4: Cell injury and fate Flashcards

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1
Q

8 causes of stress on the body

A

Aging

Physical agents (trauma/radiation)
Infectious agents
Genetic defects

Chemical agents (weed killer, drugs)
Oxygen deprivation
Immunological reactions
Nutritional imbalances (e.g obesity, lack of food)

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2
Q

4 most vulnerable parts of the cell

A

Cell membrane (immediate effects seen)
ATP generation *
Protein Synthesis
Genetic Apparatus

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3
Q

When can morphological changes be seen in a cell

A

Following cell death, although cell can already be injured

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4
Q

4 types of adaptation

A

Atrophy
Hypertrophy
Hyperplasia
Metaplasia

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5
Q

Atrophy

A

Cell shrinks in size
Each cell loses material
Organ gets smaller
Elderly not using muscle - gets smaller

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6
Q

Hypertrophy

A

Cell size increases
Organ therefore gets bigger
No new cells
e.g pregnancy

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7
Q

Hyperplasia

A

Increase in NUMBER of cells
Pathological or physiological
Physiological -liver growing after resection
Pathological - cancer

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8
Q

Metaplasia

A

Cell changes type
Reversible
Barrets oesophagus and bone development

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9
Q

Dysplasia

A

Pre-cancerous cells showing features of malignancy but has not invaded the underlying tissue

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10
Q

genetic and cytological features of cancer

A

Large nuceli
incr. nuceli to cytoplasm ratio
incr. number of mitoses

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11
Q

An athlete showed myocardial cells of increased diameter. Cell count was normal. What is the adaptation shown and what could be its cause?

A

Hypertrophy, due to intense exercise

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12
Q

Cell development after Dysplasia

A

Neoplasia (malignancy)

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13
Q

Types of cell injury

A

Reversible
Irreversible

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14
Q

Light microscopic features of reversible cell injury

A

Fatty change -white spots nothing inside
Cell swelling - white holes some cell space

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15
Q

Light microscopic features of irreversible cell injury

A

Necrotic changes (4 types)
- unexpected

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16
Q

4 types of necrosis

A

Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis

17
Q

Coagulative necrosis

A

Structure becomes fixed
e.g myocardial infarction

18
Q

Liquefactive necrosis

A

Tissue becomes liquified
e.g liquefactive cerebral infarct- brain doesn’t have much connectuve tissue to keep in place

19
Q

Caseous necrosis

A

Tissue looks Cheesy - oozy and structureless
e.g lung from Pulmonary TB

20
Q

Fat necrosis

A

Fat becomes liquified
e.g. in acute pancreatitis
Enzymes become activated in pancreas rather than duodenum –> liquifies fat

21
Q

Apoptosis

A

Intentional
needs energy
Does not cause inflammation
Can be physiological or pathological
usually a single cell

22
Q

Uses of apoptosis in the body (5)

A

Embryogenesis
Deletion of auto-reactive T cells in thymus
Withdrawal of a hormone
Cell deletion in proliferating populations
DNA damage causing cells to be eliminated

23
Q

Necroptosis

A

Spectrum of apoptosis and necrosis
energy dependent and has inflammation
-intentional

24
Q

8 main causes of cell injury

A

Genetic
Immunological
Nutritional imbalance
Chemical agents
Hypoxia
Ageing
Physical agents
Infectious agents

25
Q

4 cell mechanisms prone to injury

A

Cell membrane integrity
ATP generation
protein synthesis
genetic apparatus

  • damage to any of these most likely leads to cell death
26
Q

A woman 30 weeks pregnant, what changes has her uterus undergone

A

Physiological Hypertrophy
- incr. size of existing muscle
- normal adaptive change