Inflammation Flashcards

1
Q

a non-specific, defensive process of the body to tissue damage.

A

inflammation

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2
Q

an attempt to dispose of microbes, toxins, or foreign material at the site of injury

A

inflammation

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3
Q

5 cardinal signs and symptoms:

A

a. redness (rubor)
b. pain (dolor)
c. heat (calor)
d. swelling (tumor)
e. loss of function (functio laesa)

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4
Q

• prime symptom of inflammation

A

Pain (Dolor)

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5
Q

• due to inflammation, joints and muscles might feel pain. In particular, the inflamed areas may
be sensitive to touch.

A

Pain (Dolor)

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6
Q

due to inflammation,there is more blood flow to the area.

A

Heat (Calor)

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7
Q

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.

A

Redness (Rubor)

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8
Q

the primary cause of swelling is accumulated fluid in the tissues or outside the blood vessel

A

Swelling (tumor)

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9
Q

the immobility may result from the pain that restrains movement or from severe swelling that keeps the movement in the area.

A

Loss of function (functio laesa)

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10
Q

subdivide into two classes; microbial and non-microbial ______________.

A

Exogenous inducers

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11
Q
  • 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
A

Microbial inducers

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12
Q

include allergens, toxic compounds, irritants, and foreign bodies that are too large to be digested or cause phagosomal damage in macrophages.

A

Non-Microbial

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13
Q

signals released by tissues that are either dead,damaged, malfunctioned,orstressed.Twolargegroups- infectiousfactorsandthenon-infectiousfactors.

A

Endogenous inducers

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14
Q

category includes bacteria,viruses, and other microorganisms.

A

Infectious factors

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15
Q

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.

A

Non-Infectious factors

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16
Q

A variety of chemical mediators from circulation system, inflammatory cells, and injured tissue actively contribute to and adjust the inflammatory response include

A

(1) vasoactive amines such as histamine and serotonin,
(2) peptide (e.g., bradykinin), and
(3) eicosanoids (e.g., thromboxanes, leukotrienes, and prostaglandins).

17
Q

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

A

Mediators

18
Q

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.

A

Histamine

19
Q

polypeptide formed from inactive kininogens, induce vasodilation and increased permeability and serve chemotactic agents for phagocytes.Eg.bradykinin

A

Kinins

20
Q

lipids especially those of the E series intensify the effects of histamine and kinins. Also stimulate the emigration of phagocytes through capillary walls.

A

Prostaglandins (PGs)

21
Q

produces by basophils and mast cells, caused increased permeability;function in adherence of phagocytes to pathogens and as chemotactic agents and attract pahgocytes.

A

Leukotrienes (LTs)

22
Q

stimulate histamine release, attract neutrophils by chemotaxis, and promote phagocytosis;some components also destroy bacteria.

A

Complement

23
Q

• 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.

A

Body remove inflammation w/o drugs

24
Q

• 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

A

Pharmacological Management

25
Q

• 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

A

Non- pharmacological management

26
Q

Redness

A

Rubor

27
Q

Pain

A

Dolor

28
Q

Heat

A

Calor

29
Q

swelling

A

tumor

30
Q

Loss of function

A

function laesa

31
Q

such as aspirin, ibuprofen, or naproxen

A

Nonsteroidal anti-inflammatory drugs (NSAIDs)

32
Q

such as prednisone

A

Corticosteroids

33
Q

such as hydroxychloroquine

A

Antimalarial medications

34
Q

including azathioprine, cyclophosphamide, leflunomide, methotrexate, and sulfasalazine.

A

Disease-modifying antirheumatic drugs (DMARDs)

35
Q

such as abtacept, adalimumab,
certolizumab, etanercept, infliximab, golimumab, rituximab, and tocilizumab

A

Biologic drugs