Chapter 12 - Lung Flashcards
What are the different types of Atelectasis?
1) Resorption: airway obstruction, O2 is absorbed into circulation collapsing alveoli
2) Compression: accumulation of blood, air, fluid in pleural cavity
3) Contraction, scarring in lung parenchyma or pleura
Acute Respiratory Distress Syndrome (ARDS)
Noncardiogenic pulmonary edema, manifests as rapidly progressive dyspnea, tachypnea, and hypoxemia
Pathophysiology: occurs when a pulmonary or extrapulmonary insult causes the release of inflammatory mediators
Inflammatory cells damage the vascular endothelium and alveolar epithelium -> pulmonary edema, hyaline membrane formation, decreased lung compliance, decreased gas exchange
Most cases are associated with pneumonia or sepsis
Treatment is supportive (mechanical ventilation, prophylaxis for stress ulcers and venous thromboembolism, nutritional support, treatment of underlying injury)
What are key points of obstructive lung diseases
Reduced FEV1, normal or nearly normal forced vital capacity, FEV1:FVC is reduced, lung volume may be inc, outflow is obstructed
Forced exp. volume in 1 second (FEV1) is the volume of air that can forcibly be blown out the first 1 second, after full inspiration
Forced vital capacity (FVC) is the amount of air that can be forcibly exhaled from your lungs after taking the deepest breath possible
Asthma
Most common chronic disease in childhood (7 million children)
Inflammatory disorder of airways, episodic, reversible, bronchospasm
Symptoms: dyspnea, cough, wheezing, excessive mucus production
Eosinophils are important in both immune & non-immune types (amplify and sustain inflammatory response, can result in sustained symptoms)
Occlusion of bronchi & bronchioles by thick, tenacious, mucus plugs
Patchy necrosis & shedding of bronchial epithelial cells
Hypertrophy & hyperplasia of bronchial smooth muscle
Asthma "attack" during procedure Oral Candidiasis ( from steroid inhalers)
Immune Type (Type 1 Hypersensitivity)
Atopic - Allergic Onset 0-20 yrs Elevated blood IgE & eosinophils Th2 CD4+ T-cell driven Most common type
Nonimmune (Nonatopic) Type
Normal IgE levels
- Viral infections (Rhinovirus, influenza, RSV)
- Inhaled air pollutants (sulfur dioxide, ozone, nitrogen dioxide
- NSAID sensitivity
- Exercise-induced asthma
Mediators of Asthma: Early and Late Phase
Early: Leukotrienes C4, D4, & E4 (bronchoconstriction, inc vascular permeability, increased mucin, nasal polyps)
Prostaglandins D2, E2, F2 (Bronchoconstriction, Vasodilation)
Histamine (Bronchospasm, inc vascular permeability)
Platelet activating factor (release of more histamine from platelets, vasodilation)
Late: Inflammatory cells recruited by mast cell factors (eosinophils**, neutrophils, basophils)
Augment the TH2 CD4+ response
Chronic Obstructive Pulmonary Disease
Emphysema and chronic bronchitis
usually emphysema exists along w/ chronic bronchitis since both are related to cigarette smoking
Emphysema
Permanent (non-reversible) enlargement of airspaces distal to terminal bronchioles due to destruction of their walls
First symptom is dyspnea
Centriacinar (associated w/ cigarette smoking, involves respiratory bronchiole first)
Clinical Features: Dyspnea (shortness of breath)
Cough & wheezing (present if chronic bronchitis coexists, often the case)
Weight loss common
Barrel-chested, prolonged expiration
Gas exchange & blood gas values are normal until very late
Alpha-1-antitrypsin
Emphysema unrelated to smoking - inherited, caused by mutation in the SERPINA1 gene
Protein produced mostly in the liver
Main purpose is to destroy an enzyme called neutrophil elastase in the lungs
Distal Acinar Emphysema
emphysema unrelated to smoking
Alveolar ducts and sacs are particularly involved, related to scarring, just under pleura, may rupture into pleural space, Spontaneous pneumothorax of young adults
Chronic Bronchitis
Persistent productive cough for 3 consecutive months in at least 2 consecutive years
Causes: cigarette smoking and severe air pollution
Prominent cough and sputum production
Hypercapnia (CO2 retention) hypoxemia (low blood O2)
May terminate w/ pulmonary hypertension and cor pulmonale w/ congestive heart failure
