Week 1 - Cell Injury and Adaptations Flashcards

(55 cards)

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
Fibromatosis
Proliferation of myofibroblasts
26
Angiogenesis
New blood vessels grow into damaged tissues to supply oxygen/nutrients for cells
27
Benign prostatic hyperplasia
Too many cells/increased cell growth in transition zone
28
Atrophy
Decrease in cell size/number/both
29
Physiological atrophy
Adaptive response to decrease functional requirement for a cell/organ
30
Example of pathological atrophy
Immobilised limb -> decreased function -> loss of innervation & decreased blood supply -> decreased oxygen & nutrients
31
Mechanisms of atrophy
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
Causes of atrophy
Decreased function (disuse atrophy), loss of innervation (denervation atrophy), inadequate blood/O2 supply, pressure atrophy, lack of nutrition, systemic atrophy
33
Metaplasia
Altered differentiation, mature cell differentiates into another type
34
Mechanisms of metaplasia
Adaptive response to chronic, persistent injury/altered cellular environment => tissue change structure to better adapt to environment/stress
35
Can metaplasia be reversed?
Yes, when stimulus to change is removed e.g. stop smoking
36
Change in respiratory epithelium in smokers
Chronic irritation -> normal respiratory epithelium change to squamous epithelium -> lose functions of mucus secretion & movement
37
Barrett's oesophagus
Replacement of normal squamous epithelium in the oesophagus by glandular columnar epitheium
38
What is general pathology?
Mechanisms and characteristics of principle types of disease processes
39
What is systemic pathology?
Descriptions of specific diseases as they affect individual organs or organ systems
40
What does epidemiology study?
Incidence, prevalence, distribution, prevention
41
What is aetiology?
Cause
42
What is pathogenesis?
Mechanism causing the disease
43
What is prognosis?
Likely outcome for patient
44
What are the causes of disease?
Entirely genetic, multifactorial, entirely environmental => not always linear
45
What is the latent period?
Time lag after exposure before signs and symptoms appear
46
What are structural abnormalities?
Space occupying lesions, storage disease, loss of healthy tissue, obstruction, distension or rupture of hollow structure
47
What are functional abnormalities?
Excessive secretion of cell product, insufficient secretion, impaired neuromuscular function
48
What does pathognomonic mean?
Absolute diagnostic feature
49
What is morbidity?
Patient effects
50
What is mortality?
Rate of death
51
Why do we study epidemiology?
Providing aetiological clues, planning preventive measures, provision of adequate medical facilities, population screening for early diagnosis
52
What is incidence rate?
Number of new cases of the disease occurring in a population of defined size during a defined period
53
What is prevalence rate?
Number of cases of the disease to be found in a defined population at a stated time
54
What is remission rate?
Proportion of cases of the disease that recover
55
What is mortality rate?
Number or percentage of deaths from a disease in a defined population