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FIP > 3. Cell injury and cell death > Flashcards

3. Cell injury and cell death Flashcards

1
Q

What is atrophy

A

decrease in size or number of cells due to loss of cell substance
-resulting in a decrease in the size of the organ

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2
Q

Physiologic or pathologic atrophy

A
  • decreased workload (atrophy of disuse)
  • loss of innervation
  • diminished blood supply
  • inadequate nutrition (cachexia)
  • loss of endocrine stimulation
  • aging
  • fetal development (atrophy of thyroglossal duct)
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3
Q

What is hypertrophy

A

increase in the size of cells

  • resulting in an increase in the size of the organ
  • cells do not divide, number of cells stay the same, just the cells become larger
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4
Q

Physiologic hypertrophy

A

skeletal muscle with exercise

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5
Q

Pathologic hypertrophy

A

left ventricle hypertrophy in hypertension

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6
Q

What is hyperplasia

A

increase in number of cells and usually the size of the organ

  • occurs in organs capable of cellular division
  • often associated with hypertrophy
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7
Q

Physiologic hyperplasia

A
  • hormonal (breast/uterus during pregnancy)

- compensatory (partial hepatetectomy)

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8
Q

Pathologic hyperplasia

A

excessive hormonal/growth factor

  • thyroid
  • endometrial hyperplasia
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9
Q

What is metaplasia

A

reversible change in which one adult cell type is replaced by another adult cell type

  • genetic reprogramming of stem cells
  • e.g:
    a) cigarette smoking - respiratory pseudostratified columnar epithelium -> stratified squamous
    b) Barrett’s oesophagus - stratified squamous -> simple columnar
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10
Q

Causes of cell injury

A
  1. oxygen deprivation
    - hypoxia - low oxygen delivery to tissue
    - ishcaemia - decrease in blood flow (decrease oxygen and nutrients)
    - shock - decrease in perfusion
  2. physical agents
    - trauma, thermal injury, radiation
  3. chemical agents
    - poison, environmental pollutant, drugs
  4. infectious agents
  5. immunologic reactions
  6. genetic defects
  7. nutritional deficiency or excess
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11
Q

Mechanism of cellular injury

A
  • inhibition of aerobic respiration -> ATP depletion
  • generatin of oxygen free radicals
  • defects in membrane permeability
  • disruption of calcium homeostasis (calcium influx)
  • damage to DNA and proteins
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12
Q

How does decreased oxidative phosphorylation within mitochondria cause cellular injury

A
  1. reversible injury
    - reduced ATP
    - increased anaerobic glycolysis -> accumulation of lactic acid
    - reduced activity of sodium pump -> accumulation of sodium and water
    - reduced activity of calcium pump -> increase cytosolic free calcium -> activates enzyme:
    a) ATPase - decreased ATP
    b) phospholipase - decreased phospholipids
    c) endonuclease - nuclear chromatin damage
    d) protease - disruption of membrane and cytoskeletal proteins
  2. irreversible injury
    - mitochondrial changes
    - extensive plasma membrane damage
    - injury to lysosomal membranes:
    a) activation of enz -> degrades the damaged cell
    b) release of enz -> damage the surrounding cell
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13
Q

What is free radicals

A

extremely unstable, highly reactive chemical species with a single umpaired electron in outer orbit

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14
Q

Where does activated oxgen species come from

A
  • physiologic generation during oxidative phosphorylation
  • radiation
  • inflammation
  • oxygen toxicity
  • chemicals and drugs (paracetamol)
  • metals (copper and iron)
  • reperfusion injury
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15
Q

Example of free radicles

A
  • superoxide
  • hydrogen peroxide
  • hydroxyl ion
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16
Q

Why is there free radical degeneration

A
  • unstable with spontaneous decay
  • inactivation by enzymes
  • antioxidants (Vit E,C)
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17
Q

How does free radicals cause cell injury

A
  1. lipid peroxidation of membranes
    - free radicals and membrane lipids react to produce highly reactive lipid peroxide
  2. oxidative modification of proteins
    - cross linking of proteins -> damage to celllular enzyme
  3. react with DNA and cause mutation
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18
Q

Morphologic changes associated with reversible injury

A

decrease sodium-potassium pump -> increased cellular H2O

  1. cellular swelling
    - hydropic change, vacuolar degeneration
  2. ultra structural changes
    - plasma membrane alteration - blebbing
    - loss of microvilli
    - mitochondrial swelling
    - dilation of endoplasmic reticulum with detachments of ribosomes
    - nuclear alterations
19
Q

Morphologic changes associated with irreversible injury

A

membrane damage

  • plasma membrane -> enzyme released (e.g. troponin, amylase)
  • mitochondrial membrane
  • lysosome
20
Q

Morphologic changes associated with necrosis

A
  • death of large group of cells
  • due to pathological process
  • enzymatic digestion of cell:
    a) autolysis- digest themselves
    b) heterolysis - digest neighbouring cells
  • inflammation of surrounding tissue
  • cytoplasmic eosinophilia - become more pink than usual, protein damage so they take up the colour
  • nuclear changes:
    a) pyknosis - condensation of nucleus and clumping of chromatin (shrinking of nuclei)
    b) Karyorrhexis - fragmentation and breakdown of nucleus
    c) karyolysis - pallor and dissolution
21
Q

