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56 Cards in this Set

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Hypoxemia1. What is the alveolar air equation?2. What are 5 general causes of hypoxemia?3. What are the normal pH, PO2, PCO2 values for arterial blood?4. What arterial hemoglobin saturation and PaO2 is define hypoxemia?5. what is regional difference of ventilation?
1. PAO2=PIO2-PACO2/R= PAO2=FIO2(PB-47)-PaCO2/R (R=0.8)2. Causes§ Hypoventilation§ Diffusion defect – O2 equilibration has not occurred (exercise)§ Venous admixture – perfusion of lung areas which are poorly ventilated§ Shunt – perfusion of lung units which are not ventilated (V/Q=0)§ Decreased FIO2 (house fires/altitude)3. Values§ pH7.35-7.45§ PO2 80-100mmHg§ PCO2 35-45mmHg4. <90%; PO2 <60mmHg5. radioactive xenon measures difference in ventilation, found that ventilation decreases from lower to upper regions in upright lungs
Interpretation of spirometry1. Will an obstructive ventilatory defect show an ↑ or ↓ in FEV1/FVC? Is there a change in FVC?2. What are the 3 major pathophysiologic mechanisms for obstructive ventilatory defects?3. Will a restrictive ventilatory defect show an ↑ or ↓ in FEV1/FVC? Is there a change in FVC?4. What are the 3 major pathophysiologic mechanisms for restrictive ventilatory defects?5. What can a flow-volume curve tell you?6. What is the normal value of FEV1/FVC?7. what volumes cannot be measured by spirometry? 8. How to measure them?9. how to measure dead space?
1. ↓ FEV1/FVC; ↓ or nl FVC 2. Mechanisms§ ↑resistance in airways (upper airway obstruction/bronchitis)§ ↓lung recoil pressure (emphysema)§ ↑airway tone (asthma)3. Nl or ↑ FEV1/FVC; ↓FVC4. Mechanisms§ Stiffening of chest wall (kyphoscoliosis, ankylosing spondiltits, rib fx)§ Stiffening of lung (fibrosis, pneumonis, pulmonary edema)§ Muscle weakness (poliomyelitis, spinal cord injury, myopathies)5. Upper airway obstruction (↓inspiratory flow); Lower airway obstruction (↓expiratory flow)6. 80%7. RV residual volume, FRC functional residual capacity8. FRC can be measure either by Helium dilution and calculated with concentration volume equation [C1xV1=C2x(V1+V2)] or by body plethysmography and Boyle’s law (pressure x volume is constant at constant temperature) 9. tidal volume = mix of anatomic dead space gas and alveolar gas, use Fowler’s nitrogen wash out method for anatomic DS or Bohr’s for physiologic DS
Idiopathic pulmonary fibrosis1. What ages do patients present?2. What are main symptoms and clinical findings?3. What is the secondary effect of hypoxemia?4. What is the mean survival?5. What is the earliest detectable lesion in IPF?6. What type of cell injury is primarily responsible for the pathogenesis of IPF? Describe the pathogenesis7. Describe cellular infiltrate in interstitium and alveoli8. What 2 factors will increase PMN count and thus interfere with reading a bronchial alveolar lavage?9. What are the most useful parameters used to guide therapy of IPF?
1. 40-70yo2. Dyspnea upon exertion, ↓chest inflation, crackles in lower lung fields, clubbing3. Right-heart failure4. 3-5 years5. Lower respiratory tract inflammatory response6. Epithelial cell injury→exudate of proteins into alveolar space→inflammatory response to remove exudates and repair tissue→cytokines→collection of fibrin (and other factors) that accumulate in airways→scar7. ↑lymphocytes (B and T-cells), PMNs, macrophages8. Smoking and bronchitis9. Changes in PFTs and symptoms
Restrictive lung diseases1. Is TLC ↑ or ↓ in RLD?2. What is the most common cause of restrictive lung disease?3. Name 2 other main causes of RLD4. What are the typical presenting symptoms and lab findings in interstitial lung disease?5. What are the salient features of PFTs common to most RLDs?6. What is the treatment for RLDs?
1. ↓2. Interstitial lung disease (aka "diffuse parenchymal lung disease")3. Other causes§ Non-compliant chest wall – kyphoscoliosis, obesity, ascites, pleural thickening§ Muscle weakness – Guillain-Barré (acute), amyotriphic lateral sclerosis, multiple sclerosis, muscular dystrophies, myasthenia gravis, spinal cord injury4. Exertional dyspnea, interstitial/alveolar infiltrates, restrictive parameters on PFTs, abnormal gas exchange parameters (↓LCO)5. PFTs§ Restrictive ventilatory defect (↓TLC and VC)§ No airway obstruction§ ↓diffusing capacity§ Hypoxemia worsens w/ exercise6. Tx§ Advanced dz: supportive tx§ Specific diagnosis:specific therapy (ie. d/c amiodarone)§ Sarcoidosis/hypersensitivity pneumonitis: corticosteroids
Respiratory failure1. What values of PaO2 and PaCO2 define respiratory failure?2. Define hypercarbic respiratory failure3. What is the differential diagnosis of hypercarbic respiratory failure?4. Define hypoxemic respiratory ventilation5. Name 3 conditions that are on the differential diagnosis for hypoxemic respiratory failure6. Is acute respiratory distress syndrome hypoxemic or hypercarbic?
