Cell Injury

Question 1

List the causes of cell injury

Answer 1

Causes of Cell Injury

• Genetic defects
• Infectious agents
• Nutritional imbalances
• Chemical agents
• Hypoxia
• Ageing
• Physical agents
• Immunological reactions

GIN CHAP I

Question 2

List the mechanisms of cell injury

Answer 2

MECHANISMS

Factors affecting response to injury :

1. Type of Injury
2. Duration
3. Severity
4. Cell Type

FOUR Intracellular Mechanisms that are vulnerable to injury:

1. Cell Membrane Integrity
2. ATP Generation
3. Protein Synthesis
4. Genetic Apparatus

• The structural and biochemical components of a cell are so integrally related that multiple secondary effects rapidly occur
• Cellular function is lost before cell death occurs which in turn occurs before the morphological changes are seen

Question 3

Recall the morphological changes associated with reversible and irreversible injury

Answer 3

Reversible Changes

1. Fatty change
2. Cellular swelling

Changes Associated with Irreversible Injury

1. Coagulative – substance changes but the shape of the molecules does NOT change. The tissue retains its structure.
2. Liquefactive – tissue is broken down leaving a space which gets filled with fluid.
3. Caseous – form of granulomatous inflammation that has a characteristic ‘cheesy’ appearance. Associated with pulmonary TB.
4. Fat – characterised by the breakdown of fat cells (either by the release of lipases or due to trauma). Associated with acute pancreatitis.

Question 4

Cell fate: define and recall examples of hyperplasia, hypertrophy, atrophy, metaplasia and dysplasia; define and compare apoptosis and necrosis

Answer 4

BASIC RULE : -trophy = Growth AND - plasia = Development

Atrophy: SHRINKING in the size of a cell or organ by the loss of cell substance

• Example: Cortical atrophy in Alzheimer’s disease

Hypertrophy: INCREASE IN SIZE of cells and, consequently, an increase in the size of an organ

• Example: Left ventricular hypertrophy in response to hypertension

Hyperplasia: INCREASE IN NUMBER of cells in an organ

• Example: Physiological: oestrogen-induced endometrial hyperplasia
• Pathological: benign prostatic hyperplasia

Metaplasia: Reversible change in which one adult cell type is replaced by another

• Example: Barrett’s oesophagus: conversion of the epithelial lining of the oesophagus from squamous to columnar

Dysplasia:Precancerous cells which show genetic and cytological features of malignancy but NOT invading the underlying tissue

• Example: Cervical intraepithelial neoplasia

Apoptosis: Programmed cell death of single cells, NOT associated with inflammation. This is a normal part of an organisms growth and development

Causes:

1. Embryogenesis
2. Deletion of auto-reactive T cells in the thymus
3. Hormone-dependent physiological involution
4. Cell deletion in proliferating populations
5. A variety of mild injurious stimuli that cause irreparable DNA damage that triggers cell suicide pathways

Necrosis: Confluent cell death associated with inflammation

1. Coagulative

substance changes but the shape of the molecules does NOT change. The tissue retains its structure.

2. Liquefactive – tissue is broken down leaving a space which gets filled with fluid.
3. Caseous – form of granulomatous inflammation that has a characteristic ‘cheesy’ appearance. Associated with pulmonary TB.
4. Fat – characterised by the breakdown of fat cells (either by the release of lipases or due to trauma). Associated with acute pancreatitis

Key Differences (necrosis-apoptosis):

• Apoptosis may be physiological
• Apoptosis is active and energy-dependent
• Apoptosis is NOT associated with inflammation

Necroptosis: Programmed cell death associated with inflammation

Many causes e.g. viral infections​

Ulcer: A local defect or excavation of the surface, of an organ or tissue, produced by sloughing of necrotic inflammatory tissue

Degenerative: Change of a tissue to a lower or less functionally active form

Sub-Lethal injury: An injury that does not kill the cell/organism.