MOD Flashcards Preview

ESA 2 > MOD > Flashcards

Flashcards in MOD Deck (61)
Loading flashcards...

What is the difference between hypoxia and ischemia?

Hypoxia = oxygen deprivation
Ischemia = loss of blood supply


What are the classes of hypoxia?

Hypoxaemic - low arterial O2
Anaemic- decreased ability of haemoglobin to carry O2
Ischemic - interruption to blood supply
Histiocytic - inability to use O2 e.g. Disruption of enzymes/ cyanide


What are the causes of cell injury?

physical agents e.g. Direct trauma, radiation, pressure, electric currents, temperature.
Chemical agents and drugs
Micro organisms
Immune mechanisms
Dietary deficiencies
Genetic abnormalities.


Describe reversible hypoxia injury

Deficiency of ATP.
Na/K pump stops causing swelling.
Ca accumulates
Increased lactate so lower pH, disrupting enzymes and causing chromatids to clump.
Ribosomes dissociate from ER.


Describe irreversible hypoxic injury

Plasmamembrane and ER/mitochondrial membranes are damaged. Ca accumulates further. This activates proteases, endonucleases, phospholipases and ATPases. Lysomsomal membranes are also effected causing more damaging enzymes to be released.
Increased Ca can be detected in the blood.


What is ischemic reproduction injury?

Blood flow is restored after ischemia.
Sudden O2 can produce radicles
Neutrophils increase and can trigger inflammation and damage cell.
Complement proteins activate the complement pathway.


What is the role of a heat shock protein?

Refolds misfolded/ denatured proteins. Upkeep proteins.


How can the appearance of a tissue with cell damage change under light microscopy

Reversible - swelling so light cytoplasm or if irreversible then dark due to accumulations of ribosomes and proteins.
Nuclear changes - chromatin clumping/ shrinkage - pyknosis, karryohexis (fragmentation) or karyolysis.
Intra cellular accumulations.


Cell damage under electron microscope?

Cell and organelle swelling.
Myelin figures at membrane (damage that looks like myelin sheath)
Amorphous densities in mitochondria.


What is the difference between oncosis and necrosis?

Oncosis: the spectrum of changes that occur within an injured cell before it dies.

Necrosis: the morphological changes that occur following cell death due to degredating proteins.


What is dystrophic calcification? Why does it not happen in every case of necrosis.

Necrotic tissues harden/ calcify.

Because normally necrotic tissue is degraded by enzymes and removed via phagocytosis.


What is coagulative necrosis?

Produced mostly from ischemia.
Protein denaturation >protein breakdown (active proteases)
Produces a 'ghost outline' histologically
Results in inflammation and infiltration by phagocytes.


What is liquifactive necrosis?

Protein breakdown by active proteases > protein denaturation
Often caused by infection - neutrophil damage.
E.g. Brain
Causes acute inflammation with lots of luvly pus


What is caseous necrosis?

Cheese appearance - granulomatous inflammation
Often caused by TB


What is fat necrosis?

Destruction of adipose tissue.
Normal in acute pancreatitis (due to lipases) or from direct trauma to fatty tissues (e.g. Breasts).
FA can react with Ca to form chalky deposits in fatty tissue which can be seen on X-rays or with the naked eye.


What is gangrene?

Necrosis that can be seen with the naked eye often caused by limb ischemia.
Can be wet (liquifactive) which can result in septicaemia or dry due to coagulative necrosis.


What is an infarction? How is it different to ischemia? How is infarction different in brain and heart? What do the consequences of infarction depend on?

Ischemia is a decreased blood supply to an organ or tissue.
Infarction is a cause of necrosis. It is an area of tissue that has died from an obstruction in blood supply e.g. Twisting of a vessel/ ischemia.
So ischemia causes infarction.
In heart leads to coagulative and brain liquifactive.

Consequences depend on:
Alternate blood supply?
How quickly it has occurred (other perfusion pathways?)
How vulnerable tissue is to hypoxia
O2 conc in blood.


How is infarction described?

White or red.
White occurs in organs with good stromal support after an occlusion of an end artery.
Red occurs in organs with poor stromal support (loose tissue), dual bloody supply, previous congestion or raised Venus pressure.

*think... Will blood (red stuff) build up or not?


How does apoptosis appear under the microscope?

Chromatin condensation, pyknosis (degredation of cell nucleus) , nuclear fragmentation.
Cell shrinkage
Very eosinophilic - lots of protein in cytoplasm.

Under electron microscope 'blebbing' can be seen of apoptotic cell bodies which are eventually broken down by macrophages


How is apoptosis initiated?

Intrinsic - damage to DNA or no growth factors/hormones/p53 can initiate. Mitochondrial membranes become permeable releasing cytochrome c.

Extrinsic- ligands e.g. TRAIL or FAS bind told earth receptors.


What is p53

Guardian of genome- can trigger apoptosis if DNA is damaged


What can prevent cytochrome c release from mitochondria?



What is steatosis?

Abnormal accumulation of lipids in the liver often caused by alcohol, diabetes mellitus, obesity and toxins. No effect on function.


Where may you find abnormal accumulations of cholesterol within the body?

Within smooth muscle and macrophages in atherosclerosis.
In hyperlipideamias, in xanthomas accumulating in tendons.


When might you find abnormal accumulations of protein within the body?

Mallory's hyaline in alcoholic liver disease.
A1 antitripsin genetic defect. It accumulates in liver, and does not degradeproteases in lungs so can cause emphysema.


Describe 3 endogenous abnormal accumulations of pigments.

Lipofusin - not harmful from radicle damage - aging.
Heamosiderin- from iron e.g. Bruises and haemochromotosis (more iron uptake)
Bilirubin- from poor liver function.


Where may you find distrophic pathological calcification?

In cell death, atherosclerosis, heart valve aging, tuberculous lymph nodes.

All not from abnormal metabolism.


Where may you find metastatic pathological calcification and why?

PTH excess or ectopic Ptrh production.
Vit d disorders.
Renal failure
Destruction of bone secondary to tumours.

All errors in metabolism - usually asymptomatic


Which cells produce telomerase?

Germ and stem cells as they are rapidly dividing.
Some cancers.


What are the cofactors for alcohol dehydrogenase?

CYP2E1 and p450