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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
Note
There are rare cases of erosive
OA, polyarticular OA, and OA
with inflammatory features.
These are exceptions, and you
do not need to know them.
Intraarticular injection of hyaluronic acid has been approved for treatment of knee OA that
hasn’t responded to pharmacologic treatment. Despite this, the efficacy of hyaluronic acid has
been questioned since a large clinical trial failed to demonstrate superiority over intraarticular
injections of saline. Similarly glucosamine and chondroitin sulfate are not routinely used in
the treatment of OA since in 4 recent randomized, double blind trials both of these agents
were no more effective than placebo.
Also, clinical trial results based on analysis of x-rays suggested the possibility of glucosamine
being chondroprotective. Since the radiologic methods employed in the trial were limited,
there was concern about the interpretation of such data. A current multicenter trial sponsored
by the National Institutes of Health is under way in order to address this question.
CRYSTAL-INDUCED ARTHROPATHIES
Definition. The crystal-induced arthropathies, monosodium urate (MSU), calcium pyrophosphate (CPPD), calcium oxalate (CaOx), and calcium hydroxyapatite (HA), are caused
by microcrystal deposition in joints. In spite of differences in crystal morphology, they have
identical clinical presentations and can only be distinguished by synovial fluid analysis.
Gout
Gout is a disease that affects middle-aged men and presents most commonly with acute monoarthritis (women represent only about 5–15% of all patients with gout; premenopausal women
make up 17% of all women with gout). As gout becomes chronic, multiple joints may be
involved, and deposition of urate crystals in connective tissue (tophi) and kidneys may occur.
The metatarsophalangeal joint of the first toe is commonly affected (podagra), but other joints
like the knee, ankle, PIPs, or DIPs may be initially involved. The first episode commonly occurs
at night with severe joint pain waking the patient from sleep. The joint rapidly becomes warm,
red, and tender (it looks exactly like cellulitis). Without treatment the joint pain goes away
spontaneously within 3–14 days.
Certain events that precipitate gout sometimes precede the attack: excessive alcohol ingestion,
red meat intake, trauma, surgery, infection, steroid withdrawal, drugs (diuretics, such as HCTZ
[hydrochlorothiazide] and furosemide; anti-TB medicines, such as pyrazinamide and ethambutol), and serious medical illnesses.
MSU deposition causes an intense inflammatory process—red, warm joint. Thus, on an x-ray
of a joint that has been involved in multiple gouty attacks you would expect to find
_________________.
Diagnosis. The serum uric acid during the acute attack may be normal or low. On the other
hand, many people have elevated serum uric acid levels and never develop gout. Thus, the
serum uric acid level is of no value in the diagnosis of acute urate arthropathy. This is why the
diagnosis is made by the analysis of synovial fluid.
On synovial fluid analysis, the MSU crystals are _______ birefringent and _____ shaped. The
number of WBCs should be between ______________.
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Treatment
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Acute gouty arthritis: The goal is to decrease inflammation and thus prevent erosions and
joint destruction; also in this stage it is very important to avoid any fluctuations in serum uric
acid levels.
• NSAIDs
• Steroids, oral, rarely intraarticular, in elderly patients who cannot tolerate NSAIDs or
colchicine or in patients with renal impairment
• Colchicine is rarely to be used in acute gout but is still available.
Chapter 3
l Rheumatology
Chronic hypouricemic therapy: The goal here is to decrease uric acid levels. This is usually
required for life and initiated in patients who have had recurrent gouty attacks that cannot be
corrected by low-purine diet, limitation of alcohol, avoiding diuretics, etc. Unlike acute gout,
here the uric acid level may be helpful in following the effect of hypouricemic treatment.
• Allopurinol can be used in overproducers, undersecretors, or patients with renal failure or kidney stones
• Febuxostat is used in those intolerant of allopurinol.
• Pegloticase dissolves uric acid: used in refractory disease
• Probenecid can be used in the undersecretors (>80% of adults) only. Rarely used today.
A 32-year-old man comes with a history of right ankle swelling that occurred the
night before. He has noticed that his ankle has been red, warm, and very painful.
He occasionally drinks alcohol. On examination you find a red swollen ankle with
evidence of an effusion. The range of motion is restricted.
What is the first step in this patient? Aspiration
What do we do after confirming the diagnosis? Treat with NSAIDs
Six months after the first episode he comes back to your office with left knee
swelling. A red, warm knee is noted on examination.
