Inflammatory Response Flashcards
Inflammation
Destroy infectious and injurious organisms
Block site of infection to limit damage
Stimulates the immune response (3-4 days)
Stimulates tissue healing
Inflammationcharacteristics of IR
Occurs in vascular tissues Immediate anywhere between minutes to a few hours Nonspecific No memory Self limitating
Cytokines and mediators
INflammatory chemicals that can affect anything, host and non-host
Cells of IR
WBC’s
Endothelial cells
And platelets
Chemicals of IR
Cytokines, vasoactive inflammatory mediators, and anti-inflammatory mediators
Use them to communicate between WBC’s
Plasma protein systems IR
Complement, clotting, and kinin systems
Activation of IR
Trauma to cell membrane
Ex.) hypoxic injury, chemical injury, thermal injury, radiation, infection, immmune injury
*****Mast cells
Cells of IR
Most important activator Of the local IR
Location: tissue not blood
Activation of mast cells
Local cellular injury
Bacterial endotoxin
Complement proteins
Immunologic factors
Function of mast cells
Degranulation
Release of preformed chemicals such as: histamine
Synthesis of mediators: arachadonic acid
Histamine:
Major chemical
Vasodilation
Increased capillary permeability
Non-vascular smooth muscle contraction
Vasodilation
Increases blood flow
Quick and temporary vasoconstriction
Caused by relaxing of vascular smooth muscle cells in blood vessels
Increased capillary permeability
Plasma, proteins, etc… leave capillaries to go to the sight of infection
Non-vascular smooth muscle contraction
When they are not in the blood vessels GI tract (cramping from an infection in stomach causing you to throw up) Bronchi constriction
Synthesis of mediators
AA metabolites
- leukotrienes
- prostaglandins
Leukotrienes
Same as a histamine actions
Synthesized in mast cells
Released near capillaries would cause increase of cap permeability
Released in lungs would cause vasoconstriction due to it not being a blood vessel
Benadryl
Prostaglandins
Histamine and pain
Synthesized in mast cells
Chemical that causes pain
Counteracted by aspirin, ibuprofen, and Tylenol
Basophils
Similar to mast cells and they release histamine and leukotrienes into the blood stream
Also releases heparin(blood thinner)
Neutrophils/bands
Arrive during acute phases of inflammation (6-12 hours)
One of the first WBC’s to the sight
Phagocytosis of debris and infection
Eosinophils
Release chemicals that control inflammation
Histamine is inactivated by histaminase
Phagocytosis of parasites
Involved in allergic responses
High eosinophil countr
High count then that might mean that there is a parasitic infection or and allergic reaction happening
Monocytes/macrophages
Released into bloodstream by the bone marrow as a monocytes
Once it has reached the infected tissue then it matures to a macrophage
They don’t side right away can stay for long periods of time to fight the next infection
Phagocytosis of bacteria and debris
Complement system
10% of proteins Vasodilation Opsonizatin Chemotaxis Cell lysis
Opsonization
Bound onto outside of bacteria so that it is attractive to the phagocyte. Without it there will be no recognition
Chemotaxis
The release of chemicals that attract other histamine circling, chemical road map
Clotting system
Produces fibrin
Fibrin
Forms a meshwork to stop bleeding
Limits infection
Forms framework for scar tissue formation
Heat and redness
The blood flow (vasodilation) is causing the heat and redness
How close it is to the surface will determine the heat and redness
Pain
Prostaglandins released by the mast cell cause the pain
Edema/swelling
Means a buildup of water outside of the cells
Less oxygen which can cause hypoxic injury
Ice to try and stop edema ( less blood circulation)
Systematic manifestations of acute inflammation
Fever
Fever
Caused by bacterial endotoxin, interleukins, prostaglandins, etc…
Mainly gram - bacteria
Mechanisms of a fever
Increased cell metabolism, shivering, vasoconstriction of arterioles in skin
Purpose of a fever
Disrupt metabolism of temperature sensitive bacteria, increased WBC activity
Harmful effects of a fever
Temps above >41 degrees Celsius or 105 degrees Fahrenheit causes cell dysfunction
Leukocytes
Increased in total WBC count
Leuko: means white
Acute inflammation
Increase in neutrophil count
Increase in bands (immature neutrophils)
Chronic inflammation
Increase in monocytes count
Talks to bone marrow to increase the neutrophils due to a chronic infection or chronic inflammation
Mast cells and macrophages
Talk to the bone marrow to produce mast cells and are not in the WBC count due to not circulating in blood and are only in tissues
Increased circulating plasma proteins
Acute phase reactants
Released by liver in response to interleukins
Released to the bloodstream
C-reactive protein
Good marker for inflammation, detects early onset of cardiovascular disease (CRP)
Vascular response to systemic or severe inflammation
Occurs if vasoactive inflammatory mediators circulate systematicallly.
