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NURS 350 Exam 2 Questions And Answers (Guaranteed A+)

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©FYNDLAY EXAM SOLUTIONS 2024/2025 ALL RIGHTS RESERVED. 1 | P a g e NURS 350 Exam 2 Questions And Answers (Guaranteed A+) 1. Identify mechanisms used by pathogens to survive defenses of the body. - answero Infectious disease: infection spread from person to person o Pathogens successfully cause disease because they" Compete with normal flora Produce toxins Produce enzymes to • Avoid phagocytosis, opsonization, destroy connective tissues Avoid lysis • Stop complement cascade by degrading C3b Paralyze ciliary activity 2. Describe the different factors for infection. - answero Communicability Ability to spread disease from one to others o Infectivity Ability of pathogen to invade and multiply in host o Virulence Capacity of pathogen to cause severe disease o Pathogenicity Ability of an agent to produce diseae o Portal of entry Route by which pathogenic microorganism infects host ©FYNDLAY EXAM SOLUTIONS 2024/2025 ALL RIGHTS RESERVED. 2 | P a g e o Toxigenicity Ability to produce soluble toxins or endotoxins, factors that influence pathogen's virulence 3. Understand the significance of bacterial toxins. - answero Toxin production Exotoxins (released from living microbes) • Enzymes that damage host cell plasma membranes or can inactivate enzymes critical to protein synthesis Endotoxins (released from lysed gram-negative bacteria: LPS) • Activate inflammatory response and produce fever 4. Explain bacteremia or septicemia. - answero Bacteremia (presence) or septicemia (growth) Bacteria present in blood Failure of the body's defense mechanisms Caused by gram-negative bacteria Endotoxins released in blood activate complement and clotting systems • Capillary permeability causes plasma to escape into surrounding tissues producing widespread hypotension; severe cases= cardiovascular shock Gram negative has LPS and thinner peptidoglycan Gram positive has thicker peptidoglycan 5. Using HIV as an example, explain how viruses infect cells (be able to describe event steps and key players and what occurs). - answer• Human Immunodeficiency Virus (HIV) o Structure Gp120 proteing binds to the CD4 molecule found primarily on surface of helper T cells • Destroys CD4 Th cells o Reverses CD4: CD8 ratio o Coreceptors CXCR4 and CCR5 • Strains can be selective for these receptors; influence the tropism of the target cells ©FYNDLAY EXAM SOLUTIONS 2024/2025 ALL RIGHTS RESERVED. 3 | P a g e Steps of how HIV infects cells: 1. virion binds to CD 4 and chemokine receptors n of HIV membrane with host cell membrane entry of viral genome into cytoplasm and gp41 enters cells -RNA-> DNA 3. integration of provirus into host cell genome -DNA->mRNA 4.Cytokine activation of cell; transcription of HIV genome; transport of viral RNAs to cytoplasm -protease trim virions 5. synthesis of HIV proteins; assembly of virion core 6. Budding and release of mature virion 7. New HIV virion 6. Identify the key immunologic finding in those with HIV infection/AIDS. - answerTh cells < 200 cells/mm^3 diagnositc for AIDS CD4 T Cells (normal= 800-1000/mm^3) declines to <400/mm^3 8. Identify opportunistic infections and malignancies associated with AIDS. - answer-herpes -varicella -mycobacterium (Tb) -fungi -pneumocystis -lymphoma -cancer (Kaposi sarcoma) 9. Identify the phases in HIV infection to AIDS progression and the characteristics of each phase. - answero Early: lasts about 1-6 weeks clinical latency; active proliferation in lymph nodes headaches, fever, fatigue, non-specific, flu-like

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NURS 350 Exam 2 Questions And Answers
(Guaranteed A+)

1. Identify mechanisms used by pathogens to survive defenses of the body. - answer✔o
Infectious disease: infection spread from person to person
o Pathogens successfully cause disease because they"
Compete with normal flora
Produce toxins
Produce enzymes to
• Avoid phagocytosis, opsonization, destroy connective tissues
Avoid lysis
• Stop complement cascade by degrading C3b
Paralyze ciliary activity

2. Describe the different factors for infection. - answer✔o Communicability
Ability to spread disease from one to others
o Infectivity
Ability of pathogen to invade and multiply in host
o Virulence
Capacity of pathogen to cause severe disease
o Pathogenicity
Ability of an agent to produce diseae
o Portal of entry
Route by which pathogenic microorganism infects host

