Week 13 Fractures and Immunity Student Slides PDF

Fractures, Inflammation/Imm unity, and Burns LECTURER: KIMBERLY HELLMER MN RN A DA P T E D W I T H P E R M I S S I O N F R O M : KA RA S E A LO C K E d D M E d. B N R N C N C C ( C ) C C N E  By the End of this Lecture You Will: Critically reflect upon the overall anatomy and physiology of th...

Fractures, Inflammation/Imm unity, and Burns LECTURER: KIMBERLY HELLMER MN RN A DA P T E D W I T H P E R M I S S I O N F R O M : KA RA S E A LO C K E d D M E d. B N R N C N C C ( C ) C C N E  By the End of this Lecture You Will: Critically reflect upon the overall anatomy and physiology of the immune system and how alterations of inflammation and immunity leads to significant systemic changes. Explain pathophysiology and effects on the body related to:  Fractures  Immunity  Inflammation Begin to prioritize patient conditions related to nursing assessment and clinical manifestations Fractures  Fractures A fracture is a break in the continuity of a bone. Methods of treatment are different in pediatrics than in older adults. Rare in infants, except with motor vehicle collisions or falls from heights. The __________ clavicle is the most frequently broken bone in childhood, especially in those less than 10 years of age. Highest incidence of fractures in young males (15-24 years) and older persons (> 65 years).  Fractures: Causes Direct blow Crushing force Sudden twisting motion Cancer Osteoporosis Cushing’s syndrome https://getwellhospital.co.in/fractureofbones https://www.wataugaortho.com/2024/08/23/underst anding-bone-fractures-types-treatments-and-recove  Fracture: Types https://coastalhealth.com/conditions/spinal-com pression-fracture/ https://www.alamy.com/stock-photo/im pacted-fracture.html?sortBy=relevant Table 39.1 (Power-Keen et al., 2023, p. 965) https://www.alamy.com/comminuted-fractures-of-a rm-bones-labelled-artwork-and-corresponding-x-ra y-of-comminuted-fractures-of-the-shaft-of-the-radiu s-and-ulna-bones-in-a-pat-image334951580.html Table 39.1 (Power-Keen et al., 2023, p. 965) https://x.com/OBandarchi/status/16995047192431 Fracture: Types 45495  Classification of Fractures Name of the injured bone Location of the injury (i.e. metaphyseal, diaphyseal, epiphyseal) Orientation of the fracture (i.e. type) Condition of the overlying tissues (i.e. open or closed fracture) What type of fracture is this?  Stages of Bone Healing Figure 39.2(Power-Keen, et al., 2023, p. 96 Fractures: Clinical Manifestations Often numbness up to Pain 20 minutes following Impaired sensation injury Loss of functional ability Unnatural alignment Discoloration, bleeding at the Swelling site through an open wound Muscle spasm Crepitus Tenderness Fractures: Nursing Assessment Table 65.6 (Kwong et al., 2023, p. 1618)  Fractures: Compartment Syndrome Figure 39.7(Power-Keen et al. 2023, p. 973) Figure 65.14( Kwong et al. 2023, p. 1623) Fractures: The 5 P’s to Assess for Compartment Syndrome Pain and point of tenderness Pulse: distal to the fracture site Pallor Paresthesia: sensation distal to the fracture site Paralysis: movement distal to the fracture site https://www.osmosis.org/answers/5-ps-circulation-a ssessment-mnemonic Fractures: Limb Assessment Fractures: Complications Deep Vein Pain on passive Swelling, Thrombosis stretch or light erythema, warmth, palpation diminished pulses, pain Fracture Healing: Direct vs Indirect healing Direct Healing: occurs when bone cortices are in direct contact with one another. Most often occurs with surgical fixation No callus formation Indirect Healing: most often occurs when treatment of the fracture involves a cast or other nonsurgical method. Callus is hallmark of indirect fracture healing.  Fracture Healing Healing Time: Neonatal period: 2-3 weeks Early childhood: 4 weeks Later childhood: 6-8 weeks Adolescence: 8-12 weeks Adults vary depending on risk factors anywhere from 6-12 weeks, or months Factors Influencing Bone Healing Immunity and Inflammation  Innate and Adaptive Immunity Two main defence systems: Innate (1st Line of Defense)  Natural or native immunity  Inflammation (2nd Line of Defense) biochemical and cellular mechanisms Adaptive (3rd Line of Defense)  Slower but more specific process Separate but also interdependent Innate Immunity  FIRST LINE OF DEFENSE  SECOND LINE OF DEFENSE Innate: First Line of Defense: Physical Figure 6.1 (Power-keen et al., 2023,p. 136) Physical Barrier Compromised Neurological System Gastrointestinal Meningitis System  Clostridium difficile Respiratory System Genitourinary system Pneumonia  Urinary tract infection Cardiovascular Integumentary System System Endocarditis  Necrotizing fasciitis Common Bacteria We Encounter Staphylococcus Aureus MRSA Streptococcus VRE STI Second Line of Defense: Inflammation  Second Line of Defence: Inflammation First response to injury quick and nonspecific Figure 6.3 (Power-Keen et al. 2023, p. 138) Plasma Protein Systems Figure 6.4(Power-Keen et al., 2023, p. 139)  Second Line of Defence: Cell Components Leukocytes: Granulocytes:  Neutrophils  Band Cell – immature neutrophils  Eosinophils  Basophils  Histamine  Mast Cells  Released during inflammation and healing.  