NURS 6501 – Week 4 Study Guide, Exams of Nursing

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NURS 6501 – Week 4 Study Guide
Infection, Immunity, & Wound Healing
High-Yield Summary + 10 NCLEX-Style Questions
Infection & Host Response
1. Pathogen Types
Pathogen
Example
Notes
Virus
HIV, Influenza
Intracellular; hijack host DNA
Bacteria
Strep, E. coli
Reproduce independently; treat with antibiotics
Fungi
Candida
Opportunistic; difficult to treat
Parasites
Malaria, Giardia
Often chronic infections
Prions
Creutzfeldt-Jakob
Abnormal proteins; no nucleic acids
2. Stages of Infection
1. Incubation – time between exposure and symptom onset
2. Prodromal – mild symptoms start
3. Invasion – full infection develops
4. Convalescence – symptoms resolve, recovery begins
3. Immune Evasion Mechanisms
Antigenic variation (flu viruses)
Biofilm formation (e.g., in catheters)
Intracellular hiding (e.g., TB)
Immunocompromise
Primary = congenital (e.g., SCID)
Secondary = acquired (e.g., HIV, chemo, aging)
↑ Risk for opportunistic infections (Pneumocystis, CMV)
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NURS 6501 – Week 4 Study Guide

Infection, Immunity, & Wound Healing

High-Yield Summary + 10 NCLEX-Style Questions

Infection & Host Response

1. Pathogen Types Pathogen Example Notes Virus HIV, Influenza Intracellular; hijack host DNA Bacteria Strep, E. coli Reproduce independently; treat with antibiotics Fungi Candida Opportunistic; difficult to treat Parasites Malaria, Giardia Often chronic infections Prions Creutzfeldt-Jakob Abnormal proteins; no nucleic acids 2. Stages of Infection 1. Incubation – time between exposure and symptom onset 2. Prodromal – mild symptoms start 3. Invasion – full infection develops 4. Convalescence – symptoms resolve, recovery begins 3. Immune Evasion Mechanisms - Antigenic variation (flu viruses) - Biofilm formation (e.g., in catheters) - Intracellular hiding (e.g., TB) Immunocompromise - Primary = congenital (e.g., SCID) - Secondary = acquired (e.g., HIV, chemo, aging) - ↑ Risk for opportunistic infections (Pneumocystis, CMV)

Wound Healing Phases Phase Timeframe Main Events Hemostasis Immediate (mins–hrs) Platelets → clot formation Inflammation 1 – 3 days Neutrophils/macrophages → clean wound Proliferation 4 – 21 days Fibroblasts → collagen, new tissue forms Remodeling Weeks–months Scar maturation, tissue strength restored Clinical Case Example Patient : 68-year-old on chronic corticosteroids has a slow-healing foot ulcer. Explanation : Immunosuppression (secondary) → ↓ macrophage response → impaired wound healing. Action : Monitor for signs of infection; optimize glucose and nutrition. NCLEX-Style Practice Questions (10 Total)

1. Which stage of infection is characterized by the appearance of full-blown clinical symptoms? A. Incubation B. Prodromal C. Invasion D. Convalescence Answer: C – Invasion is when the pathogen replicates rapidly, and symptoms are pronounced. 2. Which of the following best describes a prion? A. Virus with RNA genome B. Single-celled parasite C. Infectious protein with no DNA/RNA D. Fungal toxin Answer: C – Prions are abnormal proteins that cause neurodegenerative diseases (e.g., Mad Cow). 3. What immune cell dominates the early inflammatory phase of wound healing? A. B cells B. Neutrophils C. Fibroblasts D. CD8+ T cells

9. Which immune response is most responsible for fighting intracellular viruses? A. B cell antibody production B. CD4+ T cell activation C. CD8+ cytotoxic T cells D. Complement cascade Answer: C – CD8+ T cells destroy infected host cells containing viruses. 10. Which wound healing phase involves scar formation and remodeling? A. Hemostasis B. Inflammation C. Proliferation D. Maturation/remodeling Answer: D – Remodeling strengthens the tissue and refines scar appearance. Quick Summary Sheet - Infection stages : Incubation → Prodromal → Invasion → Convalescence - Wound healing : Hemostasis → Inflammation → Proliferation → Remodeling - Immunodeficiency : o Primary : congenital (rare) o Secondary : acquired (HIV, chemo, corticosteroids) - CD4 cells = target of HIV , CD8 = kill infected cells