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NURS 516: Inflammation and Immunity, ↑ ↓ → - Coggle Diagram
NURS 516: Inflammation and Immunity
Protective Functions of Inflammation
Limiting scope of inflammatory process
Preparation of injury
Prevention of infection and further damage caused by invading microbes
Facilitate development of adaptive immunity
Plasma Protein Systems
Clotting
Prevent blood loss and provide a scaffold for healing
Key actions
Forms a fibrin clot
Works closely with platelets
Activated with tissue injury
Plasma proteins that stop bleeding
Kinin
Increase vascular permeability and cause vacsolation
Key actions
Produces bradykinin
Causes pain, swelling, and redness
↓ BP via vasodilation
Plasma proteins that mediate inflammation and pain
Complement
Kill pathogens and boost inflammation
Key actions
Opsonization
Tags pathogens for phagocytosis
Cell lysis
Punches holes in bacterial membranes
Inflammation
Attracts neutrophils and macrophages
A group of plasma proteins that enhance (complement) immune responses
Excessive/Ineffective Inflammation
Ineffective inflammation → development of chronic inflammation
Widespread, uncontrolled inflammation → systemic problems
Excessive inflammation → local tissue damage from compression
Acute Inflammation
Histamine
H2 receptor
H3 receptor
H1/H4 receptor
Types of Immunity
Active acquired
Body makes its own antibodies
Key points
Long-lasting
Takes time to develop
Immunologic memory
Immunity developed after exposure to an antigen
Examples
Getting sick and recovering
Vaccinations
Passive acquired
No immune response generated by the patient
Key points
Short-term
No memory
Immediate protection
Immunity from antibodies give to the person
Examples
Maternal antibodies (placenta, breast milk)
Immunoglobulin therapy
Tetanus immune globulin
Rabi
Innate (Natural)
Immunity you're born with
Immediate and non-specific
Key points
Ex: skin, mucous membranes, inflammation, fever, phagocytes (neutrophils, macrophages)
No memory → responds the same every time
First line of defense
Chronic Inflammation
Invasion/injury
Acute inflammation
Defective resolution OR Persistent invasion/injury
Continuation of inflammatory processes
Nonspecific proliferative chronic inflammation OR Granulomatous chronic inflammation
Chronic inflammatory disease
Resolution
Termination of inflammatory process
Hemeostasis/health
Clinical Signs
Heat
↑ Blood flow, ↑ extravasation
Pain
↑ Tissue swelling → ↑ pressure on pain receptors
Redness
↑ Blood flow to injured area
Limited mobility
Tissue swelling, guarding/avoidance of painful voluntary movement
Suppressed Immune Response
Primary immunodeficiency
Genetic or congenital defects in the immune system → compromised immunity from birth
Secondary immunodeficiency
Acquired immune system deficiencies (more common)
Present with development of unusual, recurrent and/or severe infections
Altered Immunity
Symptoms
Fever
Chronic or poor wound healing
Weight loss
Enlarged lymph nodes
Fatigue
Frequent and/or opportunistic infections
Pain
Allergic
Rhinorrhea
Cough
Sore throat
Watery eyes
Diagnostic tests
ESR
Serologic tests
CRP
CT, MRI, PET scan, colonoscopy
CBC
WBC with differential
Neutrophils - bands and segments
Autoimmunity
Self-directed immune responses (usually hypersensitivity mechanisms)
Inflammatory tissue damage
Examples
Systemic lupus erythematosus (SLE)
Sarcoidosis
Breakdown in tolerance to self-antigens
Hypersensitivity Reactions
Type II: Tissue-specific reactions
Target specific tissues or cells
Ex: transfusion reactions, transplant rejection, autoimmune hemolytic anemia
Type III: Immune complex mediated
Antibodies bind to antigens in blood or body fluids
Ex: Raynaud phenomenon, acute glomerulonephritis, celiac disease
Type I: IgE mediated
Reaction to allergens
Ex: allergic asthma, rhinitis, or conjunctivitis; hives; anaphylaxis
Type IV: Cell mediated
No antibodies involved
Ex: TB skin tests, poison ivy exposure
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