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Pathology > Cell Death & Necrosis > Flashcards

Cell Death & Necrosis Flashcards

1
Q

Is cell degeneration reversible or irreversible cell injury?

A

Reversible

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2
Q

Is cell necrosis reversible or irreversible cell injury?

A

Irreversible - too far gone

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3
Q

What is nearly all cell damage mediated by?

A

Damaged membranes or enzyme systems

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4
Q

What can be seen under the microscope with cell death/ degeneration?

A

Changes in individual cells and groups of cells

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5
Q

What can clinical biochemistry detect with damaged/ dead cells?

A

Leaked intracellular substances in body fluids - Often Enzymes

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6
Q

What is the underlying mechanism for cell injury?

A

Disruption of the Na+/K+ active membrane pump - Na+ can then move into the cell - Water follows Na+ - Cell appears to swell

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7
Q

What is severe cell swelling?

A

When the whole cell and organelles swell and are damaged - this means cellular function is impaired because the organelles no longer work as well/ at all

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8
Q

How can membrane damage be self- perpetuating?

A
  • Intracellular Ca2+ from the cytoplasm and the organelles leaks out and activates phospholipases – lyse membrane phospholipids - Cytoskeleton damage - Free radical damage - Broken down membrane fragments have a detergent effect and stop other membranes from working properly
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9
Q

What are some of the causes for cell damage?

A
  • Physical trauma - Hypoxia - Free radical damage - Immune reactions - Genetic Defects - Nutrition - Microbiological agents - Aging
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10
Q

Describe Hypoxia in terms of cell damage…

A
  • Lack of O2 - Mediated by decreased ATP production - Caused by: – respiratory disease – Anaemia – Damage to RBCs – CO poisoning – Haemorrhage – Trauma – Cardiac Dysfunction – Constriction – Thrombosis
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11
Q

What are free radicals?

A

A single unpaired electron in an outer shell - Highly reactive - Very unstable - Autocatalytic - start off with one and it makes heaps Involved in cell injury, aging anf macrophage killing

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12
Q

How are free radicals formed?

A
  • Action of radiant energy - Normal cellular reactions - Inflammation - Enzyme metabolism of certain chemicals - Reperfusion injury (hypoxic tisse gets blood flow back = lots of FRs) - Also from O2, N, C - catalysed by Fe2+
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13
Q

What are the most common free radicals?

A

Oxygen derived free radicals

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14
Q

What are the consequences of free radicals?

A
  • Lipid degradation of membranes by oxidation of unsat Fatty Acids - Damage to cell proteins - Breaks in DNA strands - Damage to mitochondria Can damage cells at every level!
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15
Q

What are some protective mechanisms against free radicals?

A
  • Natural decay of free radicals - Anti-oxidants - Enzymatic inactivation
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16
Q

What changes the morphologic appearance of cell degeneration?

A
  • Swelling and Eosinophilia - Fatty Change
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17
Q

Describe cell swelling?

A
  • Cytoplasm appears swollen, cloudy, granular or vacuolated - Reversible - Increased cell size may affect organ function
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18
Q

Describe Eosinophilia…

A

One morphological appearance of cell degeneration - Cells stain pinker - Ribosomes appear blue

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19
Q

Describe Fatty Change?

A

One morphologic appearance of cell degeneration - a.k.a. lipidosis, fatty degeneration, steatosis, fatty infiltration - Increased amounts of TAGs in cells - Normal in some tissues - Liver most often affected

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20
Q

Why is the liver most often affected by Fatty Change?

A

Because it is the main organ involved in fat metabolism - fat arrives from the diet and from adipose tissue

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21
Q

What is the pathogenesis of fatty liver?

