IMM2022 Study Guide - Final Guide: Caseous Necrosis, Apoptosis, Metaplasia
4 May 2018
School
Department
Course
Professor
Inflammatory disease
Inflammation is trying to return to a
homeostatic mechanism
Inflammation trigger inflammation
physiological purpose pathological
consequence egs
Infection inflammation host defence
against infection autoimmunity,
inflammatory tissue damage and sepsis
Tissue injury inflammation tissue repair
response fibrosis, metaplasia and/or
tumour growth
Tissue stress and malfunction inflammation
adaptation to stress and restoration of a
homeostatic state shift in homeostatic set
points, development of diseases of
homeostatic and/ or autoimmunity
Tissue necrosis
Can occur form injury, lack of oxygen, lack of
nutrients. the cells die very rapidly and
poses the cell structures to the outside. Eg
Anginga pectoris – due to mild injury lactic
acid build up (hypoxia). Eg Mycocardial
infarction – due to severe injury blockade
of artery (anoxia)
Note that when cells die WBC come to clean
up – part of the healing repair process. Some
necrotic regions can show dystrophic
calcification – a deposition of calcium that is
long standing.
Neutrophils are in AI
Macrophages in CI
TYPES OF NECROSIS
Colliquative (liquefactive)
Occurs in suppuration – due to neutrophils
lysing pyogenic bacteria and tissue. When this
occurs heterolysis is occurring (think of it like
a side effect) the neutrophils killing off the
neighbouring proteins. Eg absecess
Note that autolysis is apoptosis of a cell by its
own enzymes. Heterolysis is apoptosis
induced by hydrolytic enzymes from
surrounding (using inflammatory cells).
Caseous necrosis is a form of cell death in
which the tissue maintains a cheese-like
appearance soft and white proteinaceous
dead cell mass. This occurs in TB due to
hypersensitivity reaction and the nature of
the bacterium eg caseous necrosis of the lung.
It consists of chronic inflammatory cells
(macrophages). Can also have lymphocytes.
Fibroblasts will come in and try to stop the
spread of infection.
APOPTOSIS the inflammatory cascade is
NOT activated during apoptosis. There is no
inflammation as we tolerate our own
membranes. Apoptosis is referred to as
shrinkage necrosis.
An apoptotic body remains. PS
(phosphatidylserine) recognised by tissue
macrophages phagocytosis of membrane-
bound organelles.
• Apoptosis occurs in the immune
response as we don’t want to keep all
the immune cells around after an
immune response
• In embryogenesis – separation of
digits
• Withdrawal of hormonal growth
stimulus (uterus following child birth)
FOUR PHASES OF APOPTOSIS
1. Signalling phase
There are lots of death signals that can initiate
apoptosis.
• Cell surface R eg TNFR-mediated cell
death from cytokines (TNF-a)
• Fas FasL
• Mitochondrial cell death cell
anoxia causes changes in
mitochondrial membrane
permeability (cell damage pathway)
Document Summary
Inflammation is trying to return to a homeostatic mechanism. Inflammation trigger inflammation physiological purpose pathological consequence egs. Infection inflammation host defence against infection autoimmunity, inflammatory tissue damage and sepsis. Tissue injury inflammation tissue repair response fibrosis, metaplasia and/or tumour growth. Tissue stress and malfunction inflammation adaptation to stress and restoration of a homeostatic state shift in homeostatic set points, development of diseases of homeostatic and/ or autoimmunity. Can occur form injury, lack of oxygen, lack of nutrients. The cells die very rapidly and poses the cell structures to the outside. Anginga pectoris due to mild injury lactic acid build up (hypoxia). Eg mycocardial infarction due to severe injury blockade of artery (anoxia) Note that when cells die wbc come to clean up part of the healing repair process. Some necrotic regions can show dystrophic calcification a deposition of calcium that is long standing. Occurs in suppuration due to neutrophils lysing pyogenic bacteria and tissue.
