2.1 - Inflammation and Repair Flashcards
(171 cards)
1
Q
5 Cardinal Signs of Inflammation
A
Rubor
Calor
Tumor
Dolor
Functio laesa
2
Q
What is rubor?
A
Redness / erythema due to inflammation
3
Q
What is calor?
A
Heat due to inflammation
4
Q
What is tumor?
A
Swelling due to inflammation
5
Q
What is dolor?
A
Pain due to inflammation
6
Q
What is functio laesa?
A
Loss of function due to inflammation
7
Q
Which cardinal sign of inflammation pertains to the accumulation of fluid in the extravascular space?
A. Calor
B. Dolor
C. Rubor
D. Tumor
A
D. Tumor
8
Q
What is inflammation? A response of vascularized tissues to infections and damaged tissues that brings cells and mol- ecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offend- ing agents.
A
- A response of vascularized tissues to infections and damaged tissues that brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents.
9
Q
A 25-year-old medical student came into the ER because of thermal burn of the right hand. On inspection, the hand was swollen, erythematous, and immobile. What is the possible mechanism to explain the swollen appearance?
A. Swelling is an effect of leukocyte extravasation
B. The swollen appearance is a consequence of a burn
leakage of exudates in the area of burn
C. The swollen appearance is mainly due to direct injury to
the vessels causing vascular leakage of protein-rich fluid
in the interstitium
D. The swollen appearance is due to the formation of
endothelial gap in venules leading to vascular leakage
A
D. The swollen appearance is due to the formation of
endothelial gap in venules leading to vascular leakage
10
Q
Most common mechanism of vascular leakage inflammation
A. Decreased extravascular oncotic pressure
B. Endothelial cell necrosis
C. Formation of endothelial gaps in venules
D. Increased hydrostatic pressure
A
C. Formation of endothelial gaps in venules
11
Q
Mechanism of increased vascular permeability - 3
A
- Endothelial cell/pericyte contraction
- Direct endothelial cell injury
- Leukocyte injury of endothelium
12
Q
How does endothelial cell/pericyte contraction increase vascular permeability?
A
Contraction of endothelial cells create a gap between them resulting to an increase in vascular permeability
13
Q
How does direct endothelial cell injury increase vascular permeability?
A
In burns, or is induced by the actions of
microbes and microbial toxins that target
endothelial cells
14
Q
How does leukocyte injury of endothelium increase vascular permeability?
A
Neutrophils that adhere to the endothelium during inflammation may also injure the endothelial cells and thus amplify the reaction
15
Q
What are the typical inflammatory reaction series of sequential steps?
A
- The offending agent, which is located in extravascular tissues, is recognized by host cells and molecules.
- Leukocytes and plasma proteins are recruited from the circulation to the site where the offending agent is located.
- The leukocytes and proteins are activated and work together to destroy and eliminate the offending substance.
- The reaction is controlled and terminated.
- The damaged tissue is repaired.
16
Q
What is the first step of the typical inflammatory reaction?
A
The offending agent, which is located in extravascular tissues, is recognized by host cells and molecules.
17
Q
Diagnostic hallmark of acute inflammation
A. Fibrosis
B. Angiogenesis
C. Accumulation of neutrophils
D. Aggregatesofactivated
macrophages
A
C. Accumulation of neutrophils
18
Q
What are the major participants in the inflammatory reaction in tissues?
A
blood vessels
and
leukocytes
19
Q
What do neutrophils do in acute inflammation?
A
neutrophils release granules
20
Q
What are the categories of granules that neutrophils release? 2
A
- Primary (azurophilic) granules
2. Secondary (specific) granules
21
Q
What are the Primary (azurophilic) granules? - 7
A
o Myeloperoxidase o Phospholipase A2 o Lysozyme o Acid hydrolases o Elastase o Defensins o Bactericidal permeability increasing protein (BPI)
22
Q
What are the Secondary (specific) granules? - 6
A
o Phospholipase A2 o Lysozyme o Leukocyte alkaline phosphatase (LAP) o Collagenase o Lactoferrin o Vitamin B12 binding protein
23
Q
Which one or some of these are primary granules?
o Acid hydrolases o Collagenaseo o Leukocyte alkaline phosphatase (LAP) o Myeloperoxidase o Phospholipase A2 o Vitamin B12 binding protein
A
o Acid hydrolases
o Myeloperoxidase
o Phospholipase A2
24
Q
Which granules are both Primary and Secondary granules?
