Acute Inflammation: Vascular Events — MCQs

10 questions

A decrease in which of the following is the most likely cause of peripheral edema in a patient with long-term alcoholism and liver disease?

First mediator of inflammation to be released is

In acute inflammation, due to the contraction of the endothelial cell cytoskeleton, which of the following occurs?

Pleural effusion in rheumatoid arthritis is typically associated with the following features except

Vasodilation in acute inflammation is first shown by which blood vessels?

Which of the following is/are characteristic features of chronic inflammation?

All are vasodilators except –

Which protein primarily contributes to oncotic pressure in the blood?

Increased vascular permeability in acute inflammation is due to what?

Q10

Which of the following statements about C-reactive protein (CRP) is true?

Acute Inflammation: Vascular Events Indian Medical PG Practice Questions and MCQs

Question 1: A decrease in which of the following is the most likely cause of peripheral edema in a patient with long-term alcoholism and liver disease?

A. Interstitial colloid osmotic pressure
B. Interstitial hydrostatic pressure
C. Capillary hydrostatic pressure
D. Plasma colloid osmotic pressure (Correct Answer)

Explanation: ***Plasma colloid osmotic pressure*** - **Liver disease** leads to decreased synthesis of **albumin**, the primary protein responsible for maintaining **plasma colloid osmotic pressure** [2]. - A reduction in this pressure allows fluid to extravasate from the capillaries into the interstitial space, causing **edema** [1], [3]. *Interstitial colloid osmotic pressure* - An increase, rather than a decrease, in interstitial colloid osmotic pressure would pull more fluid into the interstitial space, contributing to edema. - However, in liver disease with reduced albumin production, the primary issue is reduced plasma, not interstitial, colloid osmotic pressure [4]. *Interstitial hydrostatic pressure* - An increase in interstitial hydrostatic pressure would tend to drive fluid back into the capillaries, thus *reducing* edema. - A decrease would allow more fluid to accumulate in the interstitium, but this is not the primary mechanism in liver disease-related edema. *Capillary hydrostatic pressure* - An increase in **capillary hydrostatic pressure** can cause edema (e.g., in heart failure) [1]. - While liver disease can lead to conditions like **portal hypertension** (an increase in pressure within the portal venous system), this primarily causes ascites and not directly peripheral edema, which is more directly linked to decreased plasma colloid osmotic pressure [4].

Question 2: First mediator of inflammation to be released is

A. Nitric oxide
B. PAF
C. Histamine (Correct Answer)
D. IL-1

Explanation: ***Histamine*** - Histamine is the **first mediator of inflammation released** by mast cells and basophils during an allergic or inflammatory response [1][3]. - It promotes **vasodilation** and increased vascular permeability, leading to typical symptoms of inflammation [1][2]. *PAF* - Platelet-activating factor (PAF) is released later in the inflammatory process and is primarily involved in **amplifying** the response rather than initiating it. - It plays a role in **platelet aggregation** and acting on vascular smooth muscle but is not the first released mediator. *Nitric oxide* - Nitric oxide is produced by endothelial cells and plays a role in **vascular relaxation and inflammation**, but it is not among the first mediators released. - It is involved in more **regulatory functions** in the inflammatory response rather than the initial trigger. *IL-1* - Interleukin-1 (IL-1) is a cytokine that is important for the **inflammatory response**, but it is produced after the initial release of mediators like histamine [2]. - It is primarily secreted by **activated macrophages** and contributes to the **amplification** of the immune response [2]. **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, p. 101. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94.

Question 3: In acute inflammation, due to the contraction of the endothelial cell cytoskeleton, which of the following occurs?

A. Early transient increase in permeability (Correct Answer)
B. Early permanent increase in permeability
C. Delayed permanent increase in permeability
D. Delayed transient increase in permeability

Explanation: ***Early transient increase in permeability*** - During acute inflammation, the **contraction of the endothelial cell cytoskeleton** leads to a rapid and temporary increase in vascular permeability [1]. - This process allows for the **exudation of fluid and plasma proteins** [1][2], contributing to the inflammatory response. *Early permanent increase in permeability* - Permanent changes in permeability do not occur early; they typically result from **severe injury** or prolonged inflammation. - Early events in inflammation are characterized by a **transient** rather than a permanent change [1]. *Delayed permanent increase in permeability* - Delayed permeability increases occur later in the inflammatory process due to **endothelial cell injury**, not the initial contraction. - This concept relates to more chronic inflammatory processes rather than **acute inflammation**. *Delayed transient increase in permeability* - Delayed transient increases are not typical and **can lead to confusion** regarding cellular responses in acute vs. chronic inflammation. - This oes not accurately represent the **initial response** during acute inflammation. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 187-188. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85.

