Flashcards in Growth, Cell Death and Neoplasia Deck (103)
programmed cell death
traumatic cell death - unintended cell death in response to cellular injury
why do we need apoptosis?
for continuous renewal of cells, working alongside mitosis
name some inhibitors of apoptosis
extracellular cell matrix
some viral proteins
name some inducers of apoptosis
growth factor withdrawal
loss of attachment of ECM
give some examples of when apoptosis is crucial for normal growth - and what occurs if apoptosis fails
separating of fingers - interdigital cell death - syndactyl (webbed fingers)
removal of redundant epithelium on fusion of palatine processes in roof of mouth - cleft palate
what is coagulative necrosis?
dead tissue is swollen and firm, then later becomes soft - digestion of macrophages
what is colliquative (liquefactive) necrosis?
occurs in brain due to lack of supporting stroma - necrotic tissue liquefies
what is caseous necrosis?
dead tissue is completely structureless. histology shows amorphous eosinophilic area with haematoxyphilic nuclear debris.
seen in TB.
what is gangrene?
necrosis with putrefaction of tissues. tissues appear black.
what is fibrinoid necrosis?
occurs in malignant hypertension - increased arterial pressure results in necrosis of SM wall.
eosinophilic and fibrinous deposits seen.
what is fat necrosis?
focal adipose tissue destruction due to direct trauma, or enzymatic lipolysis (seen in acute pancreatitis)
increase in size of a tissue caused by increase in SIZE of the constituent cells
increase in size of a tissue caused by an increase in NUMBER of constituent cells - decrease in apoptosis
decrease in size of a tissue caused by a decrease in NUMBER or SIZE of constituent cells - apoptosis
change in differentiation of a cell from one fully-differentiated type to another
morphological changes seen in cells in the progression to becoming cancer
give some examples of physiological hypertrophy/hyperplasia
muscle hypertrophy in athletes - in limbs and LV of heart.
hyperplasia of breast tissue at puberty and in pregnancy/lactation.
hypertrophy and hyperplasia of uterine smooth muscle at puberty/pregnancy.
give some examples of conditions involving pathological hypertrophy/hyperplasia
follicular epithelial hyperplasia e.g. in Graves' disease (thyroid)
present at birth - not necessarily inherited, foetus is affected by environmental factors in womb (eg FAS)
give some examples of changes to the body that are typical of ageing
loss of dermal elastosis
sarcopaenia (loss of skeletal muscle mass/strength)
transformation of normal cells to neoplastic cells through permanent genetic alterations or mututations
- malignant tumours
formation of benign and malignant tumours
agents known/suspected to cause cancer - malignant tumours.
act on DNA - mutagenic
agents known/suspected to cause tumours - benign or malignant
what problems are presented by attempts to identify carcinogens?
latent interval may be decades.
environment is complex - difficult to isolate one factor.
ethical constraints - can't deliberately give people a suspected carcinogen as part of a study
list the classes of carcinogen
hormones, parasites and mycotoxins
lesion resulting from autonomous (or relatively autonomous) abnormal growth of cells which persists after the initiating stimulus has been removed
A NEW GROWTH
what are the features of neoplasia?