My Draft Book for HARRISON INTERNAL MEDICINE

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ACUTE PAIN
The ideal treatment for any pain is to remove the cause; thus diagnosis should
always precede treatment planning. Sometimes treating the underlying condition
does not immediately relieve pain. Furthermore, some conditions are so painful that
rapid and effective analgesia is essential (e.g., the postoperative state, burns,
trauma, cancer, sickle cell crisis). Analgesic medications are a first line of treatment
in these cases, and all practitioners should be familiar with their use.
Aspirin, Acetaminophen, and Nonsteroidal Anti-Inflammatory Agents
(NSAIDS)
These drugs are considered together because they are used for similar problems
and may have a similar mechanism of action (Table 11-1). All these compounds
inhibit cyclooxygenase (COX), and, except for acetaminophen, all have antiinflammatory
actions, especially at higher dosages. They are particularly effective
for mild to moderate headache and for pain of musculoskeletal origin.Since they are effective for these common types of pain and are available without
prescription, COX inhibitors are by far the most commonly used analgesics. They
are absorbed well from the gastrointestinal tract and, with occasional use, side
effects are minimal. With chronic use, gastric irritation is a common side effect of
aspirin and NSAIDs and is the problem that most frequently limits the dose that can
be given. Gastric irritation is most severe with aspirin, which may cause erosion of
the gastric mucosa, and because aspirin irreversibly acetylates platelets and
thereby interferes with coagulation of the blood, gastrointestinal bleeding is a risk.
T he NSAIDs are less problematic,
but their risk in this regard is still significant. In addition to their well known
gastrointestinal toxicity, nephrotoxicity is a significant problem for patients using
NSAIDs on a chronic basis, and patients at risk for renal insufficiency should be
monitored closely. NSAIDs also cause an increase in blood pressure in a significant
number of individuals. Long-term treatment with NSAIDs requires regular blood
pressure monitoring and treatment if necessary. Although toxic to the liver when
taken in a high dose, acetaminophen rarely produces gastric irritation and does not
interfere with platelet function.
The introduction of a parenteral form of NSAID, ketorolac, extends the usefulness of
this class of compounds in the management of acute severe pain. Ketorolac is sufficiently potent and rapid in onset to supplant opioids for many patients with
acute severe headache and musculoskeletal pain.
There are two major classes of COX: COX-1 is constitutively expressed, and COX-2
is induced in the inflammatory state. COX-2-selective drugs have moderate
analgesic potency and produce less gastric irritation than the nonselective COX
inhibitors. It is not yet clear whether the use of COX-2-selective drugs is associated
with a lower risk of nephrotoxicity compared to nonselective NSAIDs. On the other
hand, COX-2-selective drugs offer a significant benefit in the management of acute
postoperative pain because they do not affect blood coagulation. This is a situation
in which the nonselective COX inhibitors would be contraindicated because they
impair platelet-mediated blood clotting and are thus associated with increased
bleeding at the operative site. A corollary of this is that COX-2 drugs do not provide
the same degree of protection from thromboembolic cardiovascular adverse events
such as myocardial infarction. In fact, in patients treated for arthritis, those treated
with naproxen had significantly fewer adverse thromboembolic events than those
treated with rofecoxib, a selective COX-2 inhibitor.

