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148 Cards in this Set

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  • Back
What is the disease process of someone who has an extended expiratory phase?
Obstructive lung disease
A tall, think male teenager has an abrupt-onset dyspnea and left-sided chest pain. There is hyperresonant percussion on the affected side. Breath sounds are diminished.
What is the diagnosis?
Spontaneous pneumothorax.
A young man is concerned about his wife's inability to conceive and her recurrent URIs. She has dextrocardia.
What protein is deficient?
What are the cells of the lungs?
Where do you find them?
Pseudocolumnar cilliated cells extend to the resp bronchioles
goblet cells extend only to the terminal bronchioles
Type I alveolar cells 97%
Type II alveolar cells 3%- secrete surfactant. Type II in lung damage.
What can you measure in the amniotic fluid to make sure the lung is fully developed?
lecithin to sphingomyelin ration > 2.0
mature levels of surfactant
breakdown the bronchopulmonary segments
Each segment has 3ry (segmental) bronchus and 2 arteries (bronhical and pulmonary) in the center

Veins and lymphatics drain along borders.
Arteries run with Airways
what is the relationship between the pulmonary artery and the to the bronchus at each hilus?
Right Anterior
Left Superior
What structures perforate the diaphragm? And at what level?
I 8 10 EGGs AT 12

T10- esophagus, vagus
T12: aorta, thoracid duct, azygous vein (red, white, blue)
What are the muscles of respiration? Normal breathing and excercise?
Insp- diaphragm
Exp- passive
Insp- external intercostals, scalene muscles, sternomastoids
Exp- rectus abdominis, internal and external obliques, transversus abdominis, internal intercostals.
Define the following:
Tidal volume
Inspiratory reserve volume
Expiratory Reserve volume
Residual volume
Functional Residual Capacity
Inspiratory capacity
Vital capacity
Total Lung Capacity
Forced expiratory Volume
Dead space (anatomic and physiologic)
TV- volume inspired and expired on a NORMAL breath
IRV- volume that can be inspired over and above the tidal volume
ERV- volume that can be expired after the tidal volume
Residual Volume- what's left after maximum expiration (not measurable by spirometry)
Inspiratory Capacity- TV + IRV
Vital Capacity- From max out to max in.
Total Lung Capacity- Everything
FEV1- The amount that can be expired in the first second of a max expiration (normally 80%)
Dead space
Anatomic- teh volume of the conducting airways (150ml)
Physiologic- the volume of lung that does not participate in gas exchange
When is FEV1 increased? Decreased?
increased- obstruction
FEV reduced more than FVC (FEV/FVC is decreased)
decreased- restrictive
FEV and FVC are reduced (FEV/FVC is normal or increased)
How is dead space calculated?
Vd=Vt x (Paco2 - Peco2)/Paco2
Dead space increases with V/Q defects
How do you calculate the Ventilation Rate?
Minute ventilation= Tv x B/min
Alveiolar ventilation = Tv-Vd x B/m
Breakdown compliacne
It is the distensibility of lungs and chest wall; the change in volume given the change in pressue
inverse to elastance
Surfactant increases compliance
(slope of pressure volume curve)
When does compliance change?
emphysema- lung compliance is increase, tendency for collapse is decreased.
Higher FRC- barrel chest

Fibrosis- lung compliance is decreased, lower FRC
What is Laplace's law on the pressure in the alveolus?
large alveoli- have low collapsing pressures.
small alveoli- have high collapsing pressures
(no surfactant=atelectasis
What is primatly phospholipid of surfactant?
dipalmitoyl phosphatidylcholine (DPPC)
fetus- no surfactant until week 24 or as late as wk. 35
What is the major site of airway resistance?
medium-sized bronchi
What is the relationship between lung volume and resistance?
High- decreased resistance
Why do people with COPD use pursed lips?
expire more slowly-> prevent airway collapse
What's the difference between "pink puffers" and "blue bloaters"
Pink puffers- 1ry emphysema- mild hypoxemia, normocapnia (alveolar ventilation maintained)

Blue bloaters- severe hypoxemia w/ cyanosis, hypercapnia (not maintained alveolar ventilation)
What is the respiratory response to high altitude?
1. Acute increase in ventilation
2. Chronic increase in ventilation
3. Increase in epo-> increased Hct and Hb (chronic hypoxia)
4. Increase 2,3DPG- binds to hemoglobin to release more O2
5. Increase in mitochondria
6. Increased renal excretion of bicarb (augment by acetazolamide) compensates for resp alkalosis
7. Chronic hypoxic pulm vasoconstriction results in RVH
What are some products of the lung?
ACE- AI->AII; inactivates bradykinin
Kallikrein- activates bradykinin
What is methemoglobin?
Hb with Fe3+ instead of Fe2+. Does not bind O2
What is the difference between adult and fetal hemoglobin?
Fetal- left-shift- binds O2 better. binds DPG less.
What causes the O2-heme dissociation curve to right-shift?
Decreased O2 affinity
P50 increased

