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USMLE Step 2 CK
l Internal Medicine
CENTRAL NERVOUS SYSTEM VISUALIZATION
In general, the most accurate test for evaluating the central nervous system is magnetic resonance imaging (MRI). The MRI is superior for the detection of stroke, cancer, multiple sclerosis, and infections and in the evaluation of the posterior fossa, such as the cerebellum and
brainstem.
The CT scan does not visualize the brainstem well. For example, a stroke is visible on an MRI
in >90% of cases within the first 24 hours after its onset, whereas the CT scan needs 3 to 4 days
before >90% are visible. This is because the MRI is based on the water content of tissues rather
than on the calcium content or simple density of tissue. Within a few hours after the onset of
a stroke, the cells begin to swell and increase their water content. This is immediately visible
on an MRI, whereas for a CT scan to detect an abnormality, the cells must die to decrease the
density of visible cells.
The single exception in which a CT scan is superior to an MRI is in the detection of blood.
As soon as bleeding occurs, it is visible on a CT scan. Therefore, the two cases in which a CT
scan is a better study are to evaluate head trauma and to exclude hemorrhagic stroke. When a
patient arrives within 3 hours of the onset of the symptoms of a stroke, a CT scan is first performed to exclude hemorrhage. This is to see if a patient is eligible for the use of thrombolytic
therapy within these first 3 hours.
A CT scan is also used first for the detection of subarachnoid hemorrhage. On the first day
after the stroke’s onset, the CT scan has 95% sensitivity. The sensitivity diminishes by about
5% per day as the blood is hemolyzed and removed.
Contrast on a scan of the head is indicated primarily for the detection of cancers and infection. When an abscess or neoplastic process is present, there is some disruption of the bloodbrain barrier, causing some extravasation of the contrast, which is visible as a contrast, or
“ring”-enhancing lesion around the mass.
BONE IMAGING
An x-ray is certainly the first study to implement when evaluating trauma and fracture.
Unfortunately, the bone scan has much less specificity and does not reliably distinguish
between bone infection and infection of the overlying soft tissue. The MRI is both 90 to 95%
sensitive and 90 to 95% specific.
Osteomyelitis
When there is the suspicion of osteomyelitis, then an x-ray is done first. Although plain x-rays
lack sensitivity for the first 1 to 2 weeks, the specificity for osteomyelitis is excellent. More than
50% of the calcium content of bone must be lost for osteomyelitis to be visible. The earliest
finding of osteomyelitis on an x-ray is elevation of the periosteum. If the film returns normal
and there is still suspicion of osteomyelitis, then the best test is an MRI. The MRI and technetium nuclear bone scan have the same sensitivity (90–95%); however, the MRI’s specificity
is far greater (90–95%). Both studies should become abnormal within 2 days of the onset of
osteomyelitis. Therefore, a negative bone scan is very useful if it is normal; it means that there
is no osteomyelitis. If it is abnormal, you may still need to perform an MRI.
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Ophthalmology
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Chapter Title
Learning Objectives
❏ Describe the presentation and treatment of glaucoma, cataracts, keratitis, uveitis,
periorbital cellulitis, retinal diseases, and conjunctival diseases
RETINAL DISEASES
Diabetic Retinopathy
Pathogenesis. The etiology of diabetic retinopathy is based on damage to the endothelial lining
of the small blood vessels of the eye. This is identical in pathogenesis to the damage that diabetes causes to all blood vessels in the body, such as in the heart, kidney, brain, and peripheral nervous system. The endothelial lining of the retinal vessels becomes damaged, leading to progressive occlusion on a microscopic level. The occlusion leads to obstruction and increased pressure.
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The earliest form of this adverse effect on the retina is called nonproliferative (or background) retinopathy. Nonproliferative retinopathy is characterized by dilation of veins, micro-
aneurysms, retinal edema, and retinal hemorrhages. Hemorrhages into the retina are not as
damaging as intravitreal hemorrhages because they do not obstruct sight.
Proliferative retinopathy is a more advanced form of the disease and is markedly more serious,
meaning it progresses more rapidly to blindness. As the microvascular damage to the vessels
worsens, these vessels secrete increased amounts of an angiogenesis factor. The vessels are not
providing sufficient nutrition to the retina. The vessels themselves exert an increased effort to
have more of them produced in an effort to deliver more nutrition and oxygen to the retina.
