Respiratory Flashcards
(36 cards)
Rhinitis
Inflammation of the nasal mucosa; adenovirus is the most common cause, Presents with sneezing, congestion, and runny nose (common cold)
Allergic rhinitis is a subtype of rhinitis due to a type I hypersensitivity reaction (e.g., to pollen)
- Characterized by an inflammatory infiltrate with eosinophils
- Associated with asthma and eczema
Nasal Polyp
- Protrusion of edematous, inflamed nasal mucosa
- Usually secondary to repealed bouts of rhinitis; also occurs in cystic fibrosis and aspirin-intolerant asthma
Aspirin-intolerant asthma is characterized by the triad of asthma, aspirin-induced bronchospasms, and nasal polyps; seen in 10% of asthmatic adults
Angiofibroma
- Benign tumor of nasal mucosa composed oflarge blood vessels and fibrous tissue; classically seen in adolescent males
- Presents with profuse epistaxis
Nasopharyngeal carcinoma
- Malignant tumor of nasopharyngeal epithelium
- Associated with EBV; classically seen in African children and Chinese adults
- Biopsy usually reveals pleomorphic keratin-positive epithelial cells (poorly differentiated squamous cell carcinoma) in a background of lymphocytes
- Often presents with involvement of cervical lymph nodes
Acute Epiglottitis
- Inflammation of the epiglottis; H influenzae type b is the most common cause, especially in rionimmunized children,
- Presents with high fever, sore throat, drooling with dysphagia, muffled voice, and inspiratory stridor; risk of airway obstruction
Laryngotracheobronchitis
- Croup
- Inflammation of the upper airway; parainfluenza virus Is the most common cause
- Presents with a hoarse, “barking” cough and inspiratory stridor
- Presents with hoarseness; resolves with resting of voice
Laryngeal Papilloma
- Benign papillary tumor of the vocal cord
- Due to HPV 6 and 11; papillomas are usually single in adults and multiple in children.
- Presents with hoarseness
Laryngeal Carcinoma
- Squamous cell carcinoma usually arising from the epithelial lining of the vocal cord
- Risk factors are alcohol and tobacco; can rarely arise from a laryngeal papilloma
- Presents with hoarseness; other signs include cough and stridor.
Pneumonia
- Infection of the lung parenchyma
- Occurs when normal defenses are impaired (e.g.. impaired cough reflex, damage to mucociliary escalator, or mucus plugging)
- Clinical features include fever and chills, productive cough with yellow-green (pus) or rusty (bloody) sputum, tachypnea with pleuritic chest pain, decreased breath sounds, dullness to percussion, and elevated WBC count.
- Diagnosis is made by chest x-ray, sputum gram stain and culture, and blood cultures.
Three patterns are classically seen on chest x-ray: lobar pneumonia, bronchopneumonia, and interstitial pneumonia.
Lobar Pneumonia
- Characterized by consolidation ol an entire lobe ol tile lung
- Usually bacterial; most common causes are Streptococcus pneumoniae (95%) and Klebsiella pneumoniae
- Classic gross phases of lobar pneumonia
- Congestion—due to congested vessels and edema
- Red hepatization—due to exudate, neutrophils, and hemorrhage tilling the alveolar air spaces, giving the normally spongy lung a solid consistency
- Gray hepatization—due to degradation of red cells within the exudate
- Resolution
Bronchopneumonia
- Characterized by scattered patchy consolidation centered around bronchioles; often multifocal and bilateral
- Caused by a variety of bacterial organisms (Table 9.2)
Interstitial (Atypical) Pneumonia
- Characterized by diffuse interstitial infiltrates
- Presents with relatively mild upper respiratory symptoms (minimal sputum and low fever); ‘atypical’ presentation
- Caused by bacteria or viruses
Aspiration Pneumonia
- Seen in patients at risk tor aspiration (e.g., alcoholics and comatose patients)
- Most often due to anaerobic bacteria in the oropharynx (e.g., Bacteroides, Fusobacterium, Peptococcus)
- Classically results in a right lower lobe abscess
- Anatomically- the right main stem bronchus branches at a less acute angle than the left.
