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First Aid USMLE STEP 1: Respiratory
I do not own any of the included images, which are purely for educational use.
Terms in this set (418)
How many periods does it take to develop the lung?
What are they?
1) Embryonic (weeks 4-7)
2) Pseudoglandular (weeks 5-16)
3) Canalicular (weeks 16-26)
4) Saccular (weeks 26-birth)
5) Alveolar (weeks 32-8 years)
Describe the embryonic stage
Lung bud-> trachea-> mainstem bronchi-> secondary (lobar) bronchi-> tertiary (segmental) bronchi
**Errors at this stage can lead to TE fistula
Describe the Pseudoglandular stage
Endodermal tubules-> terminal bronchioles. Surrounded by modest capillary network
**Respiration impossible, incompatible with life
Describe the Canalicular stage
Terminal bronchioles-> respiratory bronchioles-> alveolar ducts.
Surrounded by prominent capillary network
Describe the Saccular stage
Alveolar ducts-> terminal sacs.
Terminal sacs separated by primary septae. Pneumocytes develop.
Describe the Alveolar stage
Terminal sacs-> adult alveoli (d/t secondary septation).
In utero, "breathing" occurs via aspiration and expulsion of amniotic fluid-> increase in vascular resistance through gestation. At birth, fluid gets replaced w/ air-> decrease in pulmonary vascular resistance
**At birth: 20-70 million alveoli
**By 8 years: 300-400 million alveoli
What are the 2 congenital lung malformations & describe them
1) Pulmonary hypoplasia= poorly developed bronchial tree w/ abnormal histology usually involving the right lung. Associated w/ congenital diaphragmatic hernia, bilateral renal agenesis (Potter Syndrome)
2) Bronchogenic cysts= Caused by abnormal budding of foregut & dilation of terminal or large bronchi. Discrete, round, sharply defined & air-filled densities on CXR. Drain poorly & cause chronic infections.
What are Type I pneumocytes?
thin squamous cells present in the alveoli, functioning in optimal gas diffusion
Where are Type I pneumocytes found?
97% of alveolar surfaces. (line the alveoli)
Role & epithelium of Type I pneumocytes
squamous. Thin for optimal gas diffusion
How is collapsing pressure calculated?
P = (2 x surface tension) / radius
What is the function of Type II pneumocytes?
secrete pulmonary surfactant --> decrease alveolar surface tension; prevent alveolar collapse, decrease lung recoil & increase compliance
What type of cells, histologically, are Type II pneumocytes?
Do Type II cells originate from Type I cells, or are Type II cells progenitors for Type I cells?
Type II cells are progenitors for Type I cells. Type II cells can also give rise to other Type II cells.
When do Type II cells proliferate?
in LUNG DAMAGE
What is the Law of Laplace?
As the radius decreases upon expiration, alveoli have an increased tendency to collapse.
What does "atelectasis" mean, and how is it caused?
DEFINITION collapse of alveoli
CAUSES obstruction, compression, or contraction
--> damage to Type II pneumocytes --> loss of surfactant
NOTE Even reinflation may not return full function due to the loss of surfactant.
What is surfactant, chemically?
a complex mix of lecithins, most importantly DIPALMITOYLPHOSPHATIDYLCHOLINE
What are Clara (Club) cells?
nonciliated, columnar cells with secretory granules
What do Clara cells secrete?
a "watery" component of surfactant
What are the functions of Clara cells?
to secrete a component of surfactant, to degrade toxins, and to act as reserve cells
When does surfactant synthesis begin?
around week 26 of gestation
When are mature levels of surfactant reached?
around week 35 of gestation
If a child is born premature, is it likely that they will produce sufficient levels of surfactant? If not, what is the child at risk of developing?
What measurement indicates if a fetus has mature lung function?
lecithin : sphingomyelin above 2
This can be measured in the amniotic fluid.
What is the cause of neonatal respiratory distress syndrome?
inadequate surfactant --> increased surface tension --> alveolar sac collapse after expiration --> formation of hyaline membranes
What lecithin:sphingomyelin ratio in amniotic fluid is predictive of neonatal RDS?
With what is neonatal RDS associated?
prematurity: adequate surfactant levels are not reached until week 35
C-section: d/t lack of release of stress-induced steroids (fetal glucocorticoids) --> no increased synthesis of surfactant
maternal diabetes: increased fetal glucose-> increased fetal insulin-> decreased surfactant levels
What are the clinical features of neonatal RDS?
increasing respiratory effort after birth
tachypnea with use of accessory muscles
hypoxemia with cyanosis
CXR showing "ground-glass" appearance of lung
What are the complications of neonatal RDS?
(1) persistently low O2 tension --> hypoxemia --> increased risk of PDA, necrotizing enterocolitis
(2) Therapeutic supplemental oxygen--> increased risk of free radical injury (O2 can be toxic!) --> "RIB"
R= Retinopathy of prematurity
I= Intraventricular hemorrhage
B= Bronchopulmonary dysplasia
What is the treatment for neonatal RDS?
maternal steroids before birth;
artificial surfactant for infant
What is the order of structures in the Respiratory tree?
Trachea-> bronchi-> bronchioles-> terminal bronchioles-> respiratory bronchioles-> alveolar sacs
What does smoking do the epithelial lining of the trachea?
pseudo stratified ciliated columnar-> squamous (via metaplasia & now sputum cannot be cleared)
Where is the highest & lowest resistance in the Respiratory Tree?
Highest= medium-size bronchi (turbulent airflow)
Lowest= terminal bronchioles (high CSA)
What is the conducting zone?
the larger airways that warm, humidify, and filter air without participating in gas exchange (i.e. anatomic dead space)
What are the large airways of the conducting zone?
nose, pharynx, trachea, bronchi
What are the small airways of the conducting zone?
bronchioles and terminal bronchioles (large #'s in parallel-> least airway resistance)
To what level of the conducting zone will cartilage and goblet cells extend?
To what level of the conducting zone will psuedostratified ciliated columnar cells extend?
**clear mucus & debris from lungs (mucociliary escalator)
To what level of the conducting zone will smooth muscle cells extend?
What is the respiratory zone?
the airways participating in gas exchange
What are the airways of the respiratory zone?
lung parenchyma; respiratory bronchioles, alveolar ducts, alveoli
What is the histology of the respiratory bronchioles?
What is the histology of the alveoli?
simple squamous cells
You see simple squamous cells on a histology slide. From what level of the respiratory system is the slide?
alveoli or alveolar ducts
You see psuedostratified ciliated columnar cells on a histology slide. From what level of the respiratory system is the slide?
terminal bronchioles or above
You see cartilage on a histology slide. From what level of the respiratory system is the slide?
bronchi or above
You see goblet cells on a histology slide. From what level of the respiratory system is the slide?
bronchi or above
You see cuboidal cells on a histology slide. From what level of the respiratory system is the slide?
