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FOM 1 > Week 7 > Flashcards

Week 7 Flashcards

1
Q

What are the 6 categories of causes of cell damage?

A

ATP depletion/ Reduced synthesis
Mitochondria damage
Intracellular calcium
Free radical damage
Defective membrane permeability
Protein misfolding

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2
Q

What does hypoxia interfere with?

A

Aerobic oxidative respiration

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3
Q

What occurs in hypoxic injury?

A

Reduced ATP generation
Isosmotic water gain and cellular swelling
Increase in anaerobic glycolysis
Ribosomes detach from RER
Polysomes dissociate into monosomes

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4
Q

At what point in hypoxia does it become irreversible?

A

After cytoskeleton breaks down and there is a loss of ultrastructural features

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5
Q

What is a reperfusion injury?

A

Exacerbates tissue damage through paradoxical further injury

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6
Q

What is a free radical?

A

An atom, molecule or ion with one or more unpaired valence electron

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7
Q

What are ROS?

A

Reactive Oxygen Species: Free radicals by product of O2 metabolism

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8
Q

What can result in high ROS levels?

A

Membrane damage and promoted mitochondrial transition

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9
Q

What are the 3 methods of mechanical cell injury?

A

Direct mechanical damage
Freezing
Osmotic imbalance

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10
Q

What occurs during freezing?

A

Intracellular and cell membranes perforated by ice crystals

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11
Q

What is atrophy?

A

Shrinkage in the size of a cell by the loss of cell substance

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12
Q

What is hypertrophy?

A

Increase in the size of cells and consequently an increase in the size of the organ

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13
Q

What is hyperplasia?

A

Increase in number of cells in an organ or tissue

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14
Q

What is metaplasia?

A

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

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15
Q

Describe some differences between apoptosis and necrosis

A

Cell size swollen in necrosis and shrunken in apoptosis.
Membrane disrupted in necrosis and intact in apoptosis.
Inflammation nearby in necrosis not in apoptosis.
Rarely pathological in apoptosis.

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16
Q

What are the types of necrosis?

A

Coagulative necrosis
Colliquative necrosis
Caseous necrosis
Gangrenous necrosis
Fat necrosis

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17
Q

What causes coagulative necrosis?

A

Ischaemia

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18
Q

What occurs in caseous necrosis?

A

Coagulated tissue no longer resembles the cells but is in chunks of unrecognisable debris

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19
Q

Where is colliquative necrosis normally seen?

A

Brain

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20
Q

What occurs in colliquative necrosis?

A

Enzymes in neutrophils dissolve tissues nearby causing accumulation of pus effectively liquefying the tissue

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21
Q

What are the 2 types of gangrenous necrosis?

A

Wet
Dry

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22
Q

What occurs in fat necrosis?

A

Enzymes (lipases) release free fatty acids, which with calcium produce soapy deposits in tissues

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23
Q

What is autolysis?

A

Lysis of tissues by their own enzymes following the death of the organism

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24
Q

What are the 3 classifications of cell regeneration?

A

Labile
Stable
Permanent

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25
Q

What regeneration capacity do labile cells have?

A

Good capacity to regenerate

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26
Q

What regeneration capacity do stable cells have?

A

Divide slowly but can regenerate if needed

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27
Q

What regeneration capacity do permanent cells have?

A

No means of effective regeneration

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28
Q

What can cause inflammation?

A

Microbial infections
Hypersensitivity reactions
Physical agents
Chemicals
Tissue necrosis

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29
Q

How does microbial infection cause inflammation?

A

Bacterial exotoxins
Bacterial endotoxins
Viral intracellular multiplication leading to cell death
May cause hypersensitivity reactions

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30
Q

What are the cardinal signs of acute inflammation?

A

Rubor
Calor
Tumor
Dolor
Loss of function

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31
Q

What are the 6 stages of inflammation?

A

Release of chemical mediators
Vasodilation
Increased vascular permeability
Fluid accumulation
Cellular recruitment
Phagocytosis

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32
Q

What is exudation?

A

The process of increased vascular permeability and net flow of fluid out of vessels in acute inflammation

33
Q

What cells are found commonly in cellular exudate?

A

Neutrophils

34
Q

How do neutrophils move?

A

Contraction of cytoplasmic microtubules
Chemotaxis in response to inflammatory chemicals

35
Q

What are the stages of neutrophil migration out the vessel?

A

Margination
Pavementing
Passage between endothelial cells
Pass through basal lamina and migrate into adventitia

36
Q

What causes adhesion of neutrophils?

A

Interaction of paired adhesion molecules

37
Q

What chemicals are released by the original inflammatory stimulus to up regulate P-selectin and PAF?

A

Histamine
Thrombin

38
Q

What is PAF?

