MoD 1 - Cell Injury Flashcards Preview

Amars Semester Two cards > MoD 1 - Cell Injury > Flashcards

Flashcards in MoD 1 - Cell Injury Deck (26)
1

Name and briefly describe the different types of hypoxia

Hypoxaemic hypoxia - low arterial pO2
Anaemic hypoxia - capacity to transport O2 is low (low Rbc)
Ischaemic hypoxia - disrupted blood supply leading to low O2.
Histiocytic hypoxia - lack of Ox Phos enzymes so can't utilise O2.

2

Describe why low O2 leads to reversible cell injury.

Low O2 = less ATP synthesis. When ATP is at 5-10% of what it should be, then problems occur:
A) NA+/K+-ATPase fails as needs ATP. Na+ builds up inside. water follows in due to osmosis and the cell swells (oncosis).

B) protein synthesis interrupted as ribosomes detach from the ER as they need ATP to remain bound.

C) glycolysis still occurs but lactic acid is being produced (lactate dehydrogenase) which lowers cell pH - this damages organelles.

3

Briefly explain the paradox that is Ischaemic-Reperfusion injury

When a damaged (but not yet necrotic) tissue starts receiving blood flow again, it can become damaged by the blood. This is due to a few things such as free radicals, high neutrophils or complement activation, amongst others.

4

What are free radicals, name two reactions that produce them and what protection the body has? What are the main 3 radicals?

Highly reactive oxygen species with a lone electron in the outer most orbital.
H2O2, O2- and OH*

Fenton reaction and haber-Weiss reaction

Protection:
free radical scavenger
Enzymes
Storage proteins.

5

Briefly describe the role of heat shock proteins and where they are located.

Heat shock proteins try and locate damaged proteins (misfolded) and repair them and retain their viability. If this is done, there is a higher chance the damaged cell will be saved. They are NOT secreted but they are located within cells. When a cell is under stress, the synthesis of HSPs increases, and other protein synthesis decreases.

6

Describe the Dye Exclusion Technique

A dye is added to cells, and if the cell becomes stained with the dye then it is dead.

If the cell doesn't take up the stain then the membrane is still intact and it is not dead.

7

If the cytoplasm of a cell is stained heavily with pink, is the injury likely to be reversible or irreversible ?

Irreversible.

Light pink staining is reversible.

8

What is meant by the terms Pyknosis, Karolysis and Karryohexis?

Pyknosis - nucleus shrinkage
Karryohexis - nucleus fragmentation
Karyolysis - nucleus dissolution.

9

Briefly explain coagulative necrosis

Occurs when the cell dies but the proteins undergo denaturation and then clumping. This forms a mass which is why it's called coagulative. Ghost outlines of cells are seen for a short period until inflammatory response takes over.
Generally, when there is ischaemia, coagulative necrosis follows.

10

Briefly describe liquefactive necrosis

When a cell dies, if the proteins are not denatured but instead they are digested by proteases, liquefactive necrosis ensues.
Often seen when neutrophils have been present as they also secrete proteases.
Commonly seen in bacterial infections and also the brain.

11

What kind of necrosis is gangrene?

Neither. This is a trick question. Gangrene is NOT a type of necrosis, but it is necrosis that is visible to the eye. It is dead tissue that cannot be salvaged.

12

What is caseous necrosis ?

Cheese like appearance, often associated with tuberculosis.
Associated with granulomatous inflammation.

13

What is fat necrosis ?

Destruction of adipose tissue.
Often seen in acute pancreatitis when the pancreas is damaged, it secretes lipases which then digest fat in its surroundings.
Fatty acids are released which can react with Ca2+ and form 'chalky deposits' in adipose tissue - this is often seen in autopsies as wax of a candle - Known as Taches de bougie.

14

Differentiate between dry, wet and gas gangrene.

