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Pathological Processes > 2. Cell Injury > Flashcards

2. Cell Injury Flashcards

1
Q

What can severe changes in environment lead to in a cel?

A

From homeostasis, cellular adaptation, cellular injury to cell death

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2
Q

What 3 things does the degree of injury depend on?

A

Type of injury
Severity of injury
Type of tissue

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3
Q

Give 4 examples of things that can cause cell injury

A

Hypoxia
Toxins
Physical agents
Radiation

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4
Q

What is hypoxia? What is ischaemia?

A

Hypoxia - decreased O2 supply

Ischaemia - decreased blood supply (therefore lack of O2 but also other nutrients_

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5
Q

What is the cause of hypoxaemic hypoxia?

A

Arterial content of oxygen is low

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6
Q

What is the cause of anaemic hypoxia?

A

Decreased ability of haemoglobin to carry oxygen

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7
Q

What is the cause of ischaemic hypoxia?

A

Interruption of blood supply

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8
Q

What is the cause of histiocytic hypoxia?

A

Inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes

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9
Q

In what 2 ways does the immune system damage the body’s own cells?

A 
Hypersensitivity reactions (host tissue injured secondary to overly vigorous immune reaction).
Autoimmune reactions (immune system fails to distinguish self from non-self).
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10
Q

What 4 cell components are most susceptible to injury?

A

Membranes
Nucleus
Proteins
Mitochondria

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11
Q

What happens at a molecular level in hypoxia?

A

Ischemia - lack of O2, oxidative phosphorylation stops, anaerobic respiration producing lactic acid, damages chromatin. Lack of ATP affects protein channels, so influx of Ca2+, H2O, Na+, cell swelling. Ribsosomes stuck to ER is active process, so decreased protein synthesis and fat metabolism, fat accumulates.

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12
Q

What has the biggest effect cellularly in prolonged hypoxia? Is it reversible or irreversible?

A

Increased cytosolic Ca2+ - affects ATPase, phospholipase, protease and endonuclease.
Irreversible.

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13
Q

What are free radicals?

A

Single unpaired electron in an outer orbit, so is therefore a reactive oxygen species

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14
Q

What are the 3 main free radicals?

A

Hydroxyl
Superoxide
Hydrogen peroxide

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15
Q

Give 5 ways in which free radicals are produced, and an example of each

A

Normal metabolic reactions - oxidative phosphorylation
Inflammation - oxidative burst
Radiation - break down of water
Contact with unbound metals in the body - eg iron in haemachromatosis
Drugs and chemicals - eg paracetamol metabolism in the liver

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16
Q

Give 3 ways in which the body normally controls free radicals

A

Anti-oxidant system - vitamins A, C and E
Metal carrier and storage proteins - sequester iron
Enzymes neutralise free radicals - catalase

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17
Q

What part of the cell do free radicals injure primarily? What do they cause?

A

Lipids in cell membrane. Cause lipid peroxidation, leading to autolytic chain reaction

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18
Q

What do heat shock proteins aim to do?

A

Mend mis-folded proteins and maintain cell viability. Eg ubiquitin.

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19
Q

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

A

Cytoplasmic changes - picks up more pin eosin stringing as proteins denature.
Nuclear changes.
Abnormal cellular accumulations.

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20
Q

What do injured and dying cells look like under an electron microscope in hypoxia (in both reversible and irreversible injury)?

A

Blebs.
Swelling of cell and organelles.
Clumping of DNA, or complete breakdown.
Lysis of membrane and organelles.

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21
Q

What can cell death be diagnosed?

A

Put cells in fluid with fluorescence - dye enters cells with broken membrane (dead cells)

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22
Q

What is the definition of oncosis?

A

Cell death with swelling, the spectrum of changes that occur prior to death in cells injured by hypoxia and some other agents

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23
Q

What is the definition of apoptosis?

A

Cell death with shrinkage, induced by a regulated intracellular program where a cell activates enzymes that degrade its own nuclear DNA and proteins. Non-random, internucleosomal cleavage of DNA

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24
Q

What is the definition of necrosis?

A

In a living organism the morphological changes that occur after a cell has been dead some time (not a type of cell death)

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25
Q

What causes coagulation necrosis? How and where does it appear?

A

Protein denaturation
Ghost outline of cells with come neutrophils
Ischaemia of solid organs

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26
Q

What causes liquefactive necrosis? How and where does it appear?

