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ESA 2 Revision > Mechanisms of Disease > Flashcards

Mechanisms of Disease Flashcards

0
Q

What is hypoxia?

A

Oxygen deprivation

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1
Q

What are diseases the result of?

A

Intrinsic/ genetic abnormalities

External/acquired factors

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2
Q

How tolerant are cells to hypoxia?

A

It depends on the cell type
Some neurones can only tolerate a few minutes
Dermal fibroblasts can tolerate a number of hours

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3
Q

What is ischaemia?

A

Loss of blood supply due to reduced arterial supply or venous drainage

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4
Q

What are the 4 causes of hypoxia?

A

Hypoxaemic: arterial content of oxygen is low, high altitude etc
Anaemic: decreased ability of Hb to carry oxygen
Ischaemic: interruption of blood supply
Histiocytic: inability to use oxygen in cells due to disabled oxidative phosphorylation enzymes

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5
Q

Name some physical agents which cause cell injury

A

Extremes of temperature, direct trauma, electrical currents, radiation, sudden changes in atmospheric pressure

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6
Q

What are some chemical agents and drugs which can cause cell injury?

A 
Glucose or salt in hypertonic solution
High oxygen conc
Alcohol
Poisons
Insecticides
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7
Q

Give 4 causes of cell injury

A

Microorganisms
Hypersensitivity/ autoimmune disorders
Dietary deficiencies and excess
Genetic abnormalities

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8
Q

What are the four principal targets of cell injury?

A

Cell membranes
Nucleus
Mitochondria
Proteins

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9
Q

Describe the events which occur in reversible hypoxic injury

A

Levels of ATP drop due to reduced oxidative phosphorylation
Sodium potassium pump fails, sodium builds up inside the cell, organelles swell up. Calcium also comes in damaging cell components
Cell switches to glycolytic pathway, produces lactic acid, reducing the pH, affecting enzyme activity, causes chromatin clumping
Ribosomes detach from ER, disrupts protein synthesis, intracellular accumulations of denatured proteins and fat

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10
Q

How does irreversible hypoxic injury usually appear?

A

Necrosis

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11
Q

Describe the key event in irreversible hypoxic injury?

A

Disturbances in membrane activity, rise in cytosolic calcium, this activates ATPases, proteases, endonucleases
Lysosomal enzymes are released
Intracellular substances leak out into blood, eg transaminases

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12
Q

What is ischaemia reperfusion injury?

A

Blood flow returned to a tissue that has been subject of ischaemia but is not yet necrotic
Sometimes makes injury worse
Potentially free radicals, lots of neutrophils, complement activation

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13
Q

How can free radicals damage cells?

A

Lipid peroxidation
Damage proteins and nucleic acids
Mutagenic

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14
Q

How are hydroxyl radicals formed?

A

Radiation directly lyses water

Fenton and Haber Weiss reactions

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15
Q

What is the fenton reaction?

A

Iron and hydrogen peroxide make hydroxyl radicals

16
Q

What is the Haber Weiss reaction?

A

H+ and superoxide and hydrogen peroxide

Oxygen, water and hydroxyl radicals

17
Q

What is oxidative stress?

A

An imbalance between ROS production and free radical scavenging

18
Q

What makes up the anti oxidant system?

A

Enzymes such as SOD, catalase, peroxidases
Vitamins A, C, E
Storage proteins like transferrin sequester transition metals which catalyse free radical formation

19
Q

What is the role of heat shock proteins?

A

They refold proteins which are denatured

20
Q

What are the three main alterations that can be seen under a light microscope in cell injury?

A

Cytoplasmic changes
Nuclear changes
Abnormal intracellular accumulations

21
Q

What are the reversible changes seen under a light microscope with cell injury?

A

Reduced pink staining initially due to accumulation of water

Subtle clumping of chromatin

22
Q

Irreversible changes seen under a light microscope with cell injury

A

Later more pink staining of the cell due to detached ribosomes and denatured proteins
Pyknosis (shrinkage), karryolysis (dissolution), karryohexis (fragmentation) of the nucleus

23
Q

What is oncosis?

A

The spectrum of changes that occur in an injured cell prior to death

24
Q

What is necrosis?

A

The morphological changes which occur after cell death in a living tissue, largely due to the progressively degradative action of enzymes

25
Q

Apoptosis

A

Programmed cell death induced by a regulated intracellular program where a cell activates enzymes which degrades its own nuclear DNA and protein

ESA 2 Revision (4 decks)

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