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Inflammation and Infection. Nonspecific Skin 650,000 microbes/square inch; 100 trillion/ person (acts as a place holder) Sebaceous (oil) and odoriferous.

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Presentation on theme: "Inflammation and Infection. Nonspecific Skin 650,000 microbes/square inch; 100 trillion/ person (acts as a place holder) Sebaceous (oil) and odoriferous."— Presentation transcript:

1 Inflammation and Infection

2 Nonspecific Skin 650,000 microbes/square inch; 100 trillion/ person (acts as a place holder) Sebaceous (oil) and odoriferous (sweat) secrete antibacterial acids and enzymes Mucous membranes trap invaders Defense Mechanisms

3 Nonspecific Inflammatory response- isolate invader, destroy it, and clean up debris Specific much slower All cells have protein or saccharide markers called ANTIGENS Defense Mechanisms

4 Specific when an antigen of the invader is identified, lymphocytes produce ANTIBODIES This defense has ability to remember the invader and to produce more antibodies if the invader returns Defense Mechanisms


6 Nonspecific cellular and vascular response to tissue TRAUMA Only occurs where blood supply exists (no gangrene) May be so intense that it harms the tissues Anaphylactic shock Autoimmune diseases Inflammation

7 When any trauma happens, including injury, microbial infection, ischemia (decreased oxygen in cells), freezing, burning, electrocution, radiation, and chemical irritation Inflammatory Process

8 MAST CELLS (histocytes) are in all cells When injured, they produce HISTAMINE that causes blood vessels to dilate and increase blood flow HYPEREMIA causes increased redness and heat in area Hyperemia brings increased white blood cells (neutrophils also called polymorphonuclear cells- PMNs) Inflammatory Process

9 These cells also line the endothelium of the vessels (capillaries become permeable) Blood fluid called EXCUDATE leaks into tissue Leaking causes swelling (edema) With edema, pressure is put on nerve endings causing pain Inflammatory Process

10 5 Cardinal Signs of Inflammation

11 Vascular permeability also allows neutrophils to escape into tissues (DIAPEDESIS) Neutrophils arrive in great numbers and readily move into action by a process called CHEMOTAXIS Neutrophils detect chemicals released by bacteria, injured tissue, and proteins and they are then drawn to the area Inflammatory Process

12 Begin phagocytosis (cell eating) Neutrophils life is short and they die and then are mixed with blood fluid to make PUS Inflammatory Process

13 In 3-4 days, large numbers of monocytes (large eater) arrive More killing power and are on clean up crew This INFLAMMATION is considered acute Inflammatory Process

14 After 7-10 days if the inflammation is still present, then the lymphocytes are brought in They use a slower, more specific attack Inflammatory Process

15 Last mare than 2 weeks Microscope shows large amounts of macrophages and fewer neutrophils If macrophage cannot help, a granuloma might be formed These are fibrous deposits of collagen and may calcify Ex: Tuberculosis or foreign object like a splinter Chronic Inflammation

16 LEISIONS can be external or internal They can often be identified from fluid Serous exudate- clear, serum-like (Ex: blisters) Fibrinous exudate- fluid and large amounts of fibrinogen (Ex: strep throat or if dried, a scab) Purulent exudate- full of dead neutrophils, tissue debris, and pyogenic (pus forming) bacteria. If localized, it is called an abscess. If in a body cavity, it is called an empyema Inflammatory Exudates

17 Include wounds, ulcers, wheals, blisters, vesicles, pustules, tumors, etc. Abscesses Caused by streptococcal or staphylococcal bacteria Body tries to keep it contained If a large abscess ruptures, it forms a tract or opening in skin called a sinus If the tract connects two organs, it is called a fistula Inflammatory Lesions

18 Ulcers Deep loss of tissue, crater-like lesion Pressure sores or decubitus ulcers are common problems in health care Inflammatory Lesions

19 Cellulitis widespread, acute inflammatory process General edema and redness Caused by streptococcus or staphylococcus Inflammatory Lesions

20 (Khan Academy) (animated) (cartoon) Inflammation Videos

21 Tissue Repair *Cellular proliferation or division categories * mitotic- continually divide (Ex: skin and mucosa of internal organs) * facultative mitotic- cells do not divide regularly but can be stimulated to do so when needed (Ex: liver and kidney, but some tissue needs to be there) * non-dividing cells- dont divide EVER! (Ex: brain cells, heart muscle cells- repair is only scarring) Tissue Repair and Healing

22 Methods of repair Regeneration Involves mitotic cell division (bone, skin, bone marrow) Fibrous Connective Tissue Repair Scar formation – bridge between normal tissue and the wound, but DOES NOT restore function Examples: brain tissue, heart muscle Tissue Repair

23 Primary Union (First Intention) *Wound edges are clean * Steps 1. line fills with serum, forming a scab 2. in 1-2 days, new capillaries bridge the gap between the edges 3. in a few days fibroblasts grow across the deeper wound layers and begin to deposit collagen in fibrous network (granulation tissue) 4. collagen begins to contract pulling edges together and forming a scar **In a few weeks, incision will look healed but deep layers may not be for a month or more Tissue Healing

24 Secondary Union (Secondary Intention) When dirty, or deeper degree of tissue damage or cannot be pulled together Same process but with much more inflammation to resolve Large numbers of capillaries, fibroblasts, and collagen must be produced After a week, new soft tissue called granulation tissue is formed and later replaced with collagen Collagen contracts, pulling the wound edges together Healing depends on size of wound- may need skin graph Tissue Healing

25 Increased levels of dirt, bacteria, dead leukocytes, etc might make the body take months to eat up. Wounds must be cleaned or DEBRIDED Other factors effecting healing time Age, size of wound, location of wound, nutrition, immobility, and circulation Organism virulence (strength) steroids Delayed Wound Healing

26 Prolonged wound healing Poor or excessive scar formation DEHISCENSE- scar does not have enough strength and separates at margin Excessive collagen formation results in a raised scar called a keloid (more common in African- Americans) ADHESIONS form scar tissue that adheres to a nearby organ (often after surgery) Complications of Wound Healing

27 Complications or Wound Healing

28 Symptoms Fever Tachycardia Malaise Leukocytosis Septicemia Tests Cutures- organism grown in agar, often with sheeps blood Culture and sensitivity tests- microorganisms smeared on agar and small antibiotic-permeated disks are placed on the agar- killing zones are identified Antigen-antibody (reactive tests or serologic tests) Skin testing (TB- Mantoux test) for induration (positive test) Xpert test for MRSA- DNA testing Testing for Infection

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