Increase in everything but pH
CADET face right
Increased Pco2/decreased pH- Exercise- decreased pH-> increased O2 delivery.
Increased T
Increased H
High altitude, increased DPG
What causes the O2-heme curve to left-shift?
Increased affinity
decreased P50

Caused by decrease in everything but pH
Decreased Pco2
Increased pH
decreased Temp
Decreased DPG
CO poisoning
What is the difference between perfusion limited and diffusion limeted ventilation?
Perfusion- (normal)- Gas equilibrates early along the length of capillary. More blood for more diffusion

Diffusion- Blood moves too fast- exercise, emphysema, fibrosis
How is CO2 handled in the blood?
90% bicarb
5% bound to hemoglobin
5% dissolved
WHat is the haldane effect?
the bohr effect?
Haldane- Ox of heme promotes CO2 dissociation. In lungs

Bohr- increase of H shifts curve to right, unloads O2. In peripheral tissue.
Compare Zones 1, 2, 3 of the lung
1- low flow; PA>Pa>Pv (compressed capillaries in hemorrage(decreased Pa) or PPV (increased PA)) High V/Q
2- medium flow; Pa>PA>Pv
3- high flow; Pa>Pv>PA; lower V/Q
What is the best V/Q? What happens in Exercise?
1 is the best.
In excercise, increased Cardiac Ouput-> apex capillary dilation-> closer to 1.
How does allergic rhinitis come about?
IgE-type I immune. Mucosal and submucosal mast cells.
What are the major causes of Acute Rhinitis?
Adenovirus- runny nose, sneeze, congestion
Allergic Rhinitis
Bacterial- Sterp, Staph, Haemophilus
What is sinusitis?
inflam o fthe paranasal sinuses- extension of nasal or dental infection.

Obstructed drainage. Acumulation of mucoid secretions or exudate
Why is it risky?
What is the most common cause?
can kill kids
H. flu
What is croup?
harsh cough and stridor
What tumors can arise in teh nose and nasal sinuses?
Nasopharyngeal carcinoma
Asia and East Africa- EBV
Squamous cell- most frequent
Adenocarcinoma- 5%
What are the tumors of the Larynx?
Singer's nodule- benign polyp- localized to true vocal cords
Laryngeal papilloma- benign neoplasm on the true vocal cords. Kids can have mult lesions caused by HPV
Squamous Cell- most common malignant tumor. Men>40; smoke and alcohol- presents with persistant hoarseness
Glottic carcinoma- true vocal cords- good prognosis.
Supraglottic adn subglottic carcinoma- less common, worse prognosis
What is the difference between Extrinsic and Intrinsic Bronchial asthma?
Extrinsic- immune- type I with IgE bound to mast cells; begins in childhood.

Intrinsic- asthma associated with chronic bronchitis and cold/exercise induced asthma. Adult life, no Hx of allergy
What are the pathologic findings in Bronchial asthma?
Bronchial smooth muscle hypertrophy
Hyperplasia of bronchial submucosal glands and goblet cells
Thickening of basement membrane
prolif of eos
Airways plugged by viscid mucus Curschmann spirals, eos, and Charcot-Leyden crystals (Eos derive)
What are the clinical correlations with asthma?
dyspnea, wheezing
cough, tachypnea
hypoxemia, pulsus paradoxus
What are the complications of Asthma?
superimposed infection, chronic bronchitis, pulm emphysema
status asthmaticus- prolonged bout of asthma that lasts for days
What are some triggers for asthma?
viral URIs
Chronic Bronchitis:
what is the clinical definition?
What are the risk factors?
What are the pathologic changes?
What is a major complication?
What are the clinical findings?
productive cugh for 3 months over 2 years.
Cigarrettes, pollution, infection, genetic factors
Hyperplasia of mucus-secreting submucosal glands
Cor pulmonale
wheezing, crackles, cyanosis
blue bloater
What are the following:
Centrilobular emphysema
Panacinar emphysema
Paraseptal empysema
Irregular emphysema
centrilobular- dilation of brioncioles
Panacinar- dilation of the acinus- alveoli, alevolar ducts, resp bronchioles, terminal bronchioles. Deficiency of alpha antitrypsin.
Paraseptal- dilation of the distal acinus- alveoli, some duct. localizes to pleura and interlobar septa. Subpleural bullae or blebs
Irregular- irregular involvement of the acinus w/ scarring w/in the wall sof enlarged spaces.
Pathologic change
Clinical Sx
Dilation of air spaces w/ destruction of alveolar walls.
increased anteroposterior diameter of chest; increaced TVC
hypoxia, cyanosis, resp acidosis
dyspnea, decreased breath soudns, tachy

