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Pathology > Day 1- Lecture 2- Cell Injury > Flashcards

Day 1- Lecture 2- Cell Injury Flashcards

1
Q

Why might severe changes in the environment lead to physiological and morphological adaptations?

A

To attempt to remain viable- may increase or decrease level of activity

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2
Q

What does degree of cell damage depend on?

A
  • Type of injury
  • Duration of injury
  • Severity of injury
  • Type of tissue involved
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3
Q

What are the 7 causes of cell injury and death?

A
  1. Hypoxia (oxygen deprivation)- sensitivity to hypoxia/ischaemia varies between cell types e.g. Neurones only survive a few minutes without oxygen, but fibroblasts last a few hours
  2. Physical agents- e.g. Direct trauma, extremes of temperature (burns/severe cold), sudden changes in atmospheric pressure, electrical currents and radiation
  3. Chemical agents and drugs- glucose/salt in hypertonic solutions, oxygen in high concentrations, poisons, insecticides, herbicides, asbestos, alcohol, illicit drugs, therapeutic drugs
  4. Microorganisms- viruses, bacteria, fungi, other parasites
  5. Immune mechanisms
  6. Dietary insufficiency and deficiencies and dietary excess
  7. Genetic abnormalities
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4
Q

What are the mechanisms of cell injury-> the 4 components that are the principal targets for cell injury?

A
  1. Cell membranes
  2. Nucleus
  3. Proteins- structural proteins and enzymes
  4. Mitochondria
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5
Q

Describe reversible hypoxia injury

A

Leads to cell swelling, reduced cellular pH, disruption of protein synthesis

Process:
1-Ischaemia stops blood supply to a group of cells which are deprived on oxygen
2-Mitochondrial ATP production stops
3-Oxidative phosphorylation decreases so ATP decreases -> ATP driven ionic pumps are run down
4-Sodium, calcium and water enter cell
5-Glycolysis enables the cell to limp on for a while
6-The cell initiates heat shock stress response which will probably not be able to cope if hypoxia persists
7-The pH drops- increase in anaerobic respiration so the cells produce energy by glycolysis and lactic acid accumulates
8-Also… decreased protein synthesis so cannot make the proteins responsible to metabolism fats leading to lipid accumulation in the liver

Diagram in notes!

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6
Q

Describe the additional steps of prolonged hypoxia- irreversible hypoxic injury

A

It is irreversible as calcium activates lots of enzymes- it effects the cell membrane permeability, influx of calcium ions, activation and destruction of enzymes

9-Calcium enters the cell

10-Calcium activates
PHOSPHOLIPASES-> decreased phospholipids in cell membranes
PROTEASES-> damage cytoskeleton structures and attack membrane proteins
ATPASES-> reduce ATP
ENDONUCLEASES-> nuclear chromatin clumps (breakdown DNA)

11-ER and other organelles swell

12- Enzymes leak out of lysosomes and attack cytoplasmic components

13- All cell membranes are damages and start to show blebing

14- Cell dies -> possible killed by burst of bleb

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7
Q

What is ischaemia-repercussion injury? Name the 3 reasons why it may occur?

A

Blood flow is returned to a tissue which has been subject to ischaemia but is not yet necrotic- sometimes the tissue injury is worse than if the blood flow was not restored: DUE TO…

  • Increased production of oxygen free radicals with reoxygenation
  • Increased number of neutrophils following reinstatement of blood supplies, resulting in more inflammation and increased tissue injury
  • Delivery of complement proteins and activation of the complement pathways
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8
Q

Chemical injury- what is cyanide toxicity?

A

Cyanide binds to mitochondrial cytochrome oxidase and blocks oxidative phosphorylation -> leads to histocytic anaemia

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9
Q

What are free radicals?

A

Reactive oxygen species with a single unpaired electron in an outer orbit- this is an unstable configuration, and because of this, free radicals react with other molecules, often producing further free radicals

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10
Q

How are free radicals produced?

