volumes in mechanical ventilation? What are the cautions associated with low tidal volumes?
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High tidal volumes --> overstretched alveoli --> volutrauma (2ndary lung injury)
Cautions: low tidal volume --> hypercapnia and atelectasis |
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What are three reasons that PEEP (positive end-expiratory pressure) is important?
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1. Prevents alveolar collapse
2. Recruits more lung units 3. Increases FRC (functional residual capacity) 4. Redistributes fluid in the alveoli |
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What are the causes of increased airways resistance in asthma and what is primarily responsible for these changes?
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Inflammation leads to:
1)excess airway secretions 2)abnormal smooth muscle contraction 3)thickening of the airway wall |
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What cells infiltrate the airway wall in asthma?
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1) eosinophils
2) Th2 cells 3) Mast cells |
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What are the stages of inflammation in an asthma attack and what are their time durations?
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1) Early phase - starts within minutes of exposure, maximal at 30 minutes, subsides in 1-2 hours
2) Late phase - 4-6 hours after exposure, maximal at |
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What are the stages of inflammation in an asthma attack and what happens in them?
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1) Early phase - Mast cells release histamines
2) Recruited inflammatory cells and other mediators. |
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Difference between inflammatory responses in asthma and COPD
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Asthma: CD4+ lymphocytes and eosinophils
COPD: CD8+ lymphocytes, neutrophils and macrophages |
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Mild intermittent asthma: Definition and treatment
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Def: less than 2 days per week and/or less than 2 nights per month
Tx: No daily medication needed. Systemic corticoids recommended for severe exacerbations. |
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Mild persistent asthma: Definition and treatment
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Def: More than 2 days per week but less than once per day and/or more than 2 nights per month.
Tx: Low dose inhaled corticosteroids. |
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Moderate persistent asthma: Definition and treatment
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Definition: Daily symptoms plus more than 1 night per week
Tx: Low to medium dose inhaled corticosteroids AND long-acting inhaled beta2-agonists |
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Severe persistent asthma: Definition and treatment
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Definition: Continual symptoms during the day and frequent symptoms at night
Tx: High dose inhaled corticosteroids AND long-acting inhaled beta2-agonists AND (as needed) corticosteroid tablets |
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Asthma: Common symptoms
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-Dyspnea at rest/with exertion
-Cough (exacerbated frequently by deep inspiration or laughing) -Wheezing -Chest tightness/pain -Exercise intolerance -Hyperventilation syndrome |
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Pathogenesis of COPD
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1. Chronic inflammation + Imbalance between proteinases and anti-proteinases + oxidant stress + time
2. Destruction and remodeling of alveolar units 3. Lack of elastic recoil & expiratory airway collapse 4. COPD |
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Basic treatment of COPD (hint available)
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1. Smoking cessation
2. Inhaled bronchodilators (beta2-agonists, anticholinergics) 3. Systemic bronchodilators (theophylline) 4. Systemic corticosteroids (acute only) 5. Immunization 6. Nutrition 7. Oxygen 8. Pulmonary rehab |
8 treatment measures
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Define cor pulmonale
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Right ventricular hypertrophy resulting from pulmonary circulation system
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Mechanisms of pleural effusions
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1. Increased hydrostatic forces (CHF --> increased pulmonary venous pressure)
2. Reduced plasma oncotic pressure (hypoproteinemia) 3. Reduced mean intra-pleural pressure (respiration atelectasis) 4. Disruption of mesothelium and capillary walls (inflammation/tumors) 5. Lymphatics (destruction/hypoplasia/obstruction) 6. Transdiaphragmatic flow (ascites) |
6 in total
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Treatment of pleural effusions (transudate versus exudate)
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Transudate: Treat underlying problem.