A
  1. Increased energy demand by foetuses in late pregnancy combined with decreased ewe intake caused by stressors or compression of digestive organs by uterus = Negative energy balance 2. HYPOGLYCAEMIA 3. Secretion of glucocorticoids by adrenal glands + mobilisation of fat stores 4. OAA build up in blood - no ACoA due to previous hypoglycaemia 5. OAA used as substrate for ketone body formation = KETONAEMIA and KETONURIA 6. Increased deposition of TAGs into liver that can’t be oxidised = FATTY LIVER - FFA’s released from Adipose are transported to liver - re-esterified to TAGs - oxidised to ACoA - ACoA into TCA cycle to produce energy or ketone bodies
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22
Q

What happens to the TAGs sent to the liver in mobilisation of adipose?

A
  • Stored as TAGs - Oxidised to Acetyl- CoA - Used to make membranes, Steroid hormones - Exported in bloodstream stuck to lipids as VLDL
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23
Q

How does fat accumulate in the liver?

A

When more is entering than being removed - Increased dietary intake of fat OR moderate body fat supplies and decreased intake - Decreased metabolism of fat in the liver OR decreased transport of liver due to decreased apoproteins

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24
Q

What is the underlying mechanism of fatty liver disease?

A

Decreased mitochondria

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25
Q

If there is decreased apoproteins in the liver what does this indicate?

A

Protein malnutrition - apoproteins are made from AAs that come from the diet

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26
Q

What histology preparations should be used to dissolve fat out of cells?

A

Frozen sections OR Special Stains (Sudan, Oil red O)

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27
Q

What happens to the globules of fat in chronic fatty liver?

A

They start to coalesce to make big clear vacuoles of fat

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28
Q

Describe the gross appearance of a liver affected by fatty liver…

A
  • Pale - Friable - Greasy - Bulging - Floats
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29
Q

What is the definition of necrosis?

A

Local death of tissues within a living individual - A result of irreversible cell damage

30
Q

What questions should be asked to determine the significance of the necrosis?

A
  • Where is the necrosis? - How much necrosis? - How fast has the necrosis occurred? - What are the sequelae? (consequences)
31
Q

Describe a local reaction necrosis…

A
  • Irritant = inflammation - Accumulation of WBCs – neutrophils then macrophages - Line of demarcation
32
Q

Describe system reaction necrosis…

A

Release of enzymes from dead cells - Increased serum levels in clinical biochemistry Acute phase response - by generalised illness e.g. cat bite abscess

33
Q

How can the histological appearance of necrosis be described?

A
  • Cytoplasm is eosinophilic - Cells tend to be shrunken - Cells have loss of distinct membrane
34
Q

Why is it important to classify necrosis?

A
  • It may suggest possible causes of necrosis - Narrows down the differential diagnoses
35
Q

Describe coagulative necrosis…

A
  • The architecture of the organ remains
  • Enzymes are inactivated or delayed
  • Commonly due to ischaemia
36
Q

Describe Caseous necrosis…

A
  • Loss of cellular and architectural detail of the organ - Cheesy appearance - Caused by certain bacteria… – Mycobacterium sp (TB) – Corynebacterium pseudotuberculosis
37
Q

Describe Liquefactive necrosis…

A
  • Liquid mass of necrotic tissue - No cellular or architectural detail - Mostly in CNS (known as malacia)
38
Q

Describe Suppurative necrosis…

A
  • Liquefaction with pus formation - Involves pyogenic bacteria that attract neutrophils - Enzymes are released from neutrophils, bacteria and damaged cells
39
Q

What is pus?

A

Purulent exudate - Liquid necrotic debris + Neutrophils + Tissue fluid

40
Q

Describe fat necrosis…

A
  • Occurs by saponification
41
Q

What are the sequelae of necrosis?

