2804NRS · Human Pathophysiology And Pharmacology 1
Immunity and Inflammation
The immune system runs in two layers: an innate layer that is fast, fixed and forgetful, and an adaptive layer that is slow on first contact but specific and able to remember — the basis of vaccination. This chapter covers the two layers and the cells that run them, antibody structure and the five classes (IgM first, IgG most abundant + placenta, IgE allergy, IgA secretions), the primary vs secondary response and the four immunity types (active/passive, natural/artificial), then the way the same machinery damages you: the four hypersensitivity types (ACID — allergic, cytotoxic, immune-complex, delayed), anaphylaxis, immunodeficiency (HIV → CD4+), and autoimmunity. In 2804NRS this is Module 3 — examined by both MCQ and short-answer, and the hypersensitivity mediator grid is the single most tested table in the unit.
What this chapter covers
- 013.1 Innate vs adaptive immunity — the two layers
- 023.2 The immune cells — who does what
- 033.3 Antibodies — structure and the five classes
- 043.4 Primary vs secondary response & the four immunity types
- 053.5 Hypersensitivity I–IV (ACID) — immunity that harms
- 063.6 Anaphylaxis, immunodeficiency (HIV/AIDS) & autoimmunity
Name the hypersensitivity type and its mediator
- +1(a) Hay fever = Type I — allergen binds IgE on mast cells → histamine, immediate.
- +1(b) ABO transfusion reaction = Type II (cytotoxic) — IgG/IgM bind a FIXED cell-surface antigen → complement destroys the cell.
- +1(c) SLE = Type III (immune-complex) — IgG + SOLUBLE antigen form circulating complexes that deposit in tissue → complement → inflammation.
- +1(d) TB skin test = Type IV (delayed) — sensitised T cells release cytokines on re-exposure; NO antibody; delayed 24–72 h.
Key terms
- Innate vs adaptive immunity
- Innate = non-specific, immediate, NO memory (barriers, inflammation, phagocytes, NK cells, complement). Adaptive = specific, slower, HAS memory (humoral = B cells/antibodies; cell-mediated = T cells).
- Antibody (immunoglobulin)
- A Y-shaped protein of 2 heavy + 2 light chains. The variable region (Fab tips) binds antigen; the constant region (Fc stem) sets the class and effector function. Two arms = two binding sites.
- Hypersensitivity (ACID)
- An excessive immune response that damages self tissue. Type I allergic (IgE/histamine), II cytotoxic (IgG/IgM + complement, fixed antigen), III immune-complex (IgG + soluble antigen), IV delayed (T cells, no antibody).
- Active vs passive immunity
- Active = you make your own antibodies (slow onset, HAS memory, long-lasting) from infection or vaccine. Passive = pre-formed antibodies given (immediate but NO memory, decays) from maternal Ig or antivenom.
- Anaphylaxis
- A severe, systemic Type I reaction: mass histamine release → vasodilation/hypotension + bronchoconstriction + urticaria. First-line treatment is adrenaline, not an antihistamine.
Immunity and Inflammation FAQ
What is the difference between innate and adaptive immunity?
Innate immunity is non-specific, immediate and keeps no memory — barriers, inflammation, fever, phagocytes, NK cells and complement. Adaptive immunity is specific, slower on first contact and has memory — B cells make antibodies (humoral) and T cells run the cell-mediated arm. Inflammation and fever are innate even though they feel like a 'response.'
How do I tell the antibody classes apart?
IgM is the largest and the FIRST made (primary response); IgG is the MOST abundant, dominates the secondary response and is the only one that crosses the placenta; IgE binds mast cells and mediates allergy/anaphylaxis; IgA is in secretions (saliva, tears, breast milk); IgD sits on the B-cell surface. Examiners swap 'first' and 'most abundant' — lock those in.
What is the first-line drug in anaphylaxis?
Adrenaline (epinephrine), given immediately: via the β2 receptor it bronchodilates to open the airway, and via the α1 receptor it vasoconstricts to raise blood pressure. Antihistamines help early or minor reactions but are not first-line — picking 'antihistamine' is the trap answer.
Why does HIV collapse the whole immune system?
HIV destroys CD4+ helper T cells, and the CD4+ helper is the conductor that coordinates both the humoral and cell-mediated arms. Losing it cripples the entire adaptive response. AIDS is diagnosed when CD4 falls below 200 cells/mm³, opening the door to opportunistic infections and cancers.
Exam move
Memorise two grids cold: the antibody classes (IgM first/largest, IgG most abundant + placenta, IgE allergy, IgA secretions) and the four hypersensitivity types with their mediators. The hypersensitivity grid is the most tested table in the module, and the II-vs-III distinction (fixed vs soluble antigen) is the highest-value mark. Then rehearse anaphylaxis as a mechanism→manifestation chain — it is a guaranteed short-answer favourite — and lock in active vs passive and natural vs artificial as two independent axes.
