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Path Processes > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

Name some of the 7 things that can cause cell injury

A
  1. Hypoxia
  2. Toxins
  3. Physical agents (direct trauma, temp extremes)
  4. Radiation
  5. Mico-organisms
  6. Immune mechanisms
  7. Dietary insufficiency or excess
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2
Q

What are the 4 types of hypoxia?

A
  1. Hypoxaemic Hypoxia - low arterial O2 content
  2. Aneamic Hypoxia- decreased ability of Hb to carry 02
  3. Ischeamic Hypoxia- interruption to blood supply
  4. Histiocytic hypoxia- inability to utilise 02 in cells due to disabled oxidative phosphorylation enzymes
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3
Q

Give an example of when Hypoxaemic hypoxia may occur

A
  • at altitude
  • reduced 02 absorption secondary to lung disease
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4
Q

Give an example of when anaemic hypoxia may occur

A
  • Aneamia
  • Carbon monoxide poisoning
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5
Q

Give an example of when ischaemic hypoxia may occur

A
  • Heart failure
  • Blockage of a vessel
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6
Q

Give an example of when histocytic hypoxia may occur

A
  • Cyanide poisoning
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7
Q

What 4 essential cell components are the main targets of cell injury?

A
  1. Cell membrane
  2. Mitochondria
  3. Nucleus
  4. Proteins (structural and enzymes)
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8
Q

Give a summary of what happens in hypoxic cell injury (~13 steps!)

A
  1. Cell is deprived of 02
  2. Mitochondrial ATP production stops
  3. ATP driven membrane ionic pumps run down
  4. Na+ and water seep into the cell
  5. The cell swells, stretching plasma membrane
  6. Glyoclysis makes cell go limp for a while
  7. Cell initiates heat shock response
  8. pH drops as cells produce energy by glycolysis and lactic acid accumulates
  9. Ca2+ enters cell as membrane damaged. This actives: -phospholipases -proteases -ATPase -endonuclease
  10. ER and other oranelles swell
  11. Enzyme leak out of lysosomes and attack cell components
  12. Cell membranes start to bleb
  13. Cell dies
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9
Q

What is ischemia-reperfusion injury?

A

Return of blood flow to ischemic tissue can cause more injury than if blood flow wasn’t returned

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10
Q

What causes ischema-reperfusion injury?

A
  • increased production of free radicals as a result of mitochondrial burst
  • increased number of neutrophils causing more inflammation
  • Delivery of complement proteins activating complement pathway
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11
Q

What are free radicals?

A

Reactive oxygen species with single unpaired electron in outer orbit making it unstable

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12
Q

In what ways can free radicals damage cells?

A
  • mutagenic
  • cause lipid per oxidation in cell membranes
  • damage proteins, carbs and nucleic acids
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13
Q

What are the main 3 ROS?

A
  • hydroxyl OH•
  • superoxide 02-•
  • Hydrogen peroxide H202
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14
Q

What defence mechanisms make up the anti-oxidant system?

A
  1. Enzymes
  2. Free radical scavengers
  3. Storage proteins that sequester transition metals (Transferrin and ceruloplasmin sequester Fe2+ and Cu2+)
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15
Q

Name 3 anti-oxidant enzymes

A
  1. superoxide dismutase
  2. catalase
  3. peroxidases
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16
Q

Name 3 free radical scavengers

A
  • VitA
  • VitC
  • Glutathione
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17
Q

When are free radicals produces?

A
  1. Normal metabolic reaction (oxidative phosphorylation)
  2. Inflammation (oxidative burst)
  3. Radiation: H20 → OH.
  4. Contact with unbound metals the body e.g Fenton reaction
  5. Drugs and chemicals e.g in liver metabolism of paracetamol by CYPs
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18
Q

What are heat shock proteins?

A

Proteins activated by any type of cell injury that aim to mend mis-folded proteins to maintain cell viability

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19
Q

Give an example of a heat shock protein

A

Ubiquitin

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20
Q

What are the reversible changes that can be seen in damaged cells under the microscope?

A
  • Swelling - both the cell and organelles due to Na/K ATPase failure
  • Cytoplasm blebs
  • Clumped chromatin due to reduced pH
  • Ribosome separate from ER
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21
Q

What are the irreversible changes seen in damaged cells under the microscope?

A
  • Increased cell swelling
  • Nuclear changes pynokosis, karylosis, karyorrhexis
  • Swelling and rupture of lysosomes
  • Membrane defects
  • Appearance of myelin figures
  • lysis of ER
  • amorphous densities in swollen mitochondria
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22
Q

What is pynkosis?

A

Nuclear shrinking (condensation of DNA)

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23
Q

What is karyolosis?

A

Nuclear fading

DNAses and RNAses cause chromatin dissolution

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24
Q

What is karyorrhexis?

A

Nuclear membrane disruption and fragmentation

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25
Q

What is oncosis?

A

Cell death with swelling

26
Q

What is apoptosis?

A

Programmed cells death with shrinkage, controlled by regulated programme of DNAases and RNAases

27
Q

What is necrosis?

A

Morphological changes that occur after a cell has been dead some time (12-24 hours)

28
Q

What are the different types of necrosis?

A
  • Coagulative
  • Liquefactive
  • Caseous
  • Fat necrosis
29
Q

What is coagulative necrosis?

A

Necrosis by protein denaturation seen in most solid organs - ghost outlines of cell seen under microscope

30
Q

What is liquefactive necrosis?

