Pulmonology Flashcards
(251 cards)
1
Q
What is the most common cause of rhinitis?
A
rhinovirus
- non enveloped RNA virus
- attaches to ICAM-1-R (CD54) on respiratory epithelial cells
2
Q
What sets allergic rhinitis apart from viral rhinitis?
A
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
3
Q
What are nasal polyps?
A
protrusions of edematous, inflamed nasal mucosa
4
Q
What three conditions may present with nasal polyps?
A
- 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
5
Q
What is aspirin-intolerant asthma?
A
a triad of asthma, aspirin-induced bronchospasms, and nasal polyps
6
Q
Angiofibroma of the Nasopharynx
A
- a benign tumor of nasal mucosa
- composed of large blood vessels and fibrous tissue
- presents with profuse epistaxis
- really only seen in adolescent males
7
Q
Nasopharyngeal Carcinoma
A
- 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
8
Q
What is the most common cause of epiglottis?
A
Haemophilus influenza Type B
- encapsulated strain
- incidence decreased due to vaccines against polysaccharide B capsule
9
Q
Acute Epiglottitis
A
- 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
10
Q
Croup
A
- 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
11
Q
What is the most common cause of Croup?
A
parainfluenza virus
- enveloped RNA virus
- type 1 most common
12
Q
Singer’s Nodule
A
- 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
13
Q
Laryngeal Papilloma
A
- 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
14
Q
Laryngeal Carcinoma
A
- 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
15
Q
What causes pleuritic chest pain in those with pneumonia?
A
bradykinin and PGE2 released by the inflammatory response sensitize pleural sensory nerves and when breathing stretches the pleura, there is a pain sensation
16
Q
What is pneumonia?
A
an infection of the lung parenchyma
17
Q
What are the three classic patterns of pneumonia?
A
- lobar pneumonia
- bronchopneumonia
- interstitial pneumonia
18
Q
How does pneumonia present?
A
- 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
19
Q
Lobar Pneumonia
A
- 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
20
Q
Lobar pneumonia is most often due to what organisms?
A
bacterial, specifically
- Strep pneumo: gram (-) lancet-shaped diplococci, a-hemolytic
- K. pneumoniae: gram (-) rod-shaped
21
Q
What are the four phases of lobar pneumonia?
A
- 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
22
Q
What are red and grey hepatization of the lungs?
A
- 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
23
Q
What is the most common cause of community-acquired pneumonia?
A
Streptococcus pneumoniae
- gram (-) lancet-shaped diplococci, a-hemolysis (green)
24
Q
What are the two most common organisms found in secondary pneumonia? (Pneumonia superimpose on comorbid factors)
A
1) Streptococcus pneumoniae
- gram (-) lancet-shaped diplococci, a-hemolytic
2) S. aureus
- gram (+), coag (-), yellow-pigment producing
25
What is secondary pneumonia?
a bacterial pneumonia superimposed on a viral upper respiratory tract infection
26
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
27
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
28
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)
29
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)
30
Which organisms commonly cause a pneumonia superimposed on COPD?
Viral (more common)
- RSV
- influenza
- parainfluenza
Bacterial
- H. influenzae
- Moraxella catarrhalis
- strep pneumoniae
- Legionella pneumoniae (?)
31
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
32
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)
33
What is the most common cause of atypical pneumonia?
Mycoplasma pneumoniae
34
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
35
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
36
What is the most common cause of atypical pneumonia in infants?
respiratory syncytial virus
37
What is the most common cause of pneumonia in post-transplant patients?
CMV
38
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
39
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)
40
What are the most common causes of lobar, broncho-, and atypical pneumonias?
- lobar: Strep pneumo
- bronchopneumonia: S. aureus
- interstitial: Mycoplasma pneumoniae
41
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
42
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
43
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
44
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)
45
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
46
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
47
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
48
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
49
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%
50
To what disease do the terms "blue bloater" and "pink puffer" refer to?
- blue bloater: chronic bronchitis
| - pink puffer: emphysema
51
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
52
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
53
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
54
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
55
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
56
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
57
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
58
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
59
What are Curschmann spirals?
spiral-shaped mucus plugs that often come up in the productive cough of an asthmatic
60
What are Charcot-Leyden crystals?
crystalized aggregates of major basic protein found in the mucous of an asthmatic
61
Name two important microscopic findings that can help identify asthmatics.
- Curschmann spirals (mucous plugs)
| - Charcot-Leyden crystals (crystallized MBP)
62
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
63
Bronchiectasis has what long-term complications?