Question 4: Pleural effusion in rheumatoid arthritis is typically associated with the following features except

A. Glucose > 60 mg/dl (Correct Answer)
B. Protein > 3 gm/dl
C. Pleural fluid LDH to serum LDH ratio of >0.6
D. Pleural fluid protein to serum protein ratio of >0.5

Explanation: ***Glucose > 60 mg/dl*** - Pleural effusions in rheumatoid arthritis are typically characterized by **low glucose levels** (< 30 mg/dL), often due to increased cellular metabolism within the pleural space. - Therefore, a glucose level greater than 60 mg/dL would be an **atypical finding** for a rheumatoid pleural effusion. *Protein > 3 gm/dl* - Rheumatoid pleural effusions are generally **exudative**, meaning they have high protein content, typically greater than 3.0 g/dL. - This high protein level reflects increased capillary permeability and inflammation characteristic of rheumatoid disease. *Pleural fluid LDH to serum LDH ratio of >0.6* - An LDH ratio of pleural fluid to serum greater than 0.6 is a key criterion for an **exudative effusion** based on Light's criteria. - Rheumatoid effusions are almost always exudative, consistent with this elevated LDH ratio. *Pleural fluid protein to serum protein ratio of >0.5* - A pleural fluid protein to serum protein ratio greater than 0.5 also indicates an **exudative effusion**, as per Light's criteria. - This finding is common in rheumatoid pleural effusions due to increased protein leakage into the pleural space from inflammation [1].

Question 5: Vasodilation in acute inflammation is first shown by which blood vessels?

A. Venules
B. Arterioles (Correct Answer)
C. Capillaries
D. Veins

Explanation: ***Arterioles*** - **Arterioles** are the primary sites of **vasodilation** in acute inflammation [1][2], allowing increased blood flow to affected tissues. - They respond rapidly to inflammatory mediators, leading to **decreased vascular resistance** and subsequent hyperemia. *Vein* - While veins can undergo changes in response to inflammation, they typically do not initiate **vasodilation** during acute inflammatory responses. - Their primary role is in **draining blood**, rather than altering flow dynamics significantly in acute conditions. *Capillaries* - Capillaries are where **exudate** occurs, but they do not initiate vasodilation; they primarily facilitate the **exchange** of fluids and nutrients. - Their diameter remains relatively constant; changes primarily occur in arterioles before affecting capillary perfusion. *Venules* - Venules primarily function as sites for **exudation** and are influenced by the arteriolar changes that precede their dilation. - They play a role in **collecting blood** but do not exhibit initial vasodilatory responses during acute inflammation. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 185-186. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.

Question 6: Which of the following is/are characteristic features of chronic inflammation?

A. Infiltration of neutrophils
B. Tissue fibrosis and lymphocyte infiltration (Correct Answer)
C. Increased blood flow (hyperemia)
D. Presence of fluid accumulation (edema) in tissues

Explanation: ***Tissue fibrosis and lymphocyte infiltration*** - **Chronic inflammation** is characterized by the persistent presence of lymphocytes, plasma cells, and macrophages as the predominant inflammatory cells [1]. - **Tissue fibrosis** (scarring) and destruction are hallmarks of chronic inflammation as the body attempts to repair ongoing damage, often leading to loss of organ function [1]. *Infiltration of neutrophils* - **Neutrophils** are the primary inflammatory cells seen in **acute inflammation**, being the first responders to injury or infection [2]. - Their presence typically signifies an active, recent inflammatory process, usually resolving within hours to days. *Increased blood flow (hyperemia)* - **Hyperemia** is a classic sign of **acute inflammation**, contributing to the **redness and warmth** observed at the site. - While some vascular changes can persist in chronic inflammation, pronounced and primary hyperemia is characteristic of the acute phase. *Presence of fluid accumulation (edema) in tissues* - **Edema** primarily results from increased vascular permeability, a key feature of **acute inflammation**, causing swelling [2]. - While some edema may be present in chronic inflammation due to persistent vascular leakage, it is a dominant feature of acute inflammatory responses. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 109-110. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 103-104.

