NURS 5315 UTA Exam 2 Questions and
Answers
1. HIV EIA (3rd generation immunoassay): can use urine, saliva, or serum (most
accurate), need to wait until 12 weeks post exposure to see antibodies, >99% accurate
4th generation immunoassay- "gold standard"
measures P24 antigen
can test 10 days post exposure
2. Mast cell: Cellular bags of granules located in loose connective tissue close to blood vessels.
Activation initiates inflammatory process.
3. Histamine: Causes vasodilation, increases vascular permeability, increases blood flow to the
site of injury- causes erythema and swelling.
4. 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.
5. Leukotrines: Released when mast cells degranulate, prolong the inflammatory process. Cause
vasodilation, attract neutrophils, monocytes, and eosinophils.target of inhibition for singular.
6. Prostaglandins: Released when mast cells degranulate, are produced by the arachidonic
,pathway. Cause vasodilation, platelet aggregation at site of injury, pain, and fever.
7. Chemotactic factors: Biochemical substance that attracts leukocyte to the site of
inflammation
8. Neutrophils: Predominant leukocyte at work during the early stages of acute inflammation
9. 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.
10. Cytokine IL1 function: Causes fever, activates phagocytes & lymphocytes and also
increases the release of IL6a
11. Cytokine IL6 function: Stimulates production of acute phase reactants and
promotes growth and stimulation of RBCs
12. Cytokine TNF function: Causes fever, increases synthesis of proinflammatory
proteins by liver, causes muscle wasting, induces thrombosis
13. Cytokine growth factor function: Promotes production and maturation of
neutrophils
14. Complement: Functions include bacterial lysis, vasodilation and increased vascular
, permeability, triggers mast cell degranulation, chemotaxis, and opsonization.
15. Kinin: Converted to bradykinin which is responsible for pain and chemotaxis, and it
increases vascular perme- ability and vasodilation.
16. Coagulation cascade: Factor XII activates kinin. Function is to form fibrin mesh to stop
bleeding and trap micro organisms.
17. COX1: Prostaglandin of arachidonic pathway. Provides gastroprotection, platelet aggregation,
fluid/electrolyte balance
18. COX2: Prostaglandin of arachidonic pathway. Responsible for pain, fever, renal protection,
tissue repair, repro- duction development.
19. 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.
20. Arachidonic pathway purpose: Synthesis of prostaglandins
21. Non-selective NSAIDS: Inhibit COX1 and COX2, risk for gastric ulceration, GI
bleeds, edema, renal impairment
22. ASA: Blocks COX1 and COX2, also inhibits Thromboxane A2 and prostaglandins
Answers
1. HIV EIA (3rd generation immunoassay): can use urine, saliva, or serum (most
accurate), need to wait until 12 weeks post exposure to see antibodies, >99% accurate
4th generation immunoassay- "gold standard"
measures P24 antigen
can test 10 days post exposure
2. Mast cell: Cellular bags of granules located in loose connective tissue close to blood vessels.
Activation initiates inflammatory process.
3. Histamine: Causes vasodilation, increases vascular permeability, increases blood flow to the
site of injury- causes erythema and swelling.
4. 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.
5. Leukotrines: Released when mast cells degranulate, prolong the inflammatory process. Cause
vasodilation, attract neutrophils, monocytes, and eosinophils.target of inhibition for singular.
6. Prostaglandins: Released when mast cells degranulate, are produced by the arachidonic
,pathway. Cause vasodilation, platelet aggregation at site of injury, pain, and fever.
7. Chemotactic factors: Biochemical substance that attracts leukocyte to the site of
inflammation
8. Neutrophils: Predominant leukocyte at work during the early stages of acute inflammation
9. 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.
10. Cytokine IL1 function: Causes fever, activates phagocytes & lymphocytes and also
increases the release of IL6a
11. Cytokine IL6 function: Stimulates production of acute phase reactants and
promotes growth and stimulation of RBCs
12. Cytokine TNF function: Causes fever, increases synthesis of proinflammatory
proteins by liver, causes muscle wasting, induces thrombosis
13. Cytokine growth factor function: Promotes production and maturation of
neutrophils
14. Complement: Functions include bacterial lysis, vasodilation and increased vascular
, permeability, triggers mast cell degranulation, chemotaxis, and opsonization.
15. Kinin: Converted to bradykinin which is responsible for pain and chemotaxis, and it
increases vascular perme- ability and vasodilation.
16. Coagulation cascade: Factor XII activates kinin. Function is to form fibrin mesh to stop
bleeding and trap micro organisms.
17. COX1: Prostaglandin of arachidonic pathway. Provides gastroprotection, platelet aggregation,
fluid/electrolyte balance
18. COX2: Prostaglandin of arachidonic pathway. Responsible for pain, fever, renal protection,
tissue repair, repro- duction development.
19. 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.
20. Arachidonic pathway purpose: Synthesis of prostaglandins
21. Non-selective NSAIDS: Inhibit COX1 and COX2, risk for gastric ulceration, GI
bleeds, edema, renal impairment
22. ASA: Blocks COX1 and COX2, also inhibits Thromboxane A2 and prostaglandins
