How The Body Recovers From injury Flashcards Preview

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Flashcards in How The Body Recovers From injury Deck (14)
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1
Q
Tissue Growth
What do these terms mean: 
Multiplicative
Auxetic:
Accretionary (3)
A

Multiplicative: Increase in cell number by mitosis division
Auxetic: Increase in cell size
Accretionary: Increase in extracellular tissue

2
Q
What do the following terms mean? 
What are examples?
Labile Cells
Stable Cells
Permanent Cells (3)
A

Labile Cells: Cells that continuously proliferate and have short lifespan e.g leucocytes, many epithelial cells

Stable Cells: Good regenerative ability but low cell turnover e.g quinscent tissues like hepatocytes.

Permanent Cells: No/little regenerative ability e.g Kertinocytes, cardiac muscle, red blood cells

3
Q

What are the types of Cell adaptation? (4)

A
  1. Hypertrophy
  2. Hyperplasia
  3. Atrophy
  4. Metaplasia
4
Q

What is Hypertrophy (3)

A

Cell increases in size. Only adaptation possible by permanent cells.

Pathological in Cardiac muscle due to hypertension, Bladder cells due to Prostate enlargement.

5
Q

What is Hyperplasia (3)

A

Increase in cell number. Mechanism: GH and stem cells. Requires labile or stable cells.
Can he hormonal or compensatory.

E.g Liver following damage (compensatory)
Breast in pregnancy (hormonal)

Pathological: Prostatic Hyperplasia, endometrial hyperplasia

6
Q

What is Atrophy? (3)

A

Cells shrink in size and numbers. Mechanism: Degrading cell organelles by UBIQUITIN PROTEOSOME pathways.

  • Atrophy of developmental structures: Notochord, thyreoglossal
  • Atrophy of sex organs in Old age.

Pathological: Malnutrition, Vascular Atrophy in Brian, Denervation of muscle.

7
Q

What is Metaplasia? (3)

A

Reversible cell change to another type of cell.
Mechanism: Stem cell differentiates via a different pathway due to change in local micro environment.

Physiological: Cervix - change from simple columnar to epithelium to stratified Squamous due to acidic environment.
Pathological: Bronchial ciliated columnar epithelium to stratified squamous due to smoking. Vice versa in Oesophagus in response to acid reflux (Barrett’s Oesophagus).

8
Q

What are the features of Reversible Cell injury? (4)

A
  1. Reduced respiration and ATP depletion.
  2. Ion concentration and isomeric gradient change leading to swelling
  3. Intracellular organelle change
  4. Increased eosinophilia
9
Q

What are the features of irreversible cell injury? (4)

A
  1. Membrane and organelle rupture
  2. Protein Denature
  3. Nuclear changes

Results in cell death

10
Q

What is the difference between Necrosis and Apoptosis. (4)

A

Necrosis is always pathological cell death, so for as through cell injury first and then if progresses leads to cell death. INFLAMMATION occurs.

Apoptosis is programmed cell death. Tightly controlled and organised. Cell organelles condense, fragment and are PHAGOCYTED.

11
Q

What are the features of necrosis? (4)

A
  1. Organelle damages
  2. Increased Membrane permeability
  3. Influx of Calcium
  4. Loss of respiration, so depleted ATP, build up of Oxygen free radicals and lactic acid.
12
Q

What are the 3 macroscopic patterns of necrosis? (3)

A
  1. Coagulative Necrosis - Shape and architecture preserved for sometime
  2. Liquefacrive Necrosis - Liquified, viscous, soft lesions. Like in Brain from bacterial infection
  3. Caseous Necrosis - Cheese-like appearance. Usually by mycobacteria.
13
Q

What is the most common cause of cell injury?

Why is it worse than hypoxia?

A

Ischaemia.

  • In Hypoxia (lack of oxygen), anaerobic glycolysis can continue. In ischaemia no metabolites are available.

***Ischaemic Reperfusioj injury: where restoration of blood flow exacerbates tissue damage.

14
Q

What are examples of Physiological and pathological Apoptosis? 3 each

What is Autophagy?

A

Physiological: Menstral Cycle, Programmed apoptosis in embryogenesis, Apoptosis of self reactive leucocytes.

Pathological: From Viral Infections, DNA damage (chemo, radiation), Accumulation of abnormal proteins.

  • Autophagy is similar to apoptosis but cells self cannibalise to produce nutrients for other cells.