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Testicular cancer
Description
Testicular cancer is rare, but it is the most common type of cancer in young men between 15 and 35 years of age. Testicular tumors are more common in men who have had undescended testicles (cryptorchidism) or a family history of testicular cancer or anomalies.
Clinical manifestations
Testicular cancer may have a slow or rapid onset depending on the tumor.
Diagnostic studies
Nursing and collaborative management
The scrotum is easily examined, and tumors are usually palpable. Teach and encourage every man to perform a monthly testicular self-examination for the purpose of detecting testicular tumors or other scrotal abnormalities such as varicoceles. (See Table 55-9 and Fig. 55-11 for scrotum self-examination guidelines, Lewis et al.: Medical-Surgical Nursing, ed. 9, p. 1326).
Collaborative management generally involves a radical orchiectomy (surgical removal of the affected testis, spermatic cord, and regional lymph nodes). Retroperitoneal lymph node dissection and removal may also be done.
The prognosis for patients with testicular cancer has improved, and 95% of all patients obtain complete remission if the disease is detected in the early stages. All patients with testicular cancer, regardless of pathology or stage, require meticulous follow-up monitoring and regular physical examinations, chest x-ray, CT scan, and assessment of hCG and AFP. The goal is to detect relapse when tumor burden is minimal.
Thalassemia
Description
Thalassemia is a group of diseases involving inadequate production of normal hemoglobin, and therefore decreased erythrocyte production. Hemolysis also occurs in thalassemia.
Pathophysiology
Thalassemia has an autosomal recessive genetic basis that results in an absent or reduced globulin protein. α-Globin chains are absent or reduced in α-thalassemia, and β-globin chains are absent or reduced in β-thalassemia. An individual with thalassemia may have a heterozygous or homozygous form of the disease.
Clinical manifestations
■ The patient who has thalassemia major is pale and displays other general manifestations of anemia (see Anemia, pp. 31, 35). In addition, the person has marked splenomegaly, hepatomegaly, and jaundice from hemolysis of RBCs. Chronic bone marrow hyperplasia leads to expansion of the marrow space. This may cause thickening of the cranium and maxillary cavity.
Collaborative care
The laboratory findings in thalassemia major are summarized in Table 9, p. 33.
Thromboangiitis obliterans
Thromboangiitis obliterans (Buerger’s disease) is a nonatherosclerotic, segmental, recurrent inflammatory vaso-occlusive disorder of the small- and medium-sized arteries and veins of the upper and lower extremities. The disorder occurs predominantly in young men (less than 45 years of age) with a long history of tobacco use, but without other cardiovascular disease (CVD) risk factors (e.g., hypertension, hyperlipidemia, diabetes).
In the acute phase of Buerger’s disease, an inflammatory thrombus forms and blocks the vessel. Over time, the thrombus becomes more organized, and the inflammation subsides.
During the chronic phase, thrombosis and fibrosis occur in the vessel, causing tissue ischemia. The symptom complex of Buerger’s disease is often confused with peripheral artery disease (PAD) and other autoimmune diseases (e.g., scleroderma).
There are no laboratory or diagnostic tests specific to Buerger’s disease. Diagnosis is based on the age of onset, history of tobacco use, clinical symptoms, involvement of distal vessels, presence of ischemic ulcerations, and exclusion of disorders, including diabetes, autoimmune disease, thrombophilia, and other source of emboli.
Treatment is the complete cessation of tobacco use in any form. Conservative management includes avoiding limb exposure to cold temperatures, a supervised walking program, antibiotics to treat any infected ulcers, and analgesics to manage the ischemic pain. Teach patients to avoid trauma to the extremities.
Painful ulcerations may require finger or toe amputations. Amputation below the knee may occur in severe cases. The amputation rate of patients who continue tobacco use after diagnosis is much higher than in those who stop.
Thrombocytopenia
Description
Thrombocytopenia is a reduction of platelets below 150,000/μL (150 × 109/L). Acute, severe, or prolonged decreases from this normal range can result in abnormal hemostasis that manifests as prolonged bleeding from minor trauma or spontaneous bleeding without injury.
Platelet disorders can be inherited (e.g., Wiskott-Aldrich syndrome), but the vast majority are acquired. A common cause of acquired disorders is the ingestion of certain herbs or drugs (see Tables 31-11 and 31-12, Lewis et al.: Medical-Surgical Nursing, ed. 9, p. 650). Antibodies attack the platelets when the offending agent binds to the platelet surface.
Immune thrombocytopenic purpura
Immune thrombocytopenic purpura (ITP), the most common acquired thrombocytopenia, is a syndrome of abnormal destruction of circulating platelets. ITP is an autoimmune disease.
Thrombotic thrombocytopenic purpura
Thrombotic thrombocytopenic purpura (TTP) is an uncommon syndrome characterized by hemolytic anemia, thrombocytopenia, neurologic abnormalities, fever (in the absence of infection), and renal abnormalities. TTP is almost always associated with hemolytic-uremic syndrome (HUS).
Clinical manifestations
Many patients with thrombocytopenia are usually asymptomatic.
The major complication of thrombocytopenia is hemorrhage. It may occur in any area of the body, including the joints, retina, and brain. Cerebral hemorrhage may be fatal.
Diagnostic studies
Collaborative care
Immune thrombocytopenic purpura
Multiple therapies are used to manage the patient with ITP. If the patient is asymptomatic, therapy may not be used unless the platelet count is below 30,000/μL. Corticosteroids (e.g., prednisone) are used initially to suppress the phagocytic response of splenic macrophages.
Splenectomy may be indicated if the patient is not responding to the conservative treatments. Approximately 60% to 70% of patients benefit from splenectomy, resulting in a complete or partial remission. High doses of IV immunoglobulin (IVIG) and a component of IVIG, anti-Rho(D) (anti-D, WinRho), may be used in the patient who is unresponsive to corticosteroids or splenectomy, or for whom splenectomy is not an option.
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