A

Enzyme release, and so enzymatic digestion
No cell architecture left
Ischaemia in loose tissues, and presence of many neutrophils (inflammation)

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27
Q

What is caseous necrosis? How does it appear?

A 
Necrosis particularly associated with infections eg TB
Structureless debris (white lumps without microscope)
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28
Q

What is fat necrosis? How does it appear?

A

Caused by action of digestive enzymes on fat
Forms hard lump
Soaps appear as chalky white deposits, and lots of fat is seen under a microscope

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29
Q

What is gangrene? So what is wet gangrene, dry gangrene and gas gangrene?

A

Necrosis visible to the naked eye.
Wet - necrosis modified by infections (liquefactive necrosis).
Dry - necrosis modified by exposure to air (coagulation necrosis).
Gas - wet gangrene where the infection is with anaerobic bacteria that produce gas.

30
Q

What is infarction? Therefore what is an infarct?

A

Necrosis caused by reduction in arterial blood flow. So an infarct is the area of necrotic tissue caused by this.

31
Q

Name 3 common causes of infarction

A

Thrombosis
Embolism
Testicular torsion

32
Q

What two colours can infarcted tissue be? What causes each?

A

Red - haemorrhagic, liquefactive necrosis, loose tissue, dual blood supply.
White - coagulation necrosis, solid organs, occlusion of an end artery, often wedge shaped.

33
Q

What is ischaemia-reperfusion injury? Why is the damage sustained this way often worse?

A

Blood flow returned to damaged but not yet necrotic tissue.
Worse due to - increased production of oxygen free radicals, increased number of neutrophils so more inflammation and injury, delivery of complement proteins and so activation of complement pathway.

34
Q

What can the leakage of molecules out of cells with leaky membranes cause? What can they aid in?

A

Local inflammation
General toxic effects on the body eg K+ causing MI
Aid diagnosis as may appear in high concern in blood (specific enzymes and proteins to the tissue type) eg myoglobin in rhabdomyolisis

35
Q

Give an example of when apoptosis occurs physiologically

A

Embryogenesis - between fingers

36
Q

Give an example of when apoptosis occurs pathologically

A

When cells are damaged - particularly with damaged DNA.

Cytotoxic T cell killing of virus-infected or neoplastic cells.

37
Q

What does apoptosis form, and will therefore be seen under a microscope?

A

Apoptotic bodies.

38
Q

What are the three stages in which apoptosis occurs?

A

Initiation
Execution
Degradation and phagocytosis

39
Q

By what 2 mechanisms I’d the initiation and execution in apoptosis triggered?

A

Intrinsic and extrinsic

40
Q

What enzymes control and mediate apoptosis, and are activated in the initiation and execution stages? What do they do?

A

Caspases - cause cleavage of DNA and proteins of the cytoskeleton

41
Q

What are the 2 triggers of the intrinsic pathway in the initiation and execution stages of apoptosis?

A

Irreparable DNA damage

Withdrawal of growth factors or hormones

42
Q

What happens in the intrinsic pathway of initiation and execution of apoptosis?

A

p53 protein activated, outer mitochondrial membrane becomes leaky, cytochrome C released from mitochondria, caspases activated

43
Q

What is the tigger of the extrinsic pathway in initiation and execution of apoptosis?

A

Cells that are a danger eg tumour cells, virus-infected cells

44
Q

What happens in the extrinsic pathway in initiation and execution of apoptosis?

A

TNFalpha, secreted by T killer cells, binds to cell membrane receptor, activates caspases

45
Q

What happens in degradation and phagocytosis of apoptosis?

A

Apoptotic bodies express proteins on surface, recognised by phagocytes or neighbouring cells, degradation takes place within phagocyte or neighbouring cell

46
Q

What are the 3 types of nuclear changes that can be seen in cell injury due to oncosis?

A

Pyknosis
Karyorrhexis
Karyolysis

47
Q

Where are abnormal cellular accumulations derived from?

A

Cell’s own metabolism
Extracellular space
Outer environment

48
Q

What are the 5 main groups of intracellular accumulations?

A 
Water and electrolytes
Lipids
Carbohydrates
Proteins
Pigments
49
Q

When does fluid accumulate in cells?

