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General Pathology > 2.1 - Inflammation and Repair > Flashcards

2.1 - Inflammation and Repair Flashcards

1
Q

5 Cardinal Signs of Inflammation

A

Rubor

 Calor

 Tumor

 Dolor

 Functio laesa

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2
Q

What is rubor?

A

Redness / erythema due to inflammation

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3
Q

What is calor?

A

Heat due to inflammation

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4
Q

What is tumor?

A

Swelling due to inflammation

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5
Q

What is dolor?

A

Pain due to inflammation

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6
Q

What is functio laesa?

A

Loss of function due to inflammation

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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

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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.
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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

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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

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11
Q

Mechanism of increased vascular permeability - 3

A
  • Endothelial cell/pericyte contraction
  • Direct endothelial cell injury
  • Leukocyte injury of endothelium
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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

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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

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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

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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.
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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.

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17
Q

Diagnostic hallmark of acute inflammation

A. Fibrosis

B. Angiogenesis

C. Accumulation of neutrophils

D. Aggregatesofactivated
macrophages

A

C. Accumulation of neutrophils

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18
Q

What are the major participants in the inflammatory reaction in tissues?

A

blood vessels

and

leukocytes

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19
Q

What do neutrophils do in acute inflammation?

A

neutrophils release granules

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20
Q

What are the categories of granules that neutrophils release? 2

A
  1. Primary (azurophilic) granules

2. Secondary (specific) granules

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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)
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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
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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

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24
Q

Which granules are both Primary and Secondary granules?

A

o Phospholipase A2

o Lysozyme

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25
Q

Cytokines, IL-1, and TNF in the production of fever are produced by:

A. Erythrocytes
B. Leukocytes
C. Platelets
D. Histiocytes

A

B. Leukocytes

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26
Q

What are the chemical mediators of inflammation?

A

Histamine

Prostaglandins

Leukotrienes

Cytokines (TNF, IL-1, IL-6)

Chemokines

Platelet-activating factor

Complement

Kinins

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27
Q

In an acute inflammation, pain is most likely due to the release of

A. Thromboxane A2
B. Bradykinin
C. Histamine
D. Serotonin

A

B. Bradykinin

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28
Q

Secreted by sentinel cells in tissues in response to

microbes and other injurious agents

A

Cytokines

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29
Q

Recruitment of leukocytes to location of stimuli is ensured

A

Cytokines

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30
Q

The steps of the inflammatory response can be remem- bered as the five Rs:

A

(1) recognition of the injurious agent
(2) recruitment of leukocytes
(3) removal of the agent
(4) regulation (control) of the response
(5) resolution (repair)

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31
Q

What is the most notable mediator of vasodilation in inflammation?

A

histamin

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32
Q

the mechanisms by which leukocytes damage normal tissues are the same as the mechanisms involved in antimicrobial defense during these events - 3

A
  • 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
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33
Q

What is the difference between cell-derived and de novo mediators of inflammation?

A
  • 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
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34
Q

Source of:

Histamine

A
  • Mast cells
  • basophils
  • platelets
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35
Q

Action of:

Histamin

A
  • Vasodilation
  • increased vascular permeability
  • endothelial activation
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36
Q

Source of:

Prostaglandins

A
  • Mast cells

- leukocytes

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37
Q

Action of:

Prostaglandins

A
  • Vasodilation
  • pain
  • fever
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38
Q

Source of:

Leukotrienes

A
  • Mast cells

- leukocytes

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39
Q

Action of:

Leukotrienes

A
  • Increased vascular permeability
  • chemotaxis
  • leukocyte adhesion
  • activation
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40
Q

Source of:

Cytokines (TNF, IL-1, IL-6)

A
  • Macrophages
  • endothelial cells
  • mast cells
    Local: endothelial activation (expression of adhesion molecules). Systemic: fever, metabolic abnormalities, hypotension (shock)
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41
Q

Action [local and systemic]

Cytokines (TNF, IL-1, IL-6)

A 
Local: 
endothelial activation (expression of adhesion molecules)

Systemic:
fever
metabolic abnormalities
hypotension (shock)

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42
Q

Source of:

Chemokines

A
  • Leukocytes

- activated macrophages

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43
Q

Action of:

