Breast cancer may have a more indolent clinical course in women > 65 yr than in younger women. Several tumor and tumor-host observations support this hypothesis. Less aggressive hormone receptor-rich, well-differentiated tumors are more prevalent in older women. while life-threatening hepatic, cerebral, and lyrnphangitic metastases are less prevalent. In addition, the likelihood that a tumor is hormone receptor-rich increases with patient age. Overall, about 60% of tumors in postmenopausal women and > 80% of tumors in women S: 80 yr old are hormone receptor-rich. Also, slow-growing tumors, found mostly in the elderly, take longer to become delectable. Several age-related physiologic changes may slow neoplastic growth, including immune senescence and declining production of estrogens, growth hormone, and paracrine growth factors. As an example of how immune senescence affects tumor growth, one report showed thai in older women the monocellular reaction to tumor is less intense and the secretion of a monocyte-derived tumor-stimulating cytokine is reduced.
However, the suggestion thai tumors are less aggressive in older women should not prompt complacency. Breast cancer is a common cause of morbidity and death, which may be avoided by intensive preventive programs and timely treatment.
The prognosis of breast cancer is determined by the stage of the disease (see TABLE 67-4) and by different factors within each stage. In stages I and II, the number of axillary lymph nodes microscopically involved by the tumor is the most important prognostic factor. Ten years after diagnosis, 60% lo 70% of women with involvement of three or fewer lymph nodes are alive and free of disease, compared with only 15% to 20% of those with involvement of eight or more lymph nodes. When the axillary lymph nodes are not involved, the best predictors of recurrence include size of the primary tumor (recurrence rate increases
with tumor size, when the largest diameter is > I cm), low concentration of hormone receptors, high histologic grade (ie. poor histologic differentiation), high cell proliferation rate, abnormalities of the P53 protein (which is encoded by the P53 antioncogene and controls cell growth), and expression of HER/2 oncogene (which encodes for epidermal growth factor receptor). In stage 111 disease, factors indicating a poor prognosis include palpable supraclavicular or infraclavicular lymph nodes, edema, ulceration, fixation to the chesl wall, and inflammatory breast cancer. In stage IV disease, the prognosis varies markedly with the metastatic sites: the average survival is 3 to 6 mo if (he patient has liver or lymphangitic lung metastases, 24 mo if the palicnl has nodular lung metastases or pleural effusions, and > 5 yr if the me-tastases are limited to the bones.
Treatment
Treatment is guided by the stage of the disease, the patient’s general condition, and the patient’s preferences. Local treatment modalities include partial (lumpectomy), total, or radical mastectomy; axillary lymph node dissection: and external beam irradiation. Systemic treatment includes hormonal therapy and cytotoxic chemotherapy (see TABLE 67-5).

The mortality rate for patients with pulmonary embolism who receive anticoagulant therapy is only 8%; the rale for those who do not receive treatment is 30%. In the elderly, the difference between these mortality rates may be even grealer. Prognosis is poorest in patients with severe underlying cardiac or pulmonary disease. Between 75% and 90% of dealhsfrom pulmonary embolism occur within the first few hours. After that, death usually results from a recurrent embolic event.
Pulmonary embolism is believed to recur in 5% to 10% of patients despite heparin therapy. The likelihood of recurrent emboli is greatest in those who have massive pulmonary embolization and those in whom anticoagulant therapy has been inadequate. If recurrence develops in the first few days of heparin or thrombolytic therapy, treatment is usually continued. If recurrenl episodes or massive embolization occurs from a clol in the legs, interrupiion of the inferior vena cava should be considered.
The long-term prognosis for patients surviving pulmonary embolism is determined by underlying medical problems and cardiopulmonary status. Recurrent pulmonary embolism leading to chronic pulmonary hypertension and cor pulmonale is uncommon, occurring in perhaps < 2% of patients; the exact frequency in the elderly is not known

