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