Question 7: All are vasodilators except –

A. Lidocaine
B. Procaine
C. Bupivacaine
D. Cocaine (Correct Answer)

Explanation: ***Cocaine*** - Cocaine is unique among local anesthetics because it causes **vasoconstriction** rather than vasodilation. - This vasoconstrictive effect is due to its blocking of **norepinephrine reuptake** at adrenergic nerve terminals, leading to an accumulation of norepinephrine and subsequent adrenergic stimulation. *Lidocaine* - Lidocaine is a common **amide-type local anesthetic** known for its vasodilatory properties that contribute to its systemic absorption. - Its vasodilatory effect can lead to a **flushing** sensation and increased blood flow in the area of injection. *Procaine* - Procaine is an **ester-type local anesthetic** that causes vasodilation, which results in a relatively short duration of action. - This vasodilation increases **local blood flow**, speeding up the systemic absorption and metabolism of the drug. *Bupivacaine* - Bupivacaine is an **amide-type local anesthetic** with longer duration of action compared to lidocaine, and like most local anesthetics, it causes vasodilation. - The vasodilatory effect of bupivacaine can lead to increased **systemic absorption** and potential for systemic toxicity if not managed carefully.

Question 8: Which protein primarily contributes to oncotic pressure in the blood?

A. Albumin (Correct Answer)
B. Globulins
C. Fibrinogen
D. Transferrin

Explanation: ***Albumin*** - **Albumin** is the most abundant plasma protein and its small size and high concentration make it the primary determinant of **oncotic pressure** in the blood. - Its presence in the capillaries draws water from the **interstitial space** back into the blood vessels, maintaining **fluid balance** and blood volume. *Fibrinogen* - **Fibrinogen** is a crucial protein involved in **blood clotting**, where it is converted into **fibrin** to form a clot. - While a plasma protein, its contribution to **oncotic pressure** is minor compared to albumin, as it's less abundant and larger in size. *Globulins* - **Globulins** are a diverse group of proteins involved in immune function (**immunoglobulins**), transport (e.g., **alpha** and **beta globulins**), and clotting. - While they contribute to total plasma protein concentration, their collective impact on **oncotic pressure** is secondary to that of albumin due to lower concentrations and varied molecular weights. *Transferrin* - **Transferrin** is a specific **beta-globulin** that plays a vital role in **iron transport** in the blood. - Its primary function is not related to **oncotic pressure**, and its concentration is significantly lower than albumin.

Question 9: Increased vascular permeability in acute inflammation is due to what?

A. Histamine (Correct Answer)
B. IL-2
C. TGF-β
D. FGF-2

Explanation: ***Histamine*** - Histamine is a key **mediator** released during acute inflammation that causes **increased vascular permeability** by inducing **contraction of endothelial cells** [1][2]. - Its release contributes to the hallmark signs of inflammation, including **swelling** and **redness** [2]. *IL 2* - IL 2 primarily functions as a **growth factor** for T cells, not directly influencing vascular permeability in acute inflammation. - It is more involved in the **adaptive immune response** rather than in the acute phase of inflammation. *TGF beta* - TGF beta is primarily involved in **fibrosis** and **tissue repair** and does not play a direct role in increasing vascular permeability during acute phases. - It acts more as an **anti-inflammatory** cytokine rather than a pro-inflammatory mediator. *FGF* - Fibroblast growth factor (FGF) is mainly involved in **angiogenesis** and wound healing rather than direct modulation of vascular permeability during acute inflammation. - It does not contribute to **edema formation** associated with acute inflammatory responses. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 187-188. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.

Question 10: Which of the following statements about C-reactive protein (CRP) is true?

A. It is detected by agglutination test.
B. It is raised in acute pneumococcal infection. (Correct Answer)
C. It is an antibody.
D. It is detected by precipitation with carbohydrate.

Explanation: ***It is raised in acute pneumococcal infection.*** - **C-reactive protein (CRP)** is an **acute-phase reactant** whose levels rise rapidly and significantly in response to inflammation and infection [1]. - **Pneumococcal infection** (e.g., pneumonia) is an acute bacterial infection that triggers a strong inflammatory response, leading to increased CRP synthesis by the liver [1]. *It is detected by agglutination test.* - While some tests for CRP can involve **agglutination assays**, this statement describes a method of detection rather than a fundamental property or primary clinical utility of CRP itself. - CRP is more commonly quantified via methods like **nephelometry** or **turbidimetry** in modern laboratories due to their higher sensitivity. *It is an antibody.* - **CRP** is a **pentameric protein** produced by the liver, belonging to the **pentraxin family** of proteins. - It functions as a non-specific innate immune molecule, primarily involved in binding to damaged cells and pathogens to facilitate their clearance, but it does **not possess antigen-specific binding** characteristic of antibodies. *It is detected by precipitation with carbohydrate.* - **CRP** was originally named for its ability to precipitate the **C-polysaccharide** of *Streptococcus pneumoniae*. - However, this historical observation describes a specific interaction rather than the general method by which CRP is clinically detected or its primary biological function. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 109-111.

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