Respiratory Pathology Flashcards
Rhinitis
inflammation of nasal mucosa (with eosinophils)
rhinovirus (adenovirus) is most common cause
Sneezing, congestion, runny nose
Allergic rhinitis is subtype (Type I hypersensitivity)
Nasal Polyp
protrusion of edematous, inflamed nasal mucosa
secondary to bouts of rhinitis
can present as child with nasal polyps and cystic fibrosis
also aspirin-intolerant asthma can cause nasal polyps
Angiofibroma
benign tumor of nasal mucosa
large blood vessels and fibrous tissue
profuse epistaxis
Nasopharyngeal Carcinoma
malignant tumor of nasopharyngeal epithelium
Associated with EBV
Biopsy –> pleomorphic keratin-positive epithelial cells
Can involve cervical lymph nodes
Acute Epiglottitis
inflammation of epiglottis
H. flu type b (unimmunized children)
fever, sore throat, drooling, inspiratory stridor
increased risk of airway obstruction
Laryngotracheobronchitis
Croup
inflammation of upper airway by parainfluenza virus
barking cough and inspiratory stridor
Vocal Cord Nodule
Singer’s nodule –> arises on true vocal cord
due to excessive use of vocal cords (bilateral)
composed of degenerative CT
resolves with resting of voice
Laryngeal Papilloma
benign papillary tumor of vocal cord
HPV 6 and 11 (usually single in adults, multiple in children)
presents with hoarseness
Laryngeal Carcinoma
squamous cell carcinoma arising from epithelial lining of vocal cord
Tobacco and alcohol use
hoarseness and cough and stridor
Pneumonia
infection of lung parenchyma –> normal defenses impaired
Fever, chills, productive cough (rusty-sputum), tachypnea, pleuritic chest pain, decreased breath sounds
Diagnosis made by CXR
3 patterns
Lobar Pneumonia
Consolidation of entire lobe of lung –> usually bacterial (strep. pneumo, Klebsiella)
Congestion of lungs
Red hepatization –> exudate, neutrophils
Gray hepatization –> degradation of RBCs
Resolution
Bronchopneumonia
scattered patchy consolidation centered around bronchioles
Lots of organisms
Interstitial pneumonia (atypical)
diffuse interstitial infiltrates
presents with mild respiratory symptoms (mild sputum, low fever = atypical presentation)
Aspiration pneumonia
seen in patients at risk for aspiration
often due to anaerobic bacteria in oropharynx (abscess bugs)
classically seen in R lower lobe
Tuberculosis
due to inhalation of mycobacterium tuberculosis
Primary TB - initial exposure
- focal, caseating necrosis in lower lobe of lung and hilar lymph nodes –> undergoes calcification
Secondary TB - reactivation
- commonly due to immunocompromised
- occurs at APEX on lung -> forms cavitary foci of caseous necrosis
- fever, night sweats, cough with hemoptysis, weight loss
- Biopsy = caseating granulomas with acid-fast bacilli
Obstructive Pulmonary Diseases
characterized by airway obstruction –> lung doesn’t empty –> air trapping
volume of air forcefully expired is decreased (especially FEV) –> large decrease in FEV/FVC ratio
total lung capacity is actually increased because of trapping
Chronic Bronchitis
chronic, productive cough that lasts for 3 months over 2 years
HIGHLY ASSOCIATED WITH SMOKING
hypertrophy of bronchial mucinous glands –> increased thickness of mucus glands on histology (Reid index >50%)
- Productive cough, ‘blue bloaters’, increased risk of infection
Emphysema
Destruction of alveolar air sacs --> loss of elastic recoil and collapse of airways during exhalation --> air trapping due to imbalance of proteases and anti-proteases --> excessive inflammation Clinical Features 1. dyspnea with cough 2. prolonged expiration (pursed lips) 3. weight loss 4. barrel chest 5. hypoxemia
Smoking Emphysema
MAJOR type of emphysema
pollutants froms smoke lead to excessive inflammation and protease-mediated damage
centriacinar emphysema –> upper lobes
A1AT Emphysema
rare cause –> common on exams tho!
