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Quizlet
Quizlet
Aortic Stenosis: Same mechanism as that seen in MS except the LVEDP will be
elevated, whereas MS has a normal LVEDP
8. A 37-year-old woman comes to the physician because of progressive shortness of breath over the past 5 E) Pulmonary artery
years; she now has fatigue and shortness of breath with mild exertion. She has a history of mitral stenosis pressure
secondary to rheumatic fever at the age of 15 years. She was asymptomatic until 5 years ago when she
developed severe shortness of breath during pregnancy. She was treated with diuretics, low-sodium diet, Diastolic murmur =
and bed rest, and she was able to deliver the baby at term. Her only medication is hydrochlorothiazide. PR ARMS TS
Her temperature is 37 C (98.6 F), blood pressure is 110/80 mm Hg, pulse is 100/min and regular, and OS + late diastolic +
respirations are 26/min. Cardiac examination shows an obvious opening snap in S2. A grade 3/6, late apex = most likely MS
diastolic murmur is heard at the apex. A right ventricular lift is palpated along the left sternal border.
Which of the following is most likely increased in this patient? Narrowing of the MV
causes obstruction to
A) Blood flow to the lower lung fields blood flow into the
B) Diastolic filling time LV during Diastole>
C) Left-to-right shunt of blood As a result, Left atrial
D) Left ventricular end-diastolic pressure pressure increases
E) Pulmonary artery pressure and leads to a
passive rise in
backward pressure of
the pulmonary vein
9. What is the normal function of the BMPR2 gene? BMPR2 normally
functions to inhibit
vascular smooth
muscle proliferation
10. What changes to the lung vasculature result from BMPR2 gene mutation? Inactivation of
BMPR2 leads to
vascular hyper-
reactivity with
proliferation of
smooth muscle in
the pulmonary
vasculature.
11. A 25-year-old woman has had progressive dyspnea and fatigue for the past 2 years. On physical A
examination, she has pedal edema, jugular venous distention, and hepatomegaly. Lung fields are clear on
auscultation. Chest CT scan shows right heart enlargement. Cardiac catheterization is performed, and the
pulmonary arterial pressure is increased, without gradients across the pulmonic valve, and no shunts are
noted. A transbronchial biopsy is performed, and microscopic examination shows plexiform lesions of
peripheral pulmonary arteries, with striking smooth muscle hypertrophy causing marked luminal
narrowing. A mutation in a gene encoding for which of the following is most likely to cause her pulmonary
disease?
Exertional dyspnea
Fatigue
Lethargy
Atypical chest pain
Syncope of unexplained etiology
Signs of right ventricular failure later in the disease
(peripheral edema, palpitations, etc.
14. What is the normal alveolar PO2? Normal alveolar PO2 is about 100 mmHg
When does reactive hypoxic pulmonary vasoconstriction occur? <70 mmHg causes reactive vasoconstriction
15. A 30-year-old previously healthy woman
with no significant past medical history
presents to your office with gradually
worsening shortness of breath of one year's
duration. The patient reports worsening
dyspnea on exertion, fatigue, shortness of
breath, and occasional exertional chest pain.
On exam, the patient is noted to have an
increased intensity of the P2 heart sound.
Chest radiograph is seen in Figure A. What
is the next best step in management?
1. D-dimer 4. Echocardiogram
2. 12-lead EKG
3. IV furosemide
4. Echocardiogram The patient's presentation and exam is concerning for pulmonary hypertension. An
5. Pulmonary function test echocardiogram is the appropriate non-invasive test to further evaluate for
pulmonary hypertension.
The diagnosis of pulmonary hypertension is often delayed due to its similar clinical
presentation to congestive heart failure, coronary artery disease, pulmonary
embolism, and other more common diseases. Patients may initially be asymptomatic,
but as the disease progresses, may present with exertional dyspnea, fatigue,
exertional chest pain, exertional syncope, and peripheral edema. Echocardiography
can indirectly diagnose pulmonary hypertension by assessing right ventricular
hypertrophy, RA size, RV failure, and estimates of PA pressure. Right heart
catheterization is definitive diagnostic test, as it allows for direct measurement of
pulmonary artery pressures, as well as pulmonary artery occlusion pressure, which
can help differentiate pre-capillary (pulmonary arterial hypertension) and post-
capillary (pulmonary venous hypertension) etiology of pulmonary hypertension.
