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86 Cards in this Set
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Wasting of Host (Tumor Cachexia) |
Treatment Steps
Treat the malignancy; hyperalimentation if surgery planned or if hope of signicant remission or cure with therapy. |
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Symptoms
Often subtle. Mild weakness, hypokalemia, psychosis, abnormal glucose tolerance curve. |
Ectopic Adrenocorticotropic Hormone (ACTH)
Description Cushing’s syndrome: about 50% from the lung. Adrenal tumors pro- duce cortisol, but not ACTH. Increased production by cancer cells of pro-opiocortin (prohormone molecule of ACTH) |
Diagnosis
Extremely high plasma ACTH that does not suppress with dexa- methasone. Treatment Steps 1. Treat the malignancy. 2. If unable to treat CA, then try aminoglutethimide or metyrapone. |
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Symptoms
Polyuria, constipation, lethargy, personality change. |
2–2. Hypercalcemia
Description Seen in solid tumors (lung, breast, kidney, ovary), and hematologi- cal disease (multiple myeloma and adult T-cell lymphoma). Mecha- nisms include release of osteoclast-activating factor, increased renal calcium absorption. |
Treatment Steps
Acutely: Saline, loop diuretics (furosemide), IV bisphonates, gluco- corticoids, calcitonin. Chronically: Treat malignancy, mobilize patient, bisphosphonates, avoid dehydration |
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Chorionic Gonadotropin |
Cleared rapidly from serum; little clinical effect; rarely see gyneco-
mastia. |
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Hypoglycemia
PARANEOPLASTIC SYNDROMES |
Most commonly in mesotheliomas, hepatic carcinomas, adrenal cortical carcinomas. Due to factors with insulin-like activity
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Growth Hormone and Growth
Hormone-Releasing Hormone (GHRH) PARANEOPLASTIC SYNDROMES |
Acromegaly in bronchial carcinoid or pancreatic islet cell tumor.
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Calcitonin
PARANEOPLASTIC SYNDROMES |
Little or no biologic effect in normal adults, so no symptoms. Good
hormonal marker for medullary carcinoma of thyroid |
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Vasopressin
PARANEOPLASTIC SYNDROMES |
Causes syndrome of inappropriate antidiuretic hormone (SIADH).
Seen in carcinoma of the lung |
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Erythropoietin
PARANEOPLASTIC SYNDROMES |
enign and malignant renal conditions (hypernephroma, renal
cysts, hydronephrosis). Nonrenal conditions include hemangioblas- tomas, uterine fibromas, adrenal cortical neoplasms, ovarian neoplasms, hepatomas, pheochromocytomas. |
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Neurologic
PARANEOPLASTIC SYNDROMES |
ubacute cerebellar degeneration, subacute motor neuropathy, sen-
sory neuropathy, Eaton–Lambert syndrome, dermatomyositis. |
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Symptoms: Back pain in at-risk patient, bowel or bladder incontinence, loss of sphincter tone. |
Spinal Cord Compressio
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Treatment: Steroids, radiation, surgical decompression
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Symptoms: Mental status changes, polyuria, constipation.
ONCOLOGIC EMERGENCIES |
Hypercalcemia
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Treatment: IV hydration (normal saline), loop diuretics (furosemide), IV bisphosphonates.
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Symptoms: Elevated uric acid, potassium, and phosphate cause hypocalcemia and renal failure
in rapidly growing tumors. |
Tumor Lysis Syndrome
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Treatment: Allopurinol, hydration with alkalinizatin of the urine, close monitoring of electrolytes, dialysis.
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Symptoms: Change in mental status, papillary edema.
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Cerebral Herniation
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Treatment: Steroids, radiation, decompression.
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Hematologic
PARANEOPLASTIC SYNDROMES |
Hematologic
4–1. Erythrocytosis From erythropoietin secretion, renal or liver tumors (see Endocrine section). 4–2. Leukemoid Reactions From colony-stimulating factor (CSF) secretion. Also see granulocy- tosis (lung, gastric, pancreatic, brain, melanomas, lymphomas) or eosinophilia (lymphomas, Hodgkin’s, gastrointestinal [GI] carcino- mas). 4–3. Anemia See differential diagnosis in margin. 4–4. Microangiopathic Hemolytic Anemia In stomach, breast, lung cancers. 4–5. Granulocytopenia Usually from chemotherapy, radiation therapy, infection, marrow in- volvement. 4–6. Idiopathic Thrombocytopenic Purpura (ITP) In lymphomas. |
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Description |
Thromboembolic Paraneoplastic Syndromes
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Hypercoagulable state |
Migratory thrombophlebitis (Trousseau’s syndrome). |
Treatment Steps
Difcult; may require long-term heparin or enoxaparin if warfarin doesn’t work. |
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Hypercoagulable state
May be common and subclinical. |
Disseminated intravascular coagulation (DIC).
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Treatment Steps
Treat the tumor. May use heparin |
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Hypercoagulable state
Usually mucin-secreting adenocarcinomas. May embolize. |
Nonbacterial thrombotic endocarditis (marantic endocarditis)
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Treatment Steps
Treat the tumor. |
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Renal
Paraneoplastic Syndromes |
a. SIADH.
