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Year 1 - Pathological Processes > Session 1 - Cellular Injury > Flashcards

Session 1 - Cellular Injury Flashcards

1
Q

What are the agents that can injure a cell? (There are 7 altogether)

A
  • Hypoxaemic - which can be split into anaemia, hypoxaemic, iscahemic and histiocytic
  • Physical agents
  • Chemical agents
  • Genetic abnormalities
  • Dietary insufficiency
  • Immune mechanisms
  • Microorganisms
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2
Q

What are the cellular components that can become injured?

A
  • cell membranes
  • nucleus
  • protein
  • mitochondria
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3
Q

What ion causes the swelling of the cell in a hypoxic state and why?

A

Sodium will seep into the cell. This is because in a hypoxic state the cell cannot produce ATP adequately and therefore the ATP driven membrane channels cannot function properly.

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4
Q

When the cell starts to swell, the cell will initiate a stress repsonse. What is this?

A

The translation of regular cellular proteins will be downregulated and the translation of heat shock proteins will be upregulated.

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5
Q

In a cell that has been injured, what does calcium activate?

A
  1. Phospholipases - causing the cell to lose phospholipid from its membrane
  2. Proteases - damaging cytoskeletal structures and attacking membrane proteins
  3. ATPase - causing a loss of more ATP
  4. Endonucleases - this is what causes the nuclear chromatin to clump
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6
Q

What is ischaemia-reperfusion injury?

A

This is where when the cell has been subjected to ischaemia for a prolonged periof of time but isn’t yet necrotic - this is when upon perfusion the tissue injury sustained is worse than if it wasn’t reperfused at all.

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7
Q

What causes ischaemia-reperfusion injury?

A
  1. The production of oxygen free radicals upon reoxygenation.
  2. The increase in neutrophils reaching the area causes an inflammatory response and increased tissue injury
  3. Delivery of complement proteins and activation of the complement pathway
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8
Q

Give an example of 3 enzymes hat make up the anti-oxidant system?

A
  1. superoxide dismutase
  2. catalase
  3. peroxidases
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9
Q

Give an example of 4 free radical scavengers

A
  1. Glutathione
  2. Vitamin A
  3. Vitamin C
  4. Vitamin E
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10
Q

Give 2 examples of storage proteins and why they can cause damage?

A

Transferrin and ceruloplasmin. They can cause damage because they will sequester iron and copper and this can cause the catalysation of free radical formation.

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11
Q

What are the role of heat shock proteins?

A

They improve protein viability and maximise cellular survival.

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12
Q

What three main cellular alterations (occuring as a result of cellular injury) can be seen under a light microscope?

A
  • Cytoplasmic
  • Nuclear
  • Abnormal intracellular accumulations
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13
Q

What are some examples of reversible changes that occur when a cell is injured?

A
  • Swelling - of both the cells and organelles due to sodium potassium pump fialure
  • Cytoplasmic blebs
  • Clumped chromatin due to the reduced pH.
  • Ribosome separation from the ER.
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14
Q

What are some examples of cellular changes that occur in irreversible cellular damage?

A
  • Nuclear changes - pyknosis, karyorrhexis and karyolysis
  • Swelling and rupture of ribosomes
  • membrane defects
  • appearance of myelin figures
  • lysis of ER due to the membrane defects
  • amorphous densities in the swollen mitochondria
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15
Q

What is oncosis?

A

This is the spectrum of changes that the cell undergoes prior to death.

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16
Q

What is apoptosis?

A

This is cellular death with shrinkage. It is induced by a regulated intracellular program where a cell activates enzymes that degrade its own nuclear DNA and proteins.

17
Q

What is necrosis?

A

These are morphologic changes that occur AFTER a cell has been dead for some time (4-24 hours). It is an appearance not a process.

18
Q

What is dystrophic calcification?

A

This is where tissues become abnormally calcified in one area. This can occur in an area of dying tissue, atherosclerotic plaques, neoplasms (somteimes), ageing or damaged heart valves, and tuberculous lymph nodes.

19
Q

What are the four different types of necrosis?

A
  1. Coagulative
  2. Liquifactive
  3. Caseous
  4. Fat
20
Q

What is gangrene? How can it be further classified?

A

It is a clinical term used to describe necrosis that is visible to the naked eye. It can be further classified into dry and wet gangrene.

21
Q

What is dry gangrene?

A

This is where the necrosis is modified when exposed to air resulting in drying.

22
Q

What is wet gangrene?

A

This is where the gangrene is modified through exposure by an infection or with a mixed bacterial culture.

23
Q

What is gas gangrene?

A

A type of wet gangrene where the tissue has come infected with anaerobic bacteria and produce visible and palpable bubbles of gas within the tissues.

24
Q

What is an infarction?

A

This is a CAUSE of necrosis. It is an obstruction of blood supply to an organ or tissue causing death of that tissue.

Note: This is different to ischaemia which by definition is just a reduced blood supply. Ischaemia can LEAD to infarction.

25
Q

Where does a white infarct occur? Why do they occur?

A

They occur in solid organs - this means organs that have a good stromal support. This is a result of occlusion of an end artery.

26
Q

What is a red infarct? How come they occur?

A

This is something that usually happens in ‘soft’ tissues (tissues with a lack of stromal support). It is due to the occlusion of veins or occlusion of an artery with a dual blood supply. This will result with red blood cells entering the ischaemic area.

27
Q

What are some of the common locations of a red infarct?

A
  • Brain
  • Lungs
  • Gastrointestinal tract
  • Liver
28
Q

Where do white infarcts commonly occur?

A
  • Heart
  • Kidney
  • Spleen
29
Q

What is metastatic calcification?

A

This is where hydroxyapatite crystals are deposited in normal tissues throughout the body due to hypercalcaemia secondary to disturbances in calcium metabolism. Usually asymptomatic but can be lethal.

30
Q

What is replicative senescence?

A

This is the declined ability for the body to be able to replicate its DNA. This is related to telomere length and once they are at a critical length they can no longer divide.

31
Q

what enzymes can you use to assess a patients liver function?

A
  • AST
  • ALT
  • GGT
  • LDH (not specific to the liver)
32
Q

what is steatosis

A

fatty change (such as fat accumulation in the liver that occurs as a result of damage/injury)

33
Q

what are Mallory’s bodies?

A

abnormally clumped together cytokeratin filaments. This occurs in cells as a result of cellular damage.

34
Q

What are three processes that occur in apoptosis?

A
  1. loss of cellular surface contact
  2. cell shrinkage
  3. chromatin condensation

Year 1 - Pathological Processes (12 decks)

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