Note
Allopurinol should not be
initiated during an acute crisis.
However, if a patient has been
taking allopurinol and an acute
attack occurs, it should not be
discontinued.
Clinical Pearl
Use primarily allopurinol in the
chronic treatment of gout.
What is the first step now? Aspiration again
What do you do after confirming the diagnosis? NSAIDs
Answers to question
on previous page
On a routine visit the same patient has had 4 documented episodes of gout
erosive calcifications
despite limiting alcohol and diet.
negative; needle; 5,000 and
50,000
What would be the appropriate next step here? Consider allopurinol or probenecid
You have decided to place him on allopurinol. He does very well for more than
2 years with no gouty attacks. He then experiences another episode of right ankle
swelling.
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USMLE Step 2 CK
l Internal Medicine
Clinical Pearl
Always investigate patients
with pseudogout for
systemic disease, especially
hemochromatosis.
Pseudogout
Definition and Pathogenesis. CPPD crystal deposition is more common in the elderly population and in people who have preexisting joint damage.
A small percentage of the patients have metabolic abnormalities that are associated with
CPPD deposition (secondary). Remember the 4 Hs: hyperparathyroidism, hemochromatosis,
hypophosphatemia, hypomagnesemia. The presence of pseudogout in a patient <50 years of
age should raise suspicions about one of these metabolic abnormalities.
Clinical Manifestations. Pseudogout may have an acute presentation like gout. It may also
present in an asymptomatic and chronic form. The knee is the most commonly affected joint;
other joints commonly affected are the wrist, shoulder, and ankle.
Diagnosis. Definitive diagnosis requires the typical rectangular, rhomboid, positive birefringent crystals on synovial fluid evaluation.
Radiographs may reveal linear radiodense deposits in joint menisci or articular cartilage
(chondrocalcinosis). (Do not forget to look at an x-ray of chondrocalcinosis before going to
the exam.)
Treatment. The treatment is the same as gout. Prevention of frequent recurrences may be treated with low doses of colchicine.
SEPTIC ARTHRITIS
A 67-year-old woman with history of RA for many years presents with right
shoulder pain and swelling for 2 days. She has low-grade fever. The examination
reveals decreased passive and active range of motion of the right shoulder joint,
as well as erythema. She asks you if this is related to an RA flare and if she
should start steroids to decrease the pain.
What is the next step? Do an arthrocentesis
The most common cause of infectious arthritis is gonorrhea, and gonococcal arthritis
accounts for 70% of episodes in patients age <40. Women are at greater risk during menses
and pregnancy and are 2–3 times more likely than men to develop disseminated arthritis.
In older patients, Staphylococcus aureus is a common cause of infectious arthritis and occurs
in patients with preexisting joint destruction from other rheumatic diseases. Patients with RA
have the highest risk because of chronic inflamed or destroyed joints, steroid therapy, and
frequent skin breakdown over deformed joints.
Acute bacterial infection may cause rapid cartilage destruction, and thus a patient presenting
with monoarticular arthritis needs prompt diagnosis. This is done by arthrocentesis. Further,
Staph or Strep must be cleaned out of the joint space by arthocentesis or arthroscopy.
Remember that most infected joints with gonococcal will not have positive cultures, and the
Gram stain will be negative.
Treatment. Treatment should focus on the likely etiology. For example, a 30-year-old woman
with acute monoarticular arthritis who is found to have >50,000 WBCs in the synovial fluid
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without crystals should be treated with ceftriaxone. A 72-year-old man with RA with the same
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findings should be treated with nafcillin or vancomycin.
This disease is discussed further in the Infectious Diseases chapter.
VASCULITIS SYNDROMES
Definition. Vasculitis is an inflammatory process involving the blood vessels that results in
decrease of the lumen diameter and eventual ischemia of the tissues supplied.
The vasculitis syndromes are stratified according to the types of vessels involved.
Wegener Granulomatosis
Wegener granulomatosis is a small vessel vasculitis that can involve any organ system but
mainly affects the respiratory tract (sinuses, nose, trachea, and lungs) and kidneys.
The most common sign of Wegener granulomatosis is involvement of the upper respiratory
tract, which occurs in nearly all patients. Symptoms include rhinitis, sinusitis, and, rarely,
nasal ulcers. A common sign of the disease is chronic rhinitis that does not respond to usual
treatment and that becomes increasingly worse.
