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NURS 5315 UTA 2025 Exam 2 Questions & Answers

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HIV EIA (3rd generation immunoassay) - ANSWER 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 Mast cell - ANSWER Cellular bags of granules located in loose connective tisssue close to blood vessels. Activation initiates inflammatory process. Histamine - ANSWER Causes vasodilation, increases vascular permeability, increases blood flow to the site of injury- causes erythema and swelling. Cytokines - ANSWER 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 - ANSWER Released when mast cells degranulate, prolong the inflammatory process. Cause vasodilation, attract neutrophils, monocytes, and t of inhibition for singular. Prostaglandins - ANSWER Released when mast cells degranulate, are produced by the arachidonic pathway. Cause vasodilation, platelet aggregation at site of injury, pain, and fever. Chemotactic factors - ANSWER Biochemical substance that attracts leukocyte to the site of inflammation Neutrophils - ANSWER Predominant leukocyte at work during the early stages of acute inflammation Monocytes

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Publié le
10 octobre 2025
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Écrit en
2025/2026
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NURS 5315 UTA 2025 Exam 2
Questions & Answers
HIV EIA (3rd generation immunoassay) - ANSWER: Can use urine, saliva, or serum (most
accurate). Need to wait 12 weeks post-exposure to detect antibodies. >99% accurate.

4th generation immunoassay - ANSWER: "Gold standard"; detects both antibodies and
p24 antigen, can test 10 days post-exposure.

Mast cell - ANSWER: Cellular bags of granules in loose connective tissue near blood
vessels; activation initiates inflammation.

Histamine - ANSWER: Causes vasodilation, increases vascular permeability and blood flow
to injury site causing erythema and swelling.

Cytokines - ANSWER: Soluble factors regulating innate or adaptive immunity; can be pro-
or anti-inflammatory; act quickly or delayed.

Leukotrienes - ANSWER: Released during mast cell degranulation; prolong inflammation,
cause vasodilation, and attract neutrophils and monocytes.

Prostaglandins - ANSWER: Produced in arachidonic acid pathway during mast cell
degranulation; cause vasodilation, platelet aggregation, pain, fever.

Chemotactic factors - ANSWER: Chemicals attracting leukocytes to inflammation sites.

Neutrophils - ANSWER: Main leukocyte in early acute inflammation.

Monocytes - ANSWER: Circulate in blood, mature into macrophages in tissue; present
antigens to CD4 T cells and release cytokines IL-1, IL-6, TNF.

IL-1 function - ANSWER: Induces fever, activates phagocytes and lymphocytes, promotes
IL-6 release.

IL-6 function - ANSWER: Stimulates acute phase reactants, promotes RBC growth.

Causes of thrombocytopenia - ANSWER: Post-op hemodilution, splenomegaly, HIV
infection, bone marrow failure, hemolysis, multiple medications.

,Primary Immune Thrombocytopenic Purpura (ITP) - ANSWER: Autoimmune platelet
destruction; symptoms include petechiae, purpura, easy bruising, epistaxis, gingival
bleeding.

Heparin-induced thrombocytopenia (HIT) - ANSWER: Immune platelet destruction
triggered by heparin; Type 1 mild and transient, Type 2 severe with platelet drop 5-10 days
post heparin.

Hemophilia A - ANSWER: X-linked recessive; factor VIII deficiency; symptoms include joint
and GI bleeding; prolonged PTT.

Hemophilia B - ANSWER: X-linked recessive; factor IX deficiency; symptoms similar to
Hemophilia A; also called Christmas disease.

Disseminated Intravascular Coagulation (DIC) - ANSWER: Systemic coagulation
activation causing microthrombi and bleeding; triggers include sepsis, malignancy; labs
show prolonged PT/PTT, elevated D-dimer.

Complement system - ANSWER: Group of plasma proteins that opsonize pathogens,
promote inflammation, and form membrane attack complex.

Acute phase reactants - ANSWER: Proteins such as CRP, fibrinogen, and serum amyloid A
produced by liver during inflammation stimulated by IL-6.

Macrophage function - ANSWER: Phagocytosis, antigen presentation, cytokine secretion
initiating adaptive immunity.

T-lymphocytes (T cells) - ANSWER: Critical in cell-mediated immunity; differentiate into
CD4+ helper and CD8+ cytotoxic cells.

CD4+ T cells - ANSWER: Helper T cells that activate B cells, cytotoxic T cells, and
macrophages.

CD8+ T cells - ANSWER: Cytotoxic T cells that kill virus-infected and tumor cells.

B-lymphocytes (B cells) - ANSWER: Produce antibodies in adaptive humoral immunity.

Antigen-presenting cells (APCs) - ANSWER: Cells like macrophages and dendritic cells
that process and present antigens to T cells.

Humoral immunity - ANSWER: Immunity mediated by antibodies produced by B cells.

, Cell-mediated immunity - ANSWER: Immunity mediated by T cells directly acting on
infected or abnormal cells.

P24 antigen in HIV - ANSWER: Viral core protein detectable early in infection, before
antibodies develop.

Window period in HIV testing - ANSWER: Time between HIV infection and detectable
antibody or antigen levels; shorter with 4th gen tests.

Acute HIV syndrome symptoms - ANSWER: Fever, rash, lymphadenopathy, sore throat,
myalgia occurring 2-4 weeks post-infection.

Chronic HIV infection - ANSWER: Asymptomatic phase lasting years, gradual CD4 decline.

AIDS-defining illness - ANSWER: Opportunistic infections and cancers occurring with CD4
<200 cells/mm³.

Pneumocystis jiroveci pneumonia (PCP) - ANSWER: Common opportunistic infection in
AIDS causing pneumonia.

Mycobacterium avium complex (MAC) - ANSWER: Opportunistic bacterial infection in
AIDS affecting multiple organs.

Cytomegalovirus (CMV) - ANSWER: Opportunistic viral infection causing retinitis and
colitis in AIDS.

CD4 count significance - ANSWER: Indicator of immune function and HIV disease
progression.

Viral load in HIV - ANSWER: Measurement of HIV RNA to assess infection activity.

Antiretroviral therapy (ART) - ANSWER: Combination drugs that inhibit HIV replication;
reduces morbidity and mortality.

Classes of ART drugs - ANSWER: NRTIs, NNRTIs, PIs, integrase inhibitors, fusion inhibitors,
CCR5 antagonists.

HAART - ANSWER: Highly active antiretroviral therapy; multi-drug regimen.

Immune reconstitution inflammatory syndrome (IRIS) - ANSWER: Paradoxical worsening
of infections after starting ART due to immune recovery.
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