General Respiratory Pathology
Study online at quizlet.com/_259vhn
1. What is the range of normal pressure in the
pulmonary circuit?
What is the pressure in the pulmonary circuit
during pulmonary hypertension?
2. What are the 5 different groups into which
pulmonary hypertension is categorized?
3. What pulmonary conditions, if untreated, can
lead to pulmonary hypertension?
4. What cardiac conditions, if left untreated, can
lead to pulmonary hypertension??
5. What test is used to definitively diagnose a
patient with pulmonary hypertension?
6. What is the mechanism by which left sided heart
failure and/or valvular disease lead to
secondary pulmonary hypertension?
7. What is the mechanism by which mitral and
atrial stenosis leads to secondary pulmonary
hypertension?
Normal: 10-14 mmHg
Pulmonary Hypertension: >25 mmHg at rest
(>35 mmHg during exercise
Pulmonary hypertension (PH) is classified into 5 separate groups based upon the
cause of the PH.
Group 1 is pulmonary arterial hypertension (primary PH)
Group 2 is PH due to left heart disease
Group 3 is PH due to chronic lung disease/hypoxia
Group 4 is PH due to chronic thromboembolic disease
Group 5 is PH due to unknown or multifactorial causes (ex: sickle cell anemia)
Pulmonary hypertension secondary to pulmonary disease includes:
COPD
Interstitial lung disease (pneumoconioses, IPF)
Obstructive sleep apnea
Systemic sclerosis
Cardiac conditions that are known to cause pulmonary hypertension include:
*Congenital heart disease in patients with L⇒R shunts
*Valvular disease (eg. mitral and aortic stenosis)
*Left heart failure
A definitive diagnosis requires right heart catheterization demonstrating mean
pulmonary artery pressure is ≥25 mmHg at rest.
Left-sided heart and/or valvular disease can lead to congestion and backup of
blood into pulmonary veins.
This increased volume in the pulmonary circuit causes an increase in pulmonary
blood pressure as a result.
Mitral stenosis:
Mitral Stenosis: Narrowing of the MV causes obstruction to blood flow into the LV
during Diastole> As a result, Left atrial pressure increases and leads to a passive
rise in backward pressure of the pulmonary vein
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?

(A) Bone morphogenetic receptor 2 (BMPR2)

(B) Fibrillin-1
(C) Lysyl hydroxylase
(D) Endothelin
(E) Atrial natriuretic factor
(F) Renin
(G) Endothelial nitric oxide synthetase (eNOS)
12. A 55-year-old man presents to the pulmonologist with progressive
shortness of breath over the past year. He was previously healthy and
now can barely make it up the stairs in his home. A chest radiograph is
ordered and it shows enlargement of the pulmonary arteries with a
normal sized cardiac shadow and normal-appearing lung fields. An
echocardiogram is performed showing a normal-shaped left ventricle
and thickened myocardium in the right ventricle. Which diagnosis is
most likely in this patient?
2. Primary pulmonary hypertension
Given the clear lung fields with enlargement of the
pulmonary arteries on chest radiograph and the
thickened right ventricle on the echocardiogram, this
patient most likely has primary pulmonary hypertension.
In this scenario, it is most likely that the cause is
idiopathic.

1. Left heart failure In primary pulmonary hypertension, increased vascular

2. Primary pulmonary hypertension resistance in the pulmonary vasculature results in
3. Hypertrophic cardiomyopathy increased afterload for the right side of the heart. The
4. Idiopathic pulmonary fibrosis result is long-term hypertrophy of the right heart and
5. Chronic obstructive pulmonary disease ensuing difficulty filling the right heart during diastole.
Treatment includes the use of vasodilatory agents;
however, this is generally an extremely debilitating
condition that can be difficult to treat.
13. What symptoms are characteristic of patients with pulmonary The symptoms of pulmonary hypertension are
hypertension? nonspecific which often causes a delay in diagnosis.
Common symptoms include:

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
physician with complaints of fatigue and dyspnea.
Physical examination reveals normal breath sounds and
the presence of third and fourth heart sounds. Chest x-
ray shows clear lung fields but right ventricular
enlargement, main pulmonary artery enlargement, and
"pruning" of the peripheral vasculature.
Electrocardiogram shows right axis deviation and right
ventricular hypertrophy. Left ventricular function
appears normal on echocardiography. Serologic studies
show antinuclear antibodies. Which of the following
pathological findings would this patient also show,
either at autopsy or if an appropriate biopsy was taken?
A. Mural thrombus of the right atrium
B. Necrosis and scarring of the left ventricle
C. Plexogenic pulmonary vasculopathy
D. Pulmonary artery stenosis
E. Severe pulmonary fibrosis
17. What gene mutation is common in patients with familial
primary pulmonary hypertension?
18. A 55-year-old woman who is obese comes to the
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?
A) Increased pulmonary artery pressure
B) Increased right ventricular preload
C) Pulmonary embolism
D) Pulmonary valve stenosis
E) Transient hypoxia in the right ventricular myocardium
19. Name 2 drugs that can cause pulmonary arterial
hypertension.
20. Sickle Cell anemia and Pulmonary Hypertension
21. Describe the histological findings in pulmonary arteries
in a patient with pulmonary hypertension
C) Plexogenic pulmonary vasculopathy.
The presentation described is classic for pulmonary hypertension, and,
more specifically, the primary idiopathic form of pulmonary hypertension.
This rare condition is suspected of being related to the collagen vascular
diseases, since up to 50% of patients have antinuclear antibodies (despite
the absence of frank presentation of other autoimmune disease). Also, a
similar, known secondary form of pulmonary hypertension is sometimes
seen in patients with a wide variety of collagen vascular diseases,
including systemic lupus erythematosus, polymyositis, dermatomyositis,
systemic sclerosis, and adult and juvenile forms of rheumatoid arthritis. A
wide variety of other conditions have also been associated with
secondary pulmonary hypertension, including shunts, left atrial
hypertension, chronic hypoxia, pulmonary embolism, drug reaction,
hepatic cirrhosis, and sickle cell disease.
Both primary and secondary forms of pulmonary hypertension are
associated with prominent changes in the pulmonary vasculature, which
can include muscularization of smaller arterioles, concentric hypertrophy
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.
Up to 80% of patients with heritable, or familial, pulmonary hypertension
have a mutation in the BMPR2 gene.
A) Increased pulmonary artery pressure
amphetamines, cocaine
(due to vasoconstriction)
...
*Arteriosclerosis
*Medial hypertrophy
Intimal fbrosis Plexiform lesions
22. What histological feature is pathognomonic of severe,
long-standing pulmonary hypertension?

