(B2) E1, Q1 pathology

Pathology

Study of disease

General pathology

Mechanism of disease

Anatomic pathologist

Diseased tissues (biopsies, autopsies)

Clinical pathologist

Diseased fluids/ cells (labs)

Etiology

The cause

Pathogenesis

Mechanism of development of disease

Hypertrophy

Increase in cell size

Atrophy

Decrease in cell size

Hyperplasia

Increase in cell number

Metaplasia

Change in cell type

Neoplasia

New growth

Neoplasm

New and abnormal growth

Mass

3 cm or greater

Nodule

Less than 3 cm

Which tumor would have mitotic figured

Malignant

Examples of hyperplasia

Liver regeneration, thyroid, prostate

Example of metaplasia

Barrett’s esophagus (intestinal metaplasia)

Examples of lipid accumulations

Fatty liver, atherosclerosis, xanthoma

Example of protein accumulation

Mott cells

Exogenous pigment accumulations

Tattoos, coal dust

Lipofuscin

Aging “wear and tear” pigment that turn heart or liver yellow/ brown

Hemosiderin

Stored iron, gold-brown pigment

Hemosiderosis

Iron overload with no tissue damage

Hemochromatosis

Iron overload with tissue damage

Classic triad found in hemochromatosis

Cirrhosis, bronze skin, diabetes mellitus

Pre hepatic jaundice

Increased RBC destruction

Hepatic jaundice

Lover damage

Post hepatic jaundice

Biliary obstruction

Anthracosis

Deposition of dust/ carbon in lungs

Pneumoconiosis

Lung disease from inhalation of dust

Which caspase is intrinsic pathway initiator

Caspase-9

Which caspase is extrinsic pathway initiator

Caspase-8

Which caspases are executioner caspases

Caspases 3, 6, and 7