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ESA2 - Pathological Processes > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What kinds of things can cause cell injury?

A

Hypoxia, toxins, physical agents eg trauma, radiation, micro-organisms, immune mechanisms, dietry insufficiency

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2
Q

What is the difference between hypoxia and ischaemia?

A 
Hypoxia = decreased oxygen supply
Ischaemia = decreased blood supply (often worse)
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3
Q

What is hypoxaemic hypoxia?

A

Arterial oxygen content is low

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4
Q

What could cause hypoxaemic hypoxia?

A

Reduced inspired p02 eg at high altitude

Reuced absorption secondary to lung disease

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5
Q

What is anaemic hypoxia?

A

Decreased ability of haemoglobin to carry oxygen

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6
Q

What could cause anaemic hypoxia?

A

Anaemia, carbon monoxide poisoning

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7
Q

What is ischaemic hypoxia caused by?

A

Interruption to blood supply - blockage of a vessel, heart failure

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8
Q

What is histiocytic hypoxia?

A

Inability to utilise oxygen in cells due to diabled oxidative phosphorylation enzymes - caused by cyanide poisoning

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9
Q

In what ways could the immune system damage cells?

A

Hypersensitivity reactions, autoimmune reactions

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10
Q

What happens at a molecular level in hypoxia?

A

Lack of oxygen - decreased production of ATP - decreased action of sodium pump - influx of Ca2+ - increased production of lactic acid - detachment of ribosomes

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11
Q

What are some enzymes that are activated by calcium?

A

ATPase (decreased ATP)
Phospholipase (decreased phospholipids)
Protease (disruption of membrane and cytoskeleton)
Endonuclease (nuclear chromatin damage)

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12
Q

What are free radicals?

A

Reactive oxygen species - singled unpaired electron in an outer orbit which is an unstable conformation so they react with other molecules often producing more free radicals

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13
Q

What are the 3 free radicals that are of particular biological importance?

A

OH. (hydroxyl) - the most dangerous
O2- (superoxide)
H2O2 (hydrogen peroxide)

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14
Q

How are free radicals produced?

A

Normal metabolic reactions eg oxidative phosphorylation, inflammation, radiation, contact with unbound metals in the body, drugs and chemicals in the liver during metabolism

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15
Q

What are some enzymes that neutralise free radicals?

A

Superoxide dismutase, catalase, glutathione peroxidase

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16
Q

How does the body control free radicals?

A

Antioxidant system - donate electrons to free radical (vitamins A, C and E)

Metal carrier and storage proteins (transferrin and ceruloplasmin for iron and copper)

Enzymes

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17
Q

How do free radicals injure cells?

A

Cause oxidative imbalance
Target cell membranes causing lipid peroxidation which leads to the generation of more free radicals
Also oxidise proteins, carbohydrates and DNA

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18
Q

What do heat shock proteins do?

A

Facilitate the synthesis and folding of proteins

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19
Q

What is an example of a heat shock protein?

A

Ubiquitin

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20
Q

What do injured and dying cells look like under a microscope?

A

In hypoxia:

Cytoplasmic changes, nuclear changes, abnormal cellular accumulations

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21
Q

What are blebs due to?

A

Cytoskeleton being broken down by proteases - no longer held in place

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22
Q

How do we diagnose cell death?

A

Test cell function - put cells in fluid that has dye in, if dye gets taken up then membrane is damaged meaning cells with dye in are dead

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23
Q

What is the difference between oncosis and necrosis?

A

Oncosis = cell death with swelling, the spectrum of changes that occur in injured cells prior to death

Necrosis = the morphological changes that occur after a cell has been dead some time (seen after 12-24 hours)

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24
Q

What are the two main types of cell necrosis?

A

Coagulative and liquefactive

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25
Q

What is coagulative necrosis?

A

Ischaemia of solid organs (organs with a lot of connective tissue support eg kidney)

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26
Q

What is liquefactive necrosis?

A

Ischaemia in loose tissues, involves the presence of many neutrophils (eg the brain - not much connective tissue, often caused by inflammation/bacteria/infection)

Cell death in the brain due to hypoxia leads to liquefactive necrosis

27
Q

What does coagulative necrosis look like microscopically?

A

Cellular architecture is somewhat preserved - “ghost outline” of cells.

Lighter staining due to digested nuclei which no longer show up as dark purple when stained with hematoxylin, and removed cytoplasmic structures giving reduced amounts of intracellular protein, reducing the usual dark pink staining cytoplasm with eosin.

28
Q

What happens in liquefactive necrosis?

A

the affected cell is completely digested by hydrolytic enzymes, resulting in a soft, circumscribed lesion consisting of pus and the fluid remains of necrotic tissue

29
Q

What is caseous necrosis characteristic of?

A

Associated with TB

Contains structureless debris

30
Q

What is gangrene?

A

Necrosis visible to the naked eye

31
Q

What is infarction?

A

Necrosis caused by reduction in arterial blood flow

32
Q

What is the difference between dry gangrene and wet gangrene?

