1.
2 stages of acute inflammation: vascular
cellular
2.
Acute Inflammation: Chemical mediators at site of injury
Mediators enter blood
Produces systemic signs & symptoms
ACUTE PHASE RESPONSE
so overwhelming it can cause widespread acute inflammation that can lead to signs and symptoms throughout the body
3.
acute inflammation: Duration of minutes to days
Self-limited
Can overlap with chronic forms
4.
acute inflammation assessment: see changes in vital signs, redness, purulent drainage, localized edema, enlarged lymph-nodes
5.
Acute Phase Response: Total body involvement
Systemic inflammatory response (SIRS) (wide spread against suspected response; blood pressure increases and everything)
Excessive compensatory responses
6.
acute phase response: fever results in increased levels of interleukin 1
7.
acute phase response: fever anorexia
hypotension
increased HR
corticosteroid and ACTH release
8.
acute- inflammatory assessment: Physical assessment of involved area
lumph nodes- enlarged
vital signs (HR, BP, RR, Temp)
9.
an excess of prostoglandin in the area: pain is due to this
10.
arachidonic acid: this has two major pathways:
cyclooxygenase pathway
lipoxygenase pathway
11.
arachidonic acid: when cells die this is released and it causes toxic events in the patient
12.
Arachidonic Acid Increase: Lipoxygenase pathway
Cyclooxygenase pathway
13.
Arachidonic Acid Metabolites: Fatty acid found in cell membrane phospholipid
Starts many complex reactions
Leads to other inflammatory mediators
14.
arachidonic acid metabolites: excess amounts of oxygen free radicals stimulate excess release of this product
15.
Asprin: this inhibits thromboxane
helps prevent blood clotting in blood vessels
16.
Basophils: Increased with allergic reactions (due to histamine)
Release histamine & other chemical mediators
17.
C reactive protein: acute phase protein from liver
specific protein produced
widespread systemic infection
acute phase response from liver
18.
cell membrane: this has a phospholipid layer
19.
Cellular Stage: Phagocytic monocytes, granulocytes
Rapid release of chemical mediators
Result - Pain
20.
chemotactic: work with other systems
21.
chronic infection response: injured tissue chromosome changes in cells at site
microorganisms get in bone and joints
22.
Chronic Inflammation: Localized tissue infiltrated by macrophages, lymphocytes, fibroblasts
Fibroblast replicate in local area
Scar tissue forms
23.
Chronic inflammation: Durations of days to months to years
Self-promoting
Can overlap with acute forms
24.
chronic inflammation: Microorganisms
25.
chronic inflammation- injured tissue: Fracture site
Degenerative joint disease
26.
chronic inflammation- Non-biodegradable particles: Asbestos, talc, sutures
27.
clotting: promotes and prevents
28.
Cyclooxygenase pathway: *Prostaglandins
Platelet aggregation
Vasoconstriction
RX: Prostaglandin inhibitor - Aspirin, NSAIDS
29.
cyclooxygenase pathway: two pathways are
prostaglandin
thromboxane
30.
cytokines: this is a specific type of white blood cell
31.
endothelial cells: release many substances including vaso-dilators and vaso-constrictors
32.
endothelial cells: adhension molecules
cytokines
eicosanoids
chemokines
oxygen radicals
33.
Eosinophils: Allergic reactions
Parasite infestations (parcoite strongolitis)
Control release of specific mediators
34.
erythrocyte sedimentation rate: called ESR or sed rate
if elevated it indicates there is an inflammation somewhere in the body. NONSPECIFIC
35.
fibroblasts: immature cells deposited in site = scar tissue
growth of abnormal tissue
inhibits normal function over a period of time
36.
Histamine: loosing fluid
blood pressure drops
give antihistamines early because not very active later
decreased blood pressure equals profound vasodialtion, heart rate goes up and you have increased respiration's
37.