Chapter 3
l Rheumatology
The lungs are affected in most people despite lack of symptoms. If symptoms are present, they
include cough, hemoptysis, and dyspnea. Kidney involvement occurs in >80% of people with
this disorder and is a major cause of morbidity and mortality. Arthritis occurs in about 60%
of the cases.
Patients with Wegener granulomatosis usually have the presence of antineutrophil cytoplasmic antibodies (C-ANCA). Although a positive ANCA test is useful to support a suspected
diagnosis of Wegener granulomatosis, it is never diagnostic. Also, the C-ANCA test may be
negative in some people with active Wegener. The only way to confirm the diagnosis is by
performing a biopsy of an involved organ (usually the nasal septum), which demonstrates the
presence of vasculitis and granulomas.
The standard treatment consists of a combination of a glucocorticoid and an immunosuppressive agent (cyclophosphamide). In a study of 158 patients who were treated with prednisone and cyclophosphamide at the National Institutes of Health (NIH), 90% markedly
improved; after years of follow-up, 80% of the patients survived.
Polyarteritis Nodosa (PAN)
PAN is a multisystem disease that may present with nonspecific complaints such as fever, malaise, weight loss, anorexia, and abdominal pain. The disease can affect nearly any site in the body,
except the lungs. It has a predisposition for organs such as the skin, kidney, nerves, and GI tract.
Peripheral neuropathies are very common (70%). This includes tingling, numbness, and/or pain
in the hands, arms, feet, and legs, and mononeuritis (e.g., foot drop). GI manifestations are also
common, such as abdominal pain and GI bleeding (occasionally is mistaken for inflammatory
bowel disease). A minority of patients with PAN have an active hepatitis B infection.
Clinical Pearl
The diagnosis is made by biopsy of involved organs, taken more commonly from skin,
symptomatic nerves, or muscles. The diagnosis is confirmed by a biopsy showing pathologic
changes in medium-size arteries. An angiogram of the abdominal vessels may also be very
In patients with PAN, exclude
co-existing chronic active viral
hepatitis.
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USMLE Step 2 CK
l Internal Medicine
helpful in diagnosing PAN since aneurysms affecting the arteries of the kidneys and/or GI
tract are found.
Before the availability of effective therapy, untreated PAN was usually fatal within weeks to
months. Most deaths occurred as a result of kidney failure, or heart or GI complications.
Effective treatment is now available for PAN and consists of high doses of corticosteroids,
along with immunosuppressive drugs (cyclophosphamide).
Churg-Strauss Syndrome
This syndrome shares many of the clinical and pathologic features of PAN and can involve
any organ. The cardinal manifestations of Churg-Strauss syndrome are asthma, eosinophilia,
and lung involvement (for the sake of remembering this syndrome, you may consider this
Churg-Strauss as PAN in an asthmatic patient). The typical patient with Churg-Strauss is a
middle-aged individual with new-onset asthma. Asthma symptoms may begin long before the
onset of vasculitis. Other symptoms include: mononeuropathy (mononeuritis multiplex similar to PAN), transient pulmonary infiltrates on chest x-rays, paranasal sinus abnormalities,
nasal polyps, and allergic rhinitis.
Diagnosis is made by biopsy and treatment is similar to PAN (combination of prednisone and
cytotoxic agent).
Clinical Pearl
Always consider TA in patients
with new-onset headache who
are age >50–60.
PAN and Churg-Strauss syndrome both involve the small- and medium-sized arteries.
Temporal Arteritis (TA)
TA, also known as giant cell arteritis, is a vasculitis affecting the large arteries that supply the
head, eyes, and optic nerves. New-onset headache in any patient age >50 prompts consideration of this diagnosis, which if left untreated may result in permanent vision loss.
The most common symptoms of giant cell arteritis are headache and pain that usually occurs
in one or both temples. Other common symptoms include scalp tenderness (pain when
combing hair), jaw claudication (jaw pain when chewing), decreased vision or blurry vision,
tongue numbness, or, rarely, sudden loss of vision. Sometimes the patient may have proximal
stiffness (neck, arms, hips) due to polymyalgia rheumatica, a coexisting condition with TA.
Over 25% of patients with TA also have polymyalgia rheumatica.
