NURS 5315 UTA Exam 2 Complete
Questions and Answers | Verified | A+
• Mast cell -✓✓Cellular bags of granules located in loose connective tisssue close
to blood vessels. Activation initiates inflammatory process.
• Histamine -✓✓Causes vasodilation, increases vascular permeability, increases
blood flow to the site of injury- causes erythema and swelling.
• Cytokines -✓✓Soluble factors that contribute to the regulation of innate or
adaptive resistance by affecting other neighboring cells. Can be pro-inflammatory
or anti-inflammatory. Can react quickly or be more delayed.
• Leukotrines -✓✓Released when mast cells degranulate, prolong the inflammatory
process. Cause vasodilation, attract neutrophils, monocytes, and eosinophils.target
of inhibition for singular.
• Prostaglandins -✓✓Released when mast cells degranulate, are produced by the
arachidonic pathway. Cause vasodilation, platelet aggregation at site of injury,
pain, and fever.
• Chemotactic factors -✓✓Biochemical substance that attracts leukocyte to the site
of inflammation
• Neutrophils -✓✓Predominant leukocyte at work during the early stages of acute
inflammation
• Monocytes -✓✓Become macrophages when entering the tissue, responsible for
presenting antigens to the CD4 cell which triggers T-cell immunity and B-cell
immunity.
Releases additional cytokines IL1, IL6, TNF.
• Cytokine IL1 function -✓✓Causes fever, activates phagocytes & lymphocytes
and also increases the release of IL6a
• Cytokine IL6 function -✓✓Stimulates production of acute phase reactants and
promotes growth and stimulation of RBCs
, • Cytokine TNF function -✓✓Causes fever, increases synthesis of proinflammatory
proteins by liver, causes muscle wasting, induces thrombosis
• Cytokine growth factor function -✓✓Promotes production and maturation of
neutrophils
• Complement -✓✓Functions include bacterial lysis, vasodilation and increased
vascular permeability, triggers mast cell degranulation, chemotaxis, and
opsonization.
• Kinin -✓✓Converted to bradykinin which is responsible for pain and chemotaxis,
and it increases vascular permeability and vasodilation.
• Coagulation cascade -✓✓Factor XII activates kinin. Function is to form fibrin
mesh to stop bleeding and trap micro organisms.
• COX1 -✓✓Prostaglandin of arachidonic pathway. Provides gastroprotection,
platelet aggregation, fluid/electrolyte balance
• COX2 -✓✓Prostaglandin of arachidonic pathway. Responsible for pain, fever,
renal protection, tissue repair, reproduction development.
• COX2 inhibitors- clinical implications -✓✓Protect gastric mucosa- prevent ulcers
and bleeding. Removed from market r/t cardiac events except for Celebrex. Can
impair renal function , monitor labs.
• Arachidonic pathway purpose -✓✓Synthesis of prostaglandins
• Non-selective NSAIDS -✓✓Inhibit COX1 and COX2, risk for gastric ulceration,
GI bleeds, edema, renal impairment
• ASA -✓✓Blocks COX1 and COX2, also inhibits Thromboxane A2 and
prostaglandins
• Corticosteroids -✓✓Inhibit phospholipase A2, preventing formation of
prostaglandins, thromboxane A2, prostacyclin, and leukotrines
Questions and Answers | Verified | A+
• Mast cell -✓✓Cellular bags of granules located in loose connective tisssue close
to blood vessels. Activation initiates inflammatory process.
• Histamine -✓✓Causes vasodilation, increases vascular permeability, increases
blood flow to the site of injury- causes erythema and swelling.
• Cytokines -✓✓Soluble factors that contribute to the regulation of innate or
adaptive resistance by affecting other neighboring cells. Can be pro-inflammatory
or anti-inflammatory. Can react quickly or be more delayed.
• Leukotrines -✓✓Released when mast cells degranulate, prolong the inflammatory
process. Cause vasodilation, attract neutrophils, monocytes, and eosinophils.target
of inhibition for singular.
• Prostaglandins -✓✓Released when mast cells degranulate, are produced by the
arachidonic pathway. Cause vasodilation, platelet aggregation at site of injury,
pain, and fever.
• Chemotactic factors -✓✓Biochemical substance that attracts leukocyte to the site
of inflammation
• Neutrophils -✓✓Predominant leukocyte at work during the early stages of acute
inflammation
• Monocytes -✓✓Become macrophages when entering the tissue, responsible for
presenting antigens to the CD4 cell which triggers T-cell immunity and B-cell
immunity.
Releases additional cytokines IL1, IL6, TNF.
• Cytokine IL1 function -✓✓Causes fever, activates phagocytes & lymphocytes
and also increases the release of IL6a
• Cytokine IL6 function -✓✓Stimulates production of acute phase reactants and
promotes growth and stimulation of RBCs
, • Cytokine TNF function -✓✓Causes fever, increases synthesis of proinflammatory
proteins by liver, causes muscle wasting, induces thrombosis
• Cytokine growth factor function -✓✓Promotes production and maturation of
neutrophils
• Complement -✓✓Functions include bacterial lysis, vasodilation and increased
vascular permeability, triggers mast cell degranulation, chemotaxis, and
opsonization.
• Kinin -✓✓Converted to bradykinin which is responsible for pain and chemotaxis,
and it increases vascular permeability and vasodilation.
• Coagulation cascade -✓✓Factor XII activates kinin. Function is to form fibrin
mesh to stop bleeding and trap micro organisms.
• COX1 -✓✓Prostaglandin of arachidonic pathway. Provides gastroprotection,
platelet aggregation, fluid/electrolyte balance
• COX2 -✓✓Prostaglandin of arachidonic pathway. Responsible for pain, fever,
renal protection, tissue repair, reproduction development.
• COX2 inhibitors- clinical implications -✓✓Protect gastric mucosa- prevent ulcers
and bleeding. Removed from market r/t cardiac events except for Celebrex. Can
impair renal function , monitor labs.
• Arachidonic pathway purpose -✓✓Synthesis of prostaglandins
• Non-selective NSAIDS -✓✓Inhibit COX1 and COX2, risk for gastric ulceration,
GI bleeds, edema, renal impairment
• ASA -✓✓Blocks COX1 and COX2, also inhibits Thromboxane A2 and
prostaglandins
• Corticosteroids -✓✓Inhibit phospholipase A2, preventing formation of
prostaglandins, thromboxane A2, prostacyclin, and leukotrines