Chronic Bronchitis vs Emphysema
Emphysema: dyspnea, no cough, no wheezing, weight loss, barrel chested, good gas exchange until late, not hypoxic until advanced
Bronchitis: cough, wheezing, much sputum constant inflammation of airways w/ scarring as disease progresses, poor gas exchange, hypoxic
Bronchiectasis
Permanent dilation of bronchi & bronchioles
Caused by destruction of the muscular and elastic supporting tissue
Affects lower lobes, bilaterally
Airways dilated to as much as 4X normal diameter
Localized: Bronchial obstruction by tumors, foreign bodies or mucus plugs
Widespread: Cystic fibrosis, necrotizing pneumonias, immunoglobulin deficiency states, Kartagener syndrome
Cystic Fibrosis
Most common lethal AR disorder to affect caucasians, uncommon in asians and blacks, severity of clinical disease may depend upon which mutation is present
Pathogenesis: primary defect is the transport of chloride ions across epithelia
Defective cAMP-dependent Cl- channels, called cystic fibrosis transmembrane conductance regulators (CFTRs)
Mutation in the CFTR gene renders epithelial cells impermeable to Cl
Respiratory tract: absorption of Na+ and water from airspace to blood resulting in thick, viscid mucus
Pseudomonas aeruginosa resistant to neutrophilic phagocytosis. Neutrophils damage normal tissue while bacteria go home free (S. aureus & H. influenzae)
Genetics: CFTR gene on chromosome 7, 1300 mutations
Features: widespread defect in secretory function of exocrine glands, chronic pulmonary infections, pancreatic insufficiency
Consequences:
Pancreas-85% are affected, Atrophy of exocrine glands: pancreatic insufficiency
Pulmonary-Retention of viscid secretions leads to dilation of bronchioles and bronchi w/ infection: bronchiectasis
Course of Disease:
pulmonary infections main problem, median life expectancy is 30 yrs, pancreatic insufficiency, sweat chloride
Dental Implications:
no definitive alterations, incidence of caries actually less presumably, mild enamel defects
Restrictive Lung Disease
Characterized by reduced lung compliance, reduced FVC & FEV1, FEV1:FVC is normal
Chronic Restrictive Lung Disease
Different causes or etiologies, share common gross and microscopic findings, Interstitial scarring common to all
Idiopathic Pulmonary Fibrosis
Diffuse interstitial fibrosis of unknown cause - 60% of afflicted > 60 Insidious onset (dry cough, progressive dyspnea)
Collagen Vascular Disorders
Changes are similar to those seen w/ idiopathic pulmonary fibrosis, but secondary to autoimmune disease (SLE, Rheumatoid arthritis, Scleroderma)
Asbestos
Natural mineral product resistant to heat and corrosion
Used in insulation, cement, and some floor tiles
Chronic lung disease caused by inhaling asbestos fibers
Prolonged exposure to these fibers can cause lung tissue scarring and shortness of breath
Sharp, straight shape of the fibers makes them difficult for a body to dislodge and expel
Nonsmokers - 5x risk inc
Smokers - 55X inc
Silicosis
Occupational inhalation of silica, usually as quartz
Miners, rock workers
May be asymptomatic or eventuate as progressive massive fibrosis
Lung cancer risk inc somewhat
Coal Worker’s Pneumoconiosis “Black Lung Disease”
Simple CWP (little or no pulmonary dysfunction Complicated CWP (Progressive massive fibrosis, compromised pulmonary function) No inc in cancer
Sarcoidosis
Multi-systemic granulomatous disease of unknown etiology
Producing noncaseating granulomas in many organs & tissues
Etiology: disordered immune regulation in genetically predisposed individuals, triggered by exposure to unknown environmental antigen
Symptoms: shortness of breath, cough, chest pain, fever, weight loss, night sweats
May have inc serum calcium, involve eye & lacrimal glands, may cause unilateral bilateral parotitis as well as xerostomia (form of restrictive lung disease)
Oral Cavity: Lesions are a rare occurrence, biopsy required for confirmation
Pulmonary Thromboembolism (Vascular Lung Disease)
95% originate in deep leg veins Predisposing caues (prolonged bed rest, surgery on legs, severe trauma, protein S & C deficiency Consequences: depends on size of pulmonary artery, ranges from silent to sudden death, right-sided heart failure (acute cor pulmonale)
