Pulmonology Flashcards
What is the most common cause of rhinitis?
rhinovirus
- non enveloped RNA virus
- attaches to ICAM-1-R (CD54) on respiratory epithelial cells
What sets allergic rhinitis apart from viral rhinitis?
allergic is due to a type I hypersensitivity and thus is characterized by an inflammatory infiltrate with eosinophils as well as an association with asthma and eczema
What are nasal polyps?
protrusions of edematous, inflamed nasal mucosa
What three conditions may present with nasal polyps?
- most often due to repeated bouts of rhinitis
- if seen in children, they often indicate cystic fibrosis
- in adults they may be due to aspirin-intolerant asthma
What is aspirin-intolerant asthma?
a triad of asthma, aspirin-induced bronchospasms, and nasal polyps
Angiofibroma of the Nasopharynx
- a benign tumor of nasal mucosa
- composed of large blood vessels and fibrous tissue
- presents with profuse epistaxis
- really only seen in adolescent males
Nasopharyngeal Carcinoma
- a malignant tumor of nasopharyngeal epithelium
- associated with EBV
- classically seen in African children and Chinese adults
- presenting symptom is often cervical lymph node enlargement
- biopsy will reveal pleomorphic keratin-positive epithelial cells (poorly differentiated squamous cell carcinoma) in a background of lymphocytes
What is the most common cause of epiglottis?
Haemophilus influenza Type B
- encapsulated strain
- incidence decreased due to vaccines against polysaccharide B capsule
Acute Epiglottitis
- an inflammation of the epiglottis
- most often due to H. influenzae, type b
- presents with high fever, sore throat, drooling with dysphagia, muffled voice, and inspiratory stridor
- often find a swollen mass in the mouth/throat, which poses a risk of airway obstruction
Croup
- aka laryngotracheobronchitis
- it is an inflammation of the upper airway
- most often due to parainfluenza virus
- enveloped RNA virus; Type 1 mc
- presents with a hoarse, “barking” cough and inspiratory stridor
What is the most common cause of Croup?
parainfluenza virus
- enveloped RNA virus
- type 1 most common
Singer’s Nodule
- a nodule that arises on the true vocal cord composed of connective tissue with myxoid degeneration (tissues replaced by gelatinous or mucoid material)
- presents with hoarseness
- due to excessive use, so they are usually bilateral and dissipate with rest
Laryngeal Papilloma
- a benign papillary tumor the vocal cord due to HPV 6 and 11
- double-stranded, non-enveloped, circular DNA virus with icosahedral capsule
- usually single in adults and multiple in children
- presents with hoarseness
Laryngeal Carcinoma
- a squamous cell carcinoma arising from the epithelial lining of the vocal cord
- risk factors include alcohol and tobacco
- occasionally arise from malignant transformation of laryngeal papilloma
- presents with hoarseness, cough, and stridor
What causes pleuritic chest pain in those with pneumonia?
bradykinin and PGE2 released by the inflammatory response sensitize pleural sensory nerves and when breathing stretches the pleura, there is a pain sensation
What is pneumonia?
an infection of the lung parenchyma
What are the three classic patterns of pneumonia?
- lobar pneumonia
- bronchopneumonia
- interstitial pneumonia
How does pneumonia present?
- fever and chills
- productive cough with yellow-green or rusty sputum
- tachypnea with pleuritic chest pain
- decreased breath sounds and dullness to percussion (as air is replaced by exudate)
- crackles
- increased bronchophony, egophony, tactile fremitus
- elevated WBC
Lobar Pneumonia
- pneumonia that presents with consolidation of an entire lobe of the lung as seen on CXR
- usually bacterial, and most commonly due to Strep pneumoniae or K. pneumoniae (those with aspiration risk)
- goes through the phases of congestion (vessels + edema), red hepatization (neutrophils + hemorrhage), grey hepatization (RBC degradation), and resolution
Lobar pneumonia is most often due to what organisms?
bacterial, specifically
- Strep pneumo: gram (-) lancet-shaped diplococci, a-hemolytic
- K. pneumoniae: gram (-) rod-shaped
What are the four phases of lobar pneumonia?
