01 Patho of Neoplasia

Question 1

Neoplasia

Answer 1

New growth/disorder of cell growth

Tumor

Question 2

Two basic components of tumors

Answer 2

Tumor parenchyma (basis)
Reactive stroma (for growth and spread)

Question 3

Desmoplasia

Answer 3

Parenchymal cells stimulating formation of abundant collagenous stroma

Scirrhous = stony hard desmoplasmic tumors

Question 4

Benign vs malignant tumors

Answer 4

Benign (3): adenoma, papilloma, cystadenoma, polyp, adenomatous polyp
Malignant (4)

Question 5

Types of malignant tumors

Answer 5

1 Mesenchymal (sarcoma)
2 Epithelial (carcinomas): ecto/meso/endoderm; squamous cell carcinoma, adenocarcinoma; undifferentiated malignant carcinoma
3 Hematolymphoid tumors (leukemia, lymphoma)

Question 6

Mixed tumors

Answer 6

Divergent differentiation of a single neoplastic clone

From single germ layer

Question 7

Teratomas

Answer 7

Mature/immature cells from more than one germ cell layer

From totipotent cells

Question 8

Special cases: malignant tumors with “-oma” as suffix

Answer 8

Melanoma 
Seminomas (testicular origin)
Hepatoma (hepatocellularcarcinoma)
Lymphoma (WBCs or lymphocytes)
Mesothelioma (linings of lungs, abdomen, heart)

Question 9

Uncharacteristic tumors

Answer 9

Hamartoma: benign tumor, disorganized, cells of the site
Coristoma: benign tumor, for heterotopic rest of cells (excess cells found exogenous to original site)

Question 10

Distinguishing characteristics of benign vs malignant neoplasms

Answer 10

Differentiation and anaplasia
Local invasion
Metastasis

Question 11

Differentiation

Answer 11

Well-differentiated: cells resemble mature normal cells of tissue origin

Benign tumors: almost always well-differentiated (e.g. lipoma)

Malignant tumors
Hallmark: anaplasia
Well differentiated: usually endocrine organs that secrete hormones (e.g. Adenocarcinomas, squamous cell carcinoma + keratin, hepatocellular carcinoma + bile)

Question 12

Anaplasia

Answer 12

Lack of differentiation

Pleomorphism: variation in size and shape (not uniform), tumor giant cells (e.g. rhabdomyosarcoma)
Abnormal nuclear morphology: chromatin, large nuclei/nucleoli
Abnormal mitoses: rapid cell growth
Loss of polarity: disturbed orientation
Large central areas of ischemic necrosis
Paraneoplasia

Question 13

Metaplasia

Answer 13

Adaptation to tissue damage by replacing cell types

Pancreatic acinar metaplasia

Question 14

Dysplasia

Answer 14

Disordered growth/proliferation, mostly epithelia
Loss of uniformity of individual cells and architectural orientation

Histo: large nuclei, abundant mitotic figures, not confined in basal layers, architectural anarchy
Carcinoma in situ: preinvasive stage of cancer, does not pierce basement membrane (e.g. skin, breast, cervix)

Question 15

Local invasion

Answer 15

Benign: remain localized to site of origin; no infiltrate, invade, metastasis; capsule (stromal cells deposit ECM)
exception: hemangiomas

Malignant: poor demarcation; pseudoencapsulated; invasive

Question 16

Metastasis

Answer 16

Marks malignancy
Penetrate BV, lymph, body cavities

Exception: CNS gliomas, basal cell carcinoma of skin

Question 17

Pathways of spread

Answer 17

1 Seeding of body cavities: penetrates tissue (e.g. peritoneal cavity); colon cancer, ovarian carcinoma; pseudomyxoma peritonei
2 Lymphatic spread: breast cancer, lung cancer; sentinel node (first node) biopsy
3 Hematogenous spread: liver and lungs; skeletal muscle and spleen rare;

Question 18

Arterial spread vs venous spread

Answer 18

Arterial spread: pulmonary capillary beds, pulmo arteriovenous shunts
Venous spread: renal cell carcinoma (renal vein -> IVC -> right heart), hepatocellular carcinoma (portal and hepatic radicles)

Question 19

Environmental factors

Answer 19

infectious agents
occupational hazards
smoking
alcohol consumption
diet and obesity
reproductive history
environmental carcinogens

Question 20

Acquired predisposing conditions

Answer 20

Precursor lesions: chronic inflammation (increase pool of stem cells, produce ROS, metaplasia) (barrett esophagus, squamous metaplasia, colonic metaplasia)
Non-inflammatory hyperplasia: endometrial hyperplasia, leukoplakia, villous adenoma
Immunodeficiency states: t-cell deficit