1|Page

, ©FYNDLAY EXAM SOLUTIONS 2024/2025

ALL RIGHTS RESERVED.
o Toxigenicity
Ability to produce soluble toxins or endotoxins, factors that influence pathogen's virulence

3. Understand the significance of bacterial toxins. - answer✔o Toxin production
Exotoxins (released from living microbes)
• Enzymes that damage host cell plasma membranes or can inactivate enzymes critical to
protein synthesis
Endotoxins (released from lysed gram-negative bacteria: LPS)
• Activate inflammatory response and produce fever

4. Explain bacteremia or septicemia. - answer✔o Bacteremia (presence) or septicemia (growth)
Bacteria present in blood
Failure of the body's defense mechanisms
Caused by gram-negative bacteria
Endotoxins released in blood activate complement and clotting systems
• Capillary permeability causes plasma to escape into surrounding tissues producing
widespread hypotension; severe cases= cardiovascular shock
Gram negative has LPS and thinner peptidoglycan
Gram positive has thicker peptidoglycan
5. Using HIV as an example, explain how viruses infect cells (be able to describe event steps and
key players and what occurs). - answer✔• Human Immunodeficiency Virus (HIV)
o Structure
Gp120 proteing binds to the CD4 molecule found primarily on surface of helper T cells
• Destroys CD4 Th cells
o Reverses CD4: CD8 ratio
o Coreceptors
CXCR4 and CCR5
• Strains can be selective for these receptors; influence the tropism of the target cells




2|Page

, ©FYNDLAY EXAM SOLUTIONS 2024/2025

ALL RIGHTS RESERVED.
Steps of how HIV infects cells:
1. virion binds to CD 4 and chemokine receptors
2.fusion of HIV membrane with host cell membrane entry of viral genome into cytoplasm and
gp41 enters cells
-RNA-> DNA
3. integration of provirus into host cell genome
-DNA->mRNA
4.Cytokine activation of cell; transcription of HIV genome; transport of viral RNAs to cytoplasm
-protease trim virions
5. synthesis of HIV proteins; assembly of virion core
6. Budding and release of mature virion
7. New HIV virion

6. Identify the key immunologic finding in those with HIV infection/AIDS. - answer✔Th cells <
200 cells/mm^3 diagnositc for AIDS
CD4 T Cells (normal= 800-1000/mm^3) declines to <400/mm^3

8. Identify opportunistic infections and malignancies associated with AIDS. - answer✔-herpes
-varicella
-mycobacterium (Tb)
-fungi
-pneumocystis
-lymphoma
-cancer (Kaposi sarcoma)
9. Identify the phases in HIV infection to AIDS progression and the characteristics of each phase.
- answer✔o Early:
lasts about 1-6 weeks
clinical latency; active proliferation in lymph nodes
headaches, fever, fatigue, non-specific, flu-like


3|Page

, ©FYNDLAY EXAM SOLUTIONS 2024/2025

ALL RIGHTS RESERVED.
high virus in blood; serological antibodies against HIV may not yet be detected
o Middle:
Lasts month to years
Virus dormant in host DNA; few in blood but antibodies (basis of testing)
Few symptoms
Continuous infection death, CD4 T Cells likely own Tc (CD8 t cells)
o Late
Duration varies
Rapid decline in CD4 t cells
Weak, opportunistic begin (herpes, varicella, mycobacterium (TB), fungi, pneumocystis
Lymphoma Cancer (Kaposi Sarcoma) often fatal within 1 year
10. Define HAART, what it is and current guidelines for ART. Why is it so difficult to create an
effective vaccine against HIV? - answer✔o HAART (highly active antiretroviral therapy)
3 or more drugs
• Usually 2 target reverse transcriptase
o Fools DNA into incorporating it into new strand, then halts DNA synthesis
• 1 target viral protease (can't cleave apart precursor proteins so can't make new viral proteins)


o Antiretroviral therapy (ART), combination of the following:
Reverse transcriptase inhibitors
Protease inhibitors
Integrase inhibitors
Fusion inhbitors
CCR5 antagonist


-HIV is difficult to create a vaccine for because it mutates so quickly and targets white blood
cells; it also changes host cell DNA

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