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114 Cards in this Set

  • Front
  • Back
what part of the conducting zone is cartilage present
trachea and bronchi
associated with anatomic dead space
conducting zone
respiratory zone
respiratory bronchioles
alveolar ducts
alveoli
where does conducting zone end
terminal bronchioles
where do goblet cells end in conducting zone
bronchi
where does pseudostratified ciliated columnar cells extend to
respiratory bronchioles
what lecithin-to-sphingomyelin ratio indicates fetal lung maturity
ratrio of > 2.0
which type of pneumocyte is the majority of alveolar surface and is optimal for gas diffusion due to being thin
type I pneumocytes
these pneumocytes secrete surfactant which decreases alveolar surface tension
type II pneumocytes
dipalmitoyl phosphatidylcholine
surfactant
these pneumocytes proliferate during lung damage and can serve as precursors for type I penumocytes
type II
nonciliated columnar cells with secretory granules that secrete a component of surfactant, degrade toxins, and act as reserve cells
Clara cells
what does a bronchopulmonary segment consist of
tertiary bronchus
2 arteries (bronchial and pulmonary) located in the center
veins and lymphatics drain along the borders
lobes of right and left lung
right - 3 lobes
left - 2 lobes and lingula
where does an foreign body aspirate while upright vs. supine
upright - lower portion of right inferior lobe
supine - superior portion of right inferior lobe
relation of the pulmonary artery to the bronchus of each lung
right lung - pulmonary artery is found anteriorly
left lung - pulmonary artery is found superiorly
structures perforating the diaphragm at T8, T10, and T12
T8 - IVC
T10 - esophagus and vagus
T12 - aorta, thoracic duct, and azygous vein
what is the diaphragm innervated by
phrenic nerve C3-5
where can pain from diaphragm be referred to
shoulder
tendency for an alveolus to collapse on expiration increases due to
decreasing alveolar radius
what part of the lung is the largest contributor of functional dead space
apex of lung
calculation of physiologic dead space
tidal volume x (PaCO2 - PeCO2)/(PaCO2)
*PeCO2 = expired air PCO2
anatomical dead space of conduction airways plus functional dead space in alveoli
physiologic dead space
what is the natural tendency of the lungs and chest wall
lungs want to collapse
chest wall wants to spring outward
what three things decrease lung compliance
1. pulmonary fibrosis
2. decreased surfactant
3. pulmonary edema
airway and alveolar pressure at FRC
0 - both lungs and chest wall are balanced
system pressure = atmospheric
differentiate T and R forms of hemoglobin
T (taut) has low affinity for O2
R (relaxed) has high affinity for O2
why does fetal hemoglobin has higher affinity for O2
lower affinity for 2,3-BPG than adult and therefore higher affinity for O2
what shifts the O2-dissociation curve to the right favoring T form over R
increased H
increased CO2
increased 2,3-BPG
increased temperature
what can methemoglobinemia be treated with
methylene blue
oxidized form of hemoglobin that does not bind O2 as readily, but has increased affinity for CN
methemoglobin
two things used to treat cyanide poisoning
1. nitrites to oxidize hemoglobin to methemoglobin allowing cytochrome oxidase to function
2. thiosulfate to bind cyanide forming thiocyanate
binds to O2 with very high affinity and causes decreased oxygen-binding capacity with a left shift in the oxygen-hemoglobin dissociation curve decreasing unloading of oxygen
CO
what makes O2-dissociation curve shift to left or right
right - increase in everything except pH (H, CO2, T, DPG, Altitude)
left - decrease in everything except pH
what does a decrease in PAO2 do to pulmonary vessels
causes vasoconstriction and shift blood away from poorly ventilated region of lung to well ventilated regions
*unlike systemic circulation which causes vasodilation
gas diffusion equation
V = A/T x Dk(P1 - P2)
*emphysema decreases A