1. PaO2<60mmHg and PaCO2>45mmHg2. ↓alveolar ventilation due to ↓minute ventilation, ↑dead space ventilation, or both3. DDx§ Impaired control of breathing§ ↓respiratory muscle strength§ ↑mechanical load on respiratory mm. due to ↑airway resistance§ Lung parenchymal abnormalities§ Altered chest wall mechanics4. Failure of oxygenation usually due to large R→L intrapulmonary shunt5. DDx§ Pulmonary edema§ Pneumonia§ Alveolar hemorrhage6. Hypoxemic
Pneumoconiosis1. Define2. What is the most prevalent chronic occupational disease in the world?3. How does classic silicosis present?4. What are the PFT abnormalities seen in silicosis?5. Describe the pathogenesis of silicosis6. How does asbestosis present?7. What are the PFT abnormalities in asbestosis?8. Describe pathogenesis of asbestosis
1. Accumulation of dust in lungs and tissue reaction to its presence2. Silicosis3. Insidiously progressive dyspnea/cough, CXR: rounded opacities in ULZ (may coalesce over time→shadows=progressive massive fibrosis), PFT abnormalities4. PFTs§ Restrictive ventilatory defect (↓TLC and VC)§ No airway obstruction§ ↓diffusing capacity§ ↓FEV1/FVC (from airflow obstruction)5. Particles deposit in alveoli→pulmonary alveolar macrophages ingest silica and migrate to interstitium→lymph nodes/release of proteolytic enzymes→lung injury6. Slow onset of dyspnea and non-productive cough7. PFTs§ Restrictive ventilatory defect (↓TLC and VC)§ No airway obstruction§ ↓diffusing capacity§ Arterial hypoxemia8. Asbestos fibers penetrate into pulmonary parenchyma→1 fiber engulfed by alveolar macrophages→multinucleated giant cell→chemotactic cytokines released→fibrosis
Pathology of ARDS 1. Name and describe the 3 phases of ARDS
§ Exudative phase (24-96h)§ Alveolar and interstitial edema, capillary congestion, inflammatory cell infiltrate, destruction of Type I alveolar cells, hyaline membrane formation§ Proliferative phase (3-10d)§ ↑Type II alveolar cells, cellular infiltration, organization of hyaline membranes§ Fibrotic phase (7-10d)§ Fibrosis of hyaline membranes, alveolar septa, alveolar ducts§ Usually resolves
ARDS1. What clinical findings define ARDS?2. What are the 3 routes of acute lung injury?3. What syndrome is the single most important predisposition to ARDS?4. What 3 risk factors account for 75% of ARDS cases?5. What is the mortality rate of ARDS?6. How do the majority of ARDS survivors present 1 year following hospitalization?
1. Clinical findings§ Acute respiratory distress§ Diffuse alveolar infiltrates on CXR§ Severe hypoxemia (PaO2/FIO2<200mmHg)§ Absence of left heart failure (pulmonary wedge pressure<18mmHg)2. 3 routes§ Blood-borne/vascular source of injury§ Inhalation or airway source§ Direct or physical source3. Sepsis4. Sepsis, severe multiple trauma, aspiration of gastric contents5. 40%6. Near normal PFTs (minority have permanent fibrosis w/dyspnea
Pathophysiology of ARDS1. What factors determine the development of edema in ARDS?2. Which is more effective, a hydrostatic pressure gradient or oncotic pressure gradient of equal magnitude? Why?3. What is the Starling equation?4. How do Kf and σ change in ARDS and what is the result?5. What happens to Pc and why?6. At what point does alveolar flooding occur?7. How does edema in ARDS differ from edema in CHF?8. Is the severe hypoxemia seen in ARDS responsive to ↑inspired O2? Why or why not?9. Describe the pathogenetic role of PMNs in ARDS10. Why should the therapeutic goal of PO2 be increased to 80-90mmHg in ARDS patients?
1. Governing factors§ Hydrostatic and oncotic pressures acting across membranes which separate blood from interstitial and air spaces§ Filtration characteristics of those membranes2. Hydrostatic; b/c membrane has some permeability to protein3. Rate of fluid filtration (Qf)=Fluid conductance (Kf)xDriving pressure[(Pc-Pi)-σ(πc-πi)]§ Since σ normally= 0.7 fluid is continuously filtered into interstitial space and removed by lymphatics at an equal rate4. ↑Kf and ↓σ→protein rich fluid enters interstitium5. ↑Pc due to pulmonary vasoconstriction6. When clearance pathways are overwhelmed and fluid storage capacity of interstitium is exceeded7. Membrane permeability is maintained→edema fluid is protein poor→oncotic pressure gradient decreases tendency for further edema formation (CHF)8. No, refractory to O2; major cause of hypoxemia is shunt (perfusion to unventilated alveoli)9. Activation of complement due to tissue inticing event→C5a (?)→PMN activation and aggregation on pulmonary endothelium→release of oxygen radicals, proteases, arachidonic acid metabolites→loss of structural integrity and pulmonary vasospasm10. Hb dissociation curve shifted to R by fever and acidosis
Mechanical properties of lung affected by ARDS1. What happens to compliance? Why?2. Which part of the lung is collapsed and de-recruited in ARDS and why?3. What are other reasons for collapse?
1. ↓; combination of interstitial and alveolar edema and damaged surfactant→closure of small airways2. Dependent region due to weight of mediastinum and edematous lung on airways3. Interstitial edema, increased surface tension due to dilution/alteration of surfactant, ↓lung volume, fibrosis (late stages)
Positive end-expiratory pressure1. What are the benefits of PEEP?2. What are the potential harmful effects of PEEP?3. How does intermittent positive pressure ventilation (IPPV) differ from PEEP?4. How might excessive mechanical ventilation cause pulmonary edema?
1. Benefits§ ↓shunt fraction (reverses atelectasis, redistributes edema)§ Allows reduction of FIO2§ ↑lung complianceer2. Harms§ ↓venous return→↓CO (compression of R atrium/great veins)→↓mixed venous oxygen→↑arterial hypoxemia§ Barotrauma (pneumothorax, pneumomediatinum)§ ↑dead space (compress alveolar capillaries)§ ↑interstitial edema (?) (b/c of ↓interstitial pressure upon ↑inflation w/ PEEP)3. Positive pressure during inspiration but end-expiratory pressure returns to atmospheric pressure (P is positive through respiratory cycle in PEEP)4. Stretch-induced lung injury from excessive tidal volumes
Complications of ARDS1. What are 2 frequent complications of ARDS?2. How can adequate transport of O2 to tissues be maintained?
