Class 3 respiratory: Obstructive airway disorders Flashcards
COPD pathophysiology
-Decrease in the exhaled air flow caused by a narrowing or obstruction of the airways
-e.g., emphysema, chronic bronchitis, bronchiectasis (Abnormal widening of the bronchi or their branches, causing a risk of infection)
Levels of COPD
-Many patients have overlapping features of damage at both the acinar level (emphysema) and bronchial level (bronchitis)
COPD is caused by
-COPD is the result of long-term heavy cigarette smoking; about 10% of pts are non-smokers
COPD elastic recoil is
Low
What happens in COPD?
-Bronchial wall becomes inflamed and fibrosed, with breakdown of alveolar tissue and loss of elasticity, mucus secretion, airway obstruction, air trapping
Emphysema definition & pathophysiology
-Loss of lung elasticity
-Enlargement on alveoli due to air trapping; hyperinflation of lungs and increased Total Lung Capacity
-“over-inflation” enlargement of airspaces unaccompanied by destruction
Manifestations of emphysema
-Barrel chest, accessory muscles, pursed lip breathing, tripod
-Weight loss and anorexia
-Prolonged expiratory phase, wheezes, decreased breath sounds
Emphysema features
-Patient is often thin and elderly
-Little sputum produced
-Edema and overt HF are rare complications
About emphysema
-“Pink puffers”
-Caused by destruction of pulmonary connective tissue
-Characterized by permanent enlargement of air sacs and rupture of interalveolar walls
-Expiration is difficult causing hyperinflation
Emphysema inspection
-Increased AP diameter
-Barrel chest
-Accessory muscles, tripod position
-SOBOE
-Respiratory distress, tachypnea
-Decreased breath sounds, prolonged expiration, muffled heart sound d/t overdistension of the lungs
Chronic bronchitis
-Blue bloaters
-Inflammed airway
-Characterized by hypersecretion of mucus and chronic productive cough for at least 3 months
Pathophysiology of chronic bronchitis
-Inspired irritants result in airway inflammation with infiltration of neutrophils, macrophages and lymphocytes
-Continued bronchial inflammation leads to bronchial edema and increases the size and number of mucous glands leading to the production of thick tenacious mucus
Chronic bronchitis is often..
Combined with emphysema
Manifestations of chronic bronchitis
-Productive cough; classic sign
-Dyspnea, wheezing, prolonged expiration, cyanosis, hypoventilation, polycythemia, & cor pulmonale
-Barrel chest
Manifestation differences between bronchitis & emphysema (cough, dyspnea, wheezing, barrel chest, cyanosis, hypoventilation polycthemia & cor pulmonale)
-Productive cough is a classic sign in bronchitis & late in infection with emphysema
-Dyspnea is late in course with bronchitis and common in emphysema
-Wheezing is intermittent in bronchitis and common with emphysema
-Barrel chest is occasional in bronchitis and a classic sign in emphysema
-Cyanosis is common in bronchitis & uncommon in emphysema
-Hypoventilation, polycythemia, & cor pulmonale are common in bronchitis & late in course with emphysema
Primary bronchitis manifestations
Dyspnea, hypoxia, cyanosis & peripheral edema
About bronchitis
-Excessive mucus secretion
-Inflammation of bronchi with partial obstruction of bronchi by secretions or constrictions
-Sections of lung distal to obstruction may be deflated
-Acute or chronic
Bronchitis inspection
-Hacking, rasping cough productive of thick mucoid sputum
-Chronic: dyspnea, fatigue, cyanosis, possible clubbing of fingers
Bronchitis auscultation
-Normal vesicular & voice sounds
-Chronic: prolonged expiration
Bronchitis adventitious sounds
Crackles over deflated areas. Wheeze may be present
Pneumonia definition
-Infection of the lower respiratory tract caused by bacteria, viruses, fungi, protozoa, or parasites
-Defined in 2 ways:
-Location in the lungs
-Lobar Pneumonia (occurs in one lobe of the lung).
