Cellular Adaptations Flashcards
1
Q
What is hypertrophy?
A
- increase in the size of existing cells
- pathologic or physiologic
- increased synthesis of structural components
- due to increased functional demand or stimulation by hormonal growth factors
- reversible
2
Q
Describe the pathogenesis of hypertrophy
A
- usually due to increased functional demand (physiologic) or growth factors (physiologic or pathologic)
- common in skeletal muscle cells with exercise
- also in cardiac muscle cells
- eccentric - cells are longer
- concentric - cells are thicker
- nuclei are larger and irregular
- usually an adaptive response ie volume, pressure overload
- eventually becomes pathologic
3
Q
Describe the pathogenesis of hyperplasia
A
- increase in number of cells due to:
- physiology or pathology
- stimulation by hormonal or growth factors
- reversible
- examples:
- endometrium in reproductive cycle
- estrogen induces more glands and epithelial cells lining them
- lactating breast in pregnancy
- proliferation of secretory epithelial cells, take up whole breast
- endometrium in reproductive cycle
4
Q
Describe the pathogenesis of atrophy
A
- cell reduction in size and activity due to:
- reduction in cellular metabolism
- reduced synthesis of structural proteins
- cellular components removed by autophagy
- see lots of lipofuscin as a sign of atrophy
- apoptosis
- physiologic changes eg age
- pathologic changes:
- inadequate nutrition
- diminished blood supply
- denervation
- disuse
- loss of endocrine stimulation
- pressure (causing ischaemia)
- often a bit fibrotic
- when there is cell loss and fibrosis, atrophy is irreversible
- revers to individual cells, tissues, or whole organs
5
Q
Describe the pathogenesis of metaplasia
A
- most commonly in epithelia, which are functionally specialized
- tf occurs in response to changing environments
- get switching from one fully differentiated adult/mature cell type to another that is better suited
- can be physiological or pathological
- due to cytokine or growth factor driven reprogramming of the line of differentiation of adult/somatic stem cells
- examples:
- simple columnar epith of endocervix changing to stratified squamous like ectocervix in menstruation, cervical cancer
- squamous metaplasia of bronchial epithelium in smokers
6
Q
What causes concentric ventricular hypertrophy?
A
- thickened muscle fibres, new sarcomeres synthesized in parallel with old
- results from:
- increased afterload = pressure overload
- dystrophic calcification of the aortic valve causing stenosis
- get LV CHT, possible LV failure; usually 70-80 years old
7
Q
What are the consequences of concentric ventricular hypertrophy?
A
- initial preservation of systolic function
- eventiually, thickened myocardium leads to:
- impaired perfusion and ischaemia
- impaired diastolif cilling
8
Q
What causes eccentric ventricular hypertrophy?
A
- lengthened muscle fibres
- new sarcomeres synthesized in series with old
- develops as a result of volume overload
9
Q
What are the consequences of eccentric ventricular hypertrophy?
A
- functional up to a point
- ultimately predisposes myocardium to ischaemia
- eventual ventricular failure due to:
- associated subcellular changes
- microscopic fibrosis and apoptosis due to wall stress
- elevated catecholamines
- elevated cytokine production
- failing ventirucle dilates (displacement of apex beat to L), leads to enlargement of heart and:
- increased ESV, increased EDV
-
eventual ventricular failure due to:
- associated subcellular changes
- microscopic fibrosis and apoptosis due to wall stress
- elevated catecholamines
elevated cytokine production
*
failing ventirucle dilates (displacement of apex beat to L), leads to enlargement of heart and:
*
increased ESV, increased EDV
10
Q
What are the common causes of cardiac valve disease?
A
- congenital abnormalities
- e.g. bicuspid aoritc valve (~1% of pop’n)
- myxomatous mitral valve (prolapse) either genetic or acquired ~2% of pop’n
- aortic stenosis - degenerative changes causing calcification (most common in Western population)
- Rheumatic fever - valve infection and immune inflamation, usually mitral, sometimes aortic (most common in developing countries)
- infective endocarditis (staph aureus, strep viridans)
11
Q
What are the consequences of cardiac valve disease?
A
- may be asymptomatic
- murmurs on examination
- predisposition to infective endocarditis
- severe may cause incompetence or stenosis of the valve
- commonly related to heart failure (SOB)
- mitral valve disease (stenosis or incompetence) can lead to atrial fibrillation
- thrombus can form and cause cerebral infarct
- can be caused by atrial hypertrophy
12
Q
Where does HPV infection and dysplasia occur?
A
- ectocervix is stratified squamous (non-keratinising)
- (endo)cervical canal is simple columnar (mucous secreting)
- can become stratified squamous due to change in environment
- eg onset of menstruation in response to increased estrogen
- HPV infection can occur here and cause dysplasia
13
Q
What metaplasia occurs in the bronchial epithelium as a result of smoking?
A
- normal pseudostratified ciliated columnar epithelia changes to stratified squamous epithelial (loss of cilia)
- pathologic change
- can become malignant
- can be reversible
14
Q
What controls adaptive changes (hypertrophy, hyperplasia, metaplasia)?
A
- different growth factors and hormones
- act on specific cell surface receptors
- linked to internal signalling pathways
- these regulate gene transcription
- changes in cell division, protein production, cell differentiation
15
Q
How does neoplasia differ from adaptive changes?
A
- neoplasia = new growth
- incorporates malignancy and beningn neoplastic changes
- changes are unregulated (adaptive changes are regulated by growth hormones and cytokines)
- changes in the genetic material that lead to abnormal proliferation
- ie hyperplasia is not related to malignancy because no mutation is occuring; it does predispose to malignancy through increased proliferation and risk of errors
- pathologic influences of metaplasia may also intitate malignancy of the metaplastic epithelium
- eg smoking causes the epithelial change, malignancy results from the environmental change (not the metaplasia)
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