Inflammation and Repair Flashcards
Name of the organ or tissue + “itis”
= inflammation in that organ or tissue
Tonsil =
Tonsillitis
Appendix =
Appendicitis
Peritoneum =
Peritonitis
Lymph Node =
Lymphadenitis
Salpingitis –
fallopian tube
Keratitis -
cornea
Balanitis –
glans penis
– Reiter’s syndrome
Cystitis -
bladder
skin -
dermatitis
nasal mucosa -
rhinitis
renal glomerulus -
glomerulonephritis
hair follicle or sebaceous gland -
folliculitis
paranasal sinus -
sinusitis
renal interstitium -
pyelonephritis
lips -
chelitis
ear -
otitis
ureter -
urethritis, urethritis
oral mucosa
stomatitis
eyelid -
blepharitis
urinary bladder -
cystitis
gingiva -
gingivitis
conjunctiva -
conjunctivitis
prostate -
prostatitis
perdiodontium -
periodontitis
cornea -
keratitis
urethra -
urethritis
dental pulp -
pulpitis
Classification of Inflammation
3
- Acute or chronic inflammation
- Exudative or non-exudative inflammation
- Morphologic Patterns
Morphologic Patterns
4
– Serous
– Fibrinous
– Suppurative
– Ulcerative
Acute inflammation
3
– Rapid onset, short duration (minutes to days)
– Emigration of leukocytes, predominately neutrophils
– Exudation of fluid and plasma proteins
Chronic inflammation
3
– Longer duration
– Mononuclear cells –macrophages, lymphocytes, plasma cells
– Proliferation of blood vessels and fibroblasts
Exudative - — inflammation tends to be
more exudative
acute
Non-Exudative - — inflammation is
frequently non-exudative and is often
associated with (2)
chronic
fibrosis and scarring
Inflammation –
the body’s response to injury
inflammation (5)
– Thermal – Physical – Chemical – Allergic – Immune mediated disease
Immunity –
comes into play when inflammation
is caused by a living organism (infection)
Infection may provoke
inflammation & immunity
— may exist without infection
Inflammation
–Inflammation DOES NOT imply infection
Hypersensitivity (allergic disease) may cause
inflammation
Autoimmune disease may cause
—
inflammation
The Body’s Defenses:
3 Lines of Defense
Barriers
Inflammatory Response
Immune Response
Barriers
3
– Skin
– Mucous membranes
– Secretions
Inflammatory Response
2
– Cells (leukocytes)
– Molecules (mediators)
Immune Response
2
– Antibodies (humoral)
– Cytotoxic T cells (cellular)
Components Of
Inflammatory Responses
(3)
- Circulating blood cells and plasma proteins
- Cells of the blood vessel walls
- Cells and proteins of the extracellular matrix
Inflammation Is The
Body’s Response To —
Injury
Most of the defensive elements are located in the —
blood
Inflammation is the means by which defensive cells and chemicals leave the blood and enter the —
tissue
Inflammation is a complex reaction to injury:
4
– Vascular responses
– Cellular responses
– Systemic reactions
– Repair
— is beneficial. Excess or prolonged — may be harmful.
Inflammation
Leukocytes –
defensive cells
Plasma –
defensive proteins
The Inflammatory Response:
5 R’s
- Recognition of the injurious agent
- Recruitment of leukocytes
- Removal of the agent
- Regulation (control) of the response
- Resolution (repair)
Causes of Acute Inflammation
7
- Mechanical injury
- Chemical injury
- Radiation injury
- Thermal injury
- Infection
- Compromise of blood supply
- Immune injury
Cardinal Signs of Acute Inflammation
5
- Calor –heat
- Rubor - redness
- Tumor - swelling
- Dolor - pain
- Loss of function
Cellular Events in Acute Inflammation
7
- Margination
- Rolling
- Adhesion
- Diapedesis
- Chemotaxis
- Phagocytosis
- Killing
Systemic Manifestations of Acute
Inflammation (3)
fever
Leukocytosis
Acute phase response
Fever –due to —
pyrogens
Fever (2)
– Cytokines - TNF, IL-1 released by leukocytes
– Prostaglandins –from membrane phospholipids
Leukocytosis
3
– Leukemoid reaction
– Neutrophilia - shift-to-left
– Lymphocytosis
Acute phase response –
cytokines stimulate hepatocytes to synthesize and secrete acute phase proteins
Acute phase response (2)
– C-reactive protein (CRP) –acts as an opsonin
– Mannose-binding lectin - acts as an opsonin
Lymphangitis
• Lymphatic spread of
bacterial infection
Lymphangitis description
Painful red streaks and
regional
lymphadenopathy
Chemical Mediators Of Inflammation (2) derived
cell
plasma protein
preformed mediators in secretory granules (3)
histamine
serotonin
lysosomal enzymes
mediator: histamine
source: (3)
mast cells
basophils
platelets
mediator: serotonin
source:
platelets
mediator: lysosomal enzymes
source: (2)
neutrophils
macrophages
newly synthesized (6)
prostaglandins leukotrienes platelet activating factors activated oxygen species NO cytokines
mediator: prostaglandins
source: (3)
all leukocytes
platelets
EC
mediator: leukotrienes
source:
all leukocytes
mediator: platelet activating factors
source: (2)
all leukocytes
EC
mediator: activated oxygen species
source:
all lleukocytes
mediator: NO
source:
macrophages
mediator: cytokines
source: (3)
lymphocytes
macrophages
EC
factor 12 activation (2)
kinin system (bradykinin) coaggulation/fibrinolysis system
complement activation (4)
C3A
C5A
C3B
C5b-9
Vasoactive Amines (2)
HISTAMINE AND SEROTONIN
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
The first mediators to be released after injury
Histamine and Serotonin
Histamine and Serotonin cause (2)
dilation and leakage
Antigen (Ag) -
A substance that can induce an immune response when introduced into an animal.
