Oncology



Oncology



1 What are the key differential points for the commonly tested blood dyscrasias?










































































TYPE AGE WHAT TO LOOK FOR IN CASE DESCRIPTION/TRIGGER WORDS
ALL Children (peak age: 3-5 yr) Pancytopenia (bleeding, fever, anemia), history of radiation therapy, Down syndrome
AML >30 yr Pancytopenia (bleeding, fever, anemia), Auer rods (Fig. 26-1; Plate 55), DIC
CML (Fig. 26-2; Plate 56) 30-50 yr White blood cell count greater than 50,000, Philadelphia chromosome, blast crisis, splenomegaly
CLL >50 yr Male gender, lymphadenopathy, lymphocytosis, infections, smudge cells, splenomegaly
Hairy cell leukemia Adults Blood smear (hairlike projections), splenomegaly
Mycosis fungoides/Sézary syndrome >50 yr Plaquelike, itchy skin rash that does not improve with treatment, blood smear (cerebriform nuclei known as “butt cells”), Pautrier abscesses in epidermis
Burkitt lymphoma (Fig. 26-3; Plate 57) Children Associated with EBV (in Africa)
CNS B-cell lymphoma Adults Seen in patients with HIV infection, AIDS
T-cell leukemia Adults Caused by HTLV-1 virus
Hodgkin disease 15-34 yr Reed-Sternberg cell, cervical lymphadenopathy, night sweats
Non-Hodgkin lymphoma Any age Small follicular type has best prognosis, large diffuse type has worst; primary tumor may be located in GI tract
Myelodysplasia/myelofibrosis >50 yr Anemia, teardrop cells, “dry tap” on bone marrow biopsy, high MCV and RDW; associated with CML
Multiple myeloma >40 yr Bence-Jones protein (IgG = 50%, IgA = 25%), osteolytic lesions, high serum calcium
Waldenström macroglobulinemia >40 yr Hyperviscosity, IgM spike, cold agglutinins (Raynaud phenomenon with cold sensitivity)
Polycythemia vera >40 yr High hematocrit/hemoglobin, pruritus (especially after hot bath or shower); use phlebotomy
Primary thrombocythemia >50 yr Platelet count usually greater than 1,000,000; may have bleeding or thrombosis

ALL, Acute lymphoblastic leukemia; AML, acute myelogenous leukemia; CLL, chronic lymphocytic leukemia; CML, chronic myelogenous leukemia; CNS, central nervous system; DIC, disseminated intravascular coagulation; EBV, Epstein-Barr virus; GI, gastrointestinal; MCV, mean corpuscular volume; RDW, red cell distribution width.


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Figure 26-1 Auer rods vary from prominent, as in this cell, to thin and delicate. See Plate 55. (From McPherson RA, Pincus MR. Henry’s clinical diagnosis and management by laboratory methods. 22nd ed. Philadelphia: Saunders, 2011, Fig. 33-25.)

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Figure 26-2 Chronic myelogenous leukemia showing myeloid blast phase. See Plate 56. (From Hoffman R, Benz EJ Jr, Shattil SJ, et al. Hematology: basic principles and practice. 5th ed. Philadelphia: Churchill Livingstone, 2008, Figure 69-5A.)

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Figure 26-3 A young boy from South America with typical endemic Burkitt lymphoma presenting in the mandible. See Plate 57. (From Jaffe ES, Harris NL, Vardiman JW, et al. Hematopathology. 1st ed. St. Louis: Saunders, 2010, Fig. 24-1. Courtesy Prof. Georges Delsol, Toulouse, France.)







7 Name the mode of inheritance and types of cancer found in the following conditions






































































DISEASE/SYNDROME INHERITANCE TYPE OF CANCER (IN ORDER OF MOST LIKELY)/OTHER INFORMATION
Retinoblastoma Autosomal dominant Retinoblastoma, osteogenic sarcoma (later in life)
MEN, type I Autosomal dominant Parathyroid, pituitary, pancreas (islet cell tumors)
MEN, type IIa Autosomal dominant Thyroid (medullary cancer), parathyroid, pheochromocytoma
MEN, type IIb Autosomal dominant Thyroid (medullary cancer), pheochromocytoma, mucosal neuromas
Familial polyposis coli Autosomal dominant Hundreds of colon polyps that always become cancer
Gardner syndrome Autosomal dominant Familial polyposis plus osteomas and soft tissue tumors
Turcot syndrome Autosomal dominant Familial polyposis plus CNS tumors
Peutz-Jeghers syndrome Autosomal dominant Look for perioral freckles and multiple noncancerous GI polyps; increased incidence of noncolon cancer (stomach, breast, ovaries); no increased risk of colon cancer
Neurofibromatosis, type I (Fig. 26-5; Plate 58) Autosomal dominant Multiple neurofibromas, café-au-lait spots; increased number of pheochromocytomas, bone cysts, Wilms tumor, leukemia
Neurofibromatosis, type II Autosomal dominant Bilateral acoustic neuromas
Tuberous sclerosis Autosomal dominant Adenoma sebaceum, seizures, mental retardation, glial nodules in brain; increased renal angiomyolipomas and cardiac rhabdomyomas
Von Hippel-Lindau disease Autosomal dominant Hemangioblastomas in cerebellum, renal cell cancer; cysts in liver and/or kidney
Xeroderma pigmentosa Autosomal recessive Skin cancer
Albinism Autosomal recessive Skin cancer
Down syndrome Trisomy 21 Leukemia

CNS, Central nervous system; GI, gastrointestinal; MEN, multiple endocrine neoplasia.