1. Hypotension and renal failure2. Transport§ Maintainance of CO: Administration of fluids, blood, inotropic agents§ Maintainance of arterial O2 content: PEEP, ↓pulmonary capillary pressure, treatment of fever and acidosis, maintain [Hb]
Pulmonary hypertension1. How can causes of pulmonary hypertension be grouped?2. What left heart conditions can lead to pulmonary hypertension and why?3. What is the most important mechanism of pulmonary hypertension?4. What disease of the pulmonary veins causes pulmonary hypertension?5. Name 3 mechanisms that lead to passive increase in resistance6. Name 3 mechanisms that lead to active increase in resistance7. Name 1 other mechanism that leads to vascular remodeling and thus pulmonary hypertension
1. Causes: Ppa=(CO x R) + Pla§ CO§ Resistance (in pulmonary vasculature)§ Pla2. LH conditions§ LHF (acute MI, aortic valve disease, cardiomyopathy)§ Mitral valve stenosis§ Sclerosing mediastinitis (TB or histoplasmosis) (rare)§ → chronic elevation of back pressure→vascular remodeling of pulmonary arteries and veins3. Elevated resistance4. Pulmonary veno-occulsive disease5. Passive§ ↓capillary cross-sectional area§ Distortion/compression of capillaries§ Hyperinflation (elevation of FRC)6. Active§ Alveolar hypoxia§ Circulating mediators§ Pulmonary artery obliteration/obstruction7. ↑pulmonary blood flow
Cardiovascular pressures1. What is the normal and mean Ppa?2. What is the normal Pla3. What is the normal Paorta?4. What is the normal Pra?5. What is the normal pressure gradient across pulmonary circulation?6. What is the normal pressure gradient across systemic circulation?7. What is normal CO?8. Define pulmonary hypertension
1. 25/10mmHg; 15mmHg2. 5mmHg3. 120/0mmHg4. 2mmHg5. 10mmHg6. 100mmHg7. <25L/min (during exercise)8. Ppa>25mmHg
PULMONARY HYPERTENSIONChanges in pulmonary parenchymaPassive ↑ in resistance1. What % of normal lung needs to be removed to ↑PVR?2. Name 2 conditions in which less lung removal may cause pulmonary hypertension3. Name 2 processes that distort/compress capillaries→↓FRC4. What 2 conditions may cause hyperinflation (↑FRC)
2. Lung removal§ Lung resection – carcinoma§ Emphysema – loss of capillary units – obstructive disease with ↓CO diffusing capacity3. Distort/compress capillaries§ Intersitital lung disease – pulmonary fibrosis, scleroderma, sarcoidosis§ ARDS4. Hyperinflation§ Asthma – air trapping§ PEEP – for ARDS
PULMONARY HYPERTENSIONPulmonary veno-occlusive disease1. What is the usual presentation?2. What are the etiologic associations?3. What is the prognosis?
1. Young adult w/ insidious exertional dyspnea, pulmonary edema2. Bleomycin therapy, viral infections, collagen vascular diseases3. 3 years
PULMONARY HYPERTENSIONCirculating mediators1. What mediators can cause pulmonary vasoconstriction?2. What may stimulate production of these mediators?
12. Mediators§ Lipoxygenase products (leukotrienes)§ Cyclooxygenase (prostaglandin, thromboxane)§ Cytokines (TNF, Il-1)13. Gram negative bacteria
PULMONARY HYPERTENSIONAlveolar hypoxia1. What is the response of pulmonary arteries/arterioles to hypoxia?2. What is the response of systemic arteries/arterioles to hypoxia?3. What is the threshold for this response?4. Name 4 causes of pulmonary hypertension due to hypoxia
§ Vasoconstriction§ Vasodilation14. PAO2<60mmHg15. Causes§ COPD§ Altitude§ High altitude pulmonary edema§ Hypoventilation
PULMONARY HYPERTENSIONIncreased pulmonary blood flow1. What conditions lead to pulmonary hypertension due to increased pulmonary blood flow?2. Why does increased pulmonary blood flow lead to pulmonary hypertension?3. Is the prognosis better or worse than for patients with PPH? Why?
1. Congenital heart disease§ ASD, VSD, patent ductus arteriosus, anomalous pulmonary venous return2. Vacular remodeling, and increased flow3. Better; Eisenmenger's syndrome (change to R→L shunt→↓RH work)
PULMONARY HYPERTENSIONPulmonary arteries1. What are the presenting symptoms?2. What is the pathogenesis of pulmonary hypertension due to schistosomiasis?3. What is the pathogenesis of pulmonary hypertension due to pulmonary thromboembolism?4. What is the result of thromboemboli that do not resolve?5. What are 5 other circumstances in which pulmonary vasculature may become occluded?6. What is the pathogenesis of pulmonary hypertension due to primary (idiopathic) pulmonary hypertension?7. What is the presentation of PPH?8. What is the prognosis of PPH?9. What is the treatment of PPH?10. What associations have been made to PPH?11. What are other causes of pulmonary arterial hypertension?
radiographs2. Seen in conjunction with liver disease→portal hypertension→eggs bypass liver→lodge in pulmonary arterioles→granulomatous response→ destructive vasculitis→obliteration of channels3. DVT migrates to lungs→§ If large→RHF→death§ Occlusion of pulmonary arteries§ Release of vasoactive mediators§ Hypoxic pulmonary vasoconstriction by regional bronchospasm4. Progressive occlusion of large vessels→chronic pulmonary hypertension (indistinguishable from PPH)5. Other occlusions§ Fat (bone fracture/trauma/sickle cell crisis)§ Air (iatrogenic)§ Amniotic fluid (activation of coagulation and complement cascades during childbirth)§ Tumors (breast or lung)§ Foreign bodies (IV drug abuse)6. Dysfunctional endothelium loses vasodilator tone→irreversible ↑tone7. Women 20-40yo, ↑insidious exertional dyspnea (>1y), ↑Ppa8. 3 years after diagnosis9. Prostacyclin10. Diet drug use (Redux), HIV ifx, liver cirrhosis11. Collagen vascular dz (CREST scleroderma), Vasculitis (RA, SLE, Polymyositis)
PULMONARY HYPERTENSIONAlveolar hypoxia1. What is the response of pulmonary arteries/arterioles to hypoxia?2. What is the response of systemic arteries/arterioles to hypoxia?3. What is the threshold for this response?4. Name 4 causes of pulmonary hypertension due to hypoxia
§ Vasoconstriction§ Vasodilation14. PAO2<60mmHg15. Causes§ COPD§ Altitude§ High altitude pulmonary edema§ Hypoventilation
Consequences of pulmonary hypertension1. What is the consequence of acute pulmonary hypertension as in PE?2. What is the consequence of chronic ↑PPA?3. How do patient with cor pulmonale present?4. What happens to diffusion capacity and dead space with advanced PH?
