Acute Inflammation Flashcards
(30 cards)
What is Acute Inflammation characterized by?
Neutrophils
Definition of inflammation
movements of fluid/leukocytes from tissues->blood
What type of immunity is present in acute inflammation?
Innate immunity
Hows is the vascular response different between acute and chronic inflammation?
Prominent vascular response in Acute
What kind of immunity is present in chronic inflammation?
Cell-mediated
What type of leukocyte is predominant in Chronic inflammation?
Mononuclear cell
Causes of Acute Inflammation (3)
1) Tissue necrosis
2) Immune hypersensitivity
3) Microbial infections (pyogenic bacteria)
Causes of chronic inflammation (3)
1) Autoimmune disorders
2) Primary granulatomous diseases (Chron’s, sarcoidosis)
3) Phagocytosis resistant organisms
Signs of inflammation (5)
1) Redness
2) Swelling
3) Heat
4) Pain
5) Loss of Function
Major manifestations of Acute Inflammation (6)
1) Rapid vascular response/altered microvasculature
2) Increased vascular permeability
3) Platelet stimulation
4) Chemical mediator activation
5) Neutrophil activity
6) Phagocytosis & intracellular killing
What are the 2 most common causes of fibrinous pericarditis?
1) uremia
2) renal failure
Define: Effusion
Excess fluid within body cavities
Define: Edema
Fluid accumulation within extravascular compartment and interstitium
Mechanisms of increased vascular permeability during inflammation (3)
1) Inflammatory mediators cause contraction of endothelial cells –> gaps
2) Direct injury to endothelial cells (arterioles, capillaries, venules usually)
3) Leukocyte dependent injury of endothelial cells
Define: Transudate
Edema with low protein content
Define: Exudate
Edema with high protein content
Types of Exudate
1) Serious - no cellular component
2) Fibrinous - fibrin from coagulation activation
3) Purulent - cellular components , mostly neutrophils
4) Suppurative - Purulent + liquefactive necrosis
Vasoactive Mediators of Edema
- Plasma Derived
- Hageman factor
- Fibrin split products
- Kinins
- Complement system
- C3a, C5a
- Hageman factor
- Cell Derived
- Mast cell/basophils –> Histamine
- Platelets –> Serotonin
- Inflammatory Cells –> prostaglandins/leukotrienes
- Endothelium –> NO/prostaglandins
What are the anaphylatoxins and what do they do?
- C3a, C4a, C5a
- Part of complement system
- increases vascular permeability by activating Mast Cells (histamine, leukotrienes)
- cause bronchoconstriction, vasoconstriction, edema
What makes kinins? and what do kinins do?
- Kallikrenin makes kinin
- Kinin increases vascular permeability
Vasoactive Cell Derived Mediators of Edema
1) Arachidonic acid metabolites
2) Platelet Activating Factor
3) Platelet Derived mediators
4) Mast Cell & basophil derived mediators
Arachidonic acid metabolites and their functions
- Thromboxanes (TXA2)
- Vasoconstrictor, aggregatory, increases PMN response
- Prostaglandins (PGI2)
- Vasodilator, anti-aggregatory, decrases PMN responses
Actions of Neutrophils during inflammatory resposne
1) Margination of cells along vascular wall
2) Adhereance to endothelium and basement membrane
3) Emigration through vascular wall via diapedesis
4) Chemotaxis - migration through soluble chemotactic agents
5) Haptotaxis - chemotax. along fixed insoluble chemotactic gradient
Initial PMN recruitment depends on which two molecules?
1) C5a
2) LTB4