Cell Adaptations Flashcards

0
Q

What does each stage of interphase check?

A

G1 =

  • cell big enough?
  • environment favourable?
  • DNA damaged?

R point = when activated stimulates DNA repair/apoptosis/delays cell cycle (altered in cancer)

S = DNA replication

G2 =

  • all DNA replicated?
  • cell big enough?
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1
Q

Define growth factor. Give some examples of growth factors and what they do.

A

Polypeptides that act on cell surface receptors and are coded for by proto-oncogenes.

Stimulate transcription of genes that regulate entry of a cell into the cell cycle

  • epidermal growth factor (epithelia & hepatocytes)
  • vascular endothelial growth factor (angiogenesis)
  • platelet derived growth factor (fibroblast & smooth muscle proliferation)
  • granulocyte colony-stimulating growth factor (increased neutrophil function - treat chemo with this)
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2
Q

What controls the cell cycle? What effect do growth factors have on these chemicals?

A

Cyclins and cyclin-dependent kinases

Growth factors can inhibit CDK inhibitors and/or stimulate cyclins

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3
Q

What helps power a tissue’s proliferative capacity? What is special about the replication of these?

A

Stem cells replenish loss of differentiated cells

Asymmetric replication = 1 daughter cell differentiates, and 1 daughter cell remains a stem cell

remember: adult stem cells are NOT pluripotent

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4
Q

How does the division of stem cells vary between different cell types?

A

Labile cells = stem cells divide persistently to replenish loss of cells

Stable cells = stem cells normally quiescent or proliferate very slowly but will divide persistently when required

Permanent cells = stem cells present, but cannot mount an effective proliferative response to significant cell loss

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5
Q

Define regeneration. What is it stimulated by? How can this be protective?

A

REGENERATION = identical cells multiply to replace losses to maintain tissue size

Growth factors and loss of contact inhibition stimulate

Immature regenerated cells do not have the same receptors as mature cells - can be protective (e.g. if stimulation of receptors caused degeneration in the first place)

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6
Q

What is reconstitution? In what ways can reconstitution occur in humans?

A

RECONSTITUTION = replacement of a lost part of the body

  • capillaries
  • severed nail bed can sometimes regenerate 4yrs<
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7
Q

Define hyperplasia. In what cells can this occur? Is it a physiological or pathological process?

A

HYPERPLASIA = increase in tissue size due to increased cell numbers

Occurs only in labile or stable cell populations

Physiological & reversible

note: can occur secondary to a pathological cause, but hyperplasia itself is a normal response
note: repeated cell divisions exposes the cell to risk of mutations/neoplasia

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8
Q

Give examples of physiological and pathological hyperplasia.

A

Physiological:

  • proliferative endometrium under influence of oestrogen in uterus
  • bone marrow produces RBCS in response to altitude (hypoxia)

Pathological:

  • eczema
  • goitres
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9
Q

Define hypertrophy. In what cells can this occur? Why does this occur in failing tissues?

A

HYPERTROPHY = increase in tissue size due to increased cell size

Permanent cells

note: in labile and stable cells hypertrophy can occur alongside hyperplasia

Cells contain more structural components, therefore the workload is shared by a greater mass of cellular components

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10
Q

Give examples of physiological and pathological hypertrophy.

A

Physiological =

  • skeletal muscle (bodybuilders)
  • pregnant uterus (hypertrophy & hyperplasia)

Pathological =

  • right ventricular hypertrophy
  • hypertrophy of prostate gland -> hypertrophy of bladder muscle
  • colon (diverticular disease)
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11
Q

Why don’t athletes get heart failure?

A

Athletes have hypertrophied cardiac muscle, but unlike those with heart failure it is possible for them to rest to relieve hypertension (unlike those with heart failure)

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12
Q

What is compensatory hypertrophy (& hyperplasia)?

A

e.g. if one kidney stops working the other kidney can compensate for the loss of function by hypertrophying

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13
Q

Define atrophy. Is this process reversible?

