General Pathology Practice Questions

Q: Which of the following is NOT an acute phase reactant?

Tissue factor. **Explanation:** Acute Phase Reactants (APRs) are proteins whose plasma concentrations increase (positive APRs) or decrease (negative APRs) by at least 25% in response to inflammation, infection, or tissue injury [1]. This systemic response is primarily mediated by cytokines like **IL-6, IL-1, and TNF-α**, which stimulate the liver to alter protein synthesis [1]. **Why Tissue Factor is the Correct Answer:** **Tissue Factor (Option C)** is a transmembrane glycoprotein constitutively expressed by subendothelial cells (like fibroblasts) and induced in monocytes/endothelial cells during inflammation. While it plays a critical role in the coagulation cascade (extrinsic pathway), it is **not** a plasma protein synthesized by the liver as part of the systemic acute phase response. Therefore, it is not classified as an acute phase reactant. **Analysis of Incorrect Options:** * **CRP (C-Reactive Protein):** A classic positive APR [1]. It acts as an opsonin, fixing complement and facilitating phagocytosis. It is a sensitive marker of systemic inflammation. * **Fibrinogen:** A positive APR that promotes coagulation and causes RBCs to form stacks (rouleaux), which is the physiological basis for an **elevated ESR** during inflammation. * **Serum Amyloid A (SAA):** A positive APR that acts as a chemotactic factor for inflammatory cells. Chronic elevation of SAA can lead to Secondary (AA) Amyloidosis. **High-Yield NEET-PG Pearls:** * **Positive APRs:** "F-C-S" (Fibrinogen, CRP, SAA), Ferritin, Haptoglobin, Ceruloplasmin, and Complement proteins (C3, C4). * **Negative APRs:** Albumin, Transferrin, and Transthyretin (Pre-albumin). These decrease during inflammation to conserve amino acids for positive APRs. * **IL-6** is the most potent stimulator of the hepatic production of acute phase reactants [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 111.

Q: Fibrinoid necrosis may be observed in which of the following conditions?

All the above. **Explanation:** **Fibrinoid necrosis** is a specialized form of cell death characterized by the deposition of immune complexes and plasma proteins (such as fibrin) into the walls of blood vessels [2]. On H&E staining, it appears as a bright pink, "smudgy," and circumferential eosinophilic area. **Why "All the Above" is correct:** The underlying mechanism involves damage to the vessel wall, allowing plasma proteins to leak into the media. This occurs in: 1. **Malignant Hypertension:** Extreme elevation in blood pressure causes acute hemodynamic injury to the arterioles, leading to fibrinoid necrosis (arteriolosclerosis) [2]. 2. **Polyarteritis Nodosa (PAN):** This is a systemic necrotizing vasculitis [1]. Immune complex deposition in the small-to-medium-sized arteries triggers an inflammatory response that destroys the vessel wall, resulting in a classic fibrinoid appearance [1]. 3. **Aschoff Bodies:** Found in the myocardium during **Acute Rheumatic Fever**, these pathognomonic foci of inflammation contain a central area of fibrinoid necrosis surrounded by Anitschkow cells (caterpillar cells). **High-Yield Clinical Pearls for NEET-PG:** * **Appearance:** It is the only type of necrosis that is typically **microscopic** and cannot be identified on gross examination. * **Immune-Mediated:** It is frequently associated with Type III Hypersensitivity reactions (e.g., SLE, Rheumatoid Arthritis). * **Key Site:** It is primarily seen in blood vessels, except for Aschoff bodies (heart) and Rheumatoid nodules (skin/subcutaneous tissue). * **Staining:** It stains intensely with **PAS stain** and **Martius Scarlet Blue (MSB)** due to the presence of fibrin. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 517-518. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 277-278.

Q: Which of the following statements is not true regarding necroptosis?