-Bronchopneumonia (tends to be patchy).
-Origin of Infection
-Community-acquired (pneumonia contracted outside the hospital)
-Hospital-acquired pneumonia – nosocomial; particularly gram-negative bacteria and staphylococci
Pathophysiology of pneumonia
-Macrophages release tumor necrosis factor-alpha and interleukin-1 from macrophages (inflammation)
-Inflammatory mediators and immune complex damage bronchial mucous membranes and alveolar-capillary membranes causing alveoli to fill with infectious debris and exudate causing lung damage and consolidation
-Accumulation in the acinus leads to dyspnea and V/Q mismatching and hypoxemia
How pneumonia is aquired
-Acquired through: aspiration, inhalation and hematogenous
Manifestation of pneumonia
-Sudden onset of fever, chills, productive cough of purulent sputum and pleuritic chest pain
-Confusion or stupor (related to hypoxia) may be predominant
Inspection: Pneumonia
increased work of breathing, cough, changes in perfusion and oxygenation
Auscultation: Pneumonia
may have decreased breath sounds or bronchial breath sounds or crackles
Lab values for pneumonia
Complete Blood Count (CBC), C-Reactive Protein (CRP), Electrolytes, Arterial Blood Gas (ABG)
Pneumonia complications
-Pleurisy (inflammation of the pleura)
-Pleural Effusion
-Atelectasis
-Empyema
-Pericarditis
-Endocarditis
Lobar pneumonia
-Infection in lung parenchyma leaves alveolar membrane edematous and porous, and so red blood cells (RBCs) and white blood cells (WBCs) pass from blood to alveoli; causes hypoxemia
Inspection of lobar pneumonia
Increased respiratory rate. Guarding and lag on expansion on the affected side. Children: sternal retraction, nasal flaring.
Palpation: Lobar pneumonia
Chest expansion decreased on the affected side
Auscultation: Lobar pneumonia
-Breath sounds louder with patent bronchus, as if coming directly from the larynx. Voice sounds have increased clarity, bronchophony, egophony, whispered pectoriloquy present
-Children: diminished breath sounds may occur early in pneumonia
Adventitious sounds: Lobar pneumonia
Crackles, fine to medium
Pneumonias may..
Turn into ARDS and lead to sepsis
TB
-Infection caused by mycobacterium tuberculosis, an acid-fast bacillus that affects the lungs
-Can have a latent period
TB pathophysiology
-Airborne droplets
-In immunocompromised people, it is contained by the immune system and results in latent TB infection (LTBI)
-After latent period in the upper lobe, bacilli are inspired into the lungs; activating alveolar macrophages and neutrophils
-May lay dormant but can also be reactivated
Manifestations of TB
-LTBI is asymptomatic
-Cough with purulent sputum, hemoptysis, weight loss, night sweats, fever, fatigue, anorexia, chest pain
Lab values for TB
-CBC, acid-fast bacilli (AFB)
About TB
-Initial complex is acute inflammatory response; macrophages engulf bacilli but do not kill them. Tubercle forms around the bacilli
-Scar tissue forms, and lesion calcifies
-Previously healed lesions are reactivated. Dormant bacilli now multiply, producing necrosis, cavitation, and caseous lung tissue (cheese like appearance)
-Apex of lungs has the most damage
TB subjective data
-Initially no symptoms, manifested as positive result of skin test or on radiograph
-Progressive tuberculosis involves weight loss, anorexia, easy fatigability, low-grade afternoon fevers, night sweats.
-Patients may have pleural effusion, recurrent lower respiratory infections
TB inspection
Cough initially nonproductive, later productive of purulent, yellow-green sputum, may be blood-tinged. Dyspnea, orthopnea, fatigue, weakness.
TB palpation
Skin moist from night sweats
TB auscultation
Normal or decreased vesicular breath sounds.