Chemokines

A
  • Chemotaxis

- leukocyte activation

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44
Q

Source of:

Platelet-activating factor

A
  • Leukocytes

- mast cells

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45
Q

Action of:

Platelet-activating factor

A
  • Vasodilation
  • increased vascular permeability
  • leukocyte adhesion
  • chemotaxis
  • degranulation
  • oxidative burst
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46
Q

Source of:

Complement

A
  • Plasma (produced in liver)
    Leukocyte chemotaxis and activation, direct target killing (membrane attack complex), vasodilation (mast cell stimulation)
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47
Q

Action of:

Complement

A
  • Leukocyte chemotaxis and activation
  • direct target killing (membrane attack complex)
  • vasodilation (mast cell stimulation)
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48
Q

Source of:

Kinins

A

Plasma (produced in liver)

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49
Q

Action of:

Kinins

A
  • Increased vascular permeability
  • smooth muscle contraction, vasodilation
  • pain
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50
Q

Prostaglandins and leukotrienes, cytokines are examples of:

a. cell-derived mediators
b. synthesized de novo

A

b. synthesized de novo

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51
Q

Which mediators of inflammation are produced by mast cells? 5

A

Histamine

Prostaglandins

Leukotrines

Cytokines (TNF, IL-1, IL-6)

Platelet-activating factor

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52
Q

Which mediators of inflammation are produced by leukocytes?

A

Prostaglandins

Leukotrines

Chemokines

Platelet-activating factor

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53
Q

Histamine triggers for release: - 4

A
  • IgE-mediated mast cell reactions
  • Physical injury
  • Anaphylatoxins (C3a and C5a)
  • Cytokines (IL-1)
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54
Q

IL-1 and TNF (Tumor Necrosis Factor) stimulates and activates: - 3

A

fibroblasts

endothelial cells

neutrophils

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55
Q

Kinins are derived from plasma proteins, kininigens, which are activated by…

A

kallikreins

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56
Q

Action of:

Bradykinin

A
  • Increased vascular permeability
  • Pain
  • Vasodilation
  • Bronchoconstriction
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57
Q

The following are stimuli for acute inflammation, except:

A. Blunt trauma
B. Tissue necrosis
C. Immune reactions
D. Autoimmune diseases

A

D. Autoimmune diseases

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58
Q

Acute inflammation has three major components:

A

(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

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59
Q

What is a hallmark of acute inflammation?

A

increased permeability of postcapillary venule (vascular leakage)

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60
Q

An exudate is an extravascular fluid that has protein concentration and cellular debris that is:

a. high
b. low

A

a. high

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61
Q

An transudate is an extravascular fluid that has protein concentration and cellular debris that is:

a. high
b. low

A

b. low

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62
Q

The journey of leukocytes from the vessel lumen to the tissue is a multistep process that is mediated and controlled by: - 2

A
  • adhesion molecules

- cytokines called chemokines

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63
Q

The two major families of molecules involved in leukocyte adhesion and migration are

A

selectins and integrins, and their ligands

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64
Q

The steps of leukocyte migration through blood vessels are:

A
  • rolling
  • Integrin activation by chemokines
  • Integrin activation
  • Migration through endothelium
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65
Q

What is transmigration or diapedesis?

A

leukocyte recruitment is migration of the leukocytes through the endothelium

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66
Q

Causes of chronic inflammation

A
  • Autoimmune diseases
     Response to foreign material
  • Response to malignant tumors
  •  Following a bout of acute inflammation
  •  Persistent infections
  •  Infections with certain organisms
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67
Q

Which infectious organisms cause chronic inflammation?

A
  • Viral infections
  • Mycobacteria
  • Parasitic infections
  • Fungal infections
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68
Q

Which is a step in phagocytosis?

