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Semester 2- MoD > 1 Cell Injury > Flashcards

1 Cell Injury Flashcards

0
Q

How do cells react to severe changes in environmental conditions?

A

Cell adaptation
Cell injury
Cell death

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1
Q

Define ‘disease’

A

A consequence of failed homeostasis with consequent morphological and functional disturbances to cells.

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2
Q

What determines the degree of an injury?

A

Type of injury
Severity of injury
Type of tissue affected

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3
Q

Define ‘cell injury’

A

Irreversible change within a cell

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4
Q

Name 3 causes of cell injury and cell death

A 
Hypoxia
Trauma
Toxins
Radiation
Dietary deficiencies
Micro-organisms
Immune mechanisms
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5
Q

Define ‘ischaemia’

A

Loss of blood supply to a tissue

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6
Q

Define ‘hypoxia’

A

Oxygen deprivation to tissues

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7
Q

What is ‘hypoxaemic hypoxia’?

A

Arterial content of oxygen is low

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8
Q

What is ‘anaemic hypoxia’?

A

Decreased ability of haemoglobin to carry blood

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9
Q

What is ‘ischaemic hypoxia’?

A

An interruption of blood supply

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10
Q

What is ‘histiocytic hypoxia’?

A

Disabled oxidative phosphorylation enzymes so oxygen cannot be utilised.

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11
Q

Give 3 examples of toxins

A 
Alcohol
Poison
Illegal Drugs
Asbestos
Pollutants
Medicines
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12
Q

What is a ‘hypersensitivity reaction’?

A

The host tissue is injured after an overly vigorous immune reaction

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13
Q

What is an ‘immune reaction’?

A

The immune system fails to distinguish between self and non-self

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14
Q

What are the principle targets for cell damage?

A

Cell membranes
Nucleus
Proteins
Mitochondria

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15
Q

List the 4 effects of a high intracellular Ca2+ concentration

A

Decreased ATP
Decreased phospholipids
Disruption of protein production
Nuclear chromatin damage

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16
Q

What is a ‘free-radical’?

A

A very reactive molecule with a single unpaired electron in the outer orbit.

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17
Q

How are free-radicals produced in the body? When are they excessively produced?

A

Side products of the electron transport chain.

After chemical and radiation injury

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18
Q

How are free-radicals/reactive oxygen species (ROS) neutralised?

A

Antioxidants eg. H2O2

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19
Q

What is ‘ischaemia-reperfusion injury’?

A

Blood flow returns to a damaged tissue and is reoxygenised causing the production of more ROSs. This makes the damage worse.

20
Q

What is the function of ‘heat-shock’ proteins?

A

Mend misfolded proteins and maintain cell viability.

21
Q

What is ‘oncosis’?

A

Cell death with swelling (including the spectrum of changes that occur in injured cells prior to death)

22
Q

Name some cellular symptoms associated with reversible injury

A 
Blebs
Swelling
Clumping of chromatin
Mitochondrial swelling
ER swelling
Dispersion of ribosomes
23
Q

Name some features associated with irreversible injury.

A 
Rupture of lysosomes and autolysis
Defects in the cell membrane
Lysis of ER
Nuclear damage
Myelin figures
24
Q

Describe what is seen in:

i. ) Pyknosis
ii. ) Karyorrhexis
iii. ) Karyolysis

A

i. ) Accumulation of denatured proteins
ii. ) Fragmented nucleus
iii. ) No nucleus

25
Q

What is ‘necrosis’?

A

The morphological changes that occur after a cell has been dead some time. The cell contents leak out and inflammation can be seen.

26
Q

Name the 4 types of necrosis

A

Coagulative
Liquefactive
Caseous
Fat necrosis

27
Q

What happens in ‘coagulative necrosis’?

A

The denaturing of proteins dominates over the release of active proteases.
The cellular architecture is preserved as a ‘ghost outline’

28
Q

What happens in ‘liquefactive necrosis’? Where is it found?

A

Enzyme degradation is greater than denaturation so the tissues are enzymatically degraded. Found in the brain

29
Q

What can be seen in caseous necrosis? What cause is it associated with?

A

Structureless debris

Infections, especially TB

30
Q

What happens in fat necrosis? When does it occur?

A

Adipose tissue is destroyed by lipase release. It occurs after trauma.

31
Q

What is gangrene? Name and describe the two types

A

Necrosis visible by the naked eye
Dry- modified by the air to become hard
Wet- modified by infection

32
Q

What is an infarct? How are they caused?

A

An area of ishaemic necrosis

Clots in blood vessels, compression or twisting of the blood supply

33
Q

When does a white infarct occur?

A

When there is an arterial deficiency. It only has one blood supply so is not reperfused.

34
Q

When does a red infarct occur?

A

Venous insufficiency
Tissue is reperfused
Dual blood supply

35
Q

When can a large potassium leak from a cell occur?

A

After a large amount of sudden cell death (eg. MI, burns, effective cancer treatment)

36
Q

Why can enzyme leaks from cells be useful clinically? Give an example

A

Test plasma levels for released enzymes to diagnose problem

Example: troponin levels for MI, ALT/AST levels for liver damage

37
Q

What is a side effect of a large myoglobin release?

A

Myoglobin blocks renal tubes causing dark urine

38
Q

What is ‘apoptosis’?

A

Programmed cell death with shrinkage

39
Q

How is apoptosis induced?

A

Enzymes are activated that degrade its own nuclear DNA and proteins

40
Q

How many cells are affected by apoptosis at a time?

A

1

41
Q

What enzyme mediated apoptosis

A

p53

42
Q

How are the fragments of the apoptitic cell removed?

A

Phagocytosis

43
Q

Why do abnormal accumulations occur within a cell?

A

The cell cannot metabolise the accumulation

44
Q

What is the effect of fluid accumulation?

A

Swelling

45
Q

What is the effect of lipid accumulation around the liver?

A

Steatosis and an increased liver size

46
Q

What accumulation does a Mallory’s highline-hepatocyte have?

A

Accumulation of keratin

47
Q

What is ‘dystrophic calcification’?

A

Pathological calcification of areas of localised damaged tissue

48
Q

What is ‘metastatic calcification’?

A

Pathological calcification effecting the whole body and destroying bone tissue

Semester 2- MoD (9 decks)

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