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Year 1: All Units > PP: Cell Injury > Flashcards

PP: Cell Injury Flashcards

1
Q

What is Hypoxia?

A

deficiency in the amount of oxygen reaching the tissues

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2
Q

Name 4 causes of hypoxia and decribe them.

A
  1. Hypoxaemic hypoxia: low arterial content of oxygen
  2. Anaemic hypoxia: decreased ability of haemoglobin to carry oxygen
  3. Ischaemic hypoxia - interruption to blood supply
    Ischaemic hypoxia: interruption to blood supply
  4. Histiocytic hypoxia: inability to utilise oxygen in cells due to disabled
    oxidative phosphorylation enzymes
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3
Q

What can cause Hypoxaemic hypoxia?

A
  • Low atmospheric oxygen

- Reduced adsorption due to lung disease

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4
Q

What can cause Anaemic hypoxia?

A
  • Anemia

- Carbon monoxide poisoning

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5
Q

What can cause Ischaemic hypoxia?

A
  • Blockage of a vessel

- Heart failure

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6
Q

What can cause Histiocytic hypoxia?

A
  • Cyanide poisoning
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7
Q

What can cause cell death?

A
  • Hypoxia
  • Physical agents (trauma, heat, cold, radiation)
  • Chemical agents (theraputic drugs, alcohol)
  • Microorganisms
  • Immune mechanisms
  • Dietary insufficiency and dietary excess
  • Genetic abnormalities
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8
Q

What is Grave’s

disease of thyroid an example of?

A

An Autoimmune reaction - immune system fails

to distinguish self from non-self

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9
Q

Which 4 cell components are most susceptible to injury?

A
  1. Cell membranes
  2. Nucleus
  3. Proteins
  4. Mitochondria
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10
Q

What happens during reversible hypoxic injury?

A

There is not enough oxygen supplied to the cell, therefore once the remaining oxygen is used up no more ATP can be systhesised. This means the Na/K ATP pump no longer works which leads to a build up of sodium inside the cell. Hence, this causes the cell to swell, lowers the pH and disrupts protein synthesis .

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11
Q

What happens during irreversible hypoxic injury?

A

Cell membrane increases in permeability therefore there is an influx of toxic calcium. This activates destructive enzymes.

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12
Q

Name 4 disruptive enzymes.

A
  1. ATPase
  2. Phospholipase
  3. Protease
  4. Endonuclease
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13
Q

What are free radicals?

A

An atom with a single unpaired electron in an outer orbit – an
unstable configuration hence react with other
molecules, often producing further free radicals

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14
Q

Name the 3 free radicals that are of particular biological

significance in cells.

A
  1. OH*
  2. O2-
  3. H2O2
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15
Q

How are free radicals

produced?

A
  • Metabolic reactions
  • Inflammation
  • Radiation
  • Contact with unbound metals (mainly iron and copper)
  • Drugs and chemicals
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16
Q

How does the body control free radicals?

A
  • Anti-oxidant system: donate electrons to the
    free radical – vitamins A, C and E
  • Enzymes neutralise free radicals
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17
Q

Name 3 enzymes which neutralise free radicals.

A

– Superoxide dismutase
– Catalase
– Glutathione peroxidase

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18
Q

What cellular structures are damaged by free radicals?

A

Oxidise proteins, carbohydrates and DNA become bent out of shape, broken or cross-linked resulting in them becoming Mutagenic and therefore carcinogenic

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19
Q

What is the role of heat shock proteins?

A

In cell injury heat shock response aims to ‘mend’

misfolded proteins and maintain cell viability.

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20
Q

What is Pyknosis?

A

The irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis.

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21
Q

What is karyolysis?

A

dissolution of a cell nucleus

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22
Q

What is Karyorrhexis?

A

the destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm.

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23
Q

How does an injured cell appear under light microscopy?

A

Pale pink and swollen primarily, then as proteins clump it appears pinker

24
Q

How does an injured cell appear under electron microscopy?

