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NMSKI > Inflammation > Flashcards

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
Q

systemic effects of inflammation - laboratory

A

leucocytosis
raised ESR
Anaemia
acute reactive proteins - c -reactive protein

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26
Q

outcomes of acute inflammation

A

complete resolution
abscess formation
healing by connective tissue replacement (fibrosis) after substantial tissue destruction
progression to chronic inflamamtion

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27
Q

what causes chronic inflammation

A

• 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

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28
Q

abscess

A

a walled off collection of pus

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29
Q

what are the main effector cells of chronic inflammation

A

macrophages - sense and engulf particles

induce inflammatory response

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30
Q

function of lymphocytes in chronic inflammation

A

activated by macrophages and activate other inflammatory cells

31
Q

granulomatous inflammation

A

• Specific form of chronic inflammation characterised

by nodular aggregates of macrophages and giant cells

32
Q

examples of granulomatous inflammation

A

infection - TB, Fungi

33
Q

unknown aeitology of what granulomatous inflammation

A

sarcoidosis

crohn’s disease

34
Q

initial response of a damaged tissue

A

acute inflammation

leads to complete resolution and fibrosis

35
Q

complete resolution

A

• Regeneration – through proliferation of adjacent surviving structures and tissue stem cells

36
Q

fibrosis

A

• Fibro proliferative response -> scar
• Resolution of inflammation ->
organisation

37
Q

healing process

A 
regeneration and scar
remove causative agent
clear inflammatory debris
architectural damage
chronicity of associated inflammation
38
Q

labile cells

A

• 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
Q

stable cells

A
  • Normally low level of replication
  • Liver cells
  • Cells can be stimulated to divide
  • Healing by regeneration if the supporting stroma is intact
40
Q

permanent cells

A
  • Non dividing cells
  • Neurons
  • Myocardial cells
  • No regeneration
  • Replaced by connective tissue  healing by fibrosis
41
Q

regeneration

A

• Replacement of lost cells by cells of the same type through cell division to return to its pre-injury state

42
Q

how is regeneration controlled

A

by stimulatory and inhibitory factors and interactions between
cells and extra-cellular matrix (supporting
framework)

43
Q

what must be in order for regeneration to occur

A

The supporting framework must be intact

44
Q

function of fibrosis

A

to help with limited restorative capacity -fibroproliferative response that ‘patches’ rather than restores the tissue

45
Q

when does fibrosis occur

A
  1. Destruction to both functional
    (parenchymal) cells and stromal framework
  2. Death of permanent cells
  3. Long-standing inflammation
46
Q

phases of healing

A
  1. Inflammatory phase
  2. Proliferative phase
  3. Remodelling phase
47
Q

inflammatory phase

A
  • Haematoma formation
  • Infiltration by neutrophils
  • Infiltration by macrophages
  • Removal of tissue debris
48
Q

proliferative phase

A

• Epithelial cell proliferation
• Proliferation of fibroblasts and new vessels formation
(granulation tissue)

49
Q

matrix remodelling

A
  • Replacement of the granulation tissue by a fibrous stroma (scaffold)
  • Degradation of excessive extra-cellular matrix by metalloproteinase
50
Q

purpose of matrix remodelling phase of healing

A

• Increase in the strength of the wound

51
Q

types of wound healing on the skin

A

primary intention

secondary intention

52
Q

primary intention

A
  • Wound with apposed edges
  • Minimal loss of tissue
  • Surgical incision or clean wound
53
Q

secondary intention

A
  • Large gaping wound
  • Extensive loss of cells
  • Infarction
  • Ulcer
  • Abscess
54
Q

stages of wound healing by primary intention in Day 1

A

• Wound filled with blood clot
• Acute inflammation in the surrounding
tissue
• Proliferation of epithelial cells

55
Q

stages of wound healing by primary intention in Day 2

A
  • Macrophages

* Epithelial cells start to close the wound by proliferating on the surface

56
Q

stages of wound healing by primary intention Day 3

A

• Granulation tissue formation

57
Q

stages of wound healing by primary intention Day 5

A

collagen deposition

58
Q

stages of wound healing by primary intention Day 7

A

sutures removed

59
Q

what is the wound strength after sutures are removed in 1 week

A

only 10% of unwounded

skin

60
Q

what is the wound strength after 3-4 months

A

wound strength is about

80% of unwounded skin

61
Q

what is the difference between wound healing by secondary intention

A 
similar but;
Slower
• The inflammatory reaction is more intense
• Wound contraction (myofibroblast)
• More scarring
62
Q

pathologic aspects of wound healing

A
  • Deficient scar formation
    • Wound rupture/ulceration • Excessive scar formation
  • Contracture deformity
63
Q

examples of excessive scar formation

A

hypertrophic scar

keloid scar

64
Q

hypertrophic scar

A

raised, due to excessive collagen formation

65
Q

keloid scar

A

extends beyond the original area of injury

66
Q

cause of contracture deformity

A

Excessive wound contraction 
producing claw deformities / limit joint
mobility

67
Q

examples of healing in mucosal surfaces

A
  • Erosion is healed by regeneration

* Ulceration by regeneration and fibrosis

68
Q

examples of healing in liver

A
  • A single short lived injury is healed by regeneration

* Chronic injury by cirrhosis

69
Q

examples of healing in muscle

A
  • Cardiac muscle -> Fibrosis

* Skeletal muscle -> Regeneration

70
Q

examples of healing in nervous system

A
  • Central nervous system -> Gliosis

* Peripheral nerves -> Regeneration

71
Q

healing of bone

A
  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
Q

factors that influence healing

A
  • Local factors

* Systemic factors

73
Q

local factors

A
  • Infections
  • Ischaemia
  • Mechanical forces (motion/wound tension)
  • Foreign bodies
  • Type of tissue
  • Size and location
74
Q

systemic factors

A
  • Age & Nutrition (protein, Vit C)
  • Metabolic status (DM)
  • Hormones (steroids)
  • Malignancy, Chemotherapy, Radiotherapy

NMSKI (38 decks)

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