Hypersensitivity MCQs

Type II reactions involve antibodies directed against self-cells (erythrocytes) or membranes. Certain drugs react with erythrocytes to form neoantigens. Type I responses are against foreign antigens (e.g., allergens), cause IgE responses, and do not invoke a Coomb's reaction. Type III reactions involve soluble antigen-antibody complexes, and type IV reactions do not involve antibody. Reference: Ananthanarayan and Paniker's Textbook of Microbiology 10th edition Chapter 16, Pg 164-168

Basophils and mast cells bind IgE via high affinity Fc receptors, so each cell has IgE of many different specificities on its surface. Ca2+is required Many non-lgE triggers (C3a and C5a) can produce granule release. IgE Fc receptor crosslinking triggers release of granule content from mast cell. Referene: Ananthanarayan and Paniker's Textbook of Microbiology 10th edition Chapter 16, Pg 164-168

This patient had a major anaphylactic reaction and his tracheal-bronchial smooth muscle has contracted. Epinephrine is the only treatment in this group to reverse this reaction. It will relax the smooth muscle of the respiratory tree and stimulate the heart to beat stronger to raise the blood pressure. Reference: Ananthanarayan and Paniker's Textbook of Microbiology 10th edition Chapter 16, Pg 164-168

The patient has a defect in the lymphocytic lineage. This could be permanently restored by replacement of defective stem cells through bone marrow transplantation. Isolation is beneficial but is a severe imposition on the quality of life and constitutes protection rather than restoration of function. The remaining choices require constant repetitive application but not permanent restoration of function. Reference: Ananthanarayan and Paniker's Textbook of Microbiology 10th edition Chapter 19, Pg 187-190

Myasthenia gravis: Characterized by the presence of anti-acetylcholine receptor antibodies, leading to muscle weakness due to impaired neuromuscular transmission. Hashimoto's thyroiditis: Involves autoantibodies against thyroid peroxidase and does not typically present with anti-acetylcholine receptor antibodies. Grave's disease: Involves autoantibodies against the thyroid-stimulating hormone (TSH) receptor, not acetylcholine receptors. Addison's disease: Involves adrenal cortex autoantibodies, not anti-acetylcholine receptor antibodies. Key Takeaway: Anti-acetylcholine receptor antibodies are indicative of myasthenia gravis. Tags: FMGE2023 Tag Line: Easy Reference: Shastri, A., & Bhatt, S. (2023). Essential Microbiology . Chapter 17: Autoimmunity, pp. 203-207

HLA gene variations (Human Leukocyte Antigen) are strongly associated with susceptibility to various autoimmune diseases due to their role in immune system regulation. Mitochondrial DNA mutations are related to mitochondrial disorders, not specifically autoimmune diseases. X-linked chromosomal abnormalities can affect various genetic conditions but are less directly linked to autoimmune diseases. SNPs in non-coding regions may play a role but are not as directly associated with autoimmune risk as HLA variations. Key Takeaway: HLA gene variations are significant genetic factors in autoimmune disease susceptibility. Tags: Clinical | integrated Tag Line: Genetic Insights Reference: Shastri, A., & Bhatt, S. (2023). Essential Microbiology . Chapter 17: Autoimmunity, pp. 203-207

HLA-B27: This MHC Class I allele is strongly associated with an increased risk of developing ankylosing spondylitis, a type of inflammatory arthritis. HLA-B35 and C. HLA-A2 are not specifically linked to ankylosing spondylitis. HLA-Cw6 is associated with psoriasis, not ankylosing spondylitis. Key Takeaway: HLA-B27 is a key genetic marker for susceptibility to ankylosing spondylitis. Tags: FMGE 2020 | Good to know Tag Line: Hard Reference: Shastri, A., & Bhatt, S. (2023). Essential Microbiology . Chapter 14: Autoimmunity, pp. 170-183.

Ans. is 'c' i.e., Normal B cells Most patients with common variable immunodeficiency have normal or near-normal numbers of B cells in the blood and lymphoid tissues. These B cells, however, are not able to differentiate into plasma cells. The clinical manifestations are caused by antibody deficiency. The feature common to all patients is hypogammaglobulinemia, generally affecting all the antibody classes but sometimes only IgG.