pink puffer
What are the posulated causes of emphysema?
elastase action on the alveolar walls. usually neutralized by antitrypsin

Cigarettes- attract neutrophils and macros and their elastase; inactivates alpha1

Hereditary alpha1 deficiency- panacinar;
chromosome 14.
piZ allele-> Hepatic cytoplasmic droplets-> liver damage
piZZ-> cirrhosis and emphysema
what is a risk?
What part of the lung is affected?
What are the Sx
abnl permanent bronchial dilation from chronic infection w/ inflamm and necrosis
predisposed by obstruction, sinusitis (postnasal drip), Cystic Fibrosis,
rarely- Kartagener syndrome
lower lobes
copious purulent sputum, hemoptysis, pulm infections that can cause abscess
What is Kartagener syndrome
defect in cilia from a dynein arm defect. Infertility, bronchiectasis, sinusitis. W/ situs inversus no motility in resp, auditory, sperm ciliea
What is ARDS?
Diffuse alveolar damage. increase in alveolar capillary permeability; leakage of protein-rich fluid into alveoli.
intra-alveolar hyaline membrane- fibrin and debris
bad gas exchange
What can cause ARDS?
toxic agents
aspiration of gastric contents
acute pancreatitis
inhalation of chemical irritants- chlorine, o2, OD of heroin; bleomycin
What are the pathogenic factors that influence ARDS?
1. neutrophils release toxic substances to alveolar wall
2. activation of the coag cascade. microemboli
O2 toxicity mediated by the formation of o2 free radicals
What are the predisposing factors for neonatal respiratory distress syndrome?
maternal DM

Most common cause of resp failure. Most common cause of death in premature infants
What are the path findings in NRDS?
heavy lungs with areas of atelectasis alternating with dilated
small pulm vessels are engorged.
intra-laveolar hyaline membranes.
What are the complications of NRDS
Bronchopulmonary dysplasia- From O2 and mechanical ventilation
Patent Ductus from hypoxia
Intraventricular brain hemorrhage
Necrotizing enterocolitis- inflamm of intestines
What is Anthracosis?
Inhalation of carbon- no harm; carbon macros-> black patches
What is coal miner's silicosis?
inhalation of coal- carbon and silica.
Coal macules around bronchioless
no disability
fibrotic nodules with necrotic black fluid
bronchiectasis, pulm htn
What is silicosis?
inhalation of silica dust.
miners, glass, stone cutters
damage to macrophages-> inflam
silicotic nodules
what is the Rx for NRDS?
steroids for mom during pregs
surgactant for infant
What is another name for surfactant?
dipolmitoyl phophatidylcholine
What is asbestosis?
Diffuse interstitial fibrosis from asbestos fibers.
increased risk of mesothelioma adn bronchogenic carcinoma
Long latency
Ferruginous bodies in long
Ivory-white pleural plaques
Who are at risk for abestosis?
shipbuilders and plumbers
What happens when asbestosis and smoking are combined?
increased risk of bronchogenic cancer.
What fibers stane with Prussian blue?
What is the characteristic path findings?
What group is most at risk?
When does the disease occur?
Noncaseating granulomas- multiple organ systems
African Americans
Teenage or young adults.
What are the common path changes in sarcoid?
interstitial lung disease
enlarged hilar lymph nodes
anterior uveitis
erythema nodosum of the skin
What are the immune effects of sarcoid?
reduced sensitivity of skin test antigens
poly clonal hyperglobulinemia
What are the clinical abnlties in sarcoid?
Chest x-ray
1- bilat hilar lymphadenopathy
2- interstitial lung disease- defuse reticular densities
1- hypercalcemia
2- hyper gammaglobulinemia
3. increased serum ACE
Dx- biopsy
What is idiopathic pulmonary fibrosis?
chronic inflamm and fibrosis of the alveolar wall
begins with alveolitis- progresses to fibrosis, ends in a distorted fibrotic lung filled with cystic spaces (honeycomb lung
death in 5 years.
Eosinophilic granuloma?
localized proliferation of histiocytic cells like the langerhans cells- Birbeck granules.
What is 2ry pulm hypertenstion
from increased pulm blood flow- l->r shunt.
increased resistance w/in pulm circulation
embolism or vasoconstriction from hypoxia
What are some causes of pulm edema?
Increased hydrostatic pressure- LV failure or mitral stenosis
Increased alveolar capillary permeaility- inflamm alveolar reactions, ihalation of irritant gases,pneumonia, shock, sepsis, pancreatitis, uremia or OD
Miscellaneous- Rapid ascent to high altitude.
Lobar pneumonia:
most common cause
what is it characterized by?
S. pneumoniae
intra-alveolar exudate-> consolidation
may involve whole lung
most common cause
S. aureus, h.flu, klebsiella, s. pyogenes
Acute inflamm infiltrates from bronchioles into adjacent alveoli; patchy distribution involving >1 lobe
Interstitial pneumonia:
RSV, adenoviruses, M. pneumonia, legionella, chlamydia
Diffuse patchy inflamm localized to interstitial areas at alveolar walls
distribution >1 lobe
Break down the pneumonia caused by S. pneumoniae
elderly or debilitated
those with cardiopulmonary disease
can cause empyema
Break down the pneumonia caused by S. aureus
superinfection on fluo or viral
IV drug users
hospitalized, elderly, chronic lung disease

