NEET MDS Shorts
10764
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.
80054
PathologyDebulking the tumor by surgery makes the tumor cells re-enter the cell cycle and thus become susceptible to drug therapy: This statement is the most accurate. Surgical removal of a tumor (debulking) can indeed lead to the release of tumor cells into the circulation and may also alter the tumor microenvironment. This can make residual tumor cells more susceptible to chemotherapy, as they may re-enter the cell cycle and become more actively dividing, which is when many chemotherapy agents are most effective.
46594
PathologyEpitheloid cells are a hallmark of granulomatous inflammation, which occurs in response to certain chronic infections (like tuberculosis), autoimmune diseases, and foreign body reactions. In granulomas, epitheloid cells aggregate to form a protective wall around the irritant.
25834
PathologyThe expansion of the marrow space due to increased hematopoiesis can lead to resorption of the outer cortical bone and the formation of new bone, resulting in the characteristic "crew cut" appearance on X-rays. This appearance is due to the trabecular pattern of the skull becoming more prominent as the outer layer is resorbed.
83305
Pathology
Gas Gangrene, also known as clostridial myonecrosis or anaerobic cellulitis,
is a severe and rapidly progressing form of necrotizing soft tissue infection
caused by the bacterial genus Clostridium. The condition is characterized by the
production of gas within the tissues due to the fermentation of carbohydrates by
the bacteria. The most common species implicated in gas gangrene is Clostridium
perfringens.
1. Clostridium tetani: This bacterium is the causative agent of tetanus, which
is a neurotoxic disease that leads to muscle spasms and rigidity. It is not
directly associated with gas gangrene, although both are anaerobic infections
that can occur in deep puncture wounds and both produce exotoxins. However, the
primary symptom of tetanus is muscular rigidity and spasms due to the production
of tetanospasmin, not the tissue destruction and gas production seen in gas
gangrene.
2. Clostridium perfringens: This is the most common cause of gas gangrene. C.
perfringens produces alpha toxin, which is a powerful enzyme that can break down
tissue and release gas as a byproduct. The infection typically occurs in the
deep layers of the skin and muscles following a severe trauma, surgery, or
burns, where there is a lack of oxygen, allowing the anaerobic bacteria to
thrive. The rapid spread of infection is due to the bacteria's ability to
produce multiple exotoxins that cause tissue necrosis and vasoconstriction,
leading to ischemia and further tissue damage.
3. Clostridium difficile: Although a member of the Clostridium genus, C.
difficile is mainly associated with antibiotic-associated diarrhea and
pseudomembranous colitis. It is a hospital-acquired infection that affects the
intestinal tract and is not typically involved in causing gas gangrene. While it
is an anaerobic bacterium, its pathogenicity is primarily due to the production
of toxins that damage the colon's mucosal lining rather than invading tissues
outside the gut.
4. Peptostreptococci: These are anaerobic bacteria that can be part of the
normal skin and mucosal flora. They are involved in various infections,
particularly in immunocompromised individuals or those with underlying medical
conditions. Peptostreptococci are more commonly associated with mixed anaerobic
infections such as abscesses, osteomyelitis, and other soft tissue infections,
but they are not typically the sole cause of gas gangrene.
19093
Pathology
1. 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.
83683
Pathology
The correct answer is: 1. Progression vascularization invasion
detachment embolization.
Explanation of the stages for a malignant tumor cell:
1. Progression: This is the initial stage of tumor development where the cells
acquire the ability to proliferate in an uncontrolled manner. This can be due to
genetic mutations that alter the normal regulatory mechanisms that control cell
division. The tumor grows locally within the tissue or organ of origin.
2. Vascularization: Also known as angiogenesis, this stage involves the
formation of new blood vessels that supply the tumor with nutrients and oxygen,
which is essential for its continued growth and progression. The tumor cells
secrete factors that stimulate the growth of blood vessels into the tumor mass.
3. Invasion: The malignant tumor cells develop the capability to invade
surrounding tissues. They secrete enzymes that degrade the extracellular matrix
and basement membrane, allowing them to move through these barriers and invade
neighboring tissues and organs.
4. Detachment: During this stage, tumor cells detach from the primary tumor
site. This is facilitated by the loss of cell-to-cell adhesion molecules and the
degradation of the extracellular matrix by proteolytic enzymes.
5. Embolization: Detached tumor cells can then enter the lymphatic system or
bloodstream. This process is known as intravasation. They travel through these
vessels as emboli and can potentially form new tumors at distant sites, which is
the process of metastasis.
73857
Pathology
After 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.
72853
Pathology
The 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.
93778
Pathology
Sarcoidosis is a systemic granulomatous disorder of unknown etiology that can
affect any organ in the body. It is characterized by the formation of non-caseating
granulomas, which are clumps of inflammatory cells that cluster together in
response to an unidentified antigen. The lungs and lymph nodes are most commonly
involved. Here's a detailed explanation for each of the options:
1. Dry cough: This is a common symptom of pulmonary sarcoidosis. The cough is
usually persistent and non-productive, meaning it does not bring up mucus or
phlegm. The presence of a dry cough is not contradicted in the statement "All
are true regarding Sarcoidosis except," so this option is not the correct
answer.
2. Exertional dyspnoea: Shortness of breath on exertion can occur in individuals
with pulmonary sarcoidosis due to the inflammation and granuloma formation in
the lungs. This symptom can be a result of the impaired lung function and
decreased lung capacity caused by the disease. Therefore, this is also a true
statement regarding sarcoidosis.
3. Wheezing: Wheezing is a high-pitched whistling sound that occurs during
breathing, typically heard when airways become narrowed or blocked. It can be a
symptom of pulmonary sarcoidosis, particularly if the disease involves the
bronchi and bronchioles, leading to bronchial obstruction and airflow
limitation. However, it is not the primary symptom and may be less common than
the other respiratory symptoms mentioned.
4. Hemoptysis: While hemoptysis, or coughing up blood, is not a hallmark symptom
of sarcoidosis, it can occur in some cases, particularly when the granulomas are
located in the lungs. It is usually mild and self-limited, but severe cases can
lead to significant bleeding. This is a true statement regarding sarcoidosis, as
it is a possible, although less common, respiratory symptom of the disease.
Since all the options (1, 2, and 4) are true regarding Sarcoidosis