b. Nephrotic syndrome. Hodgkin’s (lipoid nephrosis, minimal change glomerulopathy). Non-Hodgkin’s lymphoma (im- mune complex). c. Myeloma and amyloid kidney. d. Hypokalemia. Myelogenous leukemia (lysozyme related). |
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Dermatologic
Paraneoplastic Syndromes |
Acanthosis nigricans (hyperkeratosis and pigmentation of axillae,
neck, and groin), dermatomyositis, flushing in carcinoid. Leser–Tre- lat (sudden onset of seborrheic keratoses), porphyria cutanea tarda (photosensitive skin lesions), pruritus. |
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Gastrointestinal
Paraneoplastic Syndromes |
Protein-losing enteropathy, malignant hepatopathy
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Paraneoplastic Syndromes
Miscellaneous |
Miscellaneous
Fever (lymphomas, hypernephromas). Lactic acidosis (acute leukemias, lymphomas). Hypokalemia and hypertension (lung, hyper- nephroma, Wilms’). Hypertrophic pulmonary osteoarthropathy (lung, mesothelioma, other metastases to lung). Amyloidosis (myeloma, lym- phoma, carcinomas). Systemic lupus (lymphomas, leukemias, thymo- mas, testicular, lung, ovarian). |
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ANEMIA IN THE ONCOLOGY
PATIENT differential diagnosis |
Anemia of Chronic Disease
• Normo- or microcytic • Elevated ferritin, low total iron-binding capacity (TIBC) Chemotherapy Related • Cisplatin • Hydroxyurea • Cytarabine (Ara-C) Hemolytic Anemia • Immune mediated in chronic leukemias and low-grade lymphomas • Microangiopathic secondary to mitomycin Renal Insufficiency • Obstruction by tumor • Chemotherapy toxicity (i.e., cisplatinum) • Tumor lysis (hyperproliferative state) Iron Deficiency • Chronic GI or genitourinary (GU) bleed |
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CHANGE IN MENTAL STATUS
IN AN ONCOLOGY PATIENT differential diagnosis |
1. Metabolic—
hypercalcemia, hypoglycemia, hyperkalemia 2. Neurologic—cerebral metastases with edema, cerebral thrombosis, cerebral hemorrhage 3. Pulmonary—hypoxia 4. Drug-related—opioids 5. Infection 6. Dehydration |
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Hormones—β subunit of human chorionic gonadotropin
(β-hCG) TUMOR MARKERS |
testicular cancer, choriocarcinomas, hydatidiform mole.
The level assesses response to therapy. Others: Human placental lacto- gen, ACTH, vasopressin, calcitonin, gastrin-releasing peptide. |
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Oncofetal Proteins—α-Fetoprotein (AFP)
TUMOR MARKERS |
hepatoma and testicu-
lar CA. The level has predictive value in follow-up |
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Carcinoembryonic Antigen (CEA)
TUMOR MARKERS |
GI tract, breast, lung, ovar-
ian tumors. Increased by smoking and inflammatory processes, so should not be used for screening. Used to assess response and recur- rence (colon) |
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Immunoglobulins
TUMOR MARKERS |
myeloma and some other lymphoproliferative
disorders; good for following response to treatment. Heavy chains and light chains in myeloma and Waldenström’s macroglobuline- mia |
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Prostatic acid phosphatase
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one-third of occult prostate
and 75% of more advanced prostate cancer |
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Tumor Antigens—CA-125
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ovarian
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Tumor Antigens CA 19-9:
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biliary
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Tumor Antigens
β2 Microglobulin (a human leukocyte antigen [HLA] class I antigen |
assessing response in myeloma therapy.
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Prostate-specific antigen (PSA):
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prostate
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Tumor Antigens CA 27-29
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breast.
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Symptoms
Painless cervical or other adenopathy. Chest x-ray may show medi- astinal mass, inltrates, effusions. Fever, sometimes cyclic (Pel– Ebstein fever). Night sweats. Pruritis. Superior vena cava obstruc- tion. Spinal cord compression. Hepatic and splenic enlargement. In- fections (herpes zoster, cryptococcosis, Pneumocystis carinii pneumo- nia, toxoplasmosis). Immunologic abnormalities common. B Symptoms Fever > 38.5; night sweats; 10% weight loss over 6 months. A— absence of “B” symptoms. B—presence of 1 or more. |
Hodgkin’s Disease
Description Lymph node malignancy of centroblast (proliferating germinal center cell); average age 32; male more than female Pathology Anemia of chronic disease, but occasionally due to hypersplenism, marrow invasion, Coombs’-positive hemolytic anemia. Leukocytosis, eosinophilia. Pathognomonic Reed–Sternberg cell (large, bilobed cell with prominent eosinophilic nucleoli), is pathognomonic but not necessary as variants exists. Hodgkin’s • Bimodal age distribution • Contiguous spread • Very high cure rate • Linked to EBV Four basic types— nodular sclerosing (60–75%), mixed cellularity (20–35%), lymphocyte predominant (5–10%), lymphocyte depleted (2–5%) |
Diagnosis
Use computed tomography (CT) of chest and abdomen, lymphan- giography. Bilateral bone marrow biopsy in all patients suspected of diffuse or bone disease. Gallium scans can be useful. (See Fig. 6–1.) Biospsy of an involved node, needle aspiration generally not ade- quate. CT of chest, abdomen, and pelvis. Lymphangiography less commonly used now. Bilateral bone marrow biopsy in patients sus- pected of diffuse or bone disease. Positron-emission tomography (PET) and gallium also helpful. (See Fig. 6–1.) Staging: I. Single lymph node or group. II. More than one node or group; same side of diaphragm. III. Spleen and nodes; both sides of diaphragm. IV. Liver or marrow. Treatment Steps Biopsy rst. Staging before treatment. Staging laparotomy (with splenectomy) is not used as frequently but still has a place in staging. Treat with radiotherapy: 3,600 to 4,000 rads. Radiation alone initially in stage I. Stages IIA and IIIA either radiation or chemotherapy. Chemotherapy: in advanced (IIB, IIIB, and IV) disease. Standard is changing and could be ABVD (adriamycin, bleomycin, vinblastine, dacarbazine) or less commonly now MOPP (mechlorethamine, vin- cristine [oncovin], procarbazine, prednisone), four to six cycles. Ra- diation can be added to involved elds. Produces complete remis- sion in 70–80%; disease free 10–20 years later in 50% of these. Greatly improved prognosis due to staging, radiotherapy, and chemotherapy advances. |