Caspase 8 is involved, but caspase 9 is not involved.. **Explanation:** Necroptosis is a form of programmed cell death that is morphologically similar to necrosis (cell swelling and membrane rupture) but mechanistically similar to apoptosis (genetically programmed) [1]. **Why Option C is the correct (False) statement:** The hallmark of necroptosis is that it is **caspase-independent**. While the process is often triggered by the ligation of the TNF receptor (TNFR1) [1], it specifically occurs when **Caspase-8 is inhibited or inactivated**. Under normal conditions, Caspase-8 cleaves pro-necroptotic kinases; when Caspase-8 is absent, the **RIPK1-RIPK3 complex** (necrosome) forms, leading to MLKL phosphorylation and membrane rupture [1]. Therefore, neither Caspase-8 nor Caspase-9 is involved in the execution of necroptosis. **Analysis of other options:** * **Option A:** Unlike apoptosis, necroptosis involves the leakage of cellular contents (DAMPs) due to membrane rupture, which triggers an **inflammatory response** [1]. * **Option B:** The final step of necroptosis involves the **MLKL protein** forming pores in the plasma membrane, leading to direct cell membrane damage and lysis. * **Option C:** It occurs in **pathological** states (e.g., ischemia-reperfusion injury, viral infections like CMV, pancreatitis) and **physiological** states (e.g., formation of the mammalian bone growth plate). **High-Yield NEET-PG Pearls:** * **Key Molecule:** MLKL (Mixed Lineage Kinase Domain-like protein) is the "executioner" of necroptosis. * **The Necrosome:** Composed of RIPK1 and RIPK3 kinases [1]. * **Inhibitor:** Necrostatin-1 is a specific inhibitor of RIPK1 used in research. * **Distinction:** It is often called "caspase-independent programmed necrosis" [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 69-71.

Question 1

Which of the following is a Heredofamilial amyloidosis?

Accepted Answer

Systemic senile amyloidosis

Answer

Alzheimer's disease

Answer

Multiple myeloma

Answer

Familial Mediterranean fever

Question 2

Birbeck granules are seen in which of the following conditions?

Accepted Answer

Histiocytosis X

Answer

Gaucher's Disease

Answer

Albinism

Answer

All of the above

Question 3

Which of the following is NOT an acute phase reactant?

Accepted Answer

Tissue factor

Answer

CRP

Answer

Fibrinogen

Answer

Serum amyloid A

Question 4

What is an example of two alleles expressing in a heterozygous state?

Accepted Answer

Codominance expression

Answer

Dominant expression

Answer

Recessive expression

Answer

Hemizygous expression

Question 5

Alpha-1-antitrypsin deficiency is a cause of which of the following conditions?

Accepted Answer

Neonatal hepatitis

Answer

Congenital cystic disease

Answer

Pulmonary fibrosis

Answer

All of the above

Question 6

What is the arrangement of the nuclei in giant cells?

Accepted Answer

Arranged around the periphery

Answer

Present at the center

Answer

Forming a network

Answer

Arranged radially

Question 7

All of the following are examples of tumor markers, except?

Accepted Answer

Alpha-HCG (aHCG)

Answer

Alpha-Feto protein

Answer

Thyroglobulin

Answer

Beta-2-microglobulin

Question 8

Fibrinoid necrosis may be observed in which of the following conditions?

Accepted Answer

All the above

Answer

Malignant Hypertension

Answer

Polyarteritis nodosa

Answer

Aschoff bodies

Question 9

Which of the following statements is not true regarding necroptosis?

Accepted Answer

Caspase 8 is involved, but caspase 9 is not involved.

Answer

Some amount of inflammation is present.

Answer

Cell membrane damage is observed.

Answer

It can be both physiological and pathological.

Question 10

Hypersensitivity pneumonitis is classically a/an?

Accepted Answer

Immune complex mediated hypersensitivity

Answer

Allergic reaction

Answer

Type II hypersensitivity

Answer

Cell mediated hypersensitivity

General Pathology — MCQs

General Pathology — MCQs

On this page

Practice by Chapter

Want unlimited practice?