Pulmonary Diseases Flashcards by Maggie Berrigan

pink puffer phenotype
a condition of the lung characterized by abnormal permanent enlargement of airspaces distal to the terminal bronchiole, accompanied by the destruction of their walls, and without obvious fibrosis

Airway walls are destroyed –> enlargement and overdistension of the airspaces without interstitial fibrosis and minimal/absent interstitial inflammation
Interstitial framework of the lung is destroyed –> simplification of the lung parenchyma and reduced surface area of gas exchange
Little scarring or fibrosis

early dyspnea and late cough, minimal sputum production, few infectious exacerbations, loss of elastic recoil, and hyperinflation of the CXR (increased AP diameter, barrel chest)

Complications: respiratory insufficiency, CO2 retention/respiratory acidosis, secondary pulmonary hypertension, right ventricular hypertrophy, cor pulmonale, pneumothorax

smoking: increase in proteases; centriacinar pattern, severe in upper lobe

alpha 1 antitrypsin deficiency: decreased anti-proteases, panacinar pattern, severe in lower lobe, cirrhosis of the liver may occur

Decreased FEV1, Decreased FEV1/FVC ratio, Increased RV, Decreased diffusion capacity, hypoxemia

Emphysema

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blue bloater phenotype characterized by a cough productive of sputum on most days during at least three consecutive months for more than two successive years

More profound hypoxemia at rest, elevated PaCO2 with chronic respiratory acidosis, cor pulmonale with right heart failure

Associated with smoking and environmental pollutants, characterized by persistent cough with airway hypersecretion and inflammation and sputum production

Chronic asthmatic bronchitis is associated with bronchospasm

Chronic airflow obstruction and acute infectious exacerbations may develop in later stages

Predominantly involves the proximal airways without the parenchymal injury and loss associated with emphysema

Particulate/noxious inhalants –> inflamed airways with increased mucus secretions and mucopurulent exudates

Airway epithelium may show mucous metaplasia and squamous metaplasia, mucosa will have increased mucus glands with productive secretions with mucus plugs

Peribronchiolar fibrosis is present in later stages

Reid index measure the ratio of mucus gland layer to the entire mucosa (normally less than 0.4). increased mucosal inflammation and mucous plugging leads to airway obstruction, mucosal fibrosis may occur in later stages

Initial symptoms are related to bronchial and bronchiolar inflammatory irritation and cough

With increased mucus secretions, airway obstruction –> atelectasis, dyspnea on exertion, air trapping

Retained CO2 (hypercapnia) --> respiratory acidosis
Inadequate oxygenation --> hypoxemia and cyanosis

Late complications include repeated airway infections, pneumonia, right-sided heart failure, respiratory insufficiency

Treatment
Increase airflow and decrease resistance with bronchodilators (anticholinergics and beta agonists)
Corticosteroids and antibiotics are used in severe cases

Chronic bronchitis

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Abnormally dilated airway resulting from prolonged destructive inflammation/infection of the airway and supporting structures

Clinical presentation:
Airway infection, cough, purulent foul-smelling sputum production, squeaks, crackles, wheezes, airflow obstruction, CXR shows tram tracks indicating dilated airways

Damage airways are permanent and result from CF, Kartagener’s syndrome, bronchial obstruction (tumor or foreign body), immunodeficiency diseases and necrotizing bronchopneumonias

Airways show remodeling and dilation with an inflamed mucosa, luminal purulent mucoid secretions, and fibro-inflammatory airway walls

complications: hypoxemia, cor pulmonale, secondary amyloidosis

Bronchiectasis

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chronic relapsing inflammatory airway disorder
more common children, females, and African Americans

Allergic inflammation (eosinophils), goblet cell metaplasia, mucous gland hyperplasia, luminal allergic mucus, airway muscular hypertrophy 
Inflammation limits airflow via acute airway smooth muscle constriction, swelling of the airway wall, chronic mucus plug formation, and airway wall remodeling

Anti-inflammatory therapy is the cornerstone of treatment
Therapy to suppress inflammation must be long term
Early intervention with therapy may modify the disease process and prevent remodeling

Episodic attacks of dyspnea, wheeze, bronchospasm, cough, and chest tightness – vary over time and in intensity
Bronchial hyperresponsiveness is an exaggerated bronchoconstrictor response to many different stimuli

Status asthmaticus involves marked mucus plugging, air trapping, and dyspnea – may cause death

Pathophysiology: increased airway resistance (airflow limitation worse on expiration), increased work of breathing, non-uniform distribution of ventilation (V/Q mismatch, low V/Q units develop, localized alveolar hypoxia)

Diagnosis: compatible history and physical exam with documentation of variable airflow obstruction

Spirometry before and after inhalation of short-acting bronchodilator (12% improvement that is at least 200mL after use of bronchodilator indicates asthma over COPD)
Low FEV1 but no symptoms, consider poor perception of control or restricted activity
bronchoprovocation testing with methacholine or exercise may be used
Frequent symptoms in the absence of abnormal FEV1 consider cardiac disease, deconditioning