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Symptoms
Painless cervical or other adenopathy. Chest x-ray may show medi- astinal mass, inltrates, effusions. Fever, sometimes cyclic (Pel– Ebstein fever). Night sweats. Pruritis. Superior vena cava obstruc- tion. Spinal cord compression. Hepatic and splenic enlargement. In- fections (herpes zoster, cryptococcosis, Pneumocystis carinii pneumo- nia, toxoplasmosis). Immunologic abnormalities common. B Symptoms Fever > 38.5; night sweats; 10% weight loss over 6 months. A— absence of “B” symptoms. B—presence of 1 or more. |
Non-Hodgkin’s Lymphoma
Description The largest group of immune system neoplasms, characterized by monoclonal proliferation of B or T lymphocytes. An immune dys- function may contribute (e.g., acquired immune deciency syndrome [AIDS]). Possible viral etiology in Burkitt’s, adult T-cell leukemia Pathology Classifying systems: Rappaport Classication, Lukes and Collins, The NCI Working Formulation (1982), REAL classication. Special Problems Superior vena cava obstruction: chemotherapy or irradiate. Gastric lymphoma: resect. Central nervous system (CNS) disease: irradiate. Urate nephropathy: allopurinol to prevent, if severe may require dialysis support. Non-Hodgkin’s • Increasing frequency with age • Variable spread • Variable cure rates—most common types not curable • Over 30 different types • NCI working formulation: low grade, intermediate grade, high grade |
Diagnosis
Node pathology; B- and T-cell typing studies. Use CT of abdomen, pelvis, and chest. Immunoglobulins, bone scan, upper GI studies (UGI), bone marrow biopsies, PET scan, gallium scan Treatment Steps Depends on grade and stage. Modalities include multiagent chemotherapy (CHOP—cytoxan, adriamycin, vincristine, pred- nisone) or combined chemo/irradiation, and immunotherapy (rit- uxamab). |
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Symptoms
Pallor, fatigue, bleeding, fever, bone pain, adenopathy, arthralgias, hepatosplenomegaly. Pathology Marrow inltrated or replaced with lymphoblasts. |
Acute Lymphoblastic Leukemia (ALL)
Description Malignant proliferation of lymphoid precursors, with replacement of normal cells; 75% of the 2,500 new acute leukemias. |
Diagnosis
Marrow morphology, cytochemical staining, immunologic cell sur- face markers, cytogenetics. Treatment Steps Cure rate 65–70%. Multiple-drug chemotherapy (prednisone, vin- cristine, doxorubicin, methotrexate, asparaginase) + intrathecal chemotherapy (methotrexate or cytarabine) or cranial irradiation. Because of high cure rate, no marrow transplant usually with rst re- mission unless patient has poor prognostic factors, but is recommended after second remission. |
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Symptoms
Pallor, fatigue, bleeding, fever, bone pain, adenopathy, arthralgias, hepatosplenomegaly. Pathology Marrow inltrated or replaced with myeloblast |
Acute Myeloblastic Leukemia (AML)
Description Malignant proliferation of myelocytic precursors, with replacement of normal cells; 15–20% of acute leukemias. |
Diagnosis
Bone marrow biopsy. Treatment Steps Intensive chemotherapy with daunorubicin and cytarabine, some- times combined with other agents. Intrathecal chemo or irradiation in some cases. Produces 80% complete remission (CR) rate, 65% re- main in continuous CR. |
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Symptoms
Anemia, hemorrhage, infection, leukemic inltrates (bone pain, meningitis, mediastinal mass, chloromas), lymphadenopathy, splenomegaly. |
Acute Leukemia in Adults
Description Malignant unregulated proliferation of immature myeloid or lym- phoid precursors, with replacement of normal cells. Inciting agents include ionizing radiation, oncogenic viruses, genetic and congenital factors, chemical agents. Pathology Bone marrow: morphologic, histochemical techniques, surface markers (immunologic techniques), cytoplasmic markers (en- zymes), chromosomal changes. Eighty percent are acute myeloge- nous leukemia (AML). |
Diagnosis
Anemia, thrombocytopenia, and abnormal bone marrow. Immuno- histochemical stains and ow cytometry. Must distinguish from infections, other cancers, drug effects. Treatment Steps 1. Correct complications. 2. Allopurinol. 3. Chemotherapy. Acute Myelogenous (AML)—remission achieved in majority of pa- tients older than 60 with one course of cytosine arabinoside (ara- C) and daunomycin or doxorubicin. Bone marrow transplant for relapse after rst remission or in rst remission if prognostic fac- tors are unfavorable. Age limits vary from center to center and with physiologic age. Cure rate 20% in AML. Acute Promyelocytic Leukemia (APML)—induce remission with all-trans retinoic acid (ATRA), then consolidate with standard chemotherapy. Cure rates of 35–45% are clearly better than typi- cal AML. Acute Lymphoblastic (Acute Lymphocytic, ALL)—vincristine, prednisone, and a third drug, such as L-asparaginase, doxorubicin, or daunorubicin, gives 80% remission in adults. Need CNS prophy- laxis (cranial irradiation or intrathecal methotrexate), then maintenance or continuation therapy. For relapse, give systemic chemo and local irradiation. Bone marrow transplant (30% survival rate in allogeneic transplant). |
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Characterized by normal to increased marrow cellularity and ineffec-
tive erythropoiesis: refractory anemia (RA), refractory anemia with ringed sideroblasts (RARS), refractory anemia with excess blasts (RAEB), and RAEB-in transition (RAEB-IT). |
Myelodysplastic Syndromes
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Symptoms
Fatigue, anorexia, weight loss, sense of abdominal fullness. Headaches, fever, sweats, bone pain. Hemorrhages, thromboses, fever. |
Chronic Myelogenous Leukemia (CML)
Description Originates in primitive myeloid stem cell. Characteristic Philadelphia (Ph1) chromosome (see Fig. 6–3). Pathology Bone marrow aspiration reveals hypercellular marrow, increase in eosinophils, basophils, megakaryocytes. Diagnosis conrmed by Philadelphia chromosome. |
Diagnosis