A

When energy supplies are cut off eg in hypoxia (Na+ and H2O flood into cell)

50
Q

What are the 4 causes of triglyceride accumulation in cells?

A

Alcohol
Diabetes mellitus
Obesity
Toxins

51
Q

Where is triglyceride accumulation in cells most often seen? Why?

A

Liver as is major organ of fat metabolism

52
Q

Why does cholesterol build up in cells?

A

Cannot be broken down, and is insoluble. Can only be eliminated through the liver and excess is stored in cells in vesicles.

53
Q

In what cells does cholesterol accumulate?

A

Smooth muscle cells and macrophages in atherosclerotic plaques forming foam cells.
Macrophages in skin and tendons of people with hereditary hyperlipidaemia forming xanthomas.

54
Q

What are protein accumulations seen as in cells?

A

Eosinophilic droplets or aggregations in the cytoplasm

55
Q

What is Mallory’ hyaline?

A

Protein accumulation (damaged keratin filaments) found in hepatocytes in alcoholic liver disease

56
Q

What happens in alpha1-antitrypsin deficiency?

A

Liver produced incorrectly folded a1-antitrypsin protein, cannot be packed by ER, accumulated and not secreted. Leads to systematic deficiency and emphysema.

57
Q

Give 2 examples of when exogenous pigments accumulate in cells and how they accumulate

A

Carbon/coal dust/soot - inhaled and phagocytosed by alveolar macrophages leading to anthracnose and blackened peribronchial lymph nodes. In large amounts causes fibrosis and emphysema.
Tattooing - pigments pricked into skin, phagocytosed by macrophages in dermis, remains there, some reaches draining lymph nodes.

58
Q

Give an example of accumulation of endogenous pigments, and why it occurs

A

Haemosiderin - iron storage molecules, derived from haemoglobin in systemic or local excess of iron eg bruise. Can be deposited in organs (haemosiderosis) in systematic overload of iron eg hereditary haemochromatosis.

59
Q

What causes hereditary haemochromatosis?

A

Genetically inherited disorder resulting in increased intestinal absorption of dietary iron

60
Q

What are the symptoms of hereditary haemochromatosis? What is the treatment?

A

Liver damage, heart dysfunction, multiple endocrine failures, especially of the pancreas.
Repeated bleeding.

61
Q

What is jaundice?

A

Accumulation is bilirubin in blood which is then deposited in tissues extracellularly or in macrophages due to obstructed bile flow.

62
Q

What is bilirubin?

A

Breakdown product of heme

63
Q

Where is bilirubin formed and eliminated?

A

Formed - in all cells in the body

Eliminated - in bile. Taken from tissues by albumin to liver, conjugated and excreted in bile.

64
Q

What are the 4 mechanism of intracellular accumulations?

A

Abnormal metabolism
Alterations in protein folding and transport
Deficiency of critical enzymes
Inability to degrade phagocytosed particles

65
Q

What is calcification of tissues?

A

Abnormal deposition of calcium salts within tissues

66
Q

Is localised for general calcification of tissues more common? Where does it occur?

A

Local more common.
Occurs in area of dying tissue, atherosclerotic plaques, aging or damaged heart valves, tuberculus lymph nodes, some malignancies, can cause organ dysfunction

67
Q

Why does localised calcification occur?

A

A local change in cells favours nucleation of hydroxyapatite crystals

68
Q

Why does generalised calcification occur? What are the symptoms?

A

Hypercalcaemia secondary to disturbances in calcium metabolism. Hydroxyapatite crystals are deposited in normal tissues throughout the body. Usually asymptomatic but can be lethal

69
Q

Can generalised calcification be reversed?

A

Can regress if cause of Hypercalcaemia is corrected

70
Q

Give 2 causes of hypercalcaemia

A

Increased secretion of parathyroid hormone resulting in bone reabsorption eg due to parathyroid hyperplasia or tumour.
Destruction of bone tissue eg primary tumours of bone marrow such as leukaemia.

71
Q

What damage accumulates in cells as they age? What means the cell can no longer divide?

A

Cellular consituents
DNA - telomere length shortens - when reach critical length cell can no longer divide (critical length)
Lipofuscin pigment
Abnormally folded proteins

72
Q

What do germ cells, stem cells and many cancer cells contain that allows them to always continue replicating?

A

Telomerase

Pathological Processes (14 decks)

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