Inflammation & Repair Flashcards
1
Q
how to name inflammatory diseases
A
name of the organ/tissue + “itis” = inflammation in that organ/tissue
2
Q
classifications of inflammation:
A
-acute or chronic
-exudative or non-exudative
-morphologic patterns (serous, fibrinous, suppurative, ulcerative)
3
Q
acute inflammation
A
– Rapid onset, short duration (minutes to days)
– Emigration of leukocytes, predominately neutrophils
– Exudation of fluid and plasma proteins
4
Q
chronic inflammation
A
– Longer duration
– Mononuclear cells – macrophages, lymphocytes, plasma cells
– Proliferation of blood vessels and fibroblasts
5
Q
ID leukocyte
A
neutrophil
(segmented nucleus)
6
Q
ID leukocyte
A
plasma cells
(nucleus pushed to the side)
7
Q
ID leukocyte
A
macrophages
(large, pale-staining)
8
Q
ID leukocyte
A
lymphocytes
(small, dark staining)
9
Q
exudative inflammation
A
formation of exudate
-acute inflammation tends to be
more exudative
10
Q
non-exudative inflammation
A
no formation of exudate
-chronic inflammation is
frequently non-exudative and is often
associated with fibrosis and scarring.
11
Q
types of injury that can cause inflammation:
A
-thermal
-physical
-chemical
-allergic
-immune mediated disease
12
Q
inflammation
A
the body’s response to injury
13
Q
immunity
A
comes into play when inflammation is caused by a LIVING organism (infection)
14
Q
infection may provoke _____ & ______
A
inflammation and immunity
15
Q
are inflammation and immunity the same thing?
A
NO
16
Q
can inflammation exist without infection?
A
yes
-inflammation DOES NOT imply infection
17
Q
what else can cause inflammation?
A
-hypersensitivity (allergic disease)
-autoimmune diseases
18
Q
what are the 3 lines of defense for the body?
A
- barriers
- inflammatory response
- immune response
19
Q
examples of barriers
A
– Skin
– Mucous membranes
– Secretions
20
Q
examples of inflammatory responses
A
– Cells (leukocytes)
– Molecules (mediators)
21
Q
examples of immune responses
A
– Antibodies (humoral)
– Cytotoxic T cells (cellular)
22
Q
where are components of inflammatory responses found?
A
- Circulating blood cells and plasma proteins
- Cells of the blood vessel walls
- Cells and proteins of the extracellular matrix
23
Q
what are these?
A
components of inflammatory response
24
Q
where are most of the defensive elements found?
A
blood
25
inflammation is the means by which what leave the blood and enter the tissue?
defensive cells & chemicals
26
is inflammation beneficial?
yes- but excess or prolonged inflammation may be harmful
27
defensive cells
leukocytes
28
defensive proteins
plasma
29
what are the 5 R's of the inflammatory response?
* Recognition of the injurious agent
* Recruitment of leukocytes
* Removal of the agent
* Regulation (control) of the response
* Resolution (repair)
30
causes of acute inflammation:
* Mechanical injury
* Chemical injury
* Radiation injury
* Thermal injury
* Infection
* Compromise of blood supply
* Immune injury
31
what are the cardinal signs of inflammation?
calor- heat
rubor- redness
tumor- swelling
dolor- pain
functio laesa- loss of function
32
all that is red (rubor) is not
inflammation
33
what are the cellular events in acute inflammation?
* Margination
* Rolling
* Adhesion
* Diapedesis
* Chemotaxis
* Phagocytosis
* Killing
34
systemic manifestations of acute inflammation
* Fever – due to pyrogens
– Cytokines - TNF, IL-1 released by leukocytes
– Prostaglandins – from membrane phospholipids
* Leukocytosis
– Leukemoid reaction
– Neutrophilia - shift-to-left
– Lymphocytosis
* Acute phase response – 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
35
lymphangitis
* Lymphatic spread of
bacterial infection
* Painful red streaks and
regional
lymphadenopathy
36
chemical mediators of inflammation
Preformed mediators:
-histamine
-serotonin
Newly synthesized:
-prostaglandins
-leukotrienes
Factor XII activation:
-kinin system (bradykinin)
Complement activation:
-C3a
-C5a
-C5b-9
37
histamine and serotonin are examples of what?
vasoactive amines
38
which mediators are available in preformed supplies?
histamine and serotonin
39
where is histamine stored?
granules of mast cells
40
where is serotonin stored?
granules of platelets
41
what are the first mediators to be released after injury?
histamine and serotonin
42
which mediators cause vascular dilation and leakage?
histamine and serotonin
43
all acute inflammatory reactions may have one of three outcomes:
1. Complete resolution
2. Healing by connective tissue replacement
(fibrosis)
3. Progression of the response to chronic
inflammation
44
examples of what type of inflammation?
serous inflammation
45
examples of what type of inflammation?
fibrinous inflammation
46
examples of what type of inflammation?
suppurative (purulent) inflammation
47
examples of what type of inflammation?
