Pulmonary Disease Flashcards
Classifications:
Obstructive or Restrictive
Pulmonary Disease: Restrictive
↓volumes during PFT, primarily during inspiration, difficult to fully fill lungs with air.
Pulmonary Disease: Obstructive
↓flow rates during PFT, primarily during exhalation, difficult to exhale all the air from the lungs
The common cold
Etiology: viral in origin. Acute inflammation of the mucus membrane of the upper respiratory tract.
Croup
-Result of a viral infection
-laryngeal spasm
-loud, high pitched inspiratory sounds
-labored respirations
-dyspnea
-especially in young children
Epiglottitis
-bacterial infection
-epiglottis swells & blocks airflow into lungs
-stridor
-drooling
-medical emergency!!!
-“thumb sign”
-usually in older children
Acute bronchitis
-Etiology: Complication of a viral infection, bacteria, irritants.
-Pathology: inflammation of the lining of your bronchial tubes
-Manifestations: chest pain, dyspnea, cough, fever, mucus
-Treatment: self-resolves in 2-3 weeks, OTC cough suppressant, humidifier
Asthma
-A reversible inflammation of the bronchi and the bronchioles.
-Etiology: “triggers” allergens (inhaled, food), infections, stress, emotion, noxious fumes, cold air, physical exertion
Chronic bronchitis
Persistent cough with sputum production for at least 3 months in at least 2 consecutive years.
-Etiology: Chronic irritation (cigarette smoking, pollution, noxious fumes, chronic/recurrent infection)
-Pathology: Histologic changes: -goblet cells: hypertrophic, hyperplastic (increased mucus production)(inhibits action of the cilia) -Bronchial mucosal lining: metaplastic changes, PSCCE(Pseudostratified Ciliated Columnar Epithelium)becomes squamous, non-ciliated, dysplasia -cilia is damaged by irritation -weakened, fibrotic airways that collapse easily. *problem with the flow.
-Manifestations: same as acute bronchitis, but persistent! Excessive secretion of mucus, hypoxia, poor drainage of mucus=infection, cough!
-Treatment: antibiotics, bronchodilators, steroids, smoking cessation, clean air environment
Emphysema
COPD
Combination of emphysema + chronic bronchitis (occurs virtually exclusively in smokers!).
-Treatment: Supportive: smoking cessation, pulmonary rehab. Medical: steroids, bronchodilators, antibiotics, oxygen therapy. Surgical: LVRS(Lung volume reduction surgery), lung transplant
Emphysema dominant: COPD Pink Puffer
-Good color (pink)
-barrel chest (air trapping)
-works hard to maintain aceptable levels of O2 & CO2, SOB (tachypnea, accessory muscle use, tripod position)
-^WOM consumes ^ energy (emaciated appearance-thin)
-minimal sputum, heart failure occurs late.
Chronic Bronchitis dominant: COPD Blue Bloater
-Recurrent pulmonary infection
-severe hypoxia (cyanosis/blue)
-^^ sputum production
-minimal weight loss, not as SOB, doesn’t work as hard, less energy consumed
-Heart failure occurs early.
COR Pulmonale
Heart failure due to lung disease (a complication of COPD).
-Pathology: hyperinflated alveoli compress pulmonary capillaries, pulmonary hypertension develops, this ^ the work on the right heart (hypertrophies, starts to fail)
-Manifestations: Right heart hypertrophy, jugular venous distension (JVD), ankle edema, arrhythmias (usually atrial), recurrent pulmonary infections
Pneumoconiosis
environmentally induced interstitial lung disease resulting from inhaling particulate matter
-Etiology: occupational exposure, coal miner’s pneumoconiosis, silicosis, asbestos.
-Pathophysiology: Macrophages ability to scavenge particles is overwhelmed (load of dust is severe, chronic inhalation of dust), causes chronic inflammatory process, results in fibrosis (scar tissue).
-Manifestations: CXR shows interstitial fibrosis, dyspnea on exertion that progresses to dyspnea at rest, hypoxia, PFT volumes indicate restriction, lung biopsy shows presence of dust particles.
ARDS: Acute Respiratory Distress Syndrome: “Shock Lung”
Acute lung injury
-Etiology: “insults”, insults cause diffuse alveolar damage
-Pathophysiology: “Insult” (acute injury) triggers vasoactive substances which damage the alveolar-capillary membrane. -Damage allows RBC’s and protein rich fluid to leak into interstitial spaces & alveoli. -Non-cardiogenic pulmonary edema. Damage also inhibits alveolar type II cells’ ability to produce surfactant. Leads to progressive atelectasis.
-Manifestations: Rapidly progressive dyspnea & SOB. -Progressive, severe hypoxia. -Gas exchange impaired. -CXR initially lags symptoms by about 24 hours. -Patient may have dry, non-productive cough.
-Treatment: support oxygenation & ventilation (aggresive mechanical ventilation)
Pneumonia
Acute inflammation of the lungs in which alveoli become filled with inflammatory fluid (lobar pna, bronchopneumonia, interstitial pna)
-Etiology: infection and aspiration.
4 Stages: Stage 1: Congestion (1st 24h) vascular engorgement, intra-alveolar fluid, small numbers of neutrophils, often numerous bacteria. Stage 2: Consolidation -Vascular congestion persists, extravasation of RBC’s into alveolar spaces, numbers of neutrophils & fibrin, gross appearance of alveolar solidification. Stage 3: Grey Hepatization- red cells disintegrate, persistence of neutrophils & fibrin, alveoli still appear consolidated, the color is paler & surface is drier. Stage 4: Resolution- exudate is digested by enzymatic activity, cleared by macrophage activity, cleared by cough!
-Manifestations: fever & chills, dyspnea and SOB, hypoxia, pleuritic chest pain, abnormal breath sounds, cough (productive during resolution phase), leukocytosis, CXR: consolidation.
-Treatment:drug therapy for infection, fluids (IV or oral), oxygen therapy, respiratory therapy (inhaled bronchodilators, inhaled mucolytics, bland aresol, lung expansion therapy)
Pulmonary edema
Leakage of fluid from pulmonary capillaries causing the fluid to accumulate in the interstitium and then to spill into the alveoli. (Rarely primarily a lung problem)
