KMU (IPM&R) pathology

1. Effects of Neoplasia on the Host

2. 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

3. The growing tumor
• May compress or destroy adjacent structures,
• Cause inflammation, pain, vascular changes,
• Functional deficits (varying degrees)

4. • 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.

5. • Neoplasms growing in a confined area, (cranial
cavity), form space-occupying lesions
• Local compressive effects
• General—potentially lethal—increase in intracranial
pressure.

6. 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.

7. • 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

8. • 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.

9. • Nonendocrine tumors may elaborate hormones
or hormone-like products and give rise to
Paraneoplastic syndromes

10. 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.

12. `

13. 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

14. • 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

15. 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

16. 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
Space–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

17. Clinical Effect Causative Factors
Various 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 IDA
Replacement of marrow by tumor
causes leukoerythroblastic type

18. 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

19. 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).

20. 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.