Histologically, plexiform lesions can be seen in the lungs of individuals

with pulmonary hypertension.

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
medical management. What is the next step in
management?
25. What age group and gender are most likely to develop
primary pulmonary hypertension?
Lung transplantation is considered the last effective treatment option for
patients with idiopathic pulmonary hypertension refractory to medical
management.
If there is no discernible cause, pulmonary hypertension is considered to
be primary.

Primary pulmonary hypertension is rare and most often occurs in young

or middle aged women.
26. What two signs are present on physical examination in Loud P2
a patient with Pulmonary Hypertension? Right Ventricular Heave (also called parasternal heave)
27. Parasternal heave ...
28. Describe the WHO group classifications of Pulmonary ...
Hypertension
29. What two hematologic pathologies are known to cause Polycythemia Vera
pulmonary hypertension? Sickle Cell Disease
30. A 30-year-old otherwise healthy woman presents to her
physician with complaints of fatigue and dyspnea. Physical
examination reveals normal breath sounds and the presence
of third and fourth heart sounds. Chest x-ray shows clear
lung fields but right ventricular enlargement, main
pulmonary artery enlargement, and "pruning" of the
peripheral vasculature. Electrocardiogram shows right axis
deviation and right ventricular hypertrophy. Left ventricular
function appears normal on echocardiography. Serologic
studies show antinuclear antibodies. Which of the following
pathological findings would this patient also show, either at
autopsy or if an appropriate biopsy was taken?
A. Mural thrombus of the right atrium
B. Necrosis and scarring of the left ventricle
C. Plexogenic pulmonary vasculopathy
D. Pulmonary artery stenosis
E. Severe pulmonary fibrosis
31. During a drug study, a rat is injected with intravenous
epoprostenol. Which of the following effects would most
likely be observed?
A. Decreased cardiac output
B. Increased systemic vascular resistance
C. Increased platelet aggregation
D. AV node blockade
E. Decreased afterload
32. Prostacyclin
C. Plexogenic pulmonary vasculopathy
Both primary and secondary forms of pulmonary hypertension are
associated with prominent changes in the pulmonary vasculature,
which can include muscularization of smaller arterioles, concentric
hypertrophy 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
Choice (E) is the correct answer.
Epoprostenol is synthetic prostacyclin, also known as prostaglandin
I2, that is used in the treatment of acute respiratory distress
syndrome (ARDS) and primary pulmonary hypertension. It causes
vasodilation of both the pulmonary and systemic vascular beds
and also inhibits platelet aggregation. Systemic vasodilation results
in a decreased afterload. Cardiac output and stroke volume
increase in response to the decrease in afterload. Pulmonary
arterial dilation results in decreased pulmonary arterial pressures.
Dilation of the pulmonary vascular bed also acts to improve V/Q
mismatching in acute respiratory distress syndrome (ARDS),
particularly in areas of the lung that are ventilated but not perfused
(high V/Q ratio = dead space). The other choices are incorrect.
*Also known as PGI2
*Produced in endothelial cells
From prostaglandin H2 (PGH2) by the action of the enzyme
prostacyclin synthase*
Inhibits platelet activation by opposing TXA2 (by doing this it
prevents formation of the platelet plug)
(Platelet stabilizer according to kaplan)
Effective vasodilator
*Binds to PGI2 receptor (GPCR) => increase in cAMP
Half life of only 42 seconds
*
*
*
33. A 31-year-old woman with
primary pulmonary
hypertension is admitted to the
hospital because of increasing
shortness of breath, dyspnea
on exertion, and increasing
home oxygen requirements.
The agent that will selectively
decrease her pulmonary
arterial pressures is
A. hydralazine
B. nifedipine
C. nitrous oxide
D. prostacyclin I
E. sodium nitroprusside
34. PGI2 are selective in that they
cause only pulmonary and not
systemic vasodilation T/F?
35. Cor Pulmonale
36. Iloprost
37. Epoprostenol
38. Bosentan
39. Which lab values should be
followed in patients on
bosentan?
40. What is the mechanism of
bosentan in the treatment of
pulmonary hypertension?
41. Calcium channel blockers in
patients with vasoreactive
pulmonary hypertension
C. Nitrous Oxide
Nitrous oxide is the only agent listed that will ONLY decrease her pulmonary arterial pressures
Nitrous oxide is a gas that is usually given in low doses, 20-80 ppm via inhalation. It then acts via
cGMP to mediate vasodilation of the pulmonary vasculature without any systemic hemodynamic
effects. Hydralazine (choice A) is a potent generalized arterial dilator. Nifedipine (choice B) is a
calcium channel antagonist. In some persons with pulmonary hypertension, a therapeutic dose of
this agent can be given without producing dramatic systemic hypotension. The majority of patients
receiving this therapy have significant peripheral vasodilation as well.Prostacyclin I (choice D) is
used via direct pulmonary artery infusion to produce pulmonary vasodilation. However, it has
moderate to severe side effects including increased GI motility and peripheral vasodilation. Sodium
nitroprusside (choice E) is a generalized arterial and venous vasodilator.
F
PGI2 are not selective they cause systemic and pulmonary vasodilation
Nitrous oxide however is selective for only pulmonary vasodilation
...
...
*
*
*
*
*
*
*
*
*Cannot take Oral Contraceptives (OCPS) while using bosentan due to interaction
*Contraindicated in pregnancy
Since bosentan is hepatotoxic, liver function tests should be monitored in patients on this drug.
Bosentan is a competitive antagonist of endothelin-1 at endothelin receptors.
Normally, the binding of endothelin-1 to endothelin receptors causes pulmonary vasoconstriction.
Thus, competitive antagonism by bosentan acts to decrease pulmonary vascular resistance.
...
42. A 50-year-old woman comes to the physician because of progressive shortness of D. Endothelin
breath during the past 2 years. Her respirations are 20/min. physical examination
shows cyanosis and ankle edema. Her pulmonary artery pressure, pulmonary
vascular resistance, and right atrial pressure are increased, her pulmonary capillary
wedge pressure is 9.3 mmHg (N=8-16). Her ventilation improves when inhaled nitric
oxide is administered. Treatment with oral bosentan is begun for long-term therapy.
Which of the following mediators of pulmonary resistance in this patient will most
likely be antagonized by this drug?

