3 Cellular Defense To understand our repair mechanisms, let s first take a look at our defenses.
4 Surface Barriers Skin, mucous membranes, and their secretions make up the first line of defense Keratin in the skin: Presents a physical barrier to most microorganisms Is resistant to weak acids and bases, bacterial enzymes, and toxins Why? (Dead, dry, physical barrier) Mucosae provide similar mechanical barriers
5 Epithelial Chemical Barriers Epithelial membranes produce protective chemicals that destroy microorganisms Skin acidity (ph of 3 to 5) inhibits bacterial growth Sebum contains chemicals toxic to bacteria Stomach mucosae secrete concentrated HCl and protein-digesting enzymes Saliva and lacrimal fluid contain lysozyme Mucus traps microorganisms that enter the digestive and respiratory systems
6 But. Sometimes injury occurs What happens when that first line of epidermal defense is violated? (Starting Page th, th ) What is the response in the first hour, days, weeks?
7 Internal Defenses: Cells and Chemicals The body uses nonspecific cellular and chemical devices to protect itself Phagocytes and natural killer (NK) cells Antimicrobial proteins in blood and tissue fluid Inflammatory response enlists macrophages, mast cells, WBCs, and chemicals Harmful substances are identified by surface carbohydrates unique to infectious organisms
8 Tissue Trauma Causes inflammation, characterized by: Dilation of blood vessels Increase in vessel permeability Redness, heat, swelling, and pain
9 Inflammation May be a local response initiated by tissue damage or... May be a systemic response initiated by activation of the immune system. We ll assume tissue damage and a local response for our example.
10 Inflammation Sequense At the site of tissue damage a variety of inflammatory chemicals is released.
11 Inflammation: Tissue Response to Injury The inflammatory response is triggered whenever body tissues are injured Prevents the spread of damaging agents to nearby tissues Disposes of cell debris and pathogens Sets the stage for repair processes The four cardinal signs of acute inflammation are redness(rubor), heat (calor), swelling (tumor), and pain (dolor).
12 Inflammation Sequence (Pg ) Histamine (from mast cells) binds to H1 receptor sites on nearby capillaries causing dilation resulting in: Increased Blood Flow Rubor: redness and heat Increased permeability resulting in an influx of WBCs and clotting proteins... explains the clot and the pus The increased proteins in the tissue space (ECF) draw water from the plasma by osmosis... explains the swelling (edema).
13 Kinins Bind to a type of sensory receptor called chemoreceptors to initiate nerve impulses which travel to the brain and are perceived as pain. The increased pressure stimulates sensory receptors... Also explains the pain.
14 Prostaglandins Bind to and stimulate chemoreceptors for sensation of pain Trigger vasodilation like histamine. Stimulated by PMN s. (Poly Morphonuclear Neutrophils)
15 Anti-inflammatory agents Aspirin: inhibits formation of prostaglandins therefore reduces both pain and fever Benadryl: (an antihistamine) blocks the receptor sites for histamine H1 receptors on vessels in tissues Cortisone cream: inhibits release of various inflammatory chemicals
16 Inflammation Response Pg 767 Begins with a flood of inflammatory chemicals released into the extracellular fluid Inflammatory mediators: Kinins, prostaglandins (PGs), complement, and cytokines Released by injured tissue, phagocytes, lymphocytes, and mast cells Cause local small blood vessels to dilate, resulting in hyperemia
17 Toll-like Receptors (TLRs) Macrophages and cells lining the gastrointestinal and respiratory tracts bear TLRs TLRs recognize specific classes of infecting microbes Activated TLRs trigger the release of cytokines that promote inflammation
18 Inflammatory Response: Vascular Permeability Chemicals liberated by the inflammatory response increase the permeability of local capillaries Exudate fluid containing proteins, clotting factors, and antibodies Exudate seeps into tissue spaces causing local edema (swelling), which contributes to the sensation of pain
19 Inflammatory Response: Edema The surge of protein-rich fluids into tissue spaces (edema): Helps dilute harmful substances Brings in large quantities of oxygen and nutrients needed for repair Allows entry of clotting proteins, which prevents the spread of bacteria
20 Inflammatory Response: Phagocytic Mobilization Four main phases: (Pg th Edition) Leukocytosis neutrophils are released from the bone marrow in response to leukocytosis-inducing factors released by injured cells Margination neutrophils cling to the walls of capillaries in the injured area Diapedesis neutrophils squeeze through capillary walls and begin phagocytosis Chemotaxis inflammatory chemicals attract neutrophils to the injury site