A
  • Liquefaction and removal into lymphatics by macrophages - Suppuration - Sequestration (encapsulation) - Ulceration/ erosion
42
Q

Describe Erosion and Ulceration sequelae…

A

Surfaces of skin and luminal organs - Dead cells desquamate - Erosion of part of thickness of epithelium - Ulceration of Basement membrane, exposing underlying tissue

43
Q

Describe Liquefaction and removal…

A
  • Small areas of tissue AND / OR - Large amounts of fluid, enzymes and neutrophils anr absorbed into lymphatics
44
Q

Describe Sequestration…

A

Encapsulation without liquefaction - more common with coagulative or caseous necrosis - necrotic tissue becomes surrounded by fibrous capsule - necrotic centre is called sequestrum

45
Q

Describe Abscessation…

A

Liquefaction + Suppurative + Encapsulation - Abscess is pus confined within a tissue - Can burst or become ‘walled off’

46
Q

Describe Repair…

A

a.k.a Organisation Involves: - WBCs - Capillaries - Fibroblasts Results in scarring

47
Q

Describe regeneration…

A

Dead cells replaced by new cells of the same type Occurs when: - Cells in affected tissue can multiply - Some cells survive initial damage e.g. liver

48
Q

Describe Gangrene…

A

Ischaemic necrosis - Usually involves extremities - May be complicated by bacterial infection because dead tissue becomes accessible to bacteria and normal defense mechanisms don’t work

49
Q

What are the different types of gangrene?

A

Dry Moist Gas

50
Q

Describe Dry gangrene…

A

Uncomplicated ischaemic necrosis - coagulative necrosis

51
Q

Describe Moist gangrene…

A
  • Tissue with large amounts of blood and fluid - Complicated by bacterial infection - Liquefaction
52
Q

Describe Gas Gangrene…

A
  • Gas-forming bacteria - Anaerobic - Produces Exotoxins
53
Q

What happens if gangrene goes untreated?

A
  • Endogenous and bacterial toxins enter the bloodstream - Blood poisoning - Can be fatal - Debridement / amputation
54
Q

Describe the appearance of gangrene..

A
  • Dark greenish colour – poorly oxygenated blood – RBC breakdown pigments – Iron Sulphide (H2S + Fe2+) - Foul odour - Cold - Unresponsive tissue - Doesn’t bleed - Line of demarcation
55
Q

What are these cells associated with?

A

Necrosis

56
Q

What is this section stained with?

A

Oil red O

57
Q

What is the blue in this slide?

A

Ribosomes

(Eosinophilia)

58
Q

Is this chronic or acute fatty liver?

A

Chronic

  • Larger vacuoles
59
Q

Which tissue here is necrotic and which has suffered degeneration?

A

Dark pink is necrotic

Swollen cells are degenerate

60
Q

Is this chronic or acute fatty liver?

A

Acute

61
Q

What type of necrosis has this liver undergone in parts?

A

Coagulative necrosis

  • Architecture remains
  • Delayed/ inactivated enzymes
  • Commonly due to ischaemia
62
Q

What type of gangrene is this pig suffering from?

A

Dry gangrene associated with sepsis

63
Q

What is wrong with this liver?

A
  • It has fatty liver
  • Pale, greasy, friable, bulging, floats in water
64
Q

What type of necrosis can be seen here?

A

Saponification necrosis

65
Q

What type of necrosis can be seen here?

A

Liquefactive necrosis

66
Q

What is this image?

A
  • A Bone sequestrum
  • a small fragment of necrotic bone is walled off
67
Q

What does this image show?

A

A local reaction

  • Line of inflammation surrounds the central lesion
68
Q

What type of necrosis is this?

A
  • Suppurative necrosis
69
Q

What type of necrosis is this?

A
  • Caseous Necrosis
  • Cheesy
  • Loss of cellular and architectural detail
70
Q

What type of gangrene is this?

A
  • Ganreneous mastitis “Blue Bag”
  • Sharply demarcated area of black skin
71
Q

What is occurring here?

A

Erosion

  • Sequelae of necrosis
  • Basement membrane is left intact
72
Q

What is occurring here?

A

Ulceration

  • Affects basement membrane and underlying tissues

Pathology (12 decks)

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