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Pathology > Cell Injury, Adaption & Death > Flashcards

Cell Injury, Adaption & Death Flashcards

1
Q

What is cell adaptation?

A

The structural and functional changes a cell undergoes due to changes in their microenvironment

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2
Q

What are the microenvironmental changes a cell undergoes?

A
  1. Physiological (stress, increased demand or hormonal influence)
  2. Pathological (injurious stimuli)
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3
Q

Why does cell injury occur?

A

If cells cannot adapt accordingly to changes in their environment, they undergo cell injury.

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4
Q

Cellular Response to Stressors

A
  1. Adaptation
  2. Cell Injury (if cell injury is continuous > cell death
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5
Q

Role of Lysosomal Enzymes in Cell Injury

A

Lysosomal damage causes leakage of hydrolytic enzymes > break down of cellular components > damage to the surrounding tissue > necrosis

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6
Q

Role of the Sodium-Potassium Pump in Cell Injury

A

Responsible for movement of K+ into the cell while simultaneously removing Na+ out of the cell.

Failure of the sodium potassium pump can cause the cell to swell + rupture

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7
Q

ATP production in the cell

A
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8
Q

What is the main cause of cell injury and what is that caused by

A

Hypoxia: AKA oxygen deficiency
- can be caused by:

  1. Ischemia (restriction in blood supply to tissues) - most common cause
  2. Reduction on O2: anemia, CO toxicity
  3. Decreased tissue perfusion: cardiac failure and shock
  4. Poor oxygenation of blood: pulmonary diseases
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9
Q

Other causes of cell injury

A

Physical, chemical and infectious agents
Free radicals
Nutritional deficiencies
Genetic abnormalities

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10
Q

Mechanisms of cellular injury

A
  1. Mechanical disruption - trauma / osmotic pressure
  2. Deficiency of metabolites - glucose, oxygen, hormones
  3. Failure of membrane functional integrity - damage to ion pumps
  4. Membrane damage - free radicals can cause damage to DNA
  5. Blockage of metabolic pathways - interruption of protein synthesis / respiratory poisons e.g. cyanide poisoning inhibits cytochrome oxidase
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11
Q

How does thombus formation lead to ischemic induced cell injury?

A

Thrombus formation in an artery lead to ischemia of the tissue.
> anaerobic glycolysis > formation of lactic acid and an acidic pH inside the cells.

Cells try to remove H+ which leads to entry of Ca+ inside the cells > activates phospholipases > cell membrane damage

Also anaerobic glycolysis lead to less ATP formation and therefore affecting sodium-potassium pump.

All these lead to cell injury or cell death

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12
Q

Mechanisms of radiation induced cell injury

A

leads to apoptosis or necrosis
If cells are exposed to a low dose (300-1000 R) - mainly breaks down water which liberates OH- (free radical) which causes damage to the tissue ultimately leads to apoptosis

High doses (<2000 R) - cell and membrane bursts - causes cell death by necrosis

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13
Q

Free radical

A

An atom/group of atoms containing one or more unpaired electron

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14
Q

Cell injury: mediation by free radicals

A

interacts w/surrounding tissue, gains an electron - damages the structure of the tissue and impairs function

Mechanism of generation:
Oxygen therapy: > 20% Oxygen therapy
Inflammation
ionizing radiation: radiotherapy
Ultraviolet light
Drugs and chemicals: Barbiturate toxicity (induction of P-450 enzyme in SER)

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15
Q

Consequences of free radicals

A

Membrane damage
DNA damage
Protein cross-linking
Loss of enzymatic activity

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16
Q

Where are free radicals produced continuously in the body?

A

Free radicals (superoxide and hydrogen peroxide) are continuously produced in the mitochondria and cytoplasm as a result of metabolic activity

17
Q

Generation and detoxification of free radicals in a cell

A

Free radicals are detoxified by:

  1. superoxide dismutase - an enzyme that facilitates the breakdown of the superoxide into either O2 or H2O2.
    Hydrogen peroxide is also damaging, but less so than the superoxide radical
  2. catalase - degrades H2O2 in the body
  3. Glutathione peroxidase - reduces hydrogen peroxide to water to limit its harmful effects.
18
Q

What are the cells responses to injury?