- congestion: congested vessels and edema
- red hepatization: exudate, neutrophils, and hemorrhage fill the alveolar air spaces, giving the normally spongy lung a solid consistency
- grey hepatization: due to degradation of red cells within the exudate
- resolution
What are red and grey hepatization of the lungs?
- features of lobar pneumonia
- red hepatization is the process whereby the lung takes on a red, solid consistency as exudate, neutrophils, and hemorrhage fill the alveolar spaces
- grey hepatization is the change in color that follows as RBCs within the exudate are degraded
What is the most common cause of community-acquired pneumonia?
Streptococcus pneumoniae
- gram (-) lancet-shaped diplococci, a-hemolysis (green)
What are the two most common organisms found in secondary pneumonia? (Pneumonia superimpose on comorbid factors)
1) Streptococcus pneumoniae
- gram (-) lancet-shaped diplococci, a-hemolytic
2) S. aureus
- gram (+), coag (-), yellow-pigment producing
What is secondary pneumonia?
a bacterial pneumonia superimposed on a viral upper respiratory tract infection
Who is at risk for K. pneumoniae pneumonia? Why?
those who are malnourished or debilitated (e.g. nursing home residents, alcoholics, and diabetics) are most at risk because K. pneumoniae is an enteric flora that causes pneumonia when it is aspirated and these individuals have a heightened risk of aspiration
- gram (-) rod-shaped bacillus, capsular polysaccharides, urease (+), lactose-fermenting, “current jelly” sputum
What are the unique features of K. pneumoniae pneumonia and the organism itself?
- a gram-negative, immotile, urease-positive, lactose-fermenting bacteria
- presents in those with a risk for aspiration because it is an enteric flora; primarily alcoholics, nursing home residents, and diabetics
- has a thick mucoid capsule and so presents with a gelatinous sputum referred to as “currant jelly”
- often complicated by abscesses or TB-like cavitary lesions
- three A’s are alcoholics, abscesses, aspiration
Bronchopneumonia
- a form of pneumonia characterized by scattered, patchy consolidation centered around bronchioles
- often multifocal and bilateral
- typically caused by S. aureus (secondary pneumonia), H. influenzae (COPD patients), P. aeruginosa (CF patients), Moraxella catarrhalis (COPD patients), or Legionella pneumoniae (COPD/immunocompromised patients, transmitted from water source)
Those with cystic fibrosis are especially at risk for what kind of pneumonia?
P. aeruginosa bronchopneumonia
- gram (-) rod
- blue-green pus
- sweet smelling culture
- produces exotoxin A (inhibits protein synthesis through –| elongation factor 2)
- produces phospholipase C (destroy cell membrane)
- produces pyovirden, pyocyanin (helps grow in Fe-deficinect environments)
Which organisms commonly cause a pneumonia superimposed on COPD?
Viral (more common)
- RSV
- influenza
- parainfluenza
Bacterial
- H. influenzae
- Moraxella catarrhalis
- strep pneumoniae
- Legionella pneumoniae (?)
Interstitial Pneumoniae
- also known as “atypical pneumonia”
- characterized by diffuse interstitial infiltrates as seen on CXR
- presents with relatively mild upper respiratory symptoms, minimal sputum, and a low fever in contrast to other pneumonias
- more likely to be caused by a virus than lobar or bronchopneumonia
- common causes include M. pneumoniae, Chlamydia pneumoniae, respiratory syncytial virus, CMV, influenza virus, and Coxiella burnetti
Which organisms are most likely to cause a bronchopneumonia?
- S. aureus (secondary pneumonia)
- H. influenzae (COPD patients)
- P. aeruginosa (CF patients)
- M. catarrhalis (COPD patients)
- Legionella pneumoniae (COPD/immunocompromised patients)
What is the most common cause of atypical pneumonia?
