The inflammatory process


Published on

Published in: Technology, Health & Medicine
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide
  • MOST LIKELY ON A TEST!!! Hemophiliacs could be missing Factor X. Fibrin Mesh picture in the book…
  • MOST LIKELY ON A TEST!!! Phases overlap. Calor = heat, tumor = swelling (usually don’t use – cancer!), rubor = redness
  • The inflammatory process

    2. 2. Inflammation • What is Inflammation • A vascular and cellular response to trauma. Its purpose is to initiate the healing of the injured tissue • The body’s attempt to dispose of microorganisms, foreign material and dying tissues so that tissue repair can occur • An inflammatory response may result from external or internal factors (infection) • Protects to the body by localizing and removing the injuring agent
    3. 3. Signs of Swelling • • • • • Redness (Rubor) Swelling (Tumor) Pain (Bolar) Warmth (Calor) Loss ROM
    4. 4. Signs of Inflammation (Cardinal Signs) • Redness (Rubor): • Caused by blood vessel dilation (the arterioles) • Chemical mediators promote the vessel dilation (contained in the capillary walls or endothelium resulting in immediate response) • • • • • Histamine Seritonin Bradykinins Prostaglandins Note: a 1x increase in arteriole diameter yields a 4x increase in blood flow
    5. 5. Signs of Inflammation Cont. • Swelling (tumor) • Edema fluid varies with the stage of inflammation • initially vessel permeability is only slightly altered and no cells or protein escapes and the fluid is mainly water and dissolved electrolytes (transudate): like synovial fluid • As capillary permeability increases and plasma proteins escape the extravascular fluid becomes cloudy and more viscous. This is called exudate (contains a large amount of leukocytes (called pus)
    6. 6. Causes of Edema/Swelling• bleeding from torn vessels • cell death due to anoxia, allows fluid leakage (permeability increases) • increased proteins raise extracellular osmotic pressure, drawing fluids from the capillaries • Chemicals alter cell permeability to proteins and fluid • Gravity may increase swelling (Capillary filtration pressures)
    7. 7. Edema/Swelling • To cease hemorrhage/swelling/edema • Must reverse the condition • pressure gradient • vessel repair
    8. 8. Signs of Inflammation Cont. • Pain (bolar) • Results from irritation of nerve ending by physical or chemical factors • Physical trauma may irritate pain receptors • Chemical mediators release when cell damage occurs sensitize pain receptors • Trauma may result in cell anoxia because of interference with blood flow due to capillary damage
    9. 9. Signs of Inflammation Cont. • Warmth (calor) • The result of chemical activity and increased blood flow in the injured area. • Loss of Function • May occur due to pain causing reflex guarding or muscle spasm • spasm decreases metabolic activity and constricts blood flow which causes more pain due to ischemia; thus the pain/spasm cycle
    10. 10. Phases of the Inflammatory Process • Phase I: Acute Phase ( 2 subphases) • Early (Acute): inflammatory response: lasts 2-4 days • Late (Sub-Acute): continue inflammatory phase which is usually complete in 2 weeks • Phase 2: Tissue Formation (Proliferation) • Tissue rebuilding approximately 2-3 weeks • This does not include chronic inflammation • Phase 3: Remodeling Phase • Adapt to original tissue • Continues for up to 1 year post injury
    11. 11. Phase I: The Inflammatory Process • Early Phase • Insult occurs - may be internal (infection) or external (trauma) • Vasoconstriction to decrease blood flow (first 10 minutes) • Vasodilatation • Late Phase • Tissue Repair • Regeneration
    12. 12. Phase I -Early Phase: Acute Inflammation In ju ry O n s et C h em ic al M ed iators R eleas ed (C h em otaxis ) C u as es V as od ilation In c reas es B lood , P las m a, P rotien s , P h ag oc ytic m aterial P rotien s are In c reas ed at In ju ry S ite In c reas e in p rotien s c au s es os m otic relation s h ip with p las m a H 2 O flows from h ig h er p rotien s c on ten t (in ju ry) to in ters tial flu id c au s in g ed em a/s wellin g S wellin g /ed em a are d ec reas ed b y lym p h atic s ys tem
    13. 13. Inflammatory Phases 100% 90% 80% 70% 60% 50% 40% 30% 20% 10% 0% Phase III Phase II Phase I Late Phase I Early Day 1 Day 2 Day 3 Day10 Day 30 Day 90 Chart Designates Percent of phase over time
    14. 14. Phase I: Early Phase Inflammation - Vasodilatation • Chemical mediators are released: • histamine, bradykinis, serotonin, prostaglandin's increase vascular permeability released from mast cells and blood platelets into traumatized tissue. • As fluid filtrates through “gaps in the extravascular spaces this is called exudation.