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Opioid Analgesics
Opioids are the most potent pain-relieving drugs currently available. Furthermore,
of all analgesics, they have the broadest range of efficacy, providing the most
reliable and effective method for rapid pain relief. Although side effects are
common, they are usually not serious except for respiratory depression and can be
reversed rapidly with the narcotic antagonist naloxone. The physician should not
hesitate to use opioid analgesics in patients with acute severe pain. Table 11-1 lists
the most commonly used opioid analgesics.
Opioids produce analgesia by actions in the central nervous system. They activate
pain-inhibitory neurons and directly inhibit pain-transmission neurons. Most of the
commercially available opioid analgesics act at the same opioid receptor (mu
receptor), differing mainly in potency, speed of onset, duration of action, and
optimal route of administration. Although the dose-related side effects (sedation,
respiratory depression, pruritus, constipation) are similar among the different
opioids, some side effects are due to accumulation of nonopioid metabolites that
are unique to individual drugs. One striking example of this is normeperidine, a
metabolite of meperidine. Normeperidine produces hyperexcitability and seizures
that are not reversible with naloxone. Normeperidine accumulation is increased in
patients with renal failure.
The most rapid relief with opioids is obtained by intravenous administration; relief
with oral administration is significantly slower. Common acute side effects include
nausea, vomiting, and sedation. The most serious side effect is respiratory
depression. Patients with any form of respiratory compromise must be kept under
close observation following opioid administration; an oxygen saturation monitor may
b e useful. The opioid antagonist, naloxone, should be readily
available. Opioid effects are dose-related, and there is great variability among
patients in the doses that relieve pain and produce side effects. Because of this,
initiation of therapy requires titration to optimal dose and interval. The most
important principle is to provide adequate pain relief. This requires determining
whether the drug has adequately relieved the pain and the duration of the relief.
The most common error made by physicians in managing severe pain with opioids is to prescribe an inadequate dose. Since many patients are reluctant to complain,
this practice leads to needless suffering. In the absence of sedation at the expected
time of peak effect, a physician should not hesitate to repeat the initial dose to
achieve satisfactory pain relief.
An innovative approach to the problem of achieving adequate pain relief is the use
of patient-controlled analgesia (PCA). PCA requires a device that delivers a
baseline continuous dose of an opioid drug, and preprogrammed additional doses
whenever the patient pushes a button. The device can be programmed to limit the
total hourly dose so that overdosing is impossible. The patient can then titrate the
dose to the optimal level. This approach is used most extensively for the
management of postoperative pain, but there is no reason why it should not be used
for any hospitalized patient with persistent severe pain. PCA is also used for shortterm
home care of patients with intractable pain, such as is caused by metastatic
cancer.
Many physicians, nurses, and patients have a certain trepidation about using
opioids that is based on an exaggerated fear of addiction. In fact, there is a
vanishingly small chance of patients becoming addicted to narcotics as a result of
their appropriate medical use.
The availability of new routes of administration has extended the usefulness of
opioid analgesics. Most important is the availability of spinal administration. Opioids
can be infused through a spinal catheter placed either intrathecally or epidurally. By
applying opioids directly to the spinal cord, regional analgesia can be obtained
using a relatively low total dose. In this way, such side effects as sedation, nausea,
and respiratory depression can be minimized. This approach has been used
extensively in obstetric procedures and for lower-body postoperative pain. Opioids
can also be given intranasally (butorphanol), rectally, and transdermally (fentanyl),
thus avoiding the discomfort of frequent injections in patients who cannot be given
oral medication. The fentanyl transdermal patch has the advantage of providing
fairly steady plasma levels, which maximizes patient comfort.

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OPIOID AND CYCLOOXYGENASE INHIBITOR COMBINATIONS
When used in combination, opioids and COX inhibitors have additive effects.
Because a lower dose of each can be used to achieve the same degree of pain
relief and their side effects are nonadditive, such combinations can be used to
lower the severity of dose-related side effects. Fixed-ratio combinations of an opioid
with acetaminophen carry a special risk. Dose escalation as a result of increased
severity of pain or decreased opioid effect as a result of tolerance may lead to
levels of acetaminophen that are toxic to the liver