Treatment requires a step-wise approach; persistent disease is most effectively controlled with daily anti-inflammatory therapy with inhaled glucocorticoids
Long term control medications: corticosteroids, long-acting beta agonists, leukotriene modifiers, anti-IgE
Rescue medications: short-acting beta agonists (relief of acute symptoms, preventative prior to exercise)

asthma

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Onset is usually in childhood and is often preceded by allergic rhinitis, urticaria, or eczema
Family history of atopy is common
Disease is triggered by environmental antigen
Skin prick tests for antigen are positive (IgE mediated reaction)

atopic asthma

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The mechanism of inflammation and airway hyperresponsiveness is less clear; may involve viral infections of respiratory tract, inhaled air pollutants (sulfur dioxide, ozone, nitrogen dioxide)
Airway hyperresponsiveness is more severe and sustained
Family history, associated allergies, and abnormal IgE levels are uncommon

intrinsic asthma

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immunologically mediated lung disease that arises from inhalation of organic dusts, animal proteins, and/or molds

Inciting antigen may be occupational or recreational and in a sensitized individual it induces a type III and type IV hypersensitivity reaction

Bronchiolitis with interstitial lympho-plasmacytic infiltration with poorly formed interstitial granuloma

Infiltration of lymphocytes and macrophages (not mast cells, eosinophils)

Clinical presentation: dyspnea, cough, fever

Acute and sub-acute presentations with rapidly progressive flu like signs and symptoms

Chronic exposure may lead to chronic disease that may progress to interstitial fibrosis and restrictive lung disease

CXR shows nodular diffuse infiltrates

Treatment: remove antigen (usually improves symptoms and reverses the pathological process); glucocorticoids to reverse the inflammatory condition
By removing exposure, condition may be reversed if no scarring or fibrosis has occurred

hypersensitivity pneumonitis

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single pitch, inspiratory or expiratory sound that is produced by large airways with severe narrowing
May be caused by severe obstruction of any proximal airway (larger airways)

Acute –> immediate consultation with ENT or anesthesia

Inspiratory = Supraglottic: epiglottis, larynx, aryepiglottic fold, false vocal cords
Epiglottitis, retropharyngeal abscess, diphtheria

Expiratory = Intrathoracic: portion of the trachea within the thorax and mainstem bronchi
Congenital disorders, foreign bodies, compression by lymph nodes or tumors

Biphasic = Glottis and subglottic: vocal cords to the extrathoracic segment of the trachea
Laryngotracheitis (croup), vocal cord paralysis, critical obstruction

Stridor

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musical sound pronounced primarily during expiration by airways of any size (usually in smaller airways)

chronic: asthma, COPD, bronchiectasis, HF
acute: asthma, HF, aspiration, URI

wheeze

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inflammation of the bronchioles
Predominantly affects the smallest air passages of the lungs
Symptoms include increased effort for work of breathing
Scattered areas of expiratory wheezes
Usually occurs in children less than two years of age with the majority of cases due to viral pathology
Most common virus is RSV which is easily spread via mucosal droplets and is most common in late fall to early spring; premature infants are at the highest risk, Palivizumab monthly injections
Most cases are mild and self-limiting, symptoms last for 2-3 weeks
Early symptoms: runny noses, cough, similar to a cold
Severe cases may require hospitalization or frequent bronchodilator therapy for wheezing responsive to therapy

bronchiolitis

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Idiopathic pulmonary fibrosis

Process of rapidly progressive respiratory failure with diffuse homogeneous interstitial infiltrates on CXR

Fibrosing alveolitis, interstitial fibroblastic proliferation, interstitial fibrosis, proliferative interstitial scarring

Lung proceeds to fibrosis, cystic changes and diffuse scarring

Acute Interstitial Pneumonia = Hamman-Rich Syndrome

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Idiopathic pulmonary fibrosis

Chronic fibrosing interstitial lung changes that present in adults with slowly progressive onset
Dyspnea and sometimes cough
Patchy distribution, CXR show subpleural and bibasilar reticulo-nodular opacities
Respiratory failure occurs over 2-5 years
Patchy interstitial fibrosis alternating with areas of spared lung, accentuation of interstitial fibrosis in a subpleural location, presence of interstitial inflammation and active fibroblastic proliferative regions with dense collagen interstitial deposition
Earliest interstitial lesions = fibroblastic foci = proliferative fibroblasts with myxoid collagenous matrix
Progresses to end stage lung with pulmonary fibrosis and cystic change (honeycomb lung)

Usual interstitial pneumonitis

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idiopathic pulmonary fibrosis

Clinical features similar to UIP but there is a more homogenous chronic interstitial pneumonia throughout the lung
Pulmonary intersitium is expanded with lympho-plasmacytic infiltrate that appears temporally uniform (unlike in UIP)
Better clinical outcome than UIP, may also be responsive to steroid therapy

