Chapter 6 - Innate Immunity: Inflammation & Wound Healing Flashcards
1
Q
Innate immunity involves the ____ and ____ lines of defense
A
first and second
2
Q
What is the first line of defense?
A
physical (skin), mechanical (mucous membrane), biochemical barriers
3
Q
What is the second line of defense?
A
the firing squad - inflammation response, macrophages, and neutrophils
4
Q
Adaptive immunity is the ____ line of defence.
A
third
5
Q
What is the third line of defense?
A
acquired or specific immunity via B and T cells
6
Q
Which type of T cell is involved in both innate and adaptive immunity?
A
Natural Killer T Cell
7
Q
What do Mast cells release?
A
histamines (cytokines)
8
Q
What does histamine do?
A
induce vasodilation
9
Q
What do platelets do?
A
induce clotting to stop blood loss
10
Q
What is the role of macrophages and neutrophils during the inflammatory response?
A
phagocytosis of the pathogen
11
Q
What element do macrophages follow?
A
cytokines
12
Q
What is pus accumulation?
A
the gathering of dead phagocytes and pathogens
13
Q
What leaks out and is followed by fluid to induce swelling?
A
ions, followed by water
14
Q
What is the role of prostaglandins in the inflammatory response?
A
Overseer/coordinator of events
15
Q
What is another principal coordinator during inflammation?
A
vascular epithelium
16
Q
What 2 cells are contained in the tissue close to vessels?
A
mast and dendritic cells
17
Q
Which cells are an inflammation activator? What do they release?
A
mast cells release cytokines
18
Q
Dendritic Cells
A
connect the innate and adaptive immune response
19
Q
What recruits the innate and adaptive immune systems?
A
chemical molecules
20
Q
Where are chemical molecules released from?
A
Damaged or destroyed cells
21
Q
What are cytokines?
A
a general term for released chemical molecules (messengers) that regulate innate and adaptive immunity
22
Q
Cytokines can be ___inflammatory or ___-inflammatory
A
pro or anti (shut down)
23
Q
Lymphokines
A
cytokines released from lymphocytes
24
Q
Monokines
A
cytokines released from monocytes
25
What do monocytes change into?
macrophages
26
What produces IL-1?
macrophages
27
What produces IL-6?
macrophages, lymphocytes, fibroblasts
28
What is different about interleukins than cytokines?
ILs have self-limiting abilities
29
What is the order of cells in the immune response?
mast cell, neutrophil, macrophage, basophil, eosinophil, natural killer cell
30
Cytokine Storm Syndrome
activated by Covid-19, a severe systemic immune response that can be damaging to the body
31
What is the cytokine released during CSS?
IL-6 (lymphokine) which plays a major role in the excessive recruitment of lymphocytes
32
What is the treatment for Covid-19?
IL-6 antibody production to counteract the effects
33
TNF-a is a _____ but not an _______
cytokine but not an interleukin
34
What releases TNF-a?
macrophages and mast cells
35
What are the pro-inflammatory effects of TNF-a?
fever, cachexia, fatal shock (gram- bacteria), granuloma
36
Cachexia
muscle wasting
37
What is a main anti-inflammatory cytokine?
IL-10 aka lymphokine
38
How do monocytes move out of blood vessels?
through interstitial spaces between cells
39
How does capillary permeability change during inflammation?
increased permeability
40
Capillary widening = ______ blood flow
increased
41
Increased permeability = _____ _____ into tissues
fluid release
42
Attraction of leukocytes = leaking of leukocytes to...
injury site
43
Systemic response = _____ and increase in _____
fever and increase in leukocytes
44
What are the signs and symptoms of inflammation?
heat, redness, swelling, tenderness, pain
45
What is the goal of the inflammatory response?
limit and control bleeding and infection
46
Interventions for Inflammation:
clean wound (saline), remove loose debris, treat with antibiotics
47
What does "itis" tell us?
Where the inflammation is (ie. tonsilitis)
48
What activates inflammation?
cell injury or death
49
What are 5 things that cause cell death?
infection, damage, ischemia, temperature, radiation
50
Erythrocyte Sedimentation Rate (ESR)
determination of the rate of RBC settling in saline solution
51
An increase in infection affects RBCs how?
