Week 1 - Cell Injury and Adaptations Flashcards

1
Q

Types of growth

A

Multiplicative, auxetic, accretionary, combined

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2
Q

Multiplicative growth

A

Increase in number of cells

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3
Q

Auxetic growth

A

Increased size of individual cells

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4
Q

Accretionary growth

A

Increase in intracellular tissue components

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5
Q

Tissue growth depends on balance between

A

Cell proliferation, apoptosis and differentiation

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6
Q

Labile tissue

A

High regenerative ability & rate of turnover

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7
Q

Stable tissue

A

Good regenerative ability but usually low turnover rate

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8
Q

Permanent tissue

A

Limited regenerative ability

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9
Q

Factors affecting differentiation

A

Genes, hormones, position within fetus, growth factors, matrix proteins

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10
Q

Morphogenesis

A

Development of the shape and form of organs, limbs, facial features etc from primitive cell masses during embryogenesis

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11
Q

Physiological adaptation

A

Adaptation that involves a body part’s job of controlling a life process

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12
Q

Types of physiological adaptation

A

Structural and metabolic

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13
Q

Examples of physiological metabolic adaptation

A

Mobilise fatty acids from adipose tissue for energy (fasting), mobilise calcium from bone matrix (lack of calcium), liver metabolising drugs

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14
Q

Mechanism of structural physiological adaptation

A

Increase/decrease in hormonal stimulation or functional demand -> increase/decrease in cell size/number

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15
Q

Pathological adaptation

A

Modifications that allow the cells to cope with changed conditions, structural and functional change

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16
Q

Hypertrophy

A

Increase in cell size without cell division

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17
Q

Physiological cardiac hyperthrophy

A

Characterised by normal organisation of cardiac structure and normal/enhanced cardiac function

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18
Q

Pathological cardiac hypertrophy

A

Commonly associated with up-regulation of fetal genes, cardiac dysfunction and increased mortality

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19
Q

Hyperplasia

A

Increase in cell number

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20
Q

Example of physiological hyperplasia

A

Red blood cells in people living at high blood pressure, breast tissue during puberty, pregnancy and lactation, thyroid hyperplasia due to increased metabolic demands of puberty and pregnancy

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21
Q

Autonomous hyperplasia

A

Cells proliferate rapidly without a clear stimulus or control mechanism

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22
Q

Examples of pathological hyperplasia

A

Psioriasis, Paget’s disease, Fibromatosis

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23
Q

Psioriasis

A

Marked epidermal hyperplasia

24
Q

Paget’s disease

A

Hyperplasia of osteoblast/osteoclast => thick but weak bone

25
Q

Fibromatosis

A

Proliferation of myofibroblasts

26
Q

Angiogenesis

A

New blood vessels grow into damaged tissues to supply oxygen/nutrients for cells

27
Q

Benign prostatic hyperplasia

A

Too many cells/increased cell growth in transition zone

28
Q

Atrophy

A

Decrease in cell size/number/both

29
Q

Physiological atrophy

A

Adaptive response to decrease functional requirement for a cell/organ

30
Q

Example of pathological atrophy

A

Immobilised limb -> decreased function -> loss of innervation & decreased blood supply -> decreased oxygen & nutrients

31
Q

Mechanisms of atrophy

A

Production and destruction of cellular constituents, reversible restructuring of cell activities to facilitate survival/adapt to conditions of diminished use, decreased protein synthesis, increased protein degradation

32
Q

Causes of atrophy

A

Decreased function (disuse atrophy), loss of innervation (denervation atrophy), inadequate blood/O2 supply, pressure atrophy, lack of nutrition, systemic atrophy

33
Q

Metaplasia

A

Altered differentiation, mature cell differentiates into another type

34
Q

Mechanisms of metaplasia

A

Adaptive response to chronic, persistent injury/altered cellular environment => tissue change structure to better adapt to environment/stress

35
Q

Can metaplasia be reversed?

A

Yes, when stimulus to change is removed e.g. stop smoking

36
Q

Change in respiratory epithelium in smokers

A

Chronic irritation -> normal respiratory epithelium change to squamous epithelium -> lose functions of mucus secretion & movement

37
Q

Barrett’s oesophagus

A

Replacement of normal squamous epithelium in the oesophagus by glandular columnar epitheium

38
Q

What is general pathology?

A

Mechanisms and characteristics of principle types of disease processes

39
Q

What is systemic pathology?

A

Descriptions of specific diseases as they affect individual organs or organ systems

40
Q

What does epidemiology study?

A

Incidence, prevalence, distribution, prevention

41
Q

What is aetiology?

42
Q

What is pathogenesis?

A

Mechanism causing the disease

43
Q

What is prognosis?

A

Likely outcome for patient

44
Q

What are the causes of disease?

A

Entirely genetic, multifactorial, entirely environmental => not always linear

45
Q

What is the latent period?

A

Time lag after exposure before signs and symptoms appear

46
Q

What are structural abnormalities?

A

Space occupying lesions, storage disease, loss of healthy tissue, obstruction, distension or rupture of hollow structure

47
Q

What are functional abnormalities?

A

Excessive secretion of cell product, insufficient secretion, impaired neuromuscular function

48
Q

What does pathognomonic mean?

A

Absolute diagnostic feature

49
Q

What is morbidity?

A

Patient effects

50
Q

What is mortality?

A

Rate of death

51
Q

Why do we study epidemiology?

A

Providing aetiological clues, planning preventive measures, provision of adequate medical facilities, population screening for early diagnosis

52
Q

What is incidence rate?

A

Number of new cases of the disease occurring in a population of defined size during a defined period

53
Q

What is prevalence rate?

A

Number of cases of the disease to be found in a defined population at a stated time

54
Q

What is remission rate?

A

Proportion of cases of the disease that recover

55
Q

What is mortality rate?

A

Number or percentage of deaths from a disease in a defined population