Splenomegaly. Leukocytosis with immature cells. Thrombocytosis. Anemia with marked leukocytosis. Markedly decreased leukocyte al- kaline phosphatase. Elevated uric acid, lactic dehydrogenase (LDH), vitamin B12. Myelobrosis. Enters a blastic or accelerated phase (myeloblastic or lymphoblastic) after 3 years in 80%. Treatment Steps 1. Treat with imatinib mesylate (Gleevec), a tyrosine kinase in- hibitor. 2. For relapsing disease, hydroxyurea, and α-interferon are the main drugs, though cyclophosphamide and busulfan are also ef- fective. 3. Acute leukostatic or thrombotic complications require leuka- pheresis, or plateletpheresis. Good hydration and allopurinol. 4. Splenic radiation to reduce spleen size and white count. 5. Treatment of blastic phase very difcult. 6. In younger patients, consider bone marrow transplant in chronic phase if donor available. |
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Symptoms
Symptoms vary by extent of disease. Asymptomatic lymphocytosis. Adenopathy, splenomegaly. Malaise, fatigue, weight loss, anorexia, fever, night sweats, bacterial infections; herpes zoster is common. Diagnosis Lymphocytosis, with > 50% of small lymphs with round nuclei in the marrow. Peripheral blood ow cytometry for monoclonality of lymphocytes (CD5+) (see Fig. 6–4). |
Chronic Lymphocytic Leukemia (CLL)
Description Twenty-ve percent of all leukemias. Monoclonal proliferation of long-lived, usually B lymphocytes. Unknown etiology. May be asymp- tomatic. High incidence of second malignancies. Pathology Lymphocytosis can be massive. Anemia, thrombocytopenia, neu- tropenia. Coombs’-positive autoimmune hemolytic anemia is common. |
Diagnosis
Lymphocytosis, with > 50% of small lymphs with round nuclei in the marrow. Peripheral blood ow cytometry for monoclonality of lymphocytes (CD5+) (see Fig. 6–4). Stage 0—lymphocytosis only Stage 1—lymphocytosis with lymphadenopathy Stage 2—lymphocytosis with splenomegaly Stage 3—lymphocytosis with anemia Stage 4—lymphocytosis with throbocytopenia Treatment Steps 1. Should avoid vaccination with live vaccines. 2. Treat only if progressive and symptomatic. Chlorambucil or u- darabine. 3. Corticosteroids for acute symptoms, hemolytic anemia, thrombo- cytopenia. 4. Local radiotherapy to splenomegaly or massive adenopathy. |
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Symptoms
Of marrow suppression and hypersplenism. Pathology Medium to large lymphocyte with hairy projections. Surface monoclonal immunoglobulin. Diagnosis Progressive splenic enlargement. Pancytopenia. Hairy cells in blood and marrow are CD10+ and TRAP+ (tartrate-resistant acid phos- phatase). May need marrow biopsy (see Fig. 6–5). |
Hairy Cell Leukemia (Leukemic
Reticuloendotheliosis) Description A chronic B-cell leukemia; 2% of all leukemias Pathology Medium to large lymphocyte with hairy projections. Surface mono- clonal immunoglobulin. |
Treatment Steps
1. May observe, as it is slowly progressive. 2. Cladribine drug of choice; 75% effective. 3. Also used after relapse are α-interferon, pentostatin, and splenec- tomy. |
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Symptoms
Skin eruption with appearance of eczema or psoriasis. Pathology Prolonged course, beginning with nonspecific lesions (premycotic stage) that slowly evolve into cutaneous plaques and patches (my- cotic stage), and then into ulcerative nodules and tumors (tumor stage). May involve lymph nodes and internal organs later |
Mycosis Fungoides
Description A cutaneous T-cell lymphoma. The Sézary syndrome is the leukemic form of mycosis fungoides. |
Diagnosis
Multiple biopsies necessary. Treatment Steps Local therapy: 1. Topical chemotherapy. 2. PUVA (psoralen plus irradiation). 3. Radiotherapy. Systemic therapy: 1. Interferon. 2. Retinoids. 3. Cytotoxics—methotrexate, adriamycin, cladribine. |
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Symptoms
Headache (morning), mental changes, generalized convulsions, pa- pilledema (25%), vomiting, vasomotor/autonomic, hormonal changes. |
Primary Neoplasms of the Brain
Description Most common CA in children. “Benign” brain tumors can be lethal. Cerebral edema is a major cause of morbidity Pathology Types: 1. Neuroectodermal are the most common. These include astro- cytoma (more benign), glioblastoma multiforme (more malig- nant). 2. Mesodermal meningioma (“benign,” though grow very large and can cause death). 3. Pituitary adenoma and craniopharyngioma. 4. Pineal (produce endocrinopathies). 5. Metastatic. 6. Vascular arteriovenous malformations (AVMs), hemangioblas- tomas. |
Diagnosis
Magnetic resonance imaging (MRI) of head. Must distinguish from benign intracranial hypertension (nonfocal), stroke (acute event), subdural hematoma, Alzheimer’s. Treatment Steps 1. Surgery for cure in meningioma, benign cerebellar tumors, or acoustic schwannomas. 2. Radiation for malignant tumors or symptomatic unresectable “be- nign” tumors. 3. Medical therapy: steroids relieve edema; anticonvulsants; chemo- therapy, local and systemic. |
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Symptoms
Neurologic symptoms, seizures, headaches, motor weakness. |
Metastases to the Brain
Description Most CNS tumors are metastatic. Brain metastases are from lung and breast; melanoma has high propensity to spread to brain. |
Diagnosis
Use MRI with gadolinium or CT with contrast. Distinguish from seizure, meningeal carcinomatosis, paraneoplastic syndrome Treatment Steps Depends on the primary tumor and the extent of disease. Options include 1. For solitary lesions, surgery and steroids. 2. For multiple metastases, irradiation chemotherapy (for small-cell lung and testicular CA). |
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Symptoms
Headaches, altered mentation, cranial nerve defects, lumbosacral radiculopathies, seizures. |
Leptomeningeal Metastases
Description About 8% of CA patients develop meningeal spread |
Diagnosis
Lumbar puncture (LP) (5–100 cells, increased protein, decreased glucose). Positive cytology (repeat LPs may be needed) to confirm diagnosis. MRI and CT are usually normal, but gadolinium contrast can be suggestive reatment Steps 1. Cranial irradiation. 2. Intrathecal chemotherapy. Usually combined. |
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Symptoms
Hearing loss, tinnitus, less often vertigo |
Acoustic Neuroma
Description Schwannoma of eighth nerve. |
Diagnosis
Brain stem auditory-evoked responses (BAERs); MRI or CT with contrast. Treatment Steps Microsurgery or radiosurgery yields 85–95% control rate |
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The most common intraocular tumor of children
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Retinoblastoma
An autosomal dominant hereditary tumor of the retina |
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Symptoms
Hemorrhagic nodules with violaceous, dark brown lesions. Before AIDS epidemic, primarily on lower extremities. With AIDS, see mucocutaneous and lymph node involvement. |
