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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2664_Библиотеки_им_академика_М_И_Перельмана
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USMLE Step 2 CK
l Internal Medicine
Pneumoconiosis
Definition. The pneumoconioses are occupational lung diseases in which inhalation of certain fibers initiates an inflammatory process that eventually leads to fibrosis of the lung.
Usually, pneumoconiosis appears 20–30 years after constant exposure to offending agents
(metal mining of gold, silver, lead, copper) but can develop in <10 years when dust exposure
is extremely high.
History is of primary importance in assessing possible occupational lung diseases.
Pathology. Alveolar macrophages engulf offending agents, causing inflammation and fibrosis
of the lung parenchyma in pneumoconiosis. Respiratory insufficiency is the ultimate consequence of the pneumoconioses.
Diagnosis. Signs and symptoms include dyspnea, shortness of breath, cough, sputum production, cor pulmonale, and clubbing. PFTs show a restrictive pattern with a decreased DLco.
Hypoxemia is evident with an increased PAo2-Pao2 gradient. Chest x-ray findings include
small irregular opacities, interstitial densities, ground glass appearance, and honeycombing.
Asbestosis
Definition. Asbestosis is an occupational lung disease caused by prolonged inhalation of asbestos dust. The result is lung parenchymal fibrosis which results in respiratory compromise.
Epidemiology. Asbestos fiber exposure may be seen in mining, milling, foundry work, shipyards, or the application of asbestos products to pipes, brake linings, insulation, and boilers.
History of exposure to asbestos is needed to consider the diagnosis.
Signs and Symptoms. These include exertional dyspnea and reduced exercise tolerance, cough
and wheezing (especially among smokers), chest wall pain, and ultimately respiratory failure.
On chest x-ray, diffuse or local pleural thickening, pleural plaques, and calcifications at the
level of the diaphragm are seen. Pleural effusions are commonly seen, and the interstitial lung
process associated with asbestosis usually involves the lower lung fields.
The most common cancer associated with asbestosis is bronchogenic carcinoma (adenocarcinoma or squamous cell carcinoma).
Pleural or peritoneal mesotheliomas are also associated with asbestos exposure but are not as
common as bronchogenic cancer.
Diagnosis. A lung biopsy is usually necessary for the diagnosis of asbestosis, in which the classic barbell-shaped asbestos fiber is found.
Treatment. No specific treatment is offered. It is important that patients with asbestos exposure
stop smoking since the risk of lung cancer is 75 times higher than that of the normal population.
Silicosis
Definition. Silicosis is an occupational lung disease caused by inhalation of silica dust.
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Epidemiology. Silicosis is seen in individuals who work in mining, quarrying, tunneling, glass
and pottery making, and sandblasting.
Signs and Symptoms. Silicosis will cause similar symptoms to asbestosis (or any other pneu-
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moconiosis) except the acute form of silicosis, which is caused by massive exposure that
causes lung failure in months.
Pathology. Silica causes inflammatory reactions with pathologic lesions being the hyaline nodule.
most prominent in the upper lobes. A characteristic finding is eggshell calcifications (rare). In
progressive massive fibrosis, densities are 10 mm or more and coalesce in large masses.
Diagnosis. Same as asbestosis.
Treatment. There is no effective therapy for silicosis. Death occurs usually because of progres-
sive respiratory insufficiency.
There is an association of silicosis with pulmonary TB. Patients with silicosis should have
yearly purified protein derivative (PPD) tuberculin testing; a patient with positive reactive PPD
(>10 mm) should get isoniazid (INH) prophylaxis for 9 months.
Coal miner’s lung/coal worker’s pneumoconiosis (CWP)
Epidemiology. The risk of development and progression of CWP is related to the amount of
coal dust exposure, higher rank (hardness) of coals, and increased silica content of inhaled
dust. Simple CWP is seen in 12% of all miners.
Chapter 9
l Pulmonology
Signs and Symptoms. CWP clinically presents as any other occupational lung disease.
Chest X-Ray. Small round densities are seen in the parenchyma, usually involving the upper
half of the lungs. Complicated or progressive massive fibrosis is diagnosed by the presence of
larger densities from 1 cm in diameter to the entire lobe.
