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Flashcards in Cel injury and inflammation Deck (51)
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Give come causes of cell injury

hypoxia, toxins, trauma, tempreature, pressure, electic currents, radiation, microorganisms, dietary excess and deficiencies


What is hypoxia?
What are the 4 types of hypoxia?

Oxygen deprivation -

Hypoxaemic hypoxia, anaemic hypoxia, ischaemic hypoxia (interruption of blood supply), histotoxic hypoxia


What is hypoxaemic hypoxia and when does it occur?

oxygen content of arterial blood is low- eg at altitude or from lung disease


What is anaemic hypoxia?

decreased ability of Hb to carry blood- CO poisoning or anaemia


What is histotoxic hypoxia and when does it occur?

inability for the tissues to utilise O2 due due to inactivated oxidative phosphylation proteins - e.g.:
In cyanide poisoning


What is the difference between reversible and irreversible cell injury to hypoxia?

There is a massive influx of calcium which means that the injury becomes irreversible


When cell injury due to hypoxia is reversible, there is decreased ATP due to decreased oxidative phosphorylation, what effects to the cell does this have? (3)

1) Na/ K pump stops- influx of Na and H20 + Na/K pump reverses so Ca comes in, K+ leaves. (Na+, Ca2+ + H20 influx, K+ efflux)
2) Glycolysis increases, less glycogen and more lactate
3) detachment of ribosomes so decreased protein synthesis and more lipid deposition (leads to fatty liver)


What effects does the reversal of Na/ K pump leading to H20, Na and Ca influx and K+ efflux have?

cell swelling
loss of microvilli
ER swelling
myelin figures


What effects does massive Ca2+ influx with irreversible damage have?

- Decreased ATPase activity (decreased ATP)
- Phospholipase activated (destroys membrane integrity)
- Protease activated (membrane and cytoskeletal as well as enzymes denatured)
- Endonuclease activated (chromatin damaged)


What are signs of ischaemia?

4 Ps
- pain
- pulelessness
- paleness (pallor)
- pins and needles (paraesthesia)


What is a free radical?

A molecule with a single unpaired electron in their outer orbit.


Give 3 examples of free radicals

H202, O- (superoxide), OH˚ (hydroxyl - most dangerous)


How are free radicals produced?

Metabolic reactions (oxidative phosphylation)
Inflammation (respiratory bursts by neutrophils)
Radiation (H20 into OH* + H)
Contact with unbound iron and copper (eg in haemochromatosis)
Drugs and chemicals (metabolism of paracetamol)


Give 3 methods of protection against free radicals

1) anti oxidants (vitamins A, C and E will donate them electrons
2) Metal carriers and storage compounds such as transferrin and ceruloplasmin sequester iron and copper which will give/ take electrons
3) enzymes that neutralise free radicals


What 3 enzymes neutralise free radicals?

Superoxide dismutase (SOD) - O2* to H2O2
Catalase - H2O2 to O2 + H20
Glutathione peroxidase


how do free radicals cause cell injury?

- overwhelm antioxidant system
- cause lipid peroxidation (electrons taken from lipids in membranes, causes a chain of redox reactions which produces more free radicals and disrupts membrane integrity)
- oxidise proteins, carbs and DNA causing structural changes - i.e.: fragmentation or strand breaks


What system is in place to repair misfolded/ damaged proteins after cellular injury

Heat shock proteins/ unfoldases/ chaperonins will mend misfolded proteins


Give an example of a heat shock protein

ubiquitin, hsp70/hsp90


How can cell death be diagnosed under a microscope?

A dye exclusion test- living cells will not take up the special dye


Do injured (but not dead) cells look different under microscope to alive cells?

they look slightly swollen, small blebs may start to be seen, chromtin clumps, ER swells and ribosomes disperse, mitochondira swell


Define oncosis

The process of cell death by swelling and the associated spectrum of changes that occur due to injury prior to death


Define necrosis

The morphological changes that occur after the cell has died in a living organism. These changes take 12- 24 hrs to occur.


What process dominates in coagulative necrosis and in liquifactive necrosis ?

Coagulative- protein denaturation
Liquifactive- Enzyme release


Where does coagulative necrosis occur and what does it look like?

Occurs in ischaemia of solid organs with connective tissue (kidneys, heart, adrenal glands). Cells have more pink staining and the GHOST OUTLINE OF THE CELL IS STILL PRESENT w/some neutrophil accumulation


Where does liquifactive necrosis occur and what does it look like?

in loose tissue (brain) and/ or when there are many neutrophils present (infection). It just looks like a hole.


When does caseous necorsis occur and what does it look like?

only found in infections, by far most common cause it TB. structurless debris is found without proper cell outlines.


When does fat necrosis commonly occur?

Due to direct trauma to a fatty area- eg tennis ball hitting breast- creates hard lump which is often mistaken for cancer.
Also in pancreatitis due to lipase release


What occurs in fat necrosis?

Lipases leak out and attack lipids. This causes lipids bonding with calcium and creates a hard soap which looks like candle wax.


Why does reperfusion injury occur?

- increased production of O2 free radicals with reoxygenation
- increased number of neutrophils so more inflammation/tissue injury
- delivery of complement proteins


What will be abnormal in blood results in hepatits?

ALT and AST and LDH (from hepatocytes), bilirubin (no longer excreted), decreased albumin and raised PT and ammonia (liver not functioning properly)