Mycoplasma pneumoniae
Aspiration Pneumonia
- seen in patients at risk for aspiration (e.g. alcoholics, comatose patients, etc.)
- most often due to anaerobic bacteria in the oropharynx such as Bacteriodes, Fusobacterium, and Peptococcus
- classically results in a right lower lobe abscess
What are the unique features of Mycoplasma pneumoniae pneumonia and the organism itself?
- lack a cell wall and are therefore, gram-indeterminant; instead they have a cell membrane with cholesterol
- usually presents as an interstitial (aka atypical) pneumonia
- most often affecting young adults, especially military recruits or college students in a dorm
- may be complicated by a cold hemolytic anemia with IgM against I antigen on RBCs or by erythema multiform
- can culture on Eaton’s agar
- best treated with macrolides
What is the most common cause of atypical pneumonia in infants?
respiratory syncytial virus
What is the most common cause of pneumonia in post-transplant patients?
CMV
What are the unique features of Coxiella burnetii pneumonia and the organism itself?
- a gram-negative bacteria that won’t gram stain
- are obligate intracellular bacteria but form spore-liked structures and are spread via aerosol transmission with farm animals being a common reservoir
- causes Q fever, which can present as an atypical pneumonia with high fever, dry cough, and headache
- may be complicated by granulomatous hepatitis
Which organisms are most likely to cause an atypical, interstitial pneumonia?
- Mycoplasma pneumonia (most common, often in young adults living in confined quarters)
- Chlamydia pneumoniae (second most common cause in young adults)
- Respiratory syncytial virus (most common in infants)
- CMV (most common in immunosuppressed post-transplant patients)
- Influenza virus (common in those with pre-existing lung disease)
- Coxiella burnetii (common in farmers and vets exposed to the endospores)
What are the most common causes of lobar, broncho-, and atypical pneumonias?
- lobar: Strep pneumo
- bronchopneumonia: S. aureus
- interstitial: Mycoplasma pneumoniae
Primary Tuberculosis
- an infection due to inhalation of aerosolized M. tuberculosis
- this initial infection is known as primary TB and affects predominately the middle or lower lobes of the lungs
- although asymptomatic in most cases, primary TB will lead to a positive PPD
- the organism replicates in macrophages and may spread via the lymphatics to the hilar nodes, causing lymphadenopathy
- involvement of the hilar nodes forms a Ghon complex, which is the combination of hilar lymphadenopathy and a parenchymal, caseating granuloma in the subpleural space
- in most cases, the bacteria are walled off in these granulomas, fibrosed, and calcified, forming a Ranke complex with the infection becoming latent
- rifampin and isoniazid can be used as prophylaxis to prevent reactivation
Secondary Tuberculosis
- a symptomatic stage of TB caused by reactivation of the bacteria, typically following application of TNFa inhibitors or the onset of some other immune compromised state
- reactivated bacteria tend to involve the upper lobes of the lungs where O2 content is highest and presents with cough, hemoptysis, night sweats, and weight loss
- the hematogenous spread of progressive primary or secondary TB is known as miliary TB
- spread to the brain forms cavitary lesions known as tuberculomas; spread to the vertebral column, most often the lower thoracic or upper lumbar, is known as Pott disease
- rifampin, isoniazid, pyrazinamide and ethambutol is the preferred treatment combination
What is the difference between a Ghon focus, Ghon complex, and Ranke complex?
they are progressive stages of a TB lesion
- a Ghon focus is a small area of granulomatous inflammation
- it is said to be a Ghon complex if it also involves the adjacent lymphatics or hilar lymph nodes
- when the Ghon complex fibroses and calcifies, it becomes known as a Ranke complex
Primary TB is characterized by what type of granulomas?
caseating granulomas in the subpleural space of the lower lobe of the lung, which stain with acid-fast (AFB)
How do spirometry values change in those with an obstructive pulmonary disease?