Associated Immunologic Abnormalities. Increased levels of IgA, IgG, C3, antinuclear antibodies (ANA), and rheumatoid factor are abnormalities seen in CWP.
In Caplan syndrome there are rheumatoid nodules in the periphery of the lung in a patient
with rheumatoid arthritis and coexisting pneumoconiosis (usually CWP).
PULMONARY THROMBOEMBOLISM
A 32-year-old woman is brought to the emergency department with an acute
onset of shortness of breath and pleuritic chest pain that occurred while she was
shopping. She has never been sick and takes no medications other than oral
contraceptives. Her respiratory rate is 26/min and pulse 107/min. Auscultation
is clear, and the rest of the examination is normal. ABG shows evidence of mild
hypoxemia (7.52/70/25/93%). Chest x-ray is normal.
Overview. Thromboembolic disease is a common cause of morbidity and mortality in the
hospital and outpatient setting and poses a diagnostic challenge even for seasoned clinicians.
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l Internal Medicine
Clinically significant pulmonary emboli, for the most part, arise from proximal (above-theknee) deep vein thrombi (DVT). In turn, most proximal DVT are a consequence of propagation of distal (below-the-knee) DVT. Studies have shown that distal DVT, by themselves, do
not pose a risk for the development of a pulmonary embolus. In one-third of the cases, they
extend to the proximal veins and thus become a source of pulmonary emboli.
Pulmonary embolism can infrequently occur with upper extremity, subclavian, and internal
jugular vein thrombosis. This type of thromboembolic disease occurs in patients when IV
catheters are placed in the associated veins. Also, in the pregnant patient, thrombosis may
occur initially in the pelvic veins rather than follow the usual course of starting in the distal
and then extending to the proximal veins.
Pulmonary embolism and DVT are considered one disease.
• Be concerned about (and treat) proximal vein thrombosis because this may result in pulmonary
embolism.
• In pregnant patients and those with IV catheters, look for the source of the thromboembolism in
uncommon places (pelvic veins, upper extremity veins, etc.).
Clinical Pearl
In patients with patent
foramen ovale, venous
thromboembolism may result
in embolization involving
the systemic circulation. This
frequently presents as CVA.
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Biomedical Communications 2007—Custom Medical Stock Photo.
Figure 9-11. Unilateral Right Leg Swelling Due to Deep Venous Thrombosis
Natural Course. After a proximal DVT dislodges, it travels through the vena cava and into
the right side of the heart. It usually breaks off into multiple thrombi as it goes into the pulmonary circulation, obstructing parts of the pulmonary artery. This results in increased alveolar dead space, vascular constriction, and increased resistance to blood flow. When ~50% of
the lung vasculature is involved, significant pulmonary hypertension may occur. This is followed by an increase in right ventricular workload and may lead to right-sided heart failure.
A massive pulmonary embolus occurs when >70% of one lung is involved.
About 10% of patients with pulmonary embolus will die within 1 hour of the event, most from a
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massive pulmonary embolus or significant comorbid conditions (e.g., preexisting CHF or COPD).
When to Consider Pulmonary Embolism and DVTs:
High-risk patients
• Recent surgery, especially orthopedic surgery (knee replacement surgery carries a 70%
risk for DVT)
• Cancer history (prostate, pelvic, abdominal, and breast). Note: Studies following
patients with unexplained DVT found that 15-20% of these patients developed cancer
within the first 2 years after the diagnosis of a DVT.