Are cilia present in the respiratory zone?
Where in the respiratory system may macrophages be found?
alveoli-> clear debris & participate in the immune response
Which lung has three lobes?
Which lung has two lobes?
left lung; in place of the middle lobe, the lung accommodates the space necessary for the heart.
"Left Lung has Less Lobes
Which lung has a lingula?
**lingula is a tongue shaped portion of the left lung
Which lung is the more common site for inhaled foreign bodies and why?
right lung; right main stem bronchus is wider and more vertical
"Swallow a bite, goes down the right"
The relation of the pulmonary artery to the bronchus at each lung hilum is described by?
RALS: Right Anterior; Left Superior
If a patient aspirates a peanut while upright, where in the lungs will it be found?
inferior (AKA basilar) portion of the right inferior lobe
If a patient aspirates a peanut while supine, where in the lungs will it be found?
superior portion of the right inferior lobe OR posterior portion of the right upper lobe
What structures perforate the diaphragm at T8, T10, and T12, respectively?
T10= esophagus, vagus nerve (CN 10)
T12= aortic (red), thoracic duct (white), azygous vein (blue)
"I 8 10 Eggs At 12"
What is the innervation of the diaphragm?
C3, C4, C5 (phrenic nerve)
--C3, 4, and 5 keep the diaphragm alive--
Where might pain from the diaphragm be referred?
trapezius ridge (C3, C4)
Name the bifurcations for the common carotid, trachea & abdominal aorta
C4= common carotid
L4= abdominal aorta
In quiet breathing, what muscle is responsible for inspiration?
In quiet breathing, what muscle is responsible for expiration?
none (passive process)
In exercise, what muscles are responsible for inspiration?
external intercostals, scalenes, sternocleidomastoid
--inSpiration: external, Scalene, Scm--
In exercise, what muscles are responsible for expiration?
Graph: Normal Lung
What is the IRV?
Inspiratory Reserve Volume:
the air that can still be breathed in after normal inspiration
What is the TV?
air that moves into lung with each quiet inspiration
What is the normal TV?
What is ERV?
Expiratory Reserve Volume:
air that can still be breathed out after normal expiration
What is RV?
the air in lung after maximal expiration
Which lung volume measurement cannot be read by spirometry?
RV (residual volume)
How is IC calculated?
Inspiratory Capacity = IRV + TV
How is FRC calculated?
Functional Residual Capacity = RV + ERV
Volume of gas in lungs after normal expiration; cannot be measured on spirometry
How is VC calculated?
Vital Capacity = IRV + TV + ERV
Maximum volume of gas that can be expired after a maximal inspiration
How is TLC calculated?
Total Lung Capacity = IRV + TV + ERV + RV
Volume of gas present in the lungs after a maximal inspiration; cannot be measured on spirometry
What is physiologic dead space?
anatomic dead space of conducting airways plus alveolar dead space (capable of gas exchange but no exchange occurs) in alveoli; volume of inspired air that does NOT take place in gas exchange
How is physiologic dead space calculated?
Vd = Vt x [(PaCO2 - PeCO2) / PaCO2]
"Taco, PAco, PEco, PAco"
Vd= physiologic dead space
Vt= Tidal Volume
PaCO2 = arterial PCO2
PeCO2 = expired air PCO2
What is the largest contributor of alveolar dead space?
apex of the lung d/t not enough blood flow
When is the physiologic dead space = anatomic dead space?
When is the physiological dead space grater than the anatomic dead space?
lung diseases w/ V/Q defects
What is pathologic dead space?
when part of the respiratory zone becomes unable to perform in gas exchange. Ventilation but no perfusion
Equation for Minute Ventilation
Total volume of gas entering lungs per minute
Equation for Alveolar Ventilation
Volume of gas per unit of time that reaches alveoli
What are the normal values for RR, Vd & Vt
RR= 12-20 breaths/min
Vd= 150 mL/breath
Vt= 500 mL/breath
There is a tendency for the lungs to _____ _____ and chest wall to ____ ______.
At FRC, what is the system pressure?
atmospheric; the inward pull of the lung is balanced by the outward pull of the chest wall.
What determines the combined volume of the chest wall and lungs?
their elastic properties
At FRC, what is the airway pressure?
At FRC, what is the alveolar pressure?
At FRC, what is the intrapleural pressure?
negative (This prevents pneumothorax). PVR is at a minimum
What is compliance?
the change in lung volume for a given change in pressure
**higher compliance= lung easier to fill
**lower compliance= lung hard to fill
In what processes does compliance decrease?
**FRC decreases b/c the lungs are now exerting more inward collapsing pressure
What are the causes of pulmonary edema?
HEMODYNAMIC: increased vascular pressure, decreased oncotic pressure
MICROVASCULAR DAMAGE: infection
UNCLEAR: neurogenic, high altitude
In what processes does compliance increase?
**FRC increases because the lungs don't do a good job of resisting the outward pull of the chest wall
Pressure-Volume Curves of Lung and Chest Wall
Does surfactant increase or decrease compliance?
What happens to intra-thoracic volume when the lung collapses?
increases d/t unopposed chest expansion
Discuss PVR for extra alveolar vessels & alveolar vessels at RV & TLC
RV= extra alveolar vessels have highest PVR
TLC= alveolar vessels have highest PVR
What are the subunits of hemoglobin?
4 polypeptide subunits:
Which form of hemoglobin has a low affinity for oxygen?
T (taut; deoxygenated)-> promotes release/unloading of O2
--Taut in Tissues--
Which form of hemoglobin has a high affinity for oxygen?
R (relaxed; oxygenated)
--Relaxed in Respiratory--
Hemoglobin exhibits ____ cooperativity and negative _____.
What are the subunits of fetal hemoglobin (HbF)?
HbF has a lower affinity for _____ than adult hemoglobin, allowing it a _____ affinity for O2.
lower affinity for 2,3-BPG --> higher affinity for O2 (drives diffusion of O2 across the placenta from mother to fetus)
Which binds oxygen better: adult or fetal hemoglobin?
What factors favor the taut form over the relaxed form of hemoglobin?
Does this mean it favors unloading or loading of oxygen?
How does the dissociation curve shift?
taut: Cl-, H+, CO2, 2,3-BPG & increase temperature
Since the taut form has low affinity for O2, it favors UNLOADING of oxygen into tissues.
This then shifts the dissociation curve right.
In sickle cell anemia, why do HbS molecules sickle?