What is pyknosis

A

condensation of nucleus and clumping of chromatin (shrinking of nuclei)

22
Q

What is karyorrhexis

A

fragmentation and breakdown of nucleus

23
Q

What is karyolysis

A

pallor and dissolution

24
Q

Type of necrosis

A
  1. coagulative necrosis
  2. liquefactive necrosis
  3. caseous necrosis
  4. fat necrosis
  5. fibrinoid necrosis
  6. gangrenous necrosis
25
Q

What is Coagulative necrosis

A

specific morphologic pattern of necrosis with preservation of the structural outlines

  • characteristic of hypoxic cell death except in the brain
  • cell shape and organ structure is preserved
  • nuclei disappear
26
Q

What is Liquefactive necrosis

A

transformation of solid tissue into a liquid mass

  • complete digestion of cells
  • tissue structure destroyed
  • enzymatic lysis of cells
  • characteristic of bacterial and some fungal infection (abscess) and hypoxic cell death in the CNS
27
Q

What is Caseous necrosis

A

distinctive form of necrosis, characteristic of tuberculous infection

  • chessy, crumbly, white gross appearance
  • granular debris surrounded by a ring of granulomatoud inflammation
28
Q

What is Fat necrosis

A

necrosis of fat induced by lipases (pancreas or macrophage)

  • fatty acids complex with Ca2+ to create calcium soap
  • chalky white area (fat saponification)
29
Q

What is Fibrinoid necrosis

A

necrotic damage to blood vessel wall

-associated with malignant hypertension and vasculitis

30
Q

What is Gangrenous necrosis

A

not a distinctive pattern of cell death

  • coagulative necrosis (mummified tissue - dry gangrene)
  • liquefactive necrosis (ischaemia with secondary bacterial infection - wet gangrene)
  • characteristic of ischaemia of the lower limb
  • gas gangrene - clostridium infection
31
Q

What is apoptosis

A

programmed cell death

  • involves single cell or small clusters
  • energy dependent
32
Q

Physiological cause of apoptosis

A
  • embryogenesis
  • hormone (involution of hormone dependent tissue: regression of lactating breast, endometrial shedding)
  • death of inflammatory cells after inflammation
  • cell deletion in proliferating population - intestinal epithelium
  • deletion of autoreactive T cells in thymus (failure might result in autoimmunity)
33
Q

Pathological cause of apoptosis

A
  • virus infected cells
  • cells with DNA damage
  • tumour cells
34
Q

Characteristic of apoptosis

A
  • plama membrane remain intact
  • activation of self-degrading enzyme
  • shrinkage of cell
  • eosinophilia of cytoplasm
  • condensation of chromatin
  • fragmentation of DNA
  • formation of apoptotic bodies
  • apoptotic bodies and cells are phagocytosed without inducing an inflammatory response
35
Q

What is apoptosis triggered by

A
  1. internal signals
    - mitochondrial damage
    - DNA damage
    - decreased hormonal stimulation
  2. external signals
    - surface suicide receptor (FAS receptor) is stimulated
    - TNF/TNFR (tumour necrosis factor)
36
Q

Process of apoptosis

A
  1. activation of caspase (family of cysteine proteases) -> protein cleavage
  2. activation of endonuclease -> stepwise fragmentation of DNA
  3. phagocytosis of apoptotic cells
37
Q

Disorders associated with increased apoptosis

A
  1. AIDS

2. neurodegenerative disease

38
Q

Disorders associated with increased cell survival

A
  1. neoplasia

2. autoimmune disease

39
Q

Intracellular accumulations

A
  1. endogenous
    - normal substance produced at normal or increased rate
    - rate of metabolism inadequate for removal (fatty layer, lipofuscin)
    - normal or abnormal substance cannot be metabolised (storage diseases)
  2. exogenous
    - cell cannot degrade substance (carbon, tattoos)
40
Q

What is lipofuscin

A

pigment like waste product, rich in lipid, accumulates in old age

41
Q

What is pathologic calcification

A

abnormal deposition of calcium salts with smaller amounts of iron, magnesium and other mineral salts

  • 2 types:
    a) dystrophic calcification
    b) metastatic calcification
42
Q

What is dystrophic calcification

A

deposition of calcium in a necrotic tissue

-normal serum calcium

43
Q

What is metastatic calcification

A

deposition of calcium in a normal tissue

a) occurs with hypercalcaemia
- hyperparathyroidism
- destruction of bone occurring with tumours involving bone
- vitamin D intoxication
- sarcoidosis - abnormal collections of inflammatory cells that form lumps known as granulomas
- renal failure
b) occurs in normal tissue
c) primarily affects vessels, kidneys, lungs, and gastric mucosa

44
Q

Two theories of cellular aging

A
  1. wear and tear
    - accumulation of metabolic and genetic damage over a long period of time
    - free radical damage throughout life
  2. intrinsic cellular ageing
    - replicative senescence
    - predetermined genetic programming
    - telomere shortening (incomplete replication of chromosome ends -> cell arrest)

FIP (24 decks)

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