• Immobile patients (especially those hospitalized); patients with significant heart failure; long travel
• Acquired thrombophilia, especially lupus anticoagulant, nephrotic syndrome (loss of
antithrombin III in the urine), and oral contraceptives (the risk increases further if the
patient is a current smoker)
• Inherited thrombophilia, of which the most common is factor V Leiden mutation (protein
C resistance); others include protein C and S deficiency and antithrombin III deficiency
• Pregnancy, for which increased risk for thromboembolism will continue until 2 months
after the delivery
Chapter 9
l Pulmonology
Consistent symptoms and signs:
• Sudden onset of dyspnea (shortness of breath) and tachypnea
• Thigh or calf swelling with or without dyspnea
• Pleuritic chest pain
• Hemoptysis (occurs only with infarction, which is rare because of the dual circulation
[bronchial and pulmonary] that supports lung parenchyma)
• On exam, always increased respiratory rate with tachycardia; increased pulmonic
sound (P2)
The Wells’ Criteria risk stratifies patients for PE, and has been validated in both inpatient and
emergency department settings. While there are other scoring systems for PE and DVT, the
Wells criteria are the most widely used in the United States:
• Symptoms of DVT (3 points)
• No alternative illness that explains symptoms (3 points)
Immobilization (≥3 days) or surgery in the previous 4 weeks (1.5 points)
•
• Prior history of DVT or PE (1.5 points)
• Presence of hemoptysis (1 point)
• Presence of malignancy (1 point)
Scoring is done as follows:
• Score >6 = high probability of PE
• Score ≥2 but <6 = mean moderate probability of PE
• Score <2 = low probability of PE
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Clinical Pearl
Consider pulmonary
embolus in all patients with
dyspnea and normal chest
radiography.
l Internal Medicine
Tests for the Diagnosis of Thromboembolic Disease
General tests are nonspecific, though they may provide important clues for the diagnosis. They
are done routinely in the emergency department in the evaluation of patients with dyspnea.
Arterial blood gas (ABG) tests usually show evidence of hypoxemia with an elevated A-a gradient. In ~10% of patients with documented pulmonary thromboembolism, the A-a gradient may
be normal and the hypoxemia mild.
Chest x-rays are very important in finding other causes that may account for the patient’s
symptoms. The most common chest x-ray finding associated with pulmonary thromboembolism is a “normal” chest x-ray. Other nonspecific findings include atelectasis and pleural effusion (transudative and exudative).
• Westermark sign is the lack of vascular markings that occur distal to the pulmonary
embolus.
• Hampton hump is a wedge-shaped infiltrate (just above the diaphragm) and is due to
pulmonary infarction
The ECG may show evidence of right heart strain (due to the development of acute pulmonary hypertension), which manifests as large S waves in lead I and deep Q waves in lead III
with T-wave inversion in the same lead (mnemonic: S1, Q3, T3). The most common finding
on the ECG is sinus tachycardia. The ECG is also an important tool in excluding other causes
with similar symptoms, specifically acute pericarditis and myocardial ischemia.
Specific tests are more specific for the evaluation of thromboembolic disease (do them when
considering the diagnosis).
Wikipedia, James Heilman, MD
Figure 9-12. Pulmonary Embolism CT
• Pulmonary embolism:
– CT pulmonary angiogram (CT-PA) is the most frequently performed initial test for
the diagnosis of pulmonary embolism. It allows direct visualization of the pulmonary
embolus, and it also allows for the diagnosis of alternative diseases involving the lung
parenchyma (pneumonia, pneumothorax, etc.). The older generation of CT-PAs may
miss pulmonary emboli that involve the smaller (peripheral) pulmonary arteries.
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Chapter 9
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l Pulmonology
– Ventilation-perfusion (V•/Q•) scan is a pair of nuclear scan tests that use inhaled and
injected material to measure breathing (ventilation) and circulation (perfusion) in
all areas of the lung. A pulmonary embolus will typically cause perfusion defects
with normal ventilation. The V•/Q• scan, depending on the number of defects, is
classified as normal, low probability, intermediate probability, or high probability.
Patients that have any preexisting lung disease (COPD) will have at least intermediate scans, which make this test less helpful. A normal V•/Q• scan rules out pulmonary
embolus.
– Pulmonary angiogram is the gold standard procedure for the diagnosis of pulmo-
nary embolus. Its risk of complication (e.g., pulmonary artery rupture) is <1%.
With the new generation of CTs able to visualize the smallest peripheral vessels, the
invasive pulmonary angiogram is becoming obsolete.