16. 30-year-old otherwise healthy woman presents to her C) Plexogenic pulmonary vasculopathy.
physician with complaints of fatigue and dyspnea.
Physical examination reveals normal breath sounds and The presentation described is classic for pulmonary hypertension, and,
the presence of third and fourth heart sounds. Chest x- more specifically, the primary idiopathic form of pulmonary hypertension.
ray shows clear lung fields but right ventricular This rare condition is suspected of being related to the collagen vascular
enlargement, main pulmonary artery enlargement, and diseases, since up to 50% of patients have antinuclear antibodies (despite
"pruning" of the peripheral vasculature. the absence of frank presentation of other autoimmune disease). Also, a
Electrocardiogram shows right axis deviation and right similar, known secondary form of pulmonary hypertension is sometimes
ventricular hypertrophy. Left ventricular function seen in patients with a wide variety of collagen vascular diseases,
appears normal on echocardiography. Serologic studies including systemic lupus erythematosus, polymyositis, dermatomyositis,
show antinuclear antibodies. Which of the following systemic sclerosis, and adult and juvenile forms of rheumatoid arthritis. A
pathological findings would this patient also show, wide variety of other conditions have also been associated with
either at autopsy or if an appropriate biopsy was taken? secondary pulmonary hypertension, including shunts, left atrial
hypertension, chronic hypoxia, pulmonary embolism, drug reaction,
hepatic cirrhosis, and sickle cell disease.
A. Mural thrombus of the right atrium
B. Necrosis and scarring of the left ventricle Both primary and secondary forms of pulmonary hypertension are
C. Plexogenic pulmonary vasculopathy associated with prominent changes in the pulmonary vasculature, which
D. Pulmonary artery stenosis can include muscularization of smaller arterioles, concentric hypertrophy
E. Severe pulmonary fibrosis of the intima ("onion skinning"), and a distinctive plexiform lesion
(plexogenic pulmonary vasculopathy) in which the smallest arterioles
become markedly dilated with lumens partially occluded by endothelial
(or possibly mesenchymal) cells and sometimes, thrombus. The prognosis
of untreated pulmonary hypertension is poor. However, the use of the
vasodilator hydralazine with anticoagulation can slow the course (fatal in
about 3 years in untreated patients). If the pulmonary hypertension is
secondary, therapy of the primary disease can be helpful. Unlike cor
pulmonale, atrial fibrillation with mural thrombus (choice A) formation is
uncommon in primary pulmonary hypertension.
17. What gene mutation is common in patients with familial Up to 80% of patients with heritable, or familial, pulmonary hypertension
primary pulmonary hypertension? have a mutation in the BMPR2 gene.
18. A 55-year-old woman who is obese comes to the A) Increased pulmonary artery pressure
physician because of daytime drowsiness, early morning
headaches, and swollen ankles. During the interveiw, she
says, "My husband tells me I snore too loudly. He can't
get any sleep because of it." Echocardiography shows
an enlarged right ventricle and poor right ventricular
function. Which of the following is the most likely
responsible for the development of right ventricular
failure in this patient?
These are complex vascular formations that are seen with severe long-
standing pulmonary hypertension.
23. Plexiform Lesions
24. A patient with pulmonary hypertension is refractory to Lung transplantation is considered the last effective treatment option for
medical management. What is the next step in patients with idiopathic pulmonary hypertension refractory to medical
management? management.
25. What age group and gender are most likely to develop If there is no discernible cause, pulmonary hypertension is considered to
primary pulmonary hypertension? be primary.
A. Adenosine
B. Calcitonin gene-related peptide
C. C-reactive protein
D. Endothelin
E. Prostacyclin (PGI2)
43. A previously healthy 35-year-old woman comes to the physician because of a 3- A) Endothelin-1
month history of progressive shortness of breath with exertion. Her respirations are
26/min. Physical examination shows jugular venous distention with a prominent a 35 y.o woman with progressive SOB +
wave. The lungs are clear to auscultation. Cardiac examination shows a loud pulmonic prominent a wave + loud S2 = Pulmonary
component of S2 and a right-sided S4 gallop. This patient's condition most likely Hypertension
involves increased pulmonary expression of which of the following?
