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Inflammation Flashcards

1
Q

inflammation

A

Inflammation is the reaction of a vascularised living tissue to a local injury

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2
Q

how are inflammation lesions typically indicated

A

by suffix (ITIS -> appendicitis, bronchitis)

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3
Q

causes of inflammation

A 
• Infectious agents
• Tissue necrosis
• Foreign bodies
• Immune reactions (hypersensitivity
responses)
• Endogenous
• Exogenous
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4
Q

objectives of inflammation

A
  1. Localise and eliminate the causative
    agent
  2. Limit tissue injury
  3. Begin the process of repair
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5
Q

5 classic local signs of acute inflammation

A
  • Calor - Heat
  • Rubor - Redness
  • Tumor - Swelling
  • Dolor - Pain
  • Functio laesa – loss of function
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6
Q

difference between acute and chronic inflammation

A

acute - immediate and rapid response but resolves just as fast
chronic - longstanding, primary or followed after acute inflammation

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7
Q

onset differences of acute and chronic inflammation

A

acute - fast (minutes - hours)

chronic - slow (days)

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8
Q

cellular infiltrate difference between acute and chronic swelling

A

acute - mainly neutrophils

chronic - monocytes/macrophages and lymphocytes

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9
Q

the difference in the extent of tissue injury and fibrosis in acute an chronic inflammation

A

acute - Usually mild and self limited
chronic - Often severe and
progressive

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10
Q

difference in local and system signs between acute and chronic inflammation

A

acute - Prominent

chronic - less

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11
Q

how is acute inflammation characterised

A

accumulation of fluid, protein and acute inflammatory cells at the site of injury

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12
Q

what white blood cells are the main cells in acute inflammation

A

neutrophils

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13
Q

what is acute inflammation mediated by

A

chemical products which cause dilatation of the

vessels & start inflammatory process derived from plasma

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14
Q

vascular events of acute inflammation

A

• Vasodilatation – increased blood flow
• Increased vascular permeability
– permitting plasma proteins and white blood cells to leave the circulation

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15
Q

cellular events in acute inflammation

A

Accumulation and activation at the site of the injury – main inflammatory cell
-> neutrophil

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16
Q

vascular changes in acute inflammation

A

vasodilation - small blood vessels, inc. blood flow and hydrostatic pressure -> redness + heat
more permeable - ooze of protein rich fluid -> swelling
oedema
pus

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17
Q

describe pus

A

purulent inflammatory exudate rich in neutrophils and

cell debris

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18
Q

cells in acute inflammation

A

white blood cells - especially neutrophils and macrophages

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19
Q

what white blood cells respond to bacteria

A

neutrophils

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20
Q

what white blood cells respond to viruses

A

lymphocytes

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21
Q

what white blood cells respond to allergies/hypersensitivity

A

eosinophils

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22
Q

beneficial effects of inflammation

A
  • Dilution of toxins
  • Fibrin production  delays bacterial spread
  • Arrival of antibodies to the site of inflammation
  • Destruction of microbial agent
  • Drug transport
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23
Q

harmful effects of inflammation

A
  • Mechanical effect e.g. epiglottitis
  • Impaired flow e.g. acute meningitis
  • Impaired function
  • Tissue destruction
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24
Q

