NURS 5315 UTA Exam 2 2026 Question and
Answer | Updated Review from Previously Tested
Questions | Grade 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
Answer | Updated Review from Previously Tested
Questions | Grade 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