Nonspecific interstitial pneumonitis

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idiopathic pulmonary fibrosis despite known cause

Inflammation in the terminal bronchioles and alveolar ducts with production and desquamation of hemosiderin-laden macrophages

RBILD may continue to involve pulmonary interstitium –> restrictive disease
Appears to be associated with smoking, improvement with smoking cessation and glucocorticoids

DIP involves diffuse involvement of alveolar units with desquamated pneumocytes and macrophages
Active alveolar disease gives ground glass appearance on high resolution CT

Respiratory bronchiolitis interstitial pneumonia/desquamative interstitial pneumonia

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idiopathic pulmonary fibrosis
commonly seen in African American females

dyspnea, cough, elevated ACE, hypercalcemia

inflammatory systemic disease of unknown etiology with inflammatory foci composed of non-caseating granuloma

Pulmonary involvement begins with mediastinal and hilar granulomatous LAD and progresses to lung involvement with granulomatous inflammation in a lymphatic distribution

Proliferating CD4 cells activate macrophages –> epithelioid histiocytes in type IV hypersensitivity pattern
Increased CD4:CD8 ratio with activation of Th1 cytokines

May lead to interstitial fibrosis and end-stage lung but most cases resolve or are indolent

asteroid body = configuration of giant cells

Exclude mycobacterial and fungal infection before making the diagnosis

sarcoidosis

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interstitial fibrosis due to chronic occupational exposure

Particles lodge at bifurcations of the distal airways, terminal bronchioles, and respiratory ducts

Inflammatory response depends on size, solubility, chemical nature and other properties of the dust/fumes

Decreasing lung clearance mechanisms (smoking) increases the retained inhalant particles

Macrophages attempt to engulf and digest particles; inflammatory mediators, lysosomal enzymes, and fibrogenic factors are released causing lung damage and fibrosis

pneumoconioses

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Sclerotic nodules

Results from exposure to silica - mining, tunneling, stone cutting, excavation, road building, sandblasting, glassmaking

Macropahges interact with silica at the bifurcations of the distal bronchioles and ducts –> release of inflammatory mediators, lysosomal enzymes, ROS, fibrogenic factors
Nodules of dense collagen are formed retaining silica particles

In simple cases the nodules are scattered throughout the lung fields but do not compromise function; may progress to coalescent massive fibrosis with pulmonary dysfunction. Nodules most often seen in upper lobe.

Simple: asymptomatic, gradually progressive dyspnea on exertion

Complicated: marked dyspnea on exertion, cough, sputum, progression to cor pulmonale and respiratory failure

Clubbing is not seen

Increased incidence of mycobacteria infection due to impaired phagolysosome function

silicosis

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Interstitial fibrosis

Results from inhalation of asbestos silicates during the processing of asbestos fibers - mining, milling, transporting, manufacturing fibers; domestic exposures

Increased fiber burden in the lung over years –> pleural effusion, pleural plaques

Injury progresses to interstitial fibrosis with interstitial ferruginous bodies

Associated with malignant pleural mesothelioma and bronchogenic carcinoma (in smokers)

Inhalation and deposition of fibers at respiratory bronchioles and alveolar ducts

Pulmonary alveolar macrophage alveolitis is dependent on fiber load

Increased release of oxidants and inflammatory mediators

Damage to parenchymal cells with remodeling of connective tissue

Chronic interstitial lung disease

asbestosis

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results from the inhalation of coal dust –> anthracotic coal macules with pigmented macrophages embedded in collagen adjacent to respiratory bronchioles

Progresses overtime to massive fibrosis with coalescent dense collagen bundles –> pulmonary dysfunction

coal workers pneumoconiosis

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diverse group of pulmonary disorders that are classified together because of similar manifestations
In general, the major problem is a disruption of the distal lung parenchyma but airways, blood vessels, or pleura may be affected as well
Characterized by infiltration of cellular and noncellular material into the lung parenchyma
CXR: diffuse interstitial infiltrates, smaller lung size
Thickening of the interstitium between the blood and airspace decreases gas exchange

injury to the alveolar epithelial cells that initiates the disease
An inflammatory response ensues that results in scarring and structural remodeling
Inflammatory cells, proliferating epithelial cells, fibroblasts, and ECM components drive the repair process that results in remodeling and may become dysregulated

results in reduced lung compliance
Restrictive ventilator defect, higher pressures are needed to inflate the lung to a given volume (increased work of breathing)
Smaller tidal volumes are moved more often; this is inefficient
DLCO is decreased; there is a thickening and loss of surface area of the membrane
V = AD(P1-P2)/T where D is proportional to solubility/sqrt MW
Both FRC and TLC are lower than normal
Abnormal resting gas exchange
Exercise desaturation
PO2 is normal at rest but falls with movement
Increased PCO2 is only seen with severe disease because it is more soluble than O2

