2. Injuries to Cells

Question 1

Cell response to noxious stimuli

Answer 1

Normal cell confined to relatively narrow range of function and structure
Stress leads to cell adaptation
If cell unable to adapt then cell injury occurs

Question 2

Cell adaptatoin

Answer 2

Hyperplasia
Hypertrophy
Metaplasia
Atrophy

Question 3

Hypertrophy

Answer 3

increase in the size of cells, resulting in increase in size of the organ
physiological eg. body builders
or
Pathological eg. heart in hypertension

Question 4

Hyperplasia

Answer 4

increase in cell number resulting in a larger (hypertrophied) organ
can occur alongside hypertrophy
Physiological eg. menstrual cycle
or
Pathological eg. endometrial hyperplasia if hormone stimulus persists

Question 5

Atrophy

Answer 5

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 6

Metaplasia

Answer 6

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 7

Causes of cell injury (1)

Answer 7

hypoxia
low oxygen supply

ischaemia
loss of blood supply, therefore oxygen and nutrients

chemical exposure
eg cigarette smoke, alcohol, paracetamol

Question 8

Causes of cell injury (2)

Answer 8

infection
radiation
lack of nutrients
immunologic reactions
ageing

Question 9

Morphology of reversible cellular injury

Answer 9

cellular swelling

fatty change

Question 10

Cell death

Answer 10

necrosis

apoptosis

Question 11

Necrosis

Answer 11

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

Question 12

Apoptosis (1)

Answer 12

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

Question 13

Apoptosis (2)

Answer 13

Programmed cell death pathway
cells activate enzymes that degrade the cells’ own DNA and proteins, resulting in death
Membrane remains intact so no contents leak out and no response is triggered.
Bits of the cell break off
dead cell rapidly removed by phagocytosis

Question 14

Physiological apoptosis

Answer 14

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 15

Apoptosis in pathological conditions

Answer 15

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

Question 16

Mechanisms of apoptosis

Answer 16

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

Question 17

Types of necrosis

Answer 17

coagulative necrosis
liquefactive necrosis
caseous necrosis
fat necrosis

Question 18

Mechanisms of cell injury

Answer 18

depletion of ATP
mitochondrial damage
influx of calcium
oxidative stress
damage to the cell membrane
DNA damage

Question 19

Depletion of ATP

Answer 19

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

Question 20

Mitochondrial damage

Answer 20

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 21

Influx of calcium

Answer 21

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

Question 22

Oxidative stress

Answer 22

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 23

Defects in membrane permeability

Answer 23

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 24

Damage to DNA and proteins

Answer 24

may occur after radiation injury/oxidative stress

can result in apoptosis

Question 25

Intracellular accumulation of abnormal material

Answer 25

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 26

Neoplasia

Answer 26

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’)