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CHRONIC PAIN
Managing patients with chronic pain is intellectually and emotionally challenging. The
patient's problem is often difficult to diagnose; such patients are demanding of the
physician's time and often appear emotionally distraught. The traditional medical
approach of seeking an obscure organic pathology is usually unhelpful. On the other
hand, psychological evaluation and behaviorally based treatment paradigms are
frequently helpful, particularly in the setting of a multidisciplinary pain-management
center.
There are several factors that can cause, perpetuate, or exacerbate chronic pain. First,
of course, the patient may simply have a disease that is characteristically painful for
which there is presently no cure. Arthritis, cancer, migraine headaches, fibromyalgia,
and diabetic neuropathy are examples of this. Second, there may be secondary
perpetuating factors that are initiated by disease and persist after that disease has
resolved. Examples include damaged sensory nerves, sympathetic efferent activity, and
painful reflex muscle contraction. Finally, a variety of psychological conditions can
exacerbate or even cause pain.
There are certain areas to which special attention should be paid in the medical history.
Because depression is the most common emotional disturbance in patients with chronic
pain, patients should be questioned about their mood, appetite, sleep patterns, and
daily activity. A simple standardized questionnaire, such as the Beck Depression
Inventory, can be a useful screening device. It is important to remember that major
depression is a common, treatable, and potentially fatal illness.
Other clues that a significant emotional disturbance is contributing to a patient's chronic
pain complaint include: pain that occurs in multiple unrelated sites; a pattern of
recurrent, but separate, pain problems beginning in childhood or adolescence; pain
beginning at a time of emotional trauma, such as the loss of a parent or spouse; a
history of physical or sexual abuse; and past or present substance abuse.
On examination, special attention should be paid to whether the patient guards the
painful area and whether certain movements or postures are avoided because of pain.
Discovering a mechanical component to the pain can be useful both diagnostically and
therapeutically. Painful areas should be examined for deep tenderness, noting whether
this is localized to muscle, ligamentous structures, or joints. Chronic myofascial pain is
very common, and in these patients deep palpation may reveal highly localized trigger
points that are firm bands or knots in muscle. Relief of the pain following injection of
local anesthetic into these trigger points supports the diagnosis. A neuropathic
component to the pain is indicated by evidence of nerve damage, such as sensory
impairment, exquisitely sensitive skin, weakness and muscle atrophy, or loss of deep
tendon reflexes. Evidence suggesting sympathetic nervous system involvement includes
the presence of diffuse swelling, changes in skin color and temperature, and
hypersensitive skin and joint tenderness compared with the normal side. Relief of the
pain with a sympathetic block is diagnostic.
A guiding principle in evaluating patients with chronic pain is to assess both emotional
and organic factors before initiating therapy. Addressing these issues together, rather
than waiting to address emotional issues after organic causes of pain have been ruled
out, improves compliance in part because it assures patients that a psychological
evaluation does not mean that the physician is questioning the validity of their
complaint. Even when an organic cause for a patient's pain can be found, it is still wise
to look for other factors. For example, a cancer patient with painful bony metastases
may have additional pain due to nerve damage and may also be depressed. Optimal
therapy requires that each of these factors be looked for and treated.

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;P

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不错

zhangheng1020UID: 2130513

zhangheng1020UID: 2130513

reviewed chapter 11 just now

[ 本帖最后由 zhangheng1020 于 2006-3-9 10:13 编辑 ]

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原帖由 zhangheng1020 于 2006-3-9 08:42 发表

3万什么？字？

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12
Chest Discomfort and Palpitations

CHEST DISCOMFORT
Chest discomfort is one of the most common challenges for clinicians in the office or emergency department. The differential diagnosis includes conditions affecting organs throughout the thorax and abdomen, with prognostic implications that vary from benign to life-threatening (Table 12-1). Failure to recognize potentially serious conditions such as acute ischemic heart disease, aortic dissection, tension pneumothorax, or pulmonary embolism can lead to serious complications, including death. Conversely, overly conservative management of low-risk patients leads to unnecessary hospital admissions, tests, procedures, and anxiety.

