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Pulmonary
Pathophysiology 5 - Disorders of the Pulmonary System
| Question | Answer |
|---|---|
| the respiratory system can be divided into what 2 structures | conducting airways and respiratory tissues |
| what are the levels of branching | trachea, bronchi, bronchioles, alveoli |
| where is the site of gas exchange | alveoli |
| what cells are in the alveolar epithelium | type I and type II alveolar cells and macrophages |
| describe what happens during inspiration | during inspiration air is drawn into the lungs as the respiratory muscles expands the chest cavity |
| describe what happens during expiration | during expiration, air moves out of the lungs as the chest muscles relax and the cavity becomes smaller |
| what occurs with the diaphragm during inspiration | the diaphragm is the main muscle of inspriation. when the diaphragm contracts the chest expands and inspirations occurs |
| what occurs with the diaphragm during expiration | upon expiration, the chest cavity decreases and pressure inside increases |
| what is lung compliance | the ease with which lungs can be inflated |
| what factors effect lung compliance | - elastin v. collagen present - elastic recoil - surface tension |
| what is ventilation | the movement of gases into and out of the lungs |
| what is perfusion | the process that allows blood flow to help facilitate gas exchange |
| what is diffusion | the movement of gases across the alveolar-capillary membrane |
| what is oxyhemoglobin | the term to describe when hemoglobin is bound with oxygen |
| what is affinity | the strength of the chemical bond between the oxygen and hemoglobin in the lungs. ----- release of oxygen in the tissues is dependent on this affinity |
| how is carbon dioxide transported | - dissolved in blood - attached to hemoglobin - bicarbonate |
| how is breathing controlled | - autonomic regulation (chemoreceptors and lug receptors) |
| function of chemoreceptors | monitor blood levels for - oxygen - carbon dioxide - pH - adjust ventilation accordingly |
| function of lung receptors | monitor breathing patterns and lung function |
| what are the characteristics of COPD | inflammation and fibrosis of bronchial wall, hypertrophy of the submucosal glands and hypersecretion of mucus, and loss of elastic lung fibers and alveolar tissue |
| in COPD what causes a mismatch in ventilation and profusion | airflow obstruction |
| in COPD, ________________________ leads to a decreased surface area for gas exchange | alveolar tissue descruction |
| what is the leading risk factor for COPD | smoking |
| what are the characteristics of asthma | chronic respiratory disease characterized by airway obstruction, bronchial hyperresponsiveness, airway inflammation and (in some cases) airway remodeling |
| what is atopy | the genetic tendency for developing IgE-mediated hypersensitivity reactions in response to environmental allergens. |
| what is the one of the strongest predisposing factors for developing asthma | atopy |
| what is pneumothorax | the presence of air in the pleural space that causes partial or complete collapse of the affected lung |
| what is atelectasis | an incomplete expansion of a lung, or portion of lung, caused by airway obstruction or lung compression |
| what type of substance causes a pulmonary embolism | the embolism may be a thrombus, air accidently injected into an intravenous infusion, fat from the bone marrow after a fracture or trauma, or amniotic fluid that enters the maternal circulation after rupture of membranes |
| what is average tidal volume (number) | 500 mL |
| what is average vital capacity (number) | 4800mL |
| what is average inspiratory reserve number (number) | 3100 mL |
| what is average expiratory reserve volume (number) | 1200 mL |
| what three measurements make up vital capacity of the lung | inspiratory reserve volume + tidal volume + expiratory reserve volume |
| what is the average inspiratory capacity | 3600 mL |
| what two measurements make up inspiratory capacity | inspiratory reserve capacity + tidal volume |
| what is the average functional residual capacity (number) | 2400 mL |
| what two measurements make up the functional residual capacity | expiratory reserve volume + residual volume |
| what is the average residual volume (number) | 1200 mL |
| what is the average total lung capacity (number) | 6000 mL |
| what lung volumes make up total lung capacity | inspiratory reserve volume + tidal volume + expiratory reserve volume + residual volume |
| name the 4 lung volumes | - inspiratory reserve volume - tidal volume - expiratory reserve volume - residual volume |
| name the 4 lung capacities | - vital capacity - inspiratory capacity - functional residual capacity - total lung capacity |
| ***know Figure 5.6 in Module 5.3*** | see module |
| what is a shunt | perfusion without ventilation ---- there is a blockage in the airway |
| what is dead air space | ventilation without perfusion ---- there is a blockage in the pulmonary artery/capillary surrounding the alveoli |