- cor pulmonale (isolated right heart failure)
| - secondary amyloidosis
64
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
65
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
66
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
67
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
68
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
69
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
70
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
71
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
72
What are the features of Caplan syndrome?
- coal worker's pneumoconiosis
| - rheumatoid arthritis
73
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
74
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
75
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
76
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
77
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
78
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
79
What qualifies as pulmonary hypertension?
- normal = 10 mmHg
| - HTN > 25 mmHg
80
How does pulmonary hypertension present?
begins with exertional dyspnea and progresses to cyanosis and right-sided heart failure
81
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
82
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
83
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
84
Primary pulmonary hypertension is associated with what genetic change?
an inactivating mutation of MBPR2, which allows for proliferation of vascular smooth muscle
85
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
86
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
87
What are alveolar hyaline membranes?
a combination of protein-rich edema and necrotic epithelial cells that line alveoli and contribute to respiratory distress syndromes
88
Which cells produce surfactant in the lungs?
type II pneumocytes
89
What is the primary component of lung surfactant?
dipalmitoylphosphatidylcholine (aka lecithin)
90
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
91
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
92
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
93
What are the three most significant risk factors for lung cancer?
- cigarette smoke
- radon
- asbestos
94
What are the two most mutagenic carcinogens in cigarette smoke?
- polycyclic aromatic hydrocarbons
| - and arsenic
95
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
96
If you identify a patient with a coin lesion in their lungs, what should the next step be?
compare it to an earlier CXR
97
What are some causes of a benign coin lesion in the lungs?
- TB
- fungus, especially Histoplasmosis in the Midwest
- bronchial hamartoma
98
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
99
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
100
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
101
What is a chromogranin stain used for?
to identify poorly differentiated neuroendocrine cells
102
Squamous Cell Carcinoma of the Lung
- a non-small cell carcinoma of the lung
- arises form squamous epithelium and as such, it typically has keratin pearls or intercellular bridges (stretched desmosomal connections)
- it is the most common tumor in male smokers
- it is usually a central tumor
- it is most frequently associated with production of PTHrP
103
Adenocarcinoma of the Lung
- a non-small cell carcinoma of the lung which contains glands or mucin
- it is the most common tumor in non-smokers and female smokers
- it is usually found at the periphery of the lung
104
Large Cell Carcinoma of the Lung
- a non-small cell carcinoma of the lung that is composed of poorly differentiated large cells
- it lacks keratin pearls, intercellular bridges, glands, or mucin and thus immunohistochemistry is needed to further classify it
- it may secrete B-hCG
- it has a poor prognosis
- strong association with smoking
105
Bronchoalveolar Carcinoma
- a non-small cell carcinoma and subtype of adenocarcinoma of the lung which grows along bronchioles and alveoli
- it arises from Clara cells and is not related to smoking
- it often presents with pneumonia-like consolidation on CXR
- it has an excellent prognosis
106
Carcinoid Tumor of the Lung
- a non-small cell tumor of the lung composed of well-differentiated neuroendocrine cells (chromogranin positive)
- it classically forms a polyp-like mass in the bronchus
- a low-grade malignancy that rarely causes a carcinoid syndrome
107
What are the most common sources of metastases to the lung?
breast and colon carcinoma
108
Local invasion of a lung cancer is likely to cause what syndromes or symptoms?
- superior vena cava syndrome if the SVC is obstructed
- hoarseness if the recurrent laryngeal nerve is involved
- diaphragmatic paralysis if the phrenic nerve is involved
- Horner syndrome if the sympathetic chain is involved
- shoulder pain and hand weakness if the branchial plexus is involved
109
Superior Vena Cava Syndrome
- a syndrome that results from obstruction of the SVC by an invasive lung cancer or thrombosis related to an indwelling catheter
- impairs drainage from the head, neck, and upper extremities, which manifests as facial plethora, JVD, and upper extremity edema, respectively
- may cause intracranial pressure to rise, leading to headaches, dizziness, and risk of aneurysm or arterial rupture
110
What is a Pancoast tumor?
a lung cancer that involves the superior sulcus of the lung and often involves the sympathetic chain, causing Horner syndrome, or the brachial plexus, causing shoulder pain and hand weakness
111
What is unique about the metastasis of lung cancer?
- it uniquely spreads to the adrenal gland
| - also likes to go the brain, bone, or liver
112
Tension Pneumothorax
- due to a penetrating chest wall injury
- air enters but cannot exit the pleural space, pushing the trachea to the side opposite the injury
- presents with diminished breath sounds, dyspnea, unilateral chest expansion, reduced tactile fremitus, and hyper-resonance
113
What are the symptoms of mesothelioma?