Diagnosis
Nonspecific respiratory complaints
Dyspnea that is usually progressive, dry cough
CXR : Diffuse parenchymal infiltrates, May be normal
Chronic: ground glass opacities, alveolar filling, cystic appearance, LAD, pleural disease, pneumothorax
Interstitial infiltrates and LAD: sarcoidosis, silicosis, infections, malignancy
Interstitial infiltrates and pleural disease: infections, malignancy, collagen vascular disease, drug hypersensitivity, CVD, asbestos-related disease

Investigation of pulmonary hypertension due to the change in pulmonary vascular resistance

Patient history: family history, exposure history, smoking history, medications, previous radiation exposure, age and sex of the patient

Physical exam findings
Velcro crackles = mid to late inspiratory crackles in the lower lung field due to the lesser negative trans pulmonary pressure that is no longer able to hold open alveoli, crackling is heard with alveolar opening
Digit clubbing is seen in IPF but is not specific for IPF
Skin lesions, eye findings, peripheral LAD, CV findings, hepatosplenomegaly, musculoskeletal

Diffuse parenchymal lung disease

chronic interstitial lung disease

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Unlikely if all of the following are absent
Fever >/= 38 degrees C
Tachypnea >/= 24 breaths/min
Tachycardia >/= 100 beats/min
Evidence of consolidation: rales, egophony, fremitus

Management of community acquired pneumonia
Applies to non-immunocompromised adults (not to hospitalized patients or non-ambulatory residents of long term care facilities)
CXR to confirm diagnosis
Tests to establish microbiologic diagnosis are optional in outpatients
Additional tests to consider in hospitalized patients
Blood culture before antibiotic regimen
Sputum gram stain and culture
Urine antigen tests for pneumococcus and Legionella

Common bacterial etiologies
Streptococcus pneumoniae
Haemophila influenzae
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Legionella
Staphylococcus aureus (especially during an influenza outbreak)

Less common bacterial etiologies
Moraxella (especially in COPD patients)
Gram negative rods (especially with chronic inhaled steroids, alcoholics, COPD)

Viral etiologies
Influenza, adenovirus, RSV, parainfluenza, MERS/SARS

Empiric therapy should target bacteria unless influenza is expected

Outpatient management in a previously healthy patient that has not used antibiotics in the preceding 3 months (low risk of resistance): oral macrolide (azithromycin, clarithromycin) is preferred, oral doxycycline is an alternative
For children, amoxicillin is used due to lower incidence of atypical pneumonia (Chlamydophila and Legionella)

Outpatient management in a patient with comorbidities (CHF, diabetes, COPD, alcoholism, immunocompromised) or antibiotic use in the last 3 months (increased concern of resistance): respiratory quinolone (levofloxacin, moxifloxacin, gemifloxacin) or beta lactam with macrolide (high dose of amoxicillin or amoxicillin-clavulonate (PO)/ceftriaxone (IM)/cefpodoxime (PO)/cefuroxime (PO) with azithromycin)

Inpatient management in a non-ICU patient: respiratory quinolone (levofloxacin, moxifloxacin, gemifloxacin) or beta lactam with macrolide (high dose of amoxicillin or amoxicillin-clavulonate (PO)/ceftriaxone (IM)/cefpodoxime (PO)/cefuroxime (PO) with azithromycin)
Start with IV and switch to PO with improvement (hemodynamically stable, clinical improvement, able to take PO medications)

Treatment should last for at least 5 days
Patient should be afebrile for 48-72 hours and without signs of clinical instability before stopping treatment
Most cases are treated for 7-10 days

pneumonia

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Viral etiologies (more than 90%)
Influenza
Parainfluenza
Respiratory syncytial virus
Coronavirus
Rhinovirus
Adenovirus

Bacterial etiologies (less than 10%):
Mycoplasma pneumoniae, Chlamydophila pneumoniae, Bordatella pertussis
Usually no treatment is required
No proven benefit to antimicrobial use
Macrolide is used in pertussis to decrease transmission
Bronchodilators and antitussives may provide symptomatic relief

acute bronchitis

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Spread by airborne droplets from patients in the early stages of infection (not aerosolized)
Highly contagious
Infects 80-100% of exposed susceptible individuals
Spreads rapidly in school, hospitals, offices, and homes
Infected adults often spread infection to schools/daycares

Caused by Bordetella pertussis a gram negative coccobacillus for which humans are the reservoir
Incubation period 7-10 days
Symptoms can be similar to those of a common cold (rhinitis)
Mortality is highest in infants

