NEET MDS Shorts
979232
PathologyNuclear cytoplasmic asynchrony refers to a condition where the nucleus and
cytoplasm of a cell do not develop at the same rate. This can occur in various
forms of anemia and other pathological conditions. Here's a detailed explanation
of the concept and its relevance to the options provided:
1. Megaloblastic Anemia: Megaloblastic anemia is a type of anemia characterized
by the presence of large, immature, nucleated red blood cells (megaloblasts) in
the bone marrow and peripheral blood. This condition is primarily caused by a
deficiency in vitamin B12 or folic acid, which are essential for DNA synthesis
during cell division. The nucleus of the cells divides more slowly than the
cytoplasm, leading to an asynchronous development and the formation of large,
abnormal cells. In megaloblastic anemia, the nucleus is often large and
hyperchromatic (darkly stained), while the cytoplasm is relatively less
developed and pale. Therefore, this option is the most appropriate answer.
2. Fe Deficiency Anemia: Iron deficiency anemia is the most common type of
anemia worldwide, resulting from a lack of iron in the body. Iron is a critical
component of hemoglobin, which is responsible for carrying oxygen in red blood
cells. In this condition, the body produces smaller than normal red blood cells
(microcytic) that lack hemoglobin, leading to decreased oxygen transport. The
nucleus and cytoplasm of the erythrocytes are typically smaller than normal, and
there is no significant asynchrony in their development. Hence, this option is
not a characteristic feature of nuclear cytoplasmic asynchrony.
3. Erythroblastosis Fetalis: This is a condition that occurs when an Rh-negative
mother has an Rh-positive fetus. The mother's immune system produces antibodies
against the fetal red blood cells, leading to their destruction. This causes
anemia in the newborn. However, erythroblastosis fetalis is not typically
associated with nuclear cytoplasmic asynchrony. The anemia is a result of
hemolysis (destruction of red blood cells) rather than an intrinsic defect in
the development of the cells themselves. Thus, this option is not the correct
answer for this characteristic feature.
correct answer is:
1. Megaloblastic anemia
This is because megaloblastic anemia is the condition where nuclear cytoplasmic
asynchrony is a hallmark feature due to the disproportionate growth of the
nucleus and cytoplasm in red blood cell precursors, resulting from vitamin B12
or folic acid deficiencies affecting DNA synthesis.
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.
424640
PathologyCells die by one of two mechanisms – necrosis or
apoptosis
• Two physiologically different processes
– Necrosis – death by injury
– Apoptosis – death by suicide
Appoptosis:
Disintegration of cells into membrane-bound particles that are then eliminated by phagocytosis or by shedding.
750022
Pathology
1. Interleukin-1 (IL-1): Interleukin-1 is a pro-inflammatory cytokine that
plays a crucial role in the activation and regulation of the immune system. It
is produced mainly by macrophages and monocytes in response to various stimuli,
including bacterial endotoxins, viruses, and tissue damage. IL-1 is a major
stimulator of monocytes, as it promotes their proliferation, differentiation
into macrophages, and enhances their phagocytic and antigen-presenting
capabilities. It also induces the production of other cytokines, such as
TNF-alpha and IL-6, which further amplify the inflammatory response. Thus, it
acts as a critical mediator in the early stages of the immune response and is
involved in the initiation of the acute phase reaction.
2. α-Interferon: Interferons (IFNs) are a family of cytokines that play an
essential role in the innate immune response to viral infections. They are
mainly produced by cells in response to viral infection and can induce an
antiviral state in nearby cells by upregulating the expression of proteins that
inhibit viral replication. While α-interferon does not directly stimulate
monocytes, it does have some effects on the immune system, such as enhancing the
natural killer (NK) cell activity and modulating the function of macrophages and
other immune cells. However, it is not the primary stimulator of monocytes like
IL-1 is.
3. Immunoglobulin E (IgE): IgE is a class of antibodies that are involved in the
allergic response and the immune response to parasites. It is produced in
response to allergens and parasitic antigens. While IgE is important in the
activation of mast cells and basophils, which play a key role in the immediate
allergic response, it does not serve as a major stimulator of monocytes.
Monocytes are more closely associated with the innate immune response and are
not primarily activated by antibodies.
4. Immunoglobulin G (IgG): