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Pathophysiology > Chapter Six - Innate Immunity : Inflammation And Wound Healing > Flashcards

Chapter Six - Innate Immunity : Inflammation And Wound Healing Flashcards

1
Q

Innate immunity: first line of defence

A

-physical, mechanical, biochemical barriers

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2
Q

Innate immunity : second line of defence

A

Inflammation, macrophage, neutrophils

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3
Q

Adaptive immunity

A

Third line of defence
-acquired or specific immunity
-B cell or T cell

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4
Q

Mast cells release

A

Histamine

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5
Q

Histamines =

A

Vasodilation

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6
Q

___ enter to stop blood loss

A

Platelets

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7
Q

______ arrive to phagocytize pathogen

A

Macrophages and neutrophils

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8
Q

When macrophages arrive to phagocytize, what accumulates

A

Pus
-dead phagocytes and pathogens

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9
Q

Rapid leakage and influx of

A

Leakage - ions

Influx - fluids

Since water follows sodium

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10
Q

During inflammation vascular ____ is a principle coordinator

A

Epithelium

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11
Q

Tissue close to vessel contains two involved cells

A

-mast cells
-dendritic cells

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12
Q

Mast cells

A

Important inflammation activator
-release histamine

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13
Q

Dendritic cells

A

Connect innate and adaptive immune response

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14
Q

Both innate and adaptive systems are recruited by

A

Chemical molecules

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15
Q

Chemical molecules are released from

A

Damaged or destroyed cells

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16
Q

Cytokines

A

General term for chemical molecules released
-they regulate innate and adaptive immunity

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17
Q

Cytokines can be

A

Pro inflammatory or anti inflammatory

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18
Q

Lymphokines

A

Cytokines released from lymphocytes

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19
Q

Monokines

A

Cytokines released from monocytes
-which change into macrophages

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20
Q

Macrophages and lymphocytes also released

A

Itnerleukin cytokines

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21
Q

Main interleukins are

A

IL-1 and IL-6
-self limiting compared to cytokines

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22
Q

IL-1

A

Produced by macrophages

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23
Q

IL-6

A

Produced by macrophages, lymphocytes and fibroblasts

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24
Q

COVID 19 activates a

A

Cytokine storm syndrome
-severe systemic inflammatory response

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25
Q

IL-6 has cytokine released =

A

Excessive recruitment of lymphocytes

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26
Q

COVID 19 treatment

A

Is production of IL-6 antibodies to counteract effect

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27
Q

TNF-a

A

A cytokine but not classified as an interleukin
-released by macrophages and mast cells

-induces multitude of pro inflammatory effects

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28
Q

Pro inflammatory effects

A

-fever
-cachexia
-fatal shock
-granuloma formation

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29
Q

Cachexia

A

Muscle wasting

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30
Q

Fatal shock is caused by

A

Gram negative bacterial infections

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31
Q

Antiflammatory cytokines are

A

Interleukin 10 lymphokine

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32
Q

Granuloma formation

A
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33
Q

Goal of inflammatory responses

A

-limit and control injury (limit blood and infection)
-intervention (clean wound, remove debris, antibiotics)

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34
Q

ITIS tells us

A

Where inflammation is located

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35
Q

Cell injury or death activates

A

Inflammation

36
Q

cell death can be due to

A

-infection
-mechanical damage
-ischemia
-temp extremes
-radiation

37
Q

Erythrocyte sedimentation rate or ESR

A

Determination of rate of RBC settling in saline solution

38
Q

An increase in infection =

A

RBC bind to each other, becoming heavier and settle at a faster rate

39
Q

Increased ESR =

A

Increased infection

40
Q

C reactive protein is caused by

A

Effect on liver

41
Q

C reactive protein increases in

A

Response to inflammation

42
Q

An increase in neutrophils during blood work would signal that

A

The WBC have not got a hold of the infection yet
-actively fighting

43
Q

Acute inflammation

A

-lasts less than two weeks
-swelling, pain, heat, redness
-localized and quick to diagnose