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

Pulmonary vasodilator testing is not

necessary in patients who are not
candidates to receive CCBs or who are
already benefiting from them. CCBs would
not be indicated in patients with right
heart failure or hemodynamic instability
45. What is the preferred first-line medication for primary pulmonary hypertension Calcium Channel Blockers
patients with vasoreactive pulmonary arteries?
46. What signs are present histologically in Pulmonary Hypertension? Atherosclerosis of the pulmonary trunk
*Smooth muscle hypertrophy of pulmonary
arteries
*Intimal Fibrosis
*Plexiform lesions are seen with severe,
long-standing disease
47. Sickle Cell Disease and Pulmonary Hypertension This is high yield
48. Describe the mechanism by which the following conditions cause Pulmonary hypertension 1) increased
pulmonary blood
1) Congenital left to right shunts flow/volume
2) Hypoxia overload
3) Polycythemia 2) vasoconstriction
4) ARDS secondary to
5) Living in a high altitude hypoxia
6) Obstructive sleep apnea 3) increased blood
7) COPD viscosity
4) vasoconstriction
secondary to
hypoxia
5) vasoconstriction
secondary to
hypoxia
6) vasoconstriction
secondary to
hypoxia
7) Destruction of
lung parenchyma
results in hypoxia
49. A 50-year-old woman with chronic obstructive pulmonary disease comes to the physician because of a 3- C) Endotheilial nitric
month history of progressive shortness of breath. Physical examination shows jugular venous distension. A oxide synthase
loud pulmonary component of S2 is heard on auscultation .Pulmonary function tests show an FEV1:FVC ratio production
of 20% and a severely decreased diffusing capacity for carbon monoxide. Based on these findings, which of
the following is most likely decreased in this patient's pulmonary vascular smooth muscle?

A) Adventitial collagen matrix deposition

B) Cytosolic phospholiapse A2 activity
C) Endotheilial nitric oxide synthase production
D) Endothelin expression
E) Voltage-gated calcium channel a-subunit production
50. Which 3 classes of agents are used to treat patients with pulmonary arterial hypertension (PAH)? Endothelin-1
antagonists
(Bosentan)
Prostanoids
(Epoprostenol,
iloprost)
Phosphodiesterase
5 inhibitors
(sildenafil, tadalafil)

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

Alveolar hyaline membranes consist of

fibrin-rich edema fluid mixed with the
cytoplasmic and lipid remnants of
necrotic epithelial cells

*Morphologically similar to that of

NRDS
56. In order to investigate possible treatment options for ARDS experimental animals are B) IL10
anaesthesised and subjected to smoke inhalation according to a well established
experimental protocol. The experimental animals are then given compounds designed IL-10 is considered an anti-inflammatory
to upregulate specific mediators involved in the inflammatory cascade. Upregulation of cytokine
which of the following mediators would most likely prevent or ameliorate the lung injury
induced in this experimental model of 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

Profound V/Q mismatch (due to

atelectasis) causes an increase in the A-
a gradient, which ultimately results in
hypoxemia.
59. The fluid seen in ARDS is a _____________ (Transudate/Exudate) ARDS: Exudate (Protein Rich)
The fluid seen in Cardiogenic Pulmonary Edema is a _____________ (Transudate/Exudate) Cardiogenic Pulmonary Edema:
Transudate (Does not contain Proteins);
Due to increased
intracapillary/hydrostatic pressure
60. Describe the Pathophysiology of ARDS

*Diffuse inflammatory injury to the alveoli of lungs.

*=> Activation of endothelium (increased expression of
adhesion molecules) and extravasation of neutrophils
*Neutrophils degranulate and release cytokines and
inflammatory mediators that cause more endothelial damage
*Endothelial damage => protein-rich leakage (exudate) forming
an intra-alveolar hyaline membrane
*Free water dragged into alveoli due to incresed osmotic
pressure in alveoli
*Accumulation of protein rich fluid in alveoli as a result of
diffuse alveolar damage makes the lungs stiff and they become
less distensible or compliant
*Type II cells proliferate with some epithelial cell regeneration,
fibrosis, and remodeling.
61. Both Type 1 and Type 2 Pneumocytes are damaged in ARDS T/F? T!

Type 2 Pneumocytes are more resistant to damage compared

to Type 1 Pneumocytes, however both are damaged in ARDS
62. ARDS and atelectasis *Hyperactivation of coagulation and/or inflammation damages
both type I and II pneumocytes
*Decreased type II pneumocytes results in decreased
surfactant production => low lung compliance and subsequent
atelectasis
63. Both Congestive Heart Failure and ARDS can cause significant In CHF, increased hydrostatic pressures from fluid backing up in
pulmonary edema. How does the cause of pulmonary edema the pulmonary system causes pulmonary edema
differ in these two settings?
In ARDS, increased capillary permeability is the basis for the
edema
64. What is the most important distinguishing point between ARDS Pulmonary capillary wedge pressure ((PCWP; AKA Swan-
and cardiogenic pulmonary edema? Ganz catheterization) is normal in ARDS

ARDS: Usually < 15 mmHg

Cardiogenic pulmonary edema: Usually > 18 mmHg
65. A 50-year-old male presents to the emergency department with sharp epigastric pain of 7 5. Pulmonary capillary wedge
hours duration. The pain was sudden in onset and radiates to the back. The patient has a pressure (PCWP) < 18 mmHg
history of chronic alcoholism. He does not take any medications. The patient is admitted to
the hospital and given 1 liter of normal saline. Several hours later, the patient appears This patient has acute pancreatitis,
markedly short of breath. Temperature is 36.9 degrees Celsius, blood pressure is 130/75 and later experiences symptoms of
mmHg, pulse is 110/min, and respiratory rate is 33/min. Physical examination is notable for respiratory failure consistent with
labored breathing and crackles at both lung bases. Chest X-ray is shown in Figure A. ARDS. A PCWP < 18 mmHg would
Which of the following would help confirm a diagnosis of Acute Respiratory Distress provide additional clinical evidence
Syndrome (ARDS)? that the respiratory failure was
secondary to ARDS and not
1. White blood cell (WBC) count > 18,000 cells/mm^3 hydrostatic edema.
2. Blood glucose > 220 mg/dL
3. Serum lactate dehydrogenase (LDH) > 400 ARDS is a dreaded complication of
4. PaO2 < 60 mmHg acute pancreatitis. ARDS presents
5. Pulmonary capillary wedge pressure (PCWP) < 18 mmHg with progressive hypoxemia not
responsive to supplemental oxygen
and other signs and symptoms similar
to cardiogenic pulmonary edema.
PCWP is useful in differentiating
ARDS from pulmonary edema and is >
18 mmHg in fluid overloaded states
66. A 37 year old woman with alcoholism is admitted to the intensive care unit for treatment of a. ARDS
severe alcoholic pancreatitis. She had several episodes of vomiting 2 hours before
admission. During the first 12 hours, her vitals have been the following: Pulse 100-130/min; ARDS is a complication of pancreatitis
respirations 28-36/min, and systolic blood pressure 90-110 mm Hg. Fourteen liters of and the normal PCWP rules out CHF
crystalloid solution have been infused to maintain a urine output of 30 mL/h. Because her
arterial oxygen saturation has fallen into the 80% to 89% on 100% oxygen by face mask,
she is intubated and being mechanically ventilated. One hour after intubation, her pulse is
110/min, blood pressure is 90/60 mm Hg. The lungs are clear to auscultation.

