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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
What causes coagulation necrosis? How and where does it appear?
Protein denaturation Ghost outline of cells with come neutrophils Ischaemia of solid organs
26
What causes liquefactive necrosis? How and where does it appear?
Enzyme release, and so enzymatic digestion No cell architecture left Ischaemia in loose tissues, and presence of many neutrophils (inflammation)
27
What is caseous necrosis? How does it appear?
``` Necrosis particularly associated with infections eg TB Structureless debris (white lumps without microscope) ```
28
What is fat necrosis? How does it appear?
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
29
What is gangrene? So what is wet gangrene, dry gangrene and gas gangrene?
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
What is infarction? Therefore what is an infarct?
Necrosis caused by reduction in arterial blood flow. So an infarct is the area of necrotic tissue caused by this.
31
Name 3 common causes of infarction
Thrombosis Embolism Testicular torsion
32
What two colours can infarcted tissue be? What causes each?
Red - haemorrhagic, liquefactive necrosis, loose tissue, dual blood supply. White - coagulation necrosis, solid organs, occlusion of an end artery, often wedge shaped.
33
What is ischaemia-reperfusion injury? Why is the damage sustained this way often worse?
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
What can the leakage of molecules out of cells with leaky membranes cause? What can they aid in?
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
Give an example of when apoptosis occurs physiologically
Embryogenesis - between fingers
36
Give an example of when apoptosis occurs pathologically
When cells are damaged - particularly with damaged DNA. | Cytotoxic T cell killing of virus-infected or neoplastic cells.
37
What does apoptosis form, and will therefore be seen under a microscope?
Apoptotic bodies.
38
What are the three stages in which apoptosis occurs?
Initiation Execution Degradation and phagocytosis
39
By what 2 mechanisms I'd the initiation and execution in apoptosis triggered?
Intrinsic and extrinsic
40
What enzymes control and mediate apoptosis, and are activated in the initiation and execution stages? What do they do?
Caspases - cause cleavage of DNA and proteins of the cytoskeleton
41
What are the 2 triggers of the intrinsic pathway in the initiation and execution stages of apoptosis?
Irreparable DNA damage | Withdrawal of growth factors or hormones
42
What happens in the intrinsic pathway of initiation and execution of apoptosis?
p53 protein activated, outer mitochondrial membrane becomes leaky, cytochrome C released from mitochondria, caspases activated
43
What is the tigger of the extrinsic pathway in initiation and execution of apoptosis?
Cells that are a danger eg tumour cells, virus-infected cells
44
What happens in the extrinsic pathway in initiation and execution of apoptosis?
TNFalpha, secreted by T killer cells, binds to cell membrane receptor, activates caspases
45
What happens in degradation and phagocytosis of apoptosis?
Apoptotic bodies express proteins on surface, recognised by phagocytes or neighbouring cells, degradation takes place within phagocyte or neighbouring cell
46
What are the 3 types of nuclear changes that can be seen in cell injury due to oncosis?
Pyknosis Karyorrhexis Karyolysis
47
Where are abnormal cellular accumulations derived from?
Cell's own metabolism Extracellular space Outer environment
48
What are the 5 main groups of intracellular accumulations?
``` Water and electrolytes Lipids Carbohydrates Proteins Pigments ```
49
When does fluid accumulate in cells?
When energy supplies are cut off eg in hypoxia (Na+ and H2O flood into cell)
50
What are the 4 causes of triglyceride accumulation in cells?
Alcohol Diabetes mellitus Obesity Toxins
51
Where is triglyceride accumulation in cells most often seen? Why?
Liver as is major organ of fat metabolism
52
Why does cholesterol build up in cells?
Cannot be broken down, and is insoluble. Can only be eliminated through the liver and excess is stored in cells in vesicles.
53
In what cells does cholesterol accumulate?
Smooth muscle cells and macrophages in atherosclerotic plaques forming foam cells. Macrophages in skin and tendons of people with hereditary hyperlipidaemia forming xanthomas.
54
What are protein accumulations seen as in cells?
Eosinophilic droplets or aggregations in the cytoplasm
55
What is Mallory' hyaline?
Protein accumulation (damaged keratin filaments) found in hepatocytes in alcoholic liver disease
56
What happens in alpha1-antitrypsin deficiency?
Liver produced incorrectly folded a1-antitrypsin protein, cannot be packed by ER, accumulated and not secreted. Leads to systematic deficiency and emphysema.
57
Give 2 examples of when exogenous pigments accumulate in cells and how they accumulate
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
Give an example of accumulation of endogenous pigments, and why it occurs
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
What causes hereditary haemochromatosis?
Genetically inherited disorder resulting in increased intestinal absorption of dietary iron
60
What are the symptoms of hereditary haemochromatosis? What is the treatment?
Liver damage, heart dysfunction, multiple endocrine failures, especially of the pancreas. Repeated bleeding.
61
What is jaundice?
Accumulation is bilirubin in blood which is then deposited in tissues extracellularly or in macrophages due to obstructed bile flow.
62
What is bilirubin?
Breakdown product of heme
63
Where is bilirubin formed and eliminated?
Formed - in all cells in the body | Eliminated - in bile. Taken from tissues by albumin to liver, conjugated and excreted in bile.
64
What are the 4 mechanism of intracellular accumulations?
Abnormal metabolism Alterations in protein folding and transport Deficiency of critical enzymes Inability to degrade phagocytosed particles
65
What is calcification of tissues?
Abnormal deposition of calcium salts within tissues
66
Is localised for general calcification of tissues more common? Where does it occur?
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
Why does localised calcification occur?
A local change in cells favours nucleation of hydroxyapatite crystals
68
Why does generalised calcification occur? What are the symptoms?
Hypercalcaemia secondary to disturbances in calcium metabolism. Hydroxyapatite crystals are deposited in normal tissues throughout the body. Usually asymptomatic but can be lethal
69
Can generalised calcification be reversed?
Can regress if cause of Hypercalcaemia is corrected
70
Give 2 causes of hypercalcaemia
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
What damage accumulates in cells as they age? What means the cell can no longer divide?
Cellular consituents DNA - telomere length shortens - when reach critical length cell can no longer divide (critical length) Lipofuscin pigment Abnormally folded proteins
72
What do germ cells, stem cells and many cancer cells contain that allows them to always continue replicating?
Telomerase

Pathological Processes (14 decks)

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