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X Understanding Disease > Inflammation, Healing and Repair > Flashcards

Inflammation, Healing and Repair Flashcards

1
Q

what are the 5 causes of inflammation?

A 
physical
infective
chemical
immunological: hypersensitivity
other
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2
Q

what kinds of physical inflammation are there?

A

trauma
heat/cold
radiation

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3
Q

what kinds of infective inflammation are there?

A

bacteria
parasites
viruses

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4
Q

what kinds of chemical inflammation are there?

A

simple poisons e.g. acid

organic poisons e.g. paraquat

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5
Q

what kinds of immunological: hypersensitivity reactions are there?

A

antigen-antibody

cell-mediated

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6
Q

what other kinds of inflammation are there?

A

vascular

hormonal

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7
Q

what do calor, dolor, rubor and tumor stand for?

A

calor - pain
dolor - heat
rubor - redness
tumor - swelling

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8
Q

what is congestion?

A

blood accumulates in organ or tissue as the result of decreased venous return

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9
Q

what kind of process is congestion?

A

passive

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10
Q

why does congestion occur?

A

increased central venous pressure or blockage/obstruction of venous return from a particular vascular bed

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11
Q

how does congestion differ from hyperaemia?

A

congestion is pathological

hyperaemia is an active, physiological reaction to injury

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12
Q

what kind of inflammation does congestion lead to?

A

predisposes to haemorrhaging -> inflammation -> causes fibrosis and organ dysfunction

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13
Q

explain how hepatic congestion causes inflammation

A
  1. increased central venous pressure in congestive heart failure
  2. increased pressure in central veins
  3. expansion
  4. pressure on hepatocytes
  5. disrupts function
  6. cell death (centrilobular necrosis)
  7. microhaemorrhages, fibrosis around central veins = permanent dysfunction
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14
Q

explain how chronic lung congestion causes inflammation

A
  1. chronic congestion in the lungs
  2. microhaemorrhages
  3. accumulation of haemosiderin-containing macrophages in alveoli and chronic inflammation and fibrosis in interstitial lung tissue
  4. scarring
  5. decreased lung compliance
  6. impaired gas exchange
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15
Q

what is indicative of cellular dysfunction resulting from abnormally increased central venous pressure in the liver?

A

Cytoplasmic vacuolisation of hepatocytes

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16
Q

what 3 signs/symptoms are there of inflammation at a microscopic level?

A

Hyperaemia
Exudation of fluid
Emigration of leucocytes

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17
Q

how does hyperaemia lead to vascular dilation?

A

injury causes a direct affect on vessels -> vascular dilation
injury causes a nervous reaction (axon-reflex) -> vascular dilation
injury damages cells which release chemical mediators which lead to vascular dilation

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18
Q

what is the mechanism of exudation: fluid movement?

A

hyperaemia -> capillary blood pressure rises -> increased filtration pressure

loss of protein from capillaries -> reduced plasma osmotic pressure -> increased filtration pressure

interstitial tissue protein increase -> increased tissue osmotic pressure -> increased filtration pressure

……..

increased filtration pressure -> local swelling (oedema) -> increased lymph flow from area

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19
Q

how does the net movement of plasma proteins and fluid moving into the interstitial space occur?

A

electrolytes in the artierial side and protein increase the oncotic pressure from osmotic conditions - the increased oncotic pressure moves water and protein out of the vessel from the venal side

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20
Q

what is the advantage of exudation?

A

fluid increase -> dilution of toxins (reduce toxin concentration in the area)

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21
Q

what is the contents of the exudation fluid?

A
  • globulins (protective antibodies)
  • fibrin deposition ( limit bacterial spread)
  • various factors (promoting healing)
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22
Q

what is the exudation protein passage?

A

chemical mediatiors:

  • endothelial contraction
  • increased permeability*

direct endothelial injury (e.g. burns) - increased permeability*

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23
Q

which cell is the first to the site of damage?

A

neutrophil

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24
Q

what do neutrophils do?

A

degrade cell debris (cells damaged from toxins etc)

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25
Q

what kind of cells are neutrophils?

A

phagocytes

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26
Q

where are neutrophils made?

A

bone marrow

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27
Q

how long are neutrophils around for?

A

short lives - 1-3 days

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28
Q

what enzymes do neutrophils contain and what do they do?

A
  • myeloperoxidase (generates hydrogen peroxide)
  • lysozyme
  • acid hydrolase (hydrolysis)
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29
Q

what kind of nucleus does a neutrophil have?

A

polymorphonuclear

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30
Q

how do neutrophils kill?

A
  1. engulf bacteria by opsonisation
  2. endocytosed
  3. endocytic vesicle
  4. fuses with lysozymes
  5. phagolysozome created
  6. respiratory burst
  7. oxygen free radicals from respiratory burst
  8. contributes to hydrogen peroxide formation
  9. hydrogen peroxide free radicals
  10. all react with bacteria and kill it
31
Q

how do neutrophils do ‘opsonisation’?