HbS allows hydrophobic interaction among hemoglobin molecules --> polymerization of HbS --> sickling in hypoxia
What effect do modifications to hemoglobin have on O2 saturation and content?
decreased O2 saturation and content --> TISSUE HYPOXIA
What is methemoglobin?
an oxidized form of hemoglobin (Fe2+ --> Fe3+) that does NOT bind O2 as readily
What is a ferric ion?
Fe3+ [ends w/ a "C" & "C" is the 3rd letter of the alphabet]
How is iron in Hb normally
Fe2+ (ferrous; reduced state)
"Fe2+ binds O2"
Methemoglobin does not bind O2 as readily, but what does it have an increase affinity for?
How does Methemoglobinemia present?
cyanosis & chocolate-colored blood
What effect do nitrates have on iron?
They oxidize Fe2+ --> Fe3+
NOTE there will be normal readings of PaO2 (plasma oxygen content is NOT changed; only hemoglobin binding), but DECREASED levels of Hb O2 saturation.
What does using nitrates (followed by thiosulfate) used for?
induced methemoglobinemia for tx of cyanide poisoning
How do you treat methemoglobinemia?
methylene blue & Vitamin C
--METHemoglobin needs METHylene blue.--
What is carboxyhemoglobin?
form of hemoglobin bound to CO in place of O2
Compared to O2, what is the affinity of CO for hemoglobin?
200X that of O2
How does the oxygen-hemoglobin curve shift in carboxyhemoglobinemia?
causes a decrease in O2-binding capacity w/ a left shift
**decrease O2 unloading in tissues (shuts down O2 delivery to tissues)
How are PO2, percent saturation and O2 content changed in carboxyhemoglobinemia (CO poisoning)?
percent saturation: decreased
O2 content: decreased
Oxygen-Hemoglobin Dissociation Curve: Myoglobin
What shape does the oxygen-hemoglobin dissociation curve have? Why?
sigmoidal due to positive cooperativity
[i.e. Tetrameric hemoglobin molecule can bind 4 oxygen molecules and has a HIGHER affinity for EACH subsequent oxygen molecule bound.]
What shape does oxygen-myoglobin dissociation curve have? Why?
hyperbolic due to monomeric nature that does NOT show positive cooperativity
What does a right shift of the oxygen-hemoglobin dissociation curve denote?
decreased affinity of hemoglobin for O2 = UNLOADING of O2 to tissue
What causes a right shift of the oxygen-hemoglobin dissociation curve?
CO2 (hypoxemia) / CHF / Chronic lung disease
"ACE BATs RIGHT-handed"
An increase in all factors (except pH) shifts the curve ____, while a decrease in all factors (except pH) shifts the curve ___.
What happens when there is a left shift physiologically?
left shift-> decreased O2 unloading-> renal hypoxia-> increased EPO synthesis-> compensatory erythrocytosis
Which direction is the HbF curve shifted and why?
left: fetal hemoglobin has a greater affinity for O2
Oxygen-Hemoglobin Dissociation Curve
Describe the Hb concentration, O2 saturation of Hb, Dissolved O2 (PaO2) & total O2 content for:
a) CO poisoning
a) normal Hb concentration, decreased Hb sat, normal PaO2, decrease total O2 content
b) decreased Hb concentration, normal Hb sat, normal PaO2, decrease total O2 content
c) increased Hb concentration, decreased Hb sat, normal PaO2, increased total O2 content
What happens when there is a decrease in Hb to O2 content, O2 saturation & PaO2?
decrease in O2 content of the blood, but no change in O2 saturation & PaO2
Does a decrease in PAO2 cause a vasoconstriction or vasodilation? Where does blood move due to this?
hypoxic vasoconstriction; this shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung
How can diffusion across perfusion limited lung membranes increase?
if blood flow increases (if you want more O2 in blood you need more blood through the lung)
What is the equation for diffusion?
Vgas = A x Dk x (P1-P2)/T
A = area
T = thickness
Dk(P1-P2) = difference in partial pressures
In emphysema, how does the diffusion equation change?
area decreases in emphysema
In pulmonary fibrosis, how does the diffusion equation change?
In normal, healthy lungs, is the circulation perfusion or diffusion limited?
In perfusion limited circulation, when does gas equilibrate?
early along the length of the capillary
In diffusion limited circulation, when does gas equilibrate?
at no point; gas does not equilibrate by the time the blood reaches the end of the capillary (diseased lung tissue is impeding gas delivery (Pa never reaches PA)
Perfusion or diffusion limited: O2 in normal health?
Perfusion or diffusion limited: O2 in emphysema or fibrosis?
Perfusion or diffusion limited: CO2?
Perfusion or diffusion limited: N2O?
Perfusion or diffusion limited: carbon monoxide?
What is DLCO?
the extent to which O2 passes from air sacs of lungs into the blood
Graph: perfusion limited
Graph: diffusion limited
Graph: oxygen in diffusion/perfusion
Flow of events in COPD**
lungs encounter a decrease in PAO2-> chronic pulmonary vasoconstriction-> chronic pulmonary HTN-> cor pulmonale (lung disease that causes heart failure) & subsequent right ventricular failure (JVD, edema, hepatomegaly)
What is the equation for pulmonary vascular resistance?
PVR = [P(pulmonary artery) - P(left atrium)] / CO
P(pulmonary artery) = pressure in the pulmonary artery
P(left atrium) = pulmonary wedge pressure
CO = cardiac output
What is the equation for resistance in a vessel?
R = (8ηl) / (πr^4)
η = viscosity of blood
l = vessel length
r = vessel radius
What is the normal amount of hemoglobin in the blood, and what level of hemoglobin denotes cyanosis?
-when deoxygenated Hb > 5 g/dL
How much O2 can be bound by 1 gram of normal Hb?
1.34 mL O2
What is the formula for O2 deliver to tissues?
O2 delivery to tissues= CO x O2 content of blood
What is the alveolar gas equation?
PAO2 = PIO2 - (PaCO2/R)
PAO2 = alveolar PO2 (mmHg)
PIO2 = PO2 in inspired air (mmHg)
PaCO2 = arterial PCO2 (mmHg)
R = respiratory quotient = CO2 produced per O2 consumed
How can you normally approximate the alveolar gas equation?
PAO2 = 150 - (PaCO2 / .8)
PAO2 = alveolar PO2 in mmHg
PaCO2 = arterial PCO2 in mmHg
What is the A-a gradient?
PAO2 - PaO2 = 10 to 15 mmHg
When does an increased A-a gradient occur?
What are the potential causes of increased A-a gradient?
fibrosis (impairs diffusion through an increase in barrier thickness)
If hypoxemia exists (decreased PaO2), but the A-a gradient is normal, what may be the causes?
high altitude (air w/ a decreased PO2)
hypoventilation (i.e. opioid use)
If hypoxemia exists (decreased PaO2), and the A-a gradient is increased, what may be the causes?
diffusion limitation (i.e. fibrosis)
If hypoxia exists (decreased O2 delivery to tissues), what might be the causes?
decreased cardiac output
carbon monoxide poisoning
If ischemia exists in the lung (loss of blood flow), what might be the causes?
impeded arterial flow
reduced venous drainage
ideally, what is the ventilation & perfusion ratio for adequate gas exchange
What is the V/Q mismatch at the apex of the lung?
3 (wasted ventilation) d/t a decrease in perfusion; part of the physiologic dead space
What is the V/Q mismatch at the base of the lung?
.6 (wasted perfusion) d/t too much blood (this is called shunting as there is venous blood leaving the hung without O2)
What area of the lung do organisms that thrive in high O2 prefer?
In exercise, what is the V/Q?
exercise increases the CO, there is vasodilation of apical capillaries causing an increase in perfusion-> V/Q=1
Where are both ventilation and perfusion the greatest?
base of the lung d/t gravity pulling more blood to the base
IF V/Q approaches 0, what is the cause?
airway obstruction (shunt)
NOTE giving 100% oxygen will NOT improve PO2 d/t nothing getting to the alveoli anyway
If V/Q approaches infinity, what is the cause?
blood flow obstruction (physiologic dead space)
NOTE assuming <100% dead space, 100% oxygen WILL improve PO2
What zone of the lung: PA > Pa > Pv?
Zone 1 (apex)
What zone of the lung: Pa > PA > Pv?
What zone of the lung: Pa > Pv > PA?
Compare V & Q at the base of the lung to the apex
Both V & Q are increased at the base of the lung d/t gravity, however perfusion increases way more!
What are the three forms of transported carbon dioxide?
bicarbonate= HCO3- (90%)
carbaminohemoglobin OR HbCO2 (5%)
dissolved CO2 (5%)
Where does CO2 bind hemoglobin?
N-terminus of globin, NOT heme
NOTE carbon monoxide binds the heme group
What form of hemoglobin does CO2 binding favor?
taut (O2 unloaded)
What is the Haldane effect?
oxygenation of Hb --> H+ dissociates from Hb --> equilibrium shifted to CO2 formation --> CO2 is released from RBCs
What is the Bohr effect?
increased H+ (CO2) from tissue metabolism --> curve shifted right (favors "T" form of Hb) --> O2 unloaded
How is the majority of blood CO2 carried?
What channel is necessary in the RBC membrane for release of CO2 (as HCO3-) from the RBC?
Cl- / HCO3- antiporter
What enzyme is required in the RBC for CO2 to be converted to HCO3-?
What is the acute body response ego being in high altitude?
decrease in Po2-> decrease in PaO2-> increase in ventilation-> decrease in PaCO2 (d/t breathing more you blow off more CO2)-> respiratory alkalosis-> altitude sickness
What is the chronic ventilation response to high altitude?
How does erythropoetin change in response to high altitude?
increased erythropoietin --> increased hematocrit AKA 40->65 & hemoglobin AKA 15->20 (chronic hypoxia!)
How does 2,3-BPG change in response to high altitude?
increased 2,3-BPG --> binds to hemoglobin --> curve shifts right --> O2 unloading favored --> hemoglobin releases more O2
What cellular changes are seen in response to high altitude?
How does renal excretion of bicarbonate change in response to high altitude?
respiratory alkalosis --> increased renal excretion of bicarbonate --> metabolic compensation
What is the result of chronic hypoxic pulmonary vasoconstriction?
pulmonary HTN & RVH
How does the respiratory system respond to exercise?
-increased CO2 production from muscles --> increased venous CO2 content*
-increased O2 consumption --> decreased venous O2 content*
-increased ventilation rate to meet O2 demand
-V/Q ration from apex to base becomes more uniform, approaches 1
-increased cardiac output --> increased pulmonary blood flow
-lactic acidosis --> decreased pH during strenuous exercise
* NOTE no change in PaO2 and PaCO2
What is Rhinosinusistis?
obstruction of sinus drainage into the nasal cavity->inflammation & pain over affected area (typically maxillary sinuses, which drain into the middle meatus, in adults)
What is the most common acute cause of Rhinosinusistis?
viral URI; may be superimposed bacterial infection (i.e. S. pneumoniae, H. influenzae, M. catarrhalis)
What is an Epistaxis
Where does Epistaxis most commonly occur?
anterior segment of nostril (Kiesselbach plexus).
Where do life-threatening Epistaxis hemorrhages occur?
posterior segment (i..e sphenopalatine artery, a branch of the maxillary artery)
What is the most common type of head & neck cancer?
squamous cell carcinoma
Risk factors for head & neck cancer?
tobacco, alcohol, HPV-16 (oropharyngeal), EBV (nasopharyngeal)
What is the most common, normally fatal, congenital pulmonary anomaly?
What is a DVT?
Blood clot w/in a deep vein (i.e. femoral, popliteal, iliofemoral)-> swelling, redness warmth & pain
What is Virchow's triad, and what is its significance?
TRIAD ("SHE gets a lot of clots"`
1) stasis (i.e. post-op, long drive/flight)
2) hypercoagulability (i.e. defect in coagulation cascade proteins, such as factor V Leiden)
3) endothelial damage (i.e. exposed collagen triggers clotting cascade
SIGNIFICANCE predisposition to DVT
What is the most common cause of hypercoagulability?
FACTOR V LEIDEN (most common defect in coagulation cascade proteins)
What is the complication of DVT?
What physical examination provocative test is most indicative of DVT?
HOMANS' SIGN= dorsiflexion of foot --> calf pain
What is used for prevention and acute management of DVT?
What is used for chronic prevention of DVT recurrence?
What clinical test is used to RULE OUT DVT? (high sensitivity, low specificity)
D-Dimer lab test
What clinical test is used to RULE IN DVT?
Imaging test (Ultrasound)
What is the effect to the body of getting a PE?
PE causes hypo perfusion of affected lung parenchyma, which leads to a redistribution of pulmonary blood flow & a V/Q mismatch. The resulting hypoxemia stimulates hyperventilation & acute Respiratory alkalosis. ABG shows an increase in pH & a decrease in PaCO2, along with a decrease in PaO2
Symptoms of a PE?
sudden-onset dyspnea, chest pain, tachypnea & tachycardia
What happens w/ a large or saddle embolus (straddles bi-furcation) of the pulmonary artery?
may cause sudden death
What do lines of Zahn in a pulmonary embolus indicate?
that the thrombi is pre-mortem
NOTE lines of Zahn are interdigitating areas of pink (platelets and fibrin) and red (RBCs) found only in thrombi formed before death
From where do the majority of pulmonary emboli arise?
deep leg veins
What are the types of pulmonary emboli?