Unfortunately, this “neovascularization,” or new blood vessel formation, leads to the optic
nerve getting covered with abnormal new vessel formation. In addition, hemorrhages protrude
into the vitreous chamber. Vitreal hemorrhages are much more serious than microaneurysms
or intraretinal hemorrhages because they are much more sight threatening.
The whole point of therapy for diabetic retinopathy is to first prevent the patient from ever
progressing to the proliferative phase and, second, to slow down the disease’s progress with
laser photocoagulation, if it occurs.
Clinical Presentation. The clinical presentation of diabetic retinopathy is highly variable.
There may be very advanced disease occurring with no symptoms. Vision may decrease slowly
or rapidly. Vitreal hemorrhages may develop suddenly, and patients will complain of “floaters”
in their vision.
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l Internal Medicine
Retina-Vitreous Surgeons of Central New York
Figure 14-1. Features of Diabetic Retinopathy
Diagnosis. Screening for the presence of retinopathy should be performed on an annual basis
by an ophthalmologist. This is how candidates for fluorescein angiography and laser photocoagulation are found. Fluorescein helps identify which vessels should undergo laser photocoagulation. The laser selectively destroys focal areas of the retina and diminishes the production
of the angiogenesis factor, which causes the proliferative retinopathy.
Treatment of both stages of diabetic retinopathy involves the attempt to have tight control of
glucose, blood pressure, and lipid levels. Proliferative retinopathy additionally involves immediate
treatment with laser photocoagulation. Aspirin, clopidogrel, and other platelet-inhibiting medications have shown no benefit. The more tightly the glucose is controlled within the normal range,
the slower the progression of the retinopathy. Blood pressure should be controlled to a level of
<130/80 mm Hg.
Diabetes is considered by the National Cholesterol Education Program (NCEP) to be the
equivalent to coronary artery disease in terms of its effect on cardiac mortality and on LDL
targets. Even if there is no evidence of coronary artery disease, the target LDL in a diabetic
patient is <100 mg/dL. If the patient is diabetic and has evidence of coronary disease, then the
target LDL can be as low as <70 mg/dL. Glucose control is the most effective of these methods
of retarding progression of the disease.
Retinal Detachment
A 71-year-old woman presents to the physician with blurry vision in her left eye
since that morning. She says it was as if “a curtain came down.” She has had
floaters in the periphery of her left eye over the past few weeks but has had no pain
or erythema. She has a history of stage I hypertension but is otherwise healthy.
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Pathogenesis. Retinal detachment is usually spontaneous, but it may result from trauma.
The term rhegmatogenous, which is used to describe the detachment, is from the Greek word
for “tear.” The two most common predisposing factors are myopia and surgical extraction of
cataracts. Traction on the retina can also occur from proliferative retinopathy from diabetes,
retinal vein occlusion, and age-related macular degeneration.
Clinical Presentation. The most common presentation is blurry vision developing in one eye
without pain or redness. The patient may complain of seeing “floaters,” as well as flashes at the
periphery of vision. Sometimes it is described as a “curtain coming down,” as the retina falls off
the sclera behind it.
Diagnosis is made by ophthalmologic examination.
Treatment. Various methods of trying to reattach the retina are employed. Patients should
lean their heads back to promote the chance that the retina will fall back into place. The retina
can be mechanically reattached to the sclera surgically, by laser photocoagulation, cryotherapy,
or by the injection of expansile gas into the vitreal cavity. The gas will press the retina back
into place. A “buckle,” or belt, can be placed around the sclera to push the sclera forward so
that it can come into contact with the retina. If all of these methods fail to reattach the retina,
then the vitreous can be removed and the retina can be surgically attached to the sclera. The
majority (80%) of uncomplicated rhegmatogenous retinal detachments can be cured with
one operation, with 15% needing a second operation.
l Ophthalmology
National Eye Institute/National Institutes of Health
Figure 14-2. Retinal Detachment
Age-Related Macular Degeneration
Pathogenesis. Age-related macular degeneration (ARMD) is the most common cause of legal
blindness in older persons in the Western world. The etiology is unknown. ARMD is characterized by the formation of deposits of extracellular material collecting into yellowish deposits
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l Internal Medicine
seen on ophthalmoscopy. These deposits are known as “drusen.” They are small, granular, subretinal deposits that are age related.
