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Flashcards in 2. Injuries to Cells Deck (26)
1

Cell response to noxious stimuli

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

2

Cell adaptatoin

Hyperplasia
Hypertrophy
Metaplasia
Atrophy

3

Hypertrophy

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

4

Hyperplasia

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

5

Atrophy

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

6

Metaplasia

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

7

Causes of cell injury (1)

hypoxia
low oxygen supply

ischaemia
loss of blood supply, therefore oxygen and nutrients

chemical exposure
eg cigarette smoke, alcohol, paracetamol

8

Causes of cell injury (2)

infection
radiation
lack of nutrients
immunologic reactions
ageing

9

Morphology of reversible cellular injury

cellular swelling
fatty change

10

Cell death

necrosis
apoptosis

11

Necrosis

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

12

Apoptosis (1)

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

13

Apoptosis (2)

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

14

Physiological apoptosis

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

15

Apoptosis in pathological conditions

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

16

Mechanisms of apoptosis

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

17

Types of necrosis

coagulative necrosis
liquefactive necrosis
caseous necrosis
fat necrosis

18

Mechanisms of cell injury

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

19

Depletion of ATP

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

20

Mitochondrial damage

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

21

Influx of calcium

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

22

Oxidative stress

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

23

Defects in membrane permeability

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

24

Damage to DNA and proteins

may occur after radiation injury/oxidative stress
can result in apoptosis

25

Intracellular accumulation of abnormal material

fat in hepatocytes (liver cells) due to alcohol misuse.
cholesterol in smooth muscle cells in atherosclerosis
protein in Alzheimer’s and Parkinson’s disease

26

Neoplasia

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’)