Cellular injury and adaption Flashcards
main ways cells can be injured
genetic derangements oxygen deprivation immunological responses nutritional imbalances infectious agents chemical agents and drugs physical agents
example of genetic derangement
sickle cell anaemia
example of oxygen deprivation
brain infarct
eg of immunological reactions
rash from poison ivy
eg of nnutritional imbalance
anorexia nervosa
eg of infectious agents
parasitics infection: leishmaniasis
eg o chemical agents/drugs
cough syrup
eg of physical agents
burns or shark bite
describe the morpholpgical alterations in cell injury
plasma membrane can bleb mitochondria can swell ER and swell and detach from ribosomes nucleus can clump all are reversible
what are some biochemical mechanisms of cell injury
hyooxia, toxins and ROS
can be seen in depletion of ATP, mitochondrial damage, loss of Ca homeostasis, accumulation ROS, defects in membrane permeability, DNA and protein damage
reversibility is dependent on level of damage
what can ROS cause
oxidative stress and cell injury
what can ROS cause
oxidative stress and cell injury
what are the responses to cellular injury
reocery, death, adaptation
what is necrosis, why does it occur, and what happens
death of body tissue
not enough blood flowing to tissue/injury/radiation/chemicals
enxymatic digestions, loss cell membrane integrity, release of products into IC space, inflammatory responses
what is coagulative necrosis associated with
ischaemia (except brain)
what does caogulative necrosis look like macroscopically and microscopically
macro = firm tissue, arhitecture maintined for days after death (looks white) micro= preserved cell outlines, cells become eosinophilic, loss of nuclei, infiltration by leukocytes
what is liquefactive necrosis associated with
infections
ischaemic injury to brain
what does liquefactive necrosis look like macroscopically and microscopically
micro = tissue architecture lost -> liquid through enzymatic digestion. cream yellow pus microscopically = leukocytes, neutrophils, dead cells and debris
what is caseous necrosis associated with
TB
describe caseous necrosis macro and micro
macro = white, soft, cheesy, encllosed by distinct border micro= eosinophilic centre, collar of lymphocytes and activated macs => granuloma
what is fat necrosis associated with
not specific pattern of cell death, but describes destruction of fat due to pancreatic lipases
describe fat necrosis macro + micro
macro = chalky, whitish deposit as a result of Ca soaps micro = anucleated adipocytes with Ca deposits
what is fibrinoid necrosis associated with
vascular damage
describe fibrinoid necrosis macro + micro
macro = not grossly discernable
micro = accumulation of fibrin (pink for protein) around BV
inflammation
what is gangrenous necrosis associated with and what is dry and wet
used in clinical practise to describe condition
dry is coagulative and wet is liquefactive
describe gangrenous necrosis macro and micro
macro = black skin + putrefaction micro = coagulative/liquefactive
what are some physiological classifications of apoptosis
embryogenesis, endometrial breakdown, cell loss in proliferating populations, eliminate potential harmful cells and host cells
what are the pathological classifications of apoptosis
DNA damage, misfolded proteins, infection, atrophy
what are the features of apoptosis
single cells, no inflammation, active process
what are adaptations
reversible changes to number, size, metabolic activity, function, phenotype of cells
what is chronic adaptation
due to persistent, sublethal injury
= changes in cell size/growth + differentiation
describe hypertrophy
increase in size of cells, inc synthesis of structural components, reversible, hormonal or increased functional demand
describe hyperplasia
inc in number, reversible, hormonal/inc functional demand
describe atrophy
decrease in cell size/number/activity
can progress to irreversible
due to reduced demand/dec O2, insufficient nutrients, persistent injury, endocrine insufficiency
describe metaplasia
cell replaced by another differentiated cell type (eg common columnar->squamous)
replaces stressed cells with better equipped cells
reversible
stem cells are reprogrammed
describe smokers lung
metaplasia
normal ciliated columnar epithelium in trache + bronchi replaced by rugged squamous epithelium
bc columnar cells are 1 cell thick
lose mucus and cilia
describe barret’s oesophagus
metaplasia
normal strat squam replaced with columnar + goblet cells in response to acid reflux
columnar cells = more resistant to HCl + pepsin bc mucus
describe dysplasia
disordered growth + maturation
epithelia
sequential mutations
reversible or can lead to neoplasia
describe dysplastic epithelium of uterine cervix
squamous epi gets infected (HPV)
abnormal proliferation -> mutations -> loss growth control
disordered maturation from basal to top layer
extending full thickness = carcinoma in situ
what is intracellular accumulation
build up of substances within cell
nomral body substances
endogenous = von gierkes disease (glycogen)
exogenous = tattoos
