Systemic Effects of Inflammation Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Systemic Effects of Inflammation. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Systemic Effects of Inflammation Indian Medical PG Question 1: A patient presents with pallor, glossitis, and jaundice. Labs show high MCV and hypersegmented neutrophils. What is the most likely cause?
- A. Iron deficiency
- B. Vitamin B12 deficiency (Correct Answer)
- C. Folate deficiency
- D. Hemolysis
Systemic Effects of Inflammation Explanation: ***Vitamin B12 deficiency***
- The combination of **pallor**, **glossitis**, **jaundice**, **high MCV (macrocytic anemia)**, and **hypersegmented neutrophils** is classic for megaloblastic anemia due to Vitamin B12 deficiency [1].
- **Jaundice** occurs due to ineffective erythropoiesis leading to intramedullary hemolysis and release of unconjugated bilirubin.
*Iron deficiency*
- This typically causes **microcytic, hypochromic anemia (low MCV)**, not high MCV [2].
- While it can cause pallor and glossitis, it does not cause **hypersegmented neutrophils** or jaundice.
*Folate deficiency*
- Folate deficiency also causes **macrocytic anemia** and **hypersegmented neutrophils**, along with pallor and glossitis [1].
- However, **jaundice** is more characteristic of Vitamin B12 deficiency due to the more pronounced ineffective erythropoiesis and associated hemolysis.
*Hemolysis*
- Hemolysis can cause **jaundice** and **pallor** due to the accelerated destruction of red blood cells.
- However, acute or isolated hemolysis does not typically lead to **high MCV** or **hypersegmented neutrophils**, which are hallmarks of megaloblastic anemias.
Systemic Effects of Inflammation Indian Medical PG Question 2: All of the following are classical mediators of inflammation, except which of the following?
- A. Prostaglandins
- B. Interleukin-1 (IL-1)
- C. Tumour necrosis factor-alpha (TNF-alpha)
- D. Myeloperoxidase (MPO) (Correct Answer)
Systemic Effects of Inflammation Explanation: ***Myeloperoxidase***
- **Myeloperoxidase** is primarily an enzyme involved in the microbial killing process in neutrophils, not a typical mediator of inflammation.
- It catalyzes the production of **hypochlorous acid** (HOCl) during the oxidative burst, more related to pathogen destruction than inflammation mediation.
*Tumour necrosis factor-a (TNF-a)*
- **TNF-a** is a key pro-inflammatory cytokine that plays a significant role in systemic inflammation and is involved in the acute phase response [1][3].
- It promotes the recruitment of immune cells to sites of inflammation and is involved in the activation of the inflammatory process [1][3].
*Prostaglandins*
- **Prostaglandins** are lipid mediators derived from arachidonic acid that have various roles, including enhancing inflammation and pain signaling [1][2].
- They contribute to vasodilation, increased vascular permeability, and sensitization of nociceptors during inflammatory responses [1][2].
*Interleukin-1*
- **Interleukin-1** (IL-1) is a crucial inflammatory cytokine that stimulates immune responses and is involved in both acute and chronic inflammation [1][3].
- It can induce fever and promote the expression of adhesion molecules on endothelial cells, facilitating leukocyte migration [1][3].
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.
[2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96.
[3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 97-99.
Systemic Effects of Inflammation Indian Medical PG Question 3: A peripheral smear with increased neutrophils, basophils, eosinophils, and platelets is highly suggestive of:
- A. Acute myeloid leukemia
- B. Acute lymphoblastic leukemia
- C. Chronic myelogenous leukemia (Correct Answer)
- D. Myelodysplastic syndrome
Systemic Effects of Inflammation Explanation: ***Chronic myelogenous leukemia***
- Characterized by a **marked increase in granulocytes** (including neutrophils, basophils, and eosinophils) and often presents with **thrombocytosis** (increased platelets) [1].
- The presence of these cell types in combination aligns with the typical **myeloid cell proliferation** seen in CML [2].
*Acute lymphoblastic leukemia*
- Primarily involves **lymphoblasts** and typically presents with a predominance of **lymphocytes**, not myeloid cells.
- Does not typically show the **elevated basophil and eosinophil counts** seen in this case.
*Myelodysplastic syndrome*
- Usually characterized by **ineffective hematopoiesis** leading to cytopenias in various lineages rather than increased counts.
- There's no significant rise in myeloid cells; this disorder typically presents with poor-quality cells and potential progression to leukemia.
*Acute myeloid leukemia*
- Features predominantly **myeloblasts** and usually presents with a rapid decline in blood cell counts, not an increase.
- While it presents with myeloid proliferation, it lacks the characteristic **chronic progression** and the increase in basophils and eosinophils seen in CML.
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 625-626.
[2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612.
Systemic Effects of Inflammation Indian Medical PG Question 4: Which of the following is NOT a characteristic of Systemic Inflammatory Response Syndrome (SIRS)?