Lack of antiprotease activity –> leaves air sacs vulnerable
Panacinar emphysema –> lower lobes
Liver cirrhosis –> defective A1AT proteins accumulate in endoplasmic reticulum
disease severity correlates to A1AT deficiency
Asthma
reversible airway bronchoconstriction (allergic stimuli)
presents in childhood
Type I Hypersensitivity –> allergens induce Th2 cells to secrete IL-4 (class switch IgE), IL-5 (eosinophils), IL-10 (more Th2, less Th1)
Reexposure leads to IgE mast cell degranulation –> bronchoconstriction
Clinical Features
1. episodic wheezing and dyspnea
2. productive cough
Bronchiectasis
permanent dilation of bronchioles and bronchi (loss of airway tone –> air trapping)
due to necrotizing inflammation
- cystic fibrosis
- Kartagener syndrome - inherited defect in dyenin arm of cilia
- tumor
- necrotizing infection
- hypersensitivity to aspergillus
Restrictive Lung Diseases
characterized by inadequate filling –> decreased TLC, FEV, FVC –> FEV/FVC normal
- most commonly due to interstitial disease (fibrosis of lungs)
Idiopathic Pulmonary Fibrosis
fibrosis of lung interstitium --> unknown etiology, likely from cyclic lung injury (TGF-beta) Clinical Features 1. PROGRESSIVE dyspnea and cough 2. fibrosis of lung on CT 3. Tx = transplant
Pneumoconioses
Interstitial fibrosis due to occupational exposure –> requires chronic exposure to small particles that are fibrinogenic (alveolar macrophages engulf particle –> induce fibrosis)
Coal Workers’ Pneumoconioses
Carbon dust
Massive exposure leads to ‘black lung’
Mild exposure results in anthracosis (not clinically significant)
Silicosis
Silica exposure (sandblasters) Silica impairs phagolysosome --> increased risk of TB --> lung nodules in upper lobes
Berylliosis
Beryllium (aerospace industry)
Noncaseating granulomas in lung, hilar lymph nodes, and systemic organs (similar to sarcoidosis)
Asbestosis
Asbestos fibers (construction and shipyard workers)
Fibrosis of lung and pleura
Increased risk of lung cancer and mesothelioma (lung cancer more common than meso)
Sarcoidosis
systemic disease characterized by noncaseating granulomas in multiple organs
Etiology unknown, likely due to CD4 Tcells response to unknown antigen
Granulomas commonly found in hilar lymph nodes and lung (asteroid bodies)
Clinical Features
1. Dyspnea, cough
2. Elevated serum ACE
3. Hypercalcemia
4. Tx = steroids
Hypersensitivity Pneumonitis
granulomatous reaction with eosinophils to organic antigens (inhaled) –> Pigeon breeders lung
Fever, cough, dyspnea, resolves after removal of exposure
Pulmonary HTN
high pressure in pulmonary circulation
atherosclerosis in pulmonary trunk –> plexiform lesions seen in long-standing cases
Leads to RVH, exertional dyspnea
Primary pulmonary HTN
Classic = young adult females
etiology unknown
BMPR2 –> leading to proliferation of vascular smooth muscle
Secondary pulmonary HTN
due to hypoxemia (COPD, etc), or increased volume in pulmonary circuit
Acute Respiratory Distress Syndrome
Diffuse damage to alveolar-capillary interface
Hyaline membranes in alveoli –> protein-rich fluid leads to edema
Hypoxia and cyanosis w/ resp distress (thickened diffusion barrier and collapse of air sacs)
Can be secondary to a variety of diseases
Neonatal Respiratory Distress Syndrome
Respiratory distress due to inadequate surfactant levels (phosphatidylcholine –> type II pneumocytes)
Associated with prematurity (surfactant production occurs at week 28 (ratio >2)), C-section (no stress), Maternal diabetes (insulin decreases surfactant production in fetus)
Hypoxemia increases risk for PDA
Lung Cancer Basic Principles
Most common cause of cancer mortality in US
Risk Factors –> smoking (polycyclic aromatic hydrocarbons and arsenic), radon (radioactive decay of uranium), asbestos
Non-specific presenting symptoms
Imaging –> solitary nodule (coin lesion)
Small Cell Carcinoma vs. Non-small cell carcinoma
Pneumothorax
accumulation of air in pleural space
Spontaneous - rupture of emphysematous bleb (young, tall thin adults)
Tension - air enters pleural space but cannot exit, trachea pushed to opposite side (medical emergency)
Mesothelioma
malignant neoplasm of mesothelial cells –> highly associated with asbestos exposure
Presents with recurrent pleural effusions, dyspnea, and chest pain (tumor encases lung)
Small Cell Carcinoma
poorly differentiated small cells (arises from neuroendocrine cells)
male smokers, central location
rapid growth and early metastasis and paraneoplastic syndromes
Squamous Cell Carcinoma
Keratin pearls or intercellular bridges on histology
Most common tumor in male smokers, central location
may produce PTHrP
Adenocarcinoma
Glands or mucin on histology
Most common tumor in nonsmokers/female smokers
peripheral location
Large Cell Carcinoma
poorly differentiated large cells
smoking associated, central/peripheral
poor prognosis
Bronchioloalveolar carcinoma
Columnar cells that grow along preexisting bronchioles and alveoli
Not related to smoking, peripheral location
May present with pneumonia like consolidation on imaging
Excellent prognosis
Carcinoid tumor
Well differentiated neuroendocrine cells (chromogranin positive)
Not related to smoking, central/peripheral location
Low grade malignancy
Metastasis to lung
Most common sources are breast and colon carcinoma
Multiple ‘cannon-ball’ nodules on imaging
more common than primary tumors