• DVT: compression on duplex U/S (US); venogram (rare); MRI
• Both pulmonary embolism and DVT:
– D-dimer is the most sensitive test for thromboembolic disease. Elevated D-dimer
indicates the presence of an abnormally high level of fibrin degradation products,
possibly because of thrombus formation and breakdown. An elevated D-dimer may
be due to a thromboembolism, but it may also be due to a recent surgery, infection,
trauma, pregnancy, and DIC. Normal D-dimer tests mean that there is no thrombus formation or breakdown. For the above reasons, a D-dimer can only be used
to rule out PE or DVT if the levels are normal. Trials have shown that the D-dimer
is most useful when the test is done on patients considered to be low-risk and is
recommended as an adjunct test (i.e., a negative D-dimer and a normal CT-PA scan
rule out thromboembolism 98% of the time).
– There are many types of D-dimer tests with different sensitivities. The ELISA assay
is the best test overall, whereas the latex agglutination test is less sensitive.
Clinical Pearl
• Order CT-PA as the primary
test to diagnose pulmonary
embolus.
• Use V•/Q• scan in patients
with iodine allergy, renal
insufficiency, or morbid
obesity.
General diagnostic concepts in patients suspected of pulmonary embolism:
• It makes sense to start with a CT-PA after a chest x-ray is completed.
• Normal CT scan and normal D-dimer test in low-risk patients excludes pulmonary
embolism.
• Normal CT scan and normal Doppler U/S in low-risk patients excludes
pulmonary embolism.
• Even if all tests are negative for pulmonary embolism but the patient is high risk, go
for the angiogram.
If a V•/Q• scan is completely normal (not near normal or low probability), the chance of
•
pulmonary embolism is almost 0%.
• Know how to use Doppler U/S in the evaluation of pulmonary embolism. For example, if a V•/Q• scan is reported as low probability, still be concerned about pulmonary
embolism. An angiogram is not preferred unless absolutely necessary because it is an
invasive procedure. Therefore, do an U/S of both lower extremities to look for a DVT
(remember that most pulmonary emboli are complications of DVTs arising in the
proximal veins).
• All patients (especially high risk) should be on anticoagulation while completing
diagnostic evaluations, so start heparin before sending that patient off to the radiology department for the CT or the V•/Q• scan.
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Figure 9-13. Management of Diagnosed Pulmonary Embolism
Hemodynamically stable Hemodynamically unstable
l Internal Medicine
Diagnosed Pulmonary Embolism
Anticoagulation
contraindicated
Inferior
vena cava filter
Treatment. Give oxygen and start heparin immediately before the diagnosis is confirmed and
while the diagnostic workup is being completed. Once the diagnosis is confirmed:
Anticoagulation
contraindicated
Thrombolytic
therapy
IV or LMW heparin and oral
anticoagulation (warfarin) 5-7 days
Oral anticoagulation (warfarin)
for at least 6 months
• Heparin—LMWH or unfractionated for 5-7 days (or until INR is therapeutic)
• In most institutions, LMWH has supplanted the use of unfractionated heparin as the
primary heparinoid in the treatment of PE and DVT.
• Warfarin (Coumadin®)—should be started with heparin and continued for 6 months
for both pulmonary emboli and DVT.
Pulmonary embolectomy
and interrupt inferior vena cava
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LMWH or fractionated heparin inactivates factor Xa but has no effect on thrombin (no
need to follow PTT). Dosing is based on patient’s weight, and the effect is very predictable.
The long half-life makes it ideal for a 1× or 2×/day dosing interval. Trials have shown that
LMWH is as good as unfractionated heparin in the treatment of DVT and pulmonary emboli;
also, LMWH is less likely to cause hemorrhage or heparin-induced thrombocytopenia (HIT).
HIT is a common complication of heparin treatment and occurs 5-7 days after starting treatment in about 5% of patients. Paradoxically, it is associated more with thrombotic events than
bleeding diathesis. Always stop heparin when platelets decrease by a significant amount. Also,
consider HIT in a patient with recurrent pulmonary embolism or DVT despite heparin treatment. HIT is treated with the new anticoagulants (argatroban, lepirudin).
Warfarin works by inhibiting the vitamin K–dependent factors (II, VII, IX, and X). Because
factor VII has the shortest half-life of all the affected factors, prothrombin time (PT) is monitored to assess the warfarin anticoagulant effect. International normalized ratio (INR) is a way
to report PT and is used to control for variability in PT between different laboratories. The
warfarin dose should be titrated to an INR of 2-3 for effective anticoagulation.