Causes: bloodstream infection, localized infection, massive trauma
Hypotension (VR)
Low blood pressure
Systemic edema
Fluid in ECF
Hypovolemia
They make look full of fluid but their might be low blood pressure because they are losing volume to the tissues
Immune response
Can cause cell injury and stimulate pathological inflammation
Allergic responses and hypersensitive reactions
Respond to tissue grafts
Can cause autoimmune disease
Cells of Immune response
B lymphocytes: produce antibodies
t lymphocytes
Inflammatory vs. immune
Inflammatory response is rapid, nonspecific, no memory, involves many cells.
Immune response slower, specific, memory, lymphocytes and antibodies, can be induced by vaccination
Antigen
A molecule that is recognized by lymphocytes and reacts with antibodies
Foreign antigen
Viruses
Bacteria
Pollens and allergens
Food or drugs
Self-antigen
Human leukocyte antigen RBC antigen (A, B and Rh antigen) Platenlets dont have antigen
HLA
Self surface proteins distinguishing self from non-self
Present on all cell membrane except RBC’s and platelets
Major histocompatability complex; genomic region that directs synthesis of HLA antigen
B lymphocyte response
Also called the humoral response
Mature b lymphocytes (plasma cells) produce immunoglobulins (antibodies)
Antibody
Immunoglobulin that have specificity for a particular antigen
Antibody classes
IgM
IgG
IgA
IgE
IgM
General antibody, highest tigers present during primary immune response
IgG
General antibody, highest tigers present during secondary immune response
IgA
Performed antibody found in sweat, saliva, tears, and breast milk
IgE
Antibody produced during allergic responses
Type 1 hypersensitivity reactions
Function of antibodies
Begins with antigen binding to form antigen-antibody complexes
Neutralize bacteria and viruses
Promotes phagocytosis of bacteria and viruses via opsonization
Activate the compliment cascade
Primary and secondary immune response
Confer active acquired immunity
Primary
Antigenic challenge with production of measurable immunoglobins, primarily IgM, after a latent period of about 5 days
Secondary
A second antigen challenge with more rapid and larger production of immunoglobins, primarily IgG
T lymphocyte response
Cellular response
Cytosine T cells (Tc cells)
Attack antigen directly and kill cells bearing foreign antigen
Helper T cells (Th cells)
Required to activate the primary B and T lymphocyte response
Memory T cells (Tm cells)
Induce secondary immune response
Regulatory T cell (Treg)
Develop in the thymus or peripheral tissues and suppress B cell and T cell activation
Vaccination
A process of stimulating a protective immune response against microbes through exposure to nonpathogenic forms or components of the microbes
Inactivated
Virulent microbes are killed to abolish their infectivity and pathogenicity, yet still retain their immunogenicity. May not be safe for immunocompromised individuals.
Ex) measles, mumps, rubella, varicella, flu, oral polio, rabies
Toxoid
Vaccine is made from inactivated bacterial toxin
Ex) tetanus toxoid, diphtheria toxoid, rattlesnake venom