A
o Phospholipase A2
o Lysozyme
25
Cytokines, IL-1, and TNF in the production of fever are produced by:
A. Erythrocytes
B. Leukocytes
C. Platelets
D. Histiocytes
B. Leukocytes
26
What are the chemical mediators of inflammation?
Histamine
Prostaglandins
Leukotrienes
Cytokines (TNF, IL-1, IL-6)
Chemokines
Platelet-activating factor
Complement
Kinins
27
In an acute inflammation, pain is most likely due to the release of
A. Thromboxane A2
B. Bradykinin
C. Histamine
D. Serotonin
B. Bradykinin
28
Secreted by sentinel cells in tissues in response to
| microbes and other injurious agents
Cytokines
29
Recruitment of leukocytes to location of stimuli is ensured
Cytokines
30
The steps of the inflammatory response can be remem- bered as the five Rs:
(1) recognition of the injurious agent
(2) recruitment of leukocytes
(3) removal of the agent
(4) regulation (control) of the response
(5) resolution (repair)
31
What is the most notable mediator of vasodilation in inflammation?
histamin
32
the mechanisms by which leukocytes damage normal tissues are the same as the mechanisms involved in antimicrobial defense during these events - 3
* part of a normal defense reaction against infectious microbes, when adjacent tissues suffer collateral damage
* inflammatory response is inappropriately directed against host tissues, as in certain autoimmune diseases
* host reacts excessively against usually harm- less environmental substances, as in allergic diseases, including asthma
33
What is the difference between cell-derived and de novo mediators of inflammation?
* Cell-derived mediators are normally sequestered in intracellular granules and can be rapidly secreted by granule exocytosis
* De novo mediators are synthesized in response to a stimulus
34
Source of:
Histamine
- Mast cells
- basophils
- platelets
35
Action of:
Histamin
- Vasodilation
- increased vascular permeability
- endothelial activation
36
Source of:
Prostaglandins
- Mast cells
| - leukocytes
37
Action of:
Prostaglandins
- Vasodilation
- pain
- fever
38
Source of:
Leukotrienes
- Mast cells
| - leukocytes
39
Action of:
Leukotrienes
- Increased vascular permeability
- chemotaxis
- leukocyte adhesion
- activation
40
Source of:
Cytokines (TNF, IL-1, IL-6)
- Macrophages
- endothelial cells
- mast cells
Local: endothelial activation (expression of adhesion molecules). Systemic: fever, metabolic abnormalities, hypotension (shock)
41
Action [local and systemic]
Cytokines (TNF, IL-1, IL-6)
```
Local:
endothelial activation (expression of adhesion molecules)
```
Systemic:
fever
metabolic abnormalities
hypotension (shock)
42
Source of:
Chemokines
- Leukocytes
| - activated macrophages
43
Action of:
Chemokines
- Chemotaxis
| - leukocyte activation
44
Source of:
Platelet-activating factor
- Leukocytes
| - mast cells
45
Action of:
Platelet-activating factor
- Vasodilation
- increased vascular permeability
- leukocyte adhesion
- chemotaxis
- degranulation
- oxidative burst
46
Source of:
Complement
- Plasma (produced in liver)
Leukocyte chemotaxis and activation, direct target killing (membrane attack complex), vasodilation (mast cell stimulation)
47
Action of:
Complement
- Leukocyte chemotaxis and activation
- direct target killing (membrane attack complex)
- vasodilation (mast cell stimulation)
48
Source of:
Kinins
Plasma (produced in liver)
49
Action of:
Kinins
- Increased vascular permeability
- smooth muscle contraction, vasodilation
- pain
50
Prostaglandins and leukotrienes, cytokines are examples of:
a. cell-derived mediators
b. synthesized de novo
b. synthesized de novo
51
Which mediators of inflammation are produced by mast cells? 5
Histamine
Prostaglandins
Leukotrines
Cytokines (TNF, IL-1, IL-6)
Platelet-activating factor
52
Which mediators of inflammation are produced by leukocytes?