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Figure 26-5 Café-au-lait patches as well as multiple axillary freckles in a 14-year-old boy. See Plate 58. (From Hoyt CS, Taylor D. Pediatric ophthalmology and strabismus. 4th ed. Saunders, 2012, Figure 65.4.)



9 Cover the right-hand column and specify the major environmental risk factors for the following cancers






11 How do you diagnose and treat lung cancer?


As with all cancers, you need a tissue biopsy (e.g., via bronchoscopy, computed tomography [CT]-guided biopsy, open lung biopsy) to confirm malignancy and to define the histologic type. Non–small cell lung cancer may be treated with surgery if the cancer remains within the lung parenchyma (i.e., without involvement of the opposite lung, pleura, chest wall, spine, or mediastinal structures). Early metastases of small cell lung cancer make surgery inappropriate. Small cell lung cancer and extensive non–small cell lung cancer (Fig. 26-6) are treated with chemotherapy with or without radiation. Usually a platinum-containing chemotherapy regimen (e.g., cisplatin) is used.


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Figure 26-6 Imaging non–small cell lung cancer. A,B, Posteroanterior and lateral chest radiogram of patients with non–small cell lung cancer which is locally advanced. C,D Computed tomography (CT) imaging using lung and mediastinal windows. (From Abeloff M, et al. Abeloff’s clinical oncology. 4th ed. Philadelphia: Churchill Livingstone, 2008, Fig. 76-12.)


12 What consequences can result from an apical (Pancoast) lung cancer?


Horner syndrome: From invasion of the cervical sympathetic chain. Look for unilateral ptosis, miosis, and anhidrosis (no sweating).


Superior vena cava syndrome: Caused by compression of superior vena cava with impaired venous drainage. Look for edema and plethora (redness) of the neck and face (Fig. 26-7; Plate 59) and central nervous system (CNS) symptoms (headache, visual symptoms, and altered mental status).


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Figure 26-7 A patient with superior vena cava syndrome and the characteristic venous dilation and facial edema. See Plate 59. (From Abeloff MD, Armitage JO, Niederhuber JE, et al. Abeloff’s clinical oncology. 4th ed. Philadelphia: Churchill Livingstone, 2008, Fig. 54-3.)

Unilateral diaphragm paralysis: From phrenic nerve involvement (apical tumor not required) will result in an elevated hemidiaphragm on chest x-ray.


Hoarseness: From recurrent laryngeal nerve involvement (apical tumor not required).



13 What is a paraneoplastic syndrome? What are the commonly tested paraneoplastic syndromes of lung cancer?


A paraneoplastic syndrome is a condition caused by a malignancy but not related directly to destruction or invasion by the tumor. Classic examples in lung cancer are as follows:


Cushing syndrome: From production of adrenocorticotropic hormone (histologic type: small cell carcinoma).


Syndrome of inappropriate antidiuretic hormone secretion (SIADH): From production of antidiuretic hormone (histologic type: small cell carcinoma).


Hypercalcemia: From production of parathyroid-like hormone (histologic type: squamous cell carcinoma).


Eaton-Lambert syndrome: Myasthenia gravis-like disease from lung cancer that spares the ocular muscles. The muscles become stronger with repetitive stimulation, which is the opposite of myasthenia gravis (histologic type: small cell carcinoma).



14 How should you manage a patient with a solitary pulmonary nodule on chest radiograph?


The first step is comparison with previous chest radiographs. If the nodule has remained the same size for more than 2 years, it is very unlikely to be cancer. If no old films are available and the patient is older than 35 years or has more than a 5-year history of smoking, get a CT scan (and possibly a positron emission tomography [PET] scan). If these are not definitely benign, get a biopsy of the nodule (via bronchoscopy or transthoracic needle biopsy, if possible) for tissue diagnosis.


If the patient is younger than 35 years or has no smoking history, the cause is most likely infection (tuberculosis or fungi), hamartoma, or collagen vascular disease. The patient should undergo CT scan and careful observation with follow-up imaging in 3 to 6 months. Investigate for infection if the history is suspicious.





17 What classic signs and symptoms indicate that a breast mass is cancer until proved otherwise?



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Apr 8, 2017 | Posted by in NURSING | Comments Off on Oncology

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