A
  • Chemical and radiation injury
  • Ischaemia-reperfusion injury
  • Cellular aging
  • High oxygen concentrations

Can be due to:

  • Normal metabolic reactions e.g. Oxidative phosphorylation (kept locked away in mitochondria)
  • Inflammation- oxidative burst of neutrophils
  • Radiation H20->OH.
  • Contact with unbound metals within the body- iron and copper (free radical damage occurs in haemochromatosis (excess iron) and Wilson’s disease (excess copper))
  • Drugs and chemicals e.g. In liver during metabolism of paracetamol or carbon tetrachloride by P450 system
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11
Q

How do free radicals injury cells?

A
  • Attack lipids in cell membranes and cause lipid peroxidation
  • Damage/oxidise proteins, carbohydrates and nucleic acids (molecules become bent/out of shape, broken or cross linked)
  • Are mutagenic (so could be carcinogenic)
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12
Q

What 3 free radicals are of particular biological significance?

A

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

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13
Q

What is the name given to the bodies defence system to prevent injury caused by free radicals?

A

Anti-oxidant system

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14
Q

When is a cell and tissue under oxidative stress?

A

When there is an imbalance between free radical production and free radical scavenging, leading to the build up of free radicals (oxidative imbalance when the free radicals overwhelms the anti-oxidant system)

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15
Q

How does the body control free radicals?

A

ENZYMES neutralise free radicals:

  • Superoxide dismutase (SOD) catalyses the reaction of superoxide to H2O2 which is significantly less toxic to cells
  • Catalase and peroxidases complete the process of free radical removal: H2O2 -> O2 + H2O

FREE RADICAL SCAVENGERS- anti-oxidant system, donate electrons to free radicals:

  • Neutralise free radicals
  • Examples: vitamins A, C, E and glutathione

METAL CARRIER AND STORAGE PROTEINS

  • Sequester transition metals in the extracellular matrix
  • Transferrin and ceruloplasmin sequester iron and copper which usually catalyse the formation of free radicals
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16
Q

How does the immune system damage the body’s cells?

A
  • Hypersensitivity reactions- host tissue is injured secondary to an overly vigorous immune reaction
  • Autoimmune reactions- immune system fails to distinguish self from non self e.g. Graves’ disease of the thyroid
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17
Q

Give some examples of heat shock proteins?

A
  • Stress proteins
  • Unfoldases
  • Chaperonins

Example: ubiquitin

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18
Q

Are heat shock proteins only triggered by heat?

A

No, they are triggered by any form of injury

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19
Q

How are heat shock proteins used by cells to protect against the effects of injury?

A

When cell is under stress, they turn down their usual protein synthesis and turn up the synthesis of Heat Shock Proteins. They are important in cell injury as the heat shock response plays a key role in maintaining protein inability and hence maximising cell survival as they mend mis-folded proteins.

Process:

  • Injury
  • Produce HSP
  • Bind to protein
  • Guide through refolding/repair process
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20
Q

What are the 3 main alterations to cells you can see under a light microscope with cell injury, by cell death and swelling/oncosis which is typical from hypoxia?

A

CYTOPLASMIC- membrane not working as well, water enters cells and causes swelling and pale cytoplasm

NUCLEAR CHANGES

  • Pyknosis: irreversible condensation of chromatin in a cell undergoing necrosis or apoptosis
  • Karyorrhexis: destructive fragmentation of the nucleus in a dying cell where it’s chromatin is distributed throughout the cytoplasm
  • Karyolysis: dissolution of cell nucleus- completely disappears

ABNORMAL INTRACELLULAR ACCUMULATIONS- proteins denatures and coagulated, clumped so picked up strongly by pink eosin stain

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21
Q

What alterations to cells can you see under an electron microscope during reversible cell injury?