- recurrent pleural effusions
- dyspnea
- chest pain
114
What are the five stages of lung development?
- embryonic
- pseudoglandular
- canalicular
- saccular
- alveolar
115
How does lung development begin?
with development of a lung bud from the distal end of the respiratory diverticulum in week 4
116
What happens during the embryonic stage of lung development?
the lung bud forms the trachea and divides into the mainstream bronchi, secondary (lobar) bronchi, and tertiary (segmental) bronchi
117
What happens during the pseudoglandular stage of lung development?
terminal bronchioles form from endodermal tubules and a modest capillary network surrounds these structures
118
What happens during the canalicular stage of lung development?
terminal bronchioles differentiate into respiratory bronchioles and alveolar ducts, which are now surrounded by a more prominent capillary network
119
What happens during the saccular stage of lung development?
alveolar ducts give rise to terminal sacs which are separated by primary septae and pneumocytes begin to develop
120
What happens during the alveolar stage of lung development?
terminal sacs give rise to adult alveoli with secondary septae
121
At what point during lung development does surfactant production begin and at what point does it become sufficient?
- begins around week 28
| - sufficient levels accumulate by around week 34
122
When during the process of lung development, do the immature lungs become capable of respiration?
at week 25
123
Errors during what stage of lung development give rise to tracheoesophageal fistulas?
the embryonic stage (weeks 4-7)
124
Pulmonary Hypoplasia
- most often involves the right long
| - associated with congenital diaphragmatic hernia and bilateral renal agenesis as part of Potter sequence
125
What is a bronchogenic cyst?
- a lung defect caused by abnormal budding of the foregut
- results in dilation of terminal and large bronchi
- presents with discrete, round, sharply defined and air-filled densities on CXR
- drain poorly and cause chronic infections
126
What are type I pneumocytes?
squamous cells that line most of the alveolar surface and are thin for optimal gas diffusion
127
What are type II pneumocytes?
cuboidal, clustered cells that serve to secrete pulmonary surfactant and as the regenerative cell of the lung parenchyma, giving rise to type I and other type II cells as needed
128
What are club cells in the respiratory system?
low-columnar to cuboidal cells with secretory granules that release products necessary for the protection of the bronchiolar epithelium
129
What is the Law of Laplace?
the law that states alveoli have an increase tendency to collapse on expiration as the radius decreases
130
Describe how the airways are divided and segmented.
the first half is called the conducting zone and does not participate in gas exchange
- the trachea gives rise to the left and right mainstem bronchi
- these bronchi give rise to lobar bronchi and then segmental bronchi
- bronchi give rise to bronchioles, which in turn give rise to terminal bronchioles
the second half is called the respiratory zone and does participate in gas exchange
- it begins with respiratory bronchioles, which give rise to alveolar sacs
131
What is the conducting zone of the respiratory tree?
- it includes everything from the trachea up to and including the terminal bronchioles
- it does not participate in gas exchange, but warms, humidifies, and filters inspired air
132
What is the respiratory zone of the respiratory tree?
- it includes both respiratory bronchioles and alveolar sacs
| - it is the part of the tree that is involved in gas exchange
133
Where is the least amount of airway resistance within the respiratory tree?
within the terminal bronchioles because they have the greatest cross-sectional area
134
How far into the respiratory tree does cartilage extend?
it can be found until the end of the bronchi but is not found in the bronchioles
135
How far into the respiratory tree can goblet cells be found within the wall?
they can be found, like cartilage, until the end of the bronchi but not in the bronchioles
136
Describe the epithelium as you descend further into the respiratory tract.
- the epithelium of the trachea and bronchi is pseudo stratified, ciliated columnar; it includes goblet cells and basal cells
- the epithelium then transitions to cuboidal, ciliated cells in the bronchioles and terminal bronchioles
- in the respiratory zone, this cuboidal epithelium becomes more squamous and loses it's cilia
137
Describe where each of the following are found within the respiratory tree:
- cartilage
- goblet cells
- club cells
- pseudostratified, ciliated columnar epithelium
- cuboidal, ciliated epithelium
- squamous epithelium
- smooth muscle
- cartilage extends to the end of the bronchi
- goblet cells extend to the end of the bronchi
- club cells extend from the bronchioles to the end of the respiratory bronchioles
- pseudostratified, ciliated, columnar epithelium lines the trachea and bronchi
- ciliated, cuboidal epithelium lines the bronchioles, terminal bronchioles, and early respiratory bronchioles
- squamous epithelium lines the end of the respiratory bronchioles and the alveolar sacs
- smooth muscle extends to the end of the terminal bronchioles but becomes scarce thereafter
138
Describe the lobes/divisions of the left and right lungs.