A

ATROPHY = shrinkage of tissue due to an acquired decrease in size/number of cells

Less reversible as time goes on - reduced function & residual bodies present

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14
Q

Give examples of physiological and pathological atrophy.

A

Physiological =

  • ovarian atrophy in post-menopausal women
  • post-partum uterus

Pathological =

  • disuse e.g. muscle atrophy with immobilisation
  • denervation e.g. waster thenar muscles after median nerve damage, Duchenne’s
  • inadequate blood supply (note: partial and gradual, hence why necrosis does not occur)
  • malnutrition -> muscle atrophy
  • loss of endocrine stimulus e.g. breast and reproductive organs
  • persistent injury e.g. polymyositis
  • senile atrophy due to accumulation of mutations and senescence (heart & brain -> Alzheimer’s)
  • pressure (secondary to ischaemia)
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15
Q

Define metaplasia. What cells can this occur in? What limitations are there?

A

METAPLASIA = reversible change of one differentiated cell type to another

Labile and stable cells (cannot occur in striated muscle & neurones)

Cannot occur across germ layers i.e. epithelia cannot become other types of connective tissue

16
Q

Give examples of metaplasia (pathological).

A

Smokers:
Bronchial pseudostratified ciliated epithelium -> stratified squamous epithelium

Barrett’s oesophagus:
Stratified squamous epithelium -> gastric glandular epithelium

+ squamous metaplasia of ductal epithelium of prostate/ectocervial epithelium, intestinal metaplasia of gastric mucosa

17
Q

Define hypoplasia. Why is it not the opposite of hyperplasia? Give some examples of hypoplasia.

A

Underdevelopment or incomplete development of a tissue or organ at the embryonic stage

Congenital (hyperplasia is not congenital)

Testes in Klinefelter’s syndrome, heart chambers

18
Q

Define aplasia. What kind of disorder leads to aplasia? Give some examples of aplasia.

A

Complete failure of a specific tissue or organ to develop/organ whose cells have ceased to proliferate

Embryonic developmental disorder

Thymic aplasia -> infections & autoimmune problems
Aplastic anaemia

19
Q

Define involution and give some examples.

A

Normal programmed shrinkage of an organ

Uterus after childbirth
Thymus in early life

20
Q

Define atresia.

A

No orifice

21
Q

Define dysplasia.

A

Abnormal maturation of tissues (pre-cancerous)

Cytological changes suggestive of malignancy

22
Q

What is spinal muscular atrophy?

A

Autosomal recessive

Loss of gene that makes survival motor neurone protein (maintains specialised motor neurones in spinal cord and brainstem) -> motor neuronal death -> spinal muscular atrophy

23
Q

Give some examples of how organs respond to alterations in hormone levels.

A

UTERUS

  • oestrogen: stimulates lining of uterus to thicken (menopause: menstruation ceases)
  • progesterone: prepares uterine lining for egg (egg not fertilised -> reduction in progesterone; egg fertilised -> prevents menstruation and prevents other eggs from maturing)

BREAST

  • oestrogen: pubertal female development
  • progesterone: stimulates growth of breasts during pregnancy

PROSTATE
- testosterone: stimulates prostate growth
(but in prostate cancer the prostate enlarges despite reduction in testosterone with age)

24
Q

What is psoriasis? How can it be treated?

A

Excessive production of stratum corneum (reduction in keratinocyte transit time due to hyperplasia) and inflammatory cell infiltrate

Appears as well defined erythematous plaques with silvery scales (poorly adherent stratum corneum)

Redness due to vascular hyperplasia and dilatation

Treatment: dithranol & tar (produce free radicals -> inhibits proliferation), calcipotriol (Vit. D agonist -> reduces proliferation), corticosteroids (causes local skin atrophy), methotrexate (immunosuppression), UV/PUVA

25
Q

What changes occur in the muscles with exercise? How do anabolic steroids affect muscle?

A

Skeletal muscle hypertrophy

Anabolic steroids: increase protein in cell, reduce catabolism of muscle (by blocking effect of cortisol), favour cell differentiation in muscle cells instead of adipose cells, androgenic (virilising)