Inflammation and Repair Practice Questions

Q: The tensile strength of a wound after laparoscopic cholecystectomy in a 30-year-old woman depends upon:

Extensive crosslinking of tropocollagen. ***Extensive crosslinking of tropocollagen*** - Tensile strength is significantly enhanced by the **crosslinking of tropocollagen**, which stabilizes the collagen matrix in the wound [1]. - This process is crucial for the **maturation phase** of wound healing, leading to increased strength over time [1]. *Replacement of type 3 collagen* - Although type 3 collagen is replaced by type 1 during healing, the mere replacement does not directly contribute to **tensile strength** at the early stages. - Type 1 collagen's eventual predominance is important, but it is **crosslinking** that ultimately determines strength [1]. *Granulation tissue* - Granulation tissue is important for wound healing as it provides a framework for new tissue, but it does not directly correlate with **tensile strength**. - It serves more as a temporary scaffold until collagen remodeling occurs, hence its role in strength is indirect. *Macrophage activity/invasion* - While macrophages are essential for **phagocytosis** and **regulating inflammation**, they do not directly affect the tensile strength of the wound. - Their role is more about initiating the healing process rather than contributing to the **structural integrity** of mature scars. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Q: During phagocytosis, the metabolic process called respiratory burst involves the activation of which?

Oxidase. ***Oxidase*** - During the **respiratory burst**, phagocytes activate **NADPH oxidase** (also known as phagocyte oxidase). - This enzyme catalyzes the production of **superoxide radicals** (O2-•), a highly reactive oxygen species critical for killing ingested pathogens. *Hydrolase* - **Hydrolases** are enzymes that catalyze the hydrolysis of chemical bonds, often found in lysosomes. - While lysosomal enzymes are involved in digestion within phagosomes, they are not directly responsible for the initial production of reactive oxygen species during the **respiratory burst**. *Dehydrogenase* - **Dehydrogenases** are enzymes that catalyze the removal of hydrogen atoms from a substrate, typically transferring them to an electron acceptor. - While some dehydrogenases are involved in metabolic pathways that provide precursors for the respiratory burst, they are not the enzyme directly activated to produce reactive oxygen species in the burst itself. *Peroxidase* - **Peroxidases**, such as **myeloperoxidase (MPO)**, are involved in the subsequent steps of the respiratory burst, using hydrogen peroxide (H2O2) to generate other toxic compounds like hypochlorous acid (HOCl). - However, the initial activation to produce the first reactive oxygen species (superoxide) is carried out by **NADPH oxidase**, not a peroxidase.

Q: The acute inflammatory response is predominantly mediated by which type of immune cells?

Neutrophils. ***Neutrophils*** - **Neutrophils** are the **primary mediators** of the **acute inflammatory response**, being the first immune cells recruited to sites of injury or infection (usually within minutes to hours) [1], [3]. - They are **innate immune cells** that perform phagocytosis, release antimicrobial substances, and form neutrophil extracellular traps (NETs) to combat pathogens [1]. - Neutrophils constitute **50-70% of circulating leukocytes** and are the hallmark cells found in acute inflammation [3]. *T lymphocytes* - **T lymphocytes** are central to **cell-mediated immunity** in the adaptive immune response, requiring several days for activation and clonal expansion [2]. - They recognize specific antigens through TCRs and are not involved in the immediate, non-specific phase of acute inflammation. - T cells play roles in **chronic inflammation** and coordinating adaptive immunity, not acute responses. *B lymphocytes* - **B lymphocytes** mediate **humoral immunity** by producing antibodies during the adaptive immune response [1]. - Their activation, differentiation into plasma cells, and antibody production take days to weeks, making them irrelevant to the rapid acute inflammatory response. - B cells are not recruited to acute inflammatory sites in the initial phase. *Both B and T lymphocytes* - While both are critical for **adaptive immunity** and host defense, neither B nor T lymphocytes are primary mediators of acute inflammation [4]. - The acute inflammatory response relies on **innate immune cells** (neutrophils, macrophages, mast cells) for immediate, non-specific protection before adaptive immunity develops [4].

Q: In a patient with Chronic Granulomatous Disease (CGD) experiencing recurrent bacterial and fungal infections, which specific function of phagocytic leukocytes is primarily impaired due to a defect in the NADPH oxidase system?

Production of reactive oxygen species. ***Production of reactive oxygen species*** - Chronic Granulomatous Disease (CGD) is characterized by a defect in the **NADPH oxidase system**, which is crucial for generating a **respiratory burst**. - This respiratory burst is essential for producing **reactive oxygen species (ROS)** like superoxide radicals, which are vital for killing phagocytosed bacteria and fungi [1]. *Migration to infection sites* - The ability of phagocytes to **migrate to infection sites (chemotaxis)** is generally intact in CGD patients. - Defects in migration are more typically associated with conditions like **Leukocyte Adhesion Deficiency**. *Phagocytosis of pathogens* - Phagocytes in CGD can **engulf pathogens (phagocytosis)** normally [1]. - The defect lies in the **intracellular killing** mechanism *after* phagocytosis, not in the uptake itself [1]. *Presentation of antigens to lymphocytes* - Antigen presentation is a function primarily of **antigen-presenting cells (APCs)** like dendritic cells and macrophages, which is generally unaffected in CGD. - This process is crucial for initiating an **adaptive immune response**, a separate function from the innate pathogen killing defect in CGD. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 91.

Question 1

The tensile strength of a wound after laparoscopic cholecystectomy in a 30-year-old woman depends upon:

Accepted Answer

Extensive crosslinking of tropocollagen

Answer

Granulation tissue

Answer

Macrophage activity/invasion

Answer

Replacement of type 3 collagen

Question 2

During phagocytosis, the metabolic process called respiratory burst involves the activation of which?

Accepted Answer

Oxidase

Answer

Hydrolase

Answer

Dehydrogenase

Answer

Peroxidase

Question 3

The acute inflammatory response is predominantly mediated by which type of immune cells?

Accepted Answer

Neutrophils

Answer

T lymphocytes

Answer

Both B and T lymphocytes

Answer

B lymphocytes

Question 4

In a patient with Chronic Granulomatous Disease (CGD) experiencing recurrent bacterial and fungal infections, which specific function of phagocytic leukocytes is primarily impaired due to a defect in the NADPH oxidase system?

Accepted Answer

Production of reactive oxygen species

Answer

Migration to infection sites

Answer

Phagocytosis of pathogens

Answer

Presentation of antigens to lymphocytes

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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