Pertussis

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Spores deposited into the terminal bronchioles and alveoli is aerosolized in 1-10 um particles (bioterrorism)

ingested by macrophages which migrate to peribronchial and mediastinal lymph nodes (widened mediastinum and possible pulmonary infiltrate on CXR)
incubation period of 10 days but may last up to 6 weeks
fever, fatigue, chest pain, nonproductive cough
hemorrhagic mediastinitis after 1-3 days with an abrupt onset of severe respiratory distress and stridor

septic shock and death within 24-36 hours
meningitis may occur
mortality 80-90%

management
empiric ciprofloxacin
alternatives include doxycycline and penicillin/amoxicillin/rifampin depending on sensitivities
isolation: standard precautions, no person to person transmission
post-exposure prophylaxis for 60 days with ciprofloxacin or doxycycline (penicillin/amoxicillin based on sensitivities)
prevention: vaccine is available but requires 6 doses followed by annual booster, not widely used

inhalational anthrax

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Pressure in the pulmonary vessels increases, RV systolic pressure increases to preserve CO, continuous high pressure in pulmonary vessels leads to progressive remodeling of the vasculature atherosclerosis of the pulmonary trunk, smooth muscle hypertrophy of pulmonary arteries, intimal fibrosis The ability of the RV to adapt to high pulmonary vascular pressure is inversely related to how fast the increase in pressure occurs With a progressive increase in RV systolic pressure there will be ischemic changes in the right ventricle myocardium and eventually RV failure PH: MPAP >/= 25 mmHg PAH: MPAP >/= 25 mmHg, PCWP = 15 mmHg, PVR > 3 wood units Dyspnea at rest, cough, dizziness, syncope, edema, chest pain, fatigue, dyspnea on exertion ``` Presymptomatic/compensated --> symptomatic/decompensating --> declining/decompensated (right heart dysfunction) At the time of diagnosis more than 60% of patients fall into class III or IV (on a scale of I-IV) ``` Diagnosis: physical exam, ECG, PFTs, CXR, CT scan, V/Q mismatch, right heart catheterization Treatment: General: avoid pregnancy, avoid physical exertion, sodium restricted diet, avoid ihgh altitude, diuretics, anticoagulation, oxygen Medical: vasodilator, NO, prostacyclin analogs, phosphodiesterase inhibitors, endothelin receptor antagonists Surgical: atrial sptostomy, transplant, embolectomy (for CTEPH)

pulmonary hypertension

occurs in smokers and nonsmokers, more common in females Glandular differentiation and mucin production Tumors tend to be peripheral, may be associated with a scar or produce desmoplastic stromal response in situ form (bronchioalveolar carcinoma) is a variant that spread along alveolar surfaces and shows no stromal invasion or pleural involvement; better prognosis that classical form Minimal invasive form with a lepidic peripheral growth pattern is associated with a better prognosis than the classical form

adenocarcinoma

occurs in smokers, more common in males Production of cytoplasmic keratinpearls and intercellular bridges corresponding to desmosomes and tonofilaments Tumors tend to be central and bulky with central cavitary necrosis Atypical form invades the superior sulcus and may present with superior vena cava syndrome Production of parathyroid-like peptide leading to hypercalcemia

squamous cell carcinoma

occurs in smokers Arises from endogenous neuroendocrine cells and is associated with aggressive clinical behavior, disseminated spread, and poor survival Tumors have dense core neurosecretory granules that may secrete hormonally active factors leading to paraneoplastic syndromes Production of ACTH resulting in Cushing’s syndrome Production of ADH leading to hyponatremia Commonly presents with advanced disease and distant spread Tumor staging divided into localized and disseminated or may follow staging for non-small cell types Responsive to chemo and radiation, but mean survival is one year after diagnosis

small cell undifferentiated carcinoma

occurs in smokers Undifferentiated carcinomas Tumors may present centrally and have cytologically large bizarre tumor cells, malignant giant cells, or clear cells

large cell carcinoma

Extravasation of fluid as a result of increased pressure gradient Contains low protein and low LDH Contains normal cell count and chemistry Almost always benign Heart failure, liver failure, nephrotic syndrome, peritoneal dialysis, trapped lung, lung entrapment

transudative pleural effusion

Extravasation of fluid due to inflammation Contains high protein and LDH levels Cell count and chemistry are almost always abnormal Pneumonia, malignancy, collagen vascular disease, pancreatitis, pulmonary embolism, post cardiac surgery Must meet one of the following Light criteria: PF/serum protein ratio > 0.5; PF/serum LDH ratio > 0.6; PF, LDH ratio > 2/3 normal (these criteria are sensitive but nor specific)

exudative pleural effusion

Parapneumonic in 60% of cases, may be a complication of thoracic surgery or due to trauma, esophageal performation, thoracocentesis Stages of development: Exudative phase: sterile exudative fluid in the pleural space Fibroproliferative phase: fibrinous sheath with septation and microorganisms Organization phase: inelastic fibrinous material along the pleural lining Most empyemas involve anaerobes; staph aureus, Legionella, strep pneumo are less common causes Pleural fluid: low pH, low glucose, high LDH, bacteria on gram stain, bacterial growth on culture Treatment requires drainage and long term antibiotics, surgery may be considered

empyema

Most common cause Increased amounts of fluid in the lung interstitial spaces exit across the visceral pleura Bilateral in >70%, if unilateral it is more commonly on the right N-Pro BNP > 1500 in pleural fluid (diagnostic) Treat with diuretics may appear as an exudate after treatment with diuretics