Pulmonary artery catheterization shows:

Cardiac index 4.2 L/min/m2 (N=2.5-4.2)
Central venous pressure 11 cm H2O (N=5-8)
PCWP 10 mm Hg (N=5-16)

Arterial Blood Gas Analysis on an FiO2 of 60% and PEEP of 10 cm H2O shows:

pH 7.32 PcO2 38 mmHg P02 78 mm Hg

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
injury while skiing in a remote area. Upon her
arrival to the ER, she is severely hypoxemic and
not responsive to O2 therapy. She is started on a
mechanical ventilator and 2 days later upon
auscultation, you note late inspiratory crackles.
Which of the following is most likely normal in this
patient?
1. Type I pneumocytes
2. Type II pneumocytes
3. Chest X-ray
4. Alveolar-arterial gradient
5. Left atrial pressure
68. A 72-year-old man is admitted to the hospital for
treatment of a systemic bacterial infection
secondary to obstructive uropathy. On the third
day of his hospitalization, he complains of
shortness of breath and progressive hypoxemia.
Which of the following parameters is most likely to
be normal if this patient suffers from acute
respiratory distress syndrome?
A. Lung compliance
B. Work of breathing
C. V/Q matching
D. Capillary wedge pressure
E. Capillary permeability
69. A patient becomes tachypnic with a falling O2
saturation that is not corrected with administration
of 100% O2. A chest radiograph is taken and
shown in Figure A. Which disease process is the
LEAST likely to cause this presentation?
1. Pulmonary embolism
2. Septic shock
3. Trauma
4. Acute pancreatitis
5. Gastric aspiration
5. Left atrial pressure
This patient is suffering from acute respiratory distress syndrome (ARDS). One
of the main criteria for ARDS is the absence of cardiogenic pulmonary edema,
and hence the left atrial pressure would be normal.
ARDS is a classic cause of non-cardiogenic pulmonary edema. The left atrial
pressure (usually estimated using the pulmonary capillary wedge pressure)
would most likely be normal, a finding used to distinguish ARDS from other
causes of pulmonary edema. A chest x-ray of an ARDS patient initially shows
bilateral infiltrates, progressing to widespread alveolar consolidation with air
bronchograms. Neutrophils damage both type I and type II pneumocytes in
ARDS
D. Capillary wedge pressure
Sepsis is a major risk factor for the development of adult respiratory distress
syndrome (ARDS). One of the minor diagnostic criteria for ARDS is absence of
cardiogenic pulmonary edema which means that the pulmonary capillary
wedge pressure is usually normal. An elevated wedge pressure would be more
suggestive of a cardiogenic (hemodynamic) cause of pulmonary edema, such
as pulmonary venous hypertension.
ARDS is characterized by diffuse injury to the pulmonary microvascular
endothelium and/or alveolar epithelium, resulting in increased pulmonary
capillary permeability and a leaky alveolocapillary membrane. The interstitial
and intra-alveolar edema, inflammation, and hyaline membrane formation
cause lung compliance to decrease, the work of breathing to increase, and the
oxygen diffusion capacity of the lung to decrease. More severe involvement
and/or atelectasis of regional alveoli can cause VIQ mismatch (decreased
ventilation with maintained perfusion).
(choices A, B, C, and E) These would all be expected to have abnormal values
in ARDS.
1. Pulmonary embolism
The clinical presentation is consistent with Acute Respiratory Distress
Syndrome (ARDS). ARDS is not strongly associated with a pulmonary embolism
(PE).
70. 50 yr old man comes to the physician for follow up examination. One year ago he was C) decreased diffusing capacity of
admitted to the hospital for treatment for ARDS associated with acute carbon monoxide (DLCO)
pancreatitis.Which of the following is most likely to be found in this patient with
Resolved ARDS ? DLCO is just a test to measure the
diffusion capacity of lung. CO is diffusion
A) decreased alveolar dead space :tidal volume limited while CO2 and O2 are perfusion-
b) decreased concentrations of surfactant protein D limited.
c) decreased diffusing capacity of carbon monoxide (DLCO)
d) Increased concentrations of neutrophils in bronchoalveolar lavage fluid Fibrosis resulting from ARDS impairs
e) Increased concentration of surfactant protein D diffusion
f) Increased pulmonary capillary blood volume
71. Causes of ARDS Remember causes of ARDS with the
mnemonic ARDS UP (AAAARDDDSSS
UP):

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?

1. Diffuse alveolar damage

2. Ventricular septal defect
3. Myocardial free wall rupture
4. Papillary muscle rupture
5. Myocardial reinfarction
81. ... ...
82. A 50 yr old man comes to the physician for follow up examination. One year ago he was C) Decreased diffusing capacity of
admitted to the hospital for treatment of ARDS associated with acute pancreatitis.Which carbon monoxide (DLCO)
of the following is most likely to be found in this patient with Resolved ARDS ?