Fat: associated with long bone fractures and lip suction; classic triad of hypoxemia, neurologic abnormalities, & petechial rash)
Air: Nitrogen bubbles precipitate in ascending divers (i.e. Caisson disease, decompression sickness d/t to rising too quick from scuba diving)-> tx w/ hyperbaric O2
Bacteria: associated w/ bacterial endocarditis
Amniotic fluid: can lead to DIC, especially post-partum
--an embolus moves like a FAT BAT--
What is the best imaging test of choice for a pulmonary embolism?
CT pulmonary angiography (look for filling defects)
Describe obstructive lung diseases?
obstruction of air flow resulting in air trapping in lungs. Airways close prematurely at high lung volumes .
**Extended expiratory phase; can't get rid of air in lungs!
In obstructive lung diseases, how do the RV, FRC, TLC FEV1, FVC, FEV1/FVC ratio, and V/Q change?
RV increased (main guy that goes up)
FEV1 greatly decreased
What is FEV1?
air expired in 1 second
What is FVC?
total air expired in a forced breath
Graph: Obstructive Lung Disease
Why does the FVC decrease in obstructive lung disease?
volume of air that can be forcefully expired decreases
Why is TLC increased in obstructive lung disease?
Why does diffusion decrease in Obstructive Lung diseases?
decrease in SA
At what percentage is the FEV1 considered "very severe"?
At what percentage is the FEV1 so severe that dyspnea at rest will be seen?
NOTE there will also be increased PCO2
How much of the lung capacity may be lost before onset of dyspnea?
How is COPD defined?
chronic lung disease with obstructive physiology
**(usually, chronic bronchitis + emphysema)
Epidemiologically, COPD is responsible for at least 100,000 deaths per year and accounts for 10% of all American disability.
What are the diagnostic criteria for chronic bronchitis?
productive cough for >3 months per year (not necessarily consecutive) for > 2 years
especially in a smoker
What is the pathogenesis of chronic bronchitis?
hypertrophy of mucus-seceting glands in bronchi --> Reid index > 50% (thickness of mucosal gland layer to thickness of wall between epithelium & cartilage) --> decreased air flow
**more than 1/2 of bronchial wall is compromised of mucus-secreting glands
Formula for the Reid Index?
mucosal glands layer/ (mucosal gland layer & epithelium)
**Cartilage is NOT included
Is chronic bronchitis caused by smoking?
Of what is a Reid index of <40% indicative?
Of what is a Reid index of >50% indicative?
What happens to the dLCO in chronic bronchitis
What happens to the RV & TLC in chronic bronchitis?
TLC does not increase as much as emphysema
What are the findings in chronic bronchitis?
-productive cough due to mucus production
-increased risk of infection and cor pulmonale
-wheezing, crackles, cyanosis, cyanosis (early-onset hypoxemia d/t shunting), mucus plugs trap carbon dioxide (hypercapnia), secondary polycythemia
What are the chronic complications of chronic complications?
pulmonary HTN, cor pulmonale
Trick name for chronic bronchitis pt's?
What is the effect of bronchodilators in chronic bronchitis?
some response, but will not return patient to normal
How is chronic bronchitis treated?
In emphysema, what changes will be seen in RV, FRV, TLC, and diffusion?
diffusion decreased (i.e. decreased dLCO)
Describe the overall criteria for Emphysema?
enlargement of air spaces; decrease elastic recoil, increased compliance, decrease diffusing capacity for CO from destruction of alveolar walls
Is emphysema caused by smoking?
Trick name for Emphysema
What is the cause of centriacinar emphysema? Location?
smoking (upper lobes); destruction of central portion of acini
"smoke rises to the UPPER LOBES"
What is the cause of panacinar emphysema? Location
alpha-1 antitrypsin (A1AT) deficiency (lower lobes); destruction of entire acini
What is A1AT, and what is its function?
alpha1-antitrypsin, inherited in an autosomal co-dominant pattern; neutralizes proteases (i.e. elastase) in the lower lobes
What is the result of A1AT deficiency?
misfolding of protein -->
(1) lack of antiprotease --> air sacs vulnerable to protease mediated damage --> panacinar emphysema
(2) accumulation of mutant A1AT in endoplasmic reticulum of hepatocytes --> liver damage
Describe the pathway once the A1AT deficiency goes into effect
increased elastase activity-> loss of elastic fibers-> increase lung compliance
What will a biopsy of the liver in A1AT deficiency emphysema reveal?
Note the pink, PAS-positive globules in hepatocytes
Where in the lung is panacinar emphysema most severe?
Where in the lung is centracinar emphysema most sever?
What is the normal allele in A1AT deficiency?
PiM; two copies are usually expressed (PiMM)
What is the most common clinically relevant mutation in A1AT deficiency?
What heterozygotes in A1AT deficiency are usually asymptomatic? What greatly increases this individual's risk for emphysema?
Which homozygotes are at significant risk for panacinar emphysema and cirrhosis?
What are the clinical features of emphysema?
-dyspnea and cough with minimal sputum, hyperventilation, wheezing
-prolonged expiration with pursed lips ("pink puffer;" this increases airway pressure and prevents airway collapse during respiration)
- CXR shows increased AP diameter, flattened diaphragm, increased lung field lucency
What are the late complications of emphysema?
destruction of capillaries in the alveolar sac --> hypoxemia
Bronchial hyper-responsivesness that causes REVERSIBLE bronchonconstriction
What happens to the smooth muscle during asthma?
hypertrophy (b/c muscles are working harder)
Key findings in asthmatic patients?
Curschmann spirals (shed epithelium forms whorled mucus plugs)
Charcot_Leyden crystals (eosinophilic, hexagonal, double-pointed, needle-like crystals formed from breakdown of eosinophils in sputum)
What are the triggers of asthma?
What type of hypersensitivity reaction is asthma?
Clinical diagnosis of asthma?
supported by spirometry & methacholine
What are the clinical features of asthma?
decreased inspiratory/expiratory ratio
pulsus paradoxus (drop in SBP > 10 mmHg during inspiration)
What is a finding on CXR during asthma?
I say "Curschmann's spirals," you say...?
I say "Charcot-Leyden crystals in sputum," you say...?
note the numerous eosinophils also
How will the FEV1, RV, FRC, and resistance change in asthma?
What is bronchiectasis?
permanent dilatation of bronchioles and bronchi; loss of airway tone --> air trapping
What is bronchiectasis
chronic/recurrent infections that cause destruction & dilation of bronchial walls
What is the pathogenesis of bronchiectasis?
chronic necrotizing infection/inflammation of bronchi --> damage to airway cells --> permanently dilated airways, purulent sputum, recurrent infections, hemoptysis & digital clubbing
What are the possible causes of bronchiectasis?