- A. Oral temperature more than 38 degrees C
- B. Thrombocytopenia (Correct Answer)
- C. Leukocytosis
- D. Infectious or non-infectious cause
Systemic Effects of Inflammation Explanation: Thrombocytopenia
- While **thrombocytopenia** can occur in severe cases of sepsis or disseminated intravascular coagulation (DIC), it is not one of the **defining criteria** for SIRS.
- SIRS is primarily characterized by responses such as changes in **temperature**, **heart rate**, **respiratory rate**, and **white blood cell count** [1].
*Leukocytosis*
- **Leukocytosis** (WBC count > 12,000 cells/mm³) is a **characteristic diagnostic criterion** for SIRS, indicating an inflammatory response [1].
- It reflects the body's attempt to combat an infection or injury by increasing the production of **white blood cells**.
*Oral temperature more than 38 degrees C*
- **Fever** (oral temperature > 38°C or 100.4°F) is a **key diagnostic criterion** for SIRS, indicating an inflammatory state [2].
- This elevated temperature is part of the body's systemic response to various insults, including **infection** or **trauma**.
*Infectious or non-infectious cause*
- SIRS can be triggered by a wide range of conditions, both **infectious** (e.g., bacterial sepsis) and **non-infectious** (e.g., pancreatitis, burns, trauma).
- The definition of SIRS focuses on the **physiological response** rather than the underlying etiology.
Systemic Effects of Inflammation Indian Medical PG Question 5: Which of the following is not an acute phase reactant?
- A. C-reactive protein
- B. Haptoglobin
- C. Endothelin (Correct Answer)
- D. Fibrinogen
Systemic Effects of Inflammation Explanation: ***Endothelin***
- Endothelin is a **vasoconstrictive peptide** primarily involved in regulating **blood vessel tone** and blood pressure.
- While it plays a role in processes like inflammation and tissue repair, it is not synthesized or regulated in the same rapid, systemic manner as a classic acute phase reactant.
*C-reactive protein*
- **C-reactive protein (CRP)** is a rapidly responding acute phase reactant produced by the liver in response to **inflammation**, infection, and tissue injury.
- Its levels can rise dramatically within hours of an inflammatory stimulus and are used as a marker for disease activity.
*Haptoglobin*
- **Haptoglobin** is an acute phase reactant that binds to free **hemoglobin** released from red blood cells during hemolysis, preventing oxidative damage.
- Its levels typically increase during acute inflammation or infection, although it can also decrease with severe hemolysis.
*Fibrinogen*
- **Fibrinogen** is a critical acute phase protein involved in the **coagulation cascade** and wound healing.
- Its concentration increases significantly during acute inflammation, contributing to the elevated **erythrocyte sedimentation rate (ESR)**.
Systemic Effects of Inflammation Indian Medical PG Question 6: A 17-year-old boy is admitted to the hospital with a traumatic brain injury, sustained when he fell off his motorcycle. He develops a fever of 39°C, which is unrelated to an infection or inflammation. The fever is most likely due to a lesion of which of the following?
- A. The posterior nucleus
- B. The anterior hypothalamus (Correct Answer)
- C. The arcuate nucleus
- D. The lateral hypothalamus
Systemic Effects of Inflammation Explanation: ***The anterior hypothalamus***
- The **anterior hypothalamus** is responsible for **heat dissipation**, including sweating and vasodilation. A lesion here impairs the body's ability to cool down, leading to **hyperthermia** (fever) even without infection or inflammation.
- This type of fever, often seen after traumatic brain injury, is referred to as **central fever** or **hypothalamic fever**.
*The posterior nucleus*
- The **posterior hypothalamus** is primarily involved in **heat conservation** and production, such as shivering and vasoconstriction.
- A lesion here would more likely lead to **hypothermia** due to impaired heat generation, rather than hyperthermia.
*The arcuate nucleus*
- The **arcuate nucleus** plays a crucial role in regulating **appetite** and **satiety** through the production of neuropeptides like NPY and POMC.
- It is not directly involved in the central control of body temperature, so a lesion here would not cause fever.
*The lateral hypothalamus*
- The **lateral hypothalamus** contains the **feeding center** and is primarily involved in stimulating appetite.
- Damage to this area typically leads to **anorexia** and weight loss, not an uncontrolled increase in body temperature.
Systemic Effects of Inflammation Indian Medical PG Question 7: Antecedent diagnosis of Group A streptococcal infection in Acute rheumatic fever can be made by?
- A. ASO (Correct Answer)
- B. ESR elevation
- C. Low C3 levels
- D. CRP
Systemic Effects of Inflammation Explanation: ***ASO***
- ASO (Antistreptolysin O) titer measures antibodies to **Streptolysin O**, a toxin produced by Group A Streptococcus (GAS), indicating a recent GAS infection.
- An elevated or rising ASO titer is a key diagnostic criterion for confirming a preceding GAS infection in the context of **Acute Rheumatic Fever (ARF)** [1].
*ESR elevation*
- **Erythrocyte Sedimentation Rate (ESR)** is a non-specific marker of inflammation and will be elevated in ARF, but it does not confirm a preceding GAS infection [2].