RBCs bind to each other, making them heavier and settle in saline faster
52
Increased ESR = ______ infection
increased
53
Sed Rate
distance (in mm) the RBCs fall in 1 hour
54
What causes the C-reactive protein?
the effect of acute inflammation on the liver
55
C-reactive protein ____ in response to inflammation
increases
56
Is CRP specific to the disease?
no
57
What do CRP tests monitor?
disease progress and flares
58
What does blood work for WBC count measure?
increase in neutrophils (bands)
59
What does it mean if there is an increase of neutrophils in the blood?
we have not got a hold of the infection yet
60
How long does acute inflammation last?
less than 2 weeks
61
Symptoms of acute inflammation?
swelling, pain, heat, redness
62
Is acute inflammation localized or systemic?
localized
63
What are the 3 main systemic changes due to acute inflammation? (Hint: temp, WBC, protein)
fever, leukocytosis, increase in circulating proteins
64
Leukocytosis
increase in circulating leukocytes
65
When can acute inflammation become chronic?
if the response is unsuccessful
66
How long does chronic inflammation last?
longer than two weeks, up to months or years
67
Does chronic inflammation occur only after acute inflammation?
no, it can occur without previous inflammation
68
What is 3 things cause of chronic inflammation?
microorganisms that resist phagocytosis, survive in a macrophage, and/or produce toxins
69
How does chronic inflammation present?
as a dense infiltration of macrophages and lymphocytes
70
When do granulomas form?
if macrophages are unable to stop damage, the body walls off the infected area
71
Which cytokine drives granuloma formation?
TNF-a
72
Granuloma
cluster of WBCs and other tissues
73
If acute inflammation resolves, what is restored?
cellular and tissue homeostasis
74
What is the first cell to arrive at the inflammation site, and the fastest to leave?
platelets
75
What is the first white blood cell on scene?
neutrophils
76
Which WBC arrives second to neutrophils?
macrophages
77
Fibroblasts arrive after _______ and do what?
after macrophages and begin repairing the tissue
78
Which WBC arrives last and what does it do?
lymphocytes (B and T cells) arrive if the problem isn't under control and...
79
The transition from acute inflammation to healing begins...
IMMEDIATELY
80
What do platelets do in wound healing?
initiate clot formation and formation of undamaged cells
81
What do neutrophils do in wound healing?
clean wound of debris and bacteria
82
What do macrophages do in wound healing?
-release growth factors
-recruit fibroblasts
-promote angiogenesis
83
Angiogenesis
development of new blood vessels
84
What 3 cells are involved in the 'inflammation' phase of wound healing?
platelets, neutrophils, macrophages
85
How long does the 'proliferation and new tissue formation' phase of wound healing last?
starts at 3 days and lasts 2 weeks
86
What do fibroblasts do in the 'proliferation and tissue formation' stage of wound healing?
collagen synthesis
87
What is "epithelialization"? When does it occur?
epithelial cells migrate to the wound during the proliferation and new tissue formation stage
88
When does cellular differentiation and macrophage secretions occur?
proliferation and new tissue formation stage
89
How long does the "remodelling and maturation" phase of wound healing last?
weeks to years
90
Cellular differentiation during the remodelling and maturation phase:
unspecialized cells (stem cells) mature and perform important cellular functions
91
When does scar tissue formation and remodelling occur?
during the remodelling and maturation phase of wound healing
92
What is the major remodelling cell?
fibroblasts
93
What is the primary intention of tissue repair?
-clean incision
-early suture
94
Why is early suture the best choice?
leaves a fresh wound with sufficient vascularization
95
What is the result if primary tissue repair intentions are successful?
fine scar
96
Secondary intention of tissue repair involves g_________ for gaping wounds
granulation
97
Why is granulation a secondary intention?
the wound is extensive and the edges can't be brought together to suture
98
Secondary intentions are ideal for c________ or i__________ wounds because the wound is left open to heal spontaneously.
contaminated or infected
99
Tertiary tissue repair intentions are used when delayed ______ closure happens
primary closure
100
Tertiary intentions are used on open but not ________ wounds
gaping
101
Tertiary intentions for tissue repair allow for ________ and ________
granulation and observation
102
Tertiary intentions: when the wound is clean...
it is sutured closed but has a wider scar than primary
103
Adhesions
abnormal union of membranous surfaces
104
When are adhesions common?
bowel surgery
105
When are adhesions painful?
when they stop the normal movements of the intestinal system
106
Wound Contraction
healing cells pull other cells together and contract the tissue
107
Wound contractions are common with ____ injuries
burn
108
Infections
wound is reinfected with the initial or new pathogen
109
Dehiscence
incision separates following surgery -- wound is "dehisced"
110
Evisceration
surgical complication where the incision opens and abdominal organs protrude
111
What is the result of dehiscence and/or evisceration?
excess scar formation caused by excess tension or movement
112
Low blood supply during wound healing...
inhibits the recovery process
113
High blood supply during wound healing...
increases risk for blood clots
114
Being obese predisposes wound to possible _______
infections
115
When fibrin (clotting factor) doesn't get reabsorbed it causes...
fibrous adhesions
116
Why does having diabetes prolong wound healing?
hyperglycaemia suppresses macrophages
117
Hyperglycaemia
excess glucose in blood due to malfunction of insulin
118
Why is nutrition important during wound healing?
to meet metabolic needs
119
How can being on steroids impact wound healing?
steroids prevent macrophages from migrating to infection site
120
Antineoplastic drugs used for cancer treatment to slow cell division impact wound healing by...
blocking neoplasm formation (new abnormal tissue growth)