POOR CILIARY FUNCTION: cystic fibrosis, Kartagener syndrome, smoking
OBSTRUCTION: tumor or foreign body
INFECTIOUS: necrotizing infection (H. influenza, P. aeruginosa), allergic bronchopulmonary aspergillosis
What is Kartagener syndrome?
inherited defect of the dynein arm --> no ciliary movement --> sinusitis, bronchitis, infertility, siuts inversus
Which individuals are most prone to allergic bronchopulmonary aspergillosis?
asthmatics, cystic fibrosis patients
(hypersensitivity reacion to Aspergillus --> chronic inflammatory damage)
What are the clinical features of bronchiectasis?
purulent, foul-smelling sputum
What are the complications of bronchiectasis?
hypoxemia with cor pulmonale
secondary amyloidosis (AA)
How do you treat COPD?
vaccinate against influenza, Streptococcus pneumonia
treat acute purulent bronchitis with bronchodilators (beta adrenergic, anticholinergic)
inhaled steroids for partial response
oxygen tank in chronic hypoxemia
What are the obstructive lung diseases?
What is the basic criteria for Restrictive lung diseases?
Restricted lung expansion causes a decrease in lung volumes
**can't fill lung very well; decreased diffusion d/t thickened tissue
What are the restrictive lung diseases (interstitial lung diseases; inside lung)?
**decreased diffusing capacity & increased A-a gradient
ARDS, neonatal RDS (hyaline membrane disease)
PNEUMOCONIOSES (Coal Workers' pneumoconiosis, silicosis, berylliosis, asbestosis, anthracosis)
idiopathic pulmonary fibrosis
Wegener's (granulomatosis with polyangiitis)
Pulmonary Langerhans cell histiocytosis (eosinophilic granuloma)
Drug Toxicity (bleomycin, busulfan, amiodarone, methotrexate)
CHEST WALL ABNORMALITIES
What are the restrictive lung diseases (poor breathing mechanics; outside lung)?
**extrapulmonary, peripheral hypoventilation, normal A-a gradient)
poor muscular effort (polio, myasthenia gravis, Guillain-Barre)
poor structural apparatus (scoliosis, morbid obesity)
How are TLC, FEV1, FVC, and the FEV1:FVC ratio changed in restrictive lung diseases?
FEV1/FVC ratio normal or increased (>80%)
Graph: Restrictive Lung Disease
Why does the TLC decrease in restricted lung disease?
restricted lung expansion --> decreased lung volumes --> decreased TLC
What issues of poor muscular effort may result in poor breathing mechanics sufficient enough to cause restrictive lung disease?
What issues of poor structural apparatus may result in poor breathing mechanics sufficient enough to cause restrictive lung disease?
If restrictive lung disease is due to poor breathing mechanics, what labs will be seen?
normal A-a gradient
If restrictive lung disease is due to interstitial lung diseases (the most common causes), what labs will be seen?
lowered diffusing capacity
increased A-a gradient
What drugs can cause restrictive lung disease?
NOTE always check drug history!
"A GRUELING DISEASE"
A= ACE & ca2+ increase
G= granulomas (non-caseating)- found in many organs (mainly lungs, lymph nodes w/in chest cavity, & liver)
R= Rheumatoid Arthritis
U= uveitis (eye)
E= erythema nodosum (tibial/shin)-> subcutaneous nodules
L= lymphadenopathy (bilateral, hilar)
N= non-caseating granuloma
V= Vitamin D increase
What is idiopathic pulmonary fibrosis?
repeated cycles of lung injury & wound healing w/ increased collagen deposition, "honey-comb" lung appearance & digital clubbing
Antibody for Goodpasture Syndrome? What organ does this condition effect?
Anti Glomerular-BM antibodies
**affects the lung & kidney (glomerulonephritis)
What is found on histology for Pulmonary Langerhans cell histiocytosis? Risk factor for this disease?
Langerhan's-like cells on histology with Birbeck granules inside (tennis racket shaped granules)
What direction does the Flow-Volume Loop go for Obstructive diseases?
What direction does the Flow-Volume Loop go for Restrictive diseases?
Describe FEV1 & FVC for obstructive & restrictive diseases
FEV1 & FVC are decreased for both. However, FEV1 is more dramatically reduced compared to FVC, resulting in a decreased FEV1/FVC ratio
What is the pathogenesis for Hypersensitivity pneumonitis (alveoli inflammation)?
Mixed type III/IV hypersensitivity reaction to environmental antigen-> dyspnea, cough, chest tightness, headache
**often seen in farmers & those exposed to birds
What is the overall title for pneumoconioses
"environmental lung disease"
**chronic, fibrotic lung disease d/y inhalation of environmental dust!
What do coal worker's pneumoconiosis, silicosis & asbestosis increase the risk for?
cor pulmonale, cancer & caplan syndrome (rheumatoid arthritis & pneumoconioses w/ intrapulmonary nodules)
How is asbestosis transmitted?
shipbuilding, roofing, plumbing
What lobes does Asbestosis affect?
What does having Asbestosis increase the risk of getting
1) Bronchogenic carcinoma > risk of mesothelioma
2) pleural effusions
How is Beryllioses transmitted?
exposure to beryllium in aerospace & manufacturing industries
What is seen on histology in Beryllioses?
Granulomatous (non-caseating granulomas via cell-mediated immunity induction)-> looks like Sarcoidosis
**this makes it occasionally responsive to steroids
What lobes are affected in Beryllioses?
What will be seen on chest Xray in silicosis and anthracosis?
"eggshell" calcification of hilar lymph nodes
How is Coal worker's pneumoconiosis transmitted?
prolonged coal dust exposure-> macrophages laden with carbon-> inflammation & fibrosis
What is Coal worker's pneumoconiosis also known as?
Black lung disease
What lobes are affected in Coal worker's pneumoconiosis?
What is Anthracosis?
asymptomatic condition found in many urban dwellers exposed to sooty airy
How is Silicosis transmitted?
foundries, sandblasting, mines
Pathogenesis of Silicosis?
Macrophages respond to silica & release fibrogenic factors, leading to fibrosis.
What is though that Silica disrupts & what does this potentially cause?
disrupt phagolysosomes & impair macrophages, increasing susceptibility to TB
What lobes are affected in Silicosis?
What is the only pneumoconioses that affects the lower lobes?
"Asbestos is from the roof, but affects the base"
"Silica & coal are from the base, but affect the roof"
What is the only pneumoconioses that does not increase the risk for getting cancer?
Coal worker's pneumoconiosis
What will be seen histologically in asbestosis?
