Cell injury ๐Ÿ—ธ Flashcards

1
Q

Homeostasis

A

steady state
closely maintained
stress on cells results in an attempt at adaptation

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2
Q

three adaptations to increased demand

A

hyperplasia
hypertrophy
growth receptors

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3
Q

hyperplasia

A

increase in cell number in response to external stimulus
can be physiological or pathological
reverses on withdrawal of stimulus

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4
Q

physiological example of hyperplasia

A

breast tissue in puberty
response to loss of tissue

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5
Q

pathological example of hyperplasia

A

hormonally induced e.g. excess of oestrogen = endometrial hypoplasia
hyperplasia of lymph nodes in response to infectiom

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6
Q

what happens if cells keep growing in a lack of stimulus?

A

could be cancerous

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7
Q

hypertrophy

A

increase in cell size

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8
Q

when does hypertrophy often occur?

A

in conjunction with hyperplasia
in isolation in non-dividing cells (e.g. skeletal muscle)
in response to mechanical stress

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9
Q

when does hypertrophy become pathological?

A

when heart/muscle cannot function
requires more blood supply
can cause heart failure

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10
Q

growth receptors

A

stress growth factors lead to cell division

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11
Q

to increase cell divisionโ€ฆ

A

produce more growth factors and growth factor receptors

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12
Q

three categories of growth factor receptor

A

receptors with intrinsic tyrosine kinase activity
7 transmembrane G protein coupled receptors
receptors without intrinsic tyrosine kinase receptors

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13
Q

Atrophy

A

reduction in cell size, can be physiological or pathological

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14
Q

physiological examples of atrophy

A

embryological structures
post-menopausal uterus

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15
Q

pathological examples of atrophy

A

decreased workload
blocked blood supply
loss of innervation

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16
Q

mechanisms of atrophy

A

reduced cellular components
protein degradation
some hormones promote degradation (thyroid hormone), others promote growth (insulin)

17
Q

Cell cycle overview

A

tightly controlled with checkpoints
faulty cells may not perform function
each stage of the cell cycle is controlled by CDKs which are activate by a specific cyclin

18
Q

G1

A

cells get bigger, increased protein synthesis
Cyclin D activates CDK4 with phosphorylates Rb protein
Rb is normally bound to E2F, stopping it from initiating cell division
when Rb is phosphorylated it is unable to bind to E2F and E2F will initiate cell division
p53 can cause cell arrest between G1 and S

19
Q

S phase

A

E2F initiates DNA replication and increases levels of cyclin A
Cyclin A activates CDK2 also promoting DNA replication
ends with two copies of the genome

20
Q

G2

A

Cell gets bigger, more protein synthesis
main p53 checkpoint occurs at the end of G2
- checks for mistakes
- pauses cell and attempts to repair, if its a success, the cycle continues and if it fails, the cell dies
if cells can avoid p53, the can keep dividing whilst being faulty

21
Q

M phase

A

mitosis

22
Q

Variations in the cell cylce

A

not all cells divide - some are terminally differentiated (neurons etc.)
Telomeres get smaller with each division, the cells can only divide a limited number of times

23
Q

telomeres

A

caps which protect the chromosome ends from degradation and fusion