Inflammation Flashcards
a non-specific, defensive process of the body to tissue damage.
inflammation
an attempt to dispose of microbes, toxins, or foreign material at the site of injury
inflammation
5 cardinal signs and symptoms:
a. redness (rubor)
b. pain (dolor)
c. heat (calor)
d. swelling (tumor)
e. loss of function (functio laesa)
• prime symptom of inflammation
Pain (Dolor)
• due to inflammation, joints and muscles might feel pain. In particular, the inflamed areas may
be sensitive to touch.
Pain (Dolor)
due to inflammation,there is more blood flow to the area.
Heat (Calor)
as the blood flow more to the inflamed area, the blood vessels of the area will be filled with more blood than normal. Due to which the inflamed area will appear red in the color.
Redness (Rubor)
the primary cause of swelling is accumulated fluid in the tissues or outside the blood vessel
Swelling (tumor)
the immobility may result from the pain that restrains movement or from severe swelling that keeps the movement in the area.
Loss of function (functio laesa)
subdivide into two classes; microbial and non-microbial ______________.
Exogenous inducers
- two classes of ________________.
• pathogen-associated molecular patter ns (PAMPs) which are carried by all microorganisms
• virulence factors- trigger the inflammatory response due to the effects of their activity.
• Example: enzymatic activity produced by helminths and exotoxins produced by bacteria
Microbial inducers
include allergens, toxic compounds, irritants, and foreign bodies that are too large to be digested or cause phagosomal damage in macrophages.
Non-Microbial
signals released by tissues that are either dead,damaged, malfunctioned,orstressed.Twolargegroups- infectiousfactorsandthenon-infectiousfactors.
Endogenous inducers
category includes bacteria,viruses, and other microorganisms.
Infectious factors
due to physical injuries such as frostbite,burn, physical injury, foreign b o d i e s , t r a u m a , i o n i z i n g r a d i a t i o n , c h e m i c a l c o m p o u n d s s u c h a s g l u c o s e , f a t t y a c i d s , t ox i n s , a l c o h o l , and chemical irritants such as nickel and other trace elements. There are also biological inducers, including signals released by damaged cells and physiological due to excitement.
Non-Infectious factors
A variety of chemical mediators from circulation system, inflammatory cells, and injured tissue actively contribute to and adjust the inflammatory response include
(1) vasoactive amines such as histamine and serotonin,
(2) peptide (e.g., bradykinin), and
(3) eicosanoids (e.g., thromboxanes, leukotrienes, and prostaglandins).
Mechanism of inflammation represents a chain of organized, dynamic responses including both cellular and vascular events with specific humoral secretions. These pathways involve changing physical location of white blood cells (monocytes, basophils, eosinophils, and neutrophils), plasma, and fluids at inflamed site. A group of secreted mediators and other signaling molecules are released by immune defense cells principally in the mechanism which can contribute in the event of inflammation
Mediators
mast cells in connective tissue and basophils and platelets in blood release histamine.Neutrophils and macrophages attracted to the site of injury also stimulate the release of histamine, which causes vasodilation and increased permeability of blood vessels.
Histamine
polypeptide formed from inactive kininogens, induce vasodilation and increased permeability and serve chemotactic agents for phagocytes.Eg.bradykinin
Kinins
lipids especially those of the E series intensify the effects of histamine and kinins. Also stimulate the emigration of phagocytes through capillary walls.
Prostaglandins (PGs)
produces by basophils and mast cells, caused increased permeability;function in adherence of phagocytes to pathogens and as chemotactic agents and attract pahgocytes.
Leukotrienes (LTs)
stimulate histamine release, attract neutrophils by chemotaxis, and promote phagocytosis;some components also destroy bacteria.
Complement
• as inflammatory response continues, monocytes follow the neutrophils in infected areas.
• monocytes transforms into wandering macrophages, they are large enough to engulf damaged tissue, worn-out neutrophils, and invading microbes. Eventually, macrophages also die.
• after few days, pocket of dead phagocytes and damaged tissue forms (pus). This will continue until the infection subsides.
• pus reaches the surface of the body or drains into an internal cavity and is dispersed.
• on other occasions the pus remains even after the infection is terminated. In this case, the pus is gradually destroyed over a period of days and is absorbed.
Body remove inflammation w/o drugs
• Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, or naproxen
• Corticosteroids (such as prednisone)
• Antimalarial medications (such as hydroxychloroquine)
• Disease-modifying antirheumatic drugs (DMARDs),
including azathioprine, cyclophosphamide, leflunomide, methotrexate, and sulfasalazine.
• Biologic drugs such as abtacept, adalimumab,
certolizumab, etanercept, infliximab, golimumab, rituximab, and tocilizumab
Pharmacological Management
• Home remedies
• Quit smoking
• Limit alcohol
• Keep a healthy weight
• Manage stress
• Get regular physical activity
• Supplements such as omega-3 fatty acids,white willow bark,curcumin, green tea,
or capsaicin.Magnesium and vitamins B6,C, D, and E also have some anti-inflammatory effects. Talk with your doctor before starting any supplement.
• Surgery
Non- pharmacological management
Redness
Rubor
Pain
Dolor
Heat
Calor
swelling
tumor
Loss of function
function laesa
such as aspirin, ibuprofen, or naproxen
Nonsteroidal anti-inflammatory drugs (NSAIDs)
such as prednisone
Corticosteroids
such as hydroxychloroquine
Antimalarial medications
including azathioprine, cyclophosphamide, leflunomide, methotrexate, and sulfasalazine.
Disease-modifying antirheumatic drugs (DMARDs)
such as abtacept, adalimumab,
certolizumab, etanercept, infliximab, golimumab, rituximab, and tocilizumab
Biologic drugs