Second Line of Defence: Cell Components Leukocytes Agranulocytes: Monocytes and Macrophages  Slower than neutrophils  Better suited for long term defence. Lymphocytes:  B cells  T cells  Natural Killer Cells Local Signs and Symptoms of Acute Inflammation Acute inflammation symptoms:  Swelling  Pain  Heat  Redness Early/mild inflammation:  Serous exudate Severe inflammation:  Fibrinous exudate  Purulent exudate http://www.footankle.info/blisters.html Systemic Signs and Symptoms of Acute Inflammation Fever  Normal Temperature 36C – 37C  Leukocytes and macrophage  pyrogen  Pyrogen “pryo”=fire  Mild to Moderate vs. High fever ( 39.4C-41.1 C) Leukocytosis  Increase in circulating  Inflammati on with Wounds Figure 6.13(Power-Keen et al., 2023, p. 151) Fig 6-14, p. 152, Power-Kean et al., (2023) Dysfunctional Wound Healing Dysfunctional wound healing can occur during any phase of the healing process. Causes: Ischemia Excessive bleeding Obesity Excessive fibrin deposition Diabetes mellitus Wound infection Inadequate nutrients Numerous medications Tobacco smoke Infection and Wounds Maggots Phagocytosis at its best Cleaning MRSA infection Group A streptococcus Third Line of Defense: Adaptive  Third Line of Defence: Adaptive Immunity Slower than innate in response due to priming. Antigen: substance capable of stimulating antibodies 3 main benefits:  Specific – particular target  Systemic – not restricted to local site  Memory - remembers http://trendland.com/chinese-swat-team/  Adaptive Immunity Humoral Adaptive B Lymphocytes Defense System Cell Mediated T Lymphocytes  Active and Passive Immunity Adaptive immunity can be either: Active (Active Acquired) Immunity is produced after either natural exposure to an antigen or after immunization Passive (Acquired) Immunity occurs when preformed antibodies or T lymphocytes are transferred from donor to recipient  Lymph nodes B and T Lymphocytes act as surveillance Lymph nodes are wide spread http://www.dreamstime.com/royalty-free-stock-photo-back-view- transparent-lymphatic-system-image26202865  Adaptive Immunity: Humoral Immunity Bone Marrow Humoral: Virus free in the fluids of our bodies Plasma cells secrete B lymphocytes antibodies Antibodies Memory Cells Plasma cells (Immunoglobulin) – Bind to antigens Memory cell prevents Antibodies future re-exposures  Humoral Immunity Antibody circulates in blood and binds to antigens on infectious agents Either directly inactivates microorganism or activates inflammatory mediators Antibodies are primarily responsible for protection Antigen and Antibody Complex  To Recognize and Respond An antigen is a molecule that reacts with antibodies or antigen receptors on B and T cells Most antigens are immunogenic Must be recognized by and bound to an antibody To Recognize and Respond: Immunoglobulins Immunoglobulin Purpose IgG -most abundant and crosses placenta IgA - Found in blood and body secretions IgM - Biggest in size and first to respond in primary response IgE - Least concentrated but specific to allergic responses and in the defense against parasitic infections IgD - Found in low concentrations Fig 7-9, p. 167, Power-Kean et al., (2023) Adaptive Immunity: Cell- Mediated Immunity T Lymphocytes Helper  Activates B cells, Cytotoxic T cells, NK cells, macrophages Cytotoxic (Killer)  Cell lysis Suppressors Th  Expressed as CD4 and T regulatory cells http://kstp.com/article/stories/s3111909.shtml  Adaptive Immunity: Cell- Mediated Immunity Bone Marrow Cellular: Virus infected cells T lymphocyte (matures in thymus) T cells activate lymphocytes and macrophages Helper T Cell Memory produced Suppressor T cell Cytotoxic T cellMemory Cells (Killer T cells)  Key Points to Remember Can you perform a full system assessment with knowledge of physiological landmarks and anatomy and physiology related to immunity and lab values? Explain the “why” associated with the immune system and connections to other systems Identify and apply concepts of alterations in immunity  Do you understand the pathophysiology, clinical manifestations and nursing assessment related to :  Fractures  Immunity  Inflammation