Hemosiderin-laden asbestos (ferruginous) bodies are golden-brown rods resembling dumbbells, found in alveolar septum sputum sample, visualized using Prussian Blue stain.
Aside from noncaseating granulomas, what will be seen histologically in sarcoidosis?
"asteroid bodies:" stellate inclusions within giant cells of the granulomas
Please note this finding is characteristic of a given disease but NOT specific.
What will be seen on CXR in asbestosis?
"ivory white" calcified, supradiaphragmatic & pleural plaques BUT NOT precancerous (black arrows show profile view)
most commonly found in the 6th-9th interspaces, usually sparing the apices and lung bases and involve the parietal pleura
What is ARDS?
Clinical syndrome characterized by acute onset respiratory failure, bilateral lung opacities, decreased PaO2/FIO2, no evidence ofHF/fluid overload.
What are the causes of ARDS?
P= pancreatitis; pneumonia
A= amniotic fluid embolism
**lead to damage of endothelial cells via inflammatory cells & O2-free radicals
What is the main risk factor for ARDS?
What is the pathogenesis of ARDS?
endothelial damage-> increased alveolar capillary permeability-> protein-rich leakage into alveoli-> diffuse alveolar damage & noncardiogenic pulmonary edema (normal PCWP)
**increased PCWP is suggestive of cardiogenic pulmonary edema
What does ARDS result in the formation of?
intra-alveolar hyaline membranes
What is the damage in ARDS d/t?
initial damage due to release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade & O2-derived free radicals
**activation of coagulation cascade can lead to DIC
Management of ARDS?
mechanical ventilation w/ low tidal volumes, address underlying cause
What is sleep apnea?
repeated cessation of breathing lasting 10 seconds or longer during sleep --> disrupted sleep --> daytime somnolence
What happens to the PaO2 during the day to a patient with sleep apnea?
Complications of sleep apnea?
Nocturnal hypoxia-> systemic/pulmonary hypertension, arrhythmias (atrial fibrillation/ flutter), sudden death
**Hypoxia-> EPO relea-> seerythropoiesis
What is obstructive sleep apnea?
Respiratory effort against airway obstruction.
What is associated with obstructive sleep apnea?
obesity & loud snoring
What is obstructive sleep apnea caused by?
excess pharyngeal tissue in adults, adenotonsillar hypertrophy in kids
**caused by close of upper airway d/t relaxation of pharyngeal muscle tone during sleep (upper airway dilator muscles weaken during sleep)
Tx for obstructive sleep apnea?
stimulation of CN XII, which causes the tongue to move forward & increase the AP airway diameter
Complications of obstructive sleep apnea?
lungs become hypoxic leading to vasoconstriction of lung vessels & pulmonary HTN, which may turn to for pulmonale, eventually turning into arrhythmias & sudden cardiac death
What is Central Sleep apnea?
No respiratory effort due to CNS injury/toxicity, HF, opioids
Who is central sleep apnea common in?
pre-mature infants (tx w/ caffeine)
What is obesity hypoventilation syndrome
Obesity (BMI greater than or equal to 30)-> hypoventilation-> decreases PaO2 & increases PaCO2 during sleep
**increased PaCO2 during waking hours (retention)
What is the normal pressure of the pulmonary artery?
What levels of pressure indicate pulmonary HTN, both at rest and during exercise?
rest: >25 mmHg
exercise: >35 mmHg
What is the characterization of pulmonary HTN?
arteriolosclerosis, medial hypertrophy, & intimal fibrosis of the pulmonary arteries
What is the course of disease for pulmonary HTN?
severe respiratory distress --> cyanosis and RVH --> death from decompensated COR PULMONALE
What causes primary pulmonary HTN?
inactivating mutation in the BMPR2 (Bone Morphogenic Protein Receptor II) gene, classically seen in young females
NOTE this is a poor prognosis
What is the normal function of the BMPR2 gene?
inhibition of vascular smooth mucle proliferation
What does this BMPR2 mutation lead to
decreased vessel radius, increased Resistance, & increased Pulmonary arterial pressure
What are other causes of primary Pulmonary HTN
drugs (i.e. amphetamines, cocaine)
connective tissue diseases
congenital heart disease
What are the causes of secondary pulmonary HTN?
1) Left heart disease: systolic/ diastolic dysfunction & valvular disease (i.e. metal stenosis)
2) Lung disease or hypoxia: destructive of lung parenchyma (i.e. COPD & pulmonary fibrosis), hyperemic vasoconstriction (i.e. obstructive sleep apnea, living in high altitude)
3) Chronic thromboemboli: recurrent microthrombi-> decrease in cross-sectional area of pulmonary vascular bed
4) Multifactorial: hematologic, systemic & metabolic disorders
What happens to the breath sounds, percussion, fremitus & tracheal deviation for a pleural effusion?
breath sounds= decreased
tracheal deviation= none OR away from side of lesion (if large)
What happens to the breath sounds, percussion, fremitus & tracheal deviation for a atelectasis (bronchial obstruction)?
breath sounds= decreased
tracheal deviation= toward side of lesion
What happens to the breath sounds, percussion, fremitus & tracheal deviation for a simple pneumothorax?
breath sounds= decreased
tracheal deviation= none
What happens to the breath sounds, percussion, fremitus & tracheal deviation for a tension pneumothorax?
breath sounds= decreased
tracheal deviation= away from side of lesion
What happens to the breath sounds, percussion, fremitus & tracheal deviation for a consolidation (lobar pneumonia, pulmonary edema)?
breath sounds= bronchial breath sounds; late inspiratory crackles
tracheal deviation= none
What is a pleural effusion?
excess accumulation of fluid between pleural layers-> restricted lung expansion during inspiration.
How to tx a pleural effusion?
thoracentesis to remove fluid
What is a transudate pleural effusion?
decreased protein content d/t increased hydrostatic pressure (i.e. HF) or decreased oncotic pressure (i.e. nephrotic syndrome, cirrhosis)
**HF produces too much fluid in vasculature
**cirrhosis & nephrotic syndrome do not produce enough protein
"TRANSudate is more TRANSparent"
What is a exudate pleural effusion?
increased protein content, cloudy d/t malignancy, pneumonia, collagen vascular disease, trauma (occurs in states of increased vascular permeability d/t pleural & lung inflammation)
**must be drained due to risk of infection
What is a lymphatic pleural effusion?
d/t thoracic duct (empties lymphatic fluid into pleural space by accident) injury from trauma or malignancy
**milky-appearing fluid d/t an increase in TAGs
What is a pneumothorax?
Accumulation of air in the pleural space.
Effects of a pneumothorax?
unilateral chest pain & dyspnea, unilateral chest expansion, decreased tactile fremitus, hyperresonance, diminished breath sounds, all on the affected side.
