Week 3- Cell adaptations + damage Flashcards

1
Q

What is cell adaptation? When may it happen & what can change to preserve cell vitality?

A

Reversible change in cells in response to environment

Stimuli may arise under physiological or pathological conditions

Cell number

Cell size

Cell type

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2
Q

What are the three classes of proliferative cells? Give examples

A

1) Labile
eg: skin, epithelial
2) Stable
eg: bone
3) Permanent
eg: brain

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3
Q

What are the different types of cell adaptation?

A

Hyperplasia

Hypertrophic

Meterplasia

Atrophy

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4
Q

Define Hyperplasia. What is the cell type? Give examples of physiological & pathological hyperplasia including causes

A

Increase in cell number

Labile/ stable cells

Physiologically:

1) Hormonal → Endometrium
2) Compensatory → Partial hepatcetomy

Pathologically:

  • Excessive growth hormone
  • Chronic irritation

Can occur alongside hypertrophy

Increased risk of tumour development

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5
Q

Define Hypertrophy. What cells can it occur in? Give examples of physiological & pathological hypertrophy including causes

A

Increase in cell size. More cellular structural proteins

All cells, most common: permanent cells

Physiologically:

1) Increased functional demand → Skeletal muscle
2) Hormonal/ growth factor → Uterine muscle pregnancy

Alongside hyperplasia

Pathologically:

Increased functional demand → Cardiac muscle (LV hypertrophy/ aortic stenosis)

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6
Q

Define Atrophy. What are the causes of atrophy?

A

Shrinkage in cell size with self-digestion of organelles

1) Reduced workload
2) Loss nerve supply
3) Blood supply loss
4) Inadequete nutrition
5) Loss endocrine stimulation
6) Ageing

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7
Q

Define Metaplasia. Talk about it- why it happens, what can happen, what it usually involves. Give examples of physiological & pathological metaplasia

A

Change in cell type from adult cell to another

Talk:

New cell type better adapted to the stimulus

Ground for the later development of cancer

Usually involves epithelium

Physiological:

1) Growth/ development → Glandular to squarmous eputhelium in pubertal cervix

Pathological:

1) Abnormal environemnt → Squarmous to glandular epithlium in GORD

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8
Q

What are the different types of developmental abnormalities?

A

Agenesis: Failure to form

Aplasia: Failure to differentiate into organ specific tissue

Dysgenesis: Failure of tissue to strucurally organise themselves into organ

Hypoplasia: Failure of organ to grow to full size

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9
Q

What are the types of abnormal growth?

A

Dysplasia

Neoplasia

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10
Q

What is dysplasia? Talk about it. Where can it occur?

A

Presence of cellular atypia, increased cell growth, altered differentiation premelignant condition

Ocurrs:

  • Cervix
  • Bladder
  • Stomach/ oesophagus
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11
Q

What is Neoplasia? What are the types?

A

Abnormal growth of cells which persists after stimulus removed and has escaped normally regularatory processes

Benign

Malignant

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12
Q

What is cell injury caused by? Is it reversible?

A

Inhrently injurous stimuli OR when the cell adaptability is exceeded.

Reversible if stimuli is removed, damage is minor + tx given

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13
Q

What are the causes of cell injury/death?

A

GINPIOC

Genetic derrangements

Infectious agents

Nutritional imbalance

Physical agents

Immune response

Oxygen deprivation

Chemicals/ toxins

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14
Q

What are the two types of cell death?

A

Apoptosis → Programmed

Necrosis → Unprogrammed

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15
Q

Talk about Cell Death Necrosis:

(6)

What type of cell death?

What are the causes?

What happens to the cell?

A

Pathological cell death- external factors

Hypoxia, Chemical toxins

Damage to cell physiology

Degredation of cell strucutre

Influx of ions & water

Cellular organelles swell & rupture

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16
Q

What is Cell Death by Apoptosis?

A

Programmed or Physiological

Constituent genes –> Cell death

17
Q

What are the Morphological feature of Necrosis?

A

Cell membrane integrity is lost & lysosomal hydrolase are released resulting in:

  • Small condensed nuclei
  • Deeply stained nuclei
  • Nuclei fragments in particles
  • Cytoplasm becomes deeply stained
  • Typically affects a large group of cells
  • Enzymatic digestion of cellular contents possible- may leak out
  • Frequent adjacent inflammation
  • Plasma membrane disrupted
18
Q

What are the Morphological Feature of Apoptosis?

A
  • Organelles remain intact
  • Nucleus and cytoplasm condense to form apoptotic bodies
  • Intact membranes surrounding apoptotic bodies
  • Apoptotic bodies phagocytosed by macrophages
  • No inflammatory response
  • Typically affects isolated cells
19
Q

What are the types of Necrosis?

A

Liquefactive

Fat Necrosis

Caseous

Coagulative

Gangrenous

Fibrinoid

20
Q

What is Liquefactive Cell Necrosis?

A

Tissue is replaced by liquefied material

Accompanied with enzymatic digestion of the tissues

21
Q

What is Fat necrosis Cell Necrosis?

A

Enzymatic digestions of tissue

22
Q

What is Caseous Cell Necrosis?

A

Dead tissue looks like cottage cheese (seen in TB infections)

[Midway in appearance between liquefactive & Coagulative]

23
Q

What is Coagulative Cell Necrosis?

A
  • Cells are non-vital i.e. the nucleus is not identifiable but the structure of the tissue still visible histologically
  • Reflects cell death WITHOUT enzymatic digestion of the tissues
  • Commonly seen in ischaemic injuries (except in the brain)
24
Q

What are the mechanisms of cell damage?

A
  • Free Radicals
  • Loss of calcium homeostasis
  • Oxidative stress
  • Defects in membrane permeability
  • Depletion of ATP
  • Mitochondrial damage
25
Q

What is infarction?

A

Area of ischeamic necrosis in tissue/ organ due to reduced/ absent blood supply