The site of the lesion, The nature of the surrounding anatomic structures The overall rate of growth
The growing tumor May compress or destroy adjacent structures, Cause inflammation, pain, vascular changes, Functional deficits (varying degrees)
Tumor growing near a vital structure (eg, the brain stem), Such local effects may be lethal Regardless of whether the neoplasm is benign or malignant.
Neoplasms growing in a confined area, (cranial cavity), form space-occupying lesions Local compressive effects Generalpotentially lethalincrease in intracranial pressure.
Local and Hormonal Effects Critical location is the pituitary adenoma. Benign and possibly not producing hormones, expansile growth can destroy the remaining pituitary leading to serious Endocrinopathy.
Cancers arising within or metastatic to an endocrine gland may cause an endocrine insufficiency by destroying the gland. Neoplasms in the gut, may cause obstruction as they enlarge.
Infrequently, peristaltic movement telescopes the neoplasm and its affected segment into the downstream segment, producing an obstructing intussusception
Endocrine neoplasms manifestations by elaboration of hormones. Benign tumors Cancers, which may be sufficiently undifferentiated to have lost such capability. A benign -cell adenoma of the pancreatic islets less than 1 cm in diameter may produce sufficient insulin to cause fatal hypoglycemia. Nonendocrine tumors may elaborate hormones or hormone-like products and give rise to Paraneoplastic syndromes
Cancer Cachexia (wasting syndrome ) Progressive loss of body fat and lean body mass Accompanied by profound weakness, anorexia, and anemia. The origins are obscure. The action of soluble factors Cytokines produced by the tumor & By the host in response to the tumor. ` Anorexia a common problem in patients with cancer Abnormalities in taste and central control of appetite Calorie expenditure often remains high, & BMR hi despite reduced food intake. Starvation, (daptational lowering of metabolic rate) Cancer cachexia, there is equal loss of fat and muscle, Whereas in starvation the muscle mass is relatively preserved at the expense of fat stores TNF produced by macrophages or possibly some tumor cells is a mediator of the wasting syndrome that accompanies cancer.
IL-1, IFN-, and leukemia inhibitory factor synergize with TNF Local Effect Result Mass Presentation as tissue lump or tumor Ulcer (nonhealing) Destruction of epithelial surfaces (eg, stomach, colon, mouth, bronchus) Hemorrhage From ulcerated area or eroded vessel Pain Any site with sensory nerve endings Seizures Tumor mass in brain; Cerebral dysfunction Wide variety of deficits depending on site Obstruction Of hollow viscera by tumor in the wall; bronchial obstruction leads to pneumonia; obstruction of bile ducts causes jaundice Perforation Of ulcer in viscera; in bowel may produce peritonitis Bone destruction Pathologic fracture, collapse of bone Inflammation Of serosal surface, pleural effusion, pericardial effusion, ascites Spaceoccupying lesion Raised intracranial pressure in brain neoplasms; anemia due to displacement of hematopoietic cells by metastases to the bone marrow Localized loss of sensory or motor function Compression or destruction of nerve or nerve trunk; classic example is involvement of recurrent laryngeal nerve by lung or thyroid cancer, with resulting hoarseness Edema Due to venous or lymphatic obstruction Clinical Effect Causative Factors Various hormonal effects, eg, hypoglycemia, Cushing's syndrome, gynecomastia, hypertension Hormone produced by endocrine tumors; socalled ectopic hormones produced by nonendocrine neoplasms Anemia Chronic blood loss or unknown toxic effects cause IDA Replacement of marrow by tumor causes leukoerythroblastic type Disseminated intravascular coagulation Widespread cancer (probably due to release of thromboplastic substances by dying tumor cells Polycythemia Renal cancer, hepatoma, uterine myoma, in some instances due to erythropoietinlike substance produced by tumor. Gout Hyperuricemia due to excess nucleic acid turnover; may be precipitated by cytotoxic therapy. Myasthenia gravis, myasthenic (Eaton Lambert) syndrome Thymoma especially; autoantibodies Clubbing of fingers Lung cancer and other intrathoracic neoplasms especially; mechanism unknown Immunodeficiency Lymphoma; any advanced cancer; chemotherapy Hyperviscosity syndrome, Monoclonal immunoglobulin (usually IgM) from lymphoma or myeloma Hypercalcemia Parathyroid hormone (including ectopic production), release of calcium from lysed bone (metastases), or lytic factors (as in myeloma). Cachexia, hypoalbuminemia, fever Advanced cancer; possible autoimmune, toxic, and nutritional mechanisms. Release of tumor necrosis factor (TNF). Direct Effects of Growth of Metastases
Metastatic deposits form growing tumors that may compress and destroy adjacent tissues in the same way that a primary lesion does.
The effects associated with a primary lesion are the direct result of the actions of the tumor on a single site in the body; in metastatic disease, more than one metastasis may be present and a multiplicity of effects may occur.
Effect of Constraint Induced Movement Therapy Versus Motor Relearning Programme To Enhance Upper Limb Motor Function in Stroke Patients: A Quasi Experimental Study
International Journal of Innovative Science and Research Technology