Circulatory System (Kaposi’s Sarcoma)
Description Seen after immunosuppressive therapy and HIV infection (50% of homosexual men with AIDS). Originally described in elderly male of Mediterranean origin. Cause now felt felt to be human herpesvirus-8. |
Diagnosis
Clinical picture; biopsy (see Fig. 6–6). Treatment Steps Local: Topical chemotherapy, intralesional injections, local radiation. Widespread: α-Interferon, cytotoxics (e.g., vinblastine, vincristine, Adriamycin). |
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Symptoms
Pharyngitis, lymphoid hypertrophy, voice change, conductive hear- ing loss, dysphagia, odynophagia, halitosis, weight loss. |
Carcinoma of the Nasopharynx
Pathology Most common is squamous cell. Also lymphoma, lymphoepithe- liomas (Schmincke’s tumor), anaplastic carcinoma. |
Diagnosis
Endoscopy, biopsy Treatment Steps 1. Surgery. 2. Radiation. 3. Chemotherapy as radiation sensitizer or for recurrent disease. |
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Symptoms
Hoarseness, pain, dysphagia, odynophagia, cough, hemoptysis, hali- tosis. |
Tumors of the Larynx (Malignant)
Pathology Squamous cell carcinoma, neuroendocrine, salivary gland. |
Diagnosis
Direct laryngoscopy, pharyngoscopy, biopsy. Treatment Steps 1. Radiation. 2. Laryngectomy. |
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Symptoms/Diagnosis
Hoarseness, later dyspnea, dysphagia, pain. Diagnosed via en- doscopy. |
Tumors of the Larynx (Benign)
Pathology Papilloma (caused by papillomavirus), hemangioma, angiobroma. |
Treatment Steps
Carbon dioxide laser (for papillomas) |
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Symptoms
Cough, hemoptysis, weight loss, weakness, wheezing, fever, chest pain. |
Carcinoma of the Lung
Description Produces 180,000 new cases per year in United States; 150,000 deaths. Eighty to ninety percent associated with smoking and passive smoke inhalation. Occupational risks include uranium, halo-ethers, arsenical fumes, asbestos. Asbestos and radon (heavily insulated homes) may be cocarcinogens with cigarette smoke. Pathology Four types make up 95% (see Cram Facts). LUNG CANCER 1. Adenocarcinoma: • 40% and increasing • Peripheral location • Less frequent association with tobacco • More likely spread to brain and liver at presentation (40–45%) 2. Squamous cell: • 30% • Central location • Usually associated with smoking 3. Small cell: • 20% • Neuroendocrine origin • Systemic disease, requires chemotherapy 4. Large cell: • 10% and decreasing • More often peripheral, probably poorly differentiated adenocarcinoma 5. Screening chest x-rays in smokers are of no value in decreasing mortality |
Diagnosis
Chest x-ray (mass in lung). Need tissue via sputum cytology, bron- choscopic biopsy or brushings, transbronchial biopsy or needle aspi- ration, CT-guided transthoracic biopsy, thoracotomy. Treatment Steps Depends on stage and histology. Non–small cell: TNM stages I and II: surgery. Stage III: Surgery and irradiation. Surgery results: 10–35% 5-year survival (squamous 37%, adeno 27%). Since very radiosensitive, give radiation therapy (XRT) in I, II, and III who do not have surgery. Unresectable (disseminated) non–small cell can be treated with con- comitant XRT and chemotherapy; XRT also to palliate SVC syn- drome, hemoptysis, cough, pain. Chemotherapy: 30–40% response rate. Small cell: Low survival, despite high initial response rate. Treat with chemotherapy (very sensitive) and irradiation. Not a surgical disease. Useful programs include a platinum plus a second agent (paclitaxel, etoposide). |
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Symptoms
Can be asymptomatic, dyspnea, chest pain, cough, cor pulmonale. Can occur via lymphatic or hematogenous spread. |
Metastases to the Lung
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Diagnosis
Sputum cytology, bronchoscopy, thoracotomy Treatment Steps 1. Treat the primary. 2. Consider resection if solitary metastasis from colon, melanoma or sarcoma. |
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Symptoms
Cough, chest pain, dyspnea occur late. |
Mesothelioma
Description Main primary pleural tumor. Benign or malignant. Malignant re- lated to asbestos in 80–90% Pathology Benign associated with hypertrophic pulmonary osteoarthropathy and clubbing (responds to surgical removal) |
Diagnosis
Malignant cells in pleural fluid or pleural biopsy Treatment Steps No standard treatment. Prognosis very poor Pemetrexed (Almta) is a new agent approved for mesothelioma and advanced non–small cell lung cance |
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Symptoms/Diagnosis
Slow-growing mass leading to ulceration, invasion of nerves, numb- ness or facial paralysis. Diagnose via biopsy |
Salivary Gland Neoplasms
Most common is pleomorphic adenoma (benign). Malignancies in- clude mucoepidermoid carcinoma, adenoid cystic carcinoma, adenocarcinoma. |
Treatment Steps
Surgery and/or radiation |
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Symptoms
Painful indurated ulceration. |
Carcinoma of the Mouth
Description Smoking and alcohol are risk factors. Tongue most common. Pathology Mostly squamous, with 20% chance of a second head and neck cancer. |
Diagnosis
Biopsy Treatment Steps 1. Radiation and surgery in combination can be curative. 2. Chemotherapy in more advanced cases (methotrexate, bleomycin, cisplatin). 3. Rehabilitation and prostheses important; 50% survival rate |
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Symptoms
Progressive dysphagia; steady, boring pain; halitosis; weight loss; cough after drinking uid |
Carcinoma of the Esophagus
Description Barrett’s esophagus, smoking, and alcohol are risk factors. Survival has been increased to 40% by combined modality therapy Pathology Squamous (more common; associated with head and neck cancer, lye strictures, inadequately treated achalasia). Adenocarcinoma arises in columnar epithelium (Barrett’s esophagus––see Cram Facts) |
Diagnosis
Esophagogram, endoscopy with biopsy and brushings, CT of chest, chest x-ray. (See Figure 6–7. Treatment Steps 1. Surgery: much morbidity. 2. Combined radiation and a platinum and 5-FU regimen. |
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Symptoms
Early are asymptomatic. Anorexia, weight loss, early satiety, bloating, dysphagia, epigastric pain, vomiting. |
Carcinoma of the Stomach
Description Majority are malignant; 5% are lymphomas. Gastric cancer associated with: • Virchow’s node: Enlarged supraclavicular node • Blumer’s shelf: Metastatic tumor felt via rectal exam • Sister Mary Joseph’s node: Enlarged periumbilical node • Acanthosis nigricans Pathology Usually adenocarcinoma. Spread to esophagus, liver, pancreas, trans- verse colon, lung, brain, bone. |