A

Necrosis by enzyme release caused by ischemia in loose tissues

  • no cellular outline
  • lots of dead neutrophils and pus
31
Q

What is caseous necrosis?

A

Necrosis with amorphous (structureless) debris -‘cheese like’

associated with infections, particularly TB

32
Q

What is fat necrosis?

A

The destruction of adipose tissue by lipase -seen in acute pancreatitis

33
Q

What is gangrene?

A

The visible appearance of gangrene to the naked eye

34
Q

What is an infarct?

A

An area of necrotic tissue which is the result of ischemia

35
Q

What is the difference between dry and wet gangrene?

A

Dry gangrene= caused by necrosis exposed to air

Wet gangrene= caused by necrosis modified by infection

36
Q

What is gas gangrene?

A

A type of wet gangrene which is infected by anaerobic bacteria that produce gas

37
Q

What are the 2 main types of infarction and what is the difference between the two?

A

White infarct= anaemic infarct with little haemorrhage - one end artery sole source of blood supply -often wedge shaped

Red infarct= haemorrhagic infarct - dual blood supply - repurfusion - raised venous pressure

38
Q

What are the consequences of cellular molecules being released by dead and dying tissues?

A
  • local irritation and inflammation
  • general toxic effects on body
  • Can be measured in blood to aid diagnosis
39
Q

What are the principle molecules that are released by dead and dying tissues?

A
  • Potassium
  • Enzymes
  • Myoglobin (from myocardium or striated muscle)
40
Q

Why does apoptosis occur physiologically?

A
  1. To maintain steady state
  2. Hormone controlled involution
  3. Embryogenesis (e.g in paw formation)
41
Q

When does apoptosis occur pathologically?

A
  1. When cells are damaged
  2. Cytotoxic T cell killing of virally infected or neoplastic cells
  3. Graft vs Host disease (transplants)
42
Q

What do the stages of apoptosis look like under the microscope?

A
  1. Normal cell
  2. Condensation
  3. Fragmentation
  4. Apoptotic bodies
43
Q

How is the intrinsic pathway of apoptosis initiated and carried out?

A
  • Initiating signal triggered by; irreparable DNA damage or withdrawal of hormones
  • p53 activation causes mitochondrial membrane to become leaky
  • cytochrome C release from mitochondria activates caspases
44
Q

How is extrinsic pathway of apoptosis initiated and carried out?

A
  • Initiated by extracellular signals from cells that are in danger
  • TNFa main signal secreted by T killer cells
  • binds to cell membrane on the ‘death receptor’ -activates caspases
45
Q

What happens to apoptotic bodies?

A

They are eventually phagocytosed

46
Q

What are the 5 main groups of things that can accumulate in intracellular accumulations?

A
  • water and electrolytes
  • lipids
  • carbohydrates
  • proteins
  • pigments
47
Q

When would fluid accumulate in cells?

A

In hypoxia energy supplies are cut off - Na+ and water flood into cell

48
Q

When do lipids accumulate in cells?

A

Steatosis is the accumulation of triglycerides, often seen in the liver as it’s the major organ of fat metabolism

Causes:

  • alcohol
  • diabetes mellitus
  • obesity
  • toxins
49
Q

In what conditions do proteins accumulate in cells?

A
  1. Alcoholic liver disease - Mallory’s hyaline (damaged keratin filaments)
  2. a1-antitrypsin deficiency - liver produces incorrectly folded a1-antitrypsin that cannot leave the ER
50
Q

Why do coal/soot pigments accumulate in cells?

A

Inhaled and phagocytosed by alveolar macrophages but cannot be destroyed usually harmless but in large amounts= fibrosis and emphysema

51
Q

What is pathological calcification?

A

Abnormal deposition of calcium salts within tissues

52
Q

What are the 2 main types of calcification?

A
  • Dystrophic
  • Metastatic
53
Q

What is Dystrophic calcification?

A

Calcification in dying tissue, atherosclerotic plaques and some neoplastic growths

Localised to the area - no abnormality in calcium metabolism, serum calcium or phosphate concentrations - local change favours hydroxyapatite crystals

54
Q

What is metastistic calcification?

A

Calcification throughout the body - hydroxyapatite crystals deposted in normal tissues, secondary to disturbances in calcium metabolsim can be lethal

55
Q

What different things can cause hypercalcaemia?

A
  1. Increased secretion of parathyroid hormone causing bone destruction
  2. Destruction of bone tissue - primary bone marrow tumours - skeletal metastasis
56
Q

In what 3 ways can levels of parathyroid hormone increase?

A
  1. Primary- parathyroid hyperplasia/ tumour
  2. Secondary- renal failure
  3. Ectopic- secretion of PTH related protein by malignant tumours
57
Q

What is replicative senescence?

A

The number of times a cell can replicate, determined by the length of a cells telomeres which shorten with every replication

58
Q

Why do stem cells and many cancer cells have the ability to continuously divide?

A

Telomerase enzyme -maintains the original length of telomeres

59
Q

In aortic calcification, what would you see in the bloods with regards to calcium and phosphate levels?

A

Both normal

60
Q

What causes aortic calcification?

A

It is age related

61
Q

What do heat shock proteins repair?

A

Damaged proteins NOT DNA!!

62
Q

In what condition would you see Mallory’s hyaline?

A

Alcoholic liver disease

Path Processes (12 decks)

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