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ESA2 > MOD S1&2 Cell Injury > Flashcards

MOD S1&2 Cell Injury Flashcards

1
Q

What is cell injury?

A

When the cell can no longer adapt to changes in its environment, it begins to show evidence of cell injury.

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2
Q

How may a cell be injured?

A 
Hypoxia
Toxins
Heat
Cold
Trauma
Radiation
Microorganisms
Immune mechanisms
Dietary deficiency/insufficiency
Genetic abnormalities
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3
Q

What are heat shock proteins?

A

Produced in response to cell injury due to heat
They refold denatured proteins correctly
Misfolded proteins are destroyed

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4
Q

What are the main targets of cell injury?

A

Cell membranes
Nucleus
Proteins
Mitochondria

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6
Q

What is ischaemia reperfusion injury?

A

When blood flow is reinstated to an area of ischaemic tissue, the damage sustained is worse that it would have been without circulation.

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8
Q

Define ischaemia

A

The interruption of blood supply

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9
Q

Name the types of hypoxia

A

Hypoxaemic
Anaemic
Ischaemic
Histeocytic

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11
Q

What is hypoxia?

A

Reduced O2

Often due to ischaemia

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13
Q

What are some reversible changes to cells caused by hypoxia?

A 
Reduced oxidative phosphorylation
Decreased pH
Na accumulation
Cell swelling
Reduced protein synthesis due to ribosome detachment
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14
Q

Define oncosis

A

The spectrum of changes that occur in a injured cell prior to death

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15
Q

What are irreversible changes to cells brought about by hypoxia?

A

Accumulation of cytosolic Ca2+

Activation of certain enzymes - these result in cell death

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16
Q

Do all cells react the same way to ischaemia?

A

No

Eg nerve cells would last a few minutes in ischaemic conditions whereas fibroblasts could last for hours

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17
Q

What reversible structural changes may be seen in an ischaemic cell under an electron microscope?

A 
Swelling
Chromatin clumping
Autophagy
Ribosome dispersal
Blebs
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18
Q

What are blebs?

A

Small bumps on the cell membrane where the cytoskeleton has detached

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19
Q

What irreversible effects may be seen with an electron microscope in an ischaemic cell?

A

Nuclear changes
Lysosome rupture
Membrane defects
Endoplasmic reticulum rupture

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21
Q

Define apoptosis

A

Programmed cell death

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22
Q

What are the stages of apoptosis?

A

Initiation
Execution
Degradation/phagocytosis

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23
Q

What are the two methods of initiation of apoptosis?

A

Intrinsic (mitochondrial)

Extrinsic

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24
Q

Name an inhibitor of apoptosis

A

Bcl-2

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25
Q

What is necrosis?

A

The changes which occur after cell death in living tissue

26
Q

Name a death ligand and a death receptor (involved in extrinsic apoptosis)

A

Ligand: TRAIL
Receptor: TRAIL-R

27
Q

What are caspases?

A

Important effector molecules of apoptosis eg caspase 3

28
Q

What are the important mediators of apoptosis?

A

Cytochrome c, APAF, caspase 9

29
Q

Give some examples of types of necrosis

A

Coagulative
Liquefactive
Fat
Caseous

30
Q

Describe coagulative necrosis

A

More protein denaturation that enzyme release
Consistency of tissue remains solid
Cell structure is somewhat preserved, leaving a “ghost outline”
Tend to be due to infarcts (not in brain)

31
Q

Describe liquefactive necrosis

A

More enzyme release than protein denaturation
Tissue becomes a viscous mass
Tissue is lysed and disappears
Tends to be due to infarction (eg in brain)
Also seen in massive neutrophil invasions

32
Q

Describe caseous necrosis

A

Tissue appears amorphous

Halfway between coagulative and liquefactive

33
Q

Describe fat necrosis

A

Occurs in cases of cell death in adipose tissue

The fatty acids released react with calcium to form chalky deposits (calcium soaps)

34
Q

What is p53?

A

Very important protein in apoptosis

Mediates apoptosis in response to DNA damage

35
Q

What is pathological calcification?

A

Abnormal deposition of calcium salts within tissues

36
Q

What is gangrene? Give types.

A

The clinical term for grossly visible necrosis

Dry or wet

37
Q

Name and briefly describe the types of pathological calcification

A

Dystrophic - occurs in areas of dying tissue. No abnormal serum calcium or calcium metabolism
Metastatic - occurs in normal tissues secondary to abnormal calcium metabolism

38
Q

Define “dry” gangrene and give an example

A

Grossly visible coagulative necrosis

An example is the umbilical cord after birth

39
Q

Give some examples of types of abnormal cellular accumulations

A

Normal cell constituents eg lipids, proteins
Abnormal substances eg minerals or abnormal metabolic bi-products
Pigments eg coal dust, bilirubin, tattoos

40
Q

Describe “wet” gangrene

A

Clinical term for grossly visible liquefactive necrosis

41
Q

What is an infarct? Name the types.

A

Necrosis due to ischaemia

Red or white infarct

42
Q

Describe white infarcts and give an example of where one could occur

A

Caused by the occlusion of an end artery
There are no peripheral blood vessels
Therefore area is left completely without blood
Eg kidney

43
Q

Describe red infarcts and give an example of where one could occur

A

Occlusion of blood vessels leads to build up of blood
All vessels haemorrhage at once
Increased pressure causes decreased blood flow
This causes ischaemia and red infarct
Eg bowel

44
Q

What are the main effects of chronic excessive alcohol intake on the liver?

A

Fatty deposits (steatosis) - reversible, can cause hepatomegaly
Hepatitis - usually reversible, jaundice, tenderness and fever
Cirrhosis - irreversible hardening and shrinking of liver, sometimes fatal, occurs in 10-15% of alcoholics

45
Q

What are the main effects of aspirin overdose?

A

Pulmonary alkalosis
Metabolic acidosis (caused by overcompensation to alkalosis)
Acute erosive gastritis

46
Q

Describe hypoxaemic hypoxia and when it could occur

A

Arterial oxygen content is low eg at high altitudes reduced inspired pO2

47
Q

Describe anaemic hypoxia and when it could occur

A

Decreased ability of haemoglobin to carry oxygen eg carbon monoxide poisoning

48
Q

Describe ischaemic hypoxia and when it could occur

A

Interruption to blood supply eg blockage of a vessel

49
Q

Describe histeocytic hypoxia and when it could occur

A

Inability to utilise oxygen due to disabled oxidative phosphorylation enzymes eg cyanide poisoning

50
Q

How could ischaemia reperfusion injury be explained?

A

Oxygen free radical production
Neutrophils causing inflammation and tissue injury
Activation of the complement pathway

51
Q

If there was TB in the lung, what is the most common type of necrosis?

A

Caseous

52
Q

What could cause liquefactive necrosis?

A

Infection which draws neutrophils, which secrete proteolytic enzymes

53
Q

What affects the colour of an infarct?

A

Colour depends on how much haemorrhaging occurred

54
Q

Where is fat necrosis most commonly seen?

A

In pancreatitis when lipases are released

ESA2 (39 decks)

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