suppurative (purulent) inflammation
48
abscess
A localized collection of pus that has accumulated in
a tissue cavity, producing fluctuance
49
cellulitis
Diffuse spread of an
acute inflammatory
process through the
fascial planes of soft
tissue producing
erythema, edema,
warmth, and pain,
without consolidation
50
catarrhal (seromucous) syndrom
Catarrhal
inflammation, a clinical
type of exudative
inflammation, occurs
only on mucosal
surfaces containing
mucus-secreting cells,
such as nasal or
bronchial mucosa
51
ulcerative inflammation
an ulcer is a defect in epithelial continuity
52
examples of defects in neutrophil function:
-leukocyte adhesion deficiency (LAD)
-lazy leukocyte syndrom
-Chediak-Higashi syndrome
-chronic granulomatous disease of childhood
-myeloperoxidase (MPO) deficiency
53
Chediak-Higashi syndrome
* A rare autosomal recessive
condition associated with
albinism
* Giant lysosomal inclusions
from fused primary granules
* Both chemotaxis and
phagolysosome formation are
defective
* Recurrent infections
* Platelet function is abnormal
54
chronic granulomatous disease of childhood
* X-linked (2/3) or autosomal (1/3)
recessive
* Deficient NADPH oxidase in the
cell membranes of neutrophils
and monocytes, resulting in an
absent respiratory burst
* No H2O2 produced - HOCl- is not
synthesized because of the
absence of H2O2
* Catalase-negative organisms
(e.g., Streptococcus species) are
killed
* Catalase-positive organisms
(e.g., Staphylococcus aureus) are
not killed
55
myeloperoxidase (MPO) deficiency
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-
* No great clinical consequences in
most people
* Diabetics may develop
candidiasis
56
what is caused by too few neutrophils?
-agranulocytosis
-cyclic neutropenia
57
what is caused by failure in adhesion?
-leukocyte adhesion deficiency (LAD)
58
what is caused by slow chemotaxis?
-lazy leukocyte syndrome
59
what is caused by failure to phagocytose?
-Bruton Agammaglobulinemia
-complement deficiency
60
what is caused by failure to kill?
-Chediak-Higashi syndrome
-chronic granulomatous disease of childhood
-myeloperoxidase (MPO) deficiency
61
causes of chronic inflammation
* 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
62
morphologic features of chronic inflammation
* 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
63
64
granulomatous inflammation
* A pattern of chronic
inflammation
* Aggregates of epitheliod
macrophages (activated)
* Multinucleated giant cells
* Mononuclear leukocytes,
principally lymphocytes
and occasionally plasma
cells peripherally
* Fibrosis variable
65
types of giant cells
-Langhans giant cells
-foreign body giant cells
66
classification of granulomas
-immune granulomas
-foreign body granulomas
67
mycobacterium tuberculosis (intracellular pathogen)
blocks fusion of phagosome with lysozome
68
granulation tissue
-reparative tissue
-endothelial cells & fibroblasts
-proliferation of blood vessels
69
granulomatous tissue
-epitheliod macrophages
-giant cells & lymphocytes
70
example of granulation tissue
pyogenic granuloma
71
repair
* Restoration of tissue architecture and function after an injury
* Repair may occur by regeneration or by healing (scar formation)
72
two mechanisms of tissue repair:
-regeneration
-healing
73
regeneration
growth of cells and tissues to replace lost structures
74
healing
consists of variable proportions of two distinct processes- regeneration and scarring
75
labile cell classification
continuously dividing tissues
76
quiescent cell classification
stable tissues
77
non-dividing cell classification
permanent tissues
78
labile tissues
* 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
* Labile tissues can readily regenerate after injury as long as the
pool of stem cells is preserved
* 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
Continuously Dividing Tissues – Labile
79
quiescent tissues
* 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
-with the exception of liver, stable tissues have limited capacity to regenerate
-malignant tumors of stable tissues are among the rarer forms of cancer
80
permanent tissues (non-dividing)
* Permanent cells were generated during fetal
life and never divide in postnatal life
* Cannot be replaced if lost
* Neurons
* Cardiac myocytes
-in permanent tissue, repair is dominated by scar formation
81
fibrosis (scarring) occurs if:
* The tissue is intrinsically unable to
regenerate (heart, brain)
* The underlying connective tissue scaffolding
is disrupted
* Following extensive exudates (organization)
82
objectives of wound healing
-epithelial regeneration (restore integrity of the epithelial surface)
-connective tissue repair (restore the tensile strength of the sub-epithelial tissue)
83
healing by primary intention
occurs when the wound margins are pulled together
84
what does all wound healing involve?
an inflammatory reaction even in the absence of infection
85
healing by secondary intention
occurs when the wound margins are NOT pulled together
86
hypertrophic scar
excessive scar formation within the boundaries of the original wound producing a raised scar
87
keloid
excessive scar formation that grows beyond the boundaries of the original wound
88
what is required for the hydroxylation of proline and lysine?
vitamin C