Warfarin skin necrosis is a rare procoagulant effect that occurs in patients who have preexist-
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ing protein C deficiency and receive warfarin. Protein C is also a vitamin-dependent factor
with a shorter half-life than factor VII. A “transient hypercoagulable state” occurs when
warfarin is started in patients with subclinical protein C deficiency. This leads to diffuse
thrombosis of the skin and other organs. By starting patients on heparin and warfarin at the
same time, you minimize the risk for this complication.
Anticoagulation is contraindicated in patients with recent neurosurgery or eye surgery.
Consider using an inferior vena cava filter (Greenfield filter) to prevent further embolism in
these patients.
Warfarin is contraindicated in pregnant patients. LMWH for 6 months is the best alternative.
The patient should have injections once or twice a day.
Thrombolytics (tPA, streptokinase) are not used routinely in pulmonary embolism and
should be reserved for patients that become hemodynamically unstable (indicated by hypotension, right heart failure, etc.). In clinical practice, thrombolytics are sometimes also considered in patients with massive DVT to prevent the postphlebitic syndrome.
Although the available vitamin K antagonists are highly effective for the prevention and
treatment of most thrombotic disease, significant patient variability in dose response, the
narrow therapeutic index, and the numerous drug and dietary interactions associated with
these agents have led clinicians to search for alternative agents. These new anti-thrombotic
drugs have relatively discrete targets within the coagulation pathway. Two new classes of
orally administered anticoagulants, inhibitors of factor X and thrombin inhibitors, have
been approved for the management and prevention of venous thromboembolic disease.
Rivaroxaban is a direct factor Xa inhibitor. Dabigatran is a direct thrombin inhibitor that has
been approved for venous thromboembolism prophylaxis.
Chapter 9
l Pulmonology
The postthrombotic syndrome (postphlebitic syndrome) is the most common complication
of DVT, occurring in up to two-thirds of patients. It may result from some obstructions that
remain in the vein or backflow of blood due to destruction of the valves or both. Signs and
symptoms include pain, edema, hyperpigmentation, and skin ulceration. The use of compression stockings has been shown to prevent the postthrombotic syndrome.
Other Concepts in Treatment
• Noncomplicated proximal DVTs are usually treated for a total of 6 months.
• In patients with thrombophilias (hypercoagulable states), lifelong anticoagulation is
considered with warfarin (usually reserved for at least two episodes of thrombosis).
Do not check for protein C or protein S deficiency during acute thrombosis. Both
•
warfarin (which the patient should be on) and acute clot formation lower protein C
and S.
• In patients that develop recurrent thrombosis while on anticoagulants, consider HIT or
cancer-related thrombosis (very resistant). Consider placing an inferior vena cava (IVC)
filter or using some of the newer anticoagulant classes (e.g., hirudin derivatives). IVC
filters are associated with clot formation around the filter site and may cause pulmonary thromboembolism.
• Limited distal DVT (below-the-knee DVT) are not themselves a cause of pulmo-
nary embolism, unless they extend to the proximal veins. Management of distal DVT
includes 2 options: monitor for possible extension to the proximal veins by using serial
U/S or treat with anticoagulation for 3 months.
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l Internal Medicine
Fat embolism is a rare type of embolism that occurs 3 days after long bone fracture (most
commonly seen with femur fracture). It may occur, although rarely, after CPR. The clinician
should consider this entity with presence of acute dyspnea, petechiae (neck and axilla), and
confusion. Treatment is supportive (no anticoagulation).
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
A 32-year-old man is admitted to the intensive care unit with the presumed
diagnosis of gram-negative sepsis. He is placed on double gram-negative
antibiotic coverage and remains stable for 24 hours. The blood cultures grow
pseudomonas sensitive to both ceftazidime and ciprofloxacin, which the patient
has been started on. The patient seems to improve but suddenly during day 2 of
hospitalization develops severe dyspnea. The examination reveals diffuse crackles;
an ABG shows hypoxemia and hypercarbia. Diffuse alveolar densities are seen on
chest x-ray (the admission chest x-ray was unremarkable).
ARDS is defined as an acute lung injury that is characterized by increased permeability of the
alveolar-capillary membrane and pulmonary edema. It eventually leads to severe hypoxemia
and decreased pulmonary compliance.