- the left has two lobes and a lingula, leaving space for the heart
- the right has three lobes
139
What names are give to the most superior and inferior parts of the lung?
- superior: apex
| - inferior: base
140
What is the lingula of the left lung?
it is a homolog to the right middle lobe
141
Where are foreign bodies most likely to be found in the respiratory system if aspirated? Why?
the right mainstem bronchus is wider and more vertical, so foreign matter tends to be aspirated into the inferior lobe of the right lung
142
If you aspirate a peanut, where will it end up if you are upright? Supine?
- upright: enters the inferior segment of the right inferior lobe
- supine: enters the superior segment of the right inferior lobe
143
Where do the pulmonary arteries lie in relationship to other structures in each lung hilum?
RALS
- the right artery is anterior to the right bronchus
- the left artery is superior to the left bronchus
144
There are three hiatuses in the diaphragm. What passes through each and at what vertebral level does this occur?
- T8: IVC
- T10: esophagus and vagus
- T12: aorta, thoracic duct, azygos vein (at T-1-2 is the red, white, and blue)
145
How is the diaphragm innervated?
it is innervated by the phrenic nerve arising from C3, C4, and C5
146
Where does pain from diaphragm irritation refer to?
the shoulder and trapezius ridge because it is innervated by C3, C4, and C5
147
At what vertebral level does the common carotid bifurcate?
C4
148
At what vertebral level does the trachea bifurcate?
T4
149
At what vertebral level does the abdominal aorta bifurcate?
L4
150
What structures bifurcate at C4, T4, and L4?
the common carotid, trachea, and abdominal aorta, respectively
151
Define inspiratory reserve volume.
additional volume that can be inspired after a normal inspiration
152
Define tidal volume. What is a typical volume?
- the volume of air that moves into the lungs with each quiet, normal inspiration
- typically, this is 0.5L
153
Define residual volume and functional residual capacity.
- functional residual capacity is the volume remaining in the lung after a normal inspiration and expiration
- residual volume is the volume remaining in the lung after maximal expiration
154
Define inspiratory capacity.
= inspiratory reserve volume + tidal volume
| - this is the volume added form a normal expiration to maximal inspiration
155
Define expiratory reserve volume.
the volume of air that can still be breathed out after a normal expiration down to residual volume
156
Define vital capacity and total lung capacity.
- total lung capacity is the maximal volume that can be achieved (completely deflated to completely inflated)
- the vital capacity is the total functional change in volume that is possible from residual volume to maximal inspiration
157
What is physiologic dead space?
the anatomic dead space (the conducting zone) plus alveolar dead space
158
What is anatomical dead space in the lung?
the volume of the conducting zone, which is filled with air upon respiration that does not take part in gas exchange and therefore remains oxygenated
159
How is physiologic dead space calculated?
V(D) = (tidal volume) x (PaCO2 - PECO2)/PaCO2
160
What portion of the lung is the largest contributor of alveolar dead space in a healthy individual?
the apex because it is best ventilated and worst perfused
161
What is minute ventilation and how is it calculated?
- minute ventilation is the total volume of gas entering the lungs per minute
- it is calculated as = tidal volume x respiratory rate
162
What is alveolar ventilation and how is it calculated?
- it is the volume of gas per unit time that reaches alveoli
| - V(A) = (tidal volume - physiologic dead space) x RR
163
At what volume does the inward pull of the lungs balance the outward pull of the chest wall? What is the pressure in the lungs at this point?
- at functional residual capacity (end volume of a normal expiration)
- at that moment, pressure in the lungs is equal to atmospheric pressure
164
How do we define the compliance of the lung mathematically?
compliance = change in volume/change in pressure
165
What is hysteresis of the lung?
the idea that the lung inflation curve follows a different path than the deflation curve due to the need to overcome surface tension forces during inflation
166
What is the intrapleural pressure at FRC? Why is this important?
it is negative and it prevents a pneumothorax
167
What are the T and R conformations of hemoglobin?
- T is the "taut" or "deoxygenated" form and has low affinity for oxygen
- R is the "rest" or "oxygenated" form and has high affinity for oxygen
168
Name six factors that favor the T form of hemoglobin (low affinity) and shift the oxygen dissociation curve in favor oxygen unloading.