- FVC is diminished (max expiration after maximal inspiration and forceful expiration)
- FEV1 is significantly diminished (forceful expiration in 1 sec)
- the FEV1/FVC ratio is reduced
Chronic Bronchitis
- a disease of smoking
- clinically defined as a chronic productive cough lasting at least three months per year for two or more consecutive years
- characterized by hypertrophy of the bronchial mucus glands with patients coughing up “cups of mucous” and a Reid index of >50%
- patients known as “blue bloaters” because mucus forms plugs which trap carbon dioxide
- this causes wheezing, crackles, dyspnea, hypercapnia, and a reactive polycythemia
- risk for infection and for cor pulmonale
What is the lamina propria of the respiratory tract?
it is a thin layer of connective tissue beneath the respiratory epithelium which contains many veins carrying warm blood which serves to heat inspired air
What is the purpose of the serous and mucus glands that lie beneath the lamina propria within the respiratory tract?
serous glands serve to humidify the inspired air while mucus glands secrete mucous to trap particles
What is the Reid index of the bronchial wall? What is a normal value? What does an increased value indicate?
- it is the percent of the bronchial wall thickness that is made up of mucus glands
- normally, it is <40%
- however, in those with chronic bronchitis, it expands to > 50%
To what disease do the terms “blue bloater” and “pink puffer” refer to?
- blue bloater: chronic bronchitis
- pink puffer: emphysema
Emphysema
- an obstructive pulmonary disease characterized by destruction of alveolar air sacs (balloons to grocery bags)
- loss of air sacs contributes to a loss of elastic recoil and collapse of airways during exhalation, trapping air
- due to an imbalance of protease and anti-protease activity, most often from smoking or a genetic a1-antitrypsin deficiency
- presents with dyspnea and cough with minimal sputum, weight loss due to the additional expiratory effort required, and a “barrel chest”
- often prolong inspiration while pursing their lips to assist their breathing
- CXR shows flattened diaphragm and an increase in lung field lucency
- late complications include hypoxemia and cor pulmonale
Why do airways collapse in emphysema during expiration?
- during expiration, the air moving out has a tendency to draw in the walls of the airway, collapsing the airway
- normally this is opposed by cartilage in the larger airways and elastic recoil of air sacs in smaller airways
- in emphysema these air sacs are destroyed and the smaller airways collapse as air is expired
Why do patients with emphysema prolong expiration and purse their lips?
- they purse their lips because this increases back pressure in their airways and helps prevent collapse
- pursing their lips and poor elastic recoil both contribute to a prolonged expiratory phase
How does smoking lead to emphysema?
- the pollutants in smoke lead to excessive inflammation
- this results in excess protease-mediate damage and an imbalance between proteases and anti-proteases
- as a result, air sacs are destroyed
How does smoking-related emphysema compare to emphysema caused by an a1-antitrypsin deficiency?
- smoking will cause a centriacinar emphysema that is most severe in the upper lobes (this is where the smoke goes)
- an a1-antitrypsin deficiency will cause a panacinar emphysema that is most severe in the lower lobes
A1AT (a1-antitrypsin) Deficiency
- a deficiency in the enzyme that balances protease activity
- especially in the lungs, leaving the air sacs vulnerable to destruction and leading to emphysema
- differs from smoking-related emphysema in that A1AT deficiency results in a panacinar emphysema more concentrated in the lower lobes
- liver cirrhosis may also be present as mutant A1AT accumulates in the ER of hepatocytes, which is seen as PAS-positive globules on biopsy
- normal allele is PiM and most common mutant allele is PiZ
- PiMZ heterozygotes are usually asymptomatic but have an increased risk for emphysema if they smoke
- PiZZ homozygotes are likely to develop emphysema and cirrhosis
What is the difference between being a heterozygote for a1-antitrypsin deficiency versus being a homozygote?