Prostaglandins
Leukotrines
Chemokines
Platelet-activating factor
53
Histamine triggers for release: - 4
- IgE-mediated mast cell reactions
- Physical injury
- Anaphylatoxins (C3a and C5a)
- Cytokines (IL-1)
54
IL-1 and TNF (Tumor Necrosis Factor) stimulates and activates: - 3
fibroblasts
endothelial cells
neutrophils
55
Kinins are derived from plasma proteins, kininigens, which are activated by...
kallikreins
56
Action of:
Bradykinin
- Increased vascular permeability
- Pain
- Vasodilation
- Bronchoconstriction
57
The following are stimuli for acute inflammation, except:
A. Blunt trauma
B. Tissue necrosis
C. Immune reactions
D. Autoimmune diseases
D. Autoimmune diseases
58
Acute inflammation has three major components:
(1) dilation of small vessels leading to an increase in blood flow
(2) increased permeability of the microvasculature enabling plasma proteins and leukocytes to leave the circulation
(3) emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent
59
What is a hallmark of acute inflammation?
increased permeability of postcapillary venule (vascular leakage)
60
An exudate is an extravascular fluid that has protein concentration and cellular debris that is:
a. high
b. low
a. high
61
An transudate is an extravascular fluid that has protein concentration and cellular debris that is:
a. high
b. low
b. low
62
The journey of leukocytes from the vessel lumen to the tissue is a multistep process that is mediated and controlled by: - 2
- adhesion molecules
| - cytokines called chemokines
63
The two major families of molecules involved in leukocyte adhesion and migration are
selectins and integrins, and their ligands
64
The steps of leukocyte migration through blood vessels are:
- rolling
- Integrin activation by chemokines
- Integrin activation
- Migration through endothelium
65
What is transmigration or diapedesis?
leukocyte recruitment is migration of the leukocytes through the endothelium
66
Causes of chronic inflammation
- Autoimmune diseases
Response to foreign material
- Response to malignant tumors
- Following a bout of acute inflammation
- Persistent infections
- Infections with certain organisms
67
Which infectious organisms cause chronic inflammation?
- Viral infections
- Mycobacteria
- Parasitic infections
- Fungal infections
68
Which is a step in phagocytosis?
A. Opsonization
B. Margination
C. Pavementing
D. Stasis
A. Opsonization
69
Phagocytosis involves three sequential steps
(1) recognition and attachment of the particle to be ingested by the leukocyte;
(2) engulfment, with subsequent formation of a phagocytic vacuole;
(3) killing or degradation of the ingested material.
70
Opsonins enhance...
enhance recognition and phagocytosis of bacteria
71
Important opsonins:
Fc portion of IgG
Complement system product C3b
Plasma proteins – collectins (bind bacterial cell walls)
72
Steps of engulfment
Neutrophils send out cytoplasmic processes that surround
the bacteria
The bacteria are internalized within a phagosome
The phagosome fuses with lysosomes (degranulation)
73
Blood vessel changes in the pathogenesis of acute inflammation
A. Vasoconstriction
B. Vasodilation
C. Thrombosis
D. Spasm
B. Vasodilation
74
Hemodynamic changes in acute inflammation
1. Initial transient vasoconstriction
2. Massive vasodilation mediated by histamine, bradykinin,
and prostaglandin
3. Increased vascular permeability due to endothelial gaps
4. Blood flow slows (stasis) due to increased viscosity,
allowing neutrophils to marginate
75
his involves the transmigration of leukocytes across the endothelium
A. Pavementing
B. Chemotaxis
C. Diapedesis
D. Margination
C. Diapedesis
76
Which is TRUE of diapedesis?
A. Active process
B. Dependent on hydrostatic pressure
C. Neutrophils stay in the vascular lumen
D. Occurs only in large arteries
A. Active process
77
Which of the following processes requires adhesion molecules?
A. Abscessformation
B. Diapedesis
C. Healing
D. Pavementing
D. Pavementing
78
Neutrophil margination and adhesion is also known as...
Pavementing
79
What are the steps in neutrophil margination and adhesion (pavementing)?
