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Flashcards in Pathology- injuries to cell Deck (25)
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

hypoxia

low oxygen supply

8

ischaemia

loss of blood supply, therefore oxygen and nutrients

9

chemical exposure

eg cigarette smoke, alcohol, paracetamol

10

Morphology of reversible cellular injury

cellular swelling
fatty change

11

necrosis

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

12

apoptosis

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

13

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

14

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

15

Mechanisms of apoptosis

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

16

Types of necrosis

coagulative necrosis

liquefactive necrosis

caseous necrosis

fat necrosis

17

Mechanisms of cell injury

depletion of ATP

mitochondrial damage

influx of calcium

oxidative stress

damage to the cell membrane

DNA damage

18

Depletion of ATP

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

19

Mitochondrial damage

failure of production of energy
failure of free radical production

20

Influx of calcium

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

21

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

22

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

23

Damage to DNA and proteins

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

24

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

25

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’)