A

wrap bacteria in antibodies/c3

antibodies/c3 receptors on neutrophil to engulf it

32
Q

how does having repeat bacterial infections affect neutrophils?

A

low opsonisation or low killing mechanisms

33
Q

what do eosinophil granules look like?

A

red/pink granules with H & E staining

34
Q

what events are eosinophils involved in?

A

type I hypersensitivity response

35
Q

what is the role of eosinophils?

A

damp down allergic hypersensitivity responses

36
Q

how do eosinophils reduce allergic responses?

A

produce histaminase, aryl sulphatase, phospholipase - degrade mast cell mediators

37
Q

what does histaminase do?

A

breakdown histamine made elsewhere

38
Q

what does phospholipase do?

A

degrade mast cell mediators

39
Q

what things do eosinophils kill?

A

antibody-coated parasites

e.g. worms/flukes

40
Q

what events are mast cells involved in?

A

type I hypersensitivity mediated by IgE

41
Q

what do basophils and mast cells granules contain?

A

histamine, heparin, tryptase, acid hydrolase

42
Q

when do basophils and mast cells degranulate?

A

on activation

43
Q

what is the activated function of a basophil?

44
Q

what is the activated function of a mast cell?

A

release of granules

45
Q

what is the difference between monocytes and macrophages?

A

macrophages derive from monocytes

46
Q

what are macrophages?

A

major scavenger cells

47
Q

when do macrophages arrive?

A

12-24hrs after neutrophils

48
Q

what chemotactic factors do macrophages release?

A

TNF, PDGF, TGF-β

49
Q

what is the activated function of a macrophage?

A

phagocytosis and activation of bactericidal mechanisms , antigen presentation

50
Q

what events are macrophages involved in?

A

inflammatory and specific response

51
Q

where are macrophages found?

A

in the gut lining - checking for things

52
Q

how are B and T lymphocytes made?

A

small resting lymphocytes stimulated
lymphoblasts formed
effector B cell OR effector T cell produced

53
Q

what is the difference between acute and chronic inflammation?

A

acute - rapid onset, short duration

chronic - pathological consequences

54
Q

activated neutrophils have increased receptors for?

A

chemoattractants, prostaglandins, leukotrienes, Fc, complement, etc

55
Q

what is the difference in neutrophil production during inflammation?

A

Normally produce 1010/day, increases 10x

56
Q

why is metabolic activity stimulated during inflammation?

A

activation of neutrophils -> metabolic activity stimulated -> reactive oxygen and nitrogen intermediates and release of chemical mediators

57
Q

what is inflammation damage regulated by?

A

regulation of duration and intensity of inflammatory response - e.g. TGF-β

58
Q

what is the sequence of events of inflammation?

A
  1. Bacteria enter tissues, cause damage
  2. Mast cells release histamine, also prostaglandins and leukotrienes
  3. Vasodilation of arterioles, increasing blood flow
  4. Capillary permeability is increased, causing oedema, kininogens converted to kinins
  5. Chemotaxis of neutrophils
  6. Killing of bacteria
  7. Tissue repair
59
Q

where are chemical mediators derived from?

A

Inflammatory cells

plasma

60
Q

what do mast cells release?

61
Q

what does histamine cause?

A

increased vascular permeability and vasodilation

62
Q

what does serotonin cause?

A

vasodilation

63
Q

what do prostaglandins cause?

A

vasodilation, oedema ( PGE2, PGI2)

64
Q

what leukotrienes cause?

A

vasoconstriction, increased permeability

65
Q

what do cytokines cause?

A

IL-2, IL-4

IL-10, TGF-β

IFN-γ, TNF-α

66
Q

what do IL-2, IL-4 cause?

A

stimulate lymphocyte proliferation

67
Q

what do IL-10, TGF-β cause?

A

suppress lymphocyte proliferation

68
Q

what do IFN-γ, TNF-α cause?

A

macrophage activation

69
Q

what releases serotonin?

70
Q

what are prostaglandins and leukotrienes?

A

Arachadonic acid derivatives

71
Q

where are cytokines released from?

A

inflammatory cells, endothelium, etc

72
Q

what are the outcomes of inflammation?

A
  • usually disappears in hours/days
  • tissue returns to normal
  • fluid and degraded protein drained by lymphatic system
  • exudate, debris and fibrin removed by phagocytes
  • inflammatory cells removed by apoptosis
73
Q

what must circulating neutrophils do to enter inflamed tissue?

A

adhere to and pass between endothelial cells

Expression of cell-adhesion molecules (CAMs) is critical

74
Q

what are the 4 steps for neutrophil to enter the tissue?

A
  1. rolling - low affinity binding of endothelial selectin molecules to neutrophil mucins
  2. activation - endothelial cell activates integrin on the neutrophil -> firm binding
  3. arrest/adhesion
  4. migration - in response to chemoattractants

X Understanding Disease (10 decks)

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