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Immune System Foundations, Prions, and ATI Insights

Course Logistics & ATI Dynamic Quizzing

  • Current schedule: one chapter (Chapter 22) over the next two weeks ≈ 60 slides per week.

  • ATI access will open in ≈ 10 weeks; includes “Dynamic Quizzing.”

    • Customizable NCLEX-style quizzes targeting weak subjects.

    • Pros: focused remediation, immediate feedback.

    • Cons: tends to make graded ATI assessments more challenging (higher‐level items are pulled once you demonstrate mastery).

  • Passing certain ATI proctored exams is required for course/ program progression (“a certain part of the bar”).

Spectrum of Infectious Agents Mentioned

  • Bacteria, viruses, fungi, protozoa.

  • Viruses = “nucleic acids surrounded by a capsid; may have an envelope; attach to host via spikes.”

  • Definition highlight: “Virulent” = causes serious illness.

Prion Diseases – Variant vs. Classic (Kuru/CJD)

  • Both variant Creutzfeldt–Jakob Disease (vCJD) and classic CJD are prion disorders (misfolded proteins → neurodegeneration).

  • Key difference = SOURCE/TRANSMISSION.

    • Variant CJD → ingestion of prion-contaminated beef (“mad-cow”).

    • Classic/ sporadic CJD → most commonly transmitted by unsterile neurosurgical equipment; can also arise genetically or from cadaveric tissue transplants.

  • ATI “hard” question focused on identifying transmission pathway rather than symptoms.

Hematopoiesis & WBC Families

  • All leukocytes originate in red bone marrow.

  • Three broad families:

    1. Granulocytes (neutrophils, eosinophils, basophils) – granule-filled cytoplasm.

    2. Monocytes → differentiate into macrophages & specialized phagocytes.

    3. Lymphocytes (B, T, NK) – adaptive / cytotoxic roles.

  • Mnemonic referenced: “B, T & K (NK) = the three lymphocytes.”

Granulocytes in Detail

  • General naming logic: “-phil” = “loving/attracted to,” granulo = granules.

Neutrophils

  • First cellular responders; main function = phagocytosis (they “neutralize” threats).

  • Work synergistically with macrophages.

Eosinophils

  • Two hallmark targets:

    • Allergies / hypersensitivity reactions.

    • Parasitic worms (helminths).

  • Elevated eosinophil count → think atopy or parasitic infection.

Basophils (and Mast Cells)

  • Release histamine & other eicosanoids (e.g., leukotrienes) → vasodilation, increased permeability → inflammation.

  • Mast cells are tissue-resident analogues performing same function.

  • Do not equate basophils with allergies only (that’s eosinophils); basophils = general inflammation.

Agranulocytes & Accessory Cells

  • Monocytes / Macrophages – large phagocytes; terms used interchangeably until specific tissue sub-types introduced.

  • Dendritic Cells (Langerhans cells in epidermis): found in basal stratum of skin; antigen-presenting; destroy invaders & cancer cells in integument.

  • Natural Killer (NK) Cells – lymphocytes that “kill” virally infected & tumor cells once they are marked.

Innate vs. Adaptive Immunity

  • Two overarching arms (graph on slide combined but mislabeled):

    • Innate (Nonspecific) / Natural
      • Barriers (skin, mucus, sebum).
      • Rapid, broad cellular & chemical defenses (neutrophils, macrophages, dendritic cells, eosinophils, basophils, interferons, complement, inflammation, fever).

    • Adaptive (Specific / Acquired)
      • Slower onset, memory component.
      • B-cells, T-cells, plasma cells, antibodies, NK cells after activation.

  • Synonyms emphasized:

    • Innate = “nonspecific.”

    • Adaptive = “specific” = “acquired.”

First, Second & Third Lines of Defense

  1. First Line (Physical/Chemical Barriers – Innate)

    • Intact skin & its mucus (cutaneous membrane = largest mucous membrane).

    • Sebum: oily barrier that traps microbes at hair follicles.

  2. Second Line (Internal Cellular/Chemical – Innate)

    • Phagocytes (neutrophils, macrophages, dendritic cells).

    • Eosinophils, basophils.

    • Chemicals: interferons (inhibit viral replication), complement, acute-phase proteins.

    • Inflammatory response (histamine-mediated).

  3. Third Line (Adaptive)

    • Activation & clonal expansion of B & T lymphocytes.

    • Production of antibodies & cytotoxic T-cell attack.

Cytokines, Half-Life & Signaling Molecules

  • Cytokines = small proteins that regulate immune activity.

    • Short half-life (t_{1/2}) → short-lived, rapidly shifting effects.

    • Example given for pharmacology: drug half-life = time to metabolize \frac{1}{2} the dose.

  • Interferons (IFN-α, β, γ) – innate cytokines; “interfere” with viral genome replication.

  • Complement – plasma protein cascade → opsonization, lysis, chemotaxis (lectured later).

Antigens vs. Antibodies (Immunoglobulins)

  • Antigen: any molecule the body recognizes as non-self; can be part of microbes (capsid, flagellin, etc.) or foreign RBC antigens (A, B, Rh).

  • Antibody (Ab) / Immunoglobulin (Ig): Y-shaped protein produced by B-cells/plasma cells that binds antigen to “mark” it for destruction.

    • Alternate names emphasized on ATI:
      • Antibody = Immunoglobulin (Ig).

  • Five Classes ("GAMED"):
    \text{IgG, IgA, IgM, IgE, IgD}

  • Structural features to label (slide exercise):

    • Two Heavy Chains (larger arms of the Y).

    • Two Light Chains (smaller arms).

    • Variable Region (tips) – differs between classes; forms antigen-binding sites.

    • Constant Region – shared framework among all Ig’s.

    • Disulfide Bonds – \text{S—S} links holding chains together.

Miscellaneous Clinical & Conceptual Points

  • Granulocyte Origin: all WBC types produced in red bone marrow.

  • Macrophage vs. Neutrophil synergy: both perform phagocytosis; neutrophils often arrive first ("neutralize"), macrophages sustain cleanup.

  • Eicosanoids: lipid mediators (e.g., prostaglandins, leukotrienes) released from basophils/mast cells → amplify inflammation.

  • Air Embolism: < 20\,\text{cc} of air usually dissipates harmlessly via:

    1. Gradual diffusion into tissues & alveoli (gas exchange).

    2. Splitting into micro-bubbles handled by lungs/kidneys.

    3. Phagocytic uptake by immune cells → lymphatic drainage.

  • Alcohol & Inflammation: ethanol is a hepatically prioritized toxin; concurrent meds accumulate; alcohol additionally provokes inflammatory responses (double burden).

  • Self-Markers (MHC proteins): membrane proteins identifying “self”; failure leads to autoimmunity → rheumatology referral.

  • Cardinal Signs of Inflammation (lecture teased): redness, heat, swelling, pain, (loss of function).

Key Take-Home Mnemonics & Numbers

  • "GAMED" = five antibody classes.

  • "Granulocytes NEB" = Neutrophils, Eosinophils, Basophils.

  • "20 cc rule" for venous air safety margin.

  • t_{1/2} concept applies to cytokines & pharmacologic agents alike.