Diagnosis
Epigastric mass. Recurrent thrombophlebitis (Trousseau’s syn- drome). Air-contrast UGI x-rays. Endoscopy with biopsy and brush cytology. Culture for H. pylori. Treatment Steps 1. Surgery for cure or palliation. 2. Chemotherapy for unresectable disease. 3. Radiotherapy. 4. Antibiotics for H. pylori if culture positive in MALT |
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Symptoms
Epigastric pain, weight loss, vomiting, hematemesis, melena, jaun- dice, palpable mass, palpable gallbladder (Courvoisier’s sign), thrombophlebitis, psychiatric disturbances, diabetes, anemia, blood in stool. |
Carcinoma of the Pancreas
Description Slowly progressive, highly malignant. Second most common GI tu- mor after colon. Risk factors include smoking; high-fat, high-meat diet; exposure to manufacturing of paper, oil rening, gasoline. Usually not curable but can control symptoms Pathology Usually adenocarcinoma. Occasionally endocrine tumors (apudo- mas and carcinoids). |
Diagnosis
Ultrasound and/or CT, followed by needle aspiration. If negative, endoscopic retrograde cholangiopancreatography (ERCP) (very sensitive and tissue for cytology helpful). The UGI is poor in early detection. Occasional amylase elevation. Elevated CA 19-9. Treatment Steps 1. Whipple’s resection (pancreaticoduodenectomy) for small focal mass lesions. High operative mortality; 5% 5-year survival. 2. Chemotherapy with gemcitabine improves quality of life. 3. Radiation with 5-FU may improve survival by weeks. |
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Symptoms
Obstructive jaundice, acute cholecystitis, palpable mass, right upper quadrant pain, or disseminated carcinoma |
Carcinoma of the Biliary System
Description Associated with tobacco use and cholelithiasis. Pathology Adenocarcinoma. |
Diagnosis
Ultrasound. Must distinguish from cholesterol polyp or stone. Ele- vated CA 19-9. Treatment Steps Surgery; 5% 5-year survival, even with optimal surgery. |
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Symptoms
Abdominal pain, mass, weight loss, deterioration of patient with cir- rhosis. |
Carcinoma of the Liver/Hepatocellular
Cancer Description Uncommon, but increasing in United States. Median survival 6 months RISK FACTORS FOR HEPATOCELLULAR CANCER • Cirrhosis • Hepatitis B and/or C • Aatoxins (toxic metabolites from Aspergillus avus [peanuts and grains]) • Very common in Asia |
Diagnosis
Ultrasound, CT, or MRI. Elevated alkaline phosphatase, transami- nase, CEA, and AFP. Needle biopsy, wedge biopsy at laparotomy. Treatment Steps 1. Hepatic resection effective if early. 2. Chemotherapy with doxorubicin (Adriamycin), 5-FU, cisplatin regimens yield 50% response rate, but minimal survival advan- tage. 3. Chemoembolization. 4. Cryosurgery or radioablation (RITA). |
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Symptoms
Silent; bleeding, obstruction, change in bowel habits, pain, symp- toms of localized perforation. Right-side lesions rarely obstruct. Left- side polypoid lesions cause diarrhea and signs of obstruction. |
Carcinoma of the Colon
See also Chapter 4, section V. Pathology About 60% occur from splenic flexure down, and almost all are adenocarcinomas RISK FACTORS FOR COLORECTAL CANCER • Increased fat • Animal protein • Decreased fiber • Increasing age • Inflammatory bowel disease • Family history of female genital or breast cancer • History of colonic cancer or adenoma (especially villous adenomas) • History of familial colon cancer syndromes (familial polyposis, Gardner syndrome, Peutz–Jeghers syndrome, generalized juvenile polyposis) Screening See American Cancer Society Recommendations for the Early Detection of Cancer in Asymptomatic People. High-risk patients require annual sig- moidoscopy beginning at puberty. |
Diagnosis
In suspected case, digital rectal exam followed by colonoscopy. Brushings and/or biopsy. Must distinguish from angiodysplasia, diverticulosis, benign tumors. Treatment Steps 1. Surgery with curative intent. 2. Chemotherapy for metastatic disease (especially liver) with irinotecan (Camptosar) and 5-FU. Evidence for effectiveness of adjuvant chemo in Duke’s C colon carcinoma with 5-FU plus lev- amisole or leucovorin. Follow with colonoscopy, CEA if elevated preoperatively. Two new medications approved for metastatic col- orectal cancer are cetuximab (Erbitux) and bevacizumab (Avastin). Both are monoclonal antibodies. 3. Radiation for recurrent disease. |
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Carcinoma of the Rectum
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If below the peritoneal reflection, it commonly recurs, and postop
radiation + 5-FU is recommended. Anal: chemotherapy + radiation is better than surgery as primary treatment |
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Symptoms
Cutaneous flushing (precipitated by alcohol, food, stress), facial telangiectasias, tachycardia and decreased blood pressure, headache after the flush, diarrhea, symptoms of peritoneal fibrosis, right-sided endocardial fibrosis (with congestive heart failure). Bronchocon- striction and wheezing less common |
Carcinoid Tumors
Description Tumors that arise from enterochromafn cells (Kulchitsky) and pro- duce biologically active amines and peptides (serotonin, bradykinin, histamine, prostaglandins). Survival variable but if metastatic, < 5 years Pathology Often arise in ileum and metastasize to the liver. Excrete serotonin and 5-HIAA. Carcinoids can arise in almost all organs, including ap- pendix, rectum, stomach, and lung |
Diagnosis
Clinical suspicion; markedly increased urinary 5-hydroxyindoleacetic acid (5-HIAA) hepatomegaly. Of less help are CT, ultrasound, scans. Treatment Steps 1. Surgery if resectable or symptomatic. 2. If not resectable, no treatment for mild symptoms. Symptomatic treatment (antidiarrheal agents, bronchodilators, nutritional sup- port). 3. Chemotherapy not very effective. |
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Symptoms/Diagnosis
Asymptomatic, bleeding, pain, diarrhea. Seen on colonnoscopy; biopsy needed to assess benign vs. malignant. |
Colon Polyps
Description Importance: bleeding or malignant potential. Pathology Four main types: 1. Hyperplastic—(majority of rectal polyps; not considered neo- plastic). 2. Tubular adenomas. 3. Villous adenomas—(neoplastic; villous have high malignant transformation rate than tubular). 4. Mixed type—cancer rate much higher in larger polyps |
Treatment Steps
1. Removal. 2. Follow with colonoscopy. |
