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MoD > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

List 5 different causes of hypoxia

A

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

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2
Q

What is the difference between hypoxia and ischaemia?

A

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

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3
Q

Which is more dangerous- hypoxia or ischaemia? Why?

A

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

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4
Q

What is histiocytic hypoxia?

A

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

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5
Q

What is anaemic hypoxia?

A

O2 deprivation due to decreased O2 carrying capacity of blood

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6
Q

What is circulatory/ischaemic hypoxia?

A

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

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7
Q

List some causes of cell injury

A

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

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8
Q

What is ischaemic reperfusion injury?

A

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.

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9
Q

How does ischaemic reperfusion injury cause damage?

A

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

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10
Q

Define oncosis

A

Cell death with sw

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11
Q

Why is ischaemia dangerous?

A

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

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12
Q

Define hypoxia

A

Oxygen deprivation.

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13
Q

Define necrosis

A

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

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14
Q

Define apoptosis

A

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

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15
Q

Is hypoxia reversible or irreversible?

A

Can be both!

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16
Q

What is oxidative stress?

A

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

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17
Q

List some free radicals

A

OH., O2-, H2O2

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18
Q

What do free radicals do? Useful and dangerous?

A

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

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19
Q

How is the hydroxyl free radical produced?

A

Lysis of H2O from radiation

20
Q

List some anti-oxidants

A

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

21
Q

How do storage proteins act as antioxidants?

A

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

22
Q

List some ways you could diagnose cell deathh

A

Add dye, those that take it up are dead.

23
Q

What is Pyknosis?

A

Shrinkage of nucleus

24
Q

What is karryohexis?

A

Fragmentation of nucleus

25
Q

What is karryolysis?

A

Dissolution of nucleus

26
Q

What nuclear changes are seen in irreversible damage?

A

Pyknosis, Karryhexis, Karryolysis

27
Q

What nuclear changes are seen in reversible damage?

A

Chromatin becomes slightly clumped

28
Q

What reversible changes may be seen in oncosis?

A

Cytoplamic blebbing, clumped chromatin, dissociation of ribosomes from ER

29
Q

What irreversible changes can be seen in oncosis?

A

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

30
Q

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

A

Coagulative, liquefactive. (Fat necrosis, caseous necrosis)

31
Q

How is necrotic tissue removed?

A

By enzymatic degradation and phagocytosis

32
Q

What happens if necrotic tissue is not removed?

A

It remains and becomes calcified= ‘dystrophic calcification’

33
Q

What is dystrophic calcification?

A

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

34
Q

What is the difference between liquifactive and coagulative necrosis?

A

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.

35
Q

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

A

Neutrophils, these release proteases etc

36
Q

What is fat necrosis?

A

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

37
Q

How can fat necrosis be mistaken for breast cancer?

A

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

38
Q

What is caseous necrosis?

A

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

39
Q

What common classes of things can accumulate in cell damage?

A

Water/electrolytes, lipids, proteins, pigments, carbohydrates

40
Q

E some examples of lipids that can accumulate in cell damage

A

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

41
Q

Give a few causes of steatosis

A

Alcohol abuse, drug abuse, DM, obesity/diet

42
Q

Give examples of proteins that can accumulate abnormally

A

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

43
Q

Describe respiratory burst

A

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)

44
Q

What is NOS? And what three types are there?

A

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

45
Q

What is chronic granulomatous disease?

A

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.

MoD (10 decks)

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