Inflammation and Repair Practice Questions

Q: What is the primary effect of the cytokine interleukin-1 on the acute phase response?

Increases C-reactive protein synthesis. ***Increases C-reactive protein synthesis*** - **Interleukin-1 (IL-1)**, along with **IL-6** and **TNF-α**, is a key cytokine that stimulates hepatocytes to synthesize **acute phase proteins**, including **C-reactive protein (CRP)** [1]. - Elevated CRP levels are a hallmark of the **acute phase response**, indicating systemic inflammation or infection [1]. *Promotes fibrinogen production* - While **fibrinogen** is an acute phase reactant, its production is primarily stimulated by **IL-6**, rather than IL-1 directly [1]. - Fibrinogen plays a crucial role in **coagulation** and also contributes to the **erythrocyte sedimentation rate (ESR)**. *Enhances white blood cell production* - **Granulocyte-colony stimulating factor (G-CSF)** and **granulocyte-macrophage colony-stimulating factor (GM-CSF)** are the primary cytokines responsible for enhancing **white blood cell production** (leukopoiesis) [1]. - While IL-1 can indirectly promote the release of these factors, it is not its primary and direct effect on the acute phase response. *Enhances insulin secretion* - **Insulin secretion** is primarily regulated by **blood glucose levels** and factors like **glucagon-like peptide-1 (GLP-1)**. - IL-1 is associated with **insulin resistance** and pancreatic beta-cell dysfunction in chronic inflammation, rather than directly enhancing insulin secretion [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 111.

Q: What is the PRIMARY mechanism by which Interleukin-1 (IL-1) induces fever?

Endogenous pyrogen. ***Endogenous pyrogen*** - **IL-1** is a potent **endogenous pyrogen** that acts directly on the **hypothalamus**, the body's thermoregulatory center. - It stimulates the production of **prostaglandin E2 (PGE2)** in the hypothalamus, which then resets the body's thermoregulatory set point to a higher temperature, leading to fever. *Stimulates antibody production* - While IL-1 can have broader immune functions and can influence B cell activity, its **primary role in fever** production is not through antibody stimulation. - Antibody production is a function of **B lymphocytes** and is primarily driven by antigen presentation and T cell help. *Inhibits inflammation* - **IL-1** is a key **pro-inflammatory cytokine** that promotes inflammation, rather than inhibiting it. - It induces the expression of various adhesion molecules and inflammatory mediators, contributing to the inflammatory response. *Activates complement cascade* - The **complement cascade** is a part of the innate immune system, typically activated by **antigen-antibody complexes** (classical pathway) or **microbial surfaces** (alternative and lectin pathways). - While IL-1 plays a role in overall immune responses, its direct mechanism for inducing fever does not primarily involve activating the complement system.

Q: Reactive nitrogen species for killing of microbes are mainly derived from

Nitric Oxide [NO]. ***Nitric Oxide [NO]*** - **Nitric oxide (NO)** is a key reactive nitrogen species produced by immune cells (e.g., macrophages) via nitric oxide synthase, which is crucial for killing intracellular pathogens. - It reacts with **superoxide radicals** to form other highly reactive and potent antimicrobial species like **peroxynitrite**. *Elemental nitrogen [N2]* - **Elemental nitrogen (N2)** is an inert gas constituting about 78% of the atmosphere and is not directly involved in the immune killing of microbes. - It must be "fixed" into biologically available forms by specific bacteria, a process distinct from host immune responses. *Nitrogen Dioxide [NO2]* - **Nitrogen dioxide (NO2)** can be formed from NO, particularly in the presence of oxygen, and can act as a reactive species, but **NO** is the primary precursor generated by immune cells for direct antimicrobial action. - While it has some oxidative potential, it is not the main biologically derived RNS for direct microbial control within phagocytes. *Nitrous Oxide [N2O]* - **Nitrous oxide (N2O)**, commonly known as laughing gas, is primarily used as an anesthetic agent and is not a significant **reactive nitrogen species** (RNS) involved in the host immune defense against microbes. - It is metabolically stable and does not participate in the cytotoxic reactions against pathogens like NO.

Q: Lymphotactin is which type of chemokine?

C. ***C*** - **Lymphotactin**, also known as **XCL1**, is a chemokine belonging to the C chemokine subfamily. - This subfamily is characterized by having **only one cysteine residue** at the N-terminus, distinguishing it from other chemokine subfamilies. *CC* - **CC chemokines** (or β-chemokines) have **two adjacent cysteine residues** at their N-terminus. - Examples include **MCP-1** and **MIP-1α**, which primarily attract monocytes and macrophages. *CX3C* - **CX3C chemokines** possess a unique motif with **three amino acids separating the first two cysteine residues** (C-X3-C). - **Fractalkine (CX3CL1)** is the sole member of this subfamily, acting as both an adhesion molecule and a chemoattractant. *CXC* - **CXC chemokines** (or α-chemokines) have **one amino acid separating the first two cysteine residues** at their N-terminus (C-X-C). - Examples include **IL-8** and **IP-10**, which primarily attract neutrophils and lymphocytes, respectively.

Q: Normal time for wound healing to transition from proliferative to maturation phase after injury is?

3 weeks. ***4 weeks*** - The normal time for scar formation is generally around **4 weeks**, allowing for significant collagen deposition and remodeling [1]. - This timeframe signifies the transition from initial wound healing to the maturation phase where the scar solidifies. *2 weeks* - At 2 weeks, the healing is in the **inflammatory** and early proliferative phase, not fully developed into a scar. - Scar formation generally requires a longer duration for sufficient **collagen synthesis** and tissue remodeling. *3 weeks* - By 3 weeks, the wound is progressing, but it still lacks the **structural integrity** of a mature scar. - Scar formation typically reaches its recognizable stage by **4 weeks**, with formal remodeling continuing thereafter. *5 weeks* - While healing continues past 4 weeks, **5 weeks** is longer than the typical duration for initial scar formation, possibly suggesting delayed healing. - By this point, the scar should be present, but significant remodeling will still occur beyond this period. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119.

Q: What is the primary mediator of vasodilatation following endothelial damage?

Histamine. ***Histamine*** - Histamine is a ** potent vasodilator** released during endothelial damage, leading to increased vascular permeability and blood flow [1]. - It causes **smooth muscle relaxation** in the blood vessels, contributing to vasodilatation [1]. - Histamine is one of the most important mediators of acute inflammation, normally sequestered in intracellular granules and rapidly secreted by granule exocytosis from mast cells [2]. *TGF-3* - Transforming growth factor-beta 3 (TGF-3) primarily plays a role in **cell differentiation and inflammation**, rather than immediate vasodilatation. - It is not directly involved in the acute vascular response to endothelial injury. *IL-2* - Interleukin-2 (IL-2) is mainly associated with **T-cell proliferation** and activation in the immune response, not with vasodilatation. - Its effects are more related to **adaptive immunity** rather than direct vascular effects. *FGF* - Fibroblast growth factor (FGF) is involved in **angiogenesis** and tissue repair but does not induce immediate vasodilatation post-endothelial damage. - It primarily promotes **cell proliferation** and differentiation rather than causing direct vasodilatation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94.

Q: Which of the following cytokines stimulate acute phase reactants?

All of the options. ***All of the above*** - Acute phase reactants are stimulated by various **cytokines**, including IL-6, TNF-α, and IL-1, highlighting a coordinated immune response [1]. - The presence of multiple cytokines indicates that a range of **inflammatory processes** contributes to the activation of the acute phase response [1]. *IL-6* - While IL-6 is indeed a **key mediator** in acute phase reactions, it is not the only cytokine responsible for stimulating this response [1]. - Other cytokines like **TNF-α** and **IL-1** also play significant roles, making this option incomplete [1][2]. *TNF-a* - TNF-α is a crucial cytokine that can stimulate acute phase reactants, but it does not act alone in this process [2]. - The role of **multiple cytokines** (including IL-6 and IL-1) makes this option insufficient on its own [1]. *IL-1* - IL-1 is known to activate acute phase reactants, but similar to the others, it is **not the sole factor** and works in conjunction with other cytokines [2]. - Therefore, like TNF-α and IL-6, its contribution alone does not capture the complete picture [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 97-99. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 110-111.

Question 1

What is the primary effect of the cytokine interleukin-1 on the acute phase response?

Accepted Answer

Increases C-reactive protein synthesis

Answer

Enhances insulin secretion

Answer

Promotes fibrinogen production

Answer

Enhances white blood cell production

Question 2

A patient with chronic granulomatous disease is unable to produce which of the following substances that are necessary for microbial killing?

Accepted Answer

Superoxide anion

Answer

Hydrogen peroxide

Answer

Nitric oxide

Answer

Hypochlorous acid

Question 3

What is the PRIMARY mechanism by which Interleukin-1 (IL-1) induces fever?

Accepted Answer

Endogenous pyrogen

Answer

Stimulates antibody production

Answer

Inhibits inflammation

Answer

Activates complement cascade

Question 4

Which of the following statements is MOST accurate regarding keloids?

Accepted Answer

It is associated with elevated growth factors

Answer

It does not extend beyond the wound

Answer

It does not recur after simple excision

Answer

None of the options

Question 5

Reactive nitrogen species for killing of microbes are mainly derived from

Accepted Answer

Nitric Oxide [NO]

Answer

Elemental nitrogen [N2]

Answer

Nitrogen Dioxide [NO2]

Answer

Nitrous Oxide [N2O]

Question 6

Lymphotactin is which type of chemokine?

Accepted Answer

C

Answer

CC

Answer

CX3C

Answer

CXC

Question 7

Which enzyme secreted by neutrophils catalyzes the production of hypochlorous acid for pathogen killing?

Accepted Answer

An enzyme that catalyzes the production of hypochlorous acid

Answer

A protein involved in immune response

Answer

An enzyme that breaks down proteins

Answer

A type of carbohydrate

Question 8

Normal time for wound healing to transition from proliferative to maturation phase after injury is?

Accepted Answer

3 weeks

Answer

2 weeks

Answer

4 weeks

Answer

5 weeks

Question 9

What is the primary mediator of vasodilatation following endothelial damage?

Accepted Answer

Histamine

Answer

IL-2

Answer

TGF-β3

Answer

FGF

Question 10

Which of the following cytokines stimulate acute phase reactants?

Accepted Answer

All of the options

Answer

IL-1

Answer

IL-6

Answer

TNF-α

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

On this page

Practice by Chapter

Want unlimited practice?