*pulmonary fibrosis increases T
perfusion limited gases
CO2 and N2O
diffusion limited gase
CO
what does pulmonary HTN do to pulmonary arteries
results in atherosclerosis, medial hypertrophy, and intimal fibrosis
primary pulmonary fibrsosis
due to inactivating mutation in the BMPR2 gene - normally function to inhibit vascular smooth muscle proliferation
causes of secondary pulmonary fibrosis
COPD, mitral stenosis, thromboemboli, autoimmune (SLE, CREST), left-to-right shunting, sleep apnea
most important determinant for pulmonary resistance
radius - multiplied to the fourth power
pulmonary vascular resistance equation
PVR = P(PA) - P(LA) / CO
normal O2 binding capacity
~20.1 mL O2/dL
*15 g/dL of hemoglobin x 1.34 mL O2 that each gram of Hb can bind
what happens to the O2 content, O2 saturation, and PO2 when Hb concentration falls
decreased O2 content
O2 saturation and PO2 remain the same
what does O2 content equal
(O2 binding capacity x % saturation) + dissolved O2
Alveolar gas equation
PAO2 = PIO2 - (PACO2/R)
*can be approximated to 150-PACO2/0.8
normal (A-a)O2 in lungs
10-15 mmHg
three general causes for oxygen deprivation
1. hypoxemia (decreased PaO2)
2. Hpoxia (decreased O2 delivery to tissue)
3. Ischemia
causes of hypoxemia and A-a gradient associated with each
high altitude (normal A-a)
hypoventilation (normal A-a)
V/Q mismatch (increased A-a)
diffusion limitation (increased A-a)
right-to-left shunt (increased A-a)
causes of hypoxia
decreased CO
hypoxemia
anemia
cyanide poisoning
CO poisoning
ideal V/Q ratio
1, ventilation should match perfusion
what is the average V/Q ratio of the apex vs. base of lungs
apex - V/Q = 3 (wasted ventilation)
base - V/Q = 0.6 (wasted perfusion)
what part of the lung both greater perfusion and ventilation
base of lung
why does TB prefer apex of lung
higher O2 content
V/Q ratio in shunt, does 100% O2 improve PO2
V/Q = 0, 100% O2 does nothing to PO2
V/Q ratio in physiologic dead space, does 100% O2 improve PO2
V/Q = infinity, 100% O2 helps improve PO2
what happens to capillaries in the apex of the lung
compressed due to higher alveolar pressure
how does CO2 bind to hemoglobin compared to O2
binds to N terminus of globin, not the heme
Haldane effect
oxygenation of Hb promotes dissociation of H from Hb shifting equilibrium toward CO2 formation and releases CO2 from RBC
physiologic response to high altitude
1. increase ventilation
2. increase EPO
3. increase 2,3-DPG
4. increase renal excretion of bicarb
5. pulmonary vasoconstriction
what happens to V/Q in the apex of lung during exercise
approaches 1 due to vasodilation of capillaries (normally they are compressed by higher pressure)
emboli associated with long bone fractures
fat emboli
emboli associated with DIC, especially postpartum
amniotic fluid emboli
Virchow's triad for being predisposed to developing DVT
1. stasis
2. hypercoagulability
3. endothelial damage
associated with increased RV and decreased FVC (same as VC), hallmark is decreased FEV1/FVC ratio
obstructive lung disease (COPD)
gland depth/total thickness of bronchial wall
Reid index
associated with hypertrophy of mucus-secreting glands in bronchioles resulting in increased Reid index > 50%; productive cough
chronic bronchitis
"blue bloater"
COPD associated with wheezing, crackles, and cyanosis
chronic bronchitis
associated with enlargement of air spaces and decreased recoil from destruction of alveolar walls, increased compliance
emphysema
what causes the increased compliance and destruction of alveolar walls in emphysema
increased elastase activity
differentiate cause of centriacinar vs. panacinar emphysema
centriacinar - smoking
panacinar - a1-antitrypsin deficiency
paraseptal emphysema
associated with bullae that can rupture and yeild spontaneous pneumothorax
clinical findings in emphysema
dyspnea
decreased breath sounds
tachycardia
late-onset hypoxemia
*chronic bronchitis has early-onset hypoxemia
bronchial hyperresponsiveness causes reversible bronchoconstriction
asthma