A
  • Swelling: both of the cell and the organelles (e.g. Mitochondria and ER) due to Na+/K+ pump failure
  • Cytoplasmic blebs- symptomatic of cell swelling as cytoskeleton breaks down due to the proteases, so do not get the rods that hold the cells shape and the membrane becomes looser
  • Clumped nuclear chromatin- due to reduced pH
  • Ribosome separation from the endoplasmic reticulum due to the failure of energy-dependant process of maintaining ribosomes in the correct location
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22
Q

What alterations to cells can you see under an electron microscope during irreversible cell injury?

A
  • Increased cell swelling
  • Nuclear changes- pyknosis, karyolysis or karyorrhexis
  • Swelling and rupture of lysosomes- reflects membrane damage
  • Cell membrane defects
  • The appearance of myelin figures (which are damaged membranes)
  • Lysis of the endoplasmic reticulum due to membrane defects
  • Amorphous densities in swollen mitochondria
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23
Q

What is 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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24
Q

What is apoptosis?

A

Cell death with shrinkage, cell death induced by a regulated intracellular program where a cell activates enzymes that degrade its own nuclear DNA and proteins -> it is the death of a single cell or small cluster of cells, which can be a normal physiological process or it can occur when a cell is damaged, particularly when the damage affects the cell’s DNA (pathological)

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25
Q

What is necrosis?

A

In a living organism the MORPHOLOGIC changes that occur after a cell has been dead some time e.g. 4-24 hours. (Necrosis describes morphologic changes and is not a type of cell death i.e. It is an appearance and not a process)

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26
Q

When does necrosis occur and what happens?

A
  • Nerosis is seen when there is damage to cell membranes (plasma and organelle) and lysosomal enzymes are released into the cytoplasm and digest the cell
  • Cell contents leak out of cell and inflammation is often seen
  • Necrotic changes develop over a number of hours (e.g. 4-12 hours before microscopic changes seen after MI)
  • Eventually necrotic tissue is removed by enzymatic degradation and phagocytosis by white cells
  • If some remains, and calcifies it is called dystrophic calcification
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27
Q

Name the four different types of necrosis

A
  • Coagulative
  • Liquefactive
  • Caseous
  • Fat
28
Q

What is coagulative necrosis?

A

When cells are dying and the proteins of the cell denature where the architecture of dead tissue is preserved for at lead a couple of days

  • Ischaemia of solid organs (e.g. Kidney with lots of connective tissue support)
  • Protein denature- denaturing of proteins dominates over release of active proteases (denatures structural and lysosomal enzymes so blocks proteolysis of damaged cells)

Microscope appearance-

  • Clumping and cytoplasm is more pink staining (eosinphilic)
  • Cell architecture is preserved- get a ghost outline so you can still recognise what the cell was
29
Q

What is liquefactive necrosis?

A

When cells are dying and the cells proteins undergo autolysis- where the proteins undergo dissolution by the cells own enzymes

  • Ischaemia in loose tissue (e.g. Brain)
  • Presence of many neutrophils
  • Enzyme release- hydrolytic enzyme degradation is substantially greater than protein denaturation which leads to enzymatic digestion of tissues
  • Abscesses are an example of liquefactive necrosis- original tissue has been digested away by free radicals and proteases, so it means the abscess contains lots of degenerate neutrophils and intracellular bacteria

Microscope appearance:
Enzymes degrades the proteins rather than allowing coagulation- cannot recognise the cells that were there in the first place

30
Q

What is caseous necrosis?

A
  • Occurs when the bacteria causing the necrosis are covered with a thick capsule and cannot easily be broken down by neutrophils
  • Contains amorphous (structureless debris)
  • Associated with infection e.g. Tuberculosis

Microscope: some debris, some broken down cells but not the uniform ghost outline, usually have many macrophages and giant cells

31
Q

What is fat necrosis?

A

Pancreatitis- digestive enzymes leak out of pancreas into abdominal cavity and attack triglycerides (lipids)- The enzyme lipase releases fatty acids from triglyceride that react with calcium

Microscope: can see the fat cells!

32
Q

What is gangrene?