Step 1: At sites of inflammation, the endothelial cells have increased expression of E-selectin and P-selectin
Step 2: Neutrophils weakly bind to the
endothelium and roll along the surface
Step 3: Neutrophils are stimulated by chemokines
to express their integrins
Step 4: Binding of the integrins firmly adheres the
neutrophils to the endothelial cells
80
Steps of leukocyte recruitment to sites of inflammation
Neutrophil margination and adhesion (Pavementing)
Emigration (Diapedesis) (transmigration)
Chemotaxis
81
What proteins are expressed in the initial step of Pavementing?
E-selectin
and
P-selectin
82
What stimulates neutrophils to express integrins in pavementing?
chemokines
83
Steps of Emigration (diapedesis) (transmigration)
- Leukocytes emigrate from the vasculature by extending pseudopods between the endothelial cells
- They move between endothelial cells, migrating through the basement membrane toward the inflammatory stimulus
84
Leukocytes extend what between endothelial cells in emigration? (diapedesis) (transmigration)
pseudopods
85
Steps of chemotaxis
The attraction of cells toward a chemical mediator
| that is released in the area of inflammation
86
What are the important chemotactic factors for neutrophils?
Bacterial products (N-formyl-methionine)
Leukotriene B4 (LTB4)
Complement system products C5a
Alpha-chemokines (IL-8)
87
Which is an important chemotactic factor for neutrophils?
a. Complement system products C3a
b. Complement system products C5a
c. Histamine
d. Serotonin
b. Complement system products C5a
88
Which of the following is sequela of acute inflammation?
A. Abscess
B. Diapedesis
C. Ceseation necrosis
D. Pavementing
A. Abscess
89
Sequela definiton
a condition that is the consequence of a previous disease or injury
90
Four outcomes of acute inflammation
- Complete resolution with regeneration
- Complete resolution with scarring
- Abscess formation
- Transition to chronic inflammation
91
The germinal centers of lymph nodes consist mainly of:
A. B-cells
B. T-cells
C. Interdigitating dendritic cells
D. Plasma cells
A. B-cells
92
Tissue-based macrophages in the liver are known as:
A. Microglia
B. Histiocytes
C. Kuppfercells
D. Alveolar macrophages
Answer: C
93
Chronic inflammation arises in the following settings:
Persistent infections
Hypersensitivity diseases
Prolonged exposure to potentially toxic agents, either exogenous or endogenous
94
General areas of lymphoid tissue associated with chronix inflammation
(external to internal)
Follicles
Intrafollicular area
Medullary area
95
What is produced in the follicle of lymphoid tissue?
B-cells
Follicular dendritic
cells (FDC)
96
What is produced in the intrafollicular areas of lymphoid tisue?
T-cells
NK cells
```
Interdigitating
dendritic cells (IDC)
```
97
What is produced in the medullary areas of lymphoid tisue?
Plasma cells
98
The dominant cells in most chronic inflammatory reac- tions are
Macrophages
99
How do macrophages contribute to the chronic inflammatory reaction? - 3
1. by secreting cytokines and growth factors that act on various cells
2. by destroying foreign invaders and tissues
3. by activating other cells, notably T lymphocytes.
100
What do macrophages release during chronic inflammation?
cytokines and growth factors
101
What is the most notable cell that macrophages activate in chronic inflammation?
T lymphocytes
102
What are the tissue-based macrophages in:
Connective tissue
(histiocyte)
103
What are the tissue-based macrophages in:
Lung
(pulmonary alveolar macrophages)
104
What are the tissue-based macrophages in:
Liver
(kuppfer cells)
|
105
What are the tissue-based macrophages in:
Bone
(osteoclasts)
|
106
What are the tissue-based macrophages in:
Brain
(microglia)
107
Where are macrophages derived?
Blood monocytes
108
Which of the following cause granulomatous inflammation?
A. Staphylococcus aureus
B. Bee sting
C. Suture material
D. Streptococcus pneumonia
C. Suture material
109
Chronic cranulomatous fever - 9
Tuberculosis (caseating granulomas)
Cat-scratch fever (Gram-negative bacillus)
Syphilis (Treponema pallidum)
Leprosy (Mycobacterium leprae)
Fungal infection (coccidiodomycosis)
Parasitic infections (schistosomiasis)
Foreign bodies
Beryllium
Sarcoidosis (unknown etiology)
110
What is granulomatous inflammation?
a form of chronic inflammation characterized by collections of activated macrophages, often with T lymphocytes, and sometimes associated with central necrosis.