Dry - when exposed to air, the tissue dries out (coagulative necrosis)
Wet - gets infected when exposed to infectious agent (liquefactive necrosis). Can get into the blood and cause septicaemia.
Gas - same as wet but infected with anaerobes that produce visible and palpable gas.

15

What is an infarct? Why do some infarcts appear red and others white?

An infarct is an area of tissue cell death due to reduced or no blood supply for a defined period of time.
Red - tissue has died but the vessel that was blocked was not a end artery so the collateral blood supply still has blood going into the infarct so it appears red. (Lungs).

White - the blocked artery is an end artery and so therefore there is no other blood supply so it appears white (heart, kidney, spleen)

16

What molecules Are released from injured cells?

k+ - normally high inside cell. The heart is sensitive to K+ levels.

Myoglobin - if high enough amount in the blood then it can cause rhabdomyolysis in some muscles.

Enzymes - eg transaminases from liver. Used to be used as confirmation in certain conditions such as MI. Enzymes indicate the type of tissue damaged and the time it occurred.

17

What is the difference between hypoxia and ischaemia?

Hypoxia is a low arterial pO2 (with blood is still being received)

Ischaemia is a disruption of blood flow to an area. The tissue doesn't receive oxygen as well as other nutrients and substrates such as glucose.

18

What is apoptosis?

Cell death (via shrinkage) due to the activation of internal suicide mechanisms.

19

In terms of DNA breakdown, describe the difference between the way DNA is broken down in oncosis and apoptosis.

In oncosis, the DNA is cleaved in a random, non structured way.
In apoptosis, it is cleaved in a non-random, systematic way.

20

In apoptosis, why is there is no inflammatory response,

When the cell dies, cytoplasmic budding occurs. Each bud is enveloped in membrane, so there is no spillage of the cell contents. The lack of spillage of the cell contents means there is no inflammatory response.

21

What are the 3 stages of apoptosis?

Initiation, execution and degradation/phagocytosis.

22

Briefly describe each stage of apoptosis.

Initiation/execution:
2 pathways - intrinsic and extrinsic- that both culminate in the activation of caspases (here cleave proteins that break up the cytoskeleton and also begin the breakdown of DNA).

A)intrinsic - cytochrome C released from mitochondria, and together with caspase 9 and APAF1, form an apoptosome. This then activates caspases.

B) extrinsic - ligand mediated - death ligand such as TRAIL or Fas binds to death receptor, which then increases caspases activity.

Degradation/Phagocytosis
The cell breaks into fragments known as apoptotic bodies. These fragments display molecules on their surface that induces phagocytosis.

23

Which molecule inhibits the release of cytochrome C? Where is cytochrome C normally released from?

Bcl-2. This prevents apoptosis.
Cytochrome C is released from the mitochondria.

24

Name, and very briefly describe, 4 abnormal cellular accumulations.

Proteins - if alpha-1-antitrypsin deficient then this accumulates and the person can suffer emphysema due to break down of lung tissue.
lipid - steatosis - accumulation of TAGs - fatty liver
- cholesterol - insoluble and excreted by liver in bile (HDL!) - can get foamy macrophages which aggregate and form xanthelasma.
fluid - cell swelling - dangerous in brain as limited space
pigment - bilirubin
- anthracosis - blackened lung tissue due to coal/carbon/soot

25

Describe the role of telomeres in cell duplication and how stem cells (and cancerous cells) overcome this problem and can duplicate indefinitely.

Cells lose the ability to replicate with age. This is known as replicative senescence. This is dependent on the length of the telomeres. With each successive duplication, the length of the telomere decreases and eventually it decreases to a point of no return - the point after which it cannot replicate further. This is when it is said to have reached replicative senescence.

Stem cells and cancerous cells overcome this problem by secreting telomerases, enzymes which keep the length of the telomere constant so that replicative senescence is not achieved and they can continue to replicate and proliferate.

26

What is cirrhosis of the liver?

Micro modules of regenerating hepatocytes, surrounded by collagen.