A

Not a type of necrosis- instead it is a clinical term used to describe necrosis that is visible to the naked eye

33
Q

What is the difference between dry, wet and gas gangrene?

A

Dry gangrene- Necrosis is modified by exposure to air resulting in drying (underlying process is coagulative necrosis)

Wet gangrene- Necrosis is modified by infection with mixed bacterial culture (underlying process is liquefactive necrosis)

Gas gangrene- is wet gangrene where the tissue has become infected with anaerobic bacteria that produce visible and palpable bubbles of gas within the tissues

34
Q

What is infarction and infarct>

A

This refers to a cause of necrosis- namely ischemia (reduced blood supply)

Infarction: Necrosis caused by a reduction in arterial blood flow- cause of necrosis which can result in gangrene (most common cause= embolism or thrombosis)

Infarct- an area of necrotic tissue which is the result of a loss of atherosclerosis blood supply - an area of ischaemic necrosis- could be caused by external pressure on blood vessels

ISCHAEMIA -> ISCHAEMIC NECROSIS/INFARCT -> COAGULATIVE/LIQUIFACTIVE (white or red)

35
Q

What is the different between white and red infarct?

A

White (anaemic) infarct- occurs in ‘solid’ organs (those with good stromal support) after occlusion of an ‘end’ artery (i.e. An artery that is the sole source of arterial blood to a segment of an organ) -> often wedge shaped, and associated with coagulative necrosis

Red (haemorrhagic) infarct- occurs where there is extensive haemorrhage into dead tissue, often liquefactive necrosis ->

  • Loose tissue so blood vessels are not very supported so can haemorrhage into it
  • Dual or collateral blood supply
  • Numerous anastomoses
  • Prior congestion- raised venous pressure- re-perfusion
36
Q

What does the consequence of infarction depend on?

A
  • Alternative blood supply (start off with anaemia but the body can try and bypass the blockage)
  • Speed of ischaemia
  • Tissues involved
  • Oxygen content in blood
37
Q

What are the consequences of molecules leaking out of injured cells (as their membranes loose integrity)?

A
  • They can cause local irritation and inflammation
  • They may have general toxic effects on the body (systemic)
  • They may appear in high concentrations in the blood and can be measured and thus aid diagnosis (Damage? Tissue? How bad?)
38
Q

What molecules are released from leaky membranes?

A
  • Potassium: e.g. With an MI in the heart, a lot of K+ is released
  • Enzymes: these can indicate the organ involved and the extent, timing and evolution of tissue damage (e.g. In heart can distinguish between MI and angina by troponin levels)
  • Myoglobin: this is released from dead myocardium and striated muscle
39
Q

What are the features of apoptotic cells under a light microscope?

A
  • Cells appear shrunken
  • Intensely eosinophilic
  • Chromatin condensation- pyknosis and karyorrhexis are seen and take a distinctive appearance
40
Q

What are the features of apoptotic cells under a electron microscope?

A
  • CONDENSATION OF PROTEINS WITHIN CELL: fragmentation into nucelosome size fragments- from clumps beneath nuclear membrane
  • BUDDING (not blebbing like oncosis)- progresses into FRAGMENTATION into membrane-bound APOPTOTIC BODIES which contain cytoplasms, organelles and often nuclear fragments

No leakage of cell contents occurs- no inflammation

41
Q

Is apoptosis an active or passive process?

A

Active

42
Q

Is membrane integrity maintained in apoptosis?