111
What is the cause of:
Tuberculosis
(caseating granulomas)
112
What is the cause of:
o Cat-scratch fever
(Gram-negative bacillus) o
113
What is the cause of:
Syphilis
(Treponema pallidum)
114
What is the cause of:
o Leprosy
(Mycobacterium leprae)
115
What is the cause of:
o Fungal infection
(coccidiodomycosis)
116
What is the cause of:
o Parasitic infections
(schistosomiasis)
117
What is the cause of:
o Sarcoidosis
(unknown etiology)
118
What is the tissue reaction of:
Mycobacterium tuberculosis
Tuberculosis
Caseating granuloma (tubercle): focus of activated macrophages (epithelioid cells), rimmed by fibroblasts, lymphocytes, histiocytes, occasional Langhans giant cells; central necrosis with amorphous granular debris; acid-fast bacilli
119
What is the tissue reaction of:
Mycobacterium leprae
Leprosy
Acid-fast bacilli in macrophages; noncaseating granulomas
120
What is the tissue reaction of:
Treponema pallidum
Syphilis
Gumma: microscopic to grossly visible lesion, enclosing wall of histiocytes; plasma cell infiltrate; central cells are necrotic without loss of cellular outline
121
What is the tissue reaction of:
Gram-negative bacillus
Cat-scratch fever
Rounded or stellate granuloma containing central granular debris and recognizable neutrophils; giant cells uncommon
122
What is the tissue reaction of:
Sarcoidosis
Noncaseating granulomas with abundant activated macrophages
123
What is the tissue reaction of:
Immune reaction against
intestinal bacteria, possibly self antigens
Crohn disease
Occasional noncaseating granulomas in the wall of the intestine, with dense chronic inflammatory infiltrate
124
Which of the following products of the lipooxygenase pathways plays an important role in the chemotaxis of neutrophils?
A. Leukotriene B4
B. Leukotriene C4
C. Leukotriene D4
D. Leukotrience E4
A. Leukotriene B4
125
Which of the following complements can function as an opsonin?
A. C3a
B. C3b
C. C35
D. C5b-9
B. C3b
126
Which of the following products of the cyclooxygenase pathway can cause pain?
A. Thromboxane A2
B. Prostacyclin
C. Prostaglandin E
D. Leukotriene B4
C. Prostaglandin E
127
General categories of chemical mediators of inflammation
Lipooxygenase pathway
Complement cascade
Cyclooxygenase pathway
Cyclooxygenase pathway
128
These are chemicals of Lipooxygenase pathway
o Leukotriene B4 (LTB4): neutrophil chemotaxis
o Leukotriene C4, D4, E4: vasoconstriction
129
Leukotriene B4 (LTB4) is responsible for
neutrophil chemotaxis
130
Leukotriene C4, D4, E4 is responsible for
vasoconstriction
131
Important inflammation mediators from complement cascade
C5b – C9 – membrane attack complex
C3a, C5a – anaphylatoxins stimulate the
release of histamine
C3b – opsonin
132
C5b – C9 does what?
– membrane attack complex
133
C3a, C5a does what?
– anaphylatoxins stimulate the
| release of histamine
134
C3b is a?
– opsonin
135
Mediators in Cyclooxygenase pathway?
```
Thromboxane A2 (TXA2)
[ Produced by platelets
Vasoconstriction and platelet aggregation]
```
Prostacyclin (PGI2)
[ Produced by vascular endothelium
Vasodilation and inhibits platelet
aggregation]
136
Thromboxane A2 (TXA2) is from and does what?
Produced by platelets
Vasoconstriction and platelet aggregation
137
Prostacyclin (PGI2) is from and does what?
Produced by vascular endothelium
Vasodilation and inhibits platelet aggregation
138
PG E is associated with?
pain
139
Which prostaglandin cause vasodilation?
Prostaglandins PGE2, PGD2 and PGF2
140
Prostaglandins (PGs) are produced by
mast cells, macro- phages, endothelial cells, and many other cell types, and are involved in the vascular and systemic reactions of inflammation.
141
Which is the hallmark/predominant cell in a granuloma?
