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Flashcards in Cell Injury Deck (40):
1

Describe hypoxia

Oxygen deprivation, usually due to low oxidative respiration. Can become cyanotic (hypoxaemia)

2

Explain the causes of hypoxia.

Hypoxaemic - low arterial oxygen caused by low inspiration or low absorption secondary to lung disease.

Anaemic - low ability of haemoglobin to carry oxygen caused by anaemia or carbon monoxide poisoning.

Ischaemic - interrupted blood flow due to blockage of vasculature and heart failure.

Histiocytic - cells are unable to use oxygen as oxidative phosphorylation enzymes are disrupted, such as in cyanide poisoning.

3

Describe the difference between hypersensitivity and autoimmune.

Hypersensitivity - injury secondary to a vigorous immune reaction e.g. urticaria/inflammation
Autoimmune - can't distinguish self from non-self. e.g. Graves' disease/Hashimoto's

4

Describe the effects of ischaemia caused by decreased sodium pumps due to low ATP.

Allows an influx of calcium, water and sodium, and an efflux of potassium.

Myelin figures, cell swels, lose microvilli, blebs, ER swells.

5

Describe the effects of ischaemia caused by high glycolysis due to low ATP.

Low glycogen

Lactic acidosis, low pH, chromatin clumps

6

Describe the effects of ischaemia not attributed to high glycolysis or decreased sodium pumps due to low ATP.

Detatch ribosomes, low protein synthesis, lipid deposition

7

Give an example of an enzyme activated in a cell by calcium ion influx which causes damage.

Phospholipase - membrane damage
Protease - membrane damage
Endonuclease - irreperable damage to DNA

8

Which is the most dangerous free radical and why?

OH*
Our bodies have no way of disposing of them.

9

Describe the Fenton reaction and why it is important.

Generates two hydroxyl radicles from free iron and hydrogen peroxide.

Important during bleeding as iron is normally well controlled.

10

What two systems allow the generation of hydrogen peroxide and superoxide?

Oxidative phosphorylation
p450 enzyme system in the cytoplasm.

11

What enzyme allows the formation of hydrogen peroxide from superoxide?

Superoxide dismutase

12

What enzyme formed oxygen and water from hydrogen peroxide?

Catalase

13

Give the vitamins which act as scavengers.

A, C, E

14

How is the Fenton reaction prevented?

Storage proteins in the ECM sequester iron and copper.

15

Describe the function of heat shock proteins and give an example.

Mend misfolded proteins and maintain cell viability. When a cell is stressed, production of these is increased and other proteins are stopped. They refold misfolded proteins, maintaining protein viability for cell survival.

Ubiquitin

16

Describe oncosis

Cell death with swelling. Changes occur before death without ATP. Mainly seen in hypoxia/ischaemia.

In light microscopy, seen as a decrease in pink stain as water moves into the cell (reversible). Then increases as proteins build up (irreversible).

Under an electron microscope you can see swelling. Clumped chromatin, ribosome dispertion, breakdown by autophagosomes occurs and blebbing. This is reversible.
Rupture of lysosomes/autolysis, nuclear changes, membrane defects and myelin figures are all irreversible changes.

Chromatin pumping and abnormal accumulation occurs.

Irreversible injury leads to cell death. Membrane becomes very permeable, especially to calcium ions.

17

Describe nuclear changes in oncosis.

Pyknosis - nucleus shrinks
Karyorrhexis - nucleus fragments
Karyolysis - nucleus dissolutes.

18

What are myelin figures?

Rolled up or scroll-like arrangement of lipid bilayer in a cell, superficially resembling a myelin sheath.

19

Describe apoptosis

Shrinkage induced by an intracellular programme. Degrades own DNA and proteins.
ATP dependent.

Internally controlled suicide, DNA breakdown not random.
Membrane integrity is maintained, fast, no lysosomal enzymes. Can be pathological or physiological.

20

Describe necrosis

Only occurs in living organisms.
Morphologic changes after cell death (4-24 hours)

21

What causes necrosis?

Damage to the cell membrane so it becomes very leaky.

22

What is coagulative necrosis?

Proteins denature and clump, causing ischaemia. Firm appearance, preserved cellular arch, white to the naked eye.

23

What is liquefactive necrosis?

Enzymes released causing autolysis, inflammation and influx of neutrophils.
Pus formed with lots of inflammation. Particularly seen in the brain after hypoxia/ischaemia as it is so fragile.

24

What is caseous necrosis?

Cheese-like and amorphous. Structureless debris.
Associated with TB and other infections.
Granulomatous inflammation, surrounded by macrophages.

25

What is gangrene?

Necrosis visible to the naked eye.

26

Describe the difference between wet and dry gangrene.

Wet - very serious as bacteria can leak into nearby blood vessels, causing septacaemia. Can lead to gas gangrene which is when it is infected by anaerobic bacteria which produce gas.

Dry - bacteria can't grow. Tissue is dead and cannot be salvaged.

27

Describe the difference between ischaemia and infarction.

Ischaemia - a cause of necrosis
Infarction - ischaemic necrosis

28

What is fat necrosis?

Destruction of adipose tissue. Seen in acute pancreatitis.
Releases free fatty acids which bind with calcium to give calcium salts.
Occurs after direct trauma to fatty tissue, especially the breast. can mimic breast cancer.

29

Describe the difference between a white and red infarction.

White - no haemorrhage. Solid organs limits it. Occurs after the occlusion of an end artery. Good stromal support, arterial supply is insufficient, no reperfusion, coagulation.
Kidney/heart/spleen

Red - haemorrhage. Dual blood supply, anastamoses, loose tissue, poor stromal support. If high venous pressure, blood can move back into the arteries. Reperfused.
Lung/bowl

30

What does the consequences of ischaemia depend on?

Alternative blood supply
Rate of ischaemia
Tissue
Oxygen in the blood

31

State some molecules released during infarction which cause inflammation and toxic effects.

Potassium - high concentration can cause the heart to stop beating. Released in MI, tourique shock, tumour lysis syndrome, severe burns with increased necrosis.

Enzymes - indicate the organ involved. Smallest molecular weight released first. E.g. troponin (heart attack) AST/ALT (liver damage)

Myoglobin - released by dead myocardium

32

Role of p53 in apoptosis

Mediates apoptic response to DNA damage

33

Role of death ligands in apoptosis

Activated death receptors and cascades. Part of the extrinsic pathway.

34

Role of cytochrome c in apoptosis and where it is released from.

Initiates formation of the apoptosome with APAF1 and caspase 9.

Released from mitochondria in the intrinsic pathway.

35

Role of Bcl-2 in apoptosis.

Prevents cytochrome c release.

36

Describe steatosis.

Fatty changes due to accumulation of TAGs. Mainly occurs in the liver causing an increase in size and weight.

37

What is Mallory's hyaline?

An accumulation of keratin seen in alcoholic liver disease. They are highly eosinophilic.

38

Describe the difference between dystrophic and metastatic calcification.

Dystrophic - Local, occurs in atherosclerosis, heart valves and lymph nodes. Local changes favour hydroxyapetite crystals. Can be benign. Pulmonary valve never calcifies.

Metastatic - General. Caused by hypercalcaemia, can be asymptomatic. May be caused by high PTH secretion.

39

Describe replicative senescence

Decreased ability of a cell to replicate as telomeres shorten.

40

Give three diseases that excessive alcohol can cause.

Fatty liver
Acute alcoholic hepatitis - causes focal hepatocyte necrosis
Alcoholic cirrhosis - seen in 10-15% of alcoholics. Causes a hard, shrunken liver with micronodules. Irreversible and usually fatal.