MOD 1.1 - Cell Injury Flashcards
What can cause cell injury/death? (7)
- Hypoxia
- Toxins
- Physical agents e.g. temperature extremes
- Radiation
- Micro-organisms
- Immune mechanisms e.g. allergic responses
- Dietary deficiencies
What happens during hypoxia?
- Area/body is deprived of Oxygen
- Decreases the rate of aerobic respiration
What are the four types of hypoxia?
- Hypoxaemic Hypoxia
- Anaemic Hypoxia
- Ischaemic Hypoxia
- Histiocytic Hypoxia
Describe hypoxaemic hypoxia
Low arterial oxygen content
Describe anaemic hypoxia
Compromise in ability of haemoglobin to transport Oxygen
Describe ischaemic hypoxia
Interruption of blood supply
Describe histiocytic hypoxia
Oxygen can’t be used due to disabled oxidative phosphorylation enzymes
Describe Ischaemia
- Loss of blood supply
- More serious as substrate as well as oxygen is lacking
What are the two immune mechanisms for cell injury? Describe them
- Hypersensitivity = Host tissue is injured after an over vigorous immune reaction
- Autoimmune = Immune system can’t distinguish self from non-self
Give 3 effects of the decrease in oxidative phosphorylation and therefore decrease in ATP as a result of ischaemic hypoxia
- Activity of Na+-K+ pump decreases therefore more Na+ and H20 in the cell which causes swelling, blebbing and oncosis
- Increases amount of Ca2+ in the cell
- Increases rate of Glycolysis which decreases pH and Glycogen therefore causing nuclear chromatin clumps
Describe the effects of an increase in cellular Ca2+
Activates enzymes such as:
- ATPase
- Phospholipase
- Proteases
- Endonucleases
(Irreversible effects)
What can cause non-ischaemic injury?
- Extreme cold therefore leading to frostbite
- Free radicals
What is the fenton reaction?
Fe2+ + H2O2 ==== Fe3+ + OH- + OH. (free radical)
What is the Haber-Weiss Reaction?
O2- + H+ + H2O2 === O2 + H2O + OH. (free radical)
Give four mechanisms of protection against cell injury
- Enzymes e.g. Catalase, Superoxide Dismutase
- Free radical scavengers
- Storage proteins e.g. transferrin
- Heat shock proteins e.g. Ubiquitin
What are the reversible changes of cell oncosis that can be seen with electron microscopy? (4)
- Blebbing
- Swelling
- Clumping of nuclear chromatin
- Dispersion of ribosomes
What are the irreversible changes of cell injury that can be seen with electron microscopy? (4)
- Myelin figures
- Cell membrane defects
- Rupturing of lysosomes
- Pyknosis, karyorrhexis, karyolysis
What are the reversible changes of oncosis that can be seen with light microscopy?
Decrease in pink cytoplasmic staining
What are the irreversible changes of oncosis that can be seen with light microscopy?
- Pyknosis (nuclear shrinkage)
- Karyolysis (lack of nucleus)
- Karyorrhexis (nuclear fragmentation)
Define oncosis
Cell death with swelling, changes occur in injured cells prior to death
Define necrosis
Cell death in living organisms where the morphological changes occur after a cell has been dead for some time. Leads to leakage of cell contents
Define apoptosis
Cell death with shrinkage, happens due to a regulated intracellular program where the cell activates enzymes for its own nuclear DNA and protein degradation. Forms apoptotic bodies
Which is ATP dependent/independent, necrosis or apoptosis?
- Necrosis = ATP independent
- Apoptosis = ATP dependent
What are the 4 types of necrosis?
- Coagulative necrosis
- Liquefactive necrosis
- Caseous necrosis
- Fat necrosis
Describe coagulative necrosis
- Protein denaturation is greater than active protease release
- Forms a ‘ghost outline’ of cells
Describe liquefactive necrosis
- Enzyme release is greater than protein denaturation
- Enzymatic digestion of tissues
- Proteins lyse and dissolve
Where is liquefactive necrosis common and why?
- In the brain
- Lacks coagulative factors
Describe caseous necrosis
- Forms a structureless debris (no ghost outline)
- Looks like cottage cheese
- Closely associated with TB
Describe fat necrosis. Where is it most likely to happen?
- Destruction of adipose tissue
- Increases lipase therefore increasing lipolysis
- Fatty acids are released which react with Ca2+ therefore forming calcium salts
- Happens in pancreas
What is gangrene? What are the types?
- Clinical term for necrosis that is visible to the naked eye
- Dry necrosis = air exposure e.g. umbilical cord
- Wet necrosis = infection e.g. septicaemia
- Gas necrosis
What are the two types of infarction that cause necrosis?
- White
- Red
Describe the features of white infarction (3)
- No blood
- No haemorrhage
- Single blood supply
Describe the features of red infarction (3)
- Extensive haemorrhage
- Venous insufficiency or reperfusion
- Dual blood supply
What is the consequence of infarction and what does this depend on?
- Death Depends on: - Blood supply - Speed of ischaemia - Tissue involved - Oxygen content
Name 3 molecules released by injured/dying cells and give their effects
- Potassium (Can cause heart to stop)
- Enzymes (time dependent i.e. small enzymes are first)
- Myoglobin (indicator of renal failure)
Give the two types of apoptosis
- Intrinsic
- Extrinsic
Describe intrinsic apoptosis
- Mitochondria plays the central role
- Increases permeability of membranes
- Leads to cytochrome C leakage
Describe extrinsic apoptosis
- Death ligands bind to receptors on CSM
- Directly activates caspases
Give 5 examples of abnormal intracellular accumulations
- Water and electrolytes
- Lipids e.g. cholesterol
- Carbohyrdates
- Proteins
- ‘Pigments’ e.g. tattoos, bruising
What are the mechanisms for abnormal accumulations? (4)
- Abnormal metabolism
- Changes in protein folding/transport
- Enzyme deficiencies
- Can’t degrade phagocytosed particles