- increasing Cl- ion concentration
- acidic pH
- higher temperature
- higher CO2 levels
- higher concentrations of 2,3BPG
- higher altitude
169
How does acidic pH affect the oxygen-hemoglobin dissociation curve?
- an acidic pH favors oxygen unloading/the T conformation
- as such it shifts the hemoglobin-oxygen dissociation curve to the right so that a greater PO2 is needed for the same degree of Hb saturation
170
Methemoglobin
- an oxidized form of hemoglobin containing Fe3+, which does not readily bind oxygen but has a high affinity for cyanide
- may be induced by nitrites or benzocaine, which oxidize the iron in hemoglobin
- presents with cyanosis and chocolate-colored blood
- treated with methylene blue and vitamin C
- the blood gases will resemble those of someone with anemia because normal hemoglobin molecules are unchanged but there are effectively fewer hemoglobin molecules
171
What is induced methemoglobin a treatment for? How is it induced?
- methemoglobin has a high affinity for cyanide
- as such, if someone is poisoned with cyanide, nitrites followed by thiosulfate can be used to induce methemoglobin and treat the patient
172
How does CO affect hemoglobin?
it reduces oxygen-binding capacity and reduces oxygen unloading (shifts the dissociation curve to the left)
173
How is total blood O2 content calculated?
total content = (1.34 x Hb x SaO2) + (0.003 x PaO2) which takes into account both oxygen bound to hemoglobin and free within blood
174
Normally, 1 g of hemoglobin can bind how much oxygen?
1.34 mL
175
What is the normal oxygen content of arterial blood?
20.1 mL O2/dL of blood = (1.34 x Hb x SaO2) + (0.003 x PaO2)
176
How can CO poisoning be differentiated from anemia based on lab values?
- CO has a normal Hb concentration but low SaO2 because CO competes for Hb
- anemia on the other hand has normal SaO2 but there is less Hb
177
How do pulmonary arteries respond to hypoxia?
they constrict to divert blood flow to better oxygenated alveoli
178
Which gases are said to be "perfusion limited" in the lung and what does this mean?
- O2 (in a healthy individual), CO2, and NO2
- this means that gas equilibrates early along the length of the capillary and diffusion can be increased only if blood flow increases
179
Why is it physiologically important that oxygen is perfusion limited in the lung of a healthy individual?
because O2 is perfusion limited, there is a reserve so that when cardiac output increases and blood flow through the pulmonary capillaries increases, there is room/time for the diffusion of additional oxygen
180
Which gases are said to be "diffusion limited" in the lung and what does this mean?
- O2 (in someone with emphysema or interstitial fibrosis) and CO
- this means that gas does not equilibrate by the time blood reaches the end of the capillary and if blood flow increases, there will be no increase in gas exchange
181
Give the equation for diffusion of a gas.
V(gas) = (area)(difference in partial pressures x constant)/(alveolar wall thickness)
182
What is the alveolar gas equation?
- it is an equation that tells us the oxygen content in the alveolar space
- PAO2 = PIO2 - (PaCO2/R) = 150 - PaCO2/0.8
- R is the respiratory quotient equal to CO2 produced/O2 consumed
183
What is the normal difference between PAO2 and PaO2? Why is this important?
- normal = 10-15 mmHg
- this can help us differentiate between causes of hypoxemia that have a normal gradient (e.g. high altitude, hypoventilation) and those with an increased gradient (fibrosis, V/Q mismatch, etc.)
184
How is pulmonary vascular resistance calculated?
PVR = (pulmonary artery pressure - left atrial pressure)/CO
185
What is the difference between hypoxia and hypoxemia?
- hypoxia is poor oxygen delivery to the tissue
| - hypoxemia is a particular type of hypoxia in which PaO2 is low
186
Would would cause hypoxemia with a normal A-a gradient?
- high altitude
| - hypoventilation
187
What is the normal V/Q at the apex and base of the lung? Which is better perfused and which is better ventilated?
- the base is both better perfused and better ventilated but the ratio of ventilation to perfusion is lower so at base, V/Q = 0.6
- the apex is worse perfused and worse ventilated but the ratio of ventilation to perfusion is higher so at apex, V/Q=3
188
How does exercise affect the V/Q of the lung?
it increases perfusion and the ratio approaches 1
189
What would cause the V/Q to decrease? What would cause the V/Q to increase? How does 100% O2 affect the patient in both cases?
- V/Q might decreases if there is an airway obstruction, and this won't improve with 100% O2
- V/Q might increase if there is a blood flow obstruction (e.g. pulmonary embolism) and 100% O2 will benefit the patient
190
How does perfusion, ventilation, and V/Q compare in the apex and base of the lung?
