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Pathological Processes > Cell Injury and Cell Death > Flashcards

Cell Injury and Cell Death Flashcards

1
Q

What are the 7 causes of cell injury

A
  1. Hypoxia - oxygen deprivation
  2. Physical agents
  3. Chemical agents and drugs
  4. Micro-organisms
  5. Immune mechanisms
  6. Dietary insufficiency and deficiencies, and dietary excess
  7. Genetic abnormalitles
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2
Q

Describe hypoxic cell injury?

A

Draw out:

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3
Q

What parts of hypoxic injury are reversible?

A

Cell swelling

Reduced cellular pH

Disruption of protein synthesis

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4
Q

What part of hypoxic cell injury are irreversible?

A

Cell membrane permeability,

Influx of calcium ions, activation of destructive enzymes

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5
Q

Define ischaemia?

A

An inadequate blood supply to an organ or part of the body,

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6
Q

What is ischaemia- reperfusion injury?

A

Blood flow returns to a tissue which has been subject to ischaemia but isn’t necrotic.

The tissue injury that is sustained is worse than if blood flow was not restored

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7
Q

What can cause ischaemia - reperfusion injury?

A

Increased production of oxygen free radicals with reoxygenation as a result of a burst of mitochondrial activity

Increased neutrophils following reinstatement of blood supply - results in more inflamation and tissue injury

Delivery of complement proteins and activation of the complement pathway

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8
Q

What is a free radical?

A

ROS - they have a single unpaired electron in an outer orbit.

Unstable configuration so they react with other molecules and often produce more free radicals

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9
Q

Where are free radicals produced?

A

In chemical and radiation injury

Ischaemia - reperfusion injury

Cellular aging

High oxygen concentrations

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10
Q

What do free radicals do?

A

Attack lipids in cell membranes and cause lipid peroxidation

Damage proteins, carbohydrate and nucleic acids

Mutagenic

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11
Q

What free radicals are of significance in the human body?

A

OH• - hydroxyl, most dangerous

O2- superoxide

H2O2 hydrogen perioxide

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12
Q

Describe the body’s defence to prevent injury caused by free radicles?

A

The anti-oxidant system:

Consists of superoxide dismutase (SOD), Catalase and Peroxidase enzymes.

Free radical scavengers - neutralise free radicals e.g. Vitamins A, C and E and glutathione

Storage proteins which hide transition metals such as iron that catalyses the formation of free radicals

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13
Q

What are heat shock proteins?

A

Heat shock proteins are a family of proteins that are produced by cells in response to exposure to stressful conditions.

Expressed during stresses such as exposure to heat, cold, UV light, and during wound healing or tissue remodeling

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14
Q

How do heat shock proteins protect cells from injury?

Give an example

A

When submitted to stress cells turn down normal protein synthesis and turn up HSP synthesis.

HSP play an important role in cellular injury as the the heat shock response plays a key role in maintaining protein viability - maximises survial

Example - Ubiquitin

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15
Q

Describe the morphology of cellular injury via a light microscope?

A

Light microscope can identify:

Cytoplasmic, nuclear changes and abnormal intracellular accumulations

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16
Q

Describe the morphology of cell injury via an electron microscope?

A

Reversible changes:

Swelling (cell and organelles from Na/K pump failure), Cytoplasmic blebs (swelling), Clumped chromatin (reduced pH), ribosome seperation from ER

Irreversible:

Increased swelling, Nuclear changes, lysosome swelling, myeline figures from damaged membranes, lysis of ER

17
Q

Define oncosis?

A

Cell death with swelling

Refers to the spectrum of changes that occur prior to death in cells injured by hypoxia

18
Q

Define 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 protein

19
Q

Define Necrosis?

A

The morphological (form) changes present in a cell after it has been dead for some time. 4 -24 hours

Appearance not process.

20
Q

What happens in necrosis?

A

Damage to cell membranes which causes lysosomal enzymes to be released into the cytoplasm and digest cells.

This results in cell content leaking out of cells and inflamation.

Necrotic tissue is then removed by enzymatic degradation and phagocytosis by white cells

21
Q

What is dystrophic calcification?

A

Calicifed nectrotic tissue

22
Q

What is coagulative necrosis?

A

Denatured proteins coagulate as they denature

23
Q

What is liquifactive necrosis?

A

The process where proteins denature by dissolution by the cells own enzymes

24
Q

What is gangrene?

What are the two types

A

Necrosis which is visible to the naked eye

Dry gangrene - necrosis modified by exposure to air (coagulative)

Wet gangrene - necrosis modified by exposure to infection with a mixed bacterial culture (liquifactive)

Gas - wet with anaerobic bacteria that produce visible bubbles of gas

25
Q

What is a white infarct?

A

Anaemic infarct.

Occurs in solid organs after occulsion (the blockage or closing of a blood vessel or hollow organ) of an end artery (sole source of arterial blood)

26
Q

What is a red infarct?

A

Haemorrhagic infarct - occurs when there is extensive haemorrage into dead tissue

27
Q

What consequences do leaked molecules from cells have?

A

Cause local irritation and inflammation,

Toxic effects

Aid diagnosis by appearing in the blood in high concentration

28
Q

What are the principle molecules released from injured cells?

A

Potassium

Enzymes - indicates organ involved and timing

Myoglobin - released from dead myocardium and striated muscle

29
Q

What is meant by pathological calcification?

A

Abnormal deposition of calcium salts within tissues.

30
Q

What is dystrophic calcification?

A

Localised abnormal deposition of calcium salts

Occurs in an area of dying tissue, in atherosclerotic plaques, within some neoplastic growths (abnormal growth), in aging or damaged heart valves and in tuberculous lymph nodes

31
Q

What is metastatic calcification?

A

Body wide abnormal deposition of calcium salts.

Hydroxyapatite crystal are deposited in normal tissues throughout the body when there is hypercalcaemia secondary to disturbances in calcium metabolism.

Pathological Processes (3 decks)

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