A. Opsonization
B. Margination
C. Pavementing
D. Stasis

A

A. Opsonization

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69
Q

Phagocytosis involves three sequential steps

A

(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
Q

Opsonins enhance…

A

enhance recognition and phagocytosis of bacteria

71
Q

Important opsonins:

A

Fc portion of IgG

Complement system product C3b

Plasma proteins – collectins (bind bacterial cell walls)

72
Q

Steps of engulfment

A

Neutrophils send out cytoplasmic processes that surround
the bacteria
 The bacteria are internalized within a phagosome
 The phagosome fuses with lysosomes (degranulation)

73
Q

Blood vessel changes in the pathogenesis of acute inflammation

A. Vasoconstriction
B. Vasodilation
C. Thrombosis
D. Spasm

A

B. Vasodilation

74
Q

Hemodynamic changes in acute inflammation

A
  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
Q

his involves the transmigration of leukocytes across the endothelium

A. Pavementing
B. Chemotaxis
C. Diapedesis
D. Margination

A

C. Diapedesis

76
Q

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

A. Active process

77
Q

Which of the following processes requires adhesion molecules?

A. Abscessformation
B. Diapedesis
C. Healing
D. Pavementing

A

D. Pavementing

78
Q

Neutrophil margination and adhesion is also known as…

A

Pavementing

79
Q

What are the steps in neutrophil margination and adhesion (pavementing)?

A

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
Q

Steps of leukocyte recruitment to sites of inflammation

A

Neutrophil margination and adhesion (Pavementing)

Emigration (Diapedesis) (transmigration)

Chemotaxis

81
Q

What proteins are expressed in the initial step of Pavementing?

A

E-selectin

and

P-selectin

82
Q

What stimulates neutrophils to express integrins in pavementing?

A

chemokines

83
Q

Steps of Emigration (diapedesis) (transmigration)

A
  • 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
Q

Leukocytes extend what between endothelial cells in emigration? (diapedesis) (transmigration)

A

pseudopods

85
Q

Steps of chemotaxis

A

The attraction of cells toward a chemical mediator

that is released in the area of inflammation

86
Q

What are the important chemotactic factors for neutrophils?

A

Bacterial products (N-formyl-methionine) 

Leukotriene B4 (LTB4)

Complement system products C5a

Alpha-chemokines (IL-8)

87
Q

Which is an important chemotactic factor for neutrophils?

a. Complement system products C3a
b. Complement system products C5a
c. Histamine
d. Serotonin

A

b. Complement system products C5a

88
Q

Which of the following is sequela of acute inflammation?

A. Abscess
B. Diapedesis
C. Ceseation necrosis
D. Pavementing

A

A. Abscess

89
Q

Sequela definiton

A

a condition that is the consequence of a previous disease or injury

90
Q

Four outcomes of acute inflammation

A
  •  Complete resolution with regeneration
  •  Complete resolution with scarring
  •  Abscess formation
  •  Transition to chronic inflammation
91
Q

The germinal centers of lymph nodes consist mainly of:

A. B-cells
B. T-cells
C. Interdigitating dendritic cells
D. Plasma cells

A

A. B-cells

92
Q

Tissue-based macrophages in the liver are known as:

A. Microglia
B. Histiocytes
C. Kuppfercells
D. Alveolar macrophages

A

Answer: C

93
Q

Chronic inflammation arises in the following settings:

A

Persistent infections

Hypersensitivity diseases

Prolonged exposure to potentially toxic agents, either exogenous or endogenous

94
Q

General areas of lymphoid tissue associated with chronix inflammation

(external to internal)

A

Follicles

Intrafollicular area

Medullary area

95
Q

What is produced in the follicle of lymphoid tissue?

A

B-cells

Follicular dendritic
cells (FDC)

96
Q

What is produced in the intrafollicular areas of lymphoid tisue?

A

 T-cells

NK cells

 Interdigitating
dendritic cells (IDC)
97
Q

What is produced in the medullary areas of lymphoid tisue?

A

Plasma cells

98
Q

The dominant cells in most chronic inflammatory reac- tions are

A

Macrophages

99
Q

How do macrophages contribute to the chronic inflammatory reaction? - 3

A
  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
Q

What do macrophages release during chronic inflammation?

A

cytokines and growth factors

101
Q

What is the most notable cell that macrophages activate in chronic inflammation?

