3325 Exam #1
Alright — this is the capstone.
What you asked for is not “notes,” it’s a compressed mental model of Exam 1 built from everything you provided:
Learning guides (Modules 1A, 1B, 2, 3A, 3B)
Student bullet questions
Review-session notes
Exam 1 concepts list
Sherpath emphasis
Faculty language patterns
What follows is a true Exam 1 MUST-KNOW MASTER GUIDE.
If a concept is not here, it is either low yield or redundant.
If it is here, you should be able to recognize it instantly in a scenario.
NURS 3325 — EXAM 1 MUST-KNOW MASTER GUIDE
(Cellular Injury, Inflammation, Immunity, Genetics, Cancer, Fluids & Acid-Base)
SECTION I — CELLULAR BIOLOGY & INJURY (FOUNDATION)
Cellular Adaptations (KNOW DEFINITIONS + SCENARIOS)
Atrophy → ↓ cell size
Disuse, aging, denervation, ischemia
Hypertrophy → ↑ cell size (NOT number)
Increased workload (heart, skeletal muscle)
Hyperplasia → ↑ cell number
Hormonal stimulation, wound healing
Metaplasia → replacement of one mature cell type with another
Chronic irritation (smoking → squamous cells)
Dysplasia → abnormal growth, precancerous
Anaplasia → loss of differentiation (hallmark of cancer)
👉 Failed adaptation → cell injury → cell death
Cellular Injury
MOST COMMON CAUSE: Hypoxia
Ischemia = ↓ blood flow → hypoxia
↓ ATP → Na⁺/K⁺ pump failure → cell swelling (early, reversible)
Reperfusion injury → ROS damage
Cell Death
Apoptosis
Programmed
No inflammation
Normal or pathologic
Necrosis (ALWAYS inflammatory)
Uncontrolled
Cell swelling + membrane rupture
Types of Necrosis (MATCH TO ORGAN)
Coagulative → ischemia (heart, kidney)
Liquefactive → brain, abscess
Caseous → TB
Fat → pancreatitis, breast trauma
Gangrenous → ischemic limb
Gas gangrene → Clostridium (medical emergency)
SECTION II — INFLAMMATION (VERY HIGH YIELD)
Purpose of Inflammation
Remove injury
Neutralize pathogens
Prepare for repair
Cardinal Signs
Redness (vasodilation)
Heat (↑ blood flow)
Swelling (↑ permeability)
Pain (bradykinin, prostaglandins)
Loss of function
Acute vs Chronic Inflammation
Feature | Acute | Chronic |
|---|---|---|
Duration | Short | Long |
Cells | Neutrophils | Macrophages, lymphocytes |
Outcome | Resolution | Fibrosis, scarring |
First responders = NEUTROPHILS
Plasma Protein Systems
Complement → opsonization, chemotaxis, cell lysis
Clotting → fibrin mesh, localizes injury
Kinin → bradykinin = pain + permeability
SECTION III — IMMUNITY (EXAM FAVORITE)
Lines of Defense
Skin, mucosa
Innate immunity
Adaptive immunity
Innate Immunity
Immediate, nonspecific
Neutrophils, macrophages, NK cells
Complement
No memory
Adaptive Immunity
Specific, memory-based
B cells → antibodies
T cells → cellular immunity
T Cells
CD4 (Helper) → activate immune response
CD8 (Cytotoxic) → kill infected cells
Regulatory T cells → tolerance
Memory T cells → faster re-exposure response
Immunoglobulins (MEMORIZE: “GAMED”)
IgG → most abundant
IgA → secretions (breast milk, saliva, GI)
IgM → first antibody produced
IgE → allergies, anaphylaxis
IgD → B-cell regulation
Hypersensitivity Reactions
Type I (IgE) → anaphylaxis
Type II → transfusion reactions
Type III → immune complexes (SLE)
Type IV → delayed, T-cell (TB skin test)
Anaphylaxis (MUST RECOGNIZE)
IgE mediated
Hives, airway swelling, hypotension
Medical emergency
Immune Deficiencies
Primary → congenital
Secondary → HIV, chemo, steroids
HIV
Destroys CD4 cells
AIDS = CD4 < 200
Opportunistic infections
SECTION IV — INFECTION & MICROBIOLOGY
Virulence = ability to cause disease
Endotoxins = Gram-negative (lipid A) → septic shock
Exotoxins = proteins, secreted
Viruses = require host cell
Fungi = budding
Parasites = symbiotic
Fever = hallmark of infection
SECTION V — GENETICS & EPIGENETICS
Genetics
Point mutations
Frameshift mutations
Silent mutations (no amino acid change)
Genotype ≠ phenotype
Epigenetics
Changes gene expression, NOT DNA sequence
DNA methylation → gene silencing
Histone modification
Non-coding RNA
Key idea:
Same genes ≠ same disease expression
SECTION VI — CANCER BIOLOGY (HUGE)
Cancer Cell Characteristics
Anaplasia
Invasion
Metastasis
Angiogenesis
Loss of contact inhibition
Cancer Types
Carcinoma → epithelial
Sarcoma → connective tissue
Lymphoma → lymphatic
Leukemia → bone marrow
Adenocarcinoma → glandular
Cancer Development
Initiation
Promotion (reversible)
Progression (irreversible)
Metastasis
Lymphatic
Hematogenous
Common sites: lungs, liver, brain, bone
Cancer Staging
TNM
Stage 0 = carcinoma in situ
Stage IV = distant metastasis
Cancer Risk Factors
Smoking (complete carcinogen)
Obesity
Alcohol
Age
Genetics (5–10%)
BRCA1 / BRCA2
Tumor suppressor genes
Breast & ovarian cancer risk
SECTION VII — FLUIDS & ELECTROLYTES (3A)
Fluid Compartments
ICF → potassium
ECF → sodium
Plasma
Interstitial
Water follows sodium
Edema
↑ hydrostatic pressure
↓ oncotic pressure (albumin)
↑ permeability
Lymphatic obstruction
Sodium
Hyponatremia → neuro symptoms
Hypernatremia → dehydration, thirst
Potassium
Hypokalemia → weakness, dysrhythmias
Hyperkalemia → peaked T waves, cardiac arrest
SECTION VIII — ACID–BASE (3B)
Normal Values
pH: 7.35–7.45
PaCO₂: 35–45
HCO₃⁻: 22–26
ROME METHOD
Respiratory → pH Opposite PaCO₂
Metabolic → pH Equal HCO₃⁻
Disorders
Respiratory acidosis → hypoventilation
Respiratory alkalosis → hyperventilation
Metabolic acidosis → DKA, renal failure, diarrhea
Metabolic alkalosis → vomiting, NG suction
Compensation
Lungs = fast
Kidneys = slow
Compensation never overcorrects
FINAL EXAM STRATEGY
When you read a question, immediately ask:
Cellular injury or immune?
Acute or chronic?
Innate or adaptive?
Genetic or epigenetic?
Benign or malignant?
Local or systemic?
Acid or base? Lung or kidney?
Bottom Line
If you can:
Identify the mechanism
Match the organ/system
Predict the next physiologic effect
You will score very high on Exam 1.