Can cause focal inflam exudates or abscess
empyema or other infectious complications
bacterial endocarditis
brain and kidney abscesses
Break down the pneumonia caused by S. pyogenes
complication of flu or measles
Klebsiella pneumonaie
Debilitated hospitalized patients and diabetic or alcoholic
High mortality in elderly
Alveolar wall damage-> necrosis. sometimes with abscess formation
Break down the pneumonia caused by H. flu
kids and infants
debilitaated adults

Can cause meningitis and epiglottitis in kids
Break down the pneumonia caused by Legionella
infection from inhalation of air-conditioning aerosol
what's special about measles and pneumonia?
giant cell pneumonia
What is the pneumonia caused by Coxiella burnetii?
Q fever
cattle, sheep or unpasteurized milk
What are the common hospital aquired pneumonias?
Klebsiella, Pseudomonas, E. coli
What bacteria cause lung abscesses?
What is Pancoast's tumor?
Carcinoma that occurs in the apex of the lung.
Cervical sympathetic plexus- Horner's (ptosis, miosis, anhidrosis)
Squamous cell carcinoma
Where is it found in the lung?
What are the characteristics?
What is the clinical presentation?
hilar mass and frequently results in cavitation
can have PTH and HyperCa
Presents as cough, hemoptysis, bronchial obstruction, wheezing, coin lesion
Small Cell Cancer:
Where is it found?
What are the characteristics?
What is the clinical presentation?
Undiffed tumor; aggressive carcinoma. Hard to cure by surg.
Usually mets at Dx. with ectopic production of corticotrophin or ADH
Can cause lambert eaton syndrome
Presents as cough, hemoptysis, bronchial obstruction, wheezing, coin lesion
Lung Adenocarcinoma
where is it found in the lung?
What are the characteristics?
Peripheral- most common
Develops on site of prior pulm inflammation
less linked to smoking
Bronchioloalveolar cancer
Where is it found in the lung?
What are the characteristics?
Peripheral- not related to smoking
columnar->cuboidal cells that line the alveolar walls.
can have multiple densities
Large Cell Carcinoma
Where is it located?
What are teh characteristics?
Has both squamous and adenocarcinoma cells.
Carcinoid tumor
Where is it located?
What are the characteristics?
major bronchi
Low malignancy, spreads by direct extension, may result in carcinoid syndrome
-flushing, diarrhea, wheezing, salivation
Metastatic carcinoma
What organs mets to the lung?
Very common
From Brain
What are the major complications of lung cancer?
Superior vena cava syndrome
Pancoast Tumor
Horner's syndrome
Endocrine- paraneoplastic
Recurrant Laryngeal symps- hoarseness
Effusions- pleural or pericardial
What is the role of LTB4?
neutrophil chemotactic agent
What is the role of LTC4, D4, E4?
broncho constriction, vasoconstriction, contraction of smooth muscle and increased vasc permeability
What is the role of PGI2?
inhibs platelet aggregation and promotes vasodilation
What is the role of Zafirlukast?
blocks the actionof leukotrienes
what is the role of montelukast?
blocks the action of leukotrienes
What is the role of Phospholipase A2?
What blocks this enzyme?
converts lipid to arachanodinic acid
Corticosteroids block it.
What is the role of lipoxygenase?
what blocks this enzyme?
converts Arachandonic Acid to Hydroperoxides for Leuko synth
What is the role of Zileuton?
blocks Lipoxygenase from forming hydroperoxides to form leukotrienes
What is the role of cyclo-oxygenase?
What blocks it?
turns Arachodonic Acid into endoperoxides which become Prostacyclin, prostaglandins, adn thromboxane