TB adventitious sounds
Crackles over upper lobes are common, persist after full expiration and cough
Pulmonary embolism
-Outside the lung problem
-Occlusion of the pulmonary vascular bed by an embolus
PE pathophysiology
-Embolism with or without infarction, massive occlusion, or multiple pulmonary embolism
-Obstruction of the pulmonary vasculature leads to pulmonary HTN
PE causes
Capillaries to leak into the alveoli (pink frothy sputum)
PE pathophysiology
-Release of neurohumoral substances and inflammatory mediators; increased vasoconstriction
-Leads to pulmonary HTN (increased pulmonary after load), can lead to RV dilation
-Absent blood flow causes V-Q mismatch (dead space) and decrease surfactant production resulting in atelectasis contributing to hypoxemia
Manifestations of a PE
-Sudden onset of pleuritic chest pain, dyspnea, tachypnea, tachycardia and anxiety
-Occasional syncope or hemoptysis
-Pleural friction rub, pleural effusion, fever and leukocytosis
PE auscultation
Crackles
PE lab values
CBC, d-dimer, troponin, BNP level, ABG
PE subjective data
Chest pain, worse on deep inspiration, dyspnea
Inspection of PEs
Apprehensiveness, restlessness, anxiety, mental status changes, cyanosis, tachypnea, cough, hemoptysis, PaO2 < 80 on pulse oximetry. Arterial blood gases show respiratory alkalosis
Palpation PEs
Diaphoresis, hypotension
Auscultation: PEs
Tachycardia, accentuated pulmonic component of S2 heart sound
PE adventitious sounds
Crackles, wheezes
Pulmonary arterial HTN
-High PA pressures and typically associated with COPD
Pathophysiology of arterial HTN
-Vascular growth factors cause fibrosis and thickening of vessel walls with luminal narrowing
-Increased PVR (after load) the RV has to pump against; reducing gas exchange and lung volumes
-Increases workload of the RV leading to RV hypertrophy, followed by failure (Cor Pulmonale)
Characterization of pulmonary arterial HTN
-Characterized by endothelial dysfunction with overproduction of vasoconstrictors (such as thromboxane and endothelin), decreased production of vasodilators (prostacyclin and nitric oxide)
Clinical manifestations of pulmonary arterial HTN
-Abnormal CXR
-Fatigue, chest discomfort, tachypnea, and dyspnea
-Peripheral edema, JVD, precordial heave, louder S2
Cor pulmonale
-RV enlargement (hypertrophy, dilation, or both) leading to right sided HF
-Caused by PAH
Pathophysiology of cor pulmonale
-Develops due to chronic pressure overload in the RV
-Increased work of the RV leading to failure
Manifestations of cor pulmonale
-Heart may appear normal at rest but with exercise CO falls
-Louder S2 (closure of the pulmonic valve)
-Murmur of the tricuspid valve
-JVD, hepatosplenomegaly, and peripheral edema
Respiratory dysfunction in the pediatric patient
Upper & lower respiratory tract disease
Approach to acute respirology
-Upper respiratory tract: Croup, epiglottitis
-Lower respiratory tract: Bronchiolitis/respiratory syncytial virus (RSV), pneumonia, asthma
-Upper/lower respiratory tract: Foreign body
Upper respiratory tract diseases
-Diseases above the thoracic inlet
-Characterized by inspiratory stridor, hoarseness, and suprasternal retractions
Differential diagnosis of stridor for upper respiratory tract diseases
-Croup
-Epiglottitis
-Foreign body aspiration
Croup
-Paroxysmal attacks (spasms of the larynx)
-Etiology: Influenza A&B, RSV, allergic component
Croup manifestations
-Hoarse voice, barking cough, stridor, SOB, anxiety
-Onset at night
Croup diagnostic methods
Clinical diagnosis
Chest x-ray (Steeple sign from subglottic narrowing)
Epigolittitis
-Acute, severe, and rapid progressive swelling
-Rare, usually occurs in 2-8 year olds
