Pathophysiology Flashcards

1
Q

3

Causes of altered cellular functions

A

Adaption
Injury
Ageing

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2
Q

5

Cellular adaption & types

A

Changes based on the environment to escape and protect from injury

Atrophy (decreased size)
Hypertrophy (increased size)
Hyperplasia (increase cell number)
Metaplasia (reversible replacement of mature cell to less mature cell)
Dysplasia (irreversible deranged cell growth)

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3
Q

7

Cellular Injury & causes

A

Unable to maintain homeostasis due to stimuli or stress

Hypoxia, nutritional imbalance, chemical agents, physical agents, infection, genetics, ageing

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4
Q

3

Hypoxia & causes

A

Insufficient oxygen supply to tissues in order to maintain homeostasis

  1. Lack of oxygen entering body (respiratory disease, low atmospheric O2)
  2. Lack of O2 transport (CVD, anaemia, low Hb, reduced RBC production)
  3. Ischaemia (lack of/restricted blood flow)
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5
Q

4

Mechanisms of cellular injury (list)

A

ATP depletion
Altered calcium homeostasis
Defects in membrane permeability
Free radicals

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6
Q

ATP Depletion

Mechanism of cellular injury

A

Loss of O2 reduces ATP synthesis
Failure of Na/K pump = cellular swelling
Anaerobic glycolysis = lactic acidosis
Overall decreased protein synthesis, membrane transport, lipogenesis, loss of membrane integrity

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7
Q

Altered calcium metabolism

Mechanism of cellular injury

A

Lack of ATP = reduced Ca transport out of cell
High cytosolic Ca = damages plasma membrane, cytoskeleton, activates destructive enzymes, damages mitochrondia

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8
Q

Defects in membrane permeability

A

Loss of selectivity in transport in all types of injury
* Na, Ca, water influx

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9
Q

Free radicals

Mechanisms of cellular injury

A

Atoms with unpaired electron
Lipid peroxidation, oxidative stress = alters proteins, DNA, and mitochondria
Esp during reperfusion

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10
Q

2

Types of cellular injury

A

Reversible: cellular swelling (ATP pumps), lipid accumulation (alt liver metabolism) (reversible)
Irreversible: cannot restore homeostasis (DNA & lysosomal leakage, enzyme induced autolysis)

Apoptosis and necrosis

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11
Q

2

Apoptosis & types

A

Programmed cell death, selective self destruction (condensation, blebs, fragmentation)
1. Pathologic = infected cells, damaged DNA, pre-cancerous cells
2: Physiologic = developmental, no inflammation, occurs too great in degenerative conditions (Alzheimer’s)

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12
Q

Necrosis & characteristics

A

Premature death from injury/noxious stimuli = autolysis, self destruction (ER/Mit swelling, blebs, breakdown, leakage)

  • Inflammatory cells (macro, neutro), areas of cell loss
  • Clumping of genetic material (karyolysis), cell membrane and organelle disruption
  • Lysosome disruption, digestive enzyme leakage, autolysis
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13
Q

5

Types of necrosis

A
  1. Coagulative: ischaemic injury, protein denaturation (kidneys, heart, adrenals)
  2. Liquefactive: ischeamic injury to brain (cell dissolusion due to digestive enzymes)
  3. Caseous: coag+liquefactive (cheese like, TB infection)
  4. Fat: adipose injury, lipase action (breast, pancreas, abdominal organs)
  5. Gangrenous: severe hypoxic injury, dry or wet
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14
Q

Ageing & types

A

Accumulation of changes over time

  1. Cellular ageing: genetics (DNA repair defects, genetic abnormalities, mutations, alt signalling) & environmental (free radicals, reduced enzymes, abnormal protein accumulation) = atrophy, loss of function and cells
  2. Tissue ageing: progressive stiffness, rigidity, scarcopenia
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