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HLSC 222 > Ch. 6 > Flashcards

Ch. 6 Flashcards

1
Q

Innate Immunity

wHatkind of drfense

A

First 2 lines of defense

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2
Q

First line of defense

A

-Physical
-Mechanical
-Biochemical Barriers

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3
Q

Second line of defense

A

-Inflammation
-Macrophage, Neutrophils

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4
Q

Adaptive Immunity

A

Third line of defense

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5
Q

Third line of defense

A

-Acquired Immunity
-B/T cells

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6
Q

Inflammatory Response- Mast Cells

A

-Release Histamine
Causes Vasodilation

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7
Q

Inflammatory Response-Platelets

A

Stop blood loss

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8
Q

Inflammatory Response- Macrophages/Neutrophils

A

Phagocytize pathogen

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9
Q

Inflammatory Response- Pus

A

-Dead phagocytes and pathogens accumulate

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10
Q

Inflammatory Response- Ions

A

Rapidly leak

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11
Q

Inflammatory Response- Fluids

A

Rapidly influx

Edema

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12
Q

Prostaglandins

A

Involved in inflammatory response as an overseer of events/coordinating

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13
Q

Cellular components of inflammation

A

Vascular epithelium is a principal coordinator

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14
Q

Tissues close to vessels contain 2 involved cells

A
  1. Mast Cells
  2. Dendritic cells
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15
Q

Mast Cells

A

Important inflammation activator

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16
Q

Dendritic cells

A

connect innate and adaptive immune responses

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17
Q

Chemical molecules

A

-Are recruited by both innate and adaptive immunity
-Released from damaged or destroyed cells

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18
Q

Cellular Products

A

-Cytokines
-Lymphokines
-Monokines
-Interleukin

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19
Q

Cytokines

A

General term for chemical molecules released

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20
Q

Cytokines regulate

A

Innate and adaptive immunity

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21
Q

Cytokines can be

A

-Proinflammatory
-Anti-inflammatory

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22
Q

Lymphokines

A

Cytokines released from lymphocytes

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23
Q

Monokines

A

Cytokines released from monocytes (Which change into Macrophages)

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24
Q

Macrophages and Lymphocytes release

A

Interleukin cytokines

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25
Q

Main interleukins

A

-IL-1
-IL-6

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26
Q

IL-1

A

produced by macrophages

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27
Q

IL-6

A

produced by macrophages, lymphocytes, and fibroblasts

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28
Q

COVID-19 cellular response

A

Activates cytokine storm syndrome
(Severe systemic inflammatory response)

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29
Q

Cytokine storm syndrome

A

-IL-6 cytokine released> excessive lymphocyte recruitment

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30
Q

COVID-19 Treatment

A

production of IL-6 antibodies counteract the effect

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31
Q

TNF-a

A

-Cytokine but not an interleukin

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32
Q

TNF-a released by

A

macrophages and mast cells

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33
Q

TNF-a induces

A

Proinflammatory Effects
-Fever
-Cachexia
-Fatal Shock
-Granuloma formation

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34
Q

Cachexia

A

Muscle wasting

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35
Q

Fatal Shock

cause

A

Caused by gram- bacterial infections

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36
Q

Anti-inflammatory cytokines

A

Interleukin-10 lymphokine

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37
Q

Vasodilation

A

increases vessel permeability

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38
Q

Acute local inflammation

A

tissue injury caused by physical, chemical, or pathogenic microorganisms

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39
Q

Process of acute local inflammation

fix/makr2cards

A

-Capillary widening>increases blood flow
-Increased permeability>fluid release into tissues
-Attraction of leukocytes>Extravasation of leukocytes to site of injury
-Systemic Response>Fever and proliferation of leukocytes

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40
Q

Acute local inflammation causes

A

-Heat
-Redness
-Swelling
-Tenderness
-Pain

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41
Q

Inflammatory Response Goals

A

Limit and control injury process
-Limit bleeding
-limit infection

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42
Q

Inflammation Limiation

A

-Clean wound (Saline if possible)
-Remove loose debris
-Treatment: Antibiotics

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43
Q

Itis

A

Tells where inflammation is located
-Appendicitis
-Tonsilitis

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44
Q

Inflammation activation

A

Cell injury or deathC

45
Q

Cell death is due to

A

-Infection
-Mechanical Damage
-Ischemia/Nutrient depravation
-Temp extremes
-Radiation

46
Q

Acute Inflammation Interventions

A

-ESR
-C-reactive protein
-Blood work for WBC count

47
Q

ESR

A

Erythrocyte sedimentation Rate

48
Q

Erythrocyte sedimentation Rate (ESR) Definition

A

Determination rate of RBC settling at a faster rate

49
Q

Erythrocyte sedimentation Rate (ESR) cause

A

Increase in infection=RBC bind to each other (Become heavier) and settle at a faster rate

50
Q

Increased ESR

A

= Increased infection

51
Q

C-Reactive Protein cause

A

Caused by an effect on the liver

52
Q

C-Reactive Protein

A

Increases in response to inflammation

53
Q

Blood work for WBC count

A

-Measurement of increased neutrophils (Called bands)

54
Q

Increase in (neutrophils) entering the bloodstream

A

Means infection isn’t in control yet

55
Q

Acute inflammation (AI)