Clinical Pearl
Chronic elevation of serum
bicarbonate may be seen in
patients with sleep apnea. This
is a response to respiratory
acidosis.
Etiology. Etiology of ARDS includes sepsis, trauma, disseminated intravascular coagulation,
drug overdose, inhalation of toxins, Goodpasture syndrome, systemic lupus erythematosus,
drowning, and the period after bypass surgery.
ARDS usually occurs within 5 days of the initiating event, and >50% will develop it within
the first 24 hours. A major component of ARDS seems to be accumulation of inflammatory
cells and their mediators.
Signs and Symptoms. Signs and symptoms of ARDS are dyspnea, increased respiratory rate,
and diffuse rales and rhonchi on auscultation.
Chest x-ray findings include diffuse interstitial or alveolar infiltrates; whiteout of both lung
fields may be seen. ABGs reveal decreased Pao2 and increased or normal Paco2. Swan-Ganz
catheter findings will reveal normal cardiac output and normal capillary wedge pressure but
increased pulmonary artery pressure.
Treatment. Treat underlying disorder. Mechanical support with increased positive endexpiratory pressure and permissive hypercapnea. Studies have shown that conservative fluid
replacement decreased ICU and ventilatory time but mortality remained unchanged. Steroid
use is controversial.
Prognosis. Mortality rates are approximately 50%.
SLEEP APNEA
Sleep apnea is defined as the cessation of airflow (>10 s) that occurs at least 10−15x per hour
during sleep. Oxygen saturation decreases during those apneic episodes, and pulmonary pressures increase.
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Daytime somnolence is mandatory for the diagnosis of sleep apnea. Other manifestations
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include daytime headaches and fatigue. Systemic hypertension also occurs. When severe, sleep
apnea will cause pulmonary hypertension and cor pulmonale.
The diagnosis of sleep apnea is based on evaluation of clinical symptoms (daytime sleepiness,
fatigue, sleep diary findings, and the results of objective testing with polysomnography.
There are 2 main classes of sleep apnea:
• Obstructive sleep apnea (OSA) occurs because of floppy airways despite adequate
ventilatory effort. Patients are usually obese and have abnormal airways. Treatment is
weight loss and nasal continuous positive airway pressure (CPAP). When noninasive
measures are not effective, surgical procedures (uvuloplasty) may be considered.
• Central sleep apnea (<5%) is caused by inadequate ventilatory drive. Treatment
includes conservative measures (weight loss; avoidance of alcohol, sedatives, and sleep
deprivation), acetazolamide, progesterone, and supplemental oxygen.
LUNG CANCER
Chapter 9
l Pulmonology
Bronchogenic Carcinoma
A 65-year-old man is admitted because of headache and blurry vision the past
few days. In the emergency room the physicians also notice that he has neck vein
distension and darker coloration over his face and neck. He is confused. Chest
x-ray reveals a right upper lobe lung mass, and blood tests indicate significant
hypercalcemia.
Bronchogenic carcinoma is the leading cause of death because of malignancy in men and women.
The overall 5-year survival rate for small cell cancer is 5% and non-small cell cancer is 8%.
Etiology. Ninety percent of cases of bronchogenic carcinoma are directly related to cigarette
smoking in both men and women. The occasional nonsmoker who has lung cancer develops
adenocarcinoma.
Smoking is the major cause of lung cancer. Active smokers have a 10× greater risk compared
with nonsmokers. The risk is directly related to the number of pack-years (40-pack-year history increases risk 60–70×). Asbestos exposure increases the risk of bronchogenic carcinoma
75× that in the nonexposed normal patients.
All lung cancers are associated with smoking.
There is no available screening test for lung cancer at this time.
Pathology. The most common lung cancers are adenocarcinoma (~40% in some studies) and
squamous cell carcinoma.
• Adenocarcinoma. Adenocarcinoma is a peripherally located lesion. This lesion metastasizes widely to essentially the same sites as small-cell carcinoma. Bronchioalveolar
carcinoma is a subtype of adenocarcinoma; it is a low-grade carcinoma that can occur
in single or multiple nodules. Asbestos exposure can be an underlying causative agent,
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