Cell Injury

Question 1

List 5 different causes of hypoxia

Answer 1

Hypoxaemic hypoxia (low 02 eg altitude), ishcaemic, anaemia, histiocytic, circulatory hypoxia

Question 2

What is the difference between hypoxia and ischaemia?

Answer 2

Hypoxia is a lack of O2 from any cause, ischaemia is a lack of blood supply to an area

Question 3

Which is more dangerous- hypoxia or ischaemia? Why?

Answer 3

Ischaemia as they also don’t get a supply of substrates either

Question 4

What is histiocytic hypoxia?

Answer 4

Oxygen deprivation due to decreased utilisation (eg due to CN- poisoning)

Question 5

What is anaemic hypoxia?

Answer 5

O2 deprivation due to decreased O2 carrying capacity of blood

Question 6

What is circulatory/ischaemic hypoxia?

Answer 6

O2 deprivation due to obstruction in circulation or systemic shock (meaning less 02 delivered because less blood delivered)

Question 7

List some causes of cell injury

Answer 7

Chemicals, immune mechanisms, hypoxia, physical agents, micro-organisms, genetics, dietary insufficiency/excess

Question 8

What is ischaemic reperfusion injury?

Answer 8

When blood returns to an area of previous ischaemia (not yet necrotic), the return of blood flow causes more damage than if it has been left without blood flow.

Question 9

How does ischaemic reperfusion injury cause damage?

Answer 9

Increased production of O2 radicals (thanks to return of O2), increased no of neutrophils (more inflammation, TF more damage)

Question 10

Define oncosis

Answer 10

Cell death with sw

Question 11

Why is ischaemia dangerous?

Answer 11

Cells resort to anaerobic respiration, the resulting local acidosis promotes influx of calcium triggering cell death

Question 12

Define hypoxia

Answer 12

Oxygen deprivation.

Question 13

Define necrosis

Answer 13

Morphological changes that occur after a cell has died/pathological cellular/tissue death in a living organism

Question 14

Define apoptosis

Answer 14

Cell death with shrinkage, induced by itself (degrades its own DNA with endogenous endonucleases)

Question 15

Is hypoxia reversible or irreversible?

Answer 15

Can be both!

Question 16

What is oxidative stress?

Answer 16

When the number of free radicals outweighs the body’s defences

Question 17

List some free radicals

Answer 17

OH., O2-, H2O2

Question 18

What do free radicals do? Useful and dangerous?

Answer 18

Useful: kill bacteria, cell signalling. Dangerous: attack lipids, mutagenic

Question 19

How is the hydroxyl free radical produced?

Answer 19

Lysis of H2O from radiation

Question 20

List some anti-oxidants

Answer 20

Free radical scavengers (Vitamin A,C,E, Glutathione), enzymes (SuperOxide Dismutase & catalases, peroxidases)

Question 21

How do storage proteins act as antioxidants?

Answer 21

They isolate transition metals which catalyse the formation of free radicals (eg Fe2+)

Question 22

List some ways you could diagnose cell deathh

Answer 22

Add dye, those that take it up are dead.

Question 23

What is Pyknosis?

Answer 23

Shrinkage of nucleus

Question 24

What is karryohexis?

Answer 24

Fragmentation of nucleus

Question 25

What is karryolysis?

Answer 25

Dissolution of nucleus

Question 26

What nuclear changes are seen in irreversible damage?

Answer 26

Pyknosis, Karryhexis, Karryolysis

Question 27

What nuclear changes are seen in reversible damage?

Answer 27

Chromatin becomes slightly clumped

Question 28

What reversible changes may be seen in oncosis?

Answer 28

Cytoplamic blebbing, clumped chromatin, dissociation of ribosomes from ER

Question 29

What irreversible changes can be seen in oncosis?

Answer 29

Nuclear changes. (Karryolysis, karryohexis, pynkosis), membrane defects

Question 30

What are the two main types of necrosis? Two others?

Answer 30

Coagulative, liquefactive. (Fat necrosis, caseous necrosis)

Question 31

How is necrotic tissue removed?

Answer 31

By enzymatic degradation and phagocytosis

Question 32

What happens if necrotic tissue is not removed?

Answer 32

It remains and becomes calcified= 'dystrophic calcification'

Question 33

What is dystrophic calcification?

Answer 33

When necrotic tissue has not been removed and remains and becomes calcified.

Question 34

What is the difference between liquifactive and coagulative necrosis?

Answer 34

Liquefactive: seen in tissues with little collagenous support/matrix where proteins become lysed by own cell enzymes. Coagulative: proteins denature and coagulate. You get a 'ghost outline' because surrounding collagenous stroma isn't broken down fully.

Question 35

What usually arrives to coagulative necrosis turning it more to liquefactive?

Answer 35

Neutrophils, these release proteases etc

Question 36

What is fat necrosis?

Answer 36

Where there is direct trauma to adipose tissue triggering an inflammatory response. Eg acute pancreatitis

Question 37

How can fat necrosis be mistaken for breast cancer?

Answer 37

Direct trauma to breast will heal to leave a palpable scar, which may feel like a nodule

Question 38

What is caseous necrosis?

Answer 38

Where dead tissue is structureless, it looks cheesy, eg in TB

Question 39

What common classes of things can accumulate in cell damage?

Answer 39

Water/electrolytes, lipids, proteins, pigments, carbohydrates

Question 40

E some examples of lipids that can accumulate in cell damage

Answer 40

Cholesterol (in membrane bound vesicles and macrophages), steatosis (fatty liver)

Question 41

Give a few causes of steatosis

Answer 41

Alcohol abuse, drug abuse, DM, obesity/diet

Question 42

Give examples of proteins that can accumulate abnormally

Answer 42

Alpha 1 anti-trypsin (in deficiency) is produced wrong so cant fold so remains in liver as cant be secreted.

Question 43

Describe respiratory burst

Answer 43

Phagocytes (eg macrophages) when stimulated rapidly produce a large amount of ROS & RNS. This destroys the cell and the bacteria/fungus/pathogen around it. (RNS using iNOS, ROS using NADPH oxidase)

Question 44

What is NOS? And what three types are there?

Answer 44

They all produce NO. From arginine. iNOS: inducible, used in resp burst. eNOS: endothelial, used for signalling. nNOS: neuronal, used for signalling.

Question 45

What is chronic granulomatous disease?

Answer 45

A deficiency in NADPH oxidase, this enzyme is used to form superoxide radical in resp burst TF without, cant kill bacteria TF form many granulomas.