Cell Adaptations Flashcards
What’s cell adaptation?
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
What are the 3 ways cells can adapt?
Cell number
Cell size
Cell type
What are the 3 classes of cells?
Labile cells - continuously dividing
Stable cells - infrequently divide but can rapidly divide when necessary
Permanent cells - never divide
What’s cell hyperplasia? What cell classes can it occur in?
Give examples of physiological and pathological hyperplasia
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
What’s cell hypertrophy? Give examples of physiological and pathological hypertrophy
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
What might be some stimuli causing cells to adapt?
Increased functional demand Increased work demand Metabolic demand Endocrine demand Persisting tissue injury
What’s atrophy and what does cellular atrophy involve?
Shrinkage in cell size by loss of substance
Involves autophagy = self digestion of organelles
What are some causes of atrophy?
Reduced workload Loss of nerve supply Reduced blood supply Inadequate nutrition Loss of endocrine stimulation Ageing
What’s metaplasia and why would it happen?
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
Give examples of a physiological and pathological metaplastic change
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)
What’s dysplasia and 3 sites where its likely to occur?
Altered cellular differentiation in development - premalignant condition
Cervix, bladder, oeseophagus/stomach
What’s neoplasia?
Abnormal growth of cells which persists after initiating stimulus has been removed - cell growth has escaped from normal regulatory mechanisms (malignant or benign)
What are some causes of cell injury and death?
Oxygen deprivation Physical agents Chemicals and drugs Infectious agents Immune reactions Genetic derangements Nutritional imbalance
Why is ischaemia worse than hypoxia for cell damage?
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
How can chemicals cause cell injury?
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
What type of cell damage is frostbite an example of?
Physical damage - exposure of tissue to extreme heat/cold stimuli results in irreversible injury due to pattern of coagulation necrosis
How can dietary insufficiency and excess lead to cell damage (nutrition imbalance)?
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
What can cause ATP depletion and how can the extent of damage differ between cells?
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
Outline the consequences of reduced ATP in a cell
= 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
What are some consequences of mitochondrial damage?
ATP depletion
ROS generation
Formation of pores in mitochondrial membrane = loss of organelle microenvironment and function
Mitochondiral membrane proteins released into cytosol triggering apoptosis
Why is there a loss in Ca2+ homeostasis in cell injury and what’re the consequences?
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
What are free radicals? What can they do?
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
What can increase free radical generation?
Absorption of radiant energy (x-ray/UV)
Enzymatic metabolism of exogenous chemicals
Inflammation
What can remove free radicals?
Spontaneous decay
Antioxidants as donate outer e- (vitamin E, A, glutathione)
Storage proteins (ferritin, transferrin)
Enzymes (catalase)
How can free radicals injure cells?
Membrane lipid peroxidation
Interact with proteins
DNA damage
What are 3 key membranes and what does damage to membrane permeability reflect?
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+
What’re 3 differences between necrosis and apoptosis and morphological differences
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
What are patterns of tissue necrosis?
Coagulative Liquefactive Caseous Gangrenous Fat Fibrinoid
What type of injuries is coagulative necrosis seen in?
Ischaemic (except from in the brain)
What’s caseous necrosis and where is it seen?
Tissue remnants look like cottage cheese
Tuberculosis necrosis
What are white and red infarcts?
Infarction = area of ischaemic necrosis in tissue White = arterial occlusion, solid tissues Red = venous occlusion, dual blood supply, loose tissues
What are the biochemical features of apoptosis?
Caspase activation (internal enzymes) DNA and protein breakdown Membrane alterations and recognition by phagocytes
What are some disorders associated with dysregulated apoptosis?
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