Causes of Lobar Pneumonia
- Streptococcus pneumoniae: Most common cause of community-acquired pneumonia; usually seen in middle- aged adults and elderly
- Klebsiella pneumoniae : Affects malnourished and debilitated individuals, especially elderly in nursing homes, alcoholics, and diabetics (enteric flora that is aspirated). Ihick mucoid capsule results in gelatinous sputum (currant jelly); often complicated by abscess
Causes of Bronchopneumonia
- Staphylococcus aureus: Most common cause of secondary pneumonia (bacterial pneumonia superimposed on a viral upper respiratory tract infection); often complicated by abscess or empyema
- Haemophilus: Common cause of secondary pneumonia and pneumonia superimposed on COPD (leads toxic exacerbation of COPD)
- Pseudomonas: Pneumonia in cystic fibrosis patients
- Moraxella: Community-acquired pneumonia and pneumonia super imposed on COPD (leads to exacerbation of COPD)
- Legionella: Community-acquired pneumonia, pneumonia superimposed on COPD, or pneumonia in immunocompromised states; transmitted from water source Intracellular organism that is best visualized by silver stain
Causes of interstitial pneumonia
- Mycoplasma: Most common cause of atypical pneumonia, usually alfecls young adults (classically, military recruits or college students living in a dormitory). Complications include autoimmune hemolytic anemia (IgM against I antigen on RBCs causes cold hemolytic anemia) and erythema multiforme. Not visibie on gram stain due to lack of cell wall
- Chlamydia pneumoniae: Second most common cause of atypical pneumonia in young adults
- Respiratory Syncytial Virus (RSV): Most common cause of atypical pneumonia in infants
- Ctyomegalovirus (CMV): Atypical pneumonia with posttransplant immunosuppressive therapy
- Influenza virus: Atypical pneumonia in the elderly, immunocompromised, and those with preexisting lung disease. Also increases the risk for superimposed S aureus or H influenzae bacterial pneumonia
- Coxiella: Atypical pneumonia with high fever (Q fever); seen in farmers and veterinarians (Coxiella spores arc deposited on cattle by ticks or are present in cattle placentas). Coxiella is a rickettsial organism, but it is distinct from most rickettsiae because it (I) causes pneumonia, (2) does not require arthropod vector for transmission [survives as highly heat-resistant endospores), and (3) dnes not produce a skin rash.
Tuberculosis
- Due to inhalation of aerosolized Mycobacterium tuberculosis B. Primary TB arises with initial exposure.
- Results in focal, caseating necrosis in the lower lobe of the lung and hilar lymph nodes that undergoes fibrosis and calcification, forming a Ghon complex
- Primary TB is generally asymptomatic, but leads to a positive PPD.
- Secondary TB arises with reactivation with Mycobacterium tuberculosis
- Reactivation is commonly due to AIDS; may also be seen with agin
- Occurs at apex of lung (high oxygen tension)
- Forms cavitary foci of caseous necrosis; may also lead to miliary pulmonary TB or tuberculous bronchopneumonia
- Clinical features include fevers and night sweats, cough with hemoptysis, and weight loss.
- Biopsy reveals caseating granulomas; AFB stain reveals acid-fast bacilli
- Systemic spread often occurs and can involve any tissue; common sites include meninges (meningitis), cervical lymph nodes, kidneys (sterile pyuria), and lumbar vertebrae (Pott disease).
Chronic Bronchitis
- Chronic productive cough lasting at least 3 months over a minimum of2 years; highly associated with smoking
- Characterized by hypertrophy of bronchial mucinous glandsLeads to increased thickness of mucus glands relative to overall bronchial wall thickness (Reid index increases to > 50%; normal is < 40%).
- Clinical features
- Productive cough due to excessive mucus production
- Cyanosis (‘blue bloaters’) —Mucus plugs trap carbon dioxide; increase PaCO2 and decreased PaO2
- Increased risk of infection and cor pulmonale
Emphysema
Destruction of alveolar air sacs– Loss of elastic recoil and collapse of airways during exhalation results in obstruction and air trapping.
- Due to imbalance of proteases and antiproteases
- Inflammation in the lung normally leads to release of proteases by neutrophils and macrophages.
- alpha antitrypsin (A1AT) neutralizes proteases.