- Many inflammatory conditions can cause ESR elevation, hence it's not specific for antecedent streptococcal infection.
*Low C3 levels*
- **Low C3 levels** are typically associated with complement consumption in diseases like systemic lupus erythematosus or post-streptococcal glomerulonephritis, not directly with ARF.
- While post-streptococcal glomerulonephritis can follow a GAS infection, ARF does not primarily involve significant C3 depression as a diagnostic feature.
*CRP*
- **C-reactive protein (CRP)** is another non-specific acute-phase reactant that is elevated during inflammation, including ARF [2].
- Like ESR, elevated CRP indicates inflammation but does not specifically confirm an antecedent **Group A streptococcal infection**.
Systemic Effects of Inflammation Indian Medical PG Question 8: Rolling of leucocytes on endothelial cells is mediated by which of the following proteins?
- A. Integrins
- B. Transferrin
- C. PECAM-1
- D. Selectins (Correct Answer)
Systemic Effects of Inflammation Explanation: **Selectins**
- **Selectins** mediate the initial, weak and transient adhesion of **leukocytes** to the **endothelial cells** lining blood vessels [1].
- This interaction slows down the leukocytes, causing them to **roll** along the vascular endothelium as a prerequisite for **extravasation** [1].
*Integrins*
- **Integrins** are responsible for the **firm adhesion** of leukocytes to endothelial cells, but not the rolling [1].
- They bind to **ICAM-1 (intercellular adhesion molecule-1)** on endothelial cells, leading to stable arrest of the leukocyte [1].
*PECAM-1*
- **PECAM-1 (Platelet Endothelial Cell Adhesion Molecule-1)** plays a role in **diapedesis** or **transmigration**, the movement of leukocytes *through* the endothelial cell junctions [1].
- It facilitates the passage of the leukocyte by interacting with PECAM-1 on the endothelial cells, but does not mediate rolling [1].
*Transferrin*
- **Transferrin** is an iron-binding protein found in blood plasma that regulates free **iron levels** in the body.
- It is crucial for **iron transport** and metabolic processes but has no direct role in leukocyte adhesion or rolling on endothelial cells.
**References:**
[1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89.
Systemic Effects of Inflammation Indian Medical PG Question 9: Pelvic abscess can present with all symptoms except:
- A. bleeding rectum (Correct Answer)
- B. pain abdomen
- C. diarrhea with mucus discharge
- D. fever
Systemic Effects of Inflammation Explanation: ***bleeding rectum***
- A **bleeding rectum** is not a typical presentation of a pelvic abscess. It might suggest other conditions like hemorrhoids, colorectal cancer, or inflammatory bowel disease.
- Pelvic abscesses are collections of pus in the pelvic cavity, and while they can cause various gastrointestinal symptoms due to local inflammation and pressure, direct rectal bleeding is generally not among them.
*pain abdomen*
- **Abdominal pain** is a very common symptom of a pelvic abscess, often localized to the lower abdomen.
- This pain is caused by inflammation, pressure, and irritation of surrounding organs and tissues.
*diarrhea with mucus discharge*
- A pelvic abscess can cause irritation to the adjacent **bowel segments**, leading to changes in bowel habits such as diarrhea.
- The presence of **mucus discharge** can also be a sign of bowel irritation or inflammation, which can occur secondary to a nearby abscess.
*fever*
- **Fever** is a classic systemic sign of infection and inflammation, and thus is almost always present in patients with an abscess, including a pelvic abscess.
- The body's inflammatory response to the infection typically elevates body temperature.
Systemic Effects of Inflammation Indian Medical PG Question 10: The drug of choice for Sydenham chorea is:
- A. Diazepam
- B. Sodium valproate
- C. Haloperidol (Correct Answer)
- D. Prednisolone
Systemic Effects of Inflammation Explanation: ***Haloperidol***
- **Haloperidol** is an antipsychotic with **dopamine receptor blocking** effects, which can effectively reduce the involuntary movements of Sydenham chorea.
- It works by modulating **dopaminergic pathways** in the basal ganglia, thereby diminishing choreiform movements [1].
*Diazepam*
- **Diazepam** is a **benzodiazepine** that acts as a central nervous system depressant and is used for anxiety, seizures, and muscle spasms [2].
- While it has sedative properties, it is not the primary drug of choice for specifically controlling the **hyperkinetic movements** of Sydenham chorea.
*Sodium valproate*
- **Sodium valproate** is an antiepileptic drug that can be used for various seizure types and bipolar disorder.
- While it may have some role in managing certain movement disorders, it is not the **first-line agent** for Sydenham chorea.
*Prednisolone*
- **Prednisolone** is a corticosteroid used to reduce inflammation and suppress the immune system.
- While corticosteroids may be used in severe cases of **rheumatic fever** (the underlying cause of Sydenham chorea) to address carditis or arthritis, they are not the primary treatment for the **chorea itself**.
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