NSG 3850 Exam 2 review | 2026 Update with complete solutions.
1. The Viral Life Cycle
• Attachment & Entry: The virus utilizes surface proteins to bind to specific host cell receptors
(tropism); it then enters the cell via receptor-mediated endocytosis or direct fusion with the host plasma
membrane.
• Genome Release & Uncoating: Once inside, the viral capsid is enzymatically degraded or
physically removed, releasing the viral DNA or RNA into the cytoplasm or nucleus to begin the infectious
process.
• Replication & Biosynthesis: The virus hijacks the host cell's metabolic machinery, using host
ribosomes and enzymes to synthesize viral mRNA, structural proteins, and multiple copies of the viral
genome.
• Assembly & Release: Newly synthesized components are organized into mature virions; these
are released from the host cell either through budding (acquiring an envelope) or by causing cell lysis
(rupture).
2. Status Asthmaticus Pathophysiology
• Refractory Treatment Failure: This is a severe, life-threatening asthma exacerbation that fails to
respond to initial emergency therapy, specifically repeated doses of short-acting beta-agonists (SABA)
like albuterol.
• Severe Airway Obstruction: The pathology involves a "triple threat" of intense, prolonged
bronchospasm, significant mucosal edema from inflammation, and the formation of thick, tenacious
mucus plugs in the distal bronchioles.
• The Silent Chest Phenomenon: As air trapping worsens, the patient may stop wheezing entirely;
this "silent chest" indicates that air movement is so restricted that it cannot produce sound, signaling
imminent respiratory arrest.
• Progressive Respiratory Acidosis: Severe ventilation-perfusion (V/Q) mismatch and alveolar
hypoventilation lead to hypercapnia (CO2 retention); as the patient fatigues, they can no longer
compensate, resulting in a dangerous drop in blood pH.
3. Immunocompromised Risk Factors
, • Physiological Age Extremes: Infants are at risk due to an immature, "naive" immune system,
while the elderly experience immunosenescence, characterized by thymic involution and a decreased
diversity of T-cell responses.
• Iatrogenic Myelosuppression: Cytotoxic chemotherapy treatments target rapidly dividing cells,
inadvertently suppressing bone marrow production and leading to profound neutropenia, which
removes the primary defense against bacteria.
• Secondary/Acquired Deficiencies: External factors such as long-term systemic corticosteroid use
suppress the activation of T-lymphocytes and macrophages, significantly increasing the risk of
opportunistic infections.
• Chronic Inflammatory & Autoimmune States: Conditions like Systemic Lupus Erythematosus
(SLE) require potent immunosuppressive drugs (e.g., TNF-inhibitors) that intentionally dampen the
immune response to prevent tissue damage, leaving the host vulnerable.
4. Hypersensitivity Reactions (Types I-IV)
• Type I (Immediate): IgE-mediated reaction where antigens bind to mast cells, triggering the
massive release of histamine; this leads to classic allergic symptoms or life -threatening anaphylaxis.
• Type II (Cytotoxic): IgG or IgM antibodies target specific antigens on host cell surfaces (e.g.,
mismatched blood transfusions), leading to cell destruction via the complement system or phagocytosis.
• Type III (Immune Complex): Antigen-antibody complexes deposit in tissue walls (like kidneys or
joints), triggering an inflammatory cascade that causes localized or systemic tissue damage (e.g., Serum
Sickness).
• Type IV (Delayed-Type): T-cell mediated response rather than antibody-driven; sensitized T-
lymphocytes attack target cells 24-72 hours after exposure (e.g., Poison Ivy or TB skin tests).
5. HIV/AIDS Pathophysiology
• Retroviral Mechanism: HIV is a retrovirus that uses reverse transcriptase to convert its RNA into
DNA, which is then integrated into the host's genome, primarily targeting CD4+ T-helper cells.
• The Window Period: The time between initial infection and when antibodies become detectable
(seroconversion); during this phase, the patient is highly infectious despite potentially testing negative.
• CD4+ T-Cell Depletion: As the virus replicates, it destroys CD4+ cells, leading to a progressive
collapse of the adaptive immune system and leaving the host vulnerable to opportunistic pathogen s.
• AIDS Progression: Diagnosed when the CD4+ count drops below 200 cells/mm³ or when an AIDS-
defining clinical condition (like Pneumocystis pneumonia or Kaposi sarcoma) develops.
