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Pathology > inflammation and wound repair > Flashcards

inflammation and wound repair Flashcards

1
Q

Nomenclature of Inflammatory Diseases

A

Name of the organ or tissue + “itis”= inflammation in that organ or tissue \
EXCEPTIONS ON HANDOUT

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2
Q
A

tonsilitis

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3
Q
A

appendicitis

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4
Q

classification of inflammation

A

• Acute or chronic inflammation
• Exudative or non-exudative inflammation
• Morphologic Patterns
– Serous
– Fibrinous
– Suppurative
– Ulcerative

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5
Q

acute inflam
onset?
duration?
what cells migrate? predominant type?
what exudates into tissue?

A

– Rapid onset, short duration (minutes to days)
– Emigration of leukocytes, predominately neutrophils
– Exudation of fluid and plasma proteins

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6
Q

chronic inflam
duration?
cells present?
what can proliferate during this?

A

– Longer duration
– Mononuclear cells –macrophages, lymphocytes, plasma cells
– Proliferation of blood vessels and fibroblasts

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7
Q

clinical and pathological views of inflamm

A
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8
Q
A

neutrophil

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9
Q
A

plasma cell

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10
Q
A

macrophage

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11
Q
A

lymphocyte

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12
Q

acute inflammation, exudative or not?

A

Exudative - acute inflammation tends to be more exudative, accumulation of fluid

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13
Q

chronic, exudative or not? often associated with?

A

Non-Exudative - chronic inflammation is frequently non-exudative and is often associated with fibrosis and scarring.

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14
Q

Inflammation
causes?

A

Inflammation –the body’s response to injury
– Thermal
– Physical
– Chemical
– Allergic
– Immune mediated disease

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15
Q

Immunity

A

Immunity –comes into play when inflammation is caused by a living organism (infection)

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16
Q

infections can provoke?

A

inflammation and immunity
• Inflammation may exist without infection
–Inflammation DOES NOT imply infection

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17
Q

Hypersensitivity (allergic disease) may cause

A

inflammation

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18
Q

Autoimmune disease may cause

A

Autoimmune disease may cause
inflammation

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19
Q

the body’s 3 defense lines, components of each

A

• Barriers (non-specific)
– Skin
– Mucous membranes
– Secretions
• Inflammatory Response (non-specific)
– Cells (leukocytes)
– Molecules (mediators)
• Immune Response (specific)
– Antibodies (humoral)
– Cytotoxic T cells (cellular)

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20
Q

Components Of Inflammatory Responses: what cells/proteins have roles?

A

• Circulating blood cells and plasma proteins
• Cells of the blood vessel walls
• Cells and proteins of the extracellular matrix

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21
Q

where are most inflammatory elements located

A

blood

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22
Q

inflammation allows for?

A

means by which defensive cells and chemicals leave the blood and enter the tissue

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23
Q

Inflammation is a complex reaction to injury: what kind of events occur?

A

– Vascular responses
– Cellular responses
– Systemic reactions
– Repair

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24
Q

Inflammation is good/bad? excessive?

A

Inflammation is beneficial. Excess or prolonged inflammation may be harmful.

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25
Q

defensive materials delivered by inflammation

A

• Leukocytes –defensive cells
• Plasma –defensive proteins

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26
Q

The Inflammatory Response: 5 R’s

A

• Recognition of the injurious agent
• Recruitment of leukocytes
• Removal of the agent
• Regulation (control) of the response
• Resolution (repair)

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27
Q

Causes of Acute Inflammation (types of injuries)

A

• Mechanical injury
• Chemical injury
• Radiation injury
• Thermal injury
• Infection
• Compromise of blood supply
• Immune injury

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28
Q

Cardinal Signs Inflammation

A

• Calor –heat
• Rubor - redness
• Tumor - swelling
• Dolor - pain
• Loss of function

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29
Q

is everything red inflamed?