pleural effusion due to heart failure

Occurs in less than 5% of patients with liver cirrhosis and ascites, could be a transudate or exudate Direct movement of peritoneal fluid through small opening in the diaphragm into the pleural space Right sided in 70% Frequently large enough to produce severe dyspnea Treat underlying liver disease

pleural effusion due to hepatic hydrothorax

Most common cause of exudative effusion in US Due to inflammation caused by bacterial pneumonia Empyema = grossly purulent effusion Unless contraindicated the fluid should be sampled/analyzed Aggressive drainage is needed if one of the following criteria is met pH = 7.2, pus, positive smear/culture, loculated effusion, large size, low glucose, LDH>1000 Treat pneumonia and drain fluid if needed

pleural effusion due to parapneumonic effusion

Most commonly in lung cancer, breast cancer, and lymphoma Usually presents with dyspnea Para malignant effusion = nonmalignant effusion in a patient with a known malignancy and is usually due to lymphatic obstruction Pleural fluid cytology: if negative and still suspicious treat with thoracocentesis and check cytology, is negative again pleuroscopy Lymphocytic predominant fluid Treat symptoms

pleural effusion due to malignant effusion

Almost always exudative effusion Usually serosanguinous and small in size CT angiogram to diagnose Treat underlying disease

pleural effusion due to pulmonary embolism

Hypersensitivity to tuberculous protein in the pleural fluid Usually seen with primary TB Presents with fever, weight loss, cough, pleuritic chest pain Culture fluid, PCR for TB, pleural biopsy, adenosine deaminase likely > 40 Unlikely to see high percentage of mesothelial cells Usually see bloody fluid, very low glucose, lymphocyte predominant fluid Treatment includes drainage of pus and TB medications

pleural effusion due to TB infection

Exudate with triglyceride level > 110 pleural fluid is milky white Usually due to trauma or malignancy Treat underlying condition, pleuro-peritoneal shunt

chylothorax

Hematocrit in fluid >/= 50% of the hematocrit of the blood Most common cause is trauma Fluid should be drained, surgery if severe

hemothorax

Almost exclusively in smokers Tall, thin, young individuals (more commonly male) Sudden onset of unilateral chest pain, often with dyspnea Due to superficial blebs (cystic airspaces underneath the visceral pleura) Occasionally resolves spontaneously but may need drainage, surgery on second episode Supplemental O2 may expedite resolution of small PTX There is up to a 50% chance of recurrence, stop smoking CXR for diagnosis

primary spontaneous pneumothorax

Occurs later in life Common causes include COPD, asthma Sudden onset of unilateral chest pain often with dyspnea CXR for diagnosis Almost always requires intervention: chest tube, surgery

secondary spontaneous pneumothorax

The pressure of the pleural space remains positive throughout the breathing cycle causing: Increase pressure in the chest cavity Decrease venous return to the heart Mediastinal shift to the contralateral side Hypotension and shock Difficulty breathing Often in the setting of mechanical ventilation or CPR may be due to blunt or penetrating trauma Treat with chest tube (medical emergency)

tension pneumothorax

Most common manifestation of asbestos exposure Focal, irregular, raised, white lesions on the parietal and rarely the visceral pleura Most likely formed as a result of reaction of mesothelial cells to asbestos fibers Plaques grow slowly and almost never turn into a malignant lesion PFTs show slow decline in FVC There is no treatment only surveillance

pleural plaque

Malignant tumor arising from the mesothelial layer of the pleura Most are related to asbestos exposure (long delay between exposure and cancer) Causes pleural effusion, has a poor prognosis Treatment is chemotherapy and sometimes surgery

mesothelioma

Usually due to esophageal perforation and less commonly due to post mediastinal surgery Fever and chest pain are most common symptoms Patients appear ill especially in esophageal rupture CXP is imaging of choice Surgical drainage/repair of the esophagus with antibiotics

acute mediastinitis

Usually due to TB or histoplasmosis, other less common causes include sarcoidosis and other fungal diseases Symptoms are related to compression of other organs (blood vessels or airways) Except for cases due to TB, there is no other standard treatments for this condition

chronic mediastinitis

Gas in the interstices of the mediastinum ``` Causes: Rupture of the alveoli Perforation of the trachea or esophagus Dissection of the air from the neck Iatrogenic Strenuous exercise ``` substernal chest pain CXR and CT for diagnosis Usually no need for therapy

pneumomediastinum

decreased breathing sounds increased vocal/tactile fremitus decreased tympanic percussion

consolidation

decreased breathing sounds decreased vocal/tactile fremitus decreased tympanic percussion

effusion

decreased breathing sounds decreased vocal/tactile fremitus increased tympanic percussion

pneumothorax

50-60 years old Peak incidence in midwinter, early spring Majority have underlying chronic disease: COPD, CAD, diabetes, alcohol abuse Causes: strep pneumo is the most common cause, H. flu, Staph aureus, Legionella, Klebsiella Symptoms: sudden onset of shaking chills, pleuritic chest pain, productive cough Clinical presentation: mild to moderate hypoxemia, tachycardia, tachypnea, ronchi Labs: leukocytosis, positive blood cultures, focal consolidation on CXR