| know differences between chronic bronchitis and emphysema (chronic bronchitis) | - airway obstruction (in both major and minor airways) ----- caused by excess mucous production |
| know differences between chronic bronchitis and emphysema (emphysema) | - decreased lung elasticity - enlargement of air spaces - destruction of alveolar walls and capillary beds |
| what is pink puffer (form of COPD) | - form of COPD that is predominantly emphysema ---- lack of cyanosis ---- puffer breathing ---- barrel chest ---- wheezing |
| what is blue bloater (form of COPD) | - form of COPD that is predominantly chronic bronchitis ---- characterized by cyanosis and fluid retention ---- expiration becomes more difficult ---- severe hypoxia (arterial PO2 <55, stimulates RBC production) |
| pathology of COPD | - comprised of two disorders (chronic bronchitis and emphysema), mechanisms include: ---- inflammation and fibrosis of the bronchial wall ---- hypertrophy of mucosal glands ---- hypersecretion of mucous ---- loss of elasticity ---- decreased S.A. |
| clinical presentation of COPD | - in 50's and 60's - decreased exercise tolerance - fatigue - cough (that is worse in the morning) - increased sputum production - SOB |
| describe the clinical presentation of late stages of COPD | - recurrent respiratory infections - chronic respiratory failure |
| how is COPD diagnosed | - H+ P - spirometry - PFT - CXR - lab tests |
| how is COPD dx with PFT | - FVC is prolonged and decreased - FEV1 is decreased - noticable decrease in FEV1/FVC ratio ----- differentiates obstructive from restrictive diseases - RV and TLC increased |
| how is Spirometry used in COPD diagnosis | - stage and disease severity |
| as COPD progresses, name other important measurements | - exercise tolerance - nutritional status - hemoglobin saturation - ABG |
| the only treatment that slows the progression of COPD | smoking censsation |
| ways to avoid respiratory tract infections in COPD patients | - flu and pneumococcal vaccinations |
| ways to treat COPD | - smoking ceasation - vaccinations and avoidance of respiratory infections - pulmonary rehab programs - pharmacologic treatments |
| list the pharmacological treatments | - short-acting bronchodilators - long-acting bronchodilators - inhaled corticosteroids -oxygen therapy |
| function of short and long-acting bronchodilators in COPD treatment | relax the airway smooth muscle |
| function of corticosteroids inhalers in COPD | - usually later in disease - not as useful in COPD as in asthma |
| function of oxygen therapy in COPD | - PO2 levels drop to less than 55 mmHg - helps reduce dyspnea and pulmonary hypertension - goal is to keep saturation at or above 90% |
| what are risk factors of asthma (name at lease 5) | - SES/demographics - family history - allergies - antenatal exposure to tobacco and pollution - GERD - exercise - cold air - race (AA, Puerto Rico) - allergy to ASA and NSAIDS |
| disease pathology of asthma | - airway obstruction - airway inflammation - bronchial hyperresponsiveness |
| how does asthma present in patients | - response to a trigger (resp, infection, emotional stress, weather changes) - wheezing (expiration) - breathlessness (with accessory muscle usage) - chest tightness - cough (worse at night and early morning) - distant breath sounds - SOB -anxiety |
| describe what happens during an asthma attack | - airway narrows (bronchospasms) - edema of bronchial mucosa - mucus plugging - prolonged expiration - air trapped in alveoli (reduced ventilation) - mismatch of ventilation and perfusion - leads to hypoxemia and hypercapnia |
| define hypoxemia | low o2 |
| define hypercapnia | high co2 |
| ways asthma is diagnosed | - PFT - H+P - spirometry |
| how can PFT diagnose asthma | - reduced FEV1 -FEV1-FVC ratio of <70% ***(hallmark) increase of FEV1 => 12% of a bronchodilator administration |
| how is peak expiratory flow used to dx asthma | - measures flow rates that the patient can use at home - pt records best forced exhalation - can be used to compare and contrast the readings |
| prevention measures for pt's with asthma | - reducing exposure to triggers (irritants and allergens) - annual flu vaccination |
| describe the pharmacological treatments of asthma | -step wise approach ---- short-acting bronchodilator (SABA..every patient) ---- low-dose inhaled corticosteroid (ICS) ---- long-acting beta agonist (LABA) ---- leukotriene modifiers |
| use of SABA drugs for asthma (albuterol) | - every asthma patient (quick relief...w/i 30 minutes) - relaxes bronchial smooth muscle |
| for a patient with mild persistent asthma symptoms, what type of pharmacological regiment works best | - (low-dose) inhaled corticosteroid (fluticasone) + SABA (albuterol) |
| what is the function of an inhaled corticosteroid for asthma | - control and prevent persistent asthma symptoms - improved lung function and quality of life *** anti-inflammatory and inhibits multiple inflammatory cytokines*** |
