Class #4 - Inflammation (part 2) Flashcards
Granulocyte?
a) Definition
b) other name
c) Eg
a) WBC containing granules in their cytoplasm
b) polymorphonuclear leukocytes (b/c varying shapes of nucleus)
c) Neutrophiles, Eosinophiles, Basophiles, Mast cells
Female mosquito saliva contains? causes?
Anticoagulants; Enz. to dissolve tissue
Inflammation due to release of histamine by body
Two major sources of inflammatory mediators?
1- Cell derived: Either preformed stocked in granules and secreted or de novo produced
2-Plasma p+-derived: Major source is the liver
Cell derived inflam. mediators?
HIstamine, serotonin, prostanglandins, leukotrienes, plt-activating factor, ROS, Nitric Oxide, cytokines, chemokines
Plasma p+-derived inflam. mediator?
Complement, Kinins, clotting system
Vasoactive inflam. mediators? Mostly by…cell
Histamine/prostanglandins/Nitric Oxide/plt activating factors = vasodilatation
Serotonin = Vasoconstriction
Mast cells
Complement system role (3)?
- Lysis of B
- Chemotaxis
- Opsonization
Activation of complement system (3 pathways)?
- Classical : 2IgG activating C1
- Alternative: ON its own
- Lectin:
All three pathways of complement activation leads to?
Activation of C3 => Formation of C3 convertase that cleave C3 to C3a and C3b
Complement role, chemotaxis, how?
C5a and C3a: Recruitment and activation of leuko. (also increase adhesion to endothelium)
Complement osponization effect?
C3b bound on bacteria attracts phagocytes.
Vasodilating effect of complement system by?
C3a and C5a
Lysis of bacteria by complement, how?
C5b to C9 create the membrane attack complex (MAC) that put a hole on B membrane.
Kinin system activation leads to?
Role?
Bradykinin
a) Bind to GCPR on nociceptor causing pain and
b) increase vascular permeability, arteriolar dilation
*Most important mediators that cause pain at site of injury
Histamine, prostaglandins, Bradykinins
Prostanglandins formation and actions?
Phospholilase A-2 (Enz.) that liberates Arachidonic acid from membrane ->Cyclooxygenase (COX1 and 2) type 2 more involved in inflam. -> Prostaglandin
Functions: Vasodilation and increase vascular permeability and causes pain
Cytokines role?
Orchestrate systemic effect of inflammation
Interleukins and TNFs effects?
Cause fever
What are chemokines?
Cytokines that attract cells.
Chemokines receptor family?
CXCR and CCR
Plt activating factors actions?
Vascular permeability, vasoconstriction, growth factors, clotting, chemotaxis.
Nitric oxide action?
Relaxation of smooth musc.
Resolution of inflammation?
Edema draines by lymph, neutro. die by apoptosis, macrophage get rid of debris, after macrophage goes away.
Abces definition?
Hole in tissue with collection of pus: NET
2 types of macrophages?
Classic (M1) - attack microbes
Alternatively (M2) - Tissue repair
Chronic inflammation results in?
a) Angiogenesis: continuous new vessels formed
b) Monocytes continuously getting activated
c) Fibrosis
Chronic inflammation causes?
Persistent injury
Granuloma definition?
Center: macrophage, some multinucleated giant cells around object of injury.
Surround: T-cells
Granuloma Eg.
Splinter
Tuberculosis
Morphologic patterns of inflammation?
1-Serous: blisters 2-Fibrinous: Deposition of fibrin due to more severe injury 3-Abces (purulent/suppurative) 4-Ulcer 5-Membranous
Eg of fibrinous inflammation?
a) Streptococcal inflammation: Fibrin removed at the end
b) Legionnaires’ disease: Fibrin not removed = dead alveoli
Membranous inflamm. Eg.
Diphtheria: membrane in throat
Systemic effects of inflammation (3) with cause?
1-Fever: Due to prostaglandins, reason b/c leukocytes speed increases
2-Leukocytis: Increase prod. in bone marrow
3-Acute phase response by liver: Increase mediators prod. Eg. C-Reactive p+ ->Opsonin, chemotactic
Tissue regeneration 3 major types of cells and their reaction to injury?
1) Labile cells: Turning over all the time (Eg. Keratinocytes)
2) Stable cells: Not turning over all the time, but they can (Eg. Hepatocytes, however if architecture damaged, results in scaring)
3) Permanent cells: Cant be replaced (Eg.Neurons, if cell body still alive, can repair)
What is Wallerian degeneration?
Regeneration of myelinated axons by Schwann cells (they normally myelinate axons) guidance.
If repair is impossible?
replacement happens
Granulation tissue contains?
Macrophage, fibroblast, necrotic cells, new blood vessels
Macrophage stimulate…(2) in tissue replacement?
Angiogenesis
Fibrogenesis: prod scar tissue
Fibroblast role?
- Lay down collagen for formation of Extra-Cellular Matrix (ECM)
- transform into myofibroblast and are contractile
Wound contraction occurs b/c?
fibroblast ->myofibroblast->contract
Explain: Wound -> Inflammation -> Proliferation -> Tissue remodeling
a) Inflam: 1-5 days
b) Proliferation: Granulation tissue (3-21days)
c) wound contraction, reepithelialization, scar tissue formation (14 days-2years)
Different intention repairs?
Primary: surgical with suture
Secondary: Large wound ->granulation tissue->large scar
Keloid tissue?
Too much secretory fibroblast, produce large scar tissue.
Improve with age