Antibody (Ab) -
A protein that is produced in response an antigen. The antibody binds the antigen that stimulated its production. All antibodies are immunoglobulins.
Immunoglobulin (Ig) -
A glycoprotein composed of heavy and light chains that functions as an antibody.
Schematic Structure of a Typical
Immunoglobulin (Antibody) Molecule
(4)
• Heavy chains (2) • Light chains (2) • Variable regions form antigen-binding site (Fab) • Constant end (Fc) receptor for attachment of phagocytic cells)
• IgM -
first immunoglobulin to appear in an immune response
• IgG -
principal immunoglobulin of the secondary immune response. Only immunoglobulin capable of crossing the placental barrier
• IgA -
principal immunoglobulin in external secretions of mucosal surfaces, tears, saliva, and colostrum
• IgE -
plays an important role in immediate hypersensitivity reactions and parasitic infections
• IgD -
thought to activate the B-lymphocyte
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
Complement System is
Multifunctional
(4)
• Membrane attack complex (MAC) lysis (C56789) • Opsonization (C3b) • Chemotaxis (C5a) • Vasodilation and increased vessel permeability via histamine release (C3a, C5a) anaphylatoxins
All acute inflammatory reactions may have one of three outcomes:
(3)
- Complete resolution
- Healing by connective tissue replacement (fibrosis)
- Progression of the response to chronic inflammation
Fibrinous Inflammation:
Fibrinous Pericarditis in Rheumatic Fever
Abscess
• A localized collection of pus that has accumulated in
a tissue cavity, producing fluctuance
Cellulitis
• Diffuse spread of an acute inflammatory process through the fascial planes of soft tissue producing erythema, edema, warmth, and pain, without consolidation
Catarrhal (Seromucous) Inflammation
• Catarrhal inflammation, a clinical type of exudative inflammation, occurs only on mucosal surfaces containing mucus-secreting cells, such as nasal or bronchial mucosa
Ulcerative Inflammation:
Recurrent Aphthous Stomatitis
• An ulcer is a defect in epithelial continuity
Lazy Leukocyte Syndrome
Impaired Chemotaxis –Mutation of Contractile Proteins
Chediak-Higashi Syndrome
5
- 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
Chronic Granulomatous
Disease of Childhood
(5)
- 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 notsynthesized 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
Myeloperoxidase (MPO) Deficiency
5
- 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
Too few neutrophils
2
– Agranulocytosis
– Cyclic neutropenia
Failure in adhesion
1
– Leukocyte Adhesion Deficiency (LAD)
Slow chemotaxis
1
– “Lazy” leukocyte syndrome
Failure to phagocytose
2
– Bruton Agammaglobulinemia
– Complement deficiency
Failure to kill
3
– Chronic Granulomatous Disease of Childhood
– Chediak-Higashi Syndrome
– Myeloperoxidase Deficiency
Causes of Chronic Inflammation
8
- 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
Morphologic Features Of
Chronic Inflammation
(3)
• Mononuclear cell infiltration
• Tissue destruction
• Attempts at healing by connective tissue
replacement
• Mononuclear cell infiltration – (3)
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 - (2)
angiogenesis and fibrosis
Granulomatous Inflammation
5
• A pattern of chronic inflammation • Aggregates of epitheliod macrophages (activated) • Multinucleated giant cells • Mononuclear leukocytes, principally lymphocytes and occasionally plasma cells peripherally • Fibrosis variable
Classification of Granulomas
2
- Immune granulomas
* Foreign body granulomas
Immune Granuloma:
Coccidioides immitis
Caseation Necrosis in Tuberculosis:
Necrotizing Granulomatous
Inflammation
Mycobacterium Tuberculosis:
Intracellular Pathogen
• Blocks fusion of phagosome with lysozome
Granulation Tissue (2)
Reparative Tissue
Endothelial Cells and Fibroblasts
Granulomatous Tissue (2)
Epitheliod Macrophages
Giant Cells
Pyogenic Granuloma:
Granulation Tissue NOT — Tissue
Granulomatous