A) Endothelin-1
B) Nitric oxide
C) Prostacycin (PGI2) synthase
D) Thrombomodulin
E) Voltage-gated potassium channels
44. Pulmonary Vasodilator Testing and Pulmonary Hypertension Pulmonary vasodilator testing establishes
the relative contribution of reversible
vasoconstriction versus fixed stenosis in
patients with PAH. If the magnitude of the
reversible vasoconstrictive component is
significant, it identifies patients who may
derive benefits from long-term use of
calcium channel blocker (CCB) therapy
Phosphodiesterase
5 inhibitors
-prolong the NO-
induced elevation
of cyclic GMP =>
smooth muscle
relaxation and
pulmonary
vasodilation
51. http://www.lumen.luc.edu/lumen/MedEd/medicine/pulmonar/diseases/pdis3.htm ...
http://www.meddean.luc.edu/lumen/MedEd/Radio/curriculum/Pulmonary/ARDS.htm
52. ARDS *Noncardiogenic Pulmonary edema resulting from acute alveolar-capillary damage
*The histological manifestation is referred to as Diffuse Alveolar Damage (DAD)
*Refractory hypoxemia (Not corrected by supplemental O2)
*Increased vascular permeability
*Increased dead space and intrapulmonary shunting that also contribute to the V/Q
Mismatch
*Non-cardiogenic Protein-rich pulmonary edema
*Respiratory distress: Initial symptoms are usually profound dyspnea and tachypnea
*Decreased lung compliance (due to damaged Type 2 Pneumocytes and decreased
surfactant production; as well as stiff lungs as a result of alveoli filled with fluid)
*Increased lung weight
*Normal PCWP/ Left Atrial Pressure
*Pulmonary hypertension is very common in ARDS and it occurs as a result of
hypoxemic vasoconstriction of pulmonary vasculature.
*Histology: Intra-alveolar hyaline membranes
*CXR: Diffuse bilateral infiltrates
*Poor Prognosis (40-50% Mortality Rate)
*Tx: Treat underlying cause
*Positive end expiratory pressure (PEEP) with low tidal volumes ( 6 mL/kg ideal body
weight)
*Some patients with ARDS who recover regain completely normal pulmonary function;
others have residual scarring, "honeycomb lungs," and respiratory insufficiency
53. What mnemonic can be used to SPARTAS
remember the most common causes of
ARDS Sepsis
Pancreatitis
Pneumonia
Aspiration
uRemia
Trauma
Amniotic fluid embolism
Shock
54. What is the characteristic histological
feature of ARDS?
The alveolar walls become lined with eosinophilic waxy hyaline membranes
55. Describe the composition of the Hyaline Membranes that are present in ARDS
A) IL1
B) IL10
C) Nuclear factor kappa B
D) Toll like receptors
E) TNF
57. What is the PaO2/FIO2 ratio in healthy persons? Healthy: > 450
What PaO2/FIO2 ratio is required for a diagnosis of ARDS? ARDS: <200
58. Describe the A-a gradient in ARDS? Increase in A-a gradient
Arterial Blood Gas Analysis on an FiO2 of 60% and PEEP of 10 cm H2O shows:
An xray chest shows bilateral diffuse hazy densities with cephalization of the pulmonary
vasculature and perihilar fullness. which of the following is the most likely diagnosis?
a. ARDS
b. Aspiration pneumonitis
c. Atelectasis
D. CHF
e. Fat embolism
f. Interstitial pneumonitis
67. A 48-year-old female suffers a traumatic brain 5. Left atrial pressure
injury while skiing in a remote area. Upon her
arrival to the ER, she is severely hypoxemic and This patient is suffering from acute respiratory distress syndrome (ARDS). One
not responsive to O2 therapy. She is started on a of the main criteria for ARDS is the absence of cardiogenic pulmonary edema,
mechanical ventilator and 2 days later upon and hence the left atrial pressure would be normal.
auscultation, you note late inspiratory crackles.