- both perfusion and ventilation are best in the base of the lung
- however, in the apex, ventilation is reduced less and so the V/Q is higher than it is in the base
191
CO2 is transported form the tissues in what three forms?
mostly bicarb but also as carbaminohemoglobin (HbCO2) and dissolved CO2
192
Where does CO2 bind hemoglobin?
it binds at the N-terminus and promotes the T conformation, reducing O2 affinity
193
Describe how CO2 is transported in the blood.
- for the most part, CO2 in peripheral tissues combines with H2O via carbonic anhydrase within RBCs; the bicarb is shuttled out of the cell in exchange for chloride ions and travels in the blood while the proton binds hemoglobin, promoting oxygen release
- in the lung, oxygenation of Hb pushes the proton off, and the process is reversed to form CO2 which diffuses into the alveolar space and is expelled
- carbon dioxide also travels as carbaminohemoglobin with CO2 bound to the N-terminus, favoring the deoxygenated form
- and it travels as dissolved CO2, but this is minimal
194
What causes altitude sickness?
- low PIO2 reduces PAO2 and thus PaO2
- ventilation increases and PaCO2 drops
- this creates a respiratory alkalosis, which manifests as AMS
195
Why is acetazolamide used to treat AMS?
- because AMS is caused by a respiratory alkalosis as the lungs hyperventilate to increase PaO2 in response to low PIO2
- acetazolamide augments HCO3 excretion to reduce this
196
How do PaO2 and PaCO2 change in response to exercise?
- they don't change, but PvO2 decreases and PvCO2 increase
- PaO2 and PaCO2 are the same but more oxygen and carbon dioxide exchanges occurs in the capillaries so the venous blood gases are altered
197
Rhinosinusitis
- an obstruction of sinus drainage into the nasal cavity, leading to inflammation and pain over the affected area
- most often involving the maxillary sinuses, which drain into the middle meatus
- most common acute cause is a viral URI
- superimposed bacterial infections are common, including S. pneumoniae, H. influenzae, and M. catarrhalis
198
What is the most common location for an epistaxis? What kind of epistaxis is most life-threatening?
- the anterior segment of the nostril, involving the Kiesselbach plexus is most common
- those in the posterior segment involving the sphenopalatine artery, a branch of the maxillary artery, are most likely life-threatening
199
What are the three elements of Virchow's triad?
- stasis
- hyper-coagulability
- endothelial damage
200
What is the most sensitive test for a DVT? What is the imaging test of choice?
- D-dimer is highly sensitive
| - compression ultrasound is the preferred imaging modality
201
What is Homan sign?
a dorsiflexion of the foot leading to calf pain, it is indicative of DVT
202
What is the preferred imaging test for pulmonary embolism?
CT pulmonary angiography looking for filling defects
203
What two tests can be used to diagnose asthma in addition to making a clinical diagnosis?
- spirometry
| - methacholine challenge
204
What are the two types of restrictive lung diseases?
- those due to poor breathing mechanics with a normal A-a gradient
- those due to interstitial lung diseases with an increased A-a gradient
205
How do obstructive and restrictive lung diseases affect flow-volume loops?
- obstructive shifts the loop to the left (greater volumes), while altering the shape of the expiratory curve and reducing the magnitude of both inspiration and expiration
- restrictive shifts the loop to the right (lower volumes), doesn't alter the shape dramatically, and reduces the magnitude of the expiratory and inspiratory phases
206
Sleep Apnea
- repeated cessation of breathing for more than ten seconds during sleep
- this disrupts sleep and leads to daytime sleepiness
- includes obstructive sleep apnea, central sleep apnea, and obesity hypoventilation syndrome
- PaO2 is normal during the day but nocturnal hypoxia contributes to systemic and pulmonary hypertension, arrhythmias, polycythemia, and sudden death
207
Obstructive Sleep Apnea
- a type of sleep apnea associated with obesity and loud snoring
- caused by excess parapharyngeal tissue in adults or adenotonsillar hypertrophy in children
- PaO2 is normal during the day but nocturnal hypoxia contributes to systemic and pulmonary hypertension, arrhythmias, polycythemia, and sudden death
- treatment includes weight loss, use of a CPAP, or surgery
208
Central Sleep Apnea
- a form of sleep apnea defined by no respiratory effort
- this is due to CNS injury/toxicity, heart failure, or opioids
- PaO2 is normal during the day but nocturnal hypoxia contributes to systemic and pulmonary hypertension, arrhythmias, polycythemia, and sudden death
209
Obesity Hypoventilation Syndrome
- a form of sleep apnea seen in the obese
- excess weight reduces respiratory rate, which increases PaCO2 and decreases PaO2 during sleep
- PaCO2 remains elevated during the waking hours
- PaO2 is normal during the day but nocturnal hypoxia contributes to systemic and pulmonary hypertension, arrhythmias, polycythemia, and sudden death
210
What does fremitus on lung examination indicate?
consolidation such as lobar pneumonia or pulmonary edema
211
Late inspiratory crackles indicate what on lung examination?
consolidation such as lobar pneumonia or pulmonary edema
212
What is the difference between a transudate and an exudate?
