What is the mechanism of tissue damage in Type II hypersensitivity?

Correct Answer: B

Rationale: The correct answer is B: Antibody binding to cell surface antigens, triggering complement activation or phagocytosis. In Type II hypersensitivity, antibodies bind to antigens on host cells, leading to complement activation or phagocytosis by immune cells. This results in cell damage or destruction. Immune complex deposition (A) is more characteristic of Type III hypersensitivity. Mast cell degranulation (C) is seen in Type I hypersensitivity. T cell-mediated cytotoxicity (D) is associated with Type IV hypersensitivity, not Type II. Therefore, choice B is the most accurate mechanism of tissue damage in Type II hypersensitivity.

Correct Answer: A

Rationale: The correct answer is A. If the client states they don't need to go to the hospital after using the epinephrine autoinjector, additional instruction is needed. The rationale is that after using an epinephrine autoinjector, it is crucial to seek medical attention immediately due to the potential for severe allergic reactions. Choice B is incorrect because carrying two autoinjectors is recommended in case the first dose is not effective. Choice C is incorrect as it demonstrates good practice in tracking the expiration date. Choice D is incorrect as it is acceptable to inject through clothes in an emergency situation.

Correct Answer: C

Rationale: Rationale: VDJ gene rearrangement occurs during lymphocyte development to generate diverse antigen receptors. This process occurs in the bone marrow, specifically in the early stages of B cell development. In the bone marrow, B cell precursors undergo VDJ recombination to create unique antibody specificity. Germinal centers are sites for B cell activation and proliferation, not gene rearrangement. Lymph nodes and spleen are secondary lymphoid organs where mature lymphocytes are activated, not where VDJ recombination occurs.

Correct Answer: E

Rationale: The correct answer is E because a TH2 immune response is associated with isotype switching to IgE and secretion of IL-4, which are essential for allergic responses. Activation of macrophages is not associated with a TH2 response. Resistance to Leishmania infection is mediated by a TH1 response, not TH2.

Correct Answer: E

Rationale: In this question, the correct answer is C) gp41. This protein is a component of the HIV envelope that plays a crucial role in the fusion of the virus with the host cell membrane. By targeting gp41 therapeutically, we can interfere with this binding process, preventing HIV from entering T lymphocytes and replicating within them. Option A) Reverse transcriptase (RT) is responsible for converting the viral RNA into DNA once the virus has entered the host cell, not for the initial binding process. Option B) Viral proteases are enzymes that cleave viral proteins into functional components but do not directly impact the binding of HIV to T lymphocytes. Option D) Matrix protein is involved in the assembly of the virus particle and not in the binding to host cells. Understanding the specific functions of these HIV proteins is essential for developing effective therapeutic strategies to combat the virus. By targeting gp41, researchers can potentially develop drugs that block HIV entry into host cells, thereby inhibiting viral replication and spread. This knowledge is crucial for students studying immunology, virology, and infectious diseases, as it highlights the importance of targeting specific viral components to design effective treatments.