A) Decreased alveolardead space :tidal volume

B) Decreased concentrations of surfactant protein D
C) Decreased diffusing capacity of carbon monoxide (DLCO)
D) Increased concentrations of neutrophils in bronchoalveolar lavage fluid
E) Increased concentration of surfactant protein D
F) Increased pulmonary capillary blood volume
83. Neonatal Respiratory Distress Syndrome *AKA hyaline membrane disease
*MCC of respiratory failure in premature infants
*Characterized by insufficient surfactant levels and progressive
atelectasis
*Perfused but not ventilated =>
*Infant is typically preterm but of weight appropriate for gestation age
*Presentation: respiratory difficulty soon after birth and resulting cyanosis
*
*
*
*With treatment, 90% of infants with NRDS survive.
84. Around what week of development are the levels of 35
surfactant considered mature?
85. Pathophysiology of NRDS

*Deficiency of surfactant -> increased surface tension -> progressive

86. Describe the clinical presentation of NRDS
87. What would an arterial blood gas (ABG) show in an
infant with neonatal respiratory distress syndrome?
88. What type of acid base disorder is present in NRDS
89. Describe the typical appearance on CXR in NRDS
atelectasis of alveoli
*Perfusion without ventilation -> increased CO2 and decreased
O2/hypoxemia
*Rsults in acidosis, pulmonary vasoconstriction, capillary endothelial and
alveolar epithelial damage
*Endothelial/capillary damage results in a protein rich/fibrin rich exudate
into alveolar spaces with the formation of hyaline membranes
*Hyaline membranes impair diffusion of gases and hypoxemia is
worsened
*Hypoxemia further impairs surfactant production
*Typically, increased respiratory effort is the first symptom (30 -60
minutes after birth)
*Tachypnea, grunting, nasal flaring
*Forceful intercostals retraction and use of accessory neck muscles
...
Respiratory acidosis
"Ground glass" granularity of the lung parenchyma

FIND A PIC
90. How is Maternal Diabetes associated with NRDS Increased fetal blood glucose results in increased fetal insulin production

High insulin levels decrease surfactant production

91. What are 3 important complications of excessive O2 Complications of supplemental O2 therapy include (mnemonic: RIB):
therapy in neonates? Retinopathy of prematurity
Intraventricular brain hemorrhage
Bronchopulmonary dysplasia
92. What is the mechanism by Temporary hyperoxia in the retina causes upregulation of VEGF => retinal vessel proliferation
which supplemental O2 (neovascularization)
therapy for NRDS can
cause Retinopathy of Blindness is a potential complication
prematurity?
93. A male infant is born C. Formation of a fibrovascular mass behind the lens
markedly prematurely at
25 weeks of gestation. Due Retinopathy of prematurity (ROP), also called retrolental fibroplasia (because of the formation of a
to the immaturity of his fibrovascular mass behind the lens), is a cause of blindness in premature infants that is related to the
lungs, therapy with oxygen therapeutic use of high concentrations of oxygen. Immature blood vessels in the retina, particularly in
is used. Because of the peripheral portion of the temporal retina, are prone to injury with high-dose oxygen, which inhibits
extensive medical the production of vascular endothelial growth factor (VEGF). This inhibition causes apoptosis of
intervention, this vascular endothelial cells with subsequent constriction and obliteration of the retinal blood vessels.
premature infant survives, This initial stage of ROP is referred to as the vaso-obliterative phase. Withdrawal of oxygen therapy
but unfortunately he is stimulates VEGF production and results in a marked increase in the proliferation of vascular endothelial
found to be blind resulting cells with new blood formation (neovascularization). This phase of ROP is called the vasoproliferative
from the use of oxygen. phase. The incidence of this complication has been markedly reduced due to close clinical monitoring
Which one of the following of the concentration of administered oxygen. In contrast, accumulation of abnormal material in the
pathologic abnormalities ganglion cells of the retina is seen clinically as a "cherry red macula," while fibrous obliteration of the
correctly describes the canal of Schlemm is a cause of closed-angle glaucoma. Lipid accumulation at the periphery of the
pathology that caused this cornea produces corneal arcus, a commonly found aging change. Degeneration of the macula occurs
infant's blindness? most often due to age-related maculopathy, but it can also be caused by inherited disorders or drugs,
such as chloroquine.
A. Accumulation of
abnormal material in the
ganglion cells of the retina
B. Fibrous obliteration of
the canal of Schlemm
C. Formation of a
fibrovascular mass behind
the lens
D. Lipid accumulation at
the periphery of the
cornea
E. Severe degeneration of
the macula
94. Describe the gross Lungs are solid, airless, and reddish purple (similar to the color of the liver)
appearance of the lungs in
NRDS
95. _________ results in Atelectasis
intrapulmonary (right-to-
left) shunting in both
ARDS and NRDS
96. How is C-Section birth an Neonates who undergo ceasarean delivery are at increased risk for NRDS because they are not
increased risk for NRDS exposed to the stress of vaginal delivery and may not experience the stress-induced increase in
corticosteroids that stimulates surfactant production
97. A lecithin-sphingomyelin >2: Fetal maturity
ratio of _________ is <1.5: NRDS
suggestive of fetal
maturity

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:

Cortisol (promotes synthesis)

Insulin (inhibits synthesis)
Thyroxine (promotes synthesis)
101. Compare the prognosis of NRDS vs ARDS With treatment, 90% of infants with NRDS survive.
With treatment, 40% of patients with ARDS die, even in the ICU
*** check these numbers***
102. Why should fluid volumes be kept low in a patient with acute Fluid volumes should be kept low to prevent pulmonary edema.
respiratory distress syndrome?
103. What is the primary functional component of pulmonary Lechitin/ Phosphatidylcholine
surfactant?
104. Surfactant reduces surface tension within the lung, facilitating facilitates expansion during inspiration
expansion during ________(inspiration/expiration) and prevents atelectasis during expiration
preventing atelectasis during ________(inspiration/expiration).
105. Foam Stability Index Test and NRDS ...
106. Stages of ARDS ...
107. FINISH LAST 7 MINUTES OF PATHOMA ...
108. A pneumothorax is defined as a collection of air in the A pneumothorax is a collection of air in the pleural space,
__________ between the lung and chest wall.
109. 2 Mechanisms by which a pneumothorax occurs There are 2 ways this generally occurs:

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)

Symptoms typically include pleuritic chest pain, dyspnea

111. Physical Exam findings of Tension Pnemothorax A tension pneumothorax can present with all the signs & symptoms
of a spontaneous pneumothorax, as well as
SHOCK/HYPOTENSION and JVD due to compression of the
superior vena cava.
112. What is a spontaneous pneumothorax? A spontaneous pneumothorax is a pneumothorax that occurs
without any inciting event (such as trauma).
How are the different types of spontaneous pneumothorax
classified? There are two types of spontaneous pneumothorax that are
classified based upon whether or not there is a known underlying
lung disease (Primary vs Secondary)
113. Primary vs Secondary A primary spontaneous pneumothorax (PSP) occurs in individuals with no known lung diseases.
Pneumothorax In most cases, the affected individual has a previously unrecognized lung disease and the
pneumothorax originates from the rupture of a subpleural bleb (aka bullae). The typical patient
affected by a PSP is a tall male between the ages of 20 and 40 (a PSP is rare in individuals over
40).

