NEET MDS Shorts
115498
PathologyThe newly formed collagen in the scar tissue is arranged differently compared to the organized collagen fibers in the unwounded skin, leading to a weaker structure. The 70-80% tensile strength is typically what is seen in well-healed sutured wounds. This remaining deficit is because scar tissue is less elastic and more prone to dehiscence (reopening) under tension compared to normal skin.
139486
PathologyOncofoetal 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.
585839
PathologyAfter 48 hours of inflammation, the predominant cells are typically monocytes,
which differentiate into macrophages.
1. Neutrophils: Neutrophils are the most abundant type of white blood cells
and are the first to arrive at the site of inflammation. They are the primary
cells that dominate the early stages of acute inflammation, which typically
occurs within the first few hours (around 4-6 hours) after the onset of injury
or infection. Their main function is to phagocytose (engulf and destroy)
microbes and release enzymes and proteins that help to break down and dissolve
damaged tissue. Although they play a crucial role in the early stages, their
numbers tend to decrease after this initial phase, making them less likely to be
the predominant cells after 48 hours.
2. Monocytes: Monocytes are the largest of the white blood cells and are part of
the mononuclear phagocytic system. They are recruited from the bloodstream to
the site of inflammation in response to chemical signals called chemokines.
After approximately 24-48 hours of inflammation, monocytes start to predominate
the scene. These cells differentiate into macrophages once they have infiltrated
the tissue. Macrophages are the "clean-up crew" of the immune system, engaging
in phagocytosis, antigen presentation, and the release of cytokines that help
coordinate the overall inflammatory response. They are crucial for the later
stages of inflammation, which include the removal of debris, repair, and
resolution.
3. Eosinophils: Eosinophils are white blood cells that are involved in the
immune response to parasitic infections and in the pathogenesis of certain
allergic diseases. They are not typically the predominant cells in the general
inflammatory response and are more commonly associated with allergic
inflammation and parasitic infections. After 48 hours, eosinophils are less
likely to be the main cell type unless the inflammation is of an allergic or
parasitic nature, in which case they might be present in larger numbers.
However, in a typical non-specific inflammatory process, they are not the
predominant cell type after this duration.
4. Lymphocytes: Lymphocytes are a type of white blood cell that is essential for
the adaptive immune response. There are two main types: T-lymphocytes and
B-lymphocytes. While they are involved in the later stages of inflammation,
particularly in the adaptive immune response, they are not typically the
predominant cells after 48 hours in a general acute inflammatory setting.
Lymphocytes are more likely to be found in higher numbers during the later
stages of inflammation, particularly during the resolution phase or in chronic
inflammation, when the body is mounting a more specific response to the invading
pathogen.
520701
PathologyThe correct answer for the MCQ is option 1: Pernicious anemia results from
vitamin B12 deficiency resulting from inadequate intrinsic factor. This is
because pernicious anemia is specifically caused by the body's inability to
absorb vitamin B12 due to a lack of intrinsic factor, which is required for the
absorption of vitamin B12 in the small intestine. Folic acid deficiency, while
it can also cause megaloblastic anemia, is not directly associated with
intrinsic factor and is a separate entity from pernicious anemia.
1. Vitamin B12 deficiency resulting from inadequate intrinsic factor:
Vitamin B12 is an essential nutrient that plays a critical role in the
production of healthy red blood cells. It is involved in the synthesis of DNA
and the metabolism of fatty acids and amino acids. Intrinsic factor is a protein
produced by the parietal cells of the stomach that binds to vitamin B12,
allowing it to be absorbed in the small intestine. When there is a deficiency of
intrinsic factor, vitamin B12 cannot be effectively absorbed from food, leading
to vitamin B12 deficiency anemia. This is the most common cause of pernicious
anemia.
Pernicious anemia is an autoimmune disorder where the body's immune system
mistakenly attacks the stomach cells that produce intrinsic factor. Without
sufficient intrinsic factor, vitamin B12 cannot be absorbed, resulting in a
decrease in the number of red blood cells produced. The red blood cells that are
formed are abnormally large and immature, known as megaloblasts. These cells are
not efficient at carrying oxygen and are destroyed more quickly than normal
cells, leading to the symptoms of anemia such as fatigue, weakness, and pallor.
The deficiency in vitamin B12 can also affect the nervous system, causing
neuropathy, cognitive impairment, and other neurological symptoms.
