Cell Injury Flashcards by Chloe Hill

List possible causes of cell injury

Hypoxia
Toxins
Immune mechanisms
Physical agents
Microorganisms
Radiation
Free radicals

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Define disease

A consequence of failed homeostasis with morphological and functional disturbances

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What is hypoxia?

O2 deprivation

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What are 4 forms of hypoxia?

Hypoxaemic hypoxia

Anaemic hypoxia

Ischaemic hypoxia

Histiocytic hypoxia

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Describe hypoxaemic hypoxia and its causes

Low arterial content of O2

Caused by a reduced inspired PO2 at high altitude/ reduced O2 absorption in lung disease

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Describe anaemic hypoxia and its causes

Decreased ability of Haemoglobin to carry O2

Caused by anaemia or CO poisoning

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Describe ischaemic hypoxia and its causes

Interruption to the blood supply

Caused by blockage of a vessel/ heart failure

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Describe hystiocytic hypoxia and its causes

Inability to utilise O2

Caused by defective oxidative phosphorylation enzymes/ organophosphate poisoning

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What toxins can cause cell injury?

Glucose and salt in hypertonic solutions
High O2 conc.
Poisons
Pollutants
Insecticides
Herbicides
Asbestos
Alcohol
Narcotic drugs
Medicines

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How can immune mechanisms damage cells?

Hypersensitivity reactions: overly vigorous immune reaction damages host tissue

Autoimmune reactions: immune system fails to distinguish self from non-self

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Give an example of how a hypersensitivity reaction can damage cells

Urticaria (hives)

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Give an example of how autoimmune reactions damage cells

Graves’ disease

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What physical agents can damage cells?

Direct trauma
Extreme temps
Changes in pressure
Electric currents

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When does cell injury due to hypoxia go from reversible to irreversible?

If O2 is not restored

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What reversible injury can be caused by hypoxia?

Decreased O2 -> decreased oxidative phosphorylation -> decreased ATP:
Influx of Ca, H2O, Na, efflux of K, cellular swelling (oncosis), loss of microvilli, bless, ER swelling
Detachment of ribosomes from ER, decreased protein synthesis, decreased metabolism-> lipid deposition
Increased anaerobic resp-> low pH->reduced enzyme activity

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What irreversible injury can be caused by hypoxia?

Increased membrane permeability, influx of Ca so increased Cytosolic Ca:
Activates ATPases, phospholipases, proteases, endonucleases
-> damage to membrane, cytoskeletal proteins and nuclear chromatin

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What reversible structural changes occur in hypoxia cells?

Swelling 
Chromatin clumping
Autophagy
Ribosome dispersal
Blebs (bumps on membrane where cytoskeleton has detached)

What irreversible structural changes occur in hypoxic cells?

Nuclear changes
Lysosomes rupture
Membrane defects
ER lysis

What are free radicals and how do they cause cell injury?

They are reactive oxygen species that are produced in high oxygen concentrations.
Can cause an imbalance in antioxidants leading to oxidative stress. Attack proteins and carbohydrates and mutate DNA.

Why does Ischaemic-reperfusion injury occur?

If blood flow is returned to damaged (but not necrotic) tissue, damage can worsen. This is because of:
Increased free radical production with reoxygenation.
Increased neutrophils leading to inflammation and tissue injury.
Activation of complement pathway.

What are heat shock proteins?

They protect against cell injury by mending misfolded proteins and maintain cell viability to maximise cell survival.
Eg. Unfoldases, chaperonins, ubiquitin

Define oncosis

Changes that occur in injured cells prior to cell death

Define necrosis

The morphological changes that occur after cell death in living tissue

What is coagulative necrosis and when does it occur?

More protein denaturation than enzyme release.
Cellular architecture is preserved creating a ‘ghost outline’.
More likely in hard tissues, tends to be due to infarcts (but not infarct in the brain).

What is liquefactive necrosis and when does it occur?

More enzyme release than protein denaturation. Tissue is lysed and disappears. Occurs in soft tissues, tends to be due to infection (or infarction in the brain).

Name 4 types of necrosis

Coagulative Liquefactive Caseous Fat

What is caseous necrosis and when does it occur?

Halfway between coagulative and liquefactive. Tissue appears amorphous, no ghost outline. Associated with infections, especially TB.

What is fat necrosis and when does it occur?

Destruction of adipose tissue leads to release of fatty acids which form soapy deposits. Occurs when cell death occurs in adipose tissue eg. after direct trauma to fatty tissues.

What is gangrene?

Grossly visible necrosis

What are the differences between dry and wet gangrene?

Dry = coagulative, modified by exposure to air, bacteria cannot grow Wet = liquefactive, infection with bacteria, causes increased neutrophils and proteolytic enzymes, can leak into blood vessels and cause septicaemia.

What is gas gangrene?

A type of wet gangrene where bacteria respired anaerobically, causing bubbles under the skin.

What is infarction?

Necrosis due to ischaemia

When does a White infarct occur?

When there is occlusion of an end artery with no peripheral vessels, meaning the area is not reperfused and left entirely without blood.

In what tissues does white infarct occur?

Kidney | Spleen

When does a red infarct occur?

Occlusion of an artery to a tissue with a dual blood supply. The tissue is reperfused leading to a build up of blood, which haemorrhages at once. Increased pressure decreases the blood flow leading to ischaemia and infarct.

In what tissues does red infarct occur?

Bowel | Brain

Define apoptosis

Programmed cell death

Give a physiological example of apoptosis

During embryonic development. | Cytotoxic T cells killing virally infected cells.

Give a pathological example of apoptosis

Toxic injury/ Tumours causing DNA damage. | Foreign cells attacking host cells eg. after bone marrow transplant.

What are the three phases of apoptosis?

Initiation Execution Degradation and phagocytosis

What structural changes occur during apoptosis?

DNA damage leads to activation of mitochondrial caspases. | Chromatin condenses, fragmentation of nucleus, binds to form apoptic bodies, removed by phagocytes/nearby cells.

List differences between oncosis/necrosis and apoptosis

Oncosis/necrosis: Continuous group of cells Cells are enlarged (swelling) Nucleus undergoes pyknosis, karyorrhexis & karyolysis Plasma membrane is disrupted and lysed early Cellular content undergoes enzymatic digestion Adjacent inflammation is frequent Always pathological. Apoptosis: Single cells Cell size is reduced (shrinkage) Nucleus fragments into nucleosome size Plasma membrane remains intact but with altered structure Cellular content remains intact, may be released in apoptotic bodies No adjacent inflammation Often physiological (can be pathological)