Clinical Presentation. There are 2 types of ARMD. The first is a dry, or atrophic, form char-
acterized by slowly progressive visual loss in the elderly. Diagnosis is confirmed by finding
clearly visible drusen on dilated eye exam.
The second type of ARMD is the wet, or exudative, form of the disease, characterized by the
abnormal growth of vessels from the choroidal circulation into the subretinal space. These vessels leak, leading to collections of subretinal fluid and a localized, exudative retinal detachment.
Dry-type ARMD leads to visual loss of a slow, gradual nature. Wet type can present with the
rapid distortion of vision over weeks to months. Fluorescein angiography will help confirm the
diagnosis of exudative ARMD.
Treatment. There is no clear evidence that any therapy will stop the progression of dry-type
ARMD. There is some evidence that zinc, antioxidant vitamins such as vitamins C and E,
and beta-carotene may retard the progression of the disease. Wet-type ARMD is treated with
VEGF inhibitors ranibizumab and bevacizumab.
Central Retinal Artery Occlusion
Pathogenesis. The etiology of the disorder can be from carotid artery embolic disease, temporal
arteritis, cardiac thrombi or myxoma, or any of the usual causes of thrombophilia, such as factor
V Leiden mutation.
Clinical Presentation. There is a sudden, painless, unilateral loss of vision. There is no redness
of the eye. Ophthalmoscopy reveals a pale retina, with overall diminished perfusion and a “cherry-red” spot at the fovea. There is also “box-car” segmentation of the blood in the veins.
Diagnosis. These patients should undergo evaluation with carotid artery imaging, echocardiography, and evaluation for thrombophilia.
Treatment. Central retinal artery occlusion is managed in much the same way as for a stroke
(cardiovascular accident [CVA]) or a transient ischemia attack (TIA). It includes laying the
patient flat and supplying oxygen and ocular massage in an attempt to unobstruct the vessel.
Other potential therapies are acetazolamide and thrombolytics. Anterior chamber paracentesis has been used to try to decompress the pressure in the eye and dislodge the embolus.
Central Retinal Vein Occlusion
Pathogenesis. Patients with retinal vein occlusion are at particularly high risk for developing
glaucoma. These patients should be monitored for the possible use of laser photocoagulation.
Younger patients should be investigated for inherited causes of thrombophilia, such as factor
V mutation, protein C deficiency, and antiphospholipid syndromes.
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Clinical Presentation. These patients have a clinical presentation similar to those with retinal
artery occlusion. There is the sudden loss of vision without pain, redness, or abnormality in
pupillary dilation. Ocular examination by funduscopy reveals disk swelling, venous dilation,
tortuosity, and retinal hemorrhages.
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Diagnosis. Retinal hemorrhages are the main way of distinguishing venous obstruction from
arterial obstruction. You can’t have a hemorrhage in the retina if you don’t have blood getting
into the eye.
Treatment. There is no specific therapy for retinal vein obstruction.
GLAUCOMA
Pathogenesis. The precise etiology of the majority of glaucoma is not clearly known. Acute
angle-closure glaucoma can be precipitated by the use of anticholinergic medications, such as
ipratropium bromide or tricyclic antidepressants; however, the majority of people with narrow
angles in their anterior chambers never develop glaucoma.
In those with open-angle glaucoma, the precise etiology of the decrease in the outward flow
of aqueous fluid has never been elucidated. Hence, the precise cause of the increase in intraocular pressure is not known.
Open-Angle Glaucoma
This disorder accounts for >90% of cases of glaucoma. Patients are asymptomatic for a long
time, and this is the reason why it is important to screen older patients.
l Ophthalmology
Diagnosis. The first clue to the diagnosis is a cup-to-disk ratio of >0.3, which should be confirmed by repeated measurements of an elevation in intraocular pressure as determined by
tonometry.
Treatment of glaucoma is based on decreasing the production of aqueous humor while
increasing its drainage. Medications that decrease the production of aqueous humor are betablockers (timolol, betaxolol, levobunolol), alpha-adrenergic agonists (apraclonidine, brimonidine), and carbonic anhydrase inhibitors (dorzolamide and brinzolamide).
Medications that increase the outflow of the humor are prostaglandin analogs, such as topical
latanoprost, travoprost, and bimatoprost. The prostaglandin analogs can lead to a change in the
color of the eyes and a darkening of the eyelid. Pilocarpine is a miotic agent that constricts the
pupil to allow greater outflow of the aqueous humor.