1. Consequences of acute PH§ ↑PRA→↓venous return→compensatory symp. discharge→hypotension/tachycardia or shock and death§ ↑afterload→acute RHF2. Consequences of chronic PH§ ↑PPA→compensatory mechanisms (aldosterone, symp. discharge)→constriction of peripheral vessels/volume expansion→↑venous return→↑PRA§ Progression of PH→↑PRA and ↑volume→edema, ascites, inadequate perfusion of vital organs (if RV unable to compensate)§ Cor Pulmonale→RHF due to pulmonary hypertension resulting from disease of the lung/vasculature3. edema, hepatic congestions, ↑JVP, loud S2, R-sided S3, RV heave, tricuspid regurgitation, ↓DLCO4. ↓diffusion capacity b/c of ↓blood in capillaries, ↑dead space because of adequate ventilation in non-perfused areas
Treatment of pulmonary hypertension1. What is the treatment of PH?
1. Unload RV§ Oxygen if hypoxic§ Anticoagulation§ Vasodilators: prostaglandin, endothelin§ Pulmonary vascular remodeling§ Lung transplantation
Pathophysiology of asthma1. How does airway inflammation contribute to the pathophysiology of asthma?2. What other pathological process accompanies inflammation in asthma?3. What cells are involved in the inflammatory response in asthma?4. Is airway hyperreactivity only seen in asthma?5. How is airway hyperreactivity measured?6. Describe airway obstruction in asthma
1. Inflammatory cells→release of mediators (histamines, prostaglandins, leukotrienes)→contract airway smooth mm., ↑airway edema, attract additional inflammatory cells2. Hyperplasia of submucosal glands→↑goblet cells→mucous hypersecretion→airway obstruction3. Inflammatory cells§ Eosinophils – Predominate during acute asthma attack§ Release eosinophilic major basic protein→damages airway tissues and alter airway function (including hyperresponsiveness)§ Neutrophils – Predominant infiltrate§ Mast cells§ Binding of allergen to IgE on surface→cascade of events→ immediate bronchoconstriction§ Lymphocytes§ TH2 cells→IgE production and cytokine release§ Macrophages4. No – lack of hyperresponsiveness excludes asthma5. Methacholine challenge6. Non-uniform obstruction of tracheobronchial tree caused by smooth mm. contraction, airway mucosal edema, inflammatory exudates
Neural controls of the airways1. Describe the dominant neural control of airway smooth mm.2. What aspect of this neural system might be deficient in asthma?3. What are 2 non-adrenergic, non-cholinergic inhibitory neurotransmitters released by airway nerves that cause bronchodilation?4. What kind of neurotransmitters are substance P, Neurokinin A and B (tachykinin)? What is there effect on airways?5. What adrenergic receptors are found on airway smooth mm. and what is the effect of stimulation by epinephrine?6. Is there direct stimulation of airway smooth mm. by adrenergic nerve fibers?
1. Cholinergic§ Vagus nerve synapses w/parasympathetic ganglia in wall of airway→stimulation of mAch Rs→§ Smooth mm. contraction/bronchoconstriction§ Release of mucus from airway glands§ Negative feedback to nerve endings→prevents further release of Ach2. Negative feedback to nerve endings→prevents further release of Ach3. Vasoactive intestinal polypeptide (VIP), NO4. Non-adrenergic, non-cholinergic excitatory§ Bronchoconstriction§ Mucus secretion§ Airway edema§ Recruit inflammatory cells to airways and activate them5. β2 R→bronchodilation6. No direct innervation, but innervate parasympathetic ganglia→inhibits release of Ach
Symptoms and signs of asthma1. Describe the classic symptoms of asthma2. When are symptoms worse?3. What are the lab findings?4. What is the result of hyperinflation and what physiological consequences does this have?5. What is ventricular interdependence?6. What is the physiological response to fatigue during an asthmatic attack?
1. Wheeze, dyspnea, cough, chest tightness2. Night and early morning3. CXR: hyperinflation, Spirometry:↓FEV1, FVC and lung volume testing: ↑TLC, FRC, RV4. Pleural pressure swings§ ↑work of breathing→respiratory fatigue→respiratory failure§ Inefficient work of respiratory mm.§ Hyperinflation→pulmonary hypertension5. Exaggerated pleural pressure swings→pulsus paradoxus: negative inspiratory pressure→§ ↑venous return and hyperinflation of lungs→RV distention→impedes LV filling§ Impedes emptying of LV6. Hypoventilation→↑PCO2→↓arterial O2 tension
Triggers for asthma exacerbations1. Name 6 triggers for asthma exacerbations2. What is the difference between extrinsic and intrinsic asthma?