The erythrocyte sedimentation test (ESR) is the first test to do in patients suspected to have
TA. Since the ESR is always increased in TA, all patients will have an elevated ESR (100%
sensitive). The diagnosis is always confirmed by biopsy of the temporal arteries in which the
characteristic giant cells are demonstrated. In the patient whom you suspect to have TA, if
the ESR is elevated, corticosteroids should be started immediately, before the temporal artery
biopsy is performed. Do not withhold treatment waiting for the biopsy to be done.
A 72-year-old woman comes to you because she has been bothered by a rightsided headache for the past 4 weeks. She has never had migraine headaches and
denies blurry vision, nausea, or vomiting. The headache does not get worse any
specific time of the day. She has noticed a feverish feeling and hip stiffness along
with the headache.
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What is the first step? Do an ESR; if elevated, start prednisone
INFLAMMATORY MYOPATHIES
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A 42-year-old woman is admitted to your service with severe proximal weakness
for 2 months. Her examination shows a diffuse lilac rash over the sun-exposed
areas. The motor strength is 3/5 in the upper and lower proximal muscle groups.
Definition. The inflammatory myopathies are inflammatory muscle diseases that present with
progressive muscle weakness. They include polymyositis, dermatomyositis, and inclusion body
myositis.
Clinical Findings. Patients report difficulty with tasks that involve the proximal muscles: lifting objects, combing hair, getting up from the chair, etc. Fine-motor tasks that involve the
distal muscles, e.g., writing, are only affected late in the disease. Ocular muscles are never
involved; this feature differentiates the inflammatory myopathies from myasthenia gravis and
Eaton-Lambert syndrome.
Dermatomyositis will also have skin involvement; the heliotrope rash is a purple-lilac discoloration of the face, eyelids, and sun-exposed areas of the body. Gottron’s papules are the scaly
lesions seen sometimes over the knuckles.
Chapter 3
l Rheumatology
Laboratory Findings. The inflammatory destruction of muscles causes an elevation of the
muscle enzymes (sometimes up to 50-fold), creatine phosphokinase (CPK), and aldolase.
These are the most sensitive tests to perform in patients suspected of inflammatory myopathies.
Autoantibodies (anti-Jo-1) occur in patients with inflammatory myopathies, which supports
the possible autoimmune origin of these diseases.
Diagnosis. Electromyography shows evidence of myopathic potentials characterized by shortduration, low-amplitude units. Diagnosis is confirmed by muscle biopsy.
Treatment. Steroids are useful in polymyositis and dermatomyositis. Inclusion body myositis
is resistant to immunosuppressive therapy.
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Gastroenterology
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Chapter Title
Learning Objectives
❏ List diseases that should be considered for presenting complaints of epigastric pain,
diarrhea, or constipation
❏ Describe the presentation and management of a patient with GI bleed
❏ Describe the epidemiology and management of diseases of the esophagus, liver,
pancreas, and colon including cirrhosis, acute pancreatitis, and colon cancer
❏ Describe the types of malabsorption syndrome, their causes, and treatment
❏ Differentiate diverticular disease and different forms of IBD in terms of their
presentation and treatment
00
4
DISEASES OF THE ESOPHAGUS
The majority of diseases of the esophagus result in dysphagia. Dysphagia refers specifically
to difficulty swallowing. Only a few of the diseases of the esophagus result in pain on swallowing, called odynophagia. Both dysphagia and odynophagia will result in weight loss if the
symptoms persist for more than a few days. The mere presence of dysphagia or odynophagia
is not sufficient to help one establish a diagnosis. The basic questions are, What additional
information has to be added to this presentation to sufficiently answer the question, and,
Which of the following is the most likely diagnosis?
In general, a barium swallow or barium esophagram is a good answer to questions asking
for the best initial test. This is not an absolute answer, however, and if there are clear signs of
obstruction, then the answer could also be upper endoscopy as the best initial test.
Achalasia
A 32-year-old woman with no past medical history comes to your office for the
evaluation of “difficulty swallowing” foods. She has had this problem for almost
a year, and it is most difficult for her to eat solids. Her symptoms have not
worsened at all over this time period, and her weight has been stable. Physical
examination is unremarkable. What is the next step in evaluation?
77
USMLE Step 2 CK
l Internal Medicine
Pathogenesis. Achalasia is the idiopathic loss of the normal neural structure of the lower
esophageal sphincter (LES). The LES is usually contracted to prevent the acidic gastric contents from refluxing backward into the esophagus. For swallowing to occur, there is normally
a relaxation process of the LES in order to allow food to pass into the stomach. Inhibitory
neurons are stimulated, blocking the impulses that cause constriction. In achalasia, these
inhibitory neurons have been lost, as well as the ability to relax the LES. The vast majority of
cases are of unknown etiology. A very small number can be from Chagas disease, gastric carcinoma, or diseases that can infiltrate into the area, such as lymphoma.