Histamine: Found in mast cells, basophils, platelets
Among 1st mediators released
Profound vasodilation
Increased capillary permeability
RX: Antihistamines
38.
infection or inflammation present: total white blood cell count is elevated this indicates that there is an
39.
Inflammation: Immediate reaction to tissue injury, before total-body immune response
Sequential localized defense response
Coordinated vascular-cellular effort to neutralize injury & promote healing
40.
Inflammation - Etiology: infection
injury
ischemia
41.
Inflammatory Mediators: Histamine
Proteases
Cytokines
Platelet-activating factor
Arachidonic acid metabolites
42.
inflammatory mediators key point: any time tissue damage occurs inflammatory mediators are immediately activated. The degree released depends on infection response.
43.
inflammatory response phases: endothelial cells
neutrophils
acute phase response
44.
injury: Trauma event
Surgery
45.
Injury
Inflammation
Immune reaction
Tissue healing: this is the predictable physiology of the injury and healing process
46.
Ischemia: Inadequate blood supply
Oxygen
Nutrients
47.
Laboratory Data: 1)Total White blood cell count (WBC)
2)Differential
Neutrophils
Eosinophils
Basophils
48.
Lipoxygenase pathway: causes contraction of smooth muscles (bronchi-oles of lungs)
constriction of airway
breathing will decrease
decreased permeability of micro-vascular (capillary) vessel walls (become more porous).
fluid inside capillaries leak out much easier (capillaries are responsible for gas exchange)
49.
Lipoxygenase pathway: * Leukotrienes
Bronchial constriction
Venule permeability
RX: Leukotriene inhibitor (Singulair ®)
50.
Mast Cells: Smooth mucosal surfaces
Similar to basophil actions
Release histamine
Profound vasodilation
Release Immunoglobulin E
51.
mast cells: when antigen provoke reaction mast cells are turned on rapidly. there is a sudden release of histamine that causes profound vasodilation. Decreased blood pressure ( hypotension) and increased immunoglobin E.
52.
Monocyte-macrophage system: Activates before widespread immune response
53.
Neutrophils: 1st to release at injury site
Increased with bacterial infections
54.
neutrophils: these are the first white blood cells activated
55.
neutrophils: aggregation
priming
56.
Numerous acute & chronic health alterations r/t INFLAMMATION: Asthma
Rheumatoid Arthritis
Alzheimer Disease
Atherosclerosis
57.
pain relievers: this block the activity of prostologlandin
58.
platelets: these are responsible for clotting
59.
prostaglandin: this induces vasodilation and bronchoconstriction inhibits inflammatory cell function
cause pain in tissue
60.
prostaloglandin: chemical mediator goes quickly to injured area. Gives coating to localized tissue but it causes pain. If there is an injury or would prostologlandin migrates to that area.
61.
Redness
Swelling
Heat
Pain
Functional decrease or loss: these are signs and symptoms of external inflammation
62.
systemic lab tests: erythrocyte sedimentation rate
C reactive protein
WBC and idfferential
63.
T cells: this type of cell tries to kill bacteria
64.
thromboxane (asprin, NSAIDS): vasoconstriction
bronchoconstriction
promotes platelet function
contributes to constriction in blood vessels and smooth muscles
stimulates clumption of platelets ( response can be negative for patient)
65.
tissue damage: this occurs in excess
66.
vascular: try to limit the amount of material from the external environment
rapid vasodilation of blood vessels so the site quickly gets red and inflamed. Blood gets in the area and carries white blood cells and protein. Redness and swelling try to carry cells for healing.
cellular debre trapped at the site= exudate
excess fluid and blood gathered at site is hyperemia and escemia
67.
Vascular Stage: Immediate vasoconstriction
Rapid vasodilation
Redness & heat
Exudate forms & area swells
Result -Hyperemia
68.
Vasoactive
Chemotactic
Clotting
Tissue damage: signs and symptoms related to chemical mediators
69.
vasocative: dilation or constriction
70.
WBC and differential: indicates inflammation/ infection