Close monitoring and intensive rehabilitation programs, including drug therapy and reconditioning through exercise, can improve the quality of life and reduce the number of hospitalizations for COPD patients. However, longevity probably cannot be improved significantly except in patients wilh hypoxemia.Smokers developing COPD lose FEVi at ihe rate of 50 to 100 mL/yr. while nonsmokers lose only 25 to 30 mL/yr. Survival rates correlate with FEVi. An FEV| > 1.5 L is usually associated with a norma] adjusted lifespan; an FEVi of s I L is associated with an average survival of s 5 yr. Other poor prognostic signs include resting tachycardia, ventricular arrhythmias, and hypercapnia.
Treatment
The therapeutic goal for geriatric patients with COPD is lo maintain functional independence and avoid repeated hospitalizations. Respiratory compromise eventually leads to functional impairment and loss of independence, often accompanied by anxiety, lowered self-esteem, depression, role reversal, and sexual dysfunction.
The chances of successful rehabilitation are enhanced when the patient has a positive attitude- as well as a caring family and physician. Education about exercise, nutrition, avoidance of infections, and appropriate use of drugs can help improve the patient’s quality of life.
Sexual function often improves if the person is rested, schedules sexual activity for (he “best-breathing” time of day. uses a bronchodilator 20 to 30 min beforehand, avoids consuming large amounts of food or alcohol, and assumes a position that does not put pressure on the chest or abdomen or require arm support.
Typically, a COPD patient is in poor physical condition. The physician should determine if this condition results from end-stage lung disease or other causes. If the patient has no respiratory reserve, exercise is unwarranted, and (he work of daily living should be decreased to minimize oxygen requirements. The physician may suggest that the patient live on a single level of his home, not wear shoes that require lying, and so on.
If the patient appears to have a respiratory reserve, a graduated exercise program should be instituted. Simultaneous supplemental oxygen may be required lo allow the patient to exercise long enough to benefit from the program; however. Medicare requires a resting POi of < 55 mm Hg for reimbursement for home oxygen therapy. The most efficient and inexpensive device for supplying supplemental oxygen in the home is an oxygen concentrator. This device, which plugs into a standard electrical outlet, extracts oxygen from the air and concentrates it for delivery through a nasal catheter that can allow the patient to move throughout one floor of a home. Outside the home, a patient can use a small tank of liquid oxygen (hat can be concealed in a bag with a shoulder strap. Such a tank allows patient mobility for 3 to8h, depending on its size, the flow rate, and the method of delivery (oxygen may be delivered conlinuously or through a valve that opens only when the patient inhales). Exercise shoujd be continued year-round. Activities may include walking outdoors in nice weather, in malls in bad weather, and up and down stairs in the house in winter, as well as using an exercise bicycle.

Drug therapy is directed primarily at reducing dyspnea. Other therapeutic goals include controlling cough and sputum production. Because treatment is not curative, it is considered successful when it produces a favorable balance between symptomatic relief and drug-related side effects. Clear, written directions are important for older patients because their age-adjusted cognitive skills arc further impaired by hypoxemia, leading lo poor short-term memory and an inability to concentrate.

Many studies confirm Ihe high mortality rate associated with unrepaired abdominal aortic aneurysms. The 5-yr survival rale varies from 14% to 37%. Complications of abdominal aortic aneurysms other than rupture occur infrequently. Mural thrombi may embolize to the legs. Rarely, consumption coagulopathy occurs, resulting in thrombocylope-nia, elevated thrombin time, fibrin split products in ihe blood, and a bleeding diathesis. An infection in Ihe aneurysm is even more rare, but if it occurs Salmonella is most often implicated. Patients with a recurrent Salmonella septicemia of unknown origin should be evaluated for an arterial aneurysm.
Surgical repair prolongs life. With an experienced surgical team, elective repair has an operative mortality rate of < 3%. even though most patients have other manifestations of atherosclerotic disease. Contraindications to surgery include recent transient ischemic attacks and unstable angina.
Treatment
Abdominal aortic aneurysms > 5 cm in diameter usually should be repaired. Repair of slightly smaller lesions might be considered, particularly if serial sonograms show progressive enlargement and if (he patient is otherwise healthy. 1′atients with small aneurysms can be followed up clinically and with ultrasonography every 6 mo.
Treatment of patients who have both coronary artery disease and an abdominal aneurysm is controversial. Some authorities advocale coronary angiography and bypass surgery as the first intervention, but most reserve this approach for patients with severe heart disease. Most surgeons forgo coronary angiography in patients with little or no angina and a good ejection fraction (as determined by radionuclide left ventricular cineangiography).
The management of patients with significant stable angina is open to question. One promising technique is the use of thallium scanning of the heart before and after IV injections of dipyridamole. Evidence of blood flow redistribution after dipyridamole adminislration is well correlated with postoperative myocardial infarction. Conventional sub-maximal stress tests and 48-h ambulatory ECG monitoring also can help to assess (he need for coronary bypass before aneurysm repair