1. Triggers§ Viral ifx§ Inhaled irritants§ Inhaled allergens§ Exercise/cold air§ Occupational exposures§ Non-adherence to therapy2. Intrinsic asthma has no recognizable triggers
Treatment of asthma1. What are the mainstay treatments of asthma between exacerbations? Describe their MOAs2. What other treatment blocks the effects of pro-inflammatory mediators in response to allergen exposure?3. Apart from medication, what 3 other factors are important in the treatment of asthma
1. Mainstay treatments§ Bronchodilators – β2 agonists (most effective); anticholinergic (less effective) – may be most effective in combination§ Corticosteroids – inhaled for persistent symptoms§ Leukotriene mediators - ↓bronchoconstriction, vascular permeability, mucus secretions, chemotacticity due to release of leukotrienes2. Omalizumab – Anti-IgE3. Environmental control, monitoring lung function, educating patients
COPD1. What are the diseases which comprise COPD?2. What are the risk factors for COPD?3. Compare the 2 types of emphysema
1. COPD§ Emphysema§ Chronic bronchitis§ [Asthma/asthmatic bronchitis]§ [Bronchiectasis]§ [Cystic fibrosis]2. Risk factors§ Older age§ Cigarette smoking§ Male§ Airway hyperreactivity§ Low socioeconomic status§ α-1 anti-trypsin deficiency3. Emphysema§ Pan-acinar§ Involves entire acinus§ Mostly affects lung bases§ Alpha-1-antitrypsin deficiency§ Centrilobular§ Involves respiratory bronchiole§ Mostly affects lung apex§ Cigarette smoker
COPD1. Describe emphysema2. Describe chronic bronchitis3. Explain the protease imbalance theory of emphysema4. What are the 3 main stages of COPD and why does each stage occur (refer to emphysema, chronic bronchitis, or asthmatic bronchitis)5. What features of emphysema are seen on chest x-rays?
bullae→↓elastic recoil of lung→slow max expiratory volumes2. Disorder of chronic mucus hypersecretion (>3 months chronic sputum production)→↑airway resistance causing expiratory airflow limitation3. Cigarette smoke inactivates anti-proteases and causes inflammatory cells to secrete proteases to accumulate in terminal airspaces→proteases such as elastase cause emphysema (also problem with α-1 antitrypsin deficiency)4. Stages§ EARLY: Airflow obstruction§ ↓elastic recoil – emphysema§ ↑airway resistance – chronic bronchitis§ ↑airway smooth mm. tone – asthmatic bronchitis§ MID-COURSE: Hypoxemia§ Ventilation-perfusion mismatch§ Hypoventilation – chronic bronchitis§ Diffusion impairment – emphysema w/exercise or high altitude§ LATE: Pulmonary hypertension (→RV dilation, ↑venous pressure, ↓survival)§ Chronic alveolar hypoxia§ Destruction of pulmonary capillary bed by emphysema§ VERY LATE: Cor Pulmonale5. ↑A-P diameter, flat diaphragm, ↓vascular marking, enlarged central pulmonary arteries, ↑anterior air space, ↑sternophrenic angle
Pink Puffers vs. Blue Bloaters1. Contrast pink puffers and blue bloaters2. Which is a COPD patient?
1. Pink Puffers Blue Bloaters
§ Emphysematous§ Hyperinflated§ Thin physique§ Dyspneic§ Low PaCO2§ Worsens O2 sat w/ exercise§ Wants O2 treatment § Bronchitic§ Less hyperinflated§ Obese physique§ Not dyspneic§ High PaCO2§ Improves O2 sat w/ exercise§ Needs O2 Rx
2. Has elements of both
Therapy for COPD1. What is the only treatment known to improve survival of COPD?2. What is the only treatment known to slow the progression of COPD?3. Name 3 adjuncts to therapy for COPD and when they are used4. What is the advanced treatment for COPD?5. What are the indications to begin ventilation in COPD?
1. Oxygen2. Smoking cessation3. Adjunct therapies§ Abx – exacerbations w/ change in sputum color/quantity§ Bronchodilators – prevent or minimize bronchospasm§ Corticosteroids – exacerbations (ant-cholinergics, beta-agonists, methyl-xanthines)4. Advanced treatment§ Lung transplantation§ Alpha-1 antitrypsin replacement therapy§ Lung-volume reduction§ Bullectomy§ Laser§ Bilateral lung volume reduction§ Long-term mechanical ventilation5. Indications§ Severe respiratory acidosis (pH<7.25)§ Need for sedation (agitation, pain control)§ Uncontrollable hypoxemia (PO2<50)§ Progressive deterioration despite Rx§ Inability to clear or protect airway
Respiratory muscles1. What are the effects of acute hyperventilation on respiratory muscles?2. Describe the 3 types of muscle fibers. Which predominate in the normal adult diaphragm? In the normal neonate diaphragm?3. What can be observed physically when the diaphragm fatigues?4. What happens to tidal volume, minute ventilation, and respiratory rate when diaphragm fatigues?5. How is the transdiaphragmatic pressure (Pdi) measured?
§ Shortens resting diaphragmatic length§ ↓force of contraction§ Less room to contract→↓piston action§ Ribs more horizontal§ ↓outward recoil of chest wall2. Muscle types§ Type I – highly oxidative – slow to fatigue (predominate in adult diaphragm)§ Type IIa – oxidative – relatively fatigue resistant - (neonatal)§ Type IIb – glycolytic – fatigue rapidly (neonatal)3. Abdominal paradox – exaggerated activation of accessory muscles → diaphragm drawn upward and abdominal wall inward during inspiration4. Initially minute volume preserved, ↑RR, ↓tidal volume5. Abdominal pressure-pleural pressure
Respiratory muscles in COPD1. Why is the pressure output of the respiratory muscles in COPD patients increased by about 3X that of normal patients?2. Why does hyperinflation increase muscle demands?3. Why is respiratory muscle capacity decreased in COPD?
1. Hyperinflation, ↑airway resistance, ↑dead space2. ↑mm demands:1. Lung on flat portion of PV relationship curve→↑change in Ppl necessary for given VT2. Chest wall above its relaxation volume→inspiration has less assistance on recoil from chest and more dependence on mm. contraction3. Isometric contraction of inspiratory muscles to lower alveolar pressure to ambient P before next inhalation3. ↓respiratory mm. capacity1. Hyperinflation2. Malnutrition3. Steroids (cause myopathy)4. Cytokines (↑TNF in serum of low-weight COPD patients)5. Myopathy
Respiratory muscles in sepsis/shock1. Why is muscle demand increased in shock states?2. Why is mm. capacity decreased?3. What is critical illness polyneuropathy?4. What is critical illness myopathy?
