Pulmonary Pathology Flashcards
What are the characteristics of all COPDs?
The airway becomes obstructed so air is trapped in the lung. This leads to a minor decrease in FVC, a major decrease in FEV1 and a decrease in the FEV1:FVC ratio. Also characterized by an increase in total lung capacity (TLC) due to air trapping.
What are the four chronic obstructive pulmonary disorders?
Chronic bronchitis
emphysema
Asthma
Bronchiectasis
What is the pathogenesis of chronic bronchitis? What is the clinical definition of chronic bronchitis? What are the clinical findings?
Smoking causes hyperplasia of the mucinous glands in the bronchi such that the percentage of the wall due to mucinous glands becomes >50% (Reid index >50%). Excessive mucus production occurs and most of it gets coughed up, but some of it slides down into the lungs and obstructs the airways, making CB a COPD. It is defined as a productive cough lasting at least 3 months over a minimum of 2 years. Clinical findings include cyanosis, a highly productive cough and increased risk of infection/cor pulmonale
What is the pathogenesis of emphysema?
Imbalance of proteases and antiproteases (e.g. alpha-1-antitrypsin) -> either increased protease activity (smoking) or decreased anti protease activity (A1AT deficiency) -> destruction of the alveolar air sacs -> decreased the elastic recoil of the lung. This causes obstruction in two ways:
1) Since expiration is passive and due to elastic recoil, air cannot flow out
2) Air picks up velocity as it moves toward the trachea. This increased velocity pulls on the walls of the airways, causing the airways to collapse. Normally, airways that do not have cartilage to keep them open (bronchioles) are held open by elastic recoil of alveolar air sacs.
What are the causes of emphysema? what lobes do they mostly effect? What part of the acinus do they effect?
Smoking - centriacinar emphysema, more servere in upper lobes
A1AT deficiency - panacinar emphysema, more severe in lower lobes
What are the clinical findings of emphysema?
Dyspnea and cough with minimal sputum
prolongues expiration with pursed lips (“pink puffer” - able to maintain oxygenation of RBCs)
weight loss due to extra work while breathing
increased AP diameter of chest (barrel chest), increased functional residual capacity
What cytokines do TH2 T helper cells secrete? What do those cytokines do?
IL-4 - allows plasma cells to class switch to IgE
IL-5 - recruits eosinophils
IL-10 - inhibits TH1 cells
What is the pathogenesis of asthma?
First phase - mediated by mast cells
A primary allergen stimulus arms mast cells with IgE. When the patient is exposed to the allergen for the second time, the mast cells release preformed histamine in the early phase and leukotrienes in the delayed phase. Histamine causes vasodilation and increased vascular permeability. Leukotrienes cause bronchoconstriction, vasoconstriction, increased vascular permeability.
Late phase - mediated by inflammatory cells
Over time, inflammation perpetuates bronchoconstriction
What are the clinical features of asthma?
dyspnea and wheezing
productive cough with Curschmann spirals with Charcot-Leyden crystals (aggregates of major basic protein from eosinophils)
What is the pathogenesis of bronchiectasis? What are the causes? What are the clinical features
Permanent dilation of bronchioles and bronchi results in air trapping.
Causes are necrotizing inflammation which damage to the airway wall that causes dilation of the airway
cystic fibrosis
kartagener syndrome
tumor or foreign body
necrotizing infection
allergic bronchopulmonary aspergillosis
Clinical features - cough, dyspnea and foul-smelling sputum
What are the clinical findings of pneumonia? atypical pneumonia?
pneumonia - High fevers and chills productive cough with yellow-green (pus) or rusty (bloody) sputum tachypnea pleuritic chest pain decreased breath sounds dullness to percussion elevated WBC atypical pneumonia - Minimal sputum low fever mild respiratory symptoms
What are the three classical patterns of pneumonia on chest x-ray? How can they be distinguished on x-ray? What are the typical causative organisms?
lobar pneumonia - consolidation of an entire lobe of the lung; usually caused by bacteria
bronchopneumonia - scattered, patchy consolidation centered around bronchioles and often multifocal and bilateral; caused by bacteria
interstitial pneumonia - diffuse interstitial infiltrates; caused by viruses and occasionally bacteria
What organisms typically cause a lobar pneumonia? bronchopneumonia? interstitial pneumonia? aspiration pneumonia?
lobar - strep pneumoniae, klebsiella pneumoniae
bronchopneumonia - staph aureus, haemophilus influenzae, pseudomonas aeruginosa, moraxalla catarrhalis, legionella pneumophilia
interstitial pneumonia - mycoplasma pneumoniae, chlamydia pneumoniae, respiratory syncytial virus, cytomegalovirus, influenza virus, coxiella burnetti
aspiration - bacteroides, fusobacterium, peptococcus
What is the classic complication of aspiration pneumonia?
right lower lobe abscess because the right main stem bronchus is steeper than the left
What are the characteristics and spirometry of restrictive lung diseases? What are the common causes of restrictive lung diseases?