- transudate: little protein content, primarily just fluid
| - exudate: high protein content, quite cloudy
213
What would cause a transudate pleural effusion or an exudate pleural effusion?
- transudate: increased hydrostatic pressure (heart failure) or decreased oncotic pressure (nephrotic syndrome, cirrhosis)
- exudate: increased vascular permeability (malignancy, pneumonia, trauma)
214
What is a chylothorax?
- a lymphatic pleural effusion due to thoracic duct injury from trauma or malignancy
- the fluid has a milky appearance and is high in triglycerides
215
Signs and symptoms of a pneumothorax.
- unilateral chest pain
- dyspnea
- unilateral chest expansion
- decreased tactile fremitus
- hyper-resonance
216
Spontaneous Pneumothorax
- primary or secondary
- primary: rupture of an apical subpleural bleb or cyst, most often in tall, thin, young males
- secondary: due to a diseased lung (often emphysema) or mechanical ventilation with use of high pressures
- results in collapse of a portion of the lung, causing the trachea to shift to the side of collapse
217
How is a lung abscess treated?
clindamycin
218
Which organisms are most commonly found in lung abscesses?
- anaerobes like Bacteriodes, Fusobacterium, or Peptostreptococcus
- S. aureus
219
Describe the histology of mesotheliomas.
- psammoma bodies can be seen
| - often stain cytokeratin and calretinin positive while most carcinomas are negative for these two markers
220
Lung cancers in general share what complications?
SPHERE
- superior vena cava syndrome
- Pancoast syndrome
- Horner syndrome
- endocrine (paraneoplastic)
- recurrent laryngeal nerve compression
- effusions, pleural or pericardial
221
What is Lambert-Eaton syndrome?
- a complication of small cell lung cancer in which antibodies are formed against pre-synaptic calcium channels
- results in weakness of the limbs
222
What is the most common primary lung cancer in these populations: male smoker, female smoker, non-smoker
- male smoker: small cell
- female smoker: adenocarcinoma
- non-smoker: adenocarcinoma
223
What is diphenhydramine? How is it used clinically? What are it's primary adverse effects?
- a first generation H1 anti-histamine
- used for allergies, motion sickness, and as a sleep aid
- adverse effects include sedation, antimuscarinic activity, and anti-a-adrenergic effects
224
What is dimenhydrinate? How is it used clinically? What are it's primary adverse effects?
- a first generation H1 anti-histamine
- used for allergies, motion sickness, and as a sleep aid
- adverse effects include sedation, antimuscarinic activity, and anti-a-adrenergic effects
225
What is chlorpheniramine? How is it used clinically? What are it's primary adverse effects?
- a first generation H1 anti-histamine
- used for allergies, motion sickness, and as a sleep aid
- adverse effects include sedation, antimuscarinic activity, and anti-a-adrenergic effects
226
What is loratadine? How is it used clinically? What are it's primary adverse effects?
- a second generation H1 anti-histamine
- used for allergies
- few adverse effects compared to first generation because it doesn't enter the CNS well
227
What is fexofenadine? How is it used clinically? What are it's primary adverse effects?
- a second generation H1 anti-histamine
- used for allergies
- few adverse effects compared to first generation because it doesn't enter the CNS well
228
What is desloratadine? How is it used clinically? What are it's primary adverse effects?
- a second generation H1 anti-histamine
- used for allergies
- few adverse effects compared to first generation because it doesn't enter the CNS well
229
What is cetirizine? How is it used clinically? What are it's primary adverse effects?
- a second generation H1 anti-histamine
- used for allergies
- few adverse effects compared to first generation because it doesn't enter the CNS well
230
What is guaifenesin? How is it used clinically?
an expectorant, which thins respiratory secretions without suppressing the cough reflex
231
What is N-acetylcysteine? How is it used clinically?