1. The Viral Life Cycle
• Attachment & Entry: The virus utilizes surface proteins to bind to specific host cell receptors
(tropism); it then enters the cell via receptor-mediated endocytosis or direct fusion with the host plasma
membrane.
• Genome Release & Uncoating: Once inside, the viral capsid is enzymatically degraded or
physically removed, releasing the viral DNA or RNA into the cytoplasm or nucleus to begin the infectious
process.
• Replication & Biosynthesis: The virus hijacks the host cell's metabolic machinery, using host
ribosomes and enzymes to synthesize viral mRNA, structural proteins, and multiple copies of the viral
genome.
• Assembly & Release: Newly synthesized components are organized into mature virions; these
are released from the host cell either through budding (acquiring an envelope) or by causing cell lysis
(rupture).
2. Status Asthmaticus Pathophysiology
• Refractory Treatment Failure: This is a severe, life-threatening asthma exacerbation that fails to
respond to initial emergency therapy, specifically repeated doses of short-acting beta-agonists (SABA)
like albuterol.
• Severe Airway Obstruction: The pathology involves a "triple threat" of intense, prolonged
bronchospasm, significant mucosal edema from inflammation, and the formation of thick, tenacious
mucus plugs in the distal bronchioles.
• The Silent Chest Phenomenon: As air trapping worsens, the patient may stop wheezing entirely;
this "silent chest" indicates that air movement is so restricted that it cannot produce sound, signaling
imminent respiratory arrest.
• Progressive Respiratory Acidosis: Severe ventilation-perfusion (V/Q) mismatch and alveolar
hypoventilation lead to hypercapnia (CO2 retention); as the patient fatigues, they can no longer
compensate, resulting in a dangerous drop in blood pH.
3. Immunocompromised Risk Factors
, • Physiological Age Extremes: Infants are at risk due to an immature, "naive" immune system,
while the elderly experience immunosenescence, characterized by thymic involution and a decreased
diversity of T-cell responses.
• Iatrogenic Myelosuppression: Cytotoxic chemotherapy treatments target rapidly dividing cells,
inadvertently suppressing bone marrow production and leading to profound neutropenia, which
removes the primary defense against bacteria.
• Secondary/Acquired Deficiencies: External factors such as long-term systemic corticosteroid use
suppress the activation of T-lymphocytes and macrophages, significantly increasing the risk of
opportunistic infections.
• Chronic Inflammatory & Autoimmune States: Conditions like Systemic Lupus Erythematosus
(SLE) require potent immunosuppressive drugs (e.g., TNF-inhibitors) that intentionally dampen the
immune response to prevent tissue damage, leaving the host vulnerable.
4. Hypersensitivity Reactions (Types I-IV)
• Type I (Immediate): IgE-mediated reaction where antigens bind to mast cells, triggering the
massive release of histamine; this leads to classic allergic symptoms or life -threatening anaphylaxis.
• Type II (Cytotoxic): IgG or IgM antibodies target specific antigens on host cell surfaces (e.g.,
mismatched blood transfusions), leading to cell destruction via the complement system or phagocytosis.
• Type III (Immune Complex): Antigen-antibody complexes deposit in tissue walls (like kidneys or
joints), triggering an inflammatory cascade that causes localized or systemic tissue damage (e.g., Serum
Sickness).
• Type IV (Delayed-Type): T-cell mediated response rather than antibody-driven; sensitized T-
lymphocytes attack target cells 24-72 hours after exposure (e.g., Poison Ivy or TB skin tests).
5. HIV/AIDS Pathophysiology
• Retroviral Mechanism: HIV is a retrovirus that uses reverse transcriptase to convert its RNA into
DNA, which is then integrated into the host's genome, primarily targeting CD4+ T-helper cells.
• The Window Period: The time between initial infection and when antibodies become detectable
(seroconversion); during this phase, the patient is highly infectious despite potentially testing negative.
• CD4+ T-Cell Depletion: As the virus replicates, it destroys CD4+ cells, leading to a progressive
collapse of the adaptive immune system and leaving the host vulnerable to opportunistic pathogen s.
• AIDS Progression: Diagnosed when the CD4+ count drops below 200 cells/mm³ or when an AIDS-
defining clinical condition (like Pneumocystis pneumonia or Kaposi sarcoma) develops.