- heterozygotes have an increased risk for emphysema if they smoke but otherwise are unlikely to have problems
- homozygotes are likely to have significant emphysema with cirrhosis
Describe the pathogenesis of allergen-induced asthma.
- an allergen induces Th2 differentiation in susceptible individuals
- these T cells secrete IL-4, mediating IgE class switching, IL-5, attracting eosinophils, and IL-10, inhibiting a Th1 response
- upon re-exposure, the allergen leads to IgE-mediated activation of mast cells
- histamine and leukotrienes mediate the early phase of bronchoconstriction, inflammation, and edema
- major basic protein damages cells and perpetuates bronchoconstriction in the late-phase
What are Curschmann spirals?
spiral-shaped mucus plugs that often come up in the productive cough of an asthmatic
What are Charcot-Leyden crystals?
crystalized aggregates of major basic protein found in the mucous of an asthmatic
Name two important microscopic findings that can help identify asthmatics.
- Curschmann spirals (mucous plugs)
- Charcot-Leyden crystals (crystallized MBP)
Bronchiectasis
- a permanent dilatation of bronchioles and bronchi due to necrotizing inflammation with damage to airway walls
- inflammation may be the result of CF, Kartagener syndrome, tumor or foreign body, necrotizing infection, or allergic bronchopulmonary aspergillosis
- in any case, dilation of the airway reduces the velocity of airflow and makes expiration difficult
- presents with cough, dyspnea, a foul-smelling sputum, recurrent infections, and hemoptysis
- complications include hypoxemia with cor pulmonale and secondary amyloidosis
Bronchiectasis has what long-term complications?
- cor pulmonale (isolated right heart failure)
- secondary amyloidosis
What is allergic bronchopulmonary aspergillosis?
a hypersensitivity reaction to aspergillus, which leads to chronic inflammatory damage and bronchiectasis, most often in those with asthma or cystic fibrosis
What is Kartagener syndrome?
- an inherited defect of the dynein arm, which inhibits ciliary movement
- associated with sinusitis, infertility, and situs inversus
- chronic respiratory inflammation often leads to bronchiectasis
How does spirometry often change in those with a restrictive pulmonary disease?
- TLC decreases
- FEV1 decreases but FVC decreases even more
- as such, the FEV1/FVC ratio increases
How do the spirometry values of an obstructive pulmonary disease compare to those of a restrictive pulmonary disease?
- TLC is increased in those with obstruction and decreased in those with restriction
- FEV1 and FVC are decreased in both instances; however, the FEV1/FVC ratio is reduced in obstructive disease and increased in restrictive disease
Idiopathic Pulmonary Fibrosis
- a fibrosis of the lung interstitium with unknown etiology
- likely related to cyclical lung injury and mediated by TGF-B from injured pneumocytes, which induces fibrosis
- must rule out secondary causes like bleomycin, amiodarone, or radiation therapy
- presents with progressive dyspnea and cough as well as fibrosis on lung CT progressing to end-stage “honeycomb” lung
- treatment requires lung transplant
Pneumoconioses
- an interstitial lung fibrosis due to chronic exposure to specific small particles
- alveolar macrophages engulf these particles and induce fibrosis
- most common are coal workers’ pneumoconiosis, silicosis, berylliosis, and asbestosis
Coal Worker’s Pneumoconiosis
- an interstitial lung fibrosis due to chronic exposure to carbon dust, which is engulfed by alveolar macrophages, inducing fibrosis
- leads to “black lung” and diffuse fibrosis that tends to affect the upper lobes more
- is associated with rheumatoid arthritis as part of Caplan syndrome
What is anthracosis?
a form of pneumoconiosis due to mild exposure to carbon in the form of pollution, which collects in carbon-laden macrophages but does not result in clinical problems
What are the features of Caplan syndrome?
