2 Injuries to Cells

Question 1

Injuries to Cells

Aims:

Answer 1

cellular response to stress
causes of cellular injury
morphology of cell and tissue injury
mechanisms of cellular injury

Question 2

Results

Reversible

Answer 2

reversible – cellular repair and recovery
cells adapt by:

hyperplasia

hypertrophy

metaplasia

atrophy

Question 3

Results

Irreversible

Answer 3

irreversible – damage too severe for cellular repair and recovery
cells are lost or changed by

apoptosis – cell “suicide”
apoptosis also has adaptive functions

necrosis – cell death

neoplasia – cancer and so on

Question 4

Cellular adaptations to stress

Answer 4

hypertrophy
hyperplasia
atrophy
metaplasia

Question 5

Hypertrophy

Answer 5

increase in the size of cells, resulting in increase in size of the organ
physiological
or
pathological

Question 6

Hyperplasia

Answer 6

increase in cell number resulting in a larger (hypertrophied) organ
can occur alongside hypertrophy
physiological
or
pathological

Question 7

Atrophy

Answer 7

shrinkage of the size of the cell by loss of cell substance
decreased workload
reduced blood supply
inadequate nutrition
loss of hormonal stimulation
ageing

Question 8

Metaplasia

Answer 8

one adult cell type is replaced by another adult cell type
reversible
new type of cell may be more able to withstand stress
eg chronic gastro-oesophageal reflux

Question 9

Causes of cell injury

Answer 9

hypoxia
low oxygen supply

ischaemia
loss of blood supply, therefore oxygen and nutrients

chemical exposure
eg cigarette smoke, alcohol, paracetamol

infection

radiation

lack of nutrients

immunologic reactions

ageing

Question 10

Morphology of reversible cellular injury

Answer 10

cellular swelling

fatty change

Question 11

Cell death

Answer 11

necrosis
damage to membranes allows enzymes to digest the cell
local inflammation
always pathological

apoptosis
programmed cell death
irreparable damage to cell’s protein/DNA or deprived of growth factors
can be pathological or physiological

Question 12

Apoptosis

Answer 12

cells activate enzymes that degrade the cells’ own DNA and proteins, resulting in death
fragments of the apototic cell break off
dead cell rapidly removed by phagocytosis

Question 13

Physiological apoptosis

Answer 13

embryogenesis
involution of hormone dependent tissues upon hormone deprivation
elimination of cells which have served their purpose
elimination of potentially harmful self-reactive lymphocytes

Question 14

Apoptosis in pathological conditions

Answer 14

DNA damage
accumulation of misfolded proteins
certain infections
pathological atrophy in parenchymal organs after duct obstruction
cell death induced by cytotoxic T cells

Question 15

Mechanisms of apoptosis

Answer 15

result from the activation of enzymes called caspases
mitochondrial pathway
intrinsic pathway
Fas (death) receptor pathway
extrinsic pathway

Question 16

Types of necrosis

Answer 16

coagulative necrosis

liquefactive necrosis

caseous necrosis

fat necrosis

Question 17

Mechanisms of cell injury

Answer 17

depletion of ATP

mitochondrial damage

influx of calcium

oxidative stress

damage to the cell membrane

DNA damage

Question 18

Depletion of ATP

Answer 18

energy store of cells
oxidative phosphorylation of ADP within mitochondria
reduced supply of oxygen and nutrients, mitochodrial damage, poisons
effects:
ATP dependent sodium pumps
increased intracellular lactic acid
failure of calcium pumps
damage to protein structures

Question 19

Mitochondrial damage

Answer 19

‘mini-factories’ for making ATP
sensitive to many types of stress eg hypoxia, chemical poisons, radiation
effects: 
failure of production of energy
failure of free radical production

Question 20

Influx of calcium

Answer 20

ischaemia, certain poisons
effects
increased intracellular calcium
		→ leads to activation of enzymes
	  → damage cellular components
may trigger apoptosis

Question 21

Oxidative stress

Answer 21

accumulation of reactive oxygen species (free radicals)
produced by normal cellular function
some insults increase their production
paracetamol overdose
removed by antioxidants
react with and damage proteins, fat, DNA, and create more of themselves in the process

Question 22

Defects in membrane permeability

Answer 22

result in necrosis
various sites of damage
mitochondrial membrane damage
plasma membrane damage
injury to lysosomal membranes
mechanisms of damage
↓ phospholipid synthesis ↓ATP
oxygen free radicals
lipid breakdown

Question 23

Damage to DNA and proteins

Answer 23

may occur after radiation injury/oxidative stress

can result in apoptosis

Question 24

Intracellular accumulation of abnormal material

Answer 24

fat in hepatocytes (liver cells) due to alcohol misuse.

cholesterol in smooth muscle cells in atherosclerosis

protein in Alzheimer’s and Parkinson’s disease

Question 25

Neoplasia

Answer 25

mild DNA damage → gene mutation
damage to genes controlling DNA repair → susceptible to further change
damage to the genes that control cell division lead to excess division
mutations accumulate and eventually lead to abnormal (dysplastic – ‘abnormal growth’) cells, and eventually into cancer (neoplastic –‘new growth’)

Question 26

Learning points

Answer 26

cellular response to stress
causes of cellular injury
morphology of cell and tissue injury
mechanisms of cellular injury