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?

A) Apical subpleural blebs

B) Centriacinar emphysema
C) Compensatory hyperinflation
D) Obstructive hyperinflation
A) Apical subpleural blebs
E) Panacinar emphysema

CXR of spontaneous PTX. Note the

red arrows outlining the collapsed
lung.

Unilateral chest pain +

hyperresonant to percussion +
absent breath sounds + tall thin
male + dyspnea + tachypnea =
spontaneous pneumothorax
119. A 28-year-old smoker presents to the emergency This patient is most likely suffering
department because of sudden onset of from a spontaneous
chest pain and dyspnea while at rest. His heart pneumothorax.
rate is 115/min, respiratory rate is 24/min, and Caused by the rupture of a small
blood pressure is 140/80 mm Hg in both arms. apical
Lung examination shows decreased breath bleb on the surface of the lung,
sounds and decreased fremitus on the right spontaneous
with hyperresonance to percussion. Which of pneumothoraces typically present
the following would most likely be seen on this in tall young
patient's x-ray of the chest? men. The patient usually has
sudden pain and
(A) A widened mediastinum dyspnea. Examination will show
(B) Barrel chest and flattened diaphragm decreased
(C) Consolidation in the right lower lobe breath sounds and
(D) Contralateral deviation of the trachea hyperresonance on the affected
(E) Tracheal deviation to the ipsilateral side side. Spontaneous pneumothorax
is treated by inserting a chest tube
to remove
the air from the pleural space.
120. What is the immediate treatment of a tension pneumothorax? A tension pneumothorax should
be treated immediately with a
needle decompression (aka
needle thoracostomy).
121. How do you treat a small (less than 3 cm) primary spontaneous pneumothorax that is not life Stable patients with small primary
threatening? spontaneous pneumothorax
(<3cm) on imaging can be given
supplemental oxygen & observed
as most small pneumothoraces will
resolve on their own.
122. What finding is suggestive of cardiac tamponade as opposed to
tension pneumothorax in the setting of trauma-induced shock with
distended neck veins?
In the setting of thoracic trauma, hypotensive tachycardia
with distended neck veins is suspected to be either cardiac
tamponade or a tension pneumothorax (though more rare
pathologies could be causative). *Distant, muffled heart
sounds are indicative of cardiac tamponade.

Blood will also be found in the pericardial sac on emergent

bedside ultrasound examination (the "FAST" exam).*

Pulmonary exam findings of decreased breath sounds and

hyperresonant percussion are indicative of tension
pneumothorax.
123. What two radiographic findings on chest x-ray are indicative of Diaphragmatic ruptures most commonly occur on the left,
diaphragmatic rupture? because the liver prevents right-sided rupture.

Two radiographic findings on chest x-ray are multiple air-

124. Penetrating trauma must be considered regardless of the mechanism
of injury in the setting of trauma to what part of the body
125. Pathogenesis of a Tension Pneumothorax
126. After you stabilize a patient with a tension pneumothorax, what
intervention is still required?
127. A 22-year-old basketball player who uses cocaine recreationally
suddenly develops severe shortness of breath after a routine
scrimmage. Physical examination shows respirations of 25/min. The
left lung field is hyperresonant and breath sounds are diminished.
Which of the following is the most likely diagnosis?
fluid levels and presence of nasogastric tube in the
thorax.
Thoracic trauma is unique in that blunt trauma may cause
secondary penetrating trauma via fractured rib penetration.
Therefore, penetrating trauma must be considered in any
case of thoracic trauma.
A tension pneumothorax occurs when the visceral pleura or
parietal pleura are involved in a tissue defect that forms a
one-way valve that lets air into the pleural space (but not
back out). This results in trapping of the air in the pleural
cavity.
After a needle decompression of a tension pneumothorax,
the patient still needs a chest tube.
e)Pneumothorax

a)Acute respiratory distress syndrome

b)Cor pulmonale
c)Flash pulmonary edema
d)Pleural effusion
e)Pneumothorax
128. Flail Chest *A flail chest is a segment of chest wall that exhibits
paradoxical respiratory mechanics (i.e. expansion on
expiration) correctable by PEEP (positive end-expiratory
pressure).
*It occurs when segments of ribs are broken in two places
to create a separate segment of chest wall.
*The best early treatment of a flail chest is pain control and
supplemental oxygen to maximize excursion and
oxygenation.
129. Sleep Apnea *Central sleep apnea
-no respiratory effort deriving from ↓ CNS drive
Obstructive sleep apnea
-physical airway obstruction
-may be caused by
↓ pharyngeal muscle tone
-obese neck pressing on the upper airway
↑ size of tonsils
-nasal septal deviation
*Increased risk in down syndrome
*Diagnosis: Sleep Study
*Tx: Mild Sleep apnea: Behavioral changes (i.e losing weight); Sleeping on side;
Patients should avoid sedative-hypnotics and alcohol before bedtime
*Moderate to severe: C-PAP(continuous positive airway pressure)
130. Clinical presentation of Sleep Apnea Daytime somnolence
Snoring or choking during the night
Morning headaches
Poor concentration
Decreased libido
131. What is the most common cause of Adenotonsillar hypertrophy
obstructive sleep apnea in children? (Enlarged tonsils or adenoids)
132. Sleep Apnea is equally common in men and F!
women T/F? More common in men
133. What are some signs and symptoms of Sleep *Daytime somnolence (often simulating narcolepsy)
Apnea *Loud snoring
*Irritability and impaired relationships
*Falling asleep while driving
*Poor job performance
*Depression
134. What are some complications of Sleep *Respiratory acidosis (retained CO2)
Apnea? *Systemic Hypertension
*Arrhythmias (due to prolonged hypoxia)
*Pulmonary Hypertension and Cor Pulmonale (due to hypoxic vasoconstriction)
135. What is the defining characteristic of sleep Repeated cessation of breathing > 10 seconds during sleep
apnea?
136. Why may patients with sleep apnea have a As a response to the respiratory acidosis caused by the sleep apnea
chronic elevation of serum bicarbonate?
137. Atelectasis *
*
*
*
*
*
*
*
138. Pleural Effusion *Accumulation of fluid in the pleural space (between parietal and visceral pleura)
*Depending on the etiology, can be Exudative,
Transudative, or Chylous
*
*
*
139. What are some presenting symptoms of a patient with a pleural effusion? Dyspnea on exertion
Orthopnea
Paroxysmal nocturnal
dyspnea
Fever
Cough
Chest pain with inspiration
*******************
140. Compare the pathophysiology between Transudative, Exudative, and Chylous pleural effusion Transudative: Increased
hydrostatic pressure or
decreased oncotic pressure
(capillaries still intact)