systemic effects of inflammation - clinical

A
  • Pyrexia
  • Increased tendency to sleep
  • Constitutional symptoms
  • Pain
  • Lymphadenopathy and splenomegal
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25
systemic effects of inflammation - laboratory
leucocytosis raised ESR Anaemia acute reactive proteins - c -reactive protein
26
outcomes of acute inflammation
complete resolution abscess formation healing by connective tissue replacement (fibrosis) after substantial tissue destruction progression to chronic inflamamtion
27
what causes chronic inflammation
• Acute inflammation – prolonged normal healing • Persistence/repeated bouts of acute inflammation • Low grade, smouldering persistent infection - rubercle, bacilli, viruses hypersensitivity exposure to potentially toxic subtances
28
abscess
a walled off collection of pus
29
what are the main effector cells of chronic inflammation
macrophages - sense and engulf particles | induce inflammatory response
30
function of lymphocytes in chronic inflammation
activated by macrophages and activate other inflammatory cells
31
granulomatous inflammation
• Specific form of chronic inflammation characterised | by nodular aggregates of macrophages and giant cells
32
examples of granulomatous inflammation
infection - TB, Fungi
33
unknown aeitology of what granulomatous inflammation
sarcoidosis | crohn's disease
34
initial response of a damaged tissue
acute inflammation | leads to complete resolution and fibrosis
35
complete resolution
• Regeneration – through proliferation of adjacent surviving structures and tissue stem cells
36
fibrosis
• Fibro proliferative response -> scar • Resolution of inflammation -> organisation
37
healing process
``` regeneration and scar remove causative agent clear inflammatory debris architectural damage chronicity of associated inflammation ```
38
labile cells
• Continuously dividing cells • Epithelial cells such as skin, oral cavity and GIT • Injury to such tissue can easily heal by regeneration if the supporting stroma is intact
39
stable cells
* Normally low level of replication * Liver cells * Cells can be stimulated to divide * Healing by regeneration if the supporting stroma is intact
40
permanent cells
* Non dividing cells * Neurons * Myocardial cells * No regeneration * Replaced by connective tissue  healing by fibrosis
41
regeneration
• Replacement of lost cells by cells of the same type through cell division to return to its pre-injury state
42
how is regeneration controlled
by stimulatory and inhibitory factors and interactions between cells and extra-cellular matrix (supporting framework)
43
what must be in order for regeneration to occur
The supporting framework must be intact
44
function of fibrosis
to help with limited restorative capacity -fibroproliferative response that ‘patches’ rather than restores the tissue
45
when does fibrosis occur
1. Destruction to both functional (parenchymal) cells and stromal framework 2. Death of permanent cells 3. Long-standing inflammation
46
phases of healing
1. Inflammatory phase 2. Proliferative phase 3. Remodelling phase
47
inflammatory phase
* Haematoma formation * Infiltration by neutrophils * Infiltration by macrophages * Removal of tissue debris
48
proliferative phase
• Epithelial cell proliferation • Proliferation of fibroblasts and new vessels formation (granulation tissue)
49
matrix remodelling
* Replacement of the granulation tissue by a fibrous stroma (scaffold) * Degradation of excessive extra-cellular matrix by metalloproteinase
50
purpose of matrix remodelling phase of healing
• Increase in the strength of the wound
51
types of wound healing on the skin
primary intention | secondary intention
52
primary intention
* Wound with apposed edges * Minimal loss of tissue * Surgical incision or clean wound
53
secondary intention
* Large gaping wound * Extensive loss of cells * Infarction * Ulcer * Abscess
54
stages of wound healing by primary intention in Day 1
• Wound filled with blood clot • Acute inflammation in the surrounding tissue • Proliferation of epithelial cells
55
stages of wound healing by primary intention in Day 2
* Macrophages | * Epithelial cells start to close the wound by proliferating on the surface
56
stages of wound healing by primary intention Day 3
• Granulation tissue formation
57
stages of wound healing by primary intention Day 5
collagen deposition
58
stages of wound healing by primary intention Day 7
sutures removed
59
what is the wound strength after sutures are removed in 1 week
only 10% of unwounded | skin
60
what is the wound strength after 3-4 months
wound strength is about | 80% of unwounded skin
61
what is the difference between wound healing by secondary intention
``` similar but; Slower • The inflammatory reaction is more intense • Wound contraction (myofibroblast) • More scarring ```
62
pathologic aspects of wound healing
* Deficient scar formation * Wound rupture/ulceration • Excessive scar formation * Contracture deformity
63
examples of excessive scar formation
hypertrophic scar | keloid scar
64
hypertrophic scar
raised, due to excessive collagen formation
65
keloid scar
extends beyond the original area of injury
66
cause of contracture deformity
Excessive wound contraction  producing claw deformities / limit joint mobility
67
examples of healing in mucosal surfaces
* Erosion is healed by regeneration | * Ulceration by regeneration and fibrosis
68
examples of healing in liver
* A single short lived injury is healed by regeneration | * Chronic injury by cirrhosis
69
examples of healing in muscle
* Cardiac muscle -> Fibrosis | * Skeletal muscle -> Regeneration
70
examples of healing in nervous system
* Central nervous system -> Gliosis | * Peripheral nerves -> Regeneration
71
healing of bone
1. haematoma formation 2. External callus bridges the fracture site outside the bone 3. Internal callus bridges the fracture in the medullary cavity 4. remodelling
72
factors that influence healing
* Local factors | * Systemic factors
73
local factors
* Infections * Ischaemia * Mechanical forces (motion/wound tension) * Foreign bodies * Type of tissue * Size and location
74
systemic factors
* Age & Nutrition (protein, Vit C) * Metabolic status (DM) * Hormones (steroids) * Malignancy, Chemotherapy, Radiotherapy

NMSKI (38 decks)

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