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Unstable Angina and Myocardial Infarction (See also Chaps.
227 and 228)
Patients with these acute ischemic syndromes usually complain of symptoms similar in
quality to angina pectoris, but more prolonged and severe. The onset of these
syndromes may occur with the patient at rest, or awakened from sleep, and sublingual
nitroglycerin may lead to transient or no relief. Accompanying symptoms may include
diaphoresis, dyspnea, nausea, and light-headedness.
The physical examination may be completely normal in patients with chest discomfort
due to ischemic heart disease. Careful auscultation during ischemic episodes may
reveal a third or fourth heart sound, reflecting myocardial systolic or diastolic
dysfunction. A transient murmur of mitral regurgitation suggests ischemic papillary
muscle dysfunction. Severe episodes of ischemia can lead to pulmonary congestion and
even pulmonary edema.

Other Cardiac Causes
Myocardial ischemia caused by hypertrophic cardiomyopathy, aortic stenosis, or other
conditions leads to angina pectoris similar to that caused by coronary atherosclerosis.
In such cases, a systolic murmur or other findings usually suggest the abnormalities
other than coronary atherosclerosis that may be contributing to the patient's symptoms.
Some patients with chest pain and normal coronary angiograms have functional
abnormalities of the coronary circulation, ranging from coronary spasm visible on
coronary angiography to abnormal vasodilator responses and heightened
vasoconstrictor responses. The term “Syndrome X” is used to describe patients with
angina-like chest pain and ischemic-appearing ST segment depression during stress
despite normal coronary arteriograms. Some data indicate that many such patients have
limited changes in coronary flow in response to pacing stress or coronary vasodilators.
Despite the possibility that chest pain may be due to myocardial ischemia in such
patients, their prognosis is excellent.

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PERICARDITIS (See also Chap. 222)
The pain in pericarditis is believed to be due to inflammation of the adjacent parietal
pleura, since most of the pericardium is believed to be insensitive to pain. Thus,
infectious pericarditis, which usually involves adjoining pleura surfaces, tends to be
associated with pain, while conditions that cause only local inflammation (e.g.,
myocardial infarction or uremia) and cardiac tamponade tend to result in mild or no
chest pain.
The adjacent parietal pleura receives its sensory supply from several sources, so the pain of pericarditis can be experienced in areas ranging from the shoulder and neck to
the abdomen and back. Most typically, the pain is retrosternal and is aggravated by
coughing, deep breaths, or changes in position—all of which lead to movements of
pleural surfaces. The pain is often worse in the supine position and relieved by sitting
upright and leaning forward. Less common is a steady aching discomfort that mimics
acute myocardial infarction.

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DISEASES OF THE AORTA (See also Chap. 231)
Aortic dissection is a potentially catastrophic condition that is due to spread within the
wall of the aorta of a subintimal hematoma. The hematoma may begin with a tear in the
intima of the aorta or with rupture of the vasa vasorum within the aortic media. This
syndrome can occur with trauma to the aorta, including motor vehicle accidents or
medical procedures in which catheters or intraaortic balloon pumps damage the intima
of the aorta. Nontraumatic aortic dissections are rare in the absence of hypertension
and/or conditions associated with deterioration of the elastic or muscular components of
the media within the aorta's wall. Cystic medial degeneration is a feature of several
inherited connective tissue diseases, including Marfan and Ehlers-Danlos syndromes.
About half of all aortic dissections in women under 40 years of age occur during
pregnancy.
Almost all patients with acute dissections present with severe chest pain, although
some patients with chronic dissections are identified without associated symptoms.
Unlike the pain of ischemic heart disease, symptoms of aortic dissection tend to reach
peak severity immediately, often causing the patient to collapse from its intensity. The
adjectives used to describe the pain reflect the process occurring within the wall of the
aorta—“ripping” and “tearing”—and the location usually correlates with the site and
extent of the dissection. Thus, dissections that begin in the ascending aorta and extend
to the descending aorta tend to cause pain in the front of the chest that extends into the
back, between the shoulder blades.
Physical findings may also reflect extension of the aortic dissection that compromises
flow into arteries branching off the aorta. Thus, loss of a pulse in one or both arms,
cerebrovascular accident, or paraplegia can all be catastrophic consequences of aortic
dissection. Hematomas that extend proximally and undermine the coronary arteries or
aortic valve apparatus may lead to acute myocardial infarction or acute aortic
insufficiency. Rupture of the hematoma into the pericardial space leads to pericardial
tamponade.
Another abnormality of the aorta that can cause chest pain is a thoracic aortic
aneurysm. Aortic aneurysms are frequently asymptomatic but can cause chest pain and
other symptoms by compressing adjacent structures. This pain tends to be steady,
deep, and sometimes severe.