A 
Dry = necrosis modified by exposure to air
Wet = necrosis modified by infection
33
Q

What is gas gangrene?

A

Wet gangrene where the infection is with anaerobic bacteria that produce gas - often found in soil

34
Q

What are the commonest causes of infarction?

A

(Necrosis caused by ischaemia)

Thrombosis, embolism

35
Q

Why are some infarcts white?

A

Solid organs, occlusion of an end artery (kidney, heart, spleen)
Often wedge-shaped
Coagulative necrosis

(No blood in something = white)

36
Q

Why are some infarcts red?

A

Loose tissue, dual blood supply

Complicated by haemorrhage

37
Q

What is ischaemia-repurfusion injury?

A

If blood flow is returned to a damaged but not yet necrotic tissue, damage can be worse than if blood flow was not returned

38
Q

What are some possible causes of ischaemia-repurfusion injury?

A

Increased production of free radicals, increased number of neutrophils, delivery of complement proteins

39
Q

What important things can leak out of cells?

A

Potassium (eg can have cardiac arrest secondary to severe burns as potassium leaks out)

Enzymes (can differentiate angina and MI)

Myoglobin (damage to skeletal muscle - blocks glomelurus in kidney and cause renal failure)

40
Q

What is apoptosis?

A

Cell death with shrinkage - induced by a regulated intracellular program where the cell activates enzymes that degrades its own nuclear DNA and proteins

41
Q

Are lysosomal enzymes involved in apoptosis?

A

No

42
Q

When does apoptosis occur physiologically?

A

In order to maintain a steady state, hormone-controlled involution, embryogenesis

43
Q

When does apoptosis occur pathologically?

A

Cytotoxic T cell killing of virus infected or neoplastic cells, when cells are damage, graft vs host disease

44
Q

What does apoptosis look like?

A

Cell shrinkage, chromatin gets broken down into regular sized clumps, budding, formation of apoptopic bodies

45
Q

What are the 3 phases of apoptosis?

A

Initiation, execution, degradation & phagocytosis

46
Q

What enzymes are activates in the initiation of apoptosis?

A

Caspases - cause cleavage of DNA and proteins of the cytoskeleton

47
Q

How is the intrinsic pathway initiated?

A

Signals that come from within the cell, p53 activation resulting in the outer mitochondrial membrane becoming leaky and the release of cytochrome C to activate caspases

48
Q

What can trigger the intrinsic pathway of apoptosis?

A

Irreparable DNA damage, withdrawal of growth factors

49
Q

What can trigger the extrinsic pathway of apoptosis?

A

Cells that are in danger eg tumour cells, virus infected cells

TNFa secreted by T killer cells that binds to death receptor and results in activation of caspases

50
Q

Why are the apoptopic bodies phagocytosed?

A

Express proteins on their surface that can now be recognised by phagocytes or neighbouring cells

51
Q

What kind of things can accumulate in cells?

A

Water/electrolytes, lipids, carbohydrates, proteins, pigments

52
Q

When does fluid accumulate in cells?

A

Hydropic swelling occurs when energy supplies are cut off - Na+ and water flood into cell

53
Q

Why is fluid accumulation in the brain a problem?

A

Encased by skull so when it swells it has no where to go. There is increased pressure and the brain becomes compressed against the skull

54
Q

What is steatosis?

A

Accumulation of triglycerides

55
Q

What can cause liver steatosis?

A

Alcohol, diabetes mellitus, obesity, toxins eg carbon tetrachloride

56
Q

When do lipids accumulate in cells?

A

Cholesterol cannot be broken down and is insoluble, can only be eliminated in liver, excess stored in cell in vesicles
It accumulates in smooth muscle cells and macrophages in atherosclerotic plaques (foam cells)

57
Q

What happens in a1-antitrypsin deficiency?

A

Liver produces incorrectly folded version of the protein which cannot be packaged by ER so accumulates. It inhibits proteases so deficiency means that proteases can act unchecked in body eg results in emphysema in lung

58
Q

What is hereditary haemochromatosis?

A

Genetically inherited diseorder resulting in increased intestinal absorption of dietry iron

59
Q

What accumulates in jaundice?

A

Bilirubin - breakdown product of heme, stacks of broken porphyrin rings

60
Q

Why does dystrophic calcification occur?

A

No abnormality in calcium metabolism, or serum calcium or phosphate concentrations

Local change favours nucleation of hydroxyapatite crystals

Can cause organ dysfunction eg atherosclerosis, calcified heart valves

61
Q

Why does metastatic calcification occur?

A

Due to hypercalcaemia secondary to disturbances in calcium metabolism

Hydroxyapatite crystals are deposited in normal tissues throughout the body

62
Q

What can cause hypercalcemia?

A

Increased secretion of PTH resulting in bone resoprtion, destruction of bone tissue

63
Q

What do germ cells and stem cells contain that maintains the original length of telomeres?

A

Telomerase

ESA2 - Pathological Processes (9 decks)

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