what can trigger asthma
viral URI
allergens
chronic necrotizing infection of bronchi resulting in permanently dilated airways and purulent sputum
bronchiectasis
associated with bronchial obstruction, CF, poor ciliary motility, and can develop aspergillosis
bronchiectasis
associated with decreased FVC and TLC with FEV1/FVC ratio > 80%
restrictive lung disease
three pneumoconioses and where they each affect
coal miner's - upper lobes
silicosis - upper lobes
asbestosis - lower lobes
associated with eggshell calcification of hilar lymph nodes and fibrosis due to macrophages responses to foreign body
silicosis
this can disrupt phagolysosomes and impair macrophages increasing susceptibility to TB
silica
associated with calcified pleural plaqes and increased incidence of bronchogenic carcinoma and mesothelioma
asbestosis
golden-brown fusiform rods resembing dumbbells located inside macrophages
abestos bodies
lecithin-to-sphingomyelin ratio in neonatal RDS
usually < 1.5
what can therapeutic supplemental O2 result in in neonates with RDS
retinopathy of prematurity
risk factors for neonatal RDS
prematurity
maternal diabetes (elevated insulin)
cesarean delivery (decreased release of fetal glucocorticoids)
associated with diffuse alveolar damage leading to increased alveolar capillary permeability and protein-rich leakage into alveoli
ARDS
initial damage in ARDS
neutrophilic substances toxic to alveolar wall causing alveolar damage
normal FEV1/FVC ratio
80%
what happens to FEV1 and FVC in both obstruction and restriction lung diseases
both are decreaes; however in obstructive, FEV1 is more dramatically reduced
differentiate central vs. obstructive sleep apnea
central - no respiratory effort
obstructive - respiratory effort against airway obstruction
differentiate tracheal deviation in bronchial obstruction vs. tension pneumothorax
bronchial obstruction - toward side of lesion
tension pneumothorax - away from side of lesion
associated with hyperresonant percusion and decreased breath sounds and tactile fremitus
tension pneumothorax
associated with bronchial breath sounds over lesion with dullness to percussion and increased VTF
lobar pneumonia
associated with decreased breath sounds over lesion with dullness to percussion and decreased VTF
pleural effusion
associated with absent breath sounds, dullness to percussion and decreased VTF
bronchial obstruction
common cancers that metatasize to the lung
breast
colon
prostate
bladder
lung cancer associated with central location and related to smoking
squamous cell carcinoma
lung cancer associated with parathyroid-like activity
squamous cell carcinoma
lung carcinoma not associated with smoking and females, located peripherally, and develops in sites of prior pulmonary inflammation of injury
adenocarcinoma of lung
histology of this lung carcinoma yields clara cells becoming type II pneumocytes
adenocarcinoma of lung
centrally located, undifferentiated lung carcinoma that is associated with ectopic production of ACTH or ADH
small cell carcinoma
inoperable lung carcinoma
small cell carcinoma
highly anaplastic undifferentiated lung carcinoma located in the periphery
large cell carcinoma
malignancy of the pleura associated with asbestosis, results in hemorrhagic pleural effusions and pleural thickening
mesothioma
psammoma bodies are seen in this lung malignancy
mesothioloma
carcinoma that occurs in the apex of the lung and may affect cervical sympathetic plexus and Horner's syndrome
pancoast's tumor
associated with ptosis, miosis, and anhidrosis
Horner's syndrome
two organisms associated with lobar pneumonia
strep pneumo
klebsiella
organisms associated with bronchopneumonia
S. aureus
H. influenzae
Klebsiella
S. pyogenes
organisms associated with interstitial (atypical) pneumonia
RSV
adenovirus
mycoplasma
legionella
chlamydia
pleural effusion with milky fluid high in triglycerides
lymphatic effusion
pleural effusion associated with malignancy, pneumonia, and trauma
exudate - increased protein content