A

Platelet Activating Factor

39
Q

What does histamine do?

A

Causes vascular dilation and permeability

40
Q

What is histamine mainly released by?

A

Mast cells

41
Q

What cells release lysosomal compounds?

A

Neutrophils

42
Q

What do leukotrienes do?

A

Have vasoactive properties

43
Q

What can prostaglandins do?

A

Some cause increased vascular permeability
Some cause platelet aggregation

44
Q

What is the effect of serotonin in acute inflammation?

A

Vasoconstriction

45
Q

What are chemokines?

A

Family of chemicals which attract more white blood cells to the site of inflammation

46
Q

What are the four enzyme cascade systems in plasma?

A

Coagulation system
Kinins
Fibrinolytic system
Complement system

47
Q

What do C3a and C5a do in acute inflammation?

A

Chemotaxis of neutrophils
Histamine release from mast cells
Increased vascular permeability

48
Q

What does C567 do in acute inflammation?

A

Chemotaxis of neutrophils

49
Q

What do C4b, 2a and 3b do in acute inflammation?

A

Opsonisation of bacteria

50
Q

What are the benefits of inflammation?

A

Dilution of toxins
Entry of antibodies
Transport of drugs
Fibrin formation
Delivery of nutrients and oxygen
Stimulation of immune response

51
Q

What are the 4 possible outcomes of acute inflammation?

A

Resolution
Suppuration
Scarring or fibrosis
Chronic inflammation

52
Q

What is suppuration?

A

Formation of pus, a mix of neutrophils, debris, bacteria etc.

53
Q

What is primary intention?

A

2 edges of wound can be brought together, fibrin joins them initially and over time epidermal regrowth and collagen synthesis strengthen the join

54
Q

What occurs in secondary intention?

A

Tissue defect filled by granulation tissue, epithelial regrowth over the surface, fibrous scar forms and contracts over time

55
Q

When can complete healing occur in the liver?

A

Loss of hepatocytes but no damage to architecture

56
Q

What type of damage leads to scarring/impaired function in the kidneys?

A

Destruction of glomerulus or damage to interstitium

57
Q

What kind of smooth muscle cells regenerate?

A

Vascular smooth muscle

58
Q

What kind of neural tissue can regrow?

A

Peripheral nerves depending on alignment and continuity

59
Q

What occurs in cellular exudate when inflammation progresses to chronic?

A

Neutrophils are replaced with lymphocytes, plasma cells, macrophages

60
Q

Give some examples of primary chronic inflammation?

A

TB
Leprosy
RA
Chronic inflammatory bowel
Crohn’s

61
Q

What is the most common type of acute inflammation to progress to chronic?

A

Suppurative

62
Q

What can be provoked by presence of foreign material?

A

Granulomatous inflammation, foreign body giant cells

63
Q

What are the macroscopic signs of chronic inflammation?

A

Chronic ulcer
Chronic abscess cavity
Fibrosis/thickening of tissue

64
Q

How do lymphocytes, plasma cells, macrophages and eosinophils appear microscopically?

A

Lymphocytes - Small purple dots
Plasma cells - Fried eggs
Macrophages - Large blobs
Eosinophils - Tomatoes with sunglasses

65
Q

What do lymphocytes do in chronic inflammation?

A

B - Meet antigens, turn into plasma cells
T - CD8+ cytotoxic function and recruiting other immune cells
CD4+ Activate killer T and plasma cells

66
Q

What are cytokines?

A

Small proteins that enhance cell mediated immunity and enhance the antibody response

67
Q

What is a granuloma?

A

A collection of histocytes

68
Q

What is granulomatous inflammation associated with?

A

Foreign body reactions
Infections (e.g. TB)
Sarcoidosis
Crohn’s

69
Q

How are giant cells formed?

A

Macrophages collide, potentially when trying to eat the same particle

70
Q

What are the 3 giant cell types?

A

Foreign body type
Langhans
Touton

71
Q

Does apoptosis or necrosis require energy?

A

Apoptosis

72
Q

What are the 2 mechanisms of inducing apoptosis?

A

Extrinsic
Intrinsic

73
Q

What receptors initiate the extrinsic pathway of apoptosis?

A

Death receptors (Fas and TNF)

74
Q

Where is the intrinsic pathway of apoptosis initiated?

A

Mitochondria

75
Q

What is the function of P53?

A

Assesses for cell damage halting division and if repair of DNA not possible stimulates caspases and initiates apoptosis

76
Q

What happens if too little apoptosis occurs?

A

Cancers
Autoimmune diseases

77
Q

What happens if too much apoptosis occurs?

A

Neurodegenerative diseases

78
Q

What is pyknosis?

A

Cell shrinkage

FOM 1 (14 decks)

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