    15. 15. Phase I- Early Phase: Vasodilatation Cont. • The accumulation of excess fluid is called edema (Swelling) • Vascular permeability due to action of the histamine is short-lived, lasting less than 1 hour
    16. 16. Phase I: Early Phase Inflam. Lymphatic channels are blocked • Local lymphatic channels are blocked by fibrin plugs formed during coagulation. Obstruction of the local lymphatic channels prevents drainage of fluid from the injured site, thus localizing the inflammatory reaction.
    17. 17. Phase I- Late Phase: Phagocytosis • Body’s cellular defense to remove toxic material via lymphatic system • Phagocytosis: a process when leukocytes capture and digest foreign matter and dead tissue • 1st line of defense: neutrophiles (in most abundance from 1-3 days) - phagocytic activity reaches maximum effectiveness within 7-12 days
    18. 18. Phase I- Late Phase: Phagocytosis Cont. • 2nd line of defense: monocytes (which convert into large cells called macrophages) and lymphoctes consume large amounts of bacteria and cellular debris. Monocytes are critical in the initiation of tissue repair because the attract fibroblasts Bacteria Macrophage
    19. 19. Phase I- Late Phase Phagocytosis Cont. • Pus is the end result - it contains leukocytes, dead tissue and phagogenic material • Prolonged puss accumulation can prevent fibroplasia which begins the wound healing • Fibroblasts are connective tissue responsible for collagen synthesis • Ligaments, joint capsule, tendon • Osteoblasts: responsible for bone synthesis Fibroblast Macrophages
    20. 20. Phase I: Early Phase Inflammation - Margination • When trauma occurs the endothelial wall is disrupted exposing collagen fibers creating a “stickiness” • WBC’s concentrate in the injury site to rid the body of foreign substances and dead (necrotic) tissue
    21. 21. Phase I- Late Phase: Margination Cont. • As circulation slows, leukocytes migrate and adhere to the walls of post-capillary veinuels (for approx 1 hour) • The leukocytes pass through the walls of the vessels (diapedesis) and travel to the site of injury (Chemotaxis)
    22. 22. Phase I: Late Phase Blood Clotting • Ruptured vessels release Enzyme (Factor X) • Factor X reacts with prothrombin (free floating in blood) • Thrombin then stimulates fibrogen into its individual form fibrin • Fibrin grouped together to form “lattice” around injured area • Fibrin lattice contracts to remove plasma and compress platelets forming a “patch”
    23. 23. Phase I: Late Phase Blood Clotting Factor X Prothrombin Fibrin Forms Seal Thrombin Fibrin Mesh Fibrin Monomer Fibrogen and Thrombin Meet
    24. 24. Phase II: Regeneration: • The replacement of destroyed cells by reproducing healthy cells adjacent to the wound (humans capacity to regenerate tissue is limited and further affected by age and nutritional state).
    25. 25. Phase II: Stages of Regeneration: • Stage starts with periphery • Re-eptheliaization is proliferation of peripheral epithelial tissue which then migrates to the wound until the area is covered. • Capillarization (Capillary buds proliferate and connect forming new capillaries which gives the red, granular appearance to the scar (granular tissue)
    26. 26. Phase II: Stages of Regeneration: Cont. • Fibroplasia occurs due to fibroblasts which arises from undifferentiated mesenchymal cells and migrate into the area along fibrin strands and begin to synthesize scar tissue. • Scar tissue is CT and mostly collagen and mucopolysaccharides. • Fibroblasts secrete both, contributing tensile strength to the repair. • Scar tissue very inelastic compared to surrounding tissue.