The lung cannot fill all the way Decreased total lung capacity (TLC) decreased FEV1, greatly decreased FRC increased FEV1:FRC ratio (> 80%) The most common cause of restrictive lung diseases are interstitial diseases of the lung but chest wall abnormalities (e.g. obesity) can also prevent complete filling
What are the restrictive lung diseases?
idiopathic pulmonary fibrosis
pneumoconiosis
sarcoidosis
obesity/chest wall abnormalities
What is the etiology of idiopathic pulmonary fibrosis? What are other causes of pulmonary fibrosis that must be excluded?
Unknown etiology but probably related to cyclical lung injury that causes injured pneumocytes to release TGF-beta which stimulates fibrosis Certain drugs (bleomycin and amiodarone) and radiation can also cause pulmonary fibrosis
What is pneumoconiosis? What are the four common types?
Pneumoconiosis is interstitial fibrosis due to an occupational exposure to small particles that are engulfed by macrophages which induce fibrosis. Coal workers' pneumoconiosis silicosis berylliosis asbestosis
What is the small particle that causes silicosis? What type of person typically gets silicosis? How does silicosis affect macrophages? What disease are patients with silicosis at increased risk of? What are the histological findings?
Chronic exposure to silica causes silicosis. Usually occurs in sandblasters and silica miners. Silica inhibits phagolysosome fusion in macrophages. Increased risk of TB. Find fibrotic nodules in the upper lobes of the lung
What is the small particle that causes berylliosis? What type of person typically gets berylliosis? What are the histological findings?
Beryllium. Usually occurs in workers in the aerospace industry. Find noncaseating granulomas in the lung, hilar lymph nodes and organs
What is the small particle that causes asbestosis? What type of person typically gets asbestosis? What are the histological findings? What disease are patients with asbestosis at increased risk of?
Asbestos fibers. Usually occurs in construction workers, plumbers, shipyard workers. Find asbestos bodies (long, golden-brown rods with iron). Also find fibrosis of lung and pleura. Increased risk of lung cancer and mesothelioma
What are the characteristic findings in sarcoidosis? What is the classic patient with this disease? What are the clinical features?
Noncaseating granulomas in hilar lymph nodes, lung and other organs. Less common organs:
uveitis, cutaneous nodules, erythema nodosum, salivary and lacrimal glands. Classically seen in african american females.
Clinical features = dyspnea/cough, elevated serum angiotensin converting enzyme, hypercalcemia (1-alpha hydroxyls activity in epitheloid histiocytes converts vitamin D to active form)
What are the three major preventable risk factors for lung cancer?
Smoking, radon, asbestos
How do you calculate pack years of smoking?
Number of packs smoked per day X number of years patient smoked. There are 20 cigarettes in a pack
What are the two main categories of lung cancer? How does their treatment plan differ?
Small cell carcinoma and non-small cell carcinoma. Treat SCC with chemotherapy but not surgery. Treat NSCC with surgery but not chemotherapy
What are the subtypes of non-small cell carcinoma?
Adenocarcinoma, squamous cell carcinoma, large cell carcinoma, carcinoid tumor
What are the histological markers of small cell carcinoma? Squamous cell carcinoma? Adenocarcinoma? Large cell carcinoma? Carcinoid tumor?
SCC - poorly differentiated small cells arising from neuroendocrine cells (kulchitsky cells)
Squamous cell carcinoma - keratin pearls or intercellular bridges
Adenocarcinoma - cells form gland structures and produce mucus
Large cell carcinoma - poorly differentiated large cells
Carcinoid tumor - well-differentiated neuroendocrine cells that are chromogranin positive
Which lung cancer is associated with male smokers? Which lung cancers are associated with non-smokers? which cancers are associated with female smokers?
Male smokers - small cell carcinoma, squamous cell carcinoma
Female smokers - Adenocarcinoma
Non-smokers - Adenocarcinoma
Which lung cancers produce paraneoplastic syndromes?
Small cell carcinoma- ADH, ACTH or antibodies against presynaptic calcium channels, blocking ACh release from the NMJ resulting in muscle weakness (eaton-lambert syndrome)
Squamous cell carcinoma - PTHrP
What are the complications of lung tumors?
Pleural involvement (adenocarcinoma), obstruction on SVC, involvement of recurrent laryngeal nerve (hoarseness) or phrenic nerve (diaphragmatic paralysis), compression of sympathetic chain and horner’s syndrome (pancoast tumor).
What are the most common sources of metastasis to the lung?
Breast and colon carcinoma