Which of the following is most likely normal in this ARDS is a classic cause of non-cardiogenic pulmonary edema. The left atrial
patient? pressure (usually estimated using the pulmonary capillary wedge pressure)
would most likely be normal, a finding used to distinguish ARDS from other
1. Type I pneumocytes causes of pulmonary edema. A chest x-ray of an ARDS patient initially shows
2. Type II pneumocytes bilateral infiltrates, progressing to widespread alveolar consolidation with air
3. Chest X-ray bronchograms. Neutrophils damage both type I and type II pneumocytes in
4. Alveolar-arterial gradient ARDS
5. Left atrial pressure
68. A 72-year-old man is admitted to the hospital for D. Capillary wedge pressure
treatment of a systemic bacterial infection
secondary to obstructive uropathy. On the third Sepsis is a major risk factor for the development of adult respiratory distress
day of his hospitalization, he complains of syndrome (ARDS). One of the minor diagnostic criteria for ARDS is absence of
shortness of breath and progressive hypoxemia. cardiogenic pulmonary edema which means that the pulmonary capillary
Which of the following parameters is most likely to wedge pressure is usually normal. An elevated wedge pressure would be more
be normal if this patient suffers from acute suggestive of a cardiogenic (hemodynamic) cause of pulmonary edema, such
respiratory distress syndrome? as pulmonary venous hypertension.
1. Pulmonary embolism
2. Septic shock
3. Trauma
4. Acute pancreatitis
5. Gastric aspiration
1. Pulmonary embolism
Aspiration
Acute pancreatitis
Air or Amniotic embolism
Radiation
Drug overdose
DIC
Drowning
Shock
Sepsis
Smoke inhalation
Uremia
Pneumonia
Oxygen Toxicity
72. What PaO2/FiO2 ratio do you expect for someone with ARDS? It is very difficult to oxygenate someone
with ARDS: the PaO2/FIO2 ratio is < 200.
regardless of the level of PEEP
73. If a patient is
suspected to be
suffering from adult
respiratory distress
syndrome (ARDS)
secondary to
urosepsis. Which of
the following most
likely suggests
ARDS in this
patient?
A
A. Normal
pulmonary capillary
Explanation:
wedge pressure
ARDS results from diffuse inflammatory injury to the alveoli of lungs. Inflammatory mediators are released as
B. Increased
a result of local or distant tissue injury. Neutrophils recruited to the lungs become activated and release
compliance of the
proteases and free oxygen radicals which damage alveolar endothelial and epithelial cells. Alveolar capillary
lung
permeability increases and protein is released into alveoli increasing osmotic pressure in alveoli and as a
C. Normal protein
result, free water is also dragged into the alveoli. Accumulation of protein rich fluid in alveoli as a result of
concentration in
diffuse alveolar damage makes the lungs stiff and they become less distensible or compliant. Alveolar-arterial
pumonary edema
PO2 difference is widened in cases of ARDS and hypoxemia occurs as a result. It occurs largely due to
fluid
ventilation-perfusion mismatch. Pulmonary hypertension is very common in ARDS and it occurs as a result of
D. Normal
hypoxemic vasoconstriction of pulmonary vasculature.
pulmonary arterial
pressure
Pulmonary capillary wedge pressure is normal in ARDS and it is the most important differentiating point
E. Normal alveolar-
between ARDS and cardiogenic pulmonary edema. It is usually less than 15 mmHg in ARDS while it is greater
arterial PO2
than 18 mmHg in cardiogenic pulmonary edema.
gradient
74. Acute Pancreatitis Pancreatitis is a major risk factor for ARDS as it results in the release of large amounts of inflammatory
and ARDS cytokines and pancreatic enzyms which lead to activation of neutrophils in alveolar tissues
75. What would you
expect to see on a
CXR in a patient with
acute respiratory
distress syndrome?
A CXR will show diffuse, bilateral infiltrates in all lung zones with prominent air bronchograms. Possibly
complete "white out" on CXR
76. Describe the typical *Acute dyspnea and hypoxemia within hours to days of an inciting event
presentation of *Need for a high fraction of inspired oxygen (FiO2) to maintain oxygen saturation
acute respiratory
distress syndrome?
77. In addition to Acute respiratory distress syndrome treatment is focused on addressing the underlying cause and *Positive
addressing the end expiratory pressure (PEEP) with low tidal volumes.
underlying cause,
what is the *PEEP is used to try to decrease the FiO2 levels
treatment of acute FIO2 levels > 50% are toxic to the lungs*
respiratory distress
syndrome?
