NURS 2090 Lecture Notes - Lactate Dehydrogenase, Aneuploidy, Itch

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Published on 16 Apr 2013
Department
Course
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
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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).
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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
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Document Summary

Clinical models of altered cellular proliferation and differentiation. 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: adenocarcinoma: **women/nonsmokers, leads to plural fibrosis/adhesions, squamous cell carcinomas: linked to smoking. Bronchial columnar leads to squamous metaplasia, dysplasia, carcinoma in situ and tumor. Can be detected in sputum: small cell carcinomas: highly malignant (rapid). Four subtypes: large cell carcinomas: large cells, high anaplasia, diagnosis based on exclusion, poor prognosis. 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. Small cell carcinoma (most likely to be spread at diagnosis) Non-small cell carcinoma (often based on ability to operate) Chemotherapy (may be used when cant get all cancer cells)

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