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Polyposis Syndromes
Autosomal dominant; will nearly all develop carcinoma |
Familial polyposis
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Treatment Steps
Subtotal colectomy. Also genetic counseling and intensive screening of family members. |
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Polyposis Syndromes
Dominantly transmitted; associated with bone tumors (osteomas), and soft tissue tumors (lipomas, sebaceous cysts, fibromas, fibrosarcomas); high malignant potential. |
Gardner syndrome
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Treatment Steps
Subtotal colectomy. Also genetic counseling and intensive screening of family members. |
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Polyposis Syndromes
Colon adenomas plus central nervous system tumors; high malignant potential. |
Munro syndrome
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Treatment Steps
Subtotal colectomy. Also genetic counseling and intensive screening of family members. |
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Polyposis Syndromes
Autosomal dominant; polyps plus mucocutaneous hyperpigmentation; low malignant potential. |
Peutz–Jeghers syndrome:
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Treatment Steps
Subtotal colectomy. Also genetic counseling and intensive screening of family members. |
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Polyposis Syndromes
Autosomal dominant; hamar- tomas; possible increased carcinoma incidence. |
Generalized juvenile polyposis
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Treatment Steps
Subtotal colectomy. Also genetic counseling and intensive screening of family members. |
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Symptoms
Variable headaches, visual disturbances (blindness, optic atrophy), temperature instability, hyperphagia, emotional disturbance, dis- turbed sleep patterns, hypopituitarism, hypogonadism. |
Pituitary Adenoma
Description Adenomas form 90% of all pituitary tumors; most are functioning; benign, but may have aggressive local growth pattern. |
Diagnosis
Enlarged sella by x-ray, mass on CT or MRI, visual elds, visual evoked response. Treatment Steps 1. Transsphenoidal pituitary surgery. 2. Optionally, can irradiate. 3. Will require endocrine replacement (see Chapter 3) |
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Symptoms/Diagnosis
Asymptomatic. Large functioning adenomas produce hyperthyroidism. Diagnose via needle aspiration. |
Benign Nodules
• About 96% of thyroid nodules are benign. • A “functioning” or “hot” nodule is also almost always benign. |
Treatment Steps
Follow warm (nonclinically thyrotoxic) nodules with annual thyroid function tests. Hot (clinically toxic) nodules are treated with surgery or radioactive iodine. |
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Symptoms
Thyroid nodule; symptoms of local invasion. |
Thyroid Cancer
Description Risk factors include childhood exposure to radiation and heredity; 11,000 cases per year; 1,000 deaths; 3–4% of solitary thyroid nodules are cancer. Pathology May occur as part of familial thyroid carcinoma (multiple endocrine neoplasia [MEN] types 2 and 3). FACTORS THAT WORSEN PROGNOSIS IN THYROID CANCER • Male gender • Age > 40 years old • Anaplastic histological type • Large primary tumor > 1.5 cm in diameter • Distant metastases • Extrathyroidal invasion 1. Papillary—(the most benign and the most common; pathog- nomonic is the psammoma body). 2. Follicular. 3. Medullary—(produces calcitonin). Can be associated with MEN-2. 4. Poorly differentiated (anaplastic)—(the most highly malignant). n anaplastic thyroid cancer, the patient may have hoarseness due to a rapidly growing mass. |
Diagnosis
Needle aspiration may reduce the need for surgery by 60%. Option- ally, thyroid scanning and ultrasound. Thyroxine to suppress thyroid-stimulating hormone (TSH). Treatment Steps 1. Needle aspiration. 2. Surgical resection (if hypo- or euthyroid) 3. Radiation therapy with 131I (if hyperfunctional). 4. Thyroxine suppression. 5. Irradiation and chemotherapy for thyroid lymphoma. |
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Symptoms
Abdominal mass. Obesity, plethora, hirsutism, menstrual disorders, hypertension, weakness (hypokalemia), back pain (from osteope- nia), striae, acne, depression, bruising |
Cushing’s Disease
Description A primary adrenal tumor secreting cortisol, causing signs and symp- toms of glucocorticoid excess. Pathology Adenoma and carcinoma equally. Spread to liver and lung. |
Diagnosis
Use 24-hour urine free cortisol; overnight 1 mg dexamethasone-suppression test; basal plasma ACTH levels. Tumor localization with CT & ultrasonography. Treatment Steps 1. Adrenalectomy. 2. Mitotane for residual or nonresectable carcinoma. 3. Other cytotoxics—doxorubicin. 4. Control hypersecretion—aminoglutethimide, metyrapone. 5. Steroid replacement therapy. |
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Female offspring of women given diethylstilbestrol during preg-
nancy may get adenosis of vagina and have increased risk of vaginal cancer (adenocarcinoma, clear cell type). |
Neoplasms of the Vagina
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Symptoms
Painless lump. Hard, irregular mass, skin dimpling, or nipple retraction. |
Carcinoma of the Breast
Description 203,500 new cases in 2002; 12% of women will get it; 85% are older than 40 years old. Risk factors: prior breast cancer, family history, early menarche, late menopause, late or no pregnancy; moderate alcohol intake; radiation exposure; western society diet. Oral contraceptives do not increase the risk, nor does estrogen given for osteoporosis. Pathology Assume distant metastases. Size of tumor, and presence of axillary nodes correlates with risk of recurrence. The presence of estrogen receptors (ER) and progesterone receptors (PR) indicates better prognosis. High Ki67 and the presence of the her-2 mutation a poorer prognosis. About 80% are inltrating ductal; others are inl- trating lobular, medullary, comedocarcinoma, colloid carcinoma (see Fig. 6–8). |
Diagnosis