| for a patient with more severe asthma symptoms, what type of pharmacological regiment works best | - (increased dose) inhaled corticosteroid + SABA + Long-acting beta-agonist (LABA...Advair) - OR including leukotriene modifiers (singluair) - OR short0term burst of oral steroids to achieve control |
| function of leukotriene modifiers (singulair) in asthma treatment | - decreased congestion associated with allergic rhinitis |
| list some risk factors of spontaneous pneumothorax | - tall boys/men between 10-30 - emphysema/lung diseases |
| list some risk factors of trauma pneumothorax | - penetrating chest wound - rib fx - medical procedure (transthoracic needle aspirations, CL insertion, intubation, positive-pressure ventilation) - chest compressions (CPR) |
| list some risk factors of tension pneumothorax | - penetrating chest wound |
| describe pneumothorax pathology | - presence of air in the pleural space that causes a partial or complete collapse of the affected lung |
| three types of pneumothorax | - spontaneous - traumatic - tension |
| pathology of spontaneous pneumothorax | rupture of an alveolus or an air-filled bleb (blister) on surface of lung |
| pathology of traumatic pneumothorax | penetrating chest wound (air can enter and exit the space) |
| pathology of tension pneumothorax | penetrating chest wound (air can enter but cannot exit), mediastinal structures move to the unaffected side causing compression of these structures (can be fatal) |
| clinical presentation of pneumothorax | - dependent on severity of disease process --- chest pain (on affected side) --- increased RR --- difficulty breathing --- decreased breath sounds on affected side |
| clinical presentation of tension pneumothorax | - deviation of trachea and mediastinum outside of midline - increased HR - decreased CO - increased intrathoracic pressure - jugular neck vein distention - subQ emphysema - clinical signs of shock - hypoxemia |
| diagnosis of pneumothorax | - CXR - CT chest |
| why are pulse ox and ABG important in pneumothorax | determines blood oxygenation |
| pneumothorax treatment depends on | severity |
| treatment of small spontaneous pneumothorax | - observation - supplemental oxygen - serial cxr |
| treatment of larger spontaneous pneumothorax | removal of air from chest cavity (anyone of the following will do) ---- needle aspiration ---- closed drainage system (w/ or w/o suction) |
| what is the pathology of atelectasis | an incomplete expansion of a lung, caused by airway obstruction of lung compression --- can be as small as portions of alveoli or as large as an entire lobe |
| atelectasis in infants | impaired lung expansion (ex: respiratory distress syndrome) |
| causes of atelectasis in adults | - mucous plug in airway - compression by fluid (CHF, or PE) - tumor mass (cancer) - exudate |
| risk factors for obstructive atelectasis | - status post surgery - s/p anesthesia - pain and pain meds - immobility (promotes retention of bronchial secretions) |
| prevention of atelectasis | - cough frequently - deep breathing - changing positions - adequate hydration - regular ambulation |
| clinical presentation of atelectasis | - rapid respiratory rate (tachypnea) - tachycardia - dyspnea - cyanosis - signs of hypoxemia - decreased chest expansion - decreased breath sounds - intercostal retractions |
| describe mediastinum during atelectasis | - large collapsed area: mediastinal structures shift TOWARD affected area - in compression atelectasis: mediastinal structures shifts AWAY from affected area |
| diagnosis of atelectasis | - CXR - CT scan - S/S |
| treatment of atelectasis | - depends on causes and extent of lung involvement ---reduce obstruction/compression --- reinflate collapsed area --- o2 administration --- ambulation --- deep breathing --- using body positions that favor increased lung expansion |
| pulmonary embolism pathology | when a substance lodges in a branch of the pulmonary arteryand obstructs blood flow |
| what can cause a pulmonary embolism | - thrombus - air - fat from bone marrow - amniotic fluid |
| a majority of PE's are caused by | thrombi from DVT's in BUE or BLE |
| what is the virchow triad | the three factors that predispose people to venous thrombosis --- venous stasis --- venous endothelial injury --- hypercoagulability states |
| list the inherited hypercoagulability disorders that increase risk of thrombosis | - antithrobin III deficiency - protein C - protein S - factor V Leiden mutation |
| venous stasis and venouse endothelial injury can result from | - prolonged bed rest/immobility - trauma - injury - surgery - childbirth - fractures (hip and femur specifically) - MI - Cancer - CHF - spinal cord injury |
| clinical presentation of PE depends on | size and location of obstruction |
| most common symptoms of PE include | - chest (pleuritic) pain (worsening on inspiration) - dyspnea - cough (sometimes) - increased RR - impaired gas exchange - moderate hypoxemia |
| clinical presentation of small PE in peripheral branches | asymptomatic unless pt is elderly or acutely ill |
| diagnosis of a PE is made by | - H+P - ABGs - venous thrombosis studies - troponin levels - D-dimer - lung scans - ECG - helical chest CT scan |