A

Yes- so not leaky membrane so no inflammation

43
Q

Give 3 examples of physiological apoptosis

A

1- maintaining a steady state between mitosis and apoptosis
2- hormone-controlled involution
3- embryogenesis e.g. Finger digits

44
Q

Give 3 examples of pathological apoptosis

A

1- cytotoxic T cell killing of viral of neoplastic cells
2- damaged cells particularly if the DNA is damaged
3- graft vs host disease (bone marrow cells from another person (graft) - produce new white blood cells - recognise host as being foreign)

45
Q

Outline the process of apoptosis (initiation, execution, degradation)

A
  • Triggered by intrinsic or extrinsic mechanism
  • Activates caspases which are enzymes that control and mediate apoptosis and cleave the DNA and proteins of the cytoskeleton
  • The cells shrink and break up into apoptotic bodies
  • These express proteins on their surface
  • Recognised by phagocytes or neighbouring cells
  • Degradation takes place within the phagocyte of neighbour
46
Q

Explain the intrinsic pathway leading to the activation of caspases and hence apoptosis

A

Signal comes from within the cell and trigger
-Irreparable DNA damage
-Withdrawal of growth factors or hormones
P53 protein is activates resulting in outer mitochondrial membrane to become leaky -> this causes cytochrome c to be released from the mitochondria activating caspases

47
Q

Explain the extrinsic pathway leading to the activation of caspases and hence apoptosis

A

Initiated by extracellular signals that trigger cells that are in danger (tumour/virus infected cells)
One of these signals is the TNFa (tumour necrosis factor)-
-Secreted by T killed cells
-Binds to cell membrane receptor (which initiates apoptosis)
-Results in activation of caspases

48
Q

What is the difference between oncosis and apoptosis with regards to the number of cells it affects?

A

Oncosis- affects contiguous groups of cells

Apoptosis- affects single cells

49
Q

Why do abnormal cellular accumulations occur and are they harmful?

A

Because if the cell cannot metabolise something it will remain in the cell - they often occur with sublethal or chronic injury.

They may be reversible and they an be harmless or toxic!

50
Q

What initiates abnormal cellular accumulations?

A
  • Cell’s own metabolism (
  • The extracellular space e.g. Spilled blood
  • The outer environment e.g. Dust
51
Q

What are the 5 main groups of intracellular accumulations?

A

1- Water and electrolytes e.g. Cell injury
2- Lipids: triglycerides and cholesterol -
3- Proteins e.g. Mallory hyaline, alpha-1-antitrypsin
4- Pathological ‘Pigments’- exogenous and endogenous
5- Carbohydrates

52
Q

When does fluid accumulate in cells? (Water and electrolytes)

A
  • Hydropic swelling (fluid accumulation in cells)
  • Occurs when energy supplies are cut off e.g. Hypoxia
  • Indicates severe cellular distress
  • Na+ and water flood into cell
  • Particular problem in the brain (as it sits in the skull so compression of blood vessels to vital structures - lead to cerebral oedema) and occurs with prolonged ischaemia
53
Q

When do lipids accumulate in cells?

A
  • Steatosis (accumulation of triglycerides)
  • Often seen in the liver as it is the major organ of fat metabolism
  • Mild=asymptomatic

Causes:

  • Alcohol (reversible in about 10 days)
  • Diabetes mellitus
  • Obesity
  • Toxins e.g. Carbon tetrachloride

Cholesterol:

  • Cannot be broken down and is insoluble
  • Can only be eliminated through the liver
  • Excess stored in cell in vesicles
  • Accumulates in smooth muscle cells and macrophages in atherosclerotic plaques = foam cells
  • Present in macrophages in skin and tendons of people with hereditary hyperlipidaemias (xanthomas)
54
Q

What does steatosis, atherosclerotic plaques and xanthomas look like?

A

Slide 66- Cell injury

Big fat droplets in the cells causes nuclei to be pushed to the edge

Google other two!

55
Q

What do accumulated proteins look like?

A

Seen as eosinophilic droplets or aggregations in the cytoplasm (see clumps of proteins stained in bright pink colour under electron light microscope)

56
Q

In what conditions to proteins accumulate in cells?

A

ALCOHOLIC LIVER DISEASE:
Mallory’s hyaline (damaged keratin filaments) clump together

A1- ANTITRYPSIN DEFICIENCY:

  • Liver produces incorrectly folded a1-antitrypsin protein
  • Cannot be packaged by ER, accumulates within ER and is not secreted
  • Systemic deficiency- proteases in lung act unchecked resulting in emphysema (a1-antitrypsin would usually inhibit the proteases)
57
Q

When do exogenous pigments accumulate in cells?