Acute community acquired pneumonia

More common in adolescents and young adults, most are less than 40 Mild presentation, prolonged symptoms Causes: Mycoplasma, Chlamydophila, Legionella, Chlamydia psittaci, Franciscella tularensis, Coxiella burnetti Symptoms: low grade fever, nonproductive cough mild dyspnea Labs: low WBC, CXR with patchy infiltrates

atypical pneumonia

Pleural effusion that arises as a result of pneumonia Uncomplicated, complicated, or empyema Thoracentesis for effusion > 10mm on lateral decubitus CXR

parapneumonic effusion

Hospital acquired, ventilator associated Second most frequent hospital acquired infection, highest mortality Results from colonization of oropharynx with pathogen organism followed by aspiration Risk factors: age >70, underlying disease, malnutrition, comordibities, acidosis, ventilator support, sedatives, narcotics, steroids Most due to gram negative bacilli (pseudomonas, klebsiella, Enterobacter, serratia), MRSA is increasingly common, almost never anaerobic bacteria

healthcare associated pneumonia

Occurs with an abnormal gag reflex or swallowing reflex – stroke, neurologic disease, dementia Majority of events are silent Chemical pneumonitis, bronchial obstruction or bacterial aspiration pneumonia Anaerobic bacteria and mixed infections most common

aspiration pneumonia

CAP, atypical, aspiration, and HCAP More unique pathogens: Aspergillus, Cryptococcus, Mucormycosis, Nocardia, Rhodococcus

pneumonia in the immunocompromised host

Most common cause of bacterial pneumonia Fevers, shaking chills, pleuritic chest pain, rusty colored sputum Elevated WBC, 20% have positive blood culture, 70% have positive urinary test CXR: lobar consolidation Complications: sinusitis, otitis media, endocarditis, meningitis, parapneumonic effusion/empyema Treatment: ceftriaxone, PCN if sensitive, azithromycin, doxycycline Vaccinate: 65+, chronic disease, alcoholism, splenic dysfunction, HIV, military recruits, prisoners, nursing home residents Revaccinate 5-10 years

pneumococcal pneumonia

Most common cause of lower respiratory tract infection in young adults Sore throat, nonproductive cough, headache, bulbous myringitis, low grade fever, mild dyspnea CXR appears worse than clinical findings Diagnosis is clinical and confirmed by serology Treatment: azithromycin, doxycycline

Mycoplasma pneumoniae pneumonia

Exposure to aqueous environments High fever, cough, GI symptoms, headache, temperature/pulse deficit, hyponatremia CXR: focal/multi lobar pneumonia, cavitation may occur Rapid progression Diagnosed with urinary test, sputum culture on BYCE, PCR, serology Treatment: fluoroquinolones or macrolides

Legionella pneumonia

Chronic necrotizing pneumonia Associated with alcohol, cancer, diabetes, COPD Sudden onset of prostration and toxemia Fever, chest pain, dyspnea, hemoptysis, thick currant jelly sputum Bulging fissure sign on CXR due to increased mucoid production Treatment: PCN with beta lactamase inhibitor, fluoroquinolones

Klebsiella pneumonia

Increasingly recognized as a cause of pneumonia in adults; before vaccination, common in children Associated with COPD and alcoholism Fever, chills, cough, purple sputum Pleural effusion is common Encapsulated strains are more virulent, beta lactamase production is common Treatment: PCN, fluoroquinolones

Heamophilus influenzae pneumonia

May cause CAP, often causes HCAP Primary: Following viral infection (flu) or hospital acquired infection Secondary: Hematogenous spread with multiple pulmonary nodules Fever, multiple rigors, dyspnea cough, purple sputum Cavitations due to PVL cytotoxin Treatment: linezolid, vancomycin

MRSA pneumonia

Caused more pneumonia before antibiotics, rarely causes pneumonia today Associated with preceding viral illness (flu, measles) Outbreaks associated with military training and nursing homes Frequent complication is empyema

Streptococcus pyogenes pneumonia

Viruses cause 15-50% of all pneumonias RSV is the most common cause of pneumonia in children Influenza Adenovirus – children, military Corona virus CMV – transplant patients Human metapneumovirus, HSV, VZV (less common) Risk factors: immunosuppression Treatment: supportive, antivirals

viral pneumonia

Mostly in patients with advanced immunosuppression HIV CD4 less than 50; neutropenia and broad spectrum antibiotics; high dose steroids, chronic granulomatous disease Definitive diagnosis requires biopsy showing hyphal invasion of tissue Usually fatal without neutrophil recovery Treatment: voriconazole, echinocandin, reduce immunosuppression, often prolonged treatment