A

-Lasts 2 weeks
-Swelling, pain, heat, redness
-Localized, quick to diagnose

56
Q

3 Primary Systemic Changes in AI

A
  1. Fever
  2. Leukocytes increase
  3. Circulating protein increase
57
Q

What does AI become

A

Chronic if response is unsuccessful

58
Q

Chronic Inflammation (CI)

A

-Longer then 2 weeks/months/years
-Can be preceded by unsuccessful AI or a distinct process w/o AI

59
Q

CI Cause

A

Microorganisms
-Insensitive to phagocytosis
-Can survive in a macrophage
-That produce toxins

60
Q

CI presented as

Cells

A

-Dense infiltration of lymphocytes and macrophages

61
Q

What happens in CI if macrophages can’t stop tissue damage

A

The body walls off infected area by forming a granuloma

62
Q

What drives granuloma formation

A

TNF-a

63
Q

Granuloma

A

Cluster of WBC and other tissues

64
Q

Chronic Inflammation cause

A

immune system unable to protect body

65
Q

Chronic inflammation action

A

form granulomas (walled off infected area)

66
Q

Wound healing process

A
  1. Inflammation
  2. Proliferation & new tissue formation
  3. Remodeling and maturation phase
67
Q
  1. Inflammation
A

Transition from AI to healing begin immediately

68
Q
  1. Inflammation- Platelets
A

Clot formation/initiate formation of undamaged cells

69
Q
  1. Inflammation- Neutrophils
A

Clean wound of debris and bacteria

70
Q
  1. Inflammation- Macrophages
A

-Release growth factors
-Recruit fibroblasts
-Promote angiogenesis

71
Q

Angiogenesis

A

Development of new blood vessels

72
Q
  1. Proliferation & New Tissue Formation- Peroid
A

3d-2w

73
Q
  1. Proliferation & New Tissue Formation- Fibroblast proliferation
A

collagen synthesis

74
Q
  1. Proliferation & New Tissue Formation- epithelization
A

Epithelial cells migrate to wound

75
Q
  1. Proliferation & New Tissue Formation
A

-Cellular differentiation
-Various macrophage secretions

76
Q
  1. Remodeling and Maturation Phase- Time Period

wound healing

A

weeks to years

77
Q
  1. Remodeling and Maturation Phase

Wound healing

A

-Cellular differentiation
-Scar tissue formation and remodeling
-Fibroblasts

78
Q

Cellular Differentation

A

Unspecialized cells mature (Become specialized) and perform important cellular functions

79
Q

Fibroblasts

A

Major remodeling cell

80
Q

Tissue Repair

A
  1. Primary intention
  2. Secondary intention
  3. Tertiary intention
81
Q

Primary Intention

A

-Clean incision
-early suture/best choice for fresh wound with sufficient vascularization
-Result: Fine scar

82
Q

Secondary Intention

A

-Gaping wound=granulation
-wound is extensive/edges can’t be brought together
-Ideal for contaminated or infected wounds as wound is left open to heal spontaneously

83
Q

Tertiary Intention

A

-Delayed primary closure
-open wound but not gaping
-increased granulation
-allows for observation of wound
-when clean- sutured closed but wide scar is left

84
Q

Adhesions

A

-Abnormal union of membranous surfaces (Common for bowel surgery)
-Painful if it stops normal movements of GI

85
Q

Strictures and Contractures

A

excess of wound contraction
(Healing cells tend to pull other cells towards them = contracture of tissue)

86
Q

Infections

A

Wound is reinfected with initial/new pathogen

87
Q

Dehiscence

A

incision separates following surgery
-wound is considered “dehisced”

88
Q

Evisceration

A

-Surgical complication
-incision opens, and abdominal organs protrude

89
Q

Excess scar formation

A

caused by excess tension/movement

90
Q

Dysfunctional Wound healing- cause

A

-Blood supply
-Obesity
-Excessive fibrin
-Diabetes

91
Q

Blood supply

A

Low- Ischemia/vasoconstriction: Inhibits recovery process
High- increased blood clots
high- increased blood clots

92
Q

Obesity

A

predisposed to infections

93
Q

Excessive fibrin

A

Doesn’t get reabsorbed and causes fibrous adhesions

94
Q

Diabetes

A

-Potential for smaller vessel disease/prolonged wound healing
-Hyperglycemia = suppression of macrophages

95
Q

Wound infection

A

infiltration of pathogen

96
Q

Nutrition

A

must meet metabolic needs of healing

97
Q

Medications

A

-Antineoplastic
-Steroids

98
Q

Antineoplastic

A

-Drugs used for cancer treatment to slow down cell division (negative side effects)
-Blocking formation of neoplasms

99
Q

Neoplasms

A

New, abnormal tissue growth

100
Q

Steroids

A

Prevent macrophages from migrating to the site

101
Q

Look over review box

A
102
Q

Look over diagrams

A
103
Q

Interleukins are

A

self-limiting compared to cytokines

104
Q

Immune response is

intensifiedby

A

driven by cytokines

105
Q

CRP facts 1

A

Higher CRP level, more inflammation in body

106
Q

CRP facts 2

A

CRP isn’t specific, not unique to one disease

107
Q

CRP facts 2

A

CRP tests cab help monitor disease progress + flares

108
Q

Tertiary intention breakdown

A

Primary size but if closed too soon may trap infection inside, wait till clean then close

HLSC 222 (9 decks)

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