Cell Adaptations

Question 1

What’s cell adaptation?

Answer 1

Reversible changes in cells in response to the environment (stimuli may be pathological or physiological)

It reflects an attempt to preserve cell vitality and meet the change in conditions

Question 2

What are the 3 ways cells can adapt?

Answer 2

Cell number
Cell size
Cell type

Question 3

What are the 3 classes of cells?

Answer 3

Labile cells - continuously dividing
Stable cells - infrequently divide but can rapidly divide when necessary
Permanent cells - never divide

Question 4

What’s cell hyperplasia? What cell classes can it occur in?

Give examples of physiological and pathological hyperplasia

Answer 4

Increase in the number of cells within a tissue
Only labile or stable

Physiological: endometrium
Pathological: risk of tumour development, stimulated by excessive hormone/growth factors or chronic irritation

Question 5

What’s cell hypertrophy? Give examples of physiological and pathological hypertrophy

Answer 5

Increase in cell size - more structural proteins produced
Physiological: increased function demand in muscle, uterine muscle in pregnancy due to hormone/growth factor influence
Pathological: seen in left ventricle due to increased function demand eg hypertension and aortic stenosis

Question 6

What might be some stimuli causing cells to adapt?

Answer 6

Increased functional demand
Increased work demand
Metabolic demand
Endocrine demand
Persisting tissue injury

Question 7

What’s atrophy and what does cellular atrophy involve?

Answer 7

Shrinkage in cell size by loss of substance

Involves autophagy = self digestion of organelles

Question 8

What are some causes of atrophy?

Answer 8

Reduced workload
Loss of nerve supply
Reduced blood supply
Inadequate nutrition
Loss of endocrine stimulation
Ageing

Question 9

What’s metaplasia and why would it happen?

Answer 9

Reversible change from one adult cell type to another adult cell type
Adaptive response to stimuli, so new cell type is better adapted to the stimulus - usually involves epithelium

Question 10

Give examples of a physiological and pathological metaplastic change

Answer 10

Physiological: normal growth and development eg glandular to squamous epithelium in the pubertal cervix

Pathological: abnormal environment causes adaptive response eg squamous to glandular epithelium in reflux oesophagitis (Barrett’s)

Question 11

What’s dysplasia and 3 sites where its likely to occur?

Answer 11

Altered cellular differentiation in development - premalignant condition

Cervix, bladder, oeseophagus/stomach

Question 12

What’s neoplasia?

Answer 12

Abnormal growth of cells which persists after initiating stimulus has been removed - cell growth has escaped from normal regulatory mechanisms (malignant or benign)

Question 13

What are some causes of cell injury and death?

Answer 13

Oxygen deprivation
Physical agents
Chemicals and drugs
Infectious agents
Immune reactions
Genetic derangements
Nutritional imbalance

Question 14

Why is ischaemia worse than hypoxia for cell damage?

Answer 14

Ischaemia reflects problems with local blood supply
There’s not just oxygen deprivation but also loss of delivery of nutrients/toxin build up so cell injury is more severe and quicker

Question 15

How can chemicals cause cell injury?

Answer 15

Either directly or by metabolism/generation of breakdown products
Can damage osmotic environment
Alter biochemical cell reactions so ATP levels drop
Damage integrity of cell membrane

Question 16

What type of cell damage is frostbite an example of?

Answer 16

Physical damage - exposure of tissue to extreme heat/cold stimuli results in irreversible injury due to pattern of coagulation necrosis

Question 17

How can dietary insufficiency and excess lead to cell damage (nutrition imbalance)?

Answer 17

Insufficiency: lead to injury at the cellular level due to interference in normal metabolic pathways

Excess: abnormal concentration or abnormal cellular locations also affects metabolic pathways

Question 18

What can cause ATP depletion and how can the extent of damage differ between cells?

Answer 18

Reduced synthesis or ATP depletion
Depends on glycolytic activity of that cell eg skeletal muscle would survive longer than cardiac muscle in ATP depleted states

Question 19

Outline the consequences of reduced ATP in a cell

Answer 19

= anaerobic respiration -> increased lactic acid -> more acidic pH of tissue -> clumping of nuclear chromatin

= reduced Na+ pump function -> influx of Ca2+, H20, Na+ and efflux of K+ -> cell swells

= detachment of ribosomes -> reduced protein synthesis

Question 20

What are some consequences of mitochondrial damage?

Answer 20

ATP depletion
ROS generation
Formation of pores in mitochondrial membrane = loss of organelle microenvironment and function
Mitochondiral membrane proteins released into cytosol triggering apoptosis

Question 21

Why is there a loss in Ca2+ homeostasis in cell injury and what’re the consequences?

Answer 21

Influx in Ca2+ in the cytoplasm in response to injury, from the extracellular compartment and intracellular stores

Ca2+ activates enzymes causing: cell membrane breakdown, DNA damage, ATP depletion

Question 22

What are free radicals? What can they do?

Answer 22

Chemical species with single unpaired e- in their outer orbital - activated by oxidative stress

They react with organic/inorganic compounds and generate free radicals from the molecules they react with propagating ROS generation

Question 23

What can increase free radical generation?

Answer 23

Absorption of radiant energy (x-ray/UV)
Enzymatic metabolism of exogenous chemicals
Inflammation

Question 24

What can remove free radicals?

Answer 24

Spontaneous decay
Antioxidants as donate outer e- (vitamin E, A, glutathione)
Storage proteins (ferritin, transferrin)
Enzymes (catalase)

Question 25

How can free radicals injure cells?

Answer 25

Membrane lipid peroxidation
Interact with proteins
DNA damage

Question 26

What are 3 key membranes and what does damage to membrane permeability reflect?

Answer 26

Mitochondiral, plasma and lysosomal membranes

Damage by ROS
Cytoskeletal damage by enzyme digestion
Damage by lipid breakdown products acting as a detergent on membrane
Reduced production or increased breakdown of phospholipids in the membrane (reduced ATP or increased Ca2+

Question 27

What’re 3 differences between necrosis and apoptosis and morphological differences

Answer 27

Both types of cell death
Necrosis: pathological, enzyme cell digestion, contents leak out
Apoptosis: pathologic or physiological, internally controlled, nuclear dissolution

Morphological:
In necrosis plasma membrane is disrupted whereas in apoptosis its intact
Cell swells in necrosis and shrinks in apoptosis
Nucleus dissolves in necrosis and fragments in apoptosis
Cellular contents (enzymes) leak out of cell in necrosis
Adjacent inflammation often present in necrosis

Question 28

What are patterns of tissue necrosis?

Answer 28

Coagulative
Liquefactive
Caseous
Gangrenous
Fat
Fibrinoid

Question 29

What type of injuries is coagulative necrosis seen in?

Answer 29

Ischaemic (except from in the brain)

Question 30

What’s caseous necrosis and where is it seen?

Answer 30

Tissue remnants look like cottage cheese

Tuberculosis necrosis

Question 31

What are white and red infarcts?

Answer 31

Infarction = area of ischaemic necrosis in tissue
White = arterial occlusion, solid tissues
Red = venous occlusion, dual blood supply, loose tissues

Question 32

What are the biochemical features of apoptosis?

Answer 32

Caspase activation (internal enzymes)
DNA and protein breakdown
Membrane alterations and recognition by phagocytes

Question 33

What are some disorders associated with dysregulated apoptosis?

Answer 33

Neoplastic cells / autoimmune cells are those with defective apoptosis and increased survival

Ischaemic injury / death of virus infected cells are those with defective apoptosis and decreased survival