NURS 6501 – Midterm Review Pack
Weeks 1–5: High-Yield Notes + 20 NCLEX Questions
Walden University | Bestseller
WEEK 1: Cellular Biology & Adaptation
• Atrophy = decrease in cell size (e.g., immobilization)
• Hypertrophy = increase in cell size (e.g., left ventricular hypertrophy)
• Hyperplasia = increase in cell number (e.g., uterine lining)
• Metaplasia = reversible cell type change (e.g., smokers’ bronchi)
• Dysplasia = abnormal growth; precursor to cancer
• Apoptosis = programmed cell death (no inflammation)
• Necrosis = cell death causing inflammation (e.g., MI)
• Hypoxia = most common cause of cell injury; leads to ATP depletion
WEEK 2: Inflammation & Tissue Repair
• Acute inflammation = redness, heat, swelling, pain, loss of function
• Chemical mediators: histamine (vasodilation), prostaglandins (pain), cytokines
• Cell types: neutrophils (early), macrophages (late)
• Chronic inflammation = weeks/months; lymphocytes/macrophages dominate
• Healing: Primary (minimal scarring), Secondary (larger wound, granulation tissue)
WEEK 3: Immunity
• Innate immunity = rapid, nonspecific (skin, NK cells, phagocytes)
• Adaptive immunity = slower, specific (T cells, B cells)
• B cells = produce antibodies
• T helper (CD4+) cells = coordinate response
• Cytotoxic T (CD8+) cells = kill infected cells
• IgG = most abundant antibody
• IgA = mucosal surfaces
• Autoimmunity = immune system attacks self (e.g., lupus, RA)
, WEEK 4: Infection & Wound Healing
• Pathogens: virus (HIV), bacteria (TB), fungi (Candida), parasites (malaria), prions
• Stages of infection: Incubation → Prodromal → Invasion → Convalescence
• Immunocompromised: HIV, chemo, steroids → ↑ opportunistic infection
• Wound healing:
1. Hemostasis
2. Inflammation
3. Proliferation
4. Remodeling (scar)
WEEK 5: Genetics & Cancer Biology
• Oncogenes = promote uncontrolled growth (e.g., HER2)
• Tumor suppressor genes = inhibit growth (e.g., p53, BRCA1/2)
• Carcinogenesis stages: Initiation → Promotion → Progression
• Hallmarks of cancer: evading apoptosis, angiogenesis, invasion
• Metastasis: colon → liver (portal vein), breast/prostate → bone
• Carcinoma in situ = localized, pre-invasive tumor
20 NCLEX-Style Practice Questions (Midterm Level)
1. What cellular adaptation occurs in the bronchial epithelium of smokers?
A. Atrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Answer: C – Metaplasia is a reversible change where one cell type replaces another.
2. Which mediator is most responsible for vasodilation during inflammation?
A. Histamine
B. Interleukin
C. TNF-alpha
D. IgE
Answer: A – Histamine causes rapid vasodilation and increased permeability.
Weeks 1–5: High-Yield Notes + 20 NCLEX Questions
Walden University | Bestseller
WEEK 1: Cellular Biology & Adaptation
• Atrophy = decrease in cell size (e.g., immobilization)
• Hypertrophy = increase in cell size (e.g., left ventricular hypertrophy)
• Hyperplasia = increase in cell number (e.g., uterine lining)
• Metaplasia = reversible cell type change (e.g., smokers’ bronchi)
• Dysplasia = abnormal growth; precursor to cancer
• Apoptosis = programmed cell death (no inflammation)
• Necrosis = cell death causing inflammation (e.g., MI)
• Hypoxia = most common cause of cell injury; leads to ATP depletion
WEEK 2: Inflammation & Tissue Repair
• Acute inflammation = redness, heat, swelling, pain, loss of function
• Chemical mediators: histamine (vasodilation), prostaglandins (pain), cytokines
• Cell types: neutrophils (early), macrophages (late)
• Chronic inflammation = weeks/months; lymphocytes/macrophages dominate
• Healing: Primary (minimal scarring), Secondary (larger wound, granulation tissue)
WEEK 3: Immunity
• Innate immunity = rapid, nonspecific (skin, NK cells, phagocytes)
• Adaptive immunity = slower, specific (T cells, B cells)
• B cells = produce antibodies
• T helper (CD4+) cells = coordinate response
• Cytotoxic T (CD8+) cells = kill infected cells
• IgG = most abundant antibody
• IgA = mucosal surfaces
• Autoimmunity = immune system attacks self (e.g., lupus, RA)
, WEEK 4: Infection & Wound Healing
• Pathogens: virus (HIV), bacteria (TB), fungi (Candida), parasites (malaria), prions
• Stages of infection: Incubation → Prodromal → Invasion → Convalescence
• Immunocompromised: HIV, chemo, steroids → ↑ opportunistic infection
• Wound healing:
1. Hemostasis
2. Inflammation
3. Proliferation
4. Remodeling (scar)
WEEK 5: Genetics & Cancer Biology
• Oncogenes = promote uncontrolled growth (e.g., HER2)
• Tumor suppressor genes = inhibit growth (e.g., p53, BRCA1/2)
• Carcinogenesis stages: Initiation → Promotion → Progression
• Hallmarks of cancer: evading apoptosis, angiogenesis, invasion
• Metastasis: colon → liver (portal vein), breast/prostate → bone
• Carcinoma in situ = localized, pre-invasive tumor
20 NCLEX-Style Practice Questions (Midterm Level)
1. What cellular adaptation occurs in the bronchial epithelium of smokers?
A. Atrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Answer: C – Metaplasia is a reversible change where one cell type replaces another.
2. Which mediator is most responsible for vasodilation during inflammation?
A. Histamine
B. Interleukin
C. TNF-alpha
D. IgE
Answer: A – Histamine causes rapid vasodilation and increased permeability.