Exudate: Further diagnostic tests |
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Pleural effusions: How to distinguish transudate from exudate
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Exudate if presence of at least one:
-pleural fluid protein: serum protein ratio > 0.5 -pleural fluid lactate dehydrogenase: serum LDH ratio > 0.6 |
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Pleural effusions: Symptoms and signs
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Sx: 1) Dyspnea 2) Chest pain
Si: 1) Reduced excursion over the effusion 2) dullness to percussion 3) diminished/absent breath sounds over the effusion |
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Definition: CFTR
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Cystic
Fibrosis Transmembrane conductance Regulator |
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Function of CFTR and result of its absence
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cAMP-dependent Cl transport into lumen of organs
Absence: Very viscous secretions |
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Pathogenesis of cystic fibrosis (hint available)
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1. CFTR incompetence
2. Increased viscosity of secretions 3. Airflow obstruction AND Colonization by P. aeruginosa, H. flu, or S. aureus 4. Chronic inflammation (lumen destruction) 5. Destruction of airways and bronchiectasis 6. Expiratory flow limitation |
6 steps
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Treatment of cystic fibrosis/bronchiectasis
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1. Antibiotics
2. Inhaled mucolytics 3. Bronchodilators (may worsen if loss of airway tone by making airway floppy) 4. Physical maneuvers for clearing functions |
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Common features of interstitial lung diseases
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-Exertional dyspnea
-Bilateral diffuse infiltrates on CXR -“Restrictive” physiology (decreased lung volumes) with abnormalities in gas exchange at rest or with exercise. -Immunocompetent host; absence of infection or neoplasm -Varying degrees of inflammation and fibrosis on histopathology |
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General picture: Restrictive PFTs
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1. Shift in pressure volume curve to the right
2. Reduction in: a. TLC b. VC (due to fall in compliance) c. RV 3. Classic obstruction absent |
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Signs, symptoms, and treatment: IPF (Idiopathic Pulmonary Fibrosis)
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Si
1. Interstitial infiltrates/honeycomb lung (end stage) 2. Restriction on PFTs Sx 1. Dyspnea 2. Dry cough 3. Gradual weight loss 4. Fatigue 5. Clubbing (enlargement of the fingertips or sometimes the toes) Tx: Anti-inflammatory |
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Signs, symptoms, and treatment: Sarcoidosis
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Si:
1) Non-caseating granulomas involving at least 2 organs 2) Bi-basilar end-inspiratory crackles 3) Restriction on PFTs Sx: 1) Uveitis 2) Cough (non-productive) 3) Dyspnea 4) Weakness, fatigue, weight loss Tx: Corticosteroids |
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Signs, symptoms, and treatment: Hypersensitivity Pneumonitis
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AKA Farmer's/Pigeon Breeder's/Mushroom Picker's Lung
Si: 1) Honeycomb lung 2) Restriction on PFTs Sx: 1) Fever, chills, malaise 2) Chest tightness 3) Dyspnea Tx: 1) Allergen avoidance 2) Corticosteroids |
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How do you distinguish between acute, subacute hypersensitivity pneumonitis
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Acute: More severe, shorter duration
Subacute: Less severe, longer duration |
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Definition: Occupational Asthma
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Occupational asthma includes only those individuals whose asthma is attributable to the work place and to no other outside exposure
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Most common manifestation of asbestosis
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Pleural plaques
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All manifestations of asbestosis
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Pleural manifestations (pleural plaques, benign asbestos pleural effusion, mesothelioma)
Lung parenchymal involvement (asbestosis, lung cancer) |
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Silicosis: clinical presentation
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Sx: Usually none, or dyspnea and non-productive cough.
