Pathology Lecture Review

Overview of lectures so far:

Reaction to stress – hypertrophy, hyperplasia, metaplasia and dysplasia

*emphasis on Barrett esophagus and uterine cervix

*dysplasia is reversible

seen - cervix, bronchi, GI tract

Apoptosis – performs functions in normal tissues

*loss of function important in malignant transformation

*usual initiators

GF deprivation, cytotoxic T-cell damage, DNA damage

Neoplasia cell types – parenchymal and stromal

Nomenclature suffixes

benign = "oma"

malignant = carcinoma, sarcoma

Contrast benign and malignant

differentiation

growth rate

expansile growth vs invasive growth

metastasis

necrosis

Development of malignancy – "tumor progression"

cell transformation

growth of transformed cell

local invasion

distant mets

Carcinogens

chemical – initiator, promoter

radiant energy – sun – nucleotide excision repair &

Xeroderma pigmentosa

radiation – X-ray, particle radiation

long lag period

leukemia, thyroid, breast, lung malignancies

viral – HPV, EBV, HBV, HCV

genetics – there are a host of these

Process of metastasis

loss of inter cell adhesion

penetrate basement membrane

traverse ECM

penetrate lymphatic