cell injury and cell death Flashcards
what happens in left ventricular hypertrophy?
muscle of ventricle thickens
what is necrosis?
when there is irreversible cell death - long term cell injury and therefore cannot be repaired
what is oncosis?
oncosis is the pre lethal changes to cells that precede death
what are some cellular adaptions?
atrophy and hypertrophy
what happens in necrosis?
there is severe cell swelling and rupture
what is apoptosis?
it is internally controlled cell death
why does CO reduce oxygen transport?
it binds to Hb preferentially as it has a higher affinity for Hb than oxygen does - hypoxia
what can cause cell death?
CO, physical agents - trauma, radiation, temp, chemical agents - drugs, immunological reaction, infectious agent, genetic derangement and nutritional imbalances
what is the mode of action for trauma, acid, paracetamol OD, bacteria and radiation?
mechanical disruption of tissue coagulates tissue proteins metabolites will bind to liver cell proteins and lipoproteins toxins and enzymes damage to DNA
why does ATP depletion result in death?
there is not enough energy for the cell so the tissue dies , loss of intercellular calcium hemostasis, oxygen and oxygen free radicals, defects in membrane permeability and irreversible mitochondrial damage
`what are the three types of cell injury?
reversible, irreversible or ischaemia/reperfusion
what is the basis of reperfusion?
damage on reperfusion mediated by oxygen free radicals
what is reversible?
pallor, hydropic change, vacuolar degeneration and cell swelling
what is irreversible?
lysosome or mitochondrial swelling, leakage of enzymes or damage to membrane
what happens if damage is left too long?
reversible goes to irreversible
how is a cascade of damage caused?
sever mitochondrial injury
what is characteristic of reversible?
decrease in generation of ATP, loss of cell membrane integrity and defects in protein synthesis, and DNA damage
what does persistent and excessive injury lead to and what are the characteristics of this?
irreversible damage
severe mitochondrial damage
extensive damage to plasma membranes
lysosome swelling
what happens in irreversible damage?
there is leakage of membranes, therefore leakage of enzymes leading to apoptosis
what are three types of cell death?
necrosis, oncosis and apoptosis
what are some examples of programmed cell death?
menstruation and losing webbed digits - individual cell deletion in physiological growth control and in disease
how does atrophy result?
increased apoptosis in excessive cell loss
what are the characteristics of atrophy?
cell shrinkage, DNA fragmentation, formation of apoptotic bodies
how does reversible cell injury result in cell swelling?
decrease in ATP production, decrease in acitivity of Na/K pump, increased sodium in the cell, osmosis and water movement into the cell
how does enzymatic degradation and apoptosis occur in irreversible cell damage?
there is damage to the lysosome, mitochondrial and plasma membrane resulting in lysosome enzyme release into cytosol, Calcium into the cell and Cyt C leakage. Ca activated proteases and other enzymes and with lysozymes this results in enzymatic degradation. Cyt C and Calcium activate caspaces resulting in apoptosis
what is necrosis?
cell death that results from failure in bioenergy and loss of plasma membrane integrity - includes inflammation and repair
what are the differences between apotosis and necrosis?
size: A - cell shrinkage in one cell, N - cell swelling in many cells
uptake: A - cell contents ingested by enighbouring cells with no inflammatory response, N - cell contents is ingested by macrophages and significant inflammation
membrane: A - membrane blebbing but still integrity, apoptotic bodies form and N - loss of membrane integrity and cell lysis occurs
organelles: A - mitochondria release pro-apoptotic proteins, chromatin condensation and non-random DNA degradation, N - organelle swelling and lysosomal leakage, random degradation of DNA
does autophagy have an inflammatory response?
no - there is increased quantity of autophages formation - Atg proteins participation
what can you see under microscope in necrosis?
disorganisation - inflammatory responses
what types of necrosis are there?
fat, fibrinoid, coagulative, caseous, gangrenous or liquefactive
what is an example of coagulative necrosis?
in MI
what are the characteristics of coagulative necrosis?
it is the commonest form and happens in most cells, cells retain their outline and architecture is preserved but proteins coagulate, there is no proteolysis, and metabolic activity ceases. Proteins and enzymes are lost.
what is liquefactive necrosis?
it is seen in the brain and is bacterial or fungal. It results in CNS hypoxia and is due to lack of substantial supporting stroma. It may result in neural tissue liquefying
what is an example of gangrenous necrosis?
limb ischaemia
what is gangrenous necrosis?
the types are wet, dry or gangrenous. The causes are infectious or bacterial. It is putrefaction of tissue and will appear black
what can TB in lung cause?
it is the main cause of caseous necrosis and can cause military, cavitary or primary TB necrosis
what is caseous TB?
it is structureless dead tissue that macrophages cannot digest
how will caseous TB present in histology?
amorphous pink material in centre with necrotic debris and granulomas
what are the causes of fat necrosis?
enzymes, trauma, panreatitis and excessive alcohol
how will fat necrosis present?
loss of architecture, lots of vacuoles
what 2 conditions is fibrinoid necrosis seen in and how does it present on histology?
malignant hypertension and autoimmune disease
wall of artery is bright pink with dark neutrophils
what happens in mycocyte necrosis after an Mi?
enzymes are released - LDH, troponins and CK-MB - biomarkers for diagnosis
what enzymes are released in pancreatic cell necrosis?
amylase
where is troponin released from?
complex is released from actin filament
how is apoptosis used in immune system?
death of post inflammatory neutrophils, virally infected cells and self reactive lymphocytes