• Screening. See American Cancer Society Recommendations for the Early Detection of Cancer in Asymptomatic People. • Mammograms (90% accuracy), ne-needle biopsy, excisional biopsy. Treatment Steps Two steps: outpatient ne-needle biopsy or excisional biopsy under local; discuss options, then do denitive treatment. Stage I and II Disease—local resection (lumpectomy and axillary node dissection or modied radical) followed by irradiation. Adjuvant systemic therapy for poor prognosis stage I and all stage II. Tamoxifen if postmenopausal and ER positive. Chemotherapy if ER negative. Lobular—higher risk of bilateral disease. Resectable Stage III—do mastectomy followed by radiation and chemotherapy. If patient strongly wishes breast conservation, consider preoperative chemotherapy. Unresectable Stage III or Inammatory Breast Carcinoma—give chemo- therapy followed by irradiation (and possible resection). Stage IV (Metastatic)—hormonal (bone, soft tissue, and mild pulmonary spread respond) or chemotherapy (liver, brain, and extensive lung). –1. Premenopausal Chemotherapy if adjuvant therapy indicated using such drugs as cy- clophosphamide, 5-FU, methotrexate, and Adriamycin. Consider adding a taxane if positive lymph nodes. Hormonal therapy of bene- t if ER positive. 9–2. Postmenopausal Tamoxifen if ER/PR positive (anastrazole also an option); chemo- therapy if resistant to hormone. Adjuvant chemotherapy. National Institutes of Health (NIH) Con- sensus says adjuvant chemotherapy and hormonal therapy (tamox- ifen) are effective in axillary node-positive patients (especially if ER positive). If CEA or CA 27-29 elevated preoperatively, can be used to monitor. No follow-up apart from mammogram proven to improve survival. |
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Symptoms
Painless testicular mass. May have dyspnea, abdominal or back pain, gynecomastia, supraclavicular adenopathy, or ureteral obstruction. |
Nonseminomatous
Description Germ cell tumors that include embryonal cell carcinomas, chorio- carcinomas, and teratomas. Stages I and II, 99% cure rate. Stage III, 70%. |
Diagnosis
Stage with chest x-ray, CT chest and abdomen, AFP, β-hCG. Do not perform percutaneous biopsy. Treatment Steps 1. Inguinal orchiectomy and retroperitoneal lymph node dissection for staging and initial treatment. 2. Cisplatin-based aggressive chemotherapy. |
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Description
Rare; most are malignant, derived from germ cells, 20–35 years old. Risk factor is cryptorchidism. |
Seminoma
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Diagnosis
Evaluate with AFP, β-hCG, CT of abdomen and pelvis. Treatment Steps 1. Inguinal orchiectomy and radiation produce 80–95% cure rates. 2. If increased AFP, treat like nonseminomatous germ cell tumor (GCT). |
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Symptoms
Gross or microscopic hematuria, ank pain, abdominal mass. Symp- toms of paraneoplastic syndrome (fever, hypertension, anemia, he- patic dysfunction [Stauffer syndrome]). Many unusual symptoms. Erythrocytosis. |
Hypernephroma (Renal Cell Carcinoma,
Renal Adenocarcinoma) Description Risk factors include male gender and tobacco use Pathology Three histologic types: clear cell, granular cell, and sarcomatoid |
Diagnosis
Intravenous pyelogram (IVP), ultrasound, CT, MRI. Rule out renal vein thrombus. (See Figs. 6–9 and 6–10.) Treatment Steps 1. Stages I, II, and IIIA require radical nephrectomy and yield 50– 70% 5-year survival. No signicant benet to adjuvant therapy. 2. Stage IV—combination therapies of α-interferon, IL-2, and 5-FU are used. |
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Symptoms
Asymptomatic palpable abdominal mass, hematuria, hypertension, abdominal pain. |
Wilms’ Tumor (Nephroblastoma)
Description Most patients are under 4 years old. Pathology About 80% are localized and resectable. |
Diagnosis
IVP, ultrasound, or CT. Must distinguish from neuroblastoma (with urinary vanillylmandelic acid [VMA]). Treatment Steps 1. Limited disease: surgery + chemotherapy (doxorubicin, actino- mycin D, vincristine) yields 85% disease-free survival. 2. Advanced disease: irradiation + chemotherapy. |
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Symptoms
Hematuria, bladder irritability (frequency, dysuria). |
Carcinoma of the Bladder
Description About 50,000 new cases per year; men predominate. Chemical car- cinogens are implicated (including those in cigarette smoke) Pathology Transitional cell. Rarely squamous if Schistosoma haematobium infestation. |
Diagnosis
Cystoscopy and transurethral bladder biopsy Treatment Steps Stage A: 1. Transurethral resection of bladder tumor (TURBT). 2. Cystoscopic surveillance for multiple recurrences. 3. Intravesical chemotherapy: bacillus Calmette–Guérin. Stages B and C: 1. Pelvic lymphadenectomy and radical cystectomy. Metastatic dis- ease. 2. Chemotherapy (e.g., methotrexate, vinblastine, platinums, doxorubicin, paclitaxel). |
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Symptoms
Asymptomatic early, urinary retention symptoms, bone pain. |
Carcinoma of the Prostate
Description Second leading cancer cause in males. No relationship to benign prostatic hypertrophy (BPH); little relationship to smoking or alco- hol. Of 30,000 deaths per year, 30–50% of men older than 50 have at least a focus of adenocarcinoma of prostate. African Americans’ risk two times that of Caucasians. Pathology About 50% of prostate nodules are malignant; 95% are adenocarci- nomas. Bone metastases common (pelvis, lumbar spine, femurs, tho- racic spine, ribs); lung and liver metastases the most common visceral spread. |
Diagnosis
Digital rectal exam, transrectal prostatitic ultrasound (TRUS), con- rmation with TRUS-guided needle biopsy. Do PSA before biopsy. IVP, bone scan, if biopsy positive. Treatment Steps Will vary with physiologic age of patient, being more aggressive in younger patients. Also considering importance of sexual function. Suppression with leuprolide preoperatively. • A1. Observation and rebiopsy. • A2 and B1. Radical prostatectomy. • B2 and C. Transurethral resection of prostate (TURP) followed by radiation (40% post-XRT impotence; 2% incontinence). • D (metastatic). Hormonal therapy (orchiectomy or luteinizing hormone–releasing hormone [LHRH] analog), which should be delayed until symptoms appear. Chemotherapy if hormone independent not very effective. Treating complications. Radiation for pain; erythropoietin or trans- fusion for anemia, strontium for painful blastic lesions. After treatment. Follow with periodic digital rectal exam (DRE) and PSA. |
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Head and Neck Tumors
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Description
Risk factors: tobacco and alcohol. Premalignant lesions include leukoplakia, erythroplakia. Pathology Usually squamous (epidermoid). Oral 44%; laryngeal 32%. |
Treatment Steps
1. Surgery. 2. Irradiation. 3. Chemotherapy for palliation (e.g., cisplatin and 5-FU). High re- sponse rates seen but not sustained. |