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HLSC 222 > Ch. 6 > Flashcards

Ch. 6 Flashcards

(108 cards)

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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
Main interleukins
-IL-1 -IL-6
26
IL-1
produced by macrophages
27
IL-6
produced by macrophages, lymphocytes, and fibroblasts
28
COVID-19 cellular response
Activates cytokine storm syndrome (Severe systemic inflammatory response)
29
Cytokine storm syndrome
-IL-6 cytokine released> excessive lymphocyte recruitment
30
COVID-19 Treatment
production of IL-6 antibodies counteract the effect
31
TNF-a
-Cytokine but not an interleukin
32
TNF-a released by
macrophages and mast cells
33
TNF-a induces
Proinflammatory Effects -Fever -Cachexia -Fatal Shock -Granuloma formation
34
Cachexia
Muscle wasting
35
Fatal Shock | cause
Caused by gram- bacterial infections
36
Anti-inflammatory cytokines
Interleukin-10 lymphokine
37
Vasodilation
increases vessel permeability
38
Acute local inflammation
tissue injury caused by physical, chemical, or pathogenic microorganisms
39
Process of acute local inflammation ## Footnote fix/makr2cards
-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
40
Acute local inflammation causes
-Heat -Redness -Swelling -Tenderness -Pain
41
Inflammatory Response Goals
Limit and control injury process -Limit bleeding -limit infection
42
Inflammation Limiation
-Clean wound (Saline if possible) -Remove loose debris -Treatment: Antibiotics
43
Itis
Tells where inflammation is located -Appendicitis -Tonsilitis
44
Inflammation activation
Cell injury or deathC
45
Cell death is due to
-Infection -Mechanical Damage -Ischemia/Nutrient depravation -Temp extremes -Radiation
46
Acute Inflammation Interventions
-ESR -C-reactive protein -Blood work for WBC count
47
ESR
Erythrocyte sedimentation Rate
48
Erythrocyte sedimentation Rate (ESR) Definition
Determination rate of RBC settling at a faster rate
49
Erythrocyte sedimentation Rate (ESR) cause
Increase in infection=RBC bind to each other (Become heavier) and settle at a faster rate
50
Increased ESR
= Increased infection
51
C-Reactive Protein cause
Caused by an effect on the liver
52
C-Reactive Protein
Increases in response to inflammation
53
Blood work for WBC count
-Measurement of increased neutrophils (Called bands)
54
Increase in (neutrophils) entering the bloodstream
Means infection isn't in control yet
55
Acute inflammation (AI)
-Lasts 2 weeks -Swelling, pain, heat, redness -Localized, quick to diagnose
56
3 Primary Systemic Changes in AI
1. Fever 2. Leukocytes increase 3. Circulating protein increase
57
What does AI become
Chronic if response is unsuccessful
58
Chronic Inflammation (CI)
-Longer then 2 weeks/months/years -Can be preceded by unsuccessful AI or a distinct process w/o AI
59
CI Cause
Microorganisms -Insensitive to phagocytosis -Can survive in a macrophage -That produce toxins
60
CI presented as | Cells
-Dense infiltration of lymphocytes and macrophages
61
What happens in CI if macrophages can't stop tissue damage
The body walls off infected area by forming a granuloma
62
What drives granuloma formation
TNF-a
63
Granuloma
Cluster of WBC and other tissues
64
Chronic Inflammation cause
immune system unable to protect body
65
Chronic inflammation action
form granulomas (walled off infected area)
66
Wound healing process
1. Inflammation 2. Proliferation & new tissue formation 3. Remodeling and maturation phase
67
1. Inflammation
Transition from AI to healing begin immediately
68
1. Inflammation- Platelets
Clot formation/initiate formation of undamaged cells
69
1. Inflammation- Neutrophils
Clean wound of debris and bacteria
70
1. Inflammation- Macrophages
-Release growth factors -Recruit fibroblasts -Promote angiogenesis
71
Angiogenesis
Development of new blood vessels
72
2. Proliferation & New Tissue Formation- Peroid
3d-2w
73
2. Proliferation & New Tissue Formation- Fibroblast proliferation
collagen synthesis
74
2. Proliferation & New Tissue Formation- epithelization
Epithelial cells migrate to wound
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2. Proliferation & New Tissue Formation
-Cellular differentiation -Various macrophage secretions
76
3. Remodeling and Maturation Phase- Time Period | wound healing
weeks to years
77
3. Remodeling and Maturation Phase | Wound healing
-Cellular differentiation -Scar tissue formation and remodeling -Fibroblasts
78
Cellular Differentation
Unspecialized cells mature (Become specialized) and perform important cellular functions
79
Fibroblasts
Major remodeling cell
80
Tissue Repair
1. Primary intention 2. Secondary intention 3. Tertiary intention
81
Primary Intention
-Clean incision -early suture/best choice for fresh wound with sufficient vascularization -Result: Fine scar
82
Secondary Intention
-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
Tertiary Intention
-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
Adhesions
-Abnormal union of membranous surfaces (Common for bowel surgery) -Painful if it stops normal movements of GI
85
Strictures and Contractures
excess of wound contraction (Healing cells tend to pull other cells towards them = contracture of tissue)
86
Infections
Wound is reinfected with initial/new pathogen
87
Dehiscence
incision separates following surgery -wound is considered "dehisced"
88
Evisceration
-Surgical complication -incision opens, and abdominal organs protrude
89
Excess scar formation
caused by excess tension/movement
90
Dysfunctional Wound healing- cause
-Blood supply -Obesity -Excessive fibrin -Diabetes
91
Blood supply
Low- Ischemia/vasoconstriction: Inhibits recovery process High- increased blood clots high- increased blood clots
92
Obesity
predisposed to infections
93
Excessive fibrin
Doesn't get reabsorbed and causes fibrous adhesions
94
Diabetes
-Potential for smaller vessel disease/prolonged wound healing -Hyperglycemia = suppression of macrophages
95
Wound infection
infiltration of pathogen
96
Nutrition
must meet metabolic needs of healing
97
Medications
-Antineoplastic -Steroids
98
Antineoplastic
-Drugs used for cancer treatment to slow down cell division (negative side effects) -Blocking formation of neoplasms
99
Neoplasms
New, abnormal tissue growth
100
Steroids
Prevent macrophages from migrating to the site
101
Look over review box
102
Look over diagrams
103
Interleukins are
self-limiting compared to cytokines
104
Immune response is | intensifiedby
driven by cytokines
105
CRP facts 1
Higher CRP level, more inflammation in body
106
CRP facts 2
CRP isn't specific, not unique to one disease
107
CRP facts 2
CRP tests cab help monitor disease progress + flares
108
Tertiary intention breakdown
Primary size but if closed too soon may trap infection inside, wait till clean then close

HLSC 222 (9 decks)

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