Type Four Hypersensitivity Notes

Type four hypersensitivity is complex with four distinct subtypes: type a, b, c, and d.
For this class, the focus will be on a general understanding rather than in-depth pathology.

Cell Mediated Reaction: Type four hypersensitivity involves specific immune cells that control the response.
- Differentiates from type three hypersensitivity, which is mediated by immune complexes involving antibodies and antigens.
- Type three reactions trigger inflammation via complement proteins.

Involvement of Immune Cells:
- Immune cells, particularly macrophages and monocytes, detect antigens.
- These cells engulf and process the antigens, presenting them to T cells (T lymphocytes).
- The process involves activation of the adaptive immune response, distinguishing it from innate responses.
- Presentation Process: Antigens are processed and presented to T cells—specifically via Major Histocompatibility Complex (MHC) molecules (not required to memorize for this course).
T Cell Activation:
- CD4 T Helper Cells: Activate CD8 T cells (Killer T cells).
- CD8 T cells target infected cells, including those infected by viruses or bacteria, resulting in destruction within 24 hours.
- Cytokine Release: Activated T cells may release cytokines, attracting more immune cells and exacerbating inflammation.
- This increase in inflammation can occur even when the body is already fighting an infection.

Delayed Hypersensitivity: Type four hypersensitivity reactions are often referred to as delayed reactions due to the time required for immune response buildup.
- Activation and responses of T cells lead to symptoms that manifest after some time post-exposure.

Stevens Johnson Syndrome (SJS):
- Representive of subtype four c of type four hypersensitivity.
- Trigger: Usually associated with the antibiotic vancomycin; rare, about 4-5 cases per million doses.
- Also can be triggered by some viruses like herpes simplex virus (HSV).

Mechanism: Vancomycin is recognized as a foreign agent, activating T cells to attack skin and other epithelial cells.
- This results in skin detachment from the underlying layers leading to severe skin damage.
- If detachment is less than 10%, it is classified as Stevens Johnson syndrome; over 30% detachment leads to Toxic Epidermal Necrolysis (TEN).

Symptoms: Skin rash, redness, pain/irritation, detachment of the skin and mucosal layers.
- May affect vision if eyes involved, can lead to prolonged blindness.
Management:
- Immediate action must be taken; the causative agent (often vancomycin) should be stopped.
- Monitor for early signs such as rashes or irritation.
- Supportive care includes administering normal saline to flush the agent and maintain hemodynamics, particularly given the involvement of blood circulation and systemic impact.
- Assess and support respiratory function if necessary, including oxygenation checks.
Pain Management: Administer pain medications or topical agents to reduce irritation.
- If ocular symptoms develop, use moist compresses for comfort and lubrication.
Severe Cases Treatment:
- For extensive skin detachments, adopt approaches similar to managing third-degree burns, including saline or antifungal compresses to maintain thermoregulation and prevent infections.
- Nutritional support focusing on high-protein intake to aid in tissue repair is essential.