1. ↑mm. demand§ Sepsis (esp. fever)→↑CO2→↑ metabolic acidosis →↑ventilation to compensate§ ↓compliance b/c of pulmonary edema (cardiogenic or non-cardiogenic)2. ↓blood flow to respiratory mm. and hypoxia3. Demyelination/axonal degeneration following sepsis/acute, severe inflammation and shock4. Occurs in patients who received corticosteroids, esp. in combination w/neuromuscular blocking agents
Respiratory muscle failure due to neurologic impairment1. What muscles are affected by lesions to lower cervical spinal cord and what are the physiologic consequences?2. Name 5 conditions which may result in unilateral diaphragmatic paralysis3. What is a good test to test for unilateral diaphragmatic paralysis?4. Name 2 signs of bilateral diaphragmatic paralysis
1. Paralysis of intercostals and expiratory muscles – diaphragm spared§ Upper ribs sucked inward during inspiration§ Expiratory strength lost→↓cough and clearance of bronchial secretions→↑risk of pneumonia2. Unilateral diaphragmatic paralysis→↓25% vital capacity/MIP§ Stroke§ Trauma§ Malignancy§ Herpes zoster of phrenic nerve§ 25% pts after open-heart surgery3. Sniff test and US/fluoroscopy4. Bilateral diaphragmatic paralysis§ Abdominal paradox§ Intolerant of recumbent position for more than several minutes
Treatment of respiratory failure1. Describe the 2 kinds of "training" that can be used to strengthen respiratory muscles2. What other approaches to treatment are effective?
1. Training§ Resistor breathing – builds strength§ Voluntary isocapnic hyperventilation – builds endurance2. Other treatments§ Rest using cuirass ventilator (negative pressure); positive pressure ventilation§ Mechaincal ventilation – required for hypercarbic ventilatory failure§ Diaphragmatic pacemakers – pts w/ intact phrenic nerve and muscle function (rarely used)§ Pharmacotherapy – bronchodilators, aminophylline and theophylline (improve contractility)§ Lung volume reduction surgery→↓degree of hyperinflation and improved respiratory muscle strength
Obstructive sleep apnea1. When do the earliest respiratory manifestations of obesity occur?2. What are 2 consequences of upper airway obstruction?3. What are the symptoms of obstructive sleep apnea?4. Are upper airway critical pressures in obstructive apneic patients positive or negative?5. What causes elevations in critical pressure during sleep?6. Name 5 risks for obstructive sleep apnea
1. During sleep2. Hypersomnolence, oxyhemoglobin desaturation→cardiac/respiratory dysfunction3. Symptoms (in order of ↑airway obstruction)§ Snoring, snorting, gasping, or choking at night§ Arousals from sleep, excessive movements, periods of insomnia§ Neurocognitive dysfunction, daytime hypersomnolence§ ↑risk of cardiovascular disease (HTN, glucose intolerance)§ RHF and respiratory failure (in severely obese)4. +5. Causes§ Defects in upper airway neuromuscular control§ ↓genioglossus and other mm. activity during sleep→tongue prolapse into pharynx§ Anatomic alterations§ Large tonsils§ Foreshortened jaw (micro- and retroagnathia)§ Adipose tissue deposits in and around pharyngeal structures6. Risks1. Obesity, snoring, menopause, male, central vs. peripheral fat distribution
Treatment of obstructive sleep apnea1. What are the major approaches to treatment of sleep apnea?
1. Approaches to treatment§ ↓critical pressure – Improve upper anatomy structure/neuromuscular control§ Weight loss§ Structural – body position, uvulopalatopharyngoplasty, hyoid and mandibular repositioning§ Neuromuscular – protryptyline, direct electrical hypoglossal stimulation§ ↑ nasal pressure→overcome obstruction w/positive splint to keep airway open (CPAP- nasal continuous positive airway pressure)
Hypercapnia1. What is the differential diagnosis for hypercapnia?2. Why might there be a drop in CNS sensitivity to CO2 in severe obesity?
1. DDx§ Won't breathe – low ventilatory drive§ Inborn defects (Ondine's curse)§ Metabolic alkalosis§ CNS depressants (opiates)§ Can't breathe§ Neuromuscular disease impairs transmission of ventilatory drive§ Guillain Barre§ Myasthenia gravis§ Muscular dystrophy§ Excessive mechanical loads§ Parenchymal lung or chest wall disease§ Upper airway obstruction2. Leptin insensitivity might lead to hypoventilation in severe obesity
Therapy for obesity-hypoventilation syndrome1. How is hypercapnia treated?2. How is hypoxemia treated?
1. Hypercapnia§ Progesterone – stimulates ventilation§ CPAP§ Tracheostomy§ Weight loss – lowers CO2 production and ↓mechanical load2. Hypoxemia§ Progesterone – stimulates ventilation§ CPAP§ Tracheostomy§ Weight loss§ Supplemental O2 (to ↑PIO2)
Expiratory flow limitation1. What causes flow limitation?2. At what percent of maximal effort does flow limitation occur?3. Why are maximum expiratory airflows decreased in emphysema?4. What are the primary factors that affect resistance?5. Name 3 factors that may increase the tendency of airways to close with ↑PPL6. Name 2 factors that determine the amount of air left in lungs at residual volume7. What are the 3 pathophysiologic mechanisms of flow limitation in the lungs?
1. Increase in Ppl →↑PA but also ↑airway resistance because airways become narrower2. Occurs at 60-70% maximal effort in normal subjects3. PEL is decreased because alveolar septa are destroyed4. Length and diameters of airways (bronchi)5. Factors§ Mucosal inflammation – bronchitis, asthma§ Smooth muscle spasm – asthma§ Destroyed tethering forces from parenchymal attachments – emphysema6. Factors§ Tendency of airways to close/resist closure§ Elastic characteristics of lung parenchyma7. Pathophysiologic mechanisms1. ↑airway resistance2. ↓lung recoil3. ↑tendency for airway to close
Respiratory system development1. Describe the changes in upper airways that develop in the infant and child2. What are the 5 categories of respiratory disease that can affect infants and children?
