L12 Flashcards
what 3 increases in functional demand cause hypertrophy and hyperplasia?
increases in work and metabolic demand, excess endocrine stimulation and persistent tissue injury
what is hypertrophy?
increased cell size
what is hyperplasia?
increased cell number
what are the precursors of muscle cells
myoblasts
what happens to myoblasts during development?
proliferation
what fuses to form muscle cells?
proliferated myoblasts
what can influence degree of proliferation?
genes
what slows myoblast proliferation?
myostatin
a mutated myostatin gene leads to?
more skeletal muscle fibres being produced during development
why would a ventricle have a hypertrophic wall because of a narrowing of it’s aortic valve?
increased workload
what kind of nuclei would you find in hypertrophic myocardium?
large, often polyploid nuclei
what effect does the thickened ventricular wall of hypertrophic myocardium have?
reduces outflow and impairs relaxation phase
what leads to hypertrophy of smooth muscle?
obstructions of bladder
what is an example of an obstructed bladder causing hypertrophy of smooth muscle?
prostate cancer
hyperplasia and hypertrophy can occur together in response to? example?
increased functional requirements e.g. pregnant myometrium
what is cell atrophy?
reduced cell size
what is involution of tissue?
reduced cell number
what is the severe type of muscle atrophy called?
neurogenic atrophy
when does neurogenic atrophy occur?
when there is injury or disease to a nerve
does neurogenic or disuse atrophy occur more suddenly?
neurogenic
what causes muscle fibres to decrease in size?
the cease of nervous stimulation of the muscle
what can reduced endocrine stimuli cause?
muscle atrophy
what 3 anabolic hormones cause the muscle atrophy?
testosterone, growth hormone, IGF-1
what naturally occurring process can also cause muscle atrophy?
ageing
what 2 mechanisms underlie atrophy and involution?
autophagy in cell atrophy and apoptosis
what is autophagy in cell atrophy?
the degradation and recycling of cellular components
what are the types of autophagy?
macroautophagy, microautophagy and chaperone-mediated autophagy
during macroautophagy, when are the phosphoryl groups detached?
when at optimal pH of less than 7
during macroautophagy, what protects the cell incase the lysosomal enzymes escape?
a lower lysosomal pH
what is apoptosis?
programmed cell death
what is apoptosis an important mechanism for?
in developing and adult tissues for eliminating cells that are no longer needed
what is activation of apoptosis initiated by?
extracellular or intercellular death signals
what is apoptosis mediated by?
caspases
what do caspases exist in all cells as?
inactive procaspases
what activates inactive procaspases?
cleavage by other caspases
what are the 4 phases of apoptosis?
induction/signalling, effector/executioner, degradation, phagocytic phases
what happens in the induction/signalling phase and how does the cell appear?
cell receives an internal or external signal initiating apoptosis and cell looks normal
what happens in the effector/executioner phase?
protease enzymes cause severe structural changes
what are the 3 main structural changes that protease causes in effector/executioner phase of apoptosis?
cell shrinkage, loss of surface specialisations, condensed chromatin
what happens in the degradation phase of apoptosis?
cell splits into apoptotic bodies, nucleus also fragments
in degradation phase of apoptosis, what does each fragment of the cell contain?
viable mitochondria and intact organelles
what is an apoptotic body?
when a cell has received a death signal and splits into smaller fragments
what happens during the phagocytic phase of apoptosis?
apoptotic bodies are recognised and phagocytosed by adjacent cells where they are destroyed
what else can happen to some fragments during phagocytic phase of apoptosis?
some fragments degenerate extracellularly, some fragments are ingested by phagocytic cells