2. Folic acid deficiency resulting from inadequate intrinsic factor:
Folic acid is another B-vitamin essential for the production of red blood cells
and is involved in DNA synthesis. However, folic acid deficiency is not directly
caused by a lack of intrinsic factor. Folic acid is absorbed in the small
intestine through a different mechanism than vitamin B12. While folic acid
deficiency can also lead to megaloblastic anemia, it is not typically referred
to as pernicious anemia. Pernicious anemia is specifically associated with
vitamin B12 deficiency due to intrinsic factor deficiency or malabsorption.
3. Vitamin B12 deficiency resulting from inadequate extrinsic factor:
The term "extrinsic factor" is not commonly used in the context of vitamin B12
deficiency. Vitamin B12 is derived from dietary sources such as meat, fish, and
dairy products. In the context of pernicious anemia, the issue is with the
intrinsic factor, which is necessary for the absorption of vitamin B12.
Therefore, this option is not accurate for explaining the cause of pernicious
anemia.
776926
PathologyExtensive cellulitis is most accurately described by the term "phlegmon
Phlegm is a thick, viscous substance produced by the respiratory tract,
especially during a respiratory infection, which can be coughed up from the
lungs or expelled from the nose. It is primarily composed of mucus, dead cells,
and other substances.
Phlegmon is a term that is closely related to extensive cellulitis. It refers
to a severe form of cellulitis where the infection has spread deeply into the
subcutaneous tissues and is accompanied by significant inflammation, including
the presence of pus and necrosis. Phlegmon is characterized by intense pain,
swelling, redness, and warmth in the affected area. This condition often
requires aggressive medical management, including intravenous antibiotics and
surgical drainage if an abscess forms. It is an advanced and severe stage of
cellulitis that can lead to systemic infection if not treated properly.
403336
Pathology1. People with Xeroderma Pigmentosum (XP):
Xeroderma pigmentosum is a rare genetic disorder that affects the way the skin
and eyes repair damage from UV radiation. Individuals with XP have a deficiency
in the DNA repair mechanism that normally removes UV-induced lesions. As a
result, their cells are more prone to mutations, which can lead to skin cancer.
There are several types of XP, and they vary in severity, but all are
characterized by extreme sensitivity to UV light, leading to early aging of the
skin, pigmentation changes, and a high risk of developing multiple skin cancers,
including melanoma, at a very young age.
2. Fanconi Anemia:
Fanconi anemia is another genetic disorder that affects the body's ability to
repair DNA. It is not exclusively related to UV radiation but rather to a defect
in the repair of DNA crosslinks, which can be caused by various agents,
including UV light. Patients with Fanconi anemia have an increased
susceptibility to various cancers, including skin cancers. Their cells have a
higher frequency of chromosomal instability and DNA damage, which can be
exacerbated by UV exposure. However, it's essential to note that the primary
cancer risk in Fanconi anemia is related to the underlying defect in DNA repair
and not solely to UV light.
3. Telangiectasia:
Telangiectasia is a condition where small blood vessels, especially those in the
skin, widen and become visible. While telangiectasia itself does not increase
the risk of skin cancer, individuals with certain forms of this condition may
have a higher susceptibility to UV light damage. For example, some patients with
telangiectasia may also have a genetic mutation or an acquired defect in the
skin that results in poor repair of UV-induced DNA damage. This can lead to a
higher risk of developing non-melanoma skin cancers like basal cell carcinoma
and squamous cell carcinoma. Moreover, telangiectasias are often found in areas
of the skin that have been exposed to significant UV radiation, such as the
face, neck, and hands, which are common sites for these types of skin cancers.
In summary, all of the conditions mentioned (Xeroderma Pigmentosum, Fanconi
Anemia, and Telangiectasia) can increase the susceptibility to UV light-induced
carcinogenesis due to their respective impairments in DNA repair mechanisms and
skin responses to UV radiation.
151537
PathologyAll of the listed conditions (leukoplakia, solar keratosis, and margins of long-standing draining sinuses) are known precursors to squamous cell carcinoma.
158573
PathologyEnlargement of interendothelial junctions: This option refers to the widening of the spaces between endothelial cells, which can occur during inflammation. This enlargement allows leukocytes to pass through the endothelium more easily. This is a significant mechanism in the process of leukocyte transmigration.