Si: 1) Egg shell calcifications on CXR |
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Effect of vascular disease on gas exchange
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-Pulm vascular obstruction --> increased Dead Space
-Hypoxemia: related to V/Q mismatch and shunt |
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Effect of vascular disease on pulmonary function tests
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-Either normal or restrictive pattern
-DLCO is normal or reduced |
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Primary pulmonary hypertension: clinical presentation
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Epi:
1)Young (20-50) 2)Female (2:1) Sx: 1)Easy fatigue 2)Exertional dyspnea 3)Dyspnea (especially on exertion) Si: 1) Loud P2 2) Cyanosis |
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Pulmonary embolus: Risk factors
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Virchow's triad (over 90% of cases have at least one):
1) Stasis 2) Inflammation 3) Hypercoagulability |
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Pulmonary embolus: Clinical presentation
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Sx:
1)Progressive dyspnea 2)Chest pain Si: 1)Tachypnea 2)Crackles 3)Tachycardia Imaging: 1)Multiple thrombi in small to medium sized arteries |
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Pulmonary hypertension: Treatment
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1)Anticoagulants/vasodilators/anti-
a)Calcium channel blockers b)Prostacyclins c)Endothelin receptor antagonists d)Phosphodiesterase 5 inhibitors 2)General measures a)Diuretics b)Oxygen c)Digoxin |
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Inhaled Delivery of drugs: General advantages
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1) Deliver high concentrations of drug to primary site
a. smaller total dose --> fewer systemic side effects b. faster delivery 2) Large surface area 3) Reproducible absorption kinetics |
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Bronchodilators - Beta-agonists: Mechanism
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Increases cAMP via Beta 2 receptor and increases Ca++ efflux to relax bronchial wall smooth muscle
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Bronchodilators - Anti-cholingergics: Mechanism
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Blocking of Muscarinic Receptors to block cholinergic bronchoconstiction
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Inhaled steroids: Advantage over topical steroids
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Fewer systemic effects
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Common inhaled steroids
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-Beclomethasone
-Fluticasone -Budesonide -Mometasone |
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Lung cancer: Usual symptoms
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1) Cough
2) Anorexia/weight-loss 3) Dyspnea 4) Hemoptysis 5) Chest pain |
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Lung cancer: Usual signs
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1) Localized wheezing
2) Neurologic (Horner's, vocal cord paralysis, unilateral diaphragm movement) 3) Shoulder pain with ulnar radiation 4) Prescalene/supraclavicular lymphadenopathy |
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Lung cancer: Risks
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1) Smoking
2) Atmospheric pollution 3) Asbestos & other occupational toxins 4) Diffuse Pulmonary Fibrosis 5) COPD 6) HIV |
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Factors which affect minute ventilation
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Increases:
1) Arterial and CSF PCO2 (+) 2) Voluntary hyperventilation (++) 3) Exercise (++) Decreases: 1) Sleep |
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Conditions with impaired response to hypoxia
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1) Narcotic addicts
2) Carotid endarterectomy 3) Cyanotic congenital heart disease 4) Altitude native 5) Arnold-Chiari syndrome |
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Conditions with impaired response to hypercapnia and hypoxia
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1) OHS/OSA
2) Sleep deprivation 3) Bulbar poliomyelitis 4) Metabolic alkalosis 5) Myxedema 6) Severe Hepatic Failure 7) Bilateral spinothalamic lesions |
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Conditions with augmented response to hypercapnia and hypoxia
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1) Hyperthyroid
2) Salicylism 3) Fever 4) Posthemodialysis 5) Luft’s Syndrome 6) Pregnancy 7) Mild Hepatic Failure |
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Pathophysiology of Obstructive Sleep Apnea
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1) Repetitive episodes of upper airway obstruction
2) Reduction in blood oxygen saturation 3) arousal from sleep 4) symptoms of snoring and sleepiness 5) catecholamine release |
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Apnea: definition
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cessation of airflow for greater than 10 seconds
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Hypopnea: definition
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reduction of airflow by >50% associated with an arousal or >3% desaturation
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Obstructive sleep apnea: Risk factors
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-Obesity, neck size >17 “
-Male gender -Snoring -Craniofacial abnormalities -Nasal obstruction/redundant soft palate -Endocrine abnormalities -Family History |
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Obstructive sleep apnea: associated features
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-Depression
-GERD -Impotence/loss of libido -Anxiety -Cognitive Deficits |
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Sleep deprivation: PFTs
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-20% reduction in response to hypoxia and hypercapnia
-Reduced FEV 1 -Reduced FVC |
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Sleep in COPD
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-Insomnia
-Delayed onset -Frequent awakenings -Nocturnal worsening of hypoxemia |
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Sleep in restrictive lung disease: chest wall deformity
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-Decrease in VC, TV and ERV
-Increase in pulmonary vascular resistance -Hypercarbia and hypoxemia -V/Q mismatch -Rapid shallow breathing |
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Sleep in restrictive lung disease: pregnancy
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-Decrease in FRC and RV
-Increase in V/Q mismatch -Worse in supine position |
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Sleep in restrictive lung disease: obesity
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-decreased compliance of the thoracic cage
-decreased FRC -increased V/Q mismatch Hypoventilation sydromes |
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Sleep in restrictive lung disease: neuromuscular disorders
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-Decrease in : FRC, TV, ERV, -lung compliance
-Increase in: RR -Pharyngeal and laryngeal muscles involved: increase in OSA -Hypoventilation, esp in REM -Hypoxia and hypercarbia |
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