    27. 27. Phase II: Stages of Regeneration: Cont. • Vascularization - occurs with the proliferation of collagen synthesis • Formation of blood vessels (angiogensis)
    28. 28. Phase II: Collagen Synthesis: • Occurs within 12 hours of injury to 6 weeks (average 3 weeks) • Type I: collagen: associate with muscular tissue (larger and stronger fibers) • Type III collage: smaller fibers, less cross linking and highly disorganized (ligamentous, tendinous) • Type III with time is replaced by Type I collagen
    29. 29. Phase II: Collagen Synthesis Cont. • Tissue Healing Times • Muscle : approximately 3 weeks • Tendon: 4-6 weeks • Extent of the tissue damage and vascularity will aid in determining healing time • Age may also be a factor in healing
    30. 30. Phase II: Stages of Regeneration: Cont. • Wound Contraction: • Wound contraction begins to occur in CT as the myobroblasts (actin-rich fibroblasts) contract. Myofibroblasts move toward the center of the wound, helping reduce the size of the area to be covered. • Outside-in
    31. 31. Phase III: Maturation/Remodeling Phase • Purpose of this phase • Strengthen the repaired tissue • Firoblasts, myofobrpblasts & Macrophages reduced to pre-injury state • Type III fibrin continues to be replaced by Type I
    32. 32. Phase III: Maturation/Remodeling Phase (day 9 onward) • Blends in with the repair phase, original collagen fibers were randomly oriented. During remodeling, the fibers become more organized, parallel to the wound surface which provides greater tensile strength • The type of tissue involved will determine the duration and extent of remodeling activity
    33. 33. Phase III: Maturation/Remodeling Phase Cont. • Strengthening of scar tissue continues from 3 months to 1 year, but fully mature scar in only 70% as strong as intact tissue. • Motion will influence the structure and functional capacity of scar tissue (controlled stress increases functional capacity, allows healing and reduces adhesion formation).
    34. 34. Chronic Inflammation • Inflammation which continues past 1 month • Marked by a loss of function • Fibroblast activity continues forming granuloma
    35. 35. Chronic Inflammation • Complications • Granuloma: large mass of weaker scar tissue (usually due to large inflammation and activity without regard to healing time) • Retardation of muscle fiber: with excessive granuloma fibroblasts cannot reach damaged tissue • Adhesions/contractures in tissue • Keloid/hypotrophic scars
    36. 36. Abnormal scarring: • Hypertophic scar or keloid scar. Biological difference not well understood, but clinically hypertrophic scar is contained within the boundaries of the original wound while a keloid scar extends beyond the borders of the original wound.
    37. 37. Injury R esp onse W ond H ealing Summary P hase I: A cute P hase P hase II: Tissue R ep air P hase III: M aturation P hase Inflam m ation A p p roxim ate Tim e Tab le 7-10 days (A cute p hase 3 days) R esolution M inor to no cell death R ep lacem ent of Typ e III collag en w ith Typ e I C ollag en G ranulation F ib rob lasts lay dow n collag en C ap illarization R eg eneration S car tissue form ed C ap ilarization O ccurs for up to 1 year C hm eical M ediators R elease V asodialation Lym p hatic C hannels b locked O sm otic P ressure R esult edem a/sw elling P hag ocytosis M arg ination A p p roxim ate tim e tab le 2-3 w eeks
    38. 38. THE BIG QUESTIONS! • • • • When do we use cold? When do we use heat? When do we use medications? When do we use Electrical modalities?
    39. 39. Treatment Planning for Phases of Tissue Healing P hase I P hase II T issue H ealing P hase III: M aturation C ontrol A ctive E ncourage E ncourage Inflam . L im it R epair/ T issue scope of O rig. R eplacem ent R em odeling and Injury D am aged T issue A lignm ent w ith F unc. S tresses.
