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Granulomatous inflammation

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Granulomatous inflammation

4
Q. 1 A sarcoidosis patient developed non caseating granulomas. Which type of hypersensitivity is responsible for developing granulomatous inflammation in this patient?
 A Type I
 B

Type II
 C

Type III
 D

Type IV
Q. 2

A 49 year old female with shortness of breath is found to have hilar lymphadenopathy on chest x-ray. Biopsy of one of the lymph nodes reveals granulomas, and is highly suggestive of sarcoidosis. Which of the following histological findings must have been present in the biopsy material to support the diagnosis of granulomatous inflammation?

 A

Asteroid bodies
 B

Caseous necrosis
 C

Epithelioid histiocytes
 D

Fibroblast proliferation
Q. 3

The epitheloid cell and multinucleated gaint cells of Granulomatous inflammation are derived from ‑

 A

Basophils
 B

Eosinophils
 C

CD 4 – T lymphocytes
 D

Monocytes – Macrophages
Q. 4

Which of the following is not a cyclin dependent kinase (CDK) inhibitor?

 A

p21
 B

p27
 C

p53
 D

P57
Q. 1

A sarcoidosis patient developed non caseating granulomas. Which type of hypersensitivity is responsible for developing granulomatous inflammation in this patient?

 A

Type I
 B

Type II
 C

Type III
 D

Type IV
Ans. D
Explanation:

Delayed-type hypersensitivity or or type IV hypersensitivity is a T-cell mediated or inflammatory response in which the stimulation of antigen-specific effector T cells leads to macrophage activation and localized inflammation and edema within tissues.

Three variants of type IV hypersensitivity reaction are recognized, contact, tuberculin type and granulomatous.

Contact hypersensitivity and tuberculin-type hypersensitivity both occur within 72 hours of antigen challenge.

Granulomatous hypersensitivity reactions develop over a period of 21-28 days – the granulomas are formed by the aggregation of macrophages and lymphocytes and may persist for weeks.

This is the most important type of hypersensitivity response for producing clinical consequences.

Examples of chronic diseases which manifest type IV granulomatous hypersensitivity are leprosy, tuberculosis, schistosomiasis, sarcoidosis, Crohn’s disease.

Ref: Immunology By David K. Male, 2006, Page 477, 486 ; Immunology by David K. Male, Jonathan Brostoff, Ivan Maurice Roitt, David B. Roth, Page 477-478

Q. 2

A 49 year old female with shortness of breath is found to have hilar lymphadenopathy on chest x-ray. Biopsy of one of the lymph nodes reveals granulomas, and is highly suggestive of sarcoidosis. Which of the following histological findings must have been present in the biopsy material to support the diagnosis of granulomatous inflammation?

 A

Asteroid bodies
 B

Caseous necrosis
 C

Epithelioid histiocytes
 D

Fibroblast proliferation
Ans.
C
Explanation:
A granuloma is defined as a focus of chronic inflammatory reaction in which the predominant cell type is the epithelioid macrophage or histiocyte. Epithelioid histiocytes are recognized on standard H&E preparation by their pale pink cytoplasm and indistinct cell boundaries. Granulomas are generally surrounded by a ring of lymphocytes and infrequent plasma cells.
 
The granulomas of sarcoidosis usually contain many multinucleated giant cells, and frequently these giant cells contain stellate inclusions called asteroid bodies
 
Caseous necrosis describes the gross appearance of cheesy, necrotic debris filling a nodule of active tuberculosis, but also has come to describe its characteristic amorphous and eosinophilic appearance on H&E sections. Caseous necrosis is suggestive of tuberculosis, not sarcoidosis.
 
Over time, fibroblasts proliferate within the core of old, inactive granulomas, eradicating the histiocytes and stereotypical appearance and producing a dense collagenous scar. 
 
Q. 3

The epitheloid cell and multinucleated gaint cells of Granulomatous inflammation are derived from ‑

 A

Basophils
 B

Eosinophils
 C

CD 4 – T lymphocytes
 D

Monocytes – Macrophages
Ans.
D
Explanation:

Ans. is ‘d’ i.e., Monocyte macrophages

In granulomatous inflammation

o Main cells involved                      —->          Macrophages, CD-4 helper T cells.

  • Epitheloid cells                              –          Macrophages that develop epithelial like appearance.
  • Multinucleated giant cells -4 Due to fusion of epitheloid cells.
Q. 4 Which of the following is not a cyclin dependent kinase (CDK) inhibitor?
 A p21
 B

p27
 C

p53
 D

P57
Ans.
C
Explanation:

 

p53 is a tumor supressor gene, that control some CDK inhibitors like p21, but p53 itself is not a CDK inhibitor.

Cell cycle Inhibitors

o The activity of cyclin – CDK complexes is tightly regulated by inhibitors, called CDK inhibitors.

o By inhibiting CDK they inhibit cell cycle and replication –> Act as tumor suppressors.

o There are two main classes of CDK inhibitors ‑

  1. The Cip/kip family
  2. The INK4/ARF family

o The Cip / kip family

      It has 3 components, p21, p27 and p57.

      This binds and inactivate cyclin – CDK complexes.

      Transcriptional activation of p21 is under the control of p53, a tumor suppressor gene that is mutated in a large proportion of human cancers.

o INK 4a/ARF family

      It consists p16INK4a and p14 ARF

     p16 INK4a competes with cyclin D for binding with CDK4, so it inhibits cyclin D-CDK4 complex.

     p14 ARF acts through p53 by preventing its degradation. p53 then activate p21 that inturn inhibit cyclin D-CDK4 complex.