1. Changes in upper airway§ At birth – epiglottis is large – covers soft palate→nasal breathing§ Older child – epiglottis and larynx migrate caudally2. 5 categories§ Extrathoracic§ Conducting airways§ Chest wall/muscle§ Lung parenchyma§ Nervous system effects on respiration
Pediatric extrathoracic obstruction1. What are the sign/symptoms of adenoid hypertrophy and other extrathoracic obstructions?2. Name 4 special situations in which upper airway obstruction is seen3. Is FRC and RV ↑ or ↓?
1. Signs/symptoms§ Long face§ Open mouth posture – mouth breathing§ "Nasal" voice§ ↓maxillary development§ Snore§ Muffled voice§ Drool§ Trouble swallowing§ Obstructive sleep apnea§ Stridor§ Failure to thrive2. Special situations1. Craniofacial abnormalities2. Septal deviation3. Down's syndrome4. Micrognathia3. Nl FRC, ↑↑RV
Pediatric conducting airway diseases1. Name 4 major causes of conducting airway diseases that affect the pediatric population2. What are the signs and symptoms of lower airway obstruction?3. What are the consequences of airway obstruction?
1. Conducting airway disease§ Asthma§ CF§ Bronchiolitis§ Inhalation injury2. Signs/symptoms§ Expiratory wheeze (polyphonic)§ Labored breathing§ Labored/prolonged exhalation§ Chest hyperinflation from air trapping§ Respiratory failure (acidosis and ↑CO2)§ Supraclavicular and intercostal retractions§ Anxiety3. Consequences§ Hypoxemia§ CO2 retention§ Atalectasis OR hyperexpansion§ Infants quickly lose lung volume from airway plugging atelectasis, ↑closing capacity→↓FRC→rapid desaturation→tachypnea
Pediatric restrictive lung disease1. Name 4 categories of restrictive lung disease and examples of each2. What are the consequences of restrictive lung disease?3. Is FRC, RV ↑ or ↓?
1. Category Examples
§ ↑elastic recoil § Pulmonary fibrosis§ Scar§ Bronchopulmonary dysplasia
§ Hypoplasia of lung§ Premature babies who never developed sufficient # of alveoli § Congenital diaphragmatic hernia
§ Restrictive chest wall§ Congenital syndromes causing small chest size§ Severe obesity § Scoliosis
§ Weak muscles and diaphragm→↓lung expansion § Muscular dystrophy
2. Consequences§ Low lung volumes§ ↑work of breathing§ Tachypnea§ Low resting lung volumes – viral ifx/mucous plugging→↓O2 sats§ Normal mechanisms to improve respiratory compromise are not sufficient (ie. cough, deep breaths, tachypnea)3. ↓↓FRC, ↓RV
Infants, sleep, and autonomic nervous system1. Why are infants at increased risk from disease due to hypoxia during sleep?2. What is unique about an infant's autonomic response to stress such as mechanical, acid reflux, or viral stimulation of the nose, larynx, or pharynx? Is this response the same in children? Adults?3. Under what circumstances is this response to stress increased?
1. ↑risk of hypoxia§ ↓skeletal mm. tone during REM sleep (infants in REM 50% sleep time)→↓lung volume→↓O2 saturation§ Sleep ↓respiratory response to CO2 and hypoxia§ Infants fail to arouse to hypoxemia2. Vagal response to stress→apnea, bradycardia→rapid O2 desaturation§ Vagal response absent in young children and adults3. ↑ vagal response in:§ Premature infants§ Viral infections§ Sleep§ Sedation
Bronchopulmonary dysplasia1. What are the risks of developing BPD?2. Describe the histology of BPD3. Describe the pathophysiology of BPD at the cellular level
1. Risks§ Earlier gestational age at delivery§ Smaller birth weight§ Prenatal/postnatal ifx§ Mechanical ventilation§ Respiratory distress syndrome/hyaline membrane disease2. Histology§ Enlarged and fewer alveoli§ ↓alveolar surface area§ fewer capillary endothelial cells§ +/- fibrosis§ +/- inflammation3. Pathophysiology§ Impaired cell growth of alveolar septum)§ ↑cell death§ Influx of inflammatory cells (macrophages and neutrophils)§ Imbalance of proteolytic and anti-proteolytic enzymes§ ↑ECM deposition (↑TGF-β levels)§ ↓essential growth factor levels
Respiratory distress syndrome1. What are the 5 factors involved in the pathophysiology of RDS?2. What causes surfactant deficiency and what is the result of surfactant deficiency?3. What is the cause and result of anti-oxidant enzyme deficiency?4. What are infants with RDS at increased risk for?5. What 2 characteristics of infants w/ RDS→pneumothoraces?