- Excessive inflammation or lack of AIA T leads to destruction of the alveolar air sacs.
Smoking is the most common cause of emphysema.
- Pollutants in smoke lead to excessive inflammation and protease-mediated damage.
- Results in centriacinar emphysema that is most severe in the upper lobes
AIA T deficiency is a rare cause of emphysema.
- Lack of antiprotease leaves the air sacs vulnerable to protease-mediated damage
- Results in panacinar emphysema that is most severe in the lower lobes
- Liver cirrhosis may also be present.
- A1AT deficiency is due to misfolding of the mutated protein.
- Mutant AIAT accumulates in the endoplasmic reticulum ofhepatocytes, resulting in liver damage.
- Biopsy reveals pink. PAS-positive globules in hepatocytes
- Disease severity is based on the degree of A1AT deficiency.
- PiM is the normal allele; two copies are usually expressed (PiMM).
- PiZ is the most common clinically relevant mutation; results in significantly low levels of circulating A1AT
- PiMZ heterozygotes are usually asymptomatic with decreased circulating levels of AIAT; however, significant risk for emphysema with smoking exists.
- PiZZ homozygotes are at significant risk tor panacinar emphysema
Clinical features of emphysema include
- Dyspnea and cough with minimal sputum
- Prolonged expiration with pursed lips (‘pink puffer’)
- Weight loss
- Increased anterior-posterior diameter of chest {‘barrel-chest)
- Hypoxemia (due to destruction of capillaries in the alveolar sac) and cor pulmonale are late complications.
Asthma
Reversible airway bronchoconstriction, most often due to allergic stimuli (type I hypersensitivity)
Presents in childhood; often associated with allergic rhinitis, eczema, and a family history of atopy
Pathogenesis
- Allergens induce TH2 phenotvpe in CD4’ T cells of genetically susceptible individuals
- TH2 cells secrete IL-4 (mediates class switch to IgE), 1L-5 (attracts eosinophils), and IL-10 (stimulates TH2 cells and inhibits TH1).
- Reexposure to allergen leads to lgE-mediated activation of mast cells.
- Release of preformed histamine granules and generation of leukotrienes C4, D4, and E4 lead to broncho constrict ion, inflammation, and edema (early- phase reaction)
- Inflammation, especially major basic protein derived from eosinophils, damages cells and perpetuates bronchocon strict ion (late-phase reaction).
Clinical features are episodic and related to allergen exposure.
- Dyspnea and wheezing
- Productive cough, classically with spiral-shaped mucus plugs (Curschmann spirals) and eosinophil-derived crystals (Charcot-Leyden crystals).
- Severe, unrelenting attack can result in status asthmaticus and death.
Asthma may also arise from nonallergic causes such as exercise, viral infection, aspirin (e.g., aspirin intolerant asthma), and occupational exposures.
Bronchietasis
Permanent dilatation of bronchioles and bronchi; loss of airway tone results in air trapping.
Due to necrotizing inflammation with damage to airway walls. Causes include
- Cystic fibrosis
- Kartagener syndrome—inherited defect of the dynein arm, which is necessary for ciliary movement. Associated with sinusitis, infertility (poor motility of sperm), and situs inversus (position of major organs is reversed, e.g., heart is on right side of thorax)
- Tumor or foreign body
- Necrotizing infection
- Allergic bronchopulmonary aspergillosis—Hypersensitivity reaction to
- Aspergillus leads to chronic inflammatory damage; usually seen in individuals with asthma or cystic fibrosis
- Clinical features
- Cough, dyspnea, and tbul-smelling sputum
- Complications include hypoxemia with cor pulmonale and secondary (AA) amyloidosis.
Idiopathic Pulmonary Fibrosis
Fibrosis of lung interstitial
Etiology is unknown. Likely related to cyclical lung injury; TGF-p from injured pneumocytes induces fibrosis.
- Secondary causes of interstitial fibrosis such as drugs (e.g., bleomycin and amiodarone) and radiation therapy must be excluded.
Clinical features
- Progressive dyspnea and cough
- Fibrosis on lung CT; initially seen in subpleural patches, but eventually results in diffuse fibrosis with end-stage ‘honeycomb’ lung
- Treatment is lung transplantation.