A
  • Carbon/coal dust/soot -> urban air pollutant
  • Inhaled and phagocytosed by alveolar macrophages
  • Leads to anthracosis (blackening of lungs) and blackened peribronchial lymph nodes (google pictures)
  • Usually harmless, unless in large amounts= fibrosis (breakdown of tissue in lungs) and emphysema as seen with coal worker’s pneumoconiosis

Tatoos- pigments pricked into skin

  • Phagocytosed by macrophages in dermis and remains there
  • Some pigments will reach draining lymph nodes
58
Q

When do endogenous pigments accumulate in cells?

A

Haemosiderin:

  • Iron storage molecule derived from haemoglobin (yellow/brown)
  • Formed when there is a local or systemic excess of iron
  • Local excess of iron = bruise
  • Systemic excess of iron= haemosiderin -> deposited in many organs this is called haemosiderosis and it is seen in haemolytic anaemias, blood transfusions and hereditary haemochromatosis
59
Q

What is hereditary haemochromatosis, and what is the symptoms and treatment?

A
  • Genetically inherited disorder- results in increased intestinal absorption of dietary iron
  • Iron is deposited in skin, liver, pancreas, heart and endocrine organs- often associated with scarring in liver (cirrhosis) and pancreas
  • Symptoms include liver damage, heart dysfunction and multiple endocrine failures, especially of the pancreas
  • Treatment- repeated bleeding
  • Appear bronzer in skin colour
60
Q

What causes jaundice?

A
  • Accumulation of bilirubin which is a breakdown product of heme (stacks of broken porphyrin rings)
  • Yellow colour
  • Formed in all cells of the body (all cells contain cytochromes which contain heme) but must be excreted in bile
  • If bile flow is obstructed or overwhelmed, bilirubin in the blood rises and jaundice results
  • Toxic- deposited extracellularly or in macrophages
61
Q

What are the mechanisms of intracellular accumulations?

A

1- Abnormal metabolism
2- Alterations in proteins folding and transport
3- Deficiency of critical enzymes
4- Inability to degrade phagocytosed particles

62
Q

What is pathological calcification?

A

Abnormal deposition of calcium salts within tissues

63
Q

What are the 2 causes of pathological calcification?

A

Dystrophic (localised) and metastatic (generalised) calcification (dystrophic is more common)

64
Q

Explain where and why dystrophic calcification occurs?

A

Where:

  • Area if dying tissue
  • In atherosclerotic plaques
  • In aging
  • Damaged heart valves
  • Tuberculous lymph nodes

Why?
There is no abnormality in the calcium metabolism, or in serum calcium or in potassium concentrations- due to a local change or disturbance in a tissue favours the nucleation of hydroxyapatite crystals which can cause organ dysfunction

65
Q

Explain what metastatic calcification is?

A

Cause: increased secretion of parathyroid hormone (PTH) resulting in bone resorption, or destruction of bone

  • It occurs body wide
  • Hydroxyapatite crystals are deposited in normal tissues throughout the body
  • This occurs when there is hypercalcaemia secondary to disturbances in calcium metabolism

Usually asymptomatic

66
Q

Describe how replicative senescence and telomeres have an effect on cellular aging?

A

Replicative senescence: after a certain number of divisions there is a decline in the cells ability to replicate due to the length of chromosomes

Telomeres: at the end of chromosomes there are telomeres, which with every replication become shorter. When telomeres reach a critical length, the cell can no longer divide.

Aging cells accumulate damage to cellular constituents and DNA

67
Q

What is telomerase?

A

Germ cells and stem cells contain an enzyme called telomerase- this maintains the original length of telomeres so that cells can continue to replicate indefinitely

Many cancer cells produce telomerase so they have the ability to replicate multiple times

Pathology (8 decks)

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