Oncofoetal antigens are substances that are normally present in the developing fetus but are found in abnormally high quantities in the tissues of certain cancer cells. These antigens are proteins that can be used as markers for the detection of certain types of cancers. The presence of these antigens in cancer cells suggests that the tumor cells have partially reverted to a more primitive, embryonic stage of development.

Explanation for each option:

1. á-Fetoprotein (AFP): This is an oncofoetal antigen. It is a glycoprotein that is produced by the liver cells of the developing fetus. In adults, the production of AFP is usually very low. However, in cases of certain cancers such as hepatocellular carcinoma (primary liver cancer) and some types of testicular cancer, the tumor cells start producing AFP in large amounts. Therefore, high levels of AFP in the blood can be indicative of these cancers.

2. Carcinoembryonic antigen (CEA): CEA is another example of an oncofoetal antigen. It is a glycoprotein that is present in the gastrointestinal tract, pancreas, and sometimes in the respiratory and reproductive systems of a developing fetus. In adults, CEA levels are typically very low. However, in certain types of cancers, such as colorectal cancer, gastric cancer, and some forms of lung, pancreatic, and breast cancer, the tumor cells may start producing large amounts of CEA, which can be detected in the blood and used as a tumor marker for these malignancies.

3. A and B: Both α-fetoprotein and carcinoembryonic antigen are examples of oncofoetal antigens, so this option is correct.

Enlarged hypersegmented neutrophils are typically seen in Megaloblastic anemia (option 3). Here is a detailed explanation:

1. Leukopenia: Leukopenia is a condition where there is a decrease in the total number of white blood cells (WBCs) in the bloodstream. It does not directly refer to the morphological changes in the neutrophils. The presence of enlarged or hypersegmented neutrophils is not a hallmark feature of leukopenia; rather, the condition is characterized by a low WBC count.

2. Leukocytosis: Leukocytosis is the medical term for an increase in the number of white blood cells in the bloodstream. It can occur due to various conditions like infections, inflammation, or leukemia. However, hypersegmentation of neutrophils is not a typical finding in leukocytosis. The presence of enlarged neutrophils is also not characteristic of this condition.

3. Megaloblastic anemia: Megaloblastic anemia is a type of anemia that occurs due to the lack of vitamin B12 or folic acid. These vitamins are essential for the maturation of red blood cells in the bone marrow. In the case of vitamin B12 or folic acid deficiency, the red blood cells become large and immature, leading to their inability to function properly. Additionally, neutrophils, which are a type of white blood cell, can also become enlarged and hypersegmented in megaloblastic anemia. The enlarged neutrophils are called "megaloblastic neutrophils" or "hypersegmented neutrophils." The hypersegmentation occurs due to the defect in DNA synthesis that results from the vitamin deficiency, causing the nucleus of the neutrophil to segment more than the normal 2-5 lobes.

4. Acute myeloid leukemia: While acute myeloid leukemia (AML) is characterized by an overproduction of immature myeloid cells, including neutrophils, enlarged hypersegmented neutrophils are not a typical feature of this condition. In AML, the bone marrow is filled with abnormal, immature cells called blasts, which do not mature properly and function as normal blood cells. However, AML can present with a variety of morphological changes in neutrophils, such as Auer rods, but hypersegmentation is not specific to AML.

Enlarged hypersegmented neutrophils are most commonly associated with Megaloblastic anemia, which is caused by vitamin B12 or folic acid deficiency and leads to abnormal cell maturation in the bone marrow, affecting both red and white blood cells.

Tumour cells have genetic alterations which result in expression of nonself proteins: This is the most accurate statement regarding immune surveillance. Tumor cells often undergo genetic mutations that lead to the expression of abnormal proteins (neoantigens) that are not present in normal cells. These nonself proteins can be recognized by the immune system as foreign, triggering an immune response. This recognition is a key aspect of how immune surveillance functions effectively against tumors.

All of the listed conditions (leukoplakia, solar keratosis, and margins of long-standing draining sinuses) are known precursors to squamous cell carcinoma.

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.