and COX-2s block
What is the role of PGE,F?
Increase uterine tone,
decrease vascular tone
decrease bronchial tone
What is the role of thromboxane?
increase platelet aggregation
increase vasc tone
increase bronchial tone
What is the difference between 1st and 2nd generation H1 blockers?
2nd generation are not as sedating
What are the clinical uses for 1st generation H1 blockers?
motion sickness
sleep aid
What are the SEs of 1st and 2nd generation H1 blockers?
What are the 1st generation H1 blockers?
What are the 2nd generation H1 blockers?
What is Isoproterenol?
Non-specific B-agonist
relaxes bronchial smooth muscle
Adverse effects-tachy
What is Salmeterol?
long-acting B2 agonist
used for prophylaxis
Adverse effects are tremor and arrhythmia
What is the mechanism of action of theophylline?
inhibs phosphodiesterase->decrease in cAMP hydrolysis-> bronchodilation
Cardiotox and neurotox
What are the SEs of theophylline?
cardiotox and neurotox
What is the mechanism of action of Ipratropium?
competative block of muscarinic receptors, prevents bronchoconstriction
What is cromolyn?
prevents release of mast cell mediators- prophylaxis of asthma.
Not good for acute
What is the role of corticosteroids in asthma?
inhibit the synth of cytokines.
inactivate NF-kB- transcription factor for TNF-a. 1st line
What is the mechanism of action of Zileuton?
blocks 5-lipoxygenase
what is the mechanism of action of Zafirlukast and montelukast?
block leukotriene receptors
What is the role of leukotrienes in asthma?
they are part of late response inflamm-> bronchial hyperreactivity
What is the role of histamine in asthma?
triggers the early response in asthma
What is the histologic presentation of an emphysematous lung?
destruction of the alveolar walls and associated capillary beds
What is a saddle embolus?
embolus from the legs that blocks the biforcation of the pulmonary trunk blocking all pulmonary circulation
non-cardiac cause of sudden death
What can cause asthma by an enhanced sensitivity to vagal stimulation?
viral URI
A hemoglobin drop would lead to what change in the blood?
a. arterial O2 content
b. arterial O2 sat
c. arterial pO2
d. CO
e. HR
f. SV
arterial O2 content
What would cause hemosiderin-laden macrophages?
pulm edema
from injestion of RBCs
What is the characteristic path of pulm edema?
proteinaceous granular precipitate
hemosiderin-laden macrophages
engorged alveolar capillaries
What is the path of pneumocystis?
hat-shaped, silver-staining cysts
What is the path of Candida?
hyphae and spores
What is the path of pulm infarction?
ischemic necrosis of alveoli
What would cause a wedge shaped opacity on x-ray?
pulm infarction
What is the histologic presentation of pneumocystic carinii?
cup shaped, crushed tennis ball
silver staining and frothy exudate
What is the histologic presentation of Cryptococcus?
encapsulated yeast- india ink
Broad-slimy capsule
What is the histologic presentation of histoplasma?
silver staining
but mainly seen in the cytoplasm of histiocytes
thin cell wall, no true capsule
What is the histologic presentation of Coccidiodes?
non-budding spherule
filled with endospores
What is the histologic presentation of paracoccidiodes?
yeast with multiple budding
When is one exposed to beryllium?
mining and fabrication
looks like sarcoid
What exposure leads to byssinosis?
What is the mechanism of N-Acetylcysteine?
splits the disulfide linkages in mucus.
Mucolytic for CF
What is Dextromethropan?
cough suppressant
What is Ipratropium?
what is pentamidine?
antiprotozoal for pneumocystis carinii
What are Charcot-Layden crystals? Curshman spirals?
rhomboid crystals of asthma
What are some peripheral causes of hypoventilation?
skeletal abnlties
phrenic nerve paralysis
What is the relationship between lung volume and radial traction?
when volume decreases, traction increases
What is the Reid index?
for bronchitis
gland depth to bronchial wall thickness
What B-blockers can be given in an ephysema pt?