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Cancer Cases- altered cell proliferation and differentiatation.docx

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Dalhousie University
NURS 2090
Heather Helpard

Clinical Models of Altered Cellular Proliferation and Differentiation Lung Cancer (15% prognosis) Pathophysiology  Leading cause of cancer deaths worldwide  Smoking and industrial exposures often implicated  Tumors originate most frequently in the epithelial lining of the bronchi, bronchioles, and alveoli  Tropic to the bone, liver, brain (affinity to spread to distant site) Four subtypes: 1. Adenocarcinoma: **women/nonsmokers, leads to plural fibrosis/adhesions 2. Squamous cell carcinomas: linked to smoking. Bronchial columnar leads to squamous metaplasia, dysplasia, carcinoma in situ and tumor. Can be detected in sputum 3. Small cell carcinomas: highly malignant (rapid). Smoking related (men). Linked to poor prognosis. 4. Large cell carcinomas: large cells, high anaplasia, diagnosis based on exclusion, poor prognosis Clinical Manifestations  Persistent cough  Hemoptysis- bloody sputum  Chest pain  Shortness of breath  Explained as smokers cough or bronchitis Staging of Lung Cancer Diagnostic Criteria  Bronchoscopy  Chest x-ray  Tissue biopsy/cytology  MRI/CT/Ultrasound  Carcinoembryonic antigen (CEA)- prognosis often related to the levels of this antigen  Adverse prognosis: presence of pulmonary symptoms, large tumor size, nonsquamous history, lymph node metastisis or vascular invasion. Treatment  Based on tumor type Small cell carcinoma (most likely to be spread at diagnosis)  Chemotherapy  Surgery, radiation rarely work Non-small cell carcinoma (often based on ability to operate)  Surgery  Chemotherapy (may be used when cant get ALL cancer cells)  Radiation, if surgery not feasible (Radiation can help control tumor when it cant be removed, but will not cure the cancer). Colorectal Cancer (24-40% if resectable) Pathophysiology  Multiple lifestyle risk factors (75% unknown etiology, 25% familial) ** Age is greatest risk factor (others= smoking, alcohol, diet high in fat, low in fiber, IBD, obesity and inactivity)  Disruption of p53 gene implicated in 3 of 4 cases of colorectal cancer  Cellular transformation in mucosal epithelium of the bowel begins at the base of the crypts (where mitosis occurs, mature cells move up the crypt and dies and gets sloughed off). High fiber diets- bind to mutagens and move it quickly through colon, helps prevent cancer. High fat diet- increases secretion of bile because that is needed to break down fats. Linked to cancer. Protective factors- selenium, vitamin E,C, A and veggies (Brussels, cabbage, cauliflower, broccoli. Groups: from benign polyps to invasive tumors (adenoma- adenocarcinoma) 1. Nonneoplastic polyps: non a cancer precursor 2. Neoplastic polyps: adenoma, at risk for cancer 3. Cancer: adenocarcinoma Usually start from a series of events triggering chromosomal instability or replication errors. Aneuploidy- alterations in chromosomal number. Clinical Manifestations  Change in bowel habits (First clue!!)  Occult – hidden blood, in the ascending colon  Frank- visible blood, in the descending colon  Abdominal pain  Bowel obstruction  Anemia- caused by loss of blood  Systematic/ paraneoplastic manifestations Diagnostic Criteria  Digital rectal exam  Colonoscopy  NOT CEA values!! Treatment  Surgery  Chemotherapy  Radiation Brain Cancer Dont use TNM classification Pathophysiology Metastasis much more common to brain than primary tumors (10:1 ratio) (∆ not primary tumors, usually from lung, breast, skin or colon origin) Primary tumors originate from:  Glial cells- non neurons  Meninges – emerge in middle- late adulthood, slow growing, erodes cranium  Schwann cells-Schwannomas arise in the brain, spinal nerves, peripheral nerves **rarely malignant  Ectopic tissues – originate in embryonic cells that have migrated to brain/spinal cord. Can grow slowly over a life time. Gliomas- most common tumor type. Vary in differentiation (20% well differentiated, 40% are highly undifferentiated) Benign or malignant. Rarely metastasize outside CNS. Clinical Manifestations  Headache (due to increased pressure in the brain, with inflammation + fluid)  Vomiting (due to increased pressure in the brain, with inflammation + fluid)  Seizures (from irritation + discharge of neurons)  Loss of motor or sensory function (vision changes, numbness, weakness, paralysis)  Cognitive or behavioral changes (personality, irritability, forgetfulness, depression) Diagnostic Criteria  Neurologic examination  Direct visualization Brain scan CT/MRI X-ray Cerebral angiography PET scan Treatment  Surgery- usually for primary tumors  Radiation- almost always indicated  Chemotherapy- into spinal canal for some of the ‘omas’  Palliative care Leukemia Pathophysiology  Malignant neoplasms of blood and blood-forming organs  Most often associated with overproliferation and lack of differentiation in WBC’s  Replaces cells in the bone marrow with immature, proliferating neoplasms (blast cells)  May happen to ppl treated with chemotherapy for other types of cancer. Lymphocytic (ALL)- involve immature lymphocytes that originate in bone marrow Myelogenous (AML)- myeloid stem cells in the marrow, interfere with maturation of all blood cells Acute- sudden rapid loss of function Lymphocytic (ALL)- most common cancer in children, 85% prognos
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