A

no, can be cell proliferation (hemaghenoma, RBC)

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30
Q

Cellular Events in Acute Inflammation (PMN migration)
mediated by ?

A

• Margination
• Rolling
• Adhesion
• Diapedesis
• Chemotaxis
• Phagocytosis
• Killing
each step is mediated by dif molecules (selecting, ICAM, integrins, C3b, IgG)

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31
Q

vascular response of inflamm, how does this influence PMN?

A

vasodilation allowing for PMN margination

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32
Q

Microbial Killing by Leukocytes

A

opsinization via IgG and C3b

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33
Q

Systemic Manifestations of Acute
Inflammation

A

fever
leukocytosis
Acute phase response –cytokines stimulate hepatocytes to synthesize and secrete acute phase proteins

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34
Q

Fever due to

A

due to pyrogens
– Cytokines - TNF, IL-1 released by leukocytes (increased count)
– Prostaglandins –from membrane phospholipids

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35
Q

leukocytosis results

A

– Leukemoid reaction, can mimic leukiemia
– Neutrophilia - shift-to-left, more than usual
– Lymphocytosis, increased lymphocytes

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36
Q

cytokine stim of hepatocytes

A

cytokines stimulate hepatocytes to synthesize and secrete acute phase proteins
– C-reactive protein (CRP) –acts as an opsonin
– Mannose-binding lectin - acts as an opsonin

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37
Q

Lymphangitis

A

lymphatic involvement in inflammation
• Lymphatic spread of bacterial infection
• Painful red streaks and regional lymphadenopathy

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38
Q

preformed chemical mediators stored in granules, cells?
(histamine, serotonin, lyso enzymes)

A

histamine-mast cell, baso, platelets
serotonin- platelets
lysosomal enzymes- neutrophils and macro

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39
Q

newly synthesized chemical mediators with inflammation, cells?
PGs, LTs, NO, cytokines

A

PGs- all leuko, platlets, EC
LTs- all leukocytes
NO- macro
cytokines- lymphocytes, macrophages, EC

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40
Q

Hageman factor

A

from the liver, activated in plasma
activates kinin system (bradykinin) and coagulation and fibrinolysis systems

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41
Q

complement proteins from where, general actions

A

from the liver
C3a and C5a= anaphylatoxins (neutrophils)
C3b= op
C5a-9= MAC

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42
Q

histamine and serotonin storage

A

• Unlike most other mediators, histamine and serotonin are available in preformed supplies
• Histamine is stored in granules of mast cells
• Serotonin is stored in the granules of platelets

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43
Q

first mediators released with injury, cause?

A

Histamine and Serotonin
cause vascular dilation and leakage

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44
Q

Antigen (Ag)

A

Antigen (Ag) - A substance that can induce an immune response when introduced into an animal.

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45
Q

Antibody (Ab)

A

Antibody (Ab) - A protein that is produced in response an antigen. The antibody binds the antigen that stimulated its production. All antibodies are immunoglobulins.

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46
Q

Immunoglobulin (Ig)

A

mmunoglobulin (Ig) - A glycoprotein composed of heavy and light chains that functions as an antibody.

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47
Q

Schematic Structure of a Typical
Immunoglobulin (Antibody) Molecule

A
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48
Q

IgM

A

IgM - first immunoglobulin to appear in an immune response
pentamer

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49
Q

IgG

A

IgG - principal immunoglobulin of the secondary immune response. Only immunoglobulin capable of crossing the placental barrier

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50
Q

IgA

A

IgA - principal immunoglobulin in external secretions of mucosal surfaces, tears, saliva, and colostrum
dimer

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51
Q

• IgE

A

• IgE - plays an important role in immediate hypersensitivity reactions and parasitic infections

52
Q

IgD

A

IgD - thought to activate the B-lymphocyte

53
Q

complement a machine for?

A

perforating cells

54
Q

The Complement System basics

A

The Complement System
• C1 to C9
• Critical step activation of C3
–C3 convertase cleaves C3 –C3a, C3b
• C3b deposits to microbes surface, forms C5
convertase
• C5 convertase cleaves C5 –C5a, C5b
• Initiates assembly of MAC

55
Q

functions of the complement system components

A

• Membrane attack complex (MAC) lysis
(C56789)
• Opsonization (C3b)
• Chemotaxis (C5a)
• Vasodilation and increased vessel permeability via histamine release
(C3a, C5a) anaphylatoxins

56
Q

Outcomes of Acute Inflammation
n

A
  1. Complete resolution
  2. Healing by connective tissue replacement (fibrosis)
  3. Progression of the response to chronic inflammation
57
Q

resolution of acute inflam

A

clearance of injurious stimuli
clearance of mediators and inflam cells
replace injured cells
normal function restored

58
Q

what role does fibrosis play in acute inflam?

A

healing occurs via fibrosis= loss of function

59
Q

chronic inflam progression from acute
what events occur?
what cells migrate?

A

angiogenesis occurs
mononuclear cells infiltrate
fibrosis occurs

60
Q

serous inflammation

A

fluid filled= transudate, free of proteins and cells
friction blisters

61
Q

fibrinous inflammation, example

A

due to an exudate= protein-rich, often fibrin (fibrinous exudate)

62
Q

Suppurative (Purulent) Inflammation

A

pus filled/ protein and cell rich

63
Q
A

Suppurative (Purulent) Inflammation

64
Q
A

fibrinous inflammation

65
Q

Abscess

A

• A localized collection of pus (many dead neutrophils) that has accumulated in a tissue cavity, producing fluctuance
fibrosis around liquefactive necrosis

66
Q
A

abcess

67
Q
A

abcesses

68
Q

Cellulitis

A

Cellulitis
• Diffuse spread of an acute inflammatory process through the fascial planes of soft tissue producing cardinal signs of inflamm without consolidation

69
Q

Catarrhal (Seromucous) Inflammation

A

a clinical type of exudative inflammation,

occurs only on mucosal surfaces containing mucus-secreting cells- bronchial mucosa, excess mucus

70
Q

Ulcerative Inflammation, example?

A

exudate surrounded with a red halo, defect in epithelial continuity
Recurrent Aphthous Stomatitis

71
Q
A

ulcerative inflammation

72
Q
A

ulcerative inflammation

73
Q

Leukocyte Adhesion Deficiency - LAD
inheritence?
what is defective? this leads to impairment of?
susceptible to?

A

autosomal recessive immune deficiency
due to integrin receptor defect= impaired adhesion and chemotaxis
susceptible to: bac/fungal infections, impaired wound healing, periodontitis (loss of alveolar bone), lack of pus formation

74
Q

Lazy Leukocyte Syndrome, what is mutated?

A

Impaired Chemotaxis –Mutation of Contractile Proteins

75
Q

Chediak-Higashi Syndrome
inheritance?
associated with?
granules?
defective functions?
susceptible to?
plattlets? MPO?

A

• A rare autosomal recessive condition associated with albinism
• Giant lysosomal inclusions from fused primary granules
• Both chemotaxis and phagolysosome formation are defective
• Recurrent infections, high grade lymphomas
• Platelet function is abnormal, MPO +

76
Q
A

PMN of chediak-higahsi

77
Q

Chronic Granulomatous Disease of Childhood inheritence

A

X-linked (2/3) or autosomal (1/3)

78
Q

Chronic Granulomatous Disease of Childhood defect

A

• Deficient NADPH oxidase in the cell membranes of neutrophils and monocytes, resulting in an absent respiratory burst
• No H2O2 produced - HOCl- is notsynthesized because of the absence of H2O2

79
Q

Chronic Granulomatous Disease of Childhood organisms capable of infection

A

• Catalase-negative organisms (e.g., Streptococcus species) are killed
• Catalase-positive organisms (e.g., Staphylococcus aureus) are not killed
catalase able to remove H2O2, thus no respiratory burst

80
Q

Chronic Granulomatous Disease of Childhood presentation

A

large granulatomous mass of the face

81
Q
A

Chronic Granulomatous Disease of Childhood

82
Q

Myeloperoxidase (MPO) Deficiency
common?
inheritance?
what is wrong?