Pulmonary Hypertension (Vascular Lung Disease)
Increase in pulmonary arterial pressure due to decrease in pulmonary vascular bed
Most frequently a consequence of chronic costructive or restrictive lung disease
May be “primary” or idiopathic (similar to that caused by multiple small thromboemboli)
Symptoms: usually complicate those of underlying lung disease, right-sided heart failure
Infectious Pneumonias
Defects in innate (natural) immunity: neutrophil defects, complement defects and immunoglobulin deficiency
Cell-mediated defects: AIDS, predispose to intracellular organisms such as mycobacteria and HSV
Community-acquired, nosocomial (in hospital setting), aspiration pneumonia, immunocompromised
Morphologic Patterns of Infection:
Bronchopneumonia
Patchy inflammation usually in more than one lobe, extension from bronchi & bronchioles, many different organisms involved
Morphologic Patterns of Infection: Lobar Pneumonia
All or part of a lobe homogeneously filled w/ exudate, “Lobar” on X-ray, 90% caused by Streptococcus pneumoniae
Community-acquired Atypical Pneumonias
Mycoplasma pneumoniae is most common cause
Also seen w/ influenza A&B, adenovirus, parainfluenza & RSV, Chlamydia pneumoniae inc. recognized as a cause
Findings: significant, relatively non-productive cough, minimalX-ray findings, Only slightly elevated WBC, Bacteria not isolated
Aspiration Pneumonia
gastric contents during unconsciousness or repeated vomiting (fast prior to surgery)
Debilitated individual (post-stroke)
Abnormal gag & swallowing reflexes
Partly chemical pneumonia and partly bacterial from oral flora
Lung Abscess
Aspiration of infected material from carious teeth, infected sinuses or tonsils during oral surgery (usually anaerobic bacteria)
Tuberculosis
Communicable chronic granulomatous disease Caused by Mycobacterium tuberculosis Person to person airborne spread usually T-cell-mediated immunity impaired Development of type IV hypersensitivity
Primary Tuberculosis
Previously unexposed and unsensitized person
Elderly & profoundly immunosuppressed may develop primary infection more than once
About 5% of primary infections lead to significant disease
Although most infected are resistant to developing clinical Tb, the organism remains dormant and may be “reactivated” if immunosuppression occurs
Secondary (Reactivation) TB
Disease occurring in a previously sensitized host
Most common after many decades following primary infection
May follow exposure to heavy inoculum of M. tuberculosis
May follow loss of T-cell immunity (HIV, corticosteroids, debilitating illness in elderly)
Apex of one or both upper lobes
Tuberculosis in Advanced HIV Disease
Much worse disease since patients cannot mount the initial CD4+ immune response
Granulomas do not form or are poorly formed
CD8+ T-cells are not activated to produce a killer response
“progressive primary tuberculosis”
more patients have sputum-negative smears for acid-fast bacilli
Diagnosis may be a challenge or missed
“Opportunistic” Pneumonias
Pneumocystis Pneumonia
caused by P. jiroveci, formerly P. carinii
A fungus seen especially in AIDS w/ CD4 <200
Produces interstitial pneumonia and acute respiratory distress syndrome
Carcinoma
non-small cell carcinoma (squamous cell, adenocarcinoma)
Small cell carcinoma - 90% of lung cancers arise in active smokers or recent quitters
Squamous Carcinoma
Tend to be “central” (arise in major bronchi)
Preceded for yrs by bronchial squamous metaplasia and progressive dysplasia
Most common type in smokers
Adenocarcinoma
More peripherally located just under pleura
Most common type in nonsmokers
May metastasize widely at early stage
Small Cell Carcinoma
Central lesions often w/ extensive involvement of lung parenchyma, hilar & mediastinal nodes at time of diagnosis, rarely resectable, highest association w/ smoking
Pleural Tumor - Mesothelioma
Malignant mesothelioma
50% have history of asbestos exposure, 25-40 rs latent period, almost all cases related to amphibole asbestos, smoking does not inc incidence of mesothelioma