Exudative: Increased vessel

permeability in acute
inflammation

Chylous: Interruption of the

thoracic duct
141. Thoracentesis is used to determine whether the pleural fluid is transudative or exudative using According to Light's Criteria,
Light's criteria. What is Light's Criteria? at least 1 of the following
suggests an exudative
effusion:

Pleural protein/serum protein

ratio > 0.5
Pleural LDH/serum LDH ratio
> 0.6
Pleural LDH >200 U/L
142. A 40-year-old man has the recent onset of right-sided chest pain, difficulty breathing, and fever. D) Neutrophils, increased
On auscultation he has crackles, decreased respiratory sounds, and evidence of a right-sided vascular permeability, edema
pleural effusion. Which of the following best describes the expected type of inflammatory
process involving the lung?

A) Fibroblasts, collagen deposition, replacement of intrinsic tissue

B) Macrophages, lymphocytes, increased concentrations of immunoglobulins
C) Mast cells, histamine, smooth muscle contraction
D) Neutrophils, increased vascular permeability, edema
E) Vascular budding, fibroblasts, edema, proteoglycans
143. On CXR, transudative effusions tend to be ______________(unilateral/bilateral), whereas exudative Transudative: Bilateral
effusions tend to be ______________(unilateral/bilateral Exudative: Unilateral
144. What signs on physical examination should be present in a pleural effusion? Dullness to percussion over
the area of effusion
Absent breath sounds
Absent tactile fremitus
Contralateral shift of the
mediastinum (in large
effusions)
145. A 60 year old man comes to the physician because of a 1 month history of progressive F) Pleural effusion
shortness of breath with exertion. Examination of the chest shows:
Pneumonia: Increased fremitus
Breath sounds--decreased in R lung base, normal in L lung base Pneumothorax: Hyperresonant
Percussion note--dullness in R lung base, normal in L lung base
Tactile fremitus--decreased in R lung base, normal in L lung base
Adventitious sounds--none in R lung base, crackles in L lung base

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?

Blunting of the costophrenic angle and

obscuration of the diaphragm

*Picture shows normal diaphragmatic

angle on left
147. How does nephrotic syndrome lead to pleural effusion? Nephrotic syndrome can cause a
transudative pleura due to decreased
oncotic pressure
148. A 17-year-old boy is brought to the emergency department because of a high-grade C) Exudate
fever and increasingly severe diffuse abdominal pain during the past 3 hours. The pain
started 2 days ago, but it resolved without medical treatment until hours prior to Specific gravity > 1.015 = Exudate
admission, when the abdominal pain recurred. He appears anxious, pale, and
diaphoretic. His temperature is 38* C (100.4 F). Abdominal examination shows guarding
and rebound tenderness. An exploratory operation is done. A sample of fluid obtained
from the abdominal cavity is found to have a specific gravity greater than 1.020,
numerous leukocytes (mainly segmented neutrophils), and cellular debris. Which of the
following best describes this fluid?

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:

Glucose - Pleural fluid - 80 mg/dl

Serum - 100 mg/dl
Protein - Pleural fluid - 2 g/dl
Serum - 7 g/dl
Lactate Dehydrogenase - Pleural fluid -
25 U/L
Serum - 50 U/L
Total nucleated cell count - Pleural fluid
- 500/mm3

Which of the following is the most likely

cause of her pleural effusion?

A) Decreased lymphatic drainage

B) Decreased oncotic pressure
C) Decreased serum protein
concentration
D) Increased hydrostatic pressure
E) Increased vascular permeability
150. A 61-year-old man is hospitalized. On
the fifth day of his hospital stay, a chest
x-ray film reveals a pleural effusion.
Thoracentesis is performed, yielding 250
cc of fluid with a pleural fluid
protein/serum protein ratio of 0.7, and a
lactate dehydrogenase level of 240 U/L.
Which of the following conditions may
lead to development of an exudate
within the pleural cavity?
A. Bacterial pleuritis
B. Cirrhosis of the liver
C. Congestive heart failure
D. Nephrotic syndrome
E. Protein-losing enteropathy
151. What are three options for removal of
pleural effusion fluid?
152. During thoracentesis, the needle is
inserted along what aspect of the rib
(superior or inferior)?
A. Bacterial pleuritis
Exudative effusions are characterized by one or more of the following: pleural fluid
protein/serum protein >0.5, pleural fluid LDH/serum LDH > 0.6, or pleural fluid LDH more
than two-thirds normal upper limit for serum. An exudate results from leakage of
protein-rich fluid from the plasma into the interstitium. It is usually the result of increased
vascular permeability caused by inflammation. Exudates also contain numerous acute or
chronic inflammatory cells, depending on the inciting event. Of the above choices, only
bacterial pleuritis would produce an exudate. If pleuritis is caused by pyogenic
organisms, the exudate is purulent (neutrophil-rich). If pleural inflammation is due to
mycobacterial infection or neoplastic infiltration, the resulting exudate will contain
chronic inflammatory cells.
In contrast, a transudate contains less protein and few inflammatory cells. There are two
main mechanisms of transudate formation: 1) decreased oncotic pressure, such as that
which occurs in cirrhosis of the liver, nephrotic syndrome, and protein-losing
enteropathy (choices B, D, and E); and 2) increased hydrostatic pressure, which may
result from congestive heart failure (choice C).
*Thoracocentesis: needle is used to draw fluid out of the pleural space
*Chest tube: left in place to drain pleural fluid over the course of several days
*Pleural drain: put and left in place for long periods for a more chronic condition
Superior
The needle and catheter are inserted on the superior border of the rib, in order to avoid
the neurovascular bundle.
153. What is the general rule for needle insertion site for a Thoracocentesis?