A

T lymphocytes

102
Q

What are the tissue-based macrophages in:

Connective tissue

A

(histiocyte)

103
Q

What are the tissue-based macrophages in:

 Lung

A

(pulmonary alveolar macrophages)

104
Q

What are the tissue-based macrophages in:

 Liver

A

(kuppfer cells)

105
Q

What are the tissue-based macrophages in:

Bone

A

(osteoclasts)

106
Q

What are the tissue-based macrophages in:

Brain

A

(microglia)

107
Q

Where are macrophages derived?

A

Blood monocytes

108
Q

Which of the following cause granulomatous inflammation?

A. Staphylococcus aureus
B. Bee sting
C. Suture material
D. Streptococcus pneumonia

A

C. Suture material

109
Q

Chronic cranulomatous fever - 9

A

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
Q

What is granulomatous inflammation?

A

a form of chronic inflammation characterized by collections of activated macrophages, often with T lymphocytes, and sometimes associated with central necrosis.

111
Q

What is the cause of:

Tuberculosis

A

(caseating granulomas)

112
Q

What is the cause of:

o Cat-scratch fever

A

(Gram-negative bacillus) o

113
Q

What is the cause of:

Syphilis

A

(Treponema pallidum)

114
Q

What is the cause of:

o Leprosy

A

(Mycobacterium leprae)

115
Q

What is the cause of:

o Fungal infection

A

(coccidiodomycosis)

116
Q

What is the cause of:

o Parasitic infections

A

(schistosomiasis)

117
Q

What is the cause of:

o Sarcoidosis

A

(unknown etiology)

118
Q

What is the tissue reaction of:

Mycobacterium tuberculosis

A

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
Q

What is the tissue reaction of:

Mycobacterium leprae

A

Leprosy

Acid-fast bacilli in macrophages; noncaseating granulomas

120
Q

What is the tissue reaction of:

Treponema pallidum

A

Syphilis

Gumma: microscopic to grossly visible lesion, enclosing wall of histiocytes; plasma cell infiltrate; central cells are necrotic without loss of cellular outline

121
Q

What is the tissue reaction of:

Gram-negative bacillus

A

Cat-scratch fever

Rounded or stellate granuloma containing central granular debris and recognizable neutrophils; giant cells uncommon

122
Q

What is the tissue reaction of:

Sarcoidosis

A

Noncaseating granulomas with abundant activated macrophages

123
Q

What is the tissue reaction of:

Immune reaction against
intestinal bacteria, possibly self antigens

A

Crohn disease

Occasional noncaseating granulomas in the wall of the intestine, with dense chronic inflammatory infiltrate

124
Q

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

A. Leukotriene B4

125
Q

Which of the following complements can function as an opsonin?

A. C3a
B. C3b
C. C35
D. C5b-9

A

B. C3b

126
Q

Which of the following products of the cyclooxygenase pathway can cause pain?

A. Thromboxane A2
B. Prostacyclin
C. Prostaglandin E
D. Leukotriene B4

A

C. Prostaglandin E

127
Q

General categories of chemical mediators of inflammation

A

Lipooxygenase pathway

Complement cascade

Cyclooxygenase pathway

Cyclooxygenase pathway

128
Q

These are chemicals of Lipooxygenase pathway

A

o Leukotriene B4 (LTB4): neutrophil chemotaxis

o Leukotriene C4, D4, E4: vasoconstriction

129
Q

Leukotriene B4 (LTB4) is responsible for

A

neutrophil chemotaxis

130
Q

Leukotriene C4, D4, E4 is responsible for

A

vasoconstriction

131
Q

Important inflammation mediators from complement cascade

A

C5b – C9 – membrane attack complex

C3a, C5a – anaphylatoxins stimulate the
release of histamine

 C3b – opsonin

132
Q

C5b – C9 does what?

A

– membrane attack complex

133
Q

C3a, C5a does what?

A

– anaphylatoxins stimulate the

release of histamine

134
Q

C3b is a?

A

– opsonin

135
Q

Mediators in Cyclooxygenase pathway?

A 
Thromboxane A2 (TXA2)
[ Produced by platelets
 Vasoconstriction and platelet aggregation]

Prostacyclin (PGI2)
[ Produced by vascular endothelium
 Vasodilation and inhibits platelet
aggregation]

136
Q

Thromboxane A2 (TXA2) is from and does what?