| why are lab and radiologic studies performed on people with PE | to rule out other causes of chest pain/dyspnea |
| why are venous thrombosis studies important in PE patients | to locate the cause of the PE (i.e. find the DVT) |
| what is the purpose of the D-dimer study in PE pts | measures plasma D-dimer - a degradation product of coagulation factors activated due to a thromboembolic event |
| what is the purpose of measuring troponin levels in PE patients | - may be increased (d/t stretching of the right ventricle by a large pulmonary infarction) |
| purpose of a ventilation-perfusion scan in PE pts | - examines lug segments for blood flow and distribution of radiolabeled gas that had been injected and inhaled |
| purpose of a helical (spiral) CT scan for PE pts | detects emboli in the proximal pulmonary arteries |
| how are PE's treated | - anticoagulant therapy (Lovenox) - thrombolytic therapy (if indicated for medium to large emboli) |
| the use of anticoagulants after surgery | help prevent DVT or PE, especially after major surgeries |
| prevention of DVT and PE after major surgery | - anticoagulant therapy - increasing mobility - use of compression stockings/intermittent pneumatic compression boods |
| list the major conditions that can lead to Acute Respiratory Distress Syndrome (ARDS) | - aspiration - drugs, toxins, therapeutic agents - infection - trauma - shock - disseminated intravascular coagulation (DIC) - multiple blood transfusions |
| ways aspiration lead to acute respiratory distress | - near drowning - aspirating gastric contents |
| ways drugs/toxins/therapeutic agents can cause acute respiratory distress | free-base cocaine smoking, heroine, inhaled gases (smoke/ammonia), breathing high concentrations of oxygen, radiation |
| ways infection can cause ARDS | septicemia |
| ways shock and trauma can cause ARDS | - burns - fat embolisms - chest trauma |
| acute respiratory distress syndrome pathology | - diffuse epithelial cell injury with increased permeability - blood products enter alveolar space - activated neutrophils release products that: --- damage alveolar cells --- inactivate surfactant --- form a hyaline membrane - lung stiffens |
| clinical presentation of ARDS | rapid onset or respiratory distress (12-18 hours after trigger event) - increased RR - s/s or respiratory failure -hypoxemia - multiple organ failure |
| diagnosis of ARDS | - CXR ----bilateral infiltrates of lungs from fluid ("white-out") ---- normal cardiac function |
| treatment of ARDS | - focus on supportive care of oxygen ventilator support until lunge heal and underlying cause is addressed |
| ARDS recovery | maybe complicated by lung scaring and fibrosis |
| name the 4 major causes of Respiratory Acidosis | - depression of respiratory center - lung disease - airway obstruction, disorders of chest wall + respiratory muscles - breathing air with high CO2 content |
| how can depression of respiratory center cause respiratory acidosis | - drug overdose - head injury |
| list some lung diseases that can cause Respiratory Acidosis | - bronchial asthma - COPD - pneumonia - pulmonary edema - respiratory distress syndrome |
| list some airway obstruction, disorders of the chest wall, and respiratory muscles that cause respiratory acidosis | - paralysis of respiratory muscles - chest injuries - kyphoscoliosis - extreme obesity - treatment with paralytic drugs |
| ways that respiratory acidosis manifests (in relation to blood pH, CO2, and HCO3-) | - pH decreases - PCO2 (primary) increases - HCO3- (compensatory) increases |
| ways respiratory acidosis manifests (neural function) | - dilation of cerebral vessels and depression of neural function - headache - weakness - behavior changes ( confusion, depression, paranoia, hallucinations) - tremors - paralysis - stupor - coma |
| ways respiratory acidosis manifests (skin) | - warm -flushed |
| ways respiratory acidosis manifests (signs of compensation) | - acidic urine |
| pathophysiology of respiratory acidosis | - caused by any condition that impairs alveolar ventilation - increased plasma PCO2 (hypercapnia) - decreased pH |
| define hypercapnia | increased plasma PCO2 |
| most common cause of respiratory acidosis | decreased ventilation |
| why is it important NOT to supplement with too much oxygen | the pts medullary respiratory center has adapted to elevated CO2 levels and no longer responds to increased PCO2 levels --- PO2 is new stimulus for respiration |
| in HEALTHY individuals, increased CO2 production is countered by | increased CO2 elimination in the lungs |
| clinical presentation of Respiratory acidosis | - typically depend on cause --- s/s similar to hypoxemia --- vasodilation --- headache --- blurred vision --- irritability --- muscle twitching --- other psychological manifestations |
| respiratory acidosis diagnosis | - blood pH below 7.35 AND PCO2 above 45 mmHg |
| respiratory acidosis treatment | - improving ventilation - (in some cases) mechanical ventilation is needed |
Created by:
kandriot
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