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Pathology - 3 Questions

1
Pathology
The principal chemical mediator of immediate phase, of acute inflammation is:
1. Serotonin
2. Histamine
3. Kinin-Kallikrein
4. Complement system

📝 Explanation:

The principal chemical mediator of the immediate phase of acute inflammation is Histamine. Here's a detailed explanation of the options given:

1. Serotonin: While serotonin is a vasoactive substance that can cause blood vessels to constrict or dilate, it is not the primary mediator of the immediate phase of acute inflammation. It is mainly associated with the regulation of mood, appetite, and sleep. In the context of inflammation, it plays a minor role compared to histamine.

2. Histamine: Histamine is indeed the correct answer. It is a potent chemical mediator released from mast cells and basophils in response to injury or antigenic stimulation. Upon release, histamine acts on blood vessels to cause vasodilation, increased permeability, and increased blood flow to the injured area, which are hallmark features of the immediate phase of acute inflammation. This results in the cardinal signs of inflammation: redness (rubor), heat (calor), swelling (tumor), and pain (dolor).

3. Kinin-Kallikrein system: The kinin-kallikrein system is another important mediator of inflammation, but it is more involved in the later phases. When activated, it results in the formation of kinins, such as bradykinin, which contribute to increased vascular permeability and pain. However, it is not the first line mediator in the immediate phase.

4. Complement system: The complement system is a group of proteins in the blood that work with antibodies to destroy pathogens and trigger inflammation. It is a key component of the innate immune response, but its activation and role are more pronounced in the later stages of inflammation rather than the immediate phase. The complement system is involved in the opsonization of pathogens, recruitment of phagocytes, and the formation of the membrane attack complex, which can lyse certain bacteria and cells.

The immediate phase of acute inflammation is characterized by the rapid response to tissue injury, which includes vasoactive changes and increased vascular permeability to allow fluid, cells, and proteins to move into the interstitial space. Histamine is quickly released from mast cells and basophils and acts on H1 receptors of blood vessels to induce vasodilation and increased permeability. This leads to the early symptoms of inflammation, such as swelling, redness, heat, and pain, and is crucial for the initiation of the inflammatory response to protect the body from harm.

2
Pathology
All the following can produce febrile jaundice except -
1. Leptospirosis
2. Malaria
3. Enteric fever
4. Viral Hepatitis A

📝 Explanation:

Leptospirosis, Malaria, Viral Hepatitis A can produce febrile jaundice

3
Pathology
The opsonins which leads to phagocytosis is/are:
1. lgG (Fc fragment)
2. C3b of complement cascade
3. 1gM (Fc fragment) and C5b of complement cascade
4. A and B

📝 Explanation:

Opsonins are molecules that enhance the phagocytosis of antigens by binding to their surfaces and acting as markers or labels that make them more recognizable to phagocytes.
1. lgG (Fc fragment): Immunoglobulin G (IgG) is the most common antibody isotype in human serum. It plays a crucial role in the secondary immune response. The Fc region of IgG is the fragment that interacts with Fc receptors present on the membrane of phagocytic cells. When an antigen is coated with IgG, the Fc fragments of these antibodies can bind to the Fc receptors, leading to the activation of the phagocytic process. This is known as antibody-dependent phagocytosis, where the antibody acts as an opsonin to facilitate the recognition and engulfment of the antigen by phagocytic cells.

2. C3b of complement cascade: The complement system is a cascade of proteins that can be activated in response to an infection or the presence of foreign substances. C3 is a central protein in this system, and when it is cleaved into C3a and C3b, the latter can bind directly to antigens. C3b acts as an opsonin by coating the surface of pathogens. The presence of C3b on a microbial surface allows it to be recognized by complement receptors on phagocytic cells, such as macrophages. This interaction enhances the efficiency of phagocytosis, as the receptors can recognize the bound C3b and engulf the antigen more readily.

3. IgM (Fc fragment) and C5b of complement cascade: While IgM is the first antibody isotype produced in response to an infection and can also opsonize antigens, it is less efficient than IgG due to its pentameric structure and lower affinity for phagocytic receptors. However, it is not as commonly associated with phagocytosis as IgG. Regarding C5b, it is part of the membrane attack complex (MAC) and is involved in the direct destruction of pathogens rather than acting as a classical opsonin that leads to phagocytosis. The MAC assembles on the surface of the antigen and creates pores, leading to osmotic lysis and destruction of the cell membrane.

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