    40. 40. Treatment Planning: P h ase I Im m o b ilizatio n C o ld M o d alities P u lsed U ltraso u n d C o m p ressio n E lev atio n E -S tim P h ase II T issu e H ealin g C o n trast B ath s C o m p ressio n D ev ices E -S tim P u lsed / C o n tin u o u s U S T ractio n M assag e B io feed b ack H eat M o d alities P h ase III: M atu ratio n H eat M o d alitie s C o n tin u o u s U S E -S tim M assag e
    41. 41. Treatment Planning: Maturation Phase Phase I Cryokinetics Isometics Controlled ROM (CPM) Proprioception CV conditioning Phase II Tissue Healing Manual Therapy Passive ROM Active ROM Progressive Resistance Ex Functional Ex Cv Exercise Phase III: Maturation Overload Resistance Ex Proprioception Ex Activity Specific Functional Ex Cv Exercise
    42. 42. END OF TOPIC - A
    43. 43. INFECTION
    44. 44. Review of Physiology • Resistance A. Non-specific Resistance - Body surface barriers - Anti Microbial Secretions - Internal Anti Microbial agents - Phagocytosis part of the reticoendothelial system a. phagocytes - Microphages - Macrophages
    45. 45. • B. Specific Resistance - lymphatic system - lymph vessels - lymph nodes - lymph - spleen
    46. 46. Specific Resistance (cont) • Antigen A. B-lymphocytes B. T – Lymphocytes C. Memory Cells
    47. 47. • Antibody 1. IgG 2. IgA 3. IgM 4. IgD 5. IgE
    48. 48. • Antigen – antibody reactions a. Agglutination b. Cytolysis c. Opsonization d. Neutralization (viral) e. Neutralization (toxin) f. Precipitation
    49. 49. Chain of Infection Susceptible host Portal of Entry Etiologic Agent (microorganism) Reservoir Method of transmission from reservoir to (Source) susceptible host Portal of exit
    50. 50. Pathogens • Bacteria – Aerobic – Anaerobic • Viruses - intracellular parasite capable of reproducing outside of a living cell. • Mycoplasma – similar to bacteria and have no cell wall – resistant to antibiotics that inhibit cell wall synthesis • Rickettsiae & Chlamydia - rigid cell wall; with some feature of both bacteria and viruses. – Chlamydia- transmitted by direct contact – Rickettsiae- infect cells of arthropods and are transmitted by these vectors. • Fungi - self-limited, affecting the skin and subcutaneous tissue. • Parasites
    51. 51. Reservoir -where the pathogen lives and multiplies – Endogenous – Exogenous • Mode of Transmission – Direct contact – Indirect contact • Vector – Droplet or airborne transmission
    52. 52. Host Factors • Factors that enable a host to resist infections: • Physical barriers • Hostile environment created by stomach acid secretions, urine & vaginal secretions. • Antimicrobial factors e.g. saliva, tears • Respiratory defenses • Specific and nonspecific immune responses to pathogenic invasion. • Age • Nutrition
    53. 53. Portal of Entry • Respiratory Tract • GI Tract • Genitourinary Tract • Skin and mucous membrane • Bloodstream
    54. 54. Stages of Infectious Process • Incubation period – period begins with active replication but with no symptoms • Prodromal stage – Symptoms first appear • Acute phase – proliferation and dissemination of pathogens • Convalescent stage - containment of infection and pathogens are eliminated • Resolution – total elimination of pathogens without residual manifestation Nosocomial infection – Infection acquired in a health care setting. – Typically manifest after 48 hrs. – UTI most common type
    56. 56. Standard precautions • • • • Blood All body fluids, secretions, excretions, Non-intact skin Mucous membranes • Essential elements: • Use barrier protection • Prevent inadvertent percutaneous exposure, dispose of needles • Immediate and thorough hand washing
    57. 57. Infection Control and Prevention
    58. 58. Infection Control in In-Patient Health Care Agencies • • • • Hand Hygiene Patient Placement Protective Equipment Proper disposal of Soiled Equipment
    59. 59. Infection Control In Community – Based Setting • • • • Sanitation Proper Disposal of Waste Food Preparation Report CD Occurrence