21 Phagocytes Macrophages are the chief phagocytic cells Free macrophages wander throughout a region in search of cellular debris Kupffer cells (liver) and microglia (brain) are fixed macrophages Figure 21.2a
22 Phagocytes A key weapon Neutrophils become phagocytic when encountering infectious material Eosinophils are weakly phagocytic, but defend against parasitic worms Mast cells bind and ingest a wide range of bacteria
23 Mechanism of Phagocytosis Microbes adhere to the phagocyte Pseudopods engulf the particle (antigen) into a phagosome Phagosomes fuse with a lysosome to form a phagolysosome Invaders in the phagolysosome are digested by proteolytic enzymes Indigestible and residual material is removed by exocytosis
24 1 Microbe adheres to phagocyte. (b) Figure 21.2b
25 1 Microbe adheres to phagocyte. 2 Phagocyte forms pseudopods that eventually engulf the particle. (b) Figure 21.2b
26 1 Microbe adheres to phagocyte. 2 Phagocyte forms pseudopods that eventually engulf the particle. Lysosome Phagocytic vesicle containing antigen (phagosome). (b) Figure 21.2b
27 1 Microbe adheres to phagocyte. 2 Phagocyte forms pseudopods that eventually engulf the particle. Lysosome 3 Phagocytic vesicle containing antigen (phagosome). Phagocytic vesicle is fused with a lysosome. Phagolysosome Acid hydrolase enzymes (b) Figure 21.2b
28 1 Microbe adheres to phagocyte. 2 Phagocyte forms pseudopods that eventually engulf the particle. Lysosome 3 Phagocytic vesicle containing antigen (phagosome). Phagocytic vesicle is fused with a lysosome. Phagolysosome Acid hydrolase enzymes 4 Microbe in fused vesicle is killed and digested by lysosomal enzymes within the phagolysosome, leaving a residual body. Residual body (b) Figure 21.2b
29 1 Microbe adheres to phagocyte. 2 Phagocyte forms pseudopods that eventually engulf the particle. Lysosome 3 Phagocytic vesicle containing antigen (phagosome). Phagocytic vesicle is fused with a lysosome. Phagolysosome Acid hydrolase enzymes 4 Microbe in fused vesicle is killed and digested by lysosomal enzymes within the phagolysosome, leaving a residual body. Residual body 5 Indigestible and residual material is removed by exocytosis. (b) Figure 21.2b
30 1 Microbe adheres to phagocyte. 2 Phagocyte forms pseudopods that eventually engulf the particle. Lysosome 3 Phagocytic vesicle containing antigen (phagosome). Phagocytic vesicle is fused with a lysosome. Phagolysosome Acid hydrolase enzymes 4 Microbe in fused vesicle is killed and digested by lysosomal enzymes within the phagolysosome, leaving a residual body. Residual body 5 Indigestible and residual material is removed by exocytosis. (b) Figure 21.2b
31 After Inflammation Repair Involves: Organization Regeneration Fibrosis
32 Tissue Repair Organization and restored blood supply The blood clot is replaced with granulation tissue Regeneration and fibrosis Surface epithelium regenerates and the scab detaches Figure 4.13a
33 Tissue Repair (Pg th th) Fibrous tissue matures and begins to resemble the adjacent tissue Figure 4.13b
34 Tissue Repair Results in a fully regenerated epithelium with underlying scar tissue Figure 4.
35 Organization Blood clot is replaced with granulation tissue new capillary buds begin to grow fibroblasts synthesize collagen fibers to patch the area and help pull the wound edges closer together macrophages consume the original clot plus bacteria and cellular debris. many macrophages die and accumulate as pus.
36 Regeneration Surface cells are replaced with cells identical to original
37 Fibrosis Original cells are replaced by collagen resulting in a scar.
38 Primary Union Edges are close together Minimal scar tissue
39 Secondary Union Deeper Cut More visible scar May have impaired mobility or function This is why deeper more serious cuts require closure. (Stitches, staples)
42 Regeneration Virtually no regeneration: Neurons of the CNS Cardiac Muscle
43 Scar tissue Tissues which do not regenerate are typically repaired with scar tissue and fibrosis. Does not perform like the original Internal space occupied in hollow organs In the heart it is not contractile, capacity reduced.
44 Cell aging Why do we live years? Wear and tear Mitochondrial aging free radicals Immune system loses effectiveness Telomeres cells are programmed for x divisions.
45 Burns First-degree only the epidermis is damaged Symptoms include localized redness, swelling, and pain
46 Burns Second-degree epidermis and upper regions of dermis are damaged Symptoms mimic first degree burns, but blisters also appear
47 Burns Third-degree entire thickness of the skin is damaged Burned area appears gray-white, cherry red, or black; there is no initial edema or pain (since nerve endings are destroyed)
48 Rule of Nines Estimates the severity of burns Burns considered critical if: Over 25% of the body has second-degree burns Over 10% of the body has third-degree burns There are third-degree burns on face, hands, or feet
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