Cell death Flashcards

1
Q

types of cell death

A

oncosis

necrosis

apoptosis

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2
Q

oncosis

A

cell death with swelling, the spectrum of changes that occur in injured cells prior to death

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3
Q

necrosis

A

in a living organism, the morphological changes that occur after a cell has been dead for some time e.g. 12-24h

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4
Q

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

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5
Q

types of necrosis

A

coagulative (main)

liquefactive (main)

caseous

fat necrosis

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6
Q

coagulative necrosis occurs in

A

ischaemia in solid organs

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7
Q

liquefactive necrosis occurs in

A

ischaemia in loose tissue

*presence of many neutrophils*

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8
Q

coagualtive necorsis due to

A

protein denaturation dominates over release of active proteases

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9
Q

liquefactive necrosis due to

A

enzyme release dominated over protein denaturation

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10
Q
A
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11
Q

what do cells that have undergone coagulative necrosis look like

A

cellular architecture is somewhat preserved-ghost outline

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12
Q

liquefactive necrosis lead to

A

liquefaction of tissue

  • cell architecture lost
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13
Q

caseous necrosis is a distinctive form of

A

coagulative necrosis

  • amphorous (structureless debris)
  • tissue maintains a cheese-like appearance.
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14
Q

where does caseous necrosis occur

A

mainly in the lungs

  • particularly associated with infection e.g. TB
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15
Q

fat necrosis

A
  • Destruction in the adipose tissue
  • Present in people with pancreatitis and in breast tissue after trauma
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16
Q

infarction

A

necrosis caused by reduction in arterial blood flow

• Can result in gangrene

17
Q

gangrene

A

necrosis visible to the naked eye

• An appearance of necrosis

18
Q

dry gangrene

A

necrosis modified by exposure to air (coagulative)

19
Q

wet gangrene

A

necrosis modified by infection (liquefactive)

20
Q

gas gangrene

A

Wet gangrene where the infection is with anaerobic bacteria that produce gas

21
Q

what is an infarct

A

an area of necrotic tissue which is the result of loss of arterial blood supply

• An area ischaemic necrosis

22
Q

apoptosis is

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

Characteristic microscopic appearance

23
Q

what does apoptosis look like

A
  • Characteristic microscopic appearance
  • Characteristic DNA breakdown
  • Non-random, internucleosomal cleavage of DNA (in oncosis, DNA is chopped into pieces of random length)
25
apoptosis is the .... and .... force to mitosis
equal and opposite
26
characteristics of apoptosis
* Active process * Single cell process * Enzymes activated that degrade nuclear DNA and protein * Membrane integrity is maintained * lysosomal enzymes not involved * Quick * Pathological or physiological
27
1) Physiological apoptosis
1. In order to maintain a steady state 2. Hormone-controlled involution 3. Embryogenesis e. g. sculpting a hand during development
28
2) pathological apoptosis
* Cytotoxic T cell killing of virus-infected or neoplastic cells * When cells are damaged, particularly with damaged DNA * Graft versus host disease
29
How does apoptosis occur?
1. Initiation * Triggered by either intrinsic or extrinsic pathways * Results in activation of caspases (enzymes which control and mediate apoptosis. Cause cleave of DNA and proteins of the cytoskeleton) 2. Execution 3. Degradation and phagocytosis * Both pathways cause the cells to shrink and break into apoptotic bodies, which express proteins on their surface * Now recognised by phagocytes or neighbouring cells * Finally degradation takes place within the phagocytes/neighbour
30
intrinsic pathway
* Initial signal comes from within the cell * Triggers: * Irreparable DNA damage * Withdrawal of growth factors or hormones * P53 protein is activated and this results in the outer mitochondrial membrane becoming leaky * Cytochrome C is released from mitochondria and activates caspases
31
Extrinsic
* Initiated by extracellular signals * Triggers: * Cells that are a danger e.g. tumour cells, virus-infected * One of the signals is TNFalpha * Secreted by T-killer cells * Binds to cell membrane receptor (death receptor) * Results in activation of caspases
32
Apoptosis versus oncosis/necrosis
33
Ends of chromosomes are called telomeres, with every replication the telomere
is shortened. When the telomeres reach a critical length, the cell can no longer divide
34
germ cells, stem cells and many cancer cells can produce
telemerase increasing the cells ability to replicates
35
Cell immortality
* As cells age they accumulate damage to cellular constituents and DNA * After a certain number of divisions they reach replicative senescence - related to the length of chromosomes (telomeres)