- coal worker’s pneumoconiosis
- rheumatoid arthritis
Silicosis
- an interstitial lung fibrosis due to chronic exposure to silica, which is engulfed by alveolar macrophages, inducing fibrosis
- seen in sandblasters and silica miners
- fibrotic nodules appear in the upper lobes of the lung and may resemble TB
- also increases the risk for TB and silica impairs phagolysosome formation in macrophages
- “eggshell” calcification on CXR
Berylliosis
- an interstitial lung fibrosis due to chronic exposure to beryllium, which is engulfed by alveolar macrophages, inducing fibrosis
- seen in those that work in the aerospace industry or who mine beryllium
- noncaseating granulomas can be found in the lung, hilar lymph nodes, and systemic organs (don’t confuse with sarcoidosis)
- increases the risk for lung cancer
Asbestosis
- an interstitial lung fibrosis due to chronic exposure to asbestosis, which is engulfed by alveolar macrophages, inducing fibrosis
- seen in construction workers, plumbers, and shipyard workers
- there is fibrosis of the lung and pleura, affecting the lower lobes more than the upper
- histology of these lesions reveal long, golden-brown fibers with associated iron (ferruginous bodies)
- “ivory white” calcified plaques can be seen on the pleura and on the top of the diaphragm which are pathognomonic
- increased risk for lung cancer and mesothelioma
Compare the populations, lesion distribution, and risks/complications for the four major pneuomconioses.
- coal workers: coal miners, diffuse lung fibrosis, risk for RA
- silicosis: sandblasters, fibrotic nodules in upper lobes, risk for TB
- berylliosis: aerospace workers, systemic granulomas, risk for cancer
- asbestosis: plumbers/construction workers/shipyard workers, fibrosis of lung and pleura, risk for cancer
Sarcoidosis
- a systemic disease of noncaseating granulomas
- classically seen in African American females
- likely due to a CD4 response to an unknown antigen
- granulomas are most commonly found in the hilar lymph nodes and lung, contributing to a restrictive lung disease, but can be found in any tissue
- may resemble Sjogren’s syndrome if affecting the salivary and lacrimal glands but can do a biopsy to differentiate
- presents with elevated serum ACE and hypercalcemia as the granulomas have 1-alpha hydroxylase activity and activate vitamin D; CD4/CD8 ratio is elevated in bronchoalveolar lavage fluid
- histology reveals characteristic “asteroid bodies” within giant cells of the granulomas
- treat with steroids if symptomatic
Hypersensitivity Pneumonitis
- a granulomatous reaction in the lungs to an inhaled organic antigen
- often referred to as pigeon breeder’s lung and seen in farmers/those exposed to birds
- presents with fever, cough, and dyspnea hours after exposure that resolves with removal of the exposure
- however, chronic exposure leads to interstitial fibrosis
What qualifies as pulmonary hypertension?
- normal = 10 mmHg
- HTN > 25 mmHg
How does pulmonary hypertension present?
begins with exertional dyspnea and progresses to cyanosis and right-sided heart failure
What histologic cardiovascular changes arise from pulmonary hypertension?
- atherosclerosis of the pulmonary trunk
- smooth muscle hypertrophy of pulmonary arteries with intimal fibrosis
- plexiform lesions (tufts of capillaries) are common with severe, long-standing disease
Primary Pulmonary Hypertension
- defined by MAP > 25 mmHg
- idiopathic but classically seen in young adult females
- associated with inactivating mutations of MBPR2, which leads to proliferation of vascular smooth muscle
- presents with dyspnea on exertion and right ventricle hypertrophy
- atherosclerosis of the pulmonary trunk, fibrosis of the intima of pulmonary arteries, and plexiform lesions are often seen with long-standing disease
What are the most common causes of secondary pulmonary hypertension?