1-2 intercostal spaces below the upper

level of pleural fluid at the midscapular
line or 5-10 cm lateral to the spine

Confirm the level of pleural effusion on

the posterior chest wall by
-auscultation: decreased or absent
breath sounds
-percussion: dullness
-fremitus: diminished or absent
vibrations

-Superior border of the rib to avoid

neurovascular bundle
-Should not be below the 9th rib to
avoid diaphragm or abdominal viscera
154. An 82 year old woman is admitted to the hospital for treatment of a small right pleural D) Above the 9th rib in the midscapular
effusion. physical examination shows dullness to percussion at the level of the 7th rib line
and below on the right. a thoracocentesis is done. the patient is sitting up, supported by
leaning against a bedside table. After preparing the skin and delivering a local 1-2 intercostal spaces below the upper
anesthetic, into which of the following locations on the right is it most appropriate to level of pleural fluid at the midscapular
insert the catheter? line or 5-10 cm lateral to the spin

A) Above the 5th rib in the midscapular line.

B) Above the 5th rib to the right of the sternum.
C) Above the 7th rib in the paravertebral region.
D) Above the 9th rib in the midscapular line
E) Below the 5th rib in the midaxillary line
F) Below the 5th rib in the midclavicular line
G) Below the 9th rib in the midscapular line
155. What is the most common clinically significant complication of Thoracocentesis? Pneumothorax

Pneumothorax is suspected after

thoracentesis if patients are
symptomatic (eg chest pain, dyspnea,
and hypoxemia) or if air is aspirated
during the procedure
*****
156. What is the most common cause of obstructive sleep apnea in adults? Obesity
157. An 87-year-old woman with a
history of metastatic
adenocarcinoma of the breast
presents with difficulty in
breathing. A plain chest film reveals
massive left pleural effusion. The
physician chooses to drain the fluid
with a thoracentesis. What is the
proper location for placement of
the cannula (hollow needle) to drain
the pleural effusion? (B) Midaxillary line—9th intercostal space

(A) Midaxillary line—6th intercostal
space
(B) Midaxillary line—9th intercostal
space
(C) Parasternal line—6th intercostal
space
(D) Parasternal line—2nd intercostal
space
(E) Midclavicular line—5th
intercostal space
158. Pulmonary Embolism
159. Which region of the lung is more
likely to infarct in a PE?
160. Most symptomatic pulmonary
emboli arise from deep venous
thrombosis (DVT) in which veins?
161. What type of acid base disturbance
is seen with pulmonary embolism?
162. What is a saddle embolus?
Patient is suffering from a pleural effusion (accumulation of excess fluid in the pleural cavity
surrounding the lung). The effusion causes the difficulty in breathing due to limiting the
expansion of the lungs during inspiration (like cardiac tamponade). A thoracentesis is an
invasive procedure to remove the excess fluid from the pleural sac. In the midaxillary line, the
lung resides at the 8th rib and the parietal pleura would reside at the 10th rib. The space
between the parietal pleura and the lung is the costodiaphragmatic recess, and it gives space
for the lung to inflate within the pleural cavity.
*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
Since there is greater perfusion at the lower lobes of the lung, pulmonary emboli most
commonly occur in the bases of the lungs.
Popliteal, iliac, and femoral
Respiratory alkalosis
(hypocapnia due to tachypnea and hyperventilation)

A large embolus that occludes the main branches of a pulmonary artery

163. What are lines of Zahn?

Alternating pale pink bands of platelets

and fibrin with red bands of RBC's

Lines of Zahn are only found in thrombi

formed in flowing blood, before the
death of the patient

Used to differentiate between Pre-vs

Postmortem pulmonary emboli
164. Autopsy examination of the main pulmonary arteries of a man presumed to have died E. Postmortem clot
from a massive cerebrovascular hemorrhage demonstrates a rubbery, congealed mass
of blood that is easily detached from the vessel wall. The clot has a homogeneous
color without evidence of layering on low power microscopic examination. This is an
example of which of the following?

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)

A. Bronchial arteries If there is underlying heart failure or

B. Bronchial veins other diseases causing inadequacy of
C. Pulmonary arteries bronchial arterial supply, wedge shaped
D. Pulmonary veins infarcts will be found which increases
E. Superior vena cava risk of morbidity and death
168. What imaging test is used to confirm a
diagnosis of pulmonary embolism?
What imaging finding indicates the
presence of pulmonary embolism?
169. Superior Vena Cava Syndrome
Pulmonary CT angiography is the gold-standard imaging test
Filling defects indicate the presence of pulmonary embolism.
Note that chest x-ray is most commonly NORMAL in the setting of a pulmonary
embolism.
*Obstruction of the SVC
*Impaired blood drainage from the upper body (head, neck, upper chest, arms)
*Most common cause is compression due to tumor (esp Small cell carcinoma)
*Presentation: Swelling of face, dyspnea, dilated collateral veins in the upper trunk.
Can raise ICP if obstruction is severe => headaches, dizziness
*If caused by a pancoast tumor, shoulder pain and Horner's syndrome are typically
present
170. A 47 year old man comes to physician because of a 3 week history of increasing facial K- vascular obstruction
swelling and 1 week history of headaches and mild shortness of breath. He had
previously felt well. He completed chemo course 4 months ago for small cell CA of
lung. temp 98.9, bp 142/80 w/ 8mmhg paradoxical pulse, pulse 84, resp 18/min.
Examination shows significant diffuse facial and periorbital edema. optic discs are
sharp and ocular movements intact. Lungs are hyperresonant bilaterally with
moderately prolonged expiratory phase. Mild rhonchi are heard on inspiration and
expiration. Chest Xray shows a 10 cm mass in the right upper lobe and apex. Which is
the most likely explanation for these findings?

A- chemo induced bone marrow toxicity

B- chemo related cardiac toxicity
C- hypercoagulable state 2ndary to malignancy
D- interstitial metastatic pulmonary disease
E- intracranial mets
F- lymphatic obstruction
G-malignant pericarditis
H- paraneoplastic syn
I- pleural mets
J- soft tissue mets
K- vascular obstruction
171. The development of facial flushing,distended neck and head superficial
veins(engorgement of veins ), inspiratory stridor and elevation of the jugular venous
pressure (JVP) upon raising both of the patient's arms above his/her head
simultaneously, as high as possible.

Name the sign and diagnosis?

Sign: Pemberton's sign

Dx: SVC syndrome