Macrophages
Develop from monocytes to become the chief phagocytic cell.
- free macrophages wander through tissue spaces
- fixed macrophages are permanent residents
- kupffer cells
Neutrophils
Become phagocytic on encountering infectious material in tissues.
Step 1: Mech of phagocytosis
Adherence of phagocyte to pathogen.
-facilitated by opsinization, the coating of the pathogen by complement proteins or antibodies.
Steps 2-5 of phagocytosis
- Phagocyte forms pseudopods, engulf particle and form phagosome.
- Lysosome fuses w/ phagocyte vesicle, forming phagolysosome.
- Lysosomal enzymes digest the particle, leaving residual body.
- Exocytosis of the vesicle removes indigestible and residual material.
Leukocytosis
Release of neutrophils from bone marrow in response to leokocytosis-inducing factors from injured cells.
Margination
Neutrophils cling to the walls of capillaries in the inflamed area.
Diapedesis
Movement of neutrophils across the membrane.
Chemotaxis
Inflammatory chemicals(chemotactic agent) promote positive chemotaxis of neutrophils. They move to the site.
Destruction of Pathogens (phagocytosis)
- Acidification and digestion by lysosomal enzymes
- Respiratory Burst. Release of cell-killing free radicals, activation of additional enzymes.
- Oxidizing chemicals.
Natural Killer (NK) Cells
Large granular lymphocytes.
- Target cells that lack self receptors.
- Induce apoptosis in cancer cells and virus infected cells.
- Secrete potent chemicals that enhance the inflammatory response.
Inflammatory Response (purposes)
- Triggered whenever body tissues are injured or infected
- Prevents spread of damaging agents
- DIsposes of cell debris and pathogens
- Sets stage for repair
Cardinal signs of acute inflammation
Redness Heat Swelling Pain Impairment of function (sometimes)
Inflammatory Mediators
Histamine (mast cells)
Blood proteins
Kinins, prostaglandins, leokotrienes, complement.
-Released by most cells (phago, injured tissue, lympho, baso, mast)
TLR
Toll like receptors
Release cytokines that promote inflammation
Released by macrophages and epithelial cells
Surge of Exudate
Moves foreign material into lymph
Delivers clotting proteins to form a scaffold for repair and isolate the area.
Starling forces
Cause the interchange of fluids between intravascular and interstitial space.
Three main determinants of filtration (lymph)
Net oncotic pressure
Net hydrostatic pressure
Capillary permeability
Capillary Oncotic Pressure
Defined as the colloid osmotic pressure contributed by the plasma proteins in the capillary.
Interstitial osmotic pressure
The colloid osmotic pressure exerted by the osmotically active proteins in the interstitium
T of F: Oncotic pressures are determined mostly by the salts in the compartments.
False: The salt levels are similar on both sides. Proteins determine the oncotic pressures for the compartments.
What does increased intravascular hydrostatic pressure lead to?
Edema. Caused by fluid overload, obstruction, CHF, Liver disease (with ascites)
Decreased intravascular oncotic pressure leads to?
Edema.
Hypoalbuminemia from:
-Low protein intake, malnutrition
-Liver failure (not enough protein produced)
-Nephrotic syndrome (too much protein lost in urine)
Lymphatic Obstruction can be caused by what?
Lymphoma, Metastatic Cancers.
Surgical removal of lymph nodes
Increased capillary filtration can be caused by?
- Burns (connective tissue destroyed)
- Inflammation (disrupt tight junctions, results in swelling)
- Toxic Damage (sepsis, pancreatitis, inhalation injuries)