- a mucolytic, which liquefies mucus in COPD patients by disrupting disulfide bonds
- also used as an antidote for acetaminophen overdose
232
What is dextromethorphan? How is it used clinically? What are it's primary adverse effects?
- a synthetic codeine analog and an antitussive (cough suppressant)
- works by antagonizing NMDA glutamate receptors
- mild abuse potential but can treat overdose with naloxone
- may cause serotonin syndrome if combined with other serotonergic agents
233
What is pseudoephedrine? How is it used clinically? What are it's primary adverse effects?
- an alpha adrenergic agonist
- used as a nasal decongestant to reduce hyperemia, edema, and nasal congestion
- used to open obstructed eustachian tubes
- may cause hypertension or enter the CNS and cause anxiety
234
What is phenylephrine? How is it used clinically? What are it's primary adverse effects?
- an alpha adrenergic agonist
- used as a nasal decongestant to reduce hyperemia, edema, and nasal congestion
- used to open obstructed eustachian tubes
- may cause hypertension
235
What is bosentan? How is it used clinically? What are it's primary adverse effects?
- a competitive endothelin-1 receptor antagonist (ETA/ETB)
- used to reduce pulmonary vascular resistance
- may be hepatotoxic
236
What is sildenafil? How is it used clinically? What are it's primary adverse effects?
- inhibits cGMP PDE-5
- used to prolong the vasodilatory effect of nitric oxide and to treat erectile dysfunction
- may cause hypotension
237
What is epoprostenol? How is it used clinically? What are it's primary adverse effects?
- a PGI2 analog with direct vasodilatory effects on pulmonary and systemic arteries
- inhibits platelet aggregation
- used to treat pulmonary hypertension
- side affects include flushing and jaw pain
238
What is iloprost? How is it used clinically? What are it's primary adverse effects?
- a PGI2 analog with direct vasodilatory effects on pulmonary and systemic arteries
- inhibits platelet aggregation
- used to treat pulmonary hypertension
- side affects include flushing and jaw pain
239
How do first generation anti-histamines compare to second generation in uses and adverse effects?
- first generation enter the CNS so they are used for motion sickness and sleep aid but they also cause sedation for this reason
- second generation are non-drowsy because they don't enter the CNS but this means they're really only effective at treating allergies
240
List four mediations used to treat pulmonary hypertension.
- bosentan (ETA/ETB inhibitor)
- sildenafil (PDE5 inhibitor)
- epoprostenol (PGI2 analog)
- iloprost (PGI2 analog)
241
Which two beta2 agonists are orally available and long-acting for use as asthma prophylaxis?
- salmoterol
| - formoterol
242
What is fluticasone?
an inhaled corticosteroid used to treat asthma
243
What is budesonide?
an inhaled corticosteroid used to treat asthma
244
What is ipratropium? How is it used to treat pulmonary conditions?
- it is a competitive muscarinic antagonist
- used to prevent bronchoconstriction in asthmatics and patients with COPD
- available as tiotropium, the long-acting formulation
245
What is zileuton?
- a 5-lipoxygenase inhibitor that blocks formation of leukotrienes
- used in the treatment of asthma
246
What is omalizumab?
- an antibody against IgE that prevents it from binding and activating mast cells
- used primarily in allergic asthmatics with elevated IgE levels resistant to inhaled steroids and LABAs
247
Leukotriene inhibitors are best for what kind of asthma?
aspirin-induced asthma
248
What is theophylline?
- a methylxanthine, which inhibits PDE and cAMP degradation, blocks adenosine receptors in bronchial smooth muscle, and promotes diaphragmatic muscle action
- by elevating cAMP it promotes bronchodilation
- it has a narrow therapeutic index and is a very dirty drug but is also extraordinarily cheap
- used in the management of chronic asthma
- natural compound is found in coffee and chocolate
249
What is methacholine? How is it used clinically?
it is an M3 agonist used in the bronchial challenge test to help diagnose asthma
250
Describe the stages of lung development.
weeks 4-7, 5-17, 16-25, 26-birth, and 36-8 years
- embryonic: the lung bud forms and gives rise to the trachea, bronchial buds, mainstream bronchi, secondary (lobar) bronchi, and tertiary (segmental) bronchi
- pseudoglandular: terminal bronchioles form and are surrounded by a modest capillary network
- canalicular: respiratory bronchioles and alveolar ducts form, now with a more prominent capillary network
- saccular: terminal sacs form with primary septae
- alveolar: adult alveoli with secondary septae form and in utero breathing occurs
251
What effect does CO have on the hemoglobin binding curve?
it increases affinity but lowers the capacity, shifting the curve to the left and down