What is a primary spontaneous pneumothorax?
Due to rupture of atypical sub-pleural bleb or cysts. Occurs in tall, thin young males
**NO precipitating event or lung disease
What is a primary secondary pneumothorax?
due to disease lung (i.e. bullae in emphysema, infections), mechanical ventilation with use of high pressures-> barotrauma (injury caused by change in air pressure)
What is a traumatic pneumothorax?
caused by blunt (i..e rib fracture) or penetrating (i.e. gunshot) trauma
What is a tension pneumothorax?
can be any of the above. Air enters the pleural space but cannot exit. Increased trapped air-> tension pneumothorax. Trachea deviates away from affected lung
Tx for tension pneumothorax?
immediate needle decompression & chest tube placement
Symptoms for a tension pneumothorax?
**all result from an MVA
[MVA can also cause symptoms from a fat embolism d/t a fracture]
What is pneumonia?
inflammation of alveoli
What is lobar pneumonia caused by?
S. pneumoniae most commonly, also Legionella, Klebsiella
What are the characteristics of lobar pneumonia?
intra-alveolar exudate-> consolidation; may involve entire lobe or lung
What is bronchopneumonia pneumonia caused by?
S. pneumoniae, S. aureus, H. influenzae, Klebsiella
What are the characteristics of bronchopneumonia pneumonia?
acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distribution involving greater than or equal to 1 lobe
Another name for interstitial (atypical) pneumonia?
What is interstitial (atypical) pneumonia caused by?
Mycoplasma, Chlamydia, Legionella, viruses (RSV, CMV, influenza, adenovirus)
What are the characteristics of interstitial (atypical) pneumonia?
diffuse patchy inflammation localized to interstitial areas at alveolar walls; diffuse distribution invoking greater than or equal to 1 lobe
**follows a less severe course
What is a lung abscess?
localized collection of pus w/in parenchyma (necrosis of pulmonary parenchyma)
What is a lung abscess cause by?
aspiration of oropharyngeal contents (especially in patients predisposed to LOC like alcoholics/epileptics) OR bronchial obstruction (i.e. cancer)
Tx for lung abscess?
What is seen on CXR of a lung abscess?
**fluid levels are common in cavities (presence suggest cavitation)
What is the cavitation due to?
Anaerobes (i.e. Bacteroides, Fusobacterium, Peptostreptococcus)
What is a mesothelioma?
malignancy of the pleura (outer linings of the lungs) associated with asbestosis.
What is seen on histology for a mesothelioma?
Psammoma bodies (round collection of Ca2+)
What is positive in most mesotheliomas & negative in most carcinomas
Cytokeratin & calretinin
Is smoking a risk factor for a mesothelioma?
Where else can a mesothelioma arise?
peritoneum, pericardium tunica vaginalis (testes sac)
What is another name for a Pancoast tumor?
Superior Sulcus Tumor
Where is the location of a Pancoast tumor?
apex of lung
What can a Pancoast tumor cause by compression of various structures?
Recurrent laryngeal nerve-> hoarseness
Superior cervical ganglion-> Horner Syndrome (ipsilateral ptosis, miosis, anhydrosis)
SVC-> SVC syndrome
shoulder pain radiating toward axilla & scapula
upper extremity edema d/t subclavian vessel compression
spina cord compression/ paraplegia
What causes SVC syndrome?
compression of the SVC
Effets of SVC syndrome?
impaired blood drainage from head ("facial plethora"= blanching after fingertip pressure), neck (JVD), & upper extremities (edema)
Most common causes of SVC syndrome?
pancoast tumor & thrombosis from indwelling catheter
Is SVC syndrome a medical emergency?
Yes-> can raise ICP-> headaches, dizziness, increase risk of aneurysm/rupture of intracranial arteries
1) Fluid in alveolar space d/t pulmonary edema
2) interstitial lung disease (pulmonary fibrosis)
4) pleural effusion
1) bilateral, fluffy infiltrate
2) bilateral reticular markings
3) increased lucency
4) complete hemithorax opacification
Describe what happens to your body when you have a pneumothorax?
Air accumulates in the pleural space causing it to expand & compress the underlying lung which may collapse.
Details of a Spontaneous pneumothorax
Passage of air into the pleural sac from an abnormal connection between pleura & the bronchial system as a result of bullous emphysema or some other lung disease.
Symptoms of Spontaneous pneumothorax?
sharp pain on one side of chest & SOB. Trachea deviates toward affected lung.
Details of a Tension pneumothorax
Can result from trauma, lung infection or medical procedures. Air becomes trapped in the pleural space & cannot escape.-> air & pressure accumulating within the chest each time the patient inhales. The lung on the affected side collapses & the mediastinum is push dotards the contralateral side compressing the other lung-> impaired venous return, decreased CO, decreased BP, LOC-> shock & death
What are the symptoms for typical pneumonia?
CXR shows a LOBAR INFILTRATE that "white's out" the image
What is lobar infiltrate?
well-defined lung consolidation
What us a lung consolidation?
region of lung tissue filled w/ liquid
What are the symptoms for atypical pneumonia?
LESS severe symptoms
CXR shows diffuse, patchy infiltrate
What does a CXR for a main stem bronchus lesion look like?
completely opacified ("white-out" d/t decrease of radiolucent air) hemithorax on affected side.
What does hemithorax?
1/2 of the chest
What symptoms does a patient with a main stem bronchus lesion exhibit?
decrease breath sounds & deviation of trachea to affected side suggestive a lung collapse (atelectasis)
What is a main stem bronchus lesion cause by?
lung tumor that obstructs the main stem bronchus
Why does the lung collapse in a main stem bronchus lesion?
no new air is getting in
What is the leading cause of cancer death?
What are the symptoms of lung cancer?
-pneumonic "coin" lesion on CXR or noncalcified nodule on CT
What are the risk factors for lung cancer?
What is radon?
heavy gas that settles down into coal mines
grows along alveolar septa-> apparent "thickening" of alveolar walls.
**Tall columnar cells containing mucus.
Characteristics of a Large cell Carcinoma?
poorly differentiated large cells; associated with smoking
Prognosis & metastasis for a bronchial carcinoid tumor?
good & rare
What are the symptoms of a bronchial carcinoid tumor?
due to mass effect or carcinoid syndrome (flushing, wheezing & diarrhea)
B= bronchospasm & wheezing
R= right sided heart lesions (i.e. valve, murmur)
Histology for a bronchial carcinoid tumor?
Nests of neuroendocrine cells
Chromogranin A positive
Which lung carcinomas have some relationship with smoking?
What are the 2 lung carcinomas most likely seen in non-smokers?
Adenocarcinoma & Bronchial carcinoid tumor
When will you see an increased CEA marker?
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