A
  1. Adaptation - adjusting their structure and functions for various conditions
  2. Reversible Injury
    a) Hydropic degeneration (cloudy swelling) - due to accumulating of water in the cell - commonly caused by Na-K+ pump function failure
    b) Fatty change - lipid accumulation die to ribosomal function failure
  3. Irreversible injury = cell death (necrosis/apoptosis)
19
Q

Cell Injury - Morphological changes

A

Reversible injury:
Cellular swelling, large vacuoles in the cytoplasm
Swelling of endoplasmic reticulum
Swelling of mitochondria
Disaggregation of ribosomes
Chromatin clumping
Cell blebs

20
Q

Irreversible cell injury - why & processes?

A

Severe and prolonged injury leads to the “point of no return”.
Cells cannot recover even if the pathological stimulus is removed.

Either physiological (there is pain AKA necrosis) or pathological (occurring in the body constantly - person is not aware AKA apoptosis)

21
Q

Necrotic vs Apoptotic cell death

A

Apoptosis - cell shrinks- fragmentation into membrane-bound apoptotic bodies containing cytoplasmic and nuclear contents - phagocytosed by neighboring cells

Necrosis - cell swells - cell becomes leaky - cellular and nuclear lysis causes inflammation

22
Q

Necrosis (in detail)

A

The death of cells in living tissues characterised by the breakdown of cell membranes

Pathological condition

Digestion and denaturation of cellular components by hydrolytic enzymes from damaged lysosomes

Nuclear changes:
- Pkynosis: shrunken, deeply stained
- Karyorrhexis: nucleus fragmentation scattered in cytoplasm
- Karyolysis: nucleus disappears

Associated with inflammatory reaction.

23
Q

Main types of necrosis

A
  1. Coagulative
    General architecture well preserved
    increased cytoplasmic binding of acidophilic dyes
    Nuclear changes
    Most often results from interruption of blood supply
    1. Liquifactive
      e.g. necrosis in the brain
      Enzymatic liquefaction of necrotic tissue
      Also occurs in areas of bacterial infected infarction
      Abscess formation
24
Q

Caseous

A

dead cells persist as coarse granular cheese-like debris
shares features of coagulation and liquefaction necrosis
most commonly seen in TB

25
Q

Gangrene

A

life threatening condition that occurs when coagulative necrosis is associated with infection

26
Q

Autolysis

A

degradation reaction of cells after death

27
Q

What is apoptosis

A

A vital process that helps eliminate unwanted cells during development

28
Q

Characteristic changes of apoptosis

A

Chromatin condenses and fragmentation
DNA fragments enclosed into membrane-bound apoptotic bodies
Electrophoresis of DNA: “laddered pattern”
No inflammation

29
Q

Apoptosis - Extrinsic Pathway

A

ligation of death receptors on the cell surface

leads to recruitment of FADD protein, which then is responsible for the recruitment of caspase-8
The activated caspase 8 then activates procaspases 3, 6, 7
- causes activation of endonucleases, breakdown of nuclear and cytoskeleton proteins
- resulting in apoptosis of a cell

30
Q

Apoptosis - Intrinsic pathway

A
31
Q

Cells that continuously multiply

A

Labile cells:
- proliferate continuously
- short life span
e.g. hemopoietic cells, epithelial cells

Stable cells:
- proliferate rapidly when cells are stimulated or lost e.g. liver, endothelial cells

Permanent cells:
- only proliferate during feotal life, but not after birth e.g. neurons, cardiac muscle

32
Q

Types of Cell Adaptation

A
  1. Atrophy
  2. Hypertrophy
  3. Hyperplasia
  4. Metaplasia
  5. Aplasia
  6. Hypoplasia
33
Q

Atrophy

A

Decrease in size of organ due to decrease in size of pre-existing cell.

Casual factors: disuse, malnutrition, aging

34
Q

Hypertrophy

A

Increase in the size of an organ due to increase in size of pre-existing cells

Casual factors: increased use, excessive hormone stimulation

35
Q

Hyperplasia

A

Increase in the size of an organ or tissue caused by an increase in the number of cells

e.g. glandular proliferation in the breast during pregnancy, uterine enlargement during pregnancy

36
Q

Metaplasia

A

Replacement of one differentiated cell type by another

37
Q

Aplasia

A

A failure of cell production during fetal development,
- results in the absence of an organ

38
Q

Hypoplasia

A

Partial growth of an organ

Pathology (11 decks)

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