Module 1 - Growth and Adaptation Flashcards
Important Vocabulary
Epidemiology - incidence, prevalence, distribution, prevention
Aetiology - cause
Pathogenesis - progress of disease
ClinicoPath - features both structural and functional
Prognosis - likely outcome for patient
Treatment - best option
Types of Growth
Multiplicative - increase in number of cells
Auxetic - increased size of individual cells e.g. muscle growth
Accretionary - increase in intracellular tissue components e.g. bone and cartilage
Combined - all of the above occur, different rates and direction of growth at different sites
Tissue growth depends on the balance between what?
Increase in cell numbers due to cell proliferation
Decrease in cell number due to apoptosis
Differentiation - cell differentiate to perform specialised roles
Cell categories based on their growth rate
Labile - very high regenerative ability and rate of turnover - e.g. skin epithelial cells Stable - good regenerative ability but usually a low rate of turnover (not needed to regenerate often) - e.g. liver muscle Permanent - limited regenerative ability - e.g. neurons
Physiological vs Pathological Adaptations
Physiological
- increased muscle bulk, strength and endurance
- improved respiratory and cardiovascular functions with exercise
- increase in RBC numbers when living at higher altitudes (reduced oxygen)
Pathological
- modifications that allow the cells to cope with changed conditions
- introduce structural and functional features to the body
- e.g. manifestations of disease state
Hypertrophy and Hyperplasia
Hypertrophy - increase in cell size without cell division
Hyperplasia - increase in cell number by mitosis
Example of Pathological Cardiac Hypertrophy
Myocardial infarct leads to less efficient ejection of blood so the left ventricle tries to compensate -> left ventricular hypertrophy
This however doesn’t completely compensate
If left ventricle doesn’t eject blood properly into the systemic circulation blood backs up in the pulmonary circulation
This then exerts back pressure on the right side of the heart and leads to right ventricular hypertrophy
This increases risk of stroke and heart attack
Hyperplasia occurs in response to what?
Altered endocrine environment
Increased functional demand
Chronic injury
Examples of Physiological Hyperplasia
Red blood cells in people living at high altitudes
- stimulated by erythropoietin
Increase in breast tissue during puberty and pregnancy
Proliferation of the endometrium during the proliferative phase of menstruation
Endometrial proliferation in readiness for pregnancy
Thyroid hyperplasia (not goiter)
- due to increased metabolic demands of puberty and pregnancy
Thyroid Goiter
Example of pathological hypertrophy
Thyroid responds to increased hormonal stimulation from the pituitary gland
Autonomous Hyperplasia
Pathological hyperplasia
Cells proliferate rapidly without a clear stimulus or control mechanism
Examples:
Psoriasis - marked epidermal hyperplasia (skin)
Paget’s disease - hyperplasia of osteoblasts relative to osteoclasts, thick but weak bone
Fibromatosis - proliferation of myofibroblasts, form tumour-like masses
Atrophy
Decrease in size of organ or cell (can be size and number)
For atrophy to occur
- no growth
- decrease in cell size or decrease in cell numbers via apoptosis
Physiological
- adaptive response to decrease in functional requirement for a cell/organ e.g. post menopausal atrophy of uterus
Pathological
- decrease function (immobilised limb) -> loss of innervation and decreased blood supply (decrease oxygen and nutrients)
Mechanisms of Atrophy
Production and destruction of cellular constituents
Reversible restructuring of cell activities
- facilitate survival
- adapt to conditions of diminished use
Decreased protein synthesis
Increased protein degradation
Metaplasia
Altered differentiation
- a mature cell differentiates into another type
Adaptive response to chronic, persistent injury/altered cellular environment
Tissues change structure to the point that they are visibily different to normal; better adapted to environment/stress
Non-neoplastic but can be associated with subsequent malignancy
Endometrial Hyperplasia
Thickening of the endometrial walls
Caused by too much estrogen or not enough progesterone
- estrogen - makes the cells grow
- progesterone - sheds the cells
Usually occurs after menopause when ovulation stops and progesterone isn’t made
Symptoms:
- post-menopause uterine bleeding
- heavier and increased menstrual bleeding
- menstrual bleeding between menstrual periods
- not having a period (pre-menopause)
Uterine hyperplasia can be treated with simple hormonal therapy