Effects of Neoplasia on the Host

Direct Effects of Primary Tumors Local Growth

The signs and symptoms vary with

• 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 • General—potentially lethal—increase 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 β-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.

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Anorexiaa 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-γ, and leukemia inhibitory factor synergize with TNF

Local Effect ResultMass Presentation as tissue lump or tumorUlcer (nonhealing) Destruction of epithelial surfaces (eg,

stomach, colon, mouth, bronchus)Hemorrhage From ulcerated area or eroded vesselPain Any site with sensory nerve endingsSeizures Tumor mass in brain;Cerebral dysfunction Wide variety of deficits depending on siteObstruction 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 boneInflammation Of serosal surface, pleural effusion,

pericardial effusion, ascitesSpace–occupying 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 FactorsVarious hormonal effects, eg, hypoglycemia, Cushing's syndrome, gynecomastia, hypertension

Hormone produced by endocrine tumors; so–called ectopic hormones produced by nonendocrine neoplasms

Anemia Chronic blood loss or unknown toxic effects cause IDAReplacement 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 erythropoietin–like 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.