§ Surfactant deficiency§ Anit-oxidant enzyme deficiency§ Increased inflammation exacerbated by underlying infection or sepsis§ Severe gas exchange abnormalities in extremely immature lungs/hypoplastic lungs§ Initiation of mechanical ventilation in infants w/ respiratory fatigue/failure→barotrauma to immature lungs2. Surfactant deficiency§ Cause: immature type 2 epithelial cells§ Result: ↑alveolar surface tension→↑airway pressure required to keep open alveoli3. Superoxide dismutase deficiency§ Cause: prematurity§ Result: ↑oxidative stress to lungs which is exacerbated by administration of high oxygen concentrations4. ↑Risk of§ Pneumothorax§ Worsening lung injury§ Prolonged mechanical ventilation§ BP instability§ Intra-ventricular hemorrhage§ Tracheal stenosis from intubation5. Compliant chest wall; stiff, wet lungs
Prevention and treatment of bronchopulmonary disease1. Name 5 measures to prevent BPD – which one of these measures may be associated with developmental abnormalities?2. Name 6 treatments of BPD
1. Prevention§ Decrease premature births§ Avoid mechanical ventilation§ Consider high frequency oscillator ventilation (HFOV), permissive hypercapnea§ Steroids (?) – may be associated w/ prenatal abnormalities§ Avoid infections in both pregnant mother and premature infant§ Maximize calories to prevent malnutrition which can impair lung growth2. Treatment1. Limit exposure to respiratory viruses2. Administer Synagis (mAb vs. RSV)3. Treat respiratory symptoms (consider diuretics, bronchodilators, anti-inflammatories, anti-cholinergics)4. Maintain adeqyate O2 sats5. Supplement w/ adequate calories6. Recognize infants at risk for pulmonary aspiration7. GERD, direct aspiration from oral intake8. Consider gastric tube placement/surgical reflux procedure
Complications of cystic fibrosis1. What is the complication associated with GI disease and why does this occur?2. What is the effect of CF on the pancreas?3. What leads to hepatobiliary disease in CF and what complications are seen?4. What reproductive abnormality is often seen in CF?
1. Failure to secrete Cl→accumulation of solid stool at ileal-cecal jxn→intussusception, rectal prolapse2. Pancreatitis, hyperglycemia (triggered by pregnancy, corticosteroids, pulmonary exacerbation other stresses)§ Hyperglycemia due to blockage of islets→↓insulin and glucagon→ketoacidosis is rare3. Eosinophilic concretions in bile ducts→↑incidence of gallbladder dz, gallstones, microgallbladder (cirrhosis also seen)4. Congenital absence of vas deferens→azoospermia→infertility
Cystic fibrosis1. Where is the genetic mutation and what protein does it affect?2. What are the clinical manifestations of CF?3. What is the most common mutation in CF and what process does it affect?4. Name 6 other molecular mechanisms that can be responsible for the phenotype of CF?
1. CFTR – chromosome 7→cAMP-regulated chloride channel2. Clinical manifestations§ Respiratory§ Chronic cough and bronchitis§ Bronchiectasis§ Recurrent pneumonia (s.aureus, pseudomonas aeruginosa)§ Chronic sinusitis, nasal polyps§ Hemoptysis, pneumothorax§ Irreversible chronic airway obstruction3. ΔF508 – Abnormal CFTR processing and trafficking4. Molecular mechanisms of CF§ No CFTR protein synthesis§ Defective CFTR regulation (normal trafficking)§ Decreased CFTR chloride conductance§ Reduced synthesis and trafficking of normal CFTR§ Reduced apical stability§ Defective regulation of other ion channels
Diagnosis of CF1. What are the 3 criteria for CF diagnosis?2. Name 3 tests that can be used to diagnose CF3. Which test has an 80% false positive rate?4. What are 3 drawbacks of interpreting sweat chlorides?5. What is CFTR genotype a good predictor of?6. What is CFTR genotype not a good predictor of?7. What is the main cause of morbidity and mortality in CF patients?
1. Diagnosis by clinical triad§ ↑sweat chloride§ Pancreatic insufficiency§ Chronic pulmonary disease2. Diagnostic tests§ Immunoreactive trypsin§ Interpretation of sweat chlorides§ Genotyping3. Immunoreactive trypsin4. Sweat chlorides§ Some mutations associated with normal chloride§ False-positives associated with hypothyroidism, Addison's disease, ectodermal dysplasia, glycogen storage disease, evaporation§ False-negatives associated with edema and malnutrition5. Pancreatic function: PS or PI6. Meconium ileus, liver disease, diabetes7. Pulmonary complications
Treatment of cystic fibrosisDescribe the treatments for the following abnormalities associated with CF1. High sweat chloride2. Thick airway mucous3. Chronic lung infections4. Inflammation5. Respiratory failure6. Pancreatic insufficiency7. Meconium ileus8. Islet cell loss9. Male infertility, CBAVD10. Biliary tract insufficiency
1. Dietary salt2. Chest physiotherapy/DNase3. Antibiotics4. Anti-inflammatories5. Lung transplant6. Pancreatic enzymes7. PEG, stool softeners8. Insulin9. In vitro10. Bile acid salts
Treatment and prevention of bronchiolitis1. What is the mainstay of treatment for bronchiolitis?2. What are 2 other treatments that may have some benefits in treating bronchiolitis?3. What are the main forms of prevention?4. What are the indications for use of Palivizumab?
1. Oxygen, supportive care to prevent dehydration and hypoxemia, rest2. α adrenergic R agonists→↓mucosal edema, Ribavirin (teratogen for hospital workers) for RSV infection3. Prevention§ Hand washing§ IV immunoglobulin w/ high anti-RSV titer§ Humanized monoclonal antibody – Palivizumab4. Prematurity, bronchopulmonary dysphasia, pulmonary, cardiac or immune deficiency <2yo
Bronchiolitis1. What age does bronchiolitis usually occur and why?2. Name 6 viruses that can cause bronchiolitis – which is the most common cause in the US?3. What children have higher morbidity and mortality from bronchiolitis?4. Describe the pathophysiology of bronchiolitis5. Is VT and VM ↑ or ↓?6. What is thought to cause this pathology?7. What are the typical clinical manifestations of bronchiolitis?8. What are the common physical findings?
1. <2yo as a result of viral infections during winter months2. Viruses§ RSV – most common cause§ Influenza A§ Parainfluenza§ Metapneumovirus§ Mycoplasma pneumoniae§ Adenovirus3. Children with pre-existing cardiopulmonary disease4. Combination of airway edema, musous plugging and bronchospasm→↑airway resistance, air trapping, ↓compliance, ↑work of breathing→hypoxemia, paradoxical breathing5. ↓6. Release of nerve growth factor from epithelial cells which stimulate a number of inflammatory cells7. Clinical sx§ Rhinorrhea, cough, low grade fever, apnea8. Physical findings§ Tachypnea, tachycardia, nasal flaring, retractions, rales (late inspiratory), hyperresonance to percussion