Histopathology
Heart
– permanent
- good example of non-replicating cells
- myocardial death is leading cause of morbidity and mortality in the western world
- MI: coagulative tissue necrosis (nuclei shrink, acidophilia, cell outlines maintained, scarring)
- hypertrophy: response to chronic stress
- cells don’t divide, so almost never see tumors in heart
- amyloid: EC protein deposits, beta-sheets
- fibrinous inflamation: common cause of non-ischemic chest pain; can be result of chronic inflammation
Blood Vessels
– stable
- atherosclerosis: lipid deposition on wall of blood vessel; has fibrous capsule
- can lead to vascular occlusion, thrombus
- thrombus: blood clot in the vascular system; can be good (hemorrhage) or bad (occlusion)
- Virchow’s triad: endothelial cell injury, stasis of blood (most critical factor leading to thrombosis), hypercoagulability
- if part of it breaks off
Þ embolism
embolism: traveling blood clot or foreign substance that causes an occlusion (i.e. pulmonary embolism)
chronic low grade hypercoagulability Þ deposition of platelets and fibrin on normal valvular endocardium Þ fatal embolic consequences
Lung
– stable
- cells normally don’t divide, but are capable, so often source of tumors (due to interaction between cells and environment)
- also major site of metastatic tumors because receives lots of blood flow
- pathologic processes
- compromise of ability to exchange oxygen (pulmonary emboli, edema)
- airborn infections and acute cellular injury
- can lead to regeneration or scarring with reduced function
- chronic environmental insults (lead to tumors or permanent structural alterations)
- do not get infarct with pulmonary embolism
Liver
– stable
- prototype for study of cellular dysfunction in solid organs
- blood enters through portal triad
- supplies periportal hepatocytes (zone 1) and then centrilobular hepatocytes (zone 3)
- zone 3 most subject to ischemia, anoxia, nutritional deficiency
- blood leaves central vein to right heart (backup leads to damage of cetrilobular hepatocytes)
- chronic alcoholics
- hepatocellular steatosis: accumulation of TG in sublethaly injured hepatocytes
- mallory bodies: accumulaiton of cytoskeletal elements in chronically damaged cells
- cirrhosis: scarring leading to loss of normal function
- occurs with chronic damage or ECM damage
- leads to compromised exchange and hepatic portal hypertension
- complications: ascites, GI hemorrhage, metabolic encephalopathy, coagulopathy
- hepatocellular carcinoma: increased cell replication equals increased risk of carcinoma
- also lots of bloodflow makes liver susceptible to metastasis
- inborn errors of metabolism
- hemochromatosis: accumulation of hemosiderin leads to cirrhosis and carcinoma
- amyloidosis
- tuberculosus infection: caseous necrosis; contrast to coagulative necrosis seen in ischemia
Skin
– labile
- mainly wound healing and repair
- acute inflamation, granulation tissue formation, collagen deposition and epithelial regeneration
- interference with this pattern (persistent injury) leads to ulceration
- ability to heal translates into risk for neoplasia
- skin cancer is most common form