A

• A common (1:2,000 individuals) autosomal recessive absence of myeloperoxidase enzyme in neutrophil and monocyte granules
• Respiratory burst is normal and H2O2 is produced
• Absence of MPO prevents synthesis of HOCl-

83
Q

clinical consequences of MPO def

A

• No great clinical consequences in most people
• Diabetics may develop candidiasis

84
Q

Immune Deficiency Caused by Defects in Leukocyte Function: what are potential defects?

A

• Too few neutrophils
• Failure in adhesion
• Slow chemotaxis
• Failure to phagocytose
• Failure to kill

85
Q

Too few neutrophils, Dx?

A

– Agranulocytosis
– Cyclic neutropenia

86
Q

Failure in adhesion, Dx?

A

– Leukocyte Adhesion Deficiency (LAD)

87
Q

Slow chemotaxis, Dx

A

– “Lazy” leukocyte syndrome

88
Q

Failure to phagocytose, dx?

A

– Bruton Agammaglobulinemia
– Complement deficiency

89
Q

Failure to kill, Dx?

A

– Chronic Granulomatous Disease of Childhood
– Chediak-Higashi Syndrome
– Myeloperoxidase Deficiency

90
Q

Causes of Chronic Inflammation

A

• Persistent infection - mycobacteria
• Prolonged exposure to toxic agents
• Exogenous - silicosis
• Endogenous - atherosclerosis
• Immune-mediated inflammatory disease
• Autoimmune diseases - rheumatoid arthritis
• Unregulated immune responses against microbes –inflammatory bowel disease
• Immune responses against environmental substances –(allergic disease) -bronchial asthma

91
Q

Morphologic Features Of Chronic Inflammation
what cells are present?
is tissue destruction occurring? why or why not?
attempts at healing with what processes?

A

• Mononuclear cell infiltration –lymphocytes, plasma cells and macrophages
• Tissue destruction –due to a persistent offending agent or by the inflammatory cells
• Attempts at healing by connective tissue replacement - angiogenesis and fibrosis

92
Q

are neutrophils present in chronic inflamm?

A

yes, but not predominant

93
Q

is this chronic or acute?

A

chronic, note Macros, plasma and lymphocytes present= mixed inflammatory infiltrate

94
Q

Granulomatous Inflammation
acute or chronic?
types?

A

special kind of chronic inflamm
two kinds: immune granulatomas, foreign body granulatomas

95
Q

Granulomatous Inflammation morpholgy

A

Aggregates of epitheliod macrophages (activated) which make the granulatomas
• Multinucleated giant cells
• Mononuclear leukocytes, principally lymphocytes and occasionally plasma cells peripherally
• Fibrosis variable

96
Q
A

granulatoma

97
Q
A

giant cell macrophage

98
Q
A

granulomatous inflammation with surrounding lymphocytes

99
Q
A

giant cells
right: foreign body giant cell
left: Langerhans giant cell

100
Q

Classification of Granulomas

A

• Immune granulomas
• Foreign body granulomas

101
Q

immune granuloma

A

foreign agent trapped within a giant cell: fungi

102
Q

Caseation Necrosis in Tuberculosis and granulomas

A

Necrotizing Granulomatous Inflammation will occur with giant cells and granuloma

103
Q

Mycobacterium Tuberculosis:

A

Intracellular Pathogen, acid fast bacili
• Blocks fusion of phagosome with lysozome

104
Q

kinds of granulomatous diseases

A
105
Q

Granulation Tissue -VS-Granulomatous Tissue

A

Granulation Tissue
Reparative Tissue
Endothelial Cells and Fibroblasts

Granulomatous Tissue
Epitheliod Macrophages
Giant Cells

106
Q

Pyogenic Granuloma: is it granulation tissue or granulomatous tissue

A

granulation tissue; RBC and fibroblast prolif= endothelial hyperplasia

107
Q

Repair defined
can occur by?

