Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

Chapter Six - Innate Immunity : Inflammation And Wound Healing Flashcards

(86 cards)

Start Studying
1
Q

Innate immunity: first line of defence

A

-physical, mechanical, biochemical barriers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Innate immunity : second line of defence

A

Inflammation, macrophage, neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Adaptive immunity

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Mast cells release

A

Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Histamines =

A

Vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

___ enter to stop blood loss

A

Platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

______ arrive to phagocytize pathogen

A

Macrophages and neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

When macrophages arrive to phagocytize, what accumulates

A

Pus
-dead phagocytes and pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Rapid leakage and influx of

A

Leakage - ions

Influx - fluids

Since water follows sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

During inflammation vascular ____ is a principle coordinator

A

Epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Tissue close to vessel contains two involved cells

A

-mast cells
-dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mast cells

A

Important inflammation activator
-release histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Dendritic cells

A

Connect innate and adaptive immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Both innate and adaptive systems are recruited by

A

Chemical molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chemical molecules are released from

A

Damaged or destroyed cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cytokines

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cytokines can be

A

Pro inflammatory or anti inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Lymphokines

A

Cytokines released from lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Monokines

A

Cytokines released from monocytes
-which change into macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Macrophages and lymphocytes also released

A

Itnerleukin cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Main interleukins are

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

IL-1

A

Produced by macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

IL-6

A

Produced by macrophages, lymphocytes and fibroblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

COVID 19 activates a

A

Cytokine storm syndrome
-severe systemic inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
IL-6 has cytokine released =
Excessive recruitment of lymphocytes
26
COVID 19 treatment
Is production of IL-6 antibodies to counteract effect
27
TNF-a
A cytokine but not classified as an interleukin -released by macrophages and mast cells -induces multitude of pro inflammatory effects
28
Pro inflammatory effects
-fever -cachexia -fatal shock -granuloma formation
29
Cachexia
Muscle wasting
30
Fatal shock is caused by
Gram negative bacterial infections
31
Antiflammatory cytokines are
Interleukin 10 lymphokine
32
Granuloma formation
33
Goal of inflammatory responses
-limit and control injury (limit blood and infection) -intervention (clean wound, remove debris, antibiotics)
34
ITIS tells us
Where inflammation is located
35
Cell injury or death activates
Inflammation
36
cell death can be due to
-infection -mechanical damage -ischemia -temp extremes -radiation
37
Erythrocyte sedimentation rate or ESR
Determination of rate of RBC settling in saline solution
38
An increase in infection =
RBC bind to each other, becoming heavier and settle at a faster rate
39
Increased ESR =
Increased infection
40
C reactive protein is caused by
Effect on liver
41
C reactive protein increases in
Response to inflammation
42
An increase in neutrophils during blood work would signal that
The WBC have not got a hold of the infection yet -actively fighting
43
Acute inflammation
-lasts less than two weeks -swelling, pain, heat, redness -localized and quick to diagnose
44
Three primary systemic changes in an acute inflammation
1. Fever 2. Leukocytosis or inc levels of circulating leukocytes 3. Increased circulating proteins
45
Acute inflammation if response is unsuccessful can become
Chronic
46
Chronic inflammation
-longer Thant so weeks/months/years -can be preceded by unsuccessful acute or distinct process without previous acute inflammation
47
Chronic inflammation causes microorganisms to
-be insensitive to phagocytosis -they can survive macrophages -produce toxins
48
Chronic inflammation presents as a
Dense infiltration of lymphocytes and macrophages
49
If macrophages are unable to stop tissue damage
Body walls off infected area by forming a granuloma
50
TNF -a drives ___ formation
Granuloma -a cluster of WBC and other tissues
51
Simple explanation of a chronic inflammation
When the immune system is unable to protect body -formation of granuloma -> walled off infection area
52
Transition from acute inflammatory to healing begins when
Immediately
53
Platelets
Clot formation -initiate formation of unmanaged cells
54
Neutrophils
Clea wound of debris and bacteria -last small amount of time
55
Macrophages
Release growth factors -recruit fibroblasts -promote angiogenesis
56
Angiogenesis
Development of new blood vessels
57
Proliferation and new tissue formation lasts
Three days to two weeks
58
Fibroblast proliferation =
Collagen synthesis
59
Epithelization
Epithelial cells migrate to wound
60
Remodeling and maturation phase lasts
Weeks to years
61
Remodeling and maturation phase: cellular differentiation continues
Unspeilized cells mature -become specialize and perform important cellular functions -scar tissue formation and remodeling
62
Fibroblast
Major remodeling cell
63
Primary intention
-clean incision -early suture and is best choice for fresh wound with sufficient vascularization
64
Secondary intention
Gaping would = granulation -much more extensive and edges can’t be brought together
65
What type of wound is “-ideal for contaminated or infected wounds a wound if left open to heal spontaneously”
Secondary intention
66
What wound results in a fine scar?
Primary intention
67
Tertiary intention
Delayed primary closure -open wound by not gaping -inc granulation -allowed observation of wound
68
What intention is sutured closed and results in a wide scar
Tertiary intention
69
Adhesions
Abnormal union of membranous surfaces (common in bowel surgery) -painful if it stops normal movements
70
Strictures and contractures
Excess of wound contraction -healing cells tend to pull other cells towards them, causing contracture of tissue
71
Infections
Wound is reinfected with initial or new pathogen
72
Dehiscence
Incision separates following surgery and wound is considered dehisced
73
Evisceration
Surgical complication -incision opens and abdominal organs protrude
74
Excess scar formation
Caused by excess tension and movement
75
Low blood supply =
Iscehmia, vasoconstriction and inhibits recovery process
76
High blood supply =
Increased blood clots
77
Obesity predisposed to
Infections
78
Excessive fibrin
Doesn’t get reabsorbed and cases fibrous adhesions
79
Diabetes
Potential for smaller vessel disease and prolonged wound healing -hyperglycaemia
80
Hyperglycaemia
Excess glucose in blood
81
Hyperglycaemia =
Suppression of macrophages
82
Wound infection is
Infiltration of pathogen
83
Nutrition must meet
Metabolic needs of healing
84
Antineoplastic
Drugs used for cancer treatment to slow cell division -has various side effects -blocks formation of neoplasms
85
Neoplasms
New abnormal tissue growth
86
Steroids
Prevent macrophages from migrating to site

Pathophysiology (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions