Cell Injury and Death part 1 Flashcards
What does the degree of cell injury depend on?
Type of injury
Severity of injury
Duration of injury
Type of tissue
Explain the heart’s response to hypertension
Increase workload on heart ( peripheral vascular resistance)
Hypertrophy ( myocyte cell size increases)
Increase in weight and size of heart
Additional stress may be caused by atherosclerosis or other factors
Cell injury and death
Causes of cell injury
Hypoxia Toxins Physical agents : direct trauma, extremes of temp, change in pressure, electric currents Radiation Microorganism Immune mechanism Nutritional / dietary - deficiencies or excess Genetic ( and age process)
Causes of hypoxia
Hypoxaemic hypoxia = arterial content of oxygen is low. Reduced oxygen pressure at altitude so oxygen can’t saturate haemoglobin. Or reduced absorption secondary to lung disease
Anaemia hypoxia= decreased ability of haemoglobin to carry oxygen. ( anaemia/ carbon monoxide poisoning)
Ischaemic hypoxia- interruption to blood supply by heart failure of blockage of vessel
Histiotoxic Hypoxia- inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes ( cyanide poisoning)
How long can neurones, fibroblasts, cardiac and skeletal muscle last as a result of hypoxia
Neurones- few mins
Fibroblasts- few hours
Cardiac - 20 mins
Skeletal- couple of hours
Name some toxins
Glucose and salt in hypertonic solutions High conc of oxygen Poisons Pollutants Insecticide Herbicide Asbestos Alcohol Narcotic drugs Medicines
How does the immune system damage the body’s cells
Hypersensitivity reactions- host tissue injured secondary to an overly vigorous immune reaction ( urticaria= itching from skin reaction)
Autoimmune reactions - immune system fails to distinguish self from non self
Which cell components are more susceptible to injury
Cell membranes
Nucleus
Proteins
Mitochondria
Consequences of reduced intracellular ATP during cell injury
Reduced ATP due to reduced oxidative phosphorylation.
Reduced ATP so Na pump working less efficiently so there will be and influx of Ca2+ , H2O and Na+ but efflux Of K+. This cusses swelling ,loss of micro villi and blebs
Reduced ATP also means more glycolysis so lower pH causing clumping of nuclear chromatin and enzyme issues.
Less atp also means detachment of ribosomes so less protein synthesis and lipid deposition.
consequences of influx on intracellular calcium during cell injury
increased cytosolic Ca2+ causes decreased ATP & phospholipids, disruption of membrane and cytoskeletal proteins and nuclear chromatin damage
why do we need free radicals
for microbial killing by phagocytes
name some biologically significant free radicals
.OH-hydroxyl
O2^- superoxide
H2O2-hydrogen peroxide
how are free radicals formed
normal metabolic reaction like oxidative phosphorylation
radiation
transition metals -iron and copper
drugs and chemicals - e.g in the liver during metabolism of paracetamol or carbon tetrachloride by P450 system
normal part of inflammatory response -oxidative first of neutrophils n
what is oxidative stress
imbalance between free radical damage and radical scavenging systems
how does the body control free radicals
decay spontaneously
free radical scavengers( antioxidants)- vit A,C and E donate e- to the free radical.
metal carrier and storage proteins(transferrin , ceruloplasmin): sequester iron and copper
enzymes that neutralise free radicals- superoxide dismutase, catalase and glutathione peroxidase
how does the body control free radical DAMAGE
free radicals cause proteins to cross link and fragment
during stressful events there is up regulation of heat shock proteins (hsp70,hsp90)
these help mend misfiled proteins and maintain cell viability
how do injured and dead cells look in comparison to alive cells under a light microscope
reduced prink staining because of accumulation of water ]
pyknosis-shrinkage of nuclei
karyorrhexis -fragmentation of nuclei
karyolysis-dissolution of nuclei
how does reversible injury look under an electron microscope
blebs swelling clumping of. nuclear chromatin ER and mitochondrial swelling dispersion of ribosomes
how does irreversible injury look under an electron microscope
rupture of lysosomes and autolysis
defects in cell membrane
nucleus :pyknosis/karolysis/karyorrhexis
lysis of ER
defime oncosis
cell death with swelling , the spectrum of changes that occur in injured cells prior to death
define necrosis
in living organism the morphological changes that occur after a cell has been dead some time (after 12-24 hrs )
define apoptosis
programmed cell death
what are the two main types of necrosis
coagulative necrosis- protein denaturation.usually in solid organs.
liquefactive necrosis- enzyme release . in looser tissues like the brain
what is caseous necrosis
a special type of necrosis which contains amorphous (structureless) debris.
particularly associated with infections especially TB.
looks like it has no architecture under a microscope
what is fat necrosis
destruction to adipose tissue by inflammation of the pancreas which releases lipase.
free fatty acids react with calcium forming lumps