invasive pulmonary aspergillosis

Seen in defective T cell immunity (HIV with CD4 less than 200), chronic steroid use, hematologic malignancy, BM transplant, chemotherapy Interstitial infiltrates on CXR, ground glass opacities Wright Giemsa stain or silver stain of cysts on induced sputum or bronchoalveolar lavage Treatment: TMP-SMX

pneumocystis jirovecii pneumonia

Transmitted through airborne bacilli that are ingested by alveolar macrophages which carry bacilli to the regional lymph nodes resulting in granulomatous formation Children, AIDS patients more likely to develop pneumonia in the middle and lower lobes with hilar LAD Adolescents and adults more likely to have apical infiltrates with cavitation but no LAD Pulmonary TB, early infection is asymptomatic, later symptoms are nonspecific (weight loss, fatigue, fever, chills, night sweats, productive cough, hemoptysis) Labs: normochromic, normocytic anemia, mild leukocytosis with monocytosis, hypercalcemia Diagnosis: acid fast staining, culture on LJ agar, DNA probes Treatment: rifampin, isoniazid, ethambutol, pyrazinamide

Mycobacterium tuberculosis

diffuse damage to the alveolar-capillary interface, leakage of protein rich fluid causing edema and formation of hyaline membranes in alveoli hypoxemia and cyanosis with respiratory distress white-out on CXR etiology: sepsis, infection, shock, trauma, aspiration, pancreatitis, DIC, HSR, drugs activation of neutrophils causes protease mediated and free radical mediated damage of pneumocytes treatment addresses the underlying cause, ventilation with PEEP recovery may be complicated by interstitial fibrosis due to the loss of type II cells and therefore decreased renewal ability

Acute Respiratory Distress Syndrome

respiratory distress due to inadequate surfactant levels increasing respiratory effort after birth tachypnea, use of accessory muscles, grunting hypoxemia with cyanosis diffuse granularity on CXR associated with premature birth, C-section delivery, and maternal diabetes increased risk of patent ductus arteriosus adn necrotizing enterocolitis supplemental O2 treatment increases risk of free radical injury

Neonatal Respiratory Distress Syndrome

interstitial fibrosis exposure to beryllium - miners, aerospace industry non-caseating granulomas in the lung, hilar lymph nodes, and systemic organs associated with an increased risk for lung cancer

berylliosis

fibrosis of lung interstitium cyclical lung injury involving TGF-beta released from injured pneumocytes resulting in fibrosis exclude drugs/radiation as a cause progressive dyspnea, cough, fibrosis on CT treatment is lung transplant

idiopathic pulmonary fibrosis

non-smoking related well differentiated tumor of neuroendocrine cells polyp like mass in the bronchus, low grade malignancy chromogranin positive

carcinoid tumor

subtype of adenocarcinoma, not related to smoking columnar cells grow along the bronchus and alveoli, arise from Clara cells peripheral presents with pneumonia like consolidation good prognosis

bronchioalveolar carcinoma

week 1 Rapid onset of respiratory failure in a patient with risk factors Arterial hypoxemia is refractory to treatment with supplemental O2 Radiologic findings are indistinguishable from cardiogenic pulmonary edema – bilateral infiltrates that may be patchy or asymmetric and may include pleural effusions CT shows alveolar filling, consolidation, and atelectasis in dependent lung zones Bronchoalveolar lavage indicates even the radiologically spared zone may be inflamed Diffuse alveolar damage with neutrophils, macrophages, RBCs, hyaline membranes, and protein risk edema fluid in alveolar space, capillary injury, disruption of alveolar epithelium

acute or exudative stage of ARDS

weeks 1-3 Persisitant hypoxemia, increase alveolar dead space, and a decrease in pulmonary compliance Pulmonary hypertension due to obliteration of the pulmonary capillary bed may be severe and may lead to right ventricular failure CXR: linear opacities, consistent with the presence of evolving fibrosis Pneumothorax may occur but the incidence is only 10-13% CT: diffuse interstitial opacities and bullae Fibrosis and acute and chronic inflammatory cells and partial resolution of the pulmonary edema

Proliferative or Fibrosing Alveolitis stage of ARDS

weeks 3-4 Alveolar edema and inflammatory exudates are converted to extensive alveolar duct and interstitial fibrosis Acinar architecture is markedly disrupted, leading to emphysema like changes with large bullae Intimal fibroproliferation in the pulmonary microcirculation leads to progressive vascular occlusion and pulmonary hypertension Physiologic consequences include an increased risk of pneumothorax, reductions in lung compliance, and increased pulmonary dead space Resolution is achieved by active transport of sodium and chloride from the distal airspaces into the lung interstitium. Water follows passively through transcellular water channels on type I cells Type II cells serve as the progenitors for reepithelialization of the alveolar epithelium Resolution of inflammatory infiltrate and fibrosis is unclear Apoptosis is thought to be a major mechanism for the clearance of neutrophils from sites of inflammation and from the injured lung

Recovery or fibrosis stage of ARDS

Pulmonary Diseases Flashcards

(77 cards)