Surgery is performed if maximal medical therapy is ineffective in controlling intraocular pressure.
Laser trabeculoplasty or surgical trabeculectomy are the most commonly performed procedures.
Closed-Angle Glaucoma
Pathogenesis. This disorder is often an ophthalmologic emergency precipitated by the use of
medications that have anticholinergic properties.
Clinical Presentation. It presents with an eye that is red, painful, hard to palpation, and associated with a fixed midpoint pupil. The cornea has a hazy cloudiness, and there is marked
diminishment of visual acuity.
Treatment of acute angle-closure glaucoma is an ophthalmologic emergency. IV acetazolamide,
urea, and osmotic diuretics, such as mannitol or glycerol, are used acutely. Pilocarpine can be
used to open the canal of Schlemm, and beta-blockers are used to decrease humor production. If
these medical therapies are ineffective, laser trabeculoplasty can be performed.
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l Internal Medicine
CATARACTS
Pathogenesis. Cataracts are opacifications of the lens. They are slowly progressive, with a
blurring of vision occurring over months to years. Glare from the headlights of cars is particularly a problem when driving at night. Color perception is reduced in general. The etiology
of cataracts is unknown, although there is an association with cigarette smoking.
Clinical Presentations. Mature cataracts can be easily seen on physical examination. Earlierstage disease is seen with a slit lamp.
Treatment. There is no medical therapy for cataracts. Surgical removal with the placement of
an intraocular lens is the standard of care.
CONJUNCTIVAL DISEASES
Conjunctivitis
Pathogenesis. Conjunctivitis can occur from any infectious agent, including bacteria, viruses,
and fungi.
Clinical Presentation. Bacterial conjunctivitis is more often unilateral and presents with a
marked purulent discharge from the eye. This is most symptomatic in the morning, when the
patient’s eye has developed a significant crust overnight, sometimes making it hard to open the
eye. There is less itching compared with viral conjunctivitis. Although the eye can be red, there is
a normally reactive pupil, as well as normal ocular pressure and no impairment of visual acuity.
Viral conjunctivitis is more often bilateral in nature, with much more severe ocular itching
and enlarged preauricular adenopathy. The eyes are also red, but again, the pupil reacts normally and there is no photophobia.
Treatment of bacterial conjunctivitis is with topical antibiotics, such as erythromycin ointment, sulfacetamide drops, or topical fluoroquinolones. There is no specific microbiologic
treatment for viral conjunctivitis. It is treated symptomatically with topical antihistamine/
decongestants.
Subconjunctival Hemorrhage
Subconjunctival hemorrhage is more dangerous in its appearance than in its actual damage
to vision or even the eye itself. The most common cause is trauma, particularly in the presence of thrombocytopenia. The collection of the hematoma stops at the limbus, which is the
anatomic connection between the conjunctiva and the cornea. Because this prevents the blood
from covering the cornea, there is no impairment of vision. There is no intraocular or intravitreal damage and hence no impairment of vision. No specific therapy for subconjunctival
hemorrhage is necessary.
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KERATITIS
Pathogenesis. Keratitis refers to any infection or inflammation of the cornea. Usually, keratitis
happens as a result of trauma to the cornea with the inoculation of bacterial or fungal elements into the cornea.
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Herpes Simplex Keratitis
Clinical Presentation. Herpes simplex keratitis is characterized by severe pain in the eye and a
sensation that something is caught under the eyelid.
Diagnosis. The diagnosis is based on finding a characteristic dendritic pattern over the cornea on
fluorescein staining of the eye with examination under a blue light.
Treatment. Therapy for herpes simplex keratitis is with oral acyclovir, famciclovir, or valacyclovir
and topical trifluridin 1% solution or idoxuridine. It is most important for the general physician
to never use oral or topical steroids in an attempt to relieve inflammation. This can markedly
worsen the growth of the virus and essentially acts as fertilizer for the virus.
PERIORBITAL CELLULITIS
Pathogenesis. Cellulitis is caused by Staphylococcus aureus or Streptococcus invading the dermis
and subcutaneous tissues surrounding the eye.
Treatment. Antistaphylococcal penicillins, such as oxacillin or nafcillin, should be administered.
If there is an allergic reaction to penicillins, such as a rash, then first-generation cephalosporins
can be used (i.e., cefazolin).
l Ophthalmology
UVEITIS
Pathogenesis. The uveal tract refers to the iris, ciliary body, and choroid. When these structures are inflamed, the condition is called uveitis. The etiology of uveitis is from a large
number of systemic inflammatory conditions, such as psoriasis, sarcoidosis, syphilis, Reiter
syndrome, or inflammatory bowel disease.
Clinical Presentation. Uveitis leads to a painful, red eye with marked photophobia. One of
the clues to the diagnosis is that pain occurs even when shining a light in the unaffected eye.
This is because of the consensual light reflex in which the affected pupil will constrict even
when light is shined in the normal eye.
Diagnosis. A specific diagnosis is made by slit lamp examination. Inflammation of the iris,
ciliary body, and choroid is visible. Inflammatory cells may accumulate on the inside of the
cornea after they precipitate out of the aqueous humor, rather like an accumulating snowfall.
These focal collections are called keratic precipitates.
Treatment. The basic management, despite the varied underlying conditions, is to treat with
topical or, sometimes, systemic steroids.
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Index
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Chapter Title
00
A
ABCDE mnemonic, acute coronary syndrome discharge
medications, 130–131
Abdominal aortic aneurysm, screening for, 7
Abdominal x-rays, 437–439
Abscesses
of the brain, 215–216
of the lung, 221–222
perinephric, 242
ABVD (adriamycin, bleomycin, vinblastine, dacarbazine)
chemotherapy regimen, for Hodgkin disease, 199
Acetaminophen
for osteoarthritis, 69
toxicity, 359–360
Acetylcholine, for dementia management, 405
Achalasia, 77–78
Achlorhydria, 87
Acid-base disturbances, in renal function and disease, 286–288
Acidosis
in drowning, 379
renal function and, 289–290
in salicylate toxicity, 365–366
Acids, toxic exposure to, 362
Acne, 432
Acquired immune deficiency syndrome (AIDS).
See also HIV patients
immune system monitoring in, 256–257
infectious disease and, 254–259
postexposure prophylaxis for, 259
Acromegaly, 13–14
Actinic keratosis, 426
Acute bacterial pyelonephritis, 241
Acute bronchitis, 220
Acute coronary syndrome (ACS), 123–134
chest pain in, 112
classification of, 123
complications of, 131–132
discharge medications after, 130
non-cardiac complications of, 132–133
nonatherosclerotic, 133–134
patient risk stratification in, 133
ST elevation myocardial infarction in, 126–130
unstable angina and NSTEMI in, 124–125
Acute hepatitis, 231–234
Acute idiopathic polyneuropathy (Guillain-Barré syndrome),
398–399
Acute lymphocytic leukemia (ALL), 192–193
Acute myelogenous leukemia (AML), 192–193
Acute pancreatitis, 103–105
Acute pericarditis, 157–158, 245–251
Acute renal failure, 263–271, 263–272
Acute respiratory compromise and distress, evaluation for, 313–315
Acute respiratory distress syndrome (ARDS), 314–315
drowning and, 379
in hospital patients, 314–315
pathology and management of, 338
Acute tubular necrosis (ATN), 266–267268
Adalimumab (Humira)
for ankylosing spondylitis, 67
for rheumatoid arthritis, 59
Addison disease, 47–48, 264
Adefovir, for hepatitis, 233
Adenocarcinoma
esophageal, 79
pulmonary, 339–340
Adenomas
pituitary, 11, 14
thyroid, 26
Adenosine stress test, in ischemic heart disease, 121
Adjuvant therapy, for ST elevation myocardial infarction, 129–130
Adrenal androgen excess, syndromes of, 46
Adrenal cortex, 41
Adrenal crisis, 48
Adrenal glands
anatomy and function of, 41
diseases of, 41–50
hyperfunctioning of, 41–47
hypofunctioning of, 47–50
hypopituitarism and, 15
Adrenal hyperplasia
congenital, 46–47
in Cushing syndrome, 41
Adrenal insufficiency, 47–48
Adrenal neoplasia, in Cushing syndrome, 41
Adrenocorticotropic hormone (ACTH)
in Cushing syndrome, 41–44
hypopituitarism and, 15
primary insufficiency of (Addison disease), 47–48
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