Flashcards in Acute and Chronic Inflammation Deck (41):
What does the inflammasome do?
Recognizes dead cells, activates caspase-1 which activates IL-1 which triggers leukocyte recruitment
What is the key difference between TLR and Inflammasome??
TLR recognizes extracellular microbes (located in plasma mem) and the inflammasome recognizes products of dead cells and some microbes (located in cytoplasm)
What are the main chemical mediators that induce vasodilation?
Histamine and NO
What action causes increased vascular permeability?? What are two mediators of this?
Endothelial cell contraction
Histamine and Bradykinin
What is the cytokine that can stimulate histamine release?
What are the functions of Bradykinin?
Causes vasodilation, increased permeability and pain
What causes transudate? How is it different from exudate?
Transudate is caused by osmotic/hydrostatic pressure imbalances. It results in fluid leakage due to hypocellular and low protein content. Low s.g.
Exudate is caused by an alteration in normal vessel permeability. Cellular and protein rich. High s.g. Fluid and protein leakage. Happens with inflammation.
Name the steps in leukocyte recruitment to an injury site.
Margination-- leukocyte accumulation at periphery of vessels
Rolling-- week and transient adhesions to endothelium
Adhesion-- firm adhesion to endothelium
Transmigration-- movement through endothelium to interstitium
Chemotaxis-- movement towards injury site
What are the two types of adhesion molecules and the strength of their attachment?
Selectins-- loose attachment to endothelial cells
Integrins-- stable attachment to endothelium
What two cytokines increase endothelial cell ligand expression for integrin binding?
IL-1 and TNF (secreted by macrophages)
Definition of diapedesis. Chemokine that drives this action.
Movement of leukocytes through vessel wall
CD31 (PECAM1) on leukocytes and endothelial cells
Some examples of chemotactic factors.
Bacterial products, chemokines, complement, leukotrienes
What happens after leukocyte recruitment? Results of this.
2. intracellular destruction
3. release of substances that destroy dead tissue and microbes
4. more mediator production
Molecules that mediate recognition of microbe by leukocyte for phagocytosis
Principle mediators of vasodilation
Histamine and NO
Principle mediators of increased vascular permeability
Histamine and Bradykinin
Principle mediators of chemotaxis
IL-1 and TNF, bacterial products
Principle mediators of fever
Principle mediator of pain
Principle mediator of tissue damage
What are 3 possible outcomes of acute inflammation?
Progression to chronic inflammation
Scarring or fibrosis
What are the 4 morphological patters of acute inflammation?
Mildest form of acute inflammation; outpouring of thin fluid (protein-poor) from plasma or serial cavity linings
Caused by more severe injury; larger vascular leaks, passage of fibrinogen and conversion to fibrin; May resolve or scar
Large numbers of neutrophils are present along with necrotic cells, edema fluid, and bacteria -- PUS; occurs with infections;
Suppurative (purulent) inflammation
What is an abscess?
Central area of necrotic tissue surrounded by preserved neutrophils, dilated vessels and fibroblastic proliferation
Local defect to surface of organ or tissue -- leads to sloughing of surface covering and necrotic inflammatory tissue
What is happening with chronic inflammation?
Active inflammation, tissue injury and healing all at the same time!
Some common causes of chronic inflammation.
Persistent infections that are difficult to eradicate
Prolonged exposure to toxic agents
Immune-mediated inflammatory disease (autoimmune)
What cell is mainly responsible for chronic inflammation?
Macrophages -- b/c of steady release of dead cells, microbes etc.
Other cells involved in chronic inflammation.
Lymphocytes-- T & B
Plasma cells-- from activated B-lymphocytes
Eosinophils-- in parasitic infections and IgE mediated inflammation (allergies)
Mast cells-- found in connective tissue
A distinctive pattern of chronic inflammation with prominent activated macrophages with epithelioid appearance
What are giant cells and what induces their formation?
Multinucleated cells made by fusion of many macrophages
What are some systemic effects of inflammation?
2. Elevated plasma levels of acute-phase proteins
What are some pyrogens that cause systemic effect of fever?
IL-1, TNF, PGE2
What stimulates acute-phase proteins, where are they synthesized and give some examples?
Synthesis in Liver
C-reactive protein, Fibrinogen, Serum amyloid A protein
Will a Sed rate be increased or decreased in infections? Why?
Increased because excess fibrinogen binds to erythrocytes causing stacks (rouleaux) that sediment more rapidly than normal
What type of leukocytosis indicates a bacterial infection?
What type of leukocytosis indicates a viral infection?
What type of leukocytosis indicates allergies, asthma, or parasitic infections?