A

• Restoration of tissue architecture and function after an injury
• Repair may occur by regeneration or by healing (scar formation)

108
Q

mechanisms of tissue repair/healing

A

• Healing –Consists of variable proportions of two distinct processes –regeneration and scarring (fibrosis)
• Regeneration –growth of cells and tissues to replace lost structures

109
Q

cell classes for regeneration purposes

A

• Continuously dividing tissues - labile
• Stable tissues - quiescent
• Permanent tissues –non-dividing

110
Q

Labile cells
Labile cells are derived from?
examples?

A

• Labile cells are derived from the division of stem cells
• Hematopoietic cells
• Surface epithelium
• Stratified squamous epithelium of the skin, mouth, pharynx, esophagus, vagina and cervix
• Gastrointestinal tract epithelium

111
Q

labile cells and regeneration

A

Labile tissues can readily regenerate after injury as long as the pool of stem cells is preserved

112
Q

labile cells and cancer, examples

A

The most common forms of cancer arise from labile tissues:
– Epidermis –skin cancer
– Bronchial mucosa –lung cancer
– Oral mucosa –oral cancer
– Cervical mucosa –cervical cancer
– Hematopoietic tissue –leukemias

113
Q

Quiescent/stable cells
TO rate?
replacement done by?
examples?

A

• Stable cells are quiescent and have a very low rate of turnover.
• Replacement is carried out by mitotic division of mature cells.
• Viscera (liver, kidney, pancreas)
• Endothelial cells
• Fibroblasts
• Smooth muscle cells

114
Q

stable cells capacity to regen? exception?

A

With the exception of liver, stable tissues have limited capacity to regenerate

115
Q

stable tissues and tumors

A

Malignant tumors of stable tissues are among the rarer forms of cancer

116
Q

Permanent Tissues (Non-dividing)

A

• Permanent cells were generated during fetal life and never divide in postnatal life
• Cannot be replaced if lost
• Neurons
• Cardiac myocytes

117
Q

repair mech in perm tissues?

A

In permanent tissues, repair is dominated by scar formation

118
Q

Fibrosis (Scarring) Occurs If:

A

–The tissue is intrinsically unable to regenerate (heart, brain)
–The underlying connective tissue scaffolding is disrupted
–Following extensive exudates (organization)

119
Q

Objectives Of Wound Healing

A

• Epithelial Regeneration
–Restore integrity of the epithelial surface

• Connective Tissue Repair
–Restore the tensile strength of the sub-epithelial tissue

120
Q

Healing By Primary Intention

A

• Healing by primary union occurs when the wound margins are pulled together

121
Q

all wound healing involves?

A

inflammatory rxn in absence of infection

122
Q

Healing By Secondary Intention occur when?

A

Healing by secondary union occurs when the wound margins are NOT pulled together

123
Q

Granulation Tissue contents of second intention healing

A

• Endothelial cells
• Fibroblasts
• Myofibroblasts - contractile

124
Q

myofibroblasts in second intention

A

Wound Contraction by Myofibroblasts, bring edges together

125
Q

Hypertrophic Scar

A

• Excessive scar formation within the boundaries of the original wound producing a
raised scar

126
Q

Keloid
demographic?

A

• Excessive scar formation that grows beyond the boundaries of the original wound
• African-Americans

127
Q

vitamin C
def? result?

A

Vitamin C is Required for the Hydroxylation of Proline and Lysine in collagen synthesis, necessary for wound healing
def= scurvy and delayed healing

Pathology (20 decks)

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