-Etiology: Bacterial (H. influenza type b)
Epiglottitis manifestations
-Abrupt onset-rapid progression
-Excessive drooling, stridor, SOB, anxiety, difficulty swallowing, tripod position
-Cherry red, swollen epiglottis
-Medical emergency
Diagnostic methods of epiglottitis
Clinical diagnosis
Avoid examining the throat to prevent further respiratory exacerbation
Epiglottitis big signs
Tripod & drooling combined mean airway is occluding
Lower respiratory tract diseases
-Obstruction of airways below thoracic inlet, produces more expiratory sounds
-Classic symptom is wheezing
Common differential diagnosis of wheezing
-Bronchiolitis: First episode of wheezing
-Pneumonia: Fever, cough, fatigue
-Asthma: Recurrent wheezing episodes, identifiable triggers
Bronchiolitis/respiratory syncytial virus (RSV)
-Acute viral infection of lower respiratory tract (small bronchioles), with resultant trapping of air
-Epidemiology: Infants, peak at 6 months
Bronchiolitis/respiratory syncytial virus (RSV) etiology
Respiratory syncytial virus
Bronchiolitis/respiratory syncytial virus (RSV) manifestations
-Coughing, wheezing, acute respiratory distress followed by rapid recovery, tachypnea, tachycardia, retractions, poor air entry
Investigation of bronchiolitis/respiratory syncytial virus (RSV)
Chest x-ray
Nasopharyngeal swab
CBC
Pneumonia
-Inflammation of pulmonary tissue associated with consolidation of alveolar spaces
-Common in infancy and early childhood
-Etiology: Viral agents: RSV and influenza virus
Manifestations of pneumonia
-Increased work of breathing (intercostal, suprasternal, subcostal, nasal flaring and use of accessory muscles)
-Cyanosis, tachypnea, respiratory fatigue, crackles, wheezing, decreased air entry on affected side
Diagnostic methods of pneumonia
Clinical diagnosis
Chest x-ray
Asthma
-Lower airway disorder characterized by heightened airway reactivity with bronchospasm & obstruction
-Unknown etiolgy, 75% have family hx
Asthma manifestations
-Anxiety, accessory muscle use, cough, crackles, cyanosis, SOB, tachypnea, tachycardia, & wheezing
Asthma classifications
-Mild: Occasional attacks <2/week
-Moderate: more frequent with persistent coughing, decreased activity tolerance
-Severe: Daily & nocturnal symptoms, frequent ER visits
Diagnostic methods of asthma
Clinical diagnosis
Pulmonary functional studies
Asthma progression
Wheeze can develop into crackles if asthma progresses to pulmonary edema
About asthma
Complex response characterized by bronchospasm, and inflammation, edema in walls of bronchioles, and secretion of highly viscous mucus into airways
Asthma inspection
-During severe attack: Increase RR, SOB w audible wheezing, accessory neck muscles, apprehension, cyanosis, intercostal indrawing. Labored & prolonged expiration.
-When asthma is chronic, barrel chest may develop
Auscultation of asthma
Diminished air movement. Breath sounds decreased, with prolonged expiration. Voice sounds decreased
Adventitious sounds + asthma
Bilateral wheezing on expiration; sometimes inspiratory and expiratory wheezing
Foreign body aspiration
-Child usually presents after sudden episode of coughing or choking while eating with subsequent wheezing coughing or stridor
-Usually in <5 years old
Foreign body aspiration manifestations
-Symptoms depend on: extent, size and composition of object, elapsed time since, location, degreee and duration of airway blockage
-Suddent respiratory distress
-Abnormal respiratory sounds
-Coughing, gagging, agitation
-Cyanosis
Diagnostic methods of foreign body aspiration
Clinical diagnosis
X-ray
Bronchoscopy
Larygoscopy (then remove with forceps)
Respiratory infections account for…
majority of acute illness in children
