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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
Q

Define Oncosis.

A

cell death with swelling, the spectrum of

changes that occur in injured cells prior to death

26
Q

Define Necrosis.

A

the morphologic
changes that occur after a cell has been dead some
time

27
Q

Define apoptosis.

A

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
Q

What are the 4 types of necrosis?

A
  1. Coagulative
  2. Liquefactive
  3. Caseous
  4. Fat necrosis
29
Q

When does coagulative necrosis occur?

A

Solid organs

30
Q

When does liquefactive necrosis occur?

A

loose tissue

31
Q

What does coagultive necrosis look like?

A

Ghost outline as cellular architecture is somewhat preserved

32
Q

What does liquefactive necrosis look like?

A

Enzyme degradation is substantially greater than denaturation therefore this leads to enzymatic digestion (liquefaction) of tissues.

gooey basically :///

33
Q

What does caseous necrosis look like?

A

Contains amorphous debris

ASSOCIATED WITH TB!!!

34
Q

Define Gangrene.

A

Necrosis visible to the naked eye

35
Q

Define Infarction.

A

Necrosis caused by reduction in arterial blood flow

36
Q

Define dry gangrene.

A

Necrosis modified by exposure to air

coagulative necrosis

37
Q

Define wet gangrene.

A

Necrosis modified by infection

liquefactive necrosis

38
Q

What is ischaemia-reperfusion injury?

A

Injury is the tissue damage caused when blood supply returns to the tissue after a period of ischemia or lack of oxygen

39
Q

What are some possible causes of ischaemia-reperfusion?

A
  • 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
Q

Name 3 molecules released by injured cells.

A
  1. Potassium
  2. Enzymes
  3. Myoglobin
41
Q

Describe the difference between when physiological apoptosis occurs and when pathological apoptosis occurs.

A

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
Q

What does apoptosis look like?

A

Condensation of a single cell followed by apoptic bodies.

43
Q

Name the 3 stages in apoptosis.

A
  1. Initiation
  2. Execution
  3. Degradation and Phagocytosis
44
Q

What 2 pathways can the Initiation and execution stages of apoptosis by triggered by?

A
  1. Intrinsic

2. Extrinsic

45
Q

What does the triggering of intrinsic or extrinsic pathways of apoptosis result in?

A

Activation of caspases: Cause cleavage of DNA and proteins of the cytoskeleton

46
Q

How is the intrinsic pathway

initiated and carried out?

A 
- 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
Q

How is the extrinsic pathway

initiated and carried out?

A 
- 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
Q

Where do abnormal cellular accumulations come

from?

A

If a cell can’t metabolise something it will remain

within the cell

49
Q

What can accumulate in

cells?

A 
– Water and electrolytes
– Lipids
– Carbohydrates
– Proteins
– ‘Pigments’
50
Q

Define dystrophic calcification of tissues.

A

Localised calcification of tissues

51
Q

Define Metastatic calcification of tissues.

A

Generalised calcification of tissues

52
Q

Where and why does dystrophic calcification of tissues occur?

A
  • Occurs in an area of dying tissue
  • Local change/disturbance
    favours nucleation of
    hydroxyapatite crystals
53
Q

Why does metastatic calcification occur?

A

Hypercalcaemia (secondary to disturbances in

calcium metabolism)

54
Q

What causes hypercalcaemia?

A
  • Increased secretion of parathyroid hormone (PTH)
    resulting in bone resorption
  • Destruction of bone
55
Q

Can cells live forever?

A

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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