Clinical Presentation. Achalasia presents with progressive dysphagia to both solids and liquids simultaneously and can have regurgitation several hours after eating. There can also be
weight loss. Achalasia has no relationship with alcohol or tobacco use. This is different from
esophageal cancer, which not only usually presents with dysphagia to solid foods that progresses to difficulty swallowing liquids, but also is more common in older patients with a long
history of alcohol and tobacco use.
Diagnosis. Esophagogastroduodenoscopy (EGD) is done for alarm symptoms: onset after age
60, anemia, heme-positive stools, >6-month duration of symptoms, and weight loss. Although
a chest x-ray may show an air-fluid level in the dilated esophagus, plain radiography is insufficiently accurate to be very useful. Barium esophagography is very accurate and shows dilation of
the esophagus, which narrows into a “bird’s beak” at the distal end. The most accurate test overall
(gold standard) is esophageal manometry. Manometry shows increased lower esophageal (LES)
resting pressure.
78
Wikimedia, Farnoosh Farrokhi and
Michael F. Vaezi
Figure 4-1. Achalasia
Chapter 4
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Treatment. The best initial therapy is pneumatic dilation or surgery. Pneumatic dilation should
be effective in 80–85% of patients. The procedure gives a 3–5% risk of perforation. Botulinum
toxin injections into the LES are used in those patients not willing to undergo pneumatic dilation, or in whom it has failed. Although the botulinum toxin is relatively benign, the main
limiting factor in its use is a need for additional injections in a few months. Fifty percent will
relapse in 6–9 months, and all patients will need reinjection after 2 years. Botulinum toxin is
also used in patients who are poor surgical candidates, e.g., the elderly with multiple comorbid
conditions who would not tolerate surgery. If both pneumatic dilation and botulinum toxin
injections fail, then surgical myotomy is performed. Myotomy is performed laparoscopically
and results in reflux in 20% of patients as a complication of therapy.
Esophageal Cancer
A 62-year-old man comes for evaluation of progressive “difficulty swallowing
solids and, recently, semisolids” for 4 months. He has noticed a 20-lb weight
loss. His past medical history is significant for reflux esophagitis for 15 years
and a 40-pack-year smoking history. On the physical examination, a 1.5-cm, left
supraclavicular lymph node is found. The remainder of the physical examination
is unremarkable.
l Gastroenterology
Pathogenesis. Esophageal cancer is linked to the synergistic, carcinogenic effect of alcohol
and tobacco use for cases of squamous cell cancer in the proximal two-thirds of the esophagus. Adenocarcinoma is found in the distal third of the esophagus and is associated with
long-standing gastroesophageal reflux disease and Barrett esophagus. The rate of development
of cancer from Barrett esophagus is between 0.4 and 0.8% per year. Squamous and adenocarcinoma are now of equal frequency.
Clinical Presentation. Esophageal cancer presents with progressive dysphagia first for solid
food, then for liquids. Weight loss is prominent. Rarely, halitosis, regurgitation, and hoarseness occur. Hypercalcemia may arise, as it can with most cancers.
Diagnosis. Although a barium swallow can be done first, endoscopy is mandatory because
this is a diagnosis that requires a tissue biopsy. CT scanning detects the degree of local spread,
and bronchoscopy detects asymptomatic spread into the bronchi. Endoscopic U/S is performed for staging.
Treatment. The only truly effective therapy for esophageal carcinoma is surgical resection if the
disease is sufficiently localized to the esophagus. Only 25% of patients are found to be operable.
Five-year survival is 5–20%. Chemotherapy with a 5-fluorouracil-based chemotherapy is combined with radiation to control locally metastatic disease.
Scleroderma (Progressive Systemic Sclerosis)
Pathogenesis. As many as 80 to 90% of patients with scleroderma will develop diminished
esophageal peristalsis from the atrophy and fibrosis of the esophageal smooth muscle.
Clinical Presentation. Although there is dysphagia, the main clue to the diagnosis is simply the
presence of gastroesophageal reflux symptoms in a person with a history of scleroderma. The
LES will neither contract nor relax and basically assumes the role of an immobile open tube.
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