78. What happens to functional residual capacity in Acute Respiratory Distress Syndrome? In ARDS, the functional residual
capacity is decreased.
79. DLCO and FVC in ARDS ARDS follows a restrictive pattern and
thus both DLC and FVC are reduced
80. A 45-year-old man arrives by ambulance to the emergency room after being involved
in a very severe construction accident. The patient was found unconscious with a large
metal spike protruding from his abdomen by a coworker who was unable to estimate the
amount of time the patient went without medical aid. Upon arrival to the ER, the patient
was unconscious and unresponsive. His vital signs are BP: 80/40, HR: 120 bpm, RR: 25
bpm, Temperature: 97.1 degrees, and SPO2: 99%.He is taken to the operating room to
remove the foreign body and control the bleeding. Although both objectives were
accomplished, the patient had an acute drop in his blood pressure during the surgery at
which time ST elevations were noted in multiple leads. This resolved with adequate fluid
resuscitation and numerous blood transfusions. The patient remained sedated after
surgery and continued to have relatively stable vital signs until his third day in the
intensive care unit, when he experiences an oxygen desaturation of 85% despite being
on a respirator with 100% oxygen at 15 breaths/minute. On auscultation air entry is 1. Diffuse alveolar damage
present bilaterally with the presence of crackles. A 2/6 systolic murmur is heard.
Readings from a Swan-Ganz catheter display the following: central venous pressure This individual is likely suffering from
(CVP): 4 mmHg, right ventricular pressure (RVP) 20/5 mmHg, pulmonary artery pressure Acute Respiratory Distress Syndrome
(PAP): 20/5 mmHg. Pulmonary capillary wedge pressure (PCWP): 5 mm Hg. A chest x- (ARDS) which is classified histologically
ray is shown as Image A. The patient dies soon after this episode. What is the most likely as diffuse alveolar damage (DAD)
direct cause of his death?
FIND A PIC
90. How is Maternal Diabetes associated with NRDS Increased fetal blood glucose results in increased fetal insulin production
A lecithin-sphingomyelin
ratio of _________ is
suggestive of NRDS
98. NRDS and persistent PDA Neonates depend on increased oxygen tension after birth to close
the ductus arteriosus so neonates who are hypoxemic because of
NRDS often have patent ductus arteriosus
99. NRDS and Necrotizing Enterocolitis ...
100. What 3 hormones modulate surfactant synthesis in a fetus? Hormones that modulate surfactant synthesis include:
1)Air enters the pleural space through the chest wall as a result of
trauma
2)Air enters the pleural space from the lung parenchyma through
the visceral pleura
110. What are the physical exam findings in a patient with a Physical exam typically reveals:
pneumothorax? **Unilateral absence of breath sounds (on the affected side)
*Hyper-resonant sounds upon percussion of the lungs
*Tachycardia
*Tachypnea*
In some cases, a deviated trachea
Venous congestion of the head/upper extremities (JVD) (in a
tension pneumothorax)
A secondary spontaneous pneumothorax occurs in individuals with lung disease (ex: COPD,CF,
PCP pneumonia, TB).
Two of the most common cause of 2ndary Spontaneous Pneumothorax = CF and COPD
(emedicine)
114. What is the major complication A spontaneous pneumothorax can progress to a tension pneumothorax.
of a spontaneous
pneumothorax?
115. What is the most important risk Smoking
factor for a spontaneous
pneumothorax
116. What type of emphysema is Paraseptal emphysema
associated with an increased
risk of spontaneous
pneumothorax
117. What is the cause of bleb Blebs are secondary to high negative intrapleural pressures
formation in spontaneous
pneumothorax? The superficial alveoli at the apices are typically the most negative and because pleural pressure
falls about .2 cm H2O per cm of vertical height, tall patients have an increased risk
Where do these blebs
typically form?
118. An 18-year-old man comes to the emergency department with sudden-onset right-sided
chest pain and dyspnea. The patient was at home watching a football game on television
when his symptoms abruptly started. He now has pain with deep breaths. He has no other
medical problems and takes no medications. The patient has smoked a pack of cigarettes
daily for the past 2 years. His respirations are 24/min. Physical examination shows a thin, tall
patient in acute distress. The right side of the chest is hyperresonant to percussion and lacks
audible breath sounds. His chest x-ray is shown below.