A
  • Blebs
  • Ribsomes dispersed from ER (no ATP to hold them on)
  • Clumping of chromatin
  • Swelling
25
Define Oncosis.
cell death with swelling, the spectrum of | changes that occur in injured cells prior to death
26
Define Necrosis.
the morphologic changes that occur after a cell has been dead some time
27
Define apoptosis.
Cell death with shrinkage, induced by a regulated intracellular program where a cell activates enzymes that degrade it’s own nuclear DNA and proteins
28
What are the 4 types of necrosis?
1. Coagulative 2. Liquefactive 3. Caseous 4. Fat necrosis
29
When does coagulative necrosis occur?
Solid organs
30
When does liquefactive necrosis occur?
loose tissue
31
What does coagultive necrosis look like?
Ghost outline as cellular architecture is somewhat preserved
32
What does liquefactive necrosis look like?
Enzyme degradation is substantially greater than denaturation therefore this leads to enzymatic digestion (liquefaction) of tissues. gooey basically :///
33
What does caseous necrosis look like?
Contains amorphous debris ASSOCIATED WITH TB!!!
34
Define Gangrene.
Necrosis visible to the naked eye
35
Define Infarction.
Necrosis caused by reduction in arterial blood flow
36
Define dry gangrene.
Necrosis modified by exposure to air | coagulative necrosis
37
Define wet gangrene.
Necrosis modified by infection | liquefactive necrosis
38
What is ischaemia-reperfusion injury?
Injury is the tissue damage caused when blood supply returns to the tissue after a period of ischemia or lack of oxygen
39
What are some possible causes of ischaemia-reperfusion?
- Increased production of oxygen free radicals with reoxygenation. – Increased number of neutrophils resulting in more inflammation and increased tissue injury. – Delivery of complement proteins and activation of the complement pathway.
40
Name 3 molecules released by injured cells.
1. Potassium 2. Enzymes 3. Myoglobin
41
Describe the difference between when physiological apoptosis occurs and when pathological apoptosis occurs.
Physiological: Hormone controlled, evident in embrogenesis of limb buds Pathological: Cytotoxic T cell killing of virus-infected or neoplastic cells or graft versus host disease
42
What does apoptosis look like?
Condensation of a single cell followed by apoptic bodies.
43
Name the 3 stages in apoptosis.
1. Initiation 2. Execution 3. Degradation and Phagocytosis
44
What 2 pathways can the Initiation and execution stages of apoptosis by triggered by?
1. Intrinsic | 2. Extrinsic
45
What does the triggering of intrinsic or extrinsic pathways of apoptosis result in?
Activation of caspases: Cause cleavage of DNA and proteins of the cytoskeleton
46
How is the intrinsic pathway | initiated and carried out?
``` - Initiating signal comes from within the cell - p53 protein is activated and this results in the outer mitochondrial membrane becoming leaky - Cytochrome C is released from the mitochondria and this causes activation of caspases ```
47
How is the extrinsic pathway | initiated and carried out?
``` - Initiated by extracellular signals One of the signals is TNFα – Secreted by T killer cells – Binds to cell membrane receptor (‘death receptor’) – Results in activation of caspases ```
48
Where do abnormal cellular accumulations come | from?
If a cell can’t metabolise something it will remain | within the cell
49
What can accumulate in | cells?
``` – Water and electrolytes – Lipids – Carbohydrates – Proteins – ‘Pigments’ ```
50
Define dystrophic calcification of tissues.
Localised calcification of tissues
51
Define Metastatic calcification of tissues.
Generalised calcification of tissues
52
Where and why does dystrophic calcification of tissues occur?
- Occurs in an area of dying tissue - Local change/disturbance favours nucleation of hydroxyapatite crystals
53
Why does metastatic calcification occur?
Hypercalcaemia (secondary to disturbances in | calcium metabolism)
54
What causes hypercalcaemia?
- Increased secretion of parathyroid hormone (PTH) resulting in bone resorption - Destruction of bone
55
Can cells live forever?
Mostly no, Germ cells and stem cells contain an enzyme called telomerase - maintains the original length of the telomeres. In this way they can continue to replicate, indefinitely.

Year 1: All Units (66 decks)

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