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ESA 2 - Pathological Processes > 7. Cellular adaptations > Flashcards

7. Cellular adaptations Flashcards

1
Q

Why do cells adapt?

A
  • To respond to challenges that aren’t severe enough to cause injury, by adaptations that aren’t truly pathogenic, although they may open the door to disease.
  • Adaptation is the state between a normal unstressed cell and an overstressed injured cell.
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2
Q

What are the 5 important types of cell adaptation?

A
  1. regeneration: multiply to replace losses
  2. hyperplasia
  3. hypertrophy
  4. atrophy
  5. metaplasia
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3
Q

Are cellular adaptations reversible?

A

Usually yes, though atrophy is less so

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4
Q

What is hyperplasia and why does it occur?

A

Increase in tissue/organ size due to increased cell numbers.

Response to:

i) increased functional demand, via external/hormonal stimulation
ii) tissue damage -increase in tissue mass (compensatory)

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5
Q

In which types of tissue does hyperplasia occur?

A

labile or stable tissues

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6
Q

What is the difference between hyperplasia and neoplasia?

A

Hyperplasia

  • under physiological control
  • reversible

Neoplasia

  • not under physiological control
  • irreversible
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7
Q

Why is neoplasia a risk in hyperplastic tissue?

A
  • repeated cell divisions expose the cell to mutation risk (commonly occur in DNA replication)
  • pathological hyperplasia usually occurs secondary to excessive hormonal stimulation or growth factor production
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8
Q

Give 2 examples of physiological hyperplasia.

A
  1. increased bone marrow production of erythrocytes in resp. to low oxygen/hypoxia
  2. proliferation of endometrium under influence of oestrogen
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9
Q

Give 2 examples of pathological hyperplasia.

A
  1. epidermal thickening in chronic eczema/psoriasis

2. thyroid goitre in iodine deficiency

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10
Q

What is hypertrophy?

A

Increase in tissue/organ size due to increase in cell size (without increase in cell no.)

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11
Q

In which tissue types does hypertrophy occur?

A

Labile, stable but esp. permanent tissues (as these cell pops. have no replicative potential so any increase in organ size must occur via hypertrophy)

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12
Q

What causes cellular hypertrophy?

A

Same stimuli as hyperplasia - increased functional demand or hormonal stimulation - so in labile and stable tissues, hypertrophy usually occurs with hyperplasia.

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13
Q

How do cells mediate hypertrophy?

A

Synthesise more cytoplasm (i.e. protein) - contain more structural components so cellular workload is shared by a greater mass of cellular components.

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14
Q

Give 2 examples of physiological hypertrophy.

A
  1. skeletal muscle hypertrophy of body builder
  2. smooth muscle hypertrophy (+hyperplasia) of pregnant uterus - body of uterus enlarges approx. 70x under influence of oestrogen
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15
Q

Give 3 examples of pathological hypertrophy.

A
  1. ventricular cardiac muscle hypertrophy in resp. to systemic hypertension or valvular disease
  2. smooth muscle hypertrophy proximal to an intestinal stenosis due to extra work of pushing intestinal contents through narrowing
  3. bladder smooth muscle hypertrophy with bladder obstruction due to an enlarged prostate gland (which has undergone both hypertrophy and hyperplasia)
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16
Q

Why don’t athletes get cardiac muscle hypertrophy?

A

Some hypertrophy but limited as can always rest and recuperate after effort, whereas in pathology, always relatively hypoxic.

17
Q

What is compensatory hypertrophy?

A

Enlargement of 1 organ of a pair, if the other is damaged/removed (e.g. kidney)

18
Q

What are cellular and tissue/organ atrophy?

A

Cellular = decrease in cell size to a size where survival is still possible

Tissue/organ = shrinkage of a tissue/organ due to a decrease in size and/or number ( via apoptosis) of cells

19
Q

What causes atrophy?

A

reduced supply of growth factors and/or nutrients

20
Q

What happens in cellular atrophy?

A

Reduction in amount of inessential structural components (digested via phagosomes - residual bodies), leading to reduced function.
But cell shrinkage is limited as most cellular organelles are essential for survival.

21
Q

Why do atrophic organs often contain large amounts of connective tissue?

A

In organs undergoing atrophy by cell deletion, parenchymal cells will apoptose before stromal cells.

22
Q

Give 2 examples of physiological atrophy.

A
  1. ovarian atrophy in post-menopausal women

2. decrease in uterus size after childbirth

23
Q

Give examples of pathological atrophy causes.