A

Produced by platelets

Vasoconstriction and platelet aggregation

137
Q

Prostacyclin (PGI2) is from and does what?

A

Produced by vascular endothelium

Vasodilation and inhibits platelet aggregation

138
Q

PG E is associated with?

A

pain

139
Q

Which prostaglandin cause vasodilation?

A

Prostaglandins PGE2, PGD2 and PGF2

140
Q

Prostaglandins (PGs) are produced by

A

mast cells, macro- phages, endothelial cells, and many other cell types, and are involved in the vascular and systemic reactions of inflammation.

141
Q

Which is the hallmark/predominant cell in a granuloma?

A. Lymphocyte
B. Fibroblast
C. Epithelioid histiocytes
D. Langerhans type multinucleated giant cells

A

C. Epithelioid histiocytes

142
Q

Granuloma formation is a response mediated by:

A. B-cells
B. Plasma cells
C. T-cells
D. Mast cells

A

C. T-cells

143
Q

Specialized form of chronic inflammation

A

Small aggregates of modified macrophages
(epithelioid cells and multinucleated giant cells) o

Surrounded by rim of lymphocytes

144
Q

Composition of a granuloma

A

Epithelioid cell

Multinucleated giant cells (langhans-type)

Lymphocytes and plasma cells

Central caseous necrosis

145
Q

Epithelioid cell are

A

IFN-alpha transforms macrophages to epithelioid cells

 Enlarged cell with abundant pink cytoplasm

146
Q

Multinucleated giant cells (langhans-type)

A

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
Q

Central caseous necrosis

A

Present in granulomas due to tuberculosis  Rare in other granulomatous diseases

148
Q

Which of the following cells regenerate throughout life?

A. Hepatocytes
B. Proximal tubular cells
C. Cardiac muscle cells
D. Hematopoietic cells

A

D. Hematopoietic cells

149
Q

When do Hepatocytes and proximal tubular cells regenerate?

A

when there is injury or stimulus

150
Q

Do labile cells regenerate?

A

Yes, through out life

151
Q

Do permanent cells regenerate?

A

No.

e.g. neurons and cardiac muscle

152
Q

The following are components of fibrosis, except:

A. Angiogenesis
B. Migration through basement membrane
C. Proliferation of fibroblasts
D. Remodeling

A

B. Migration through basement membrane

153
Q

Steps in scar formation

A
  1. Angiogenesis
  2. Formation of granulation tissue
  3. Remodeling of connective tissue
154
Q

What happens in Angiogenesis?

A

 Formation of new blood vessels, which supply

nutrients and oxygen needed to support the repair process

155
Q

What happens in Formation of granulation tissue?

A

 Migration and proliferation of fibroblasts, and deposition of loose connective tissue, together with the vessels and interspersed leukocytes, form granulation tissue

156
Q

What happens in Remodeling of connective tissue?

A

 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
Q

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

A

B. Atherosclerotic lesions

158
Q

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

A

D. Healing of liver with cirrhosis

159
Q

The hallmark of healing

A. Granuloma
B. Granulation tissue
C. Granulocytes
D. Germination

A

B. Granulation tissue

160
Q

This substance provides the tensile strength in wound healing

A. fibrin
B. collagen
C. elastin
D. keratin

A

B. collagen

161
Q

How many types of collagen?

A

Four

162
Q

Collagen Type I

A 
Most common

 High tensile strength

 Skin, bone, tendons and most organs
163
Q

Collagen Type II

A

cartilage

vitreous humor

164
Q

Collagen Type III

A

granulation tissue,

embryonic tissue,

uterus,

keloids

165
Q

Collagen Type IV

A

basement membranes

166
Q

Hydroxylation of collagen is mediated by

A

Vitamin C

167
Q

Cross-linking of collagen is performed by

A

lysyl oxidase. Copper is a required co-factor

168
Q

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

A. Healing by first intention

169
Q

the principal mechanism of repair is epithelial regeneration, also called primary union or healing by first intention is when

A

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
Q

In healing of skin wounds by second intention, also known as healing by secondary union occurs…

A

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
Q

What delays wound healing?

A

foreign bodies

infection

ischemia

diabetes

malnutrition

scurvy

General Pathology (5 decks)

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