44
Q

Three primary systemic changes in an acute inflammation

A
  1. Fever
  2. Leukocytosis or inc levels of circulating leukocytes
  3. Increased circulating proteins
45
Q

Acute inflammation if response is unsuccessful can become

A

Chronic

46
Q

Chronic inflammation

A

-longer Thant so weeks/months/years
-can be preceded by unsuccessful acute or distinct process without previous acute inflammation

47
Q

Chronic inflammation causes microorganisms to

A

-be insensitive to phagocytosis
-they can survive macrophages
-produce toxins

48
Q

Chronic inflammation presents as a

A

Dense infiltration of lymphocytes and macrophages

49
Q

If macrophages are unable to stop tissue damage

A

Body walls off infected area by forming a granuloma

50
Q

TNF -a drives ___ formation

A

Granuloma

-a cluster of WBC and other tissues

51
Q

Simple explanation of a chronic inflammation

A

When the immune system is unable to protect body
-formation of granuloma -> walled off infection area

52
Q

Transition from acute inflammatory to healing begins when

A

Immediately

53
Q

Platelets

A

Clot formation
-initiate formation of unmanaged cells

54
Q

Neutrophils

A

Clea wound of debris and bacteria
-last small amount of time

55
Q

Macrophages

A

Release growth factors
-recruit fibroblasts
-promote angiogenesis

56
Q

Angiogenesis

A

Development of new blood vessels

57
Q

Proliferation and new tissue formation lasts

A

Three days to two weeks

58
Q

Fibroblast proliferation =

A

Collagen synthesis

59
Q

Epithelization

A

Epithelial cells migrate to wound

60
Q

Remodeling and maturation phase lasts

A

Weeks to years

61
Q

Remodeling and maturation phase: cellular differentiation continues

A

Unspeilized cells mature
-become specialize and perform important cellular functions
-scar tissue formation and remodeling

62
Q

Fibroblast

A

Major remodeling cell

63
Q

Primary intention

A

-clean incision
-early suture and is best choice for fresh wound with sufficient vascularization

64
Q

Secondary intention

A

Gaping would = granulation
-much more extensive and edges can’t be brought together

65
Q

What type of wound is “-ideal for contaminated or infected wounds a wound if left open to heal spontaneously”

A

Secondary intention

66
Q

What wound results in a fine scar?

A

Primary intention

67
Q

Tertiary intention

A

Delayed primary closure
-open wound by not gaping
-inc granulation
-allowed observation of wound

68
Q

What intention is sutured closed and results in a wide scar

A

Tertiary intention

69
Q

Adhesions

A

Abnormal union of membranous surfaces (common in bowel surgery)
-painful if it stops normal movements

70
Q

Strictures and contractures

A

Excess of wound contraction
-healing cells tend to pull other cells towards them, causing contracture of tissue

71
Q

Infections

A

Wound is reinfected with initial or new pathogen

72
Q

Dehiscence

A

Incision separates following surgery and wound is considered dehisced

73
Q

Evisceration

A

Surgical complication
-incision opens and abdominal organs protrude

74
Q

Excess scar formation

A

Caused by excess tension and movement

75
Q

Low blood supply =

A

Iscehmia, vasoconstriction and inhibits recovery process

76
Q

High blood supply =

A

Increased blood clots

77
Q

Obesity predisposed to

A

Infections

78
Q

Excessive fibrin

A

Doesn’t get reabsorbed and cases fibrous adhesions

79
Q

Diabetes

A

Potential for smaller vessel disease and prolonged wound healing
-hyperglycaemia

80
Q

Hyperglycaemia

A

Excess glucose in blood

81
Q

Hyperglycaemia =

A

Suppression of macrophages

82
Q

Wound infection is

A

Infiltration of pathogen

83
Q

Nutrition must meet

A

Metabolic needs of healing

84
Q

Antineoplastic

A

Drugs used for cancer treatment to slow cell division
-has various side effects
-blocks formation of neoplasms

85
Q

Neoplasms

A

New abnormal tissue growth

86
Q

Steroids

A

Prevent macrophages from migrating to site

Pathophysiology (20 decks)

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