A. Lymphocyte
B. Fibroblast
C. Epithelioid histiocytes
D. Langerhans type multinucleated giant cells
C. Epithelioid histiocytes
142
Granuloma formation is a response mediated by:
A. B-cells
B. Plasma cells
C. T-cells
D. Mast cells
C. T-cells
143
Specialized form of chronic inflammation
Small aggregates of modified macrophages
(epithelioid cells and multinucleated giant cells) o
Surrounded by rim of lymphocytes
144
Composition of a granuloma
Epithelioid cell
Multinucleated giant cells (langhans-type)
Lymphocytes and plasma cells
Central caseous necrosis
145
Epithelioid cell are
IFN-alpha transforms macrophages to epithelioid cells
Enlarged cell with abundant pink cytoplasm
146
Multinucleated giant cells (langhans-type)
Formed by the fusion of epithelioid cells
Langhans-type giant cells (peripheral arrangement of nuclei)
Foreign-body type giant cells (haphazard arrangement of nuclei)
147
Central caseous necrosis
Present in granulomas due to tuberculosis Rare in other granulomatous diseases
148
Which of the following cells regenerate throughout life?
A. Hepatocytes
B. Proximal tubular cells
C. Cardiac muscle cells
D. Hematopoietic cells
D. Hematopoietic cells
149
When do Hepatocytes and proximal tubular cells regenerate?
when there is injury or stimulus
150
Do labile cells regenerate?
Yes, through out life
151
Do permanent cells regenerate?
No.
e.g. neurons and cardiac muscle
152
The following are components of fibrosis, except:
A. Angiogenesis
B. Migration through basement membrane
C. Proliferation of fibroblasts
D. Remodeling
B. Migration through basement membrane
153
Steps in scar formation
1. Angiogenesis
2. Formation of granulation tissue
3. Remodeling of connective tissue
154
What happens in Angiogenesis?
Formation of new blood vessels, which supply
| nutrients and oxygen needed to support the repair process
155
What happens in Formation of granulation tissue?
Migration and proliferation of fibroblasts, and deposition of loose connective tissue, together with the vessels and interspersed leukocytes, form granulation tissue
156
What happens in Remodeling of connective tissue?
Maturation and reorganization of the connective
tissue produce the stable fibrous scar
Amount of connective tissue increases in the
granulation tissue, eventually resulting in the formation of a scar, which may remodel over time
157
Which of these can lead to chronic inflammatory reaction?
A. Abscessoftheaxilla
B. Atherosclerotic lesions
C. Secondary burns of the arms in an immunocompent
patient
D. Streptococcal sore throat in a healthy athlete
B. Atherosclerotic lesions
158
Which condition shows fibrosis as a form of healing/repair?
A. Acute chemical injury in hepatocytes
B. Continuous sloughing of superficial squamous cells of
skin
C. Epithelial healing in primary wound healing
D. Healing of liver with cirrhosis
D. Healing of liver with cirrhosis
159
The hallmark of healing
A. Granuloma
B. Granulation tissue
C. Granulocytes
D. Germination
B. Granulation tissue
160
This substance provides the tensile strength in wound healing
A. fibrin
B. collagen
C. elastin
D. keratin
B. collagen
161
How many types of collagen?
Four
162
Collagen Type I
```
Most common
High tensile strength
Skin, bone, tendons and most organs
```
163
Collagen Type II
cartilage
vitreous humor
164
Collagen Type III
granulation tissue,
embryonic tissue,
uterus,
keloids
165
Collagen Type IV
basement membranes
166
Hydroxylation of collagen is mediated by
Vitamin C
167
Cross-linking of collagen is performed by
lysyl oxidase. Copper is a required co-factor
168
Which of the following is TRUE in surgical incision?
A. Healing by first intention
B. Healing by secondary intention
C. Significant wound contraction
D. Wounds have large tissue defects
A. Healing by first intention
169
the principal mechanism of repair is epithelial regeneration, also called primary union or healing by first intention is when
the injury involves only the epithelial layer
Occurs with clean wounds when there has been
little tissue damage and the wound edges are
closely approximated
o Classic example: surgical incision
170
In healing of skin wounds by second intention, also known as healing by secondary union occurs...
Occurs in wounds that have large tissue defects
and when the two skin edges are not in contact
Required larger amounts of granulation tissue to fill
in the defect
o Significant wound contraction o Larger residual scar
171
What delays wound healing?
foreign bodies
infection
ischemia
diabetes
malnutrition
scurvy