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PULMONARY EMBOLISM (See also Chap. 244)
Chest pain due to pulmonary embolism is believed to be due to distention of the
pulmonary artery or infarction of a segment of the lung adjacent to the pleura. Massive
pulmonary emboli may lead to substernal pain that is suggestive of acute myocardial
infarction. More commonly, smaller emboli lead to focal pulmonary infarctions that
cause pain that is lateral and pleuritic. Associated symptoms include dyspnea and,
occasionally, hemoptysis. Tachycardia is usually present. Although not always present, certain characteristic ECG changes can support the diagnosis

PNEUMOTHORAX (See also Chap. 245)
Sudden onset of pleuritic chest pain and respiratory distress should lead to
consideration of spontaneous pneumothorax, as well as pulmonary embolism. Such
events may occur without a precipitating event in people without lung disease, or as a
consequence of underlying lung disorders.

PNEUMONIA OR PLEURITIS (See also Chaps. 239 and 245)
Lung diseases that damage and cause inflammation of the pleura of the lung usually
cause a sharp, knifelike pain that is aggravated by inspiration or coughing.

GASTROINTESTINAL CONDITIONS (See also Chap. 273)
Esophageal pain from acid reflux from the stomach, spasm, obstruction, or injury can
be difficult to discern from myocardial syndromes. Acid reflux typically causes a deep
burning discomfort that may be exacerbated by alcohol, aspirin, or some foods; this
discomfort is often relieved by antacid or other acid-reducing therapies. Acid reflux
tends to be exacerbated by lying down and may be worse in early morning when the
stomach is empty of food that might otherwise absorb gastric acid.
Esophageal spasm may occur in the presence or absence of acid reflux, and leads to a
squeezing pain indistinguishable from angina. Prompt relief of esophageal spasm is
often provided by antianginal therapies such as sublingual nifedipine, further promoting
confusion between these syndromes. Chest pain can also result from injury to the
esophagus, such as a Mallory-Weiss tear caused by severe vomiting.
Chest pain can result from diseases of the gastrointestinal tract below the diaphragm,
including peptic ulcer disease, biliary disease, and pancreatitis. These conditions
usually cause abdominal pain as well as chest discomfort; symptoms are not likely to be
associated with exertion. The pain of ulcer disease typically occurs 60 to 90 min after
meals, when postprandial acid production is no longer neutralized by food in the
stomach. Cholecystitis usually causes a pain that is described as aching, occurring an
hour or more after meals.

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NEUROMUSCULOSKELETAL CONDITIONS
Cervical disk disease can cause chest pain by compression of nerve roots. Pain in a
dermatomal distribution can also be caused by intercostal muscle cramps or by herpes
zoster. Chest pain symptoms due to herpes zoster may occur before skin lesions are
apparent.
Costochondral and chondrosternal syndromes are the most common causes of anterior
c hest musculoskeletal pain. Only occasionally
are physical signs of costochondritis such as swelling, redness, and warmth (Tietze's
syndrome) present. The pain of such syndromes is usually fleeting and sharp, but some
patients experience a dull ache that lasts for hours. Direct pressure on the
chondrosternal and costochondral junctions may reproduce the pain from these and
other musculoskeletal syndromes. Arthritis of the shoulder and spine and bursitis may also cause chest pain. Some patients who have these conditions and myocardial
ischemia blur and confuse symptoms of these syndromes.