GENERAL PATHOLOGY

Necrosis and Apoptosis

The type of necrosis is dependent on the nature, intensity and duration of the injurious agent, and the type of cell involved. Note that initial membrane damage allows Ca+2 leakage with subsequent activation of Ca-dependent phosphatases and lipases.

• Coagulative necrosis – cytoplasm of the necrosed cells becomes eosinophilic and persists for many days (myocardial infarction)
• Colliquative necrosis – cells undergo lysis rapidly (brain infarcts)
• Caseous necrosis – Mycobacterium tuberculosis interacts with macrophages
• Gangrenous necrosis – primary (bacterial toxins) or secondary (ischaemia, infection)
• Fibrinoid necrosis – smooth muscle necrosis, fibrin release (malignant hypertension)
• Fat necrosis – inflammatory response to liberated fat fibrosis

There are also nuclear changes related to necrosis:

• Margination of chromatin – chromatin condensing around the periphery of the nuleus
• Pyknosis – small and dense nuclei
• Karyolysis – complete lysis of the nuclei
• Karyorrhexis – fragmented nuclei (generally seen in apoptosis)