Which of the following conditions most likely led to this patient's presentation?
Which is diagnosis?
A) Asthmatic bronchitis
B) Bronchiectasis
C) Bullous emphysema
D) Chronic bronchitis
E) Lobar pneumonia
F) Pleural effusion
G) Pneumothorax
H) Pulmonary embolism
146. What are some chest x-ray findings in a patient with a pleural effusion?
A) Ascites
B) Blood
C) Exudate
D) Lymphedema
E) Transudate
149. A 55 year old woman with CHF has D) Increased hydrostatic pressure
progressive shortness of breath and
chest pain. An x-ray of the chest shows
bilateral pleural effusions. Lab studies
done on pleural fluid and serum show:
(A) Midaxillary line—6th intercostal Patient is suffering from a pleural effusion (accumulation of excess fluid in the pleural cavity
space surrounding the lung). The effusion causes the difficulty in breathing due to limiting the
(B) Midaxillary line—9th intercostal expansion of the lungs during inspiration (like cardiac tamponade). A thoracentesis is an
space invasive procedure to remove the excess fluid from the pleural sac. In the midaxillary line, the
(C) Parasternal line—6th intercostal lung resides at the 8th rib and the parietal pleura would reside at the 10th rib. The space
space between the parietal pleura and the lung is the costodiaphragmatic recess, and it gives space
(D) Parasternal line—2nd intercostal for the lung to inflate within the pleural cavity.
space
(E) Midclavicular line—5th
intercostal space
158. Pulmonary Embolism *Occlusion of a pulmonary artery from embolization of a thrombus from a distal site
*Most PE arise from DVT that occur in the proximal deep veins of the leg (e.g. popliteal, iliac,
and femoral veins)
*Size of embolism determines proximity of occlusion to pulmonary trunk
*Infarction is rare due to collateral circulation from bronchial arteries, except in the setting
of cardiopulmonary compromise
*Presentation: Tachypnea, tachycardia, dyspnea, chest pain (often pleuritic), hypoxemia due
to V/Q mismatch
*Increase in a-a gradient
159. Which region of the lung is more Since there is greater perfusion at the lower lobes of the lung, pulmonary emboli most
likely to infarct in a PE? commonly occur in the bases of the lungs.
160. Most symptomatic pulmonary Popliteal, iliac, and femoral
emboli arise from deep venous
thrombosis (DVT) in which veins?
161. What type of acid base disturbance Respiratory alkalosis
is seen with pulmonary embolism?
(hypocapnia due to tachypnea and hyperventilation)
162. What is a saddle embolus?
A. Canalized thrombus.
B. Mural thrombus.
C. Occlusive embolus.
D. Occlusive thrombus.
E. Postmortem clot
165. What are the pink areas within Lines of Zahn made of? Pink - platelets and fibrin
What are the red areas within Lines of Zahn made of? Red - red blood cells
166. What fibrin breakdown product can be elevated and detected in the blood in the D-Dimer
setting of thromboembolic disease?
With regard to pulmonary embolism (PE), is a test for this substance more sensitive or Very sensitive; Good for screening
more specific?
Does that mean this test is better for screening or confirming that a person has a PE?
167. Four days after admission to the hospital with multiple fractures sustained in a motor A. Bronchial arteries
vehicle collision, a 27-year-old man has the sudden onset of shortness of breath. His
respiration are 30/min. Doppler ultrasonography of the lower extremities shows deep
vein thrombosis, and a spiral CT scan of the chest shows evidence of multiple
subsegmental pulmonary emboli. Anticoagulant therapy is begun. One week later, a If the cardiovascular function is
follow-up CT scan of the chest is done to evaluate atypical chest pain. Results show no adequate, the bronchial circulation will
abnormalities and the pain was considered to be musculoskeletal. Collateral circulation maintain tissue viability resulting in
from which of the following best explains the lack of identifiable pulmonary hemorrhage but no infarct. (Infarct may
parenchymal infarcts in this patient? be present in only 10% of cases)