- hypoxemia (e.g. emphysema)
- increased blood volume (e.g. congenital heart disease)
- recurrent pulmonary embolism
- left heart failure
Primary pulmonary hypertension is associated with what genetic change?
an inactivating mutation of MBPR2, which allows for proliferation of vascular smooth muscle
Acute Respiratory Distress Syndrome
- diffuse damage to the alveolar-capillary interface allows protein-rich fluid to leak into the alveoli, which combines with necrotic epithelial cells to form hyaline membranes
- secondary to diseases which activate neutrophils and induce protease and ROS damage of pneumocytes
- these include SPARTAS: sepsis, pancreatitis/pneumonia, aspiration, uremia, trauma, amniotic fluid embolism, shock
- importantly, the edema is non-cardiogenic and PCWP is normal
- presents with hypoxemia, cyanosis, and “white out” on CXR as the diffuse barrier thickens and air sacs collapse
- treat with positive end-expiratory pressure ventilation
- recovery may be complicated by interstitial fibrosis if type II pneumocytes can’t recover properly
Neonatal Respiratory Distress Syndrome
- respiratory distress due to inadequate surfactant levels, leading to collapse of air sacs and formation of hyaline membranes
- most often due to prematurity, Caesarian section, or maternal diabetes
- presents with increasing respiratory effort after birth, tachypnea with use of accessory muscles, grunting, hypoxemia with cyanosis, and diffuse granularity of the lung on CXR
- increases risk for PDA, necrotizing enterocolitis, and respiratory acidosis
- treat with supplemental oxygen; however, this may induce free radical injury of the retina, leading to blindness (called retinopathy of prematurity), or lung, leading to bronchopulmonary dysplasia
What are alveolar hyaline membranes?
a combination of protein-rich edema and necrotic epithelial cells that line alveoli and contribute to respiratory distress syndromes
Which cells produce surfactant in the lungs?
type II pneumocytes
What is the primary component of lung surfactant?
dipalmitoylphosphatidylcholine (aka lecithin)
How do prematurity, Caesarian section, and maternal diabetes contribute to neonatal respiratory distress syndrome?
- prematurity means that surfactant hasn’t had time to reach adequate levels yet
- C-section reduces the stress of delivery and therefore the release of stress-induced steroids which normally promote surfactant production and release
- maternal diabetes leads to excess insulin produced by the child, which inhibits surfactant production
When does surfactant production in a fetus begin and when does it reach adequate levels?
- begins at 28 weeks
- adequate levels are reached around week 34
What is an L/S ratio? What information does it provide about a developing fetus?
- it is the ratio of phosphatidylcholine (lecithin) to sphingomyelin
- during pregnancy sphingomyelin levels remain constant but lecithin increases as surfactant production begins
- when the ratio > 2, it indicates adequate levels of surfactant have been produced to sustain respiration after birth
What are the three most significant risk factors for lung cancer?
- cigarette smoke
- radon
- asbestos
What are the two most mutagenic carcinogens in cigarette smoke?
- polycyclic aromatic hydrocarbons
- and arsenic
How does radon form and where is it found?
- radon forms from radioactive decay of uranium, which is present in the soil
- it accumulates in closed spaces such as basements and is odorless
If you identify a patient with a coin lesion in their lungs, what should the next step be?
compare it to an earlier CXR
What are some causes of a benign coin lesion in the lungs?
- TB
- fungus, especially Histoplasmosis in the Midwest
- bronchial hamartoma
What is a bronchial hamartoma?
a benign mass of disorganized lung tissue and cartilage, which often appears as a coin lesion on CXR after it calcifies
How are lung carcinomas divided? Why is this clinically important?
- small cell carcinomas are not amenable to surgical resection and are thus treated with chemo and radiation
- non-small cell carcinomas are usually amenable to surgical resection
Small Cell Carcinoma of the Lung
- a malignant tumor of the lung composed of small, poorly differentiated neuroendocrine cells (stain chromogranin positive)
- seen in male smokers
- usually a central tumor
- associated with several endocrine and nervous system paraneoplastic syndromes: ACTH, SIADH, Lambert-Eaton syndrome, and other antibody-mediated conditions (paraneoplastic myelitis, encephalitis, subacute cerebellar degeneration)
- common to have amplification of myc oncogenes
- not usually amenable to surgical treatment