A
  1. reduced functional demand/workload (atrophy of disuse), e.g. muscle atrophy after immobilisation (reversible with activity)
  2. loss of innervation (denervation atrophy), e.g. wasted hand muscles after median nerve damage
  3. chronic inadequate blood supply, e.g. thinning of skin on legs with peripheral vascular disease
  4. inadequate nutrition, e.g. muscle wasting with malnutrition
  5. loss of endocrine stimulation, e.g. breast, reproductive organs
  6. aging (senile atrophy), usually in permanent tissues (brain and heart)
  7. pressure, e.g. tissues around an enlarging benign tumour (probably secondary to ischaemia)
24
Q

What is atrophy of extracellular matrix?

A

loss of bone substance (rather than calcium) in osteoporosis, often as a consequence of inactivity (as stimulus for bone formation is movement and pressure)

25
Q

What is metaplasia? How does this occur?

A

Reversible change of 1 differentiated cell type to another:

1- cells of original phenotype are eliminated
2- stem cells within the tissue are reprogrammed and differentiate into a different type of progeny

26
Q

Why does metaplasia occur?

A

may represent adapative substitution of cells sensitive to stress by cells better able to withstand the adverse environment

27
Q

What is the difference between metaplasia, dysplasia and cancer?

A

Metaplasic cells

  • fully differentiated
  • process is reversible
  • sometimes a prelude to dysplasia and cancer

Dysplasia = abnormal maturation of cells within a tissue.

  • disorganised and abnormal differentiation
  • potentially reversible but is often pre-cancerous.

Cancer

  • disorganised and abnormal differentiation
  • irreversible
28
Q

What cell types can metaplasia give rise to?

A
  • Only occurs in cell populations that can replicate (not known to occur in adult striated muscle or neurons) - labile or stable.
  • Occurs only within varieties of epithelia and within varieties of connective tissue (mesenchyme), but not across germ layers (e.g. bone to nerve or mesenchyme to epithelium).
29
Q

In what tissue type is metaplasia seen most commonly?

A

Epithelial tissues on surface linings - exposed to insults. Columnar epithelium (fragile) commonly undergoes metaplasia to squamous epithelium (more resilient).

30
Q

Give 2 examples of adaptive/useful metaplasia.

A
  1. If BM is destroyed, splenic tissue undergoes metaplasia to BM (myeloid metaplasia), e.g. megakaryocytes for platelet production.
  2. columnar epithelium lining ducts, e.g. in salivary glands, pancreas, bile ducts or renal pelvis, can change to stratified squamous epithelium (more resistant to mechanical abrasion) secondary to chronic irritation by stones.
31
Q

Give 2 examples of metaplasia that are detrimental.

A
  1. Transformation of bronchial pseudostratified ciliated columnar epithelium to stratified squamous epithelium due to effect of cigarette smoke. Squamous epithelium doesn’t produce cleansing mucus and lacks cilia to move mucus along.
  2. Stratified squamous epithelium to gastric glandular epithelium due to persistent acid reflux (Barrett’s oesophagus).
32
Q

What is traumatic myositis ossificans?

A
  • Metaplastic bone can develop in skeletal muscle following trauma - fibroblasts to osteoblasts.
  • Often seen in young people after a premature return to activity before proper healing has occurred.
  • Often disappears by metaplasia in opposite direction.
33
Q

Does metaplasia predispose to cancer?

A

Several types of epithelial metaplasia predispose to dysplasia and malignant epithelial cancers, e.g.

  • Barrett’s epithelium and oesophageal adenocarcinoma (with chronic infection by Helicobacter pylori)
  • Intestinal metaplasia of stomach and gastric adenocarcinoma
34
Q

What is aplasia?

A
  • Embryonic developmental disorder involving complete failure of a specific tissue or organ to develop.
  • E.g. thymic aplasia (infections and autoimmune probs), aplasia of a kidney.
  • (Also used to describe an organ whose cells have ceased to proliferate, e.g. aplasia of BM in aplastic anaemia).
35
Q

What is hypoplasia?

A
  • congenital underdevelopment or incomplete development (inadequate no. of cells) of tissue/organ at embryonic stage
  • in a spectrum with aplasia
  • e.g. testicular in Klinefelter’s syndrome, heart chambers, renal. breast
36
Q

What is involution?

A

normal programmed shrinkage of an organ, e.g. uterus after childbirth, thymus in early life, temporary foetal organs such as pro- and mesonephros - overlaps with atrophy

37
Q

What is atresia?

A

congenital imperforation of an opening (‘No orifice’), e.g. of anus or vagina

38
Q

What is reconstitution? Can it occur in humans?

A
  • Replacement of a lost body part (e.g. antlers).
  • Cannot occur in humans (e.g. pale, hairless scars) except:
    • angiogenesis (some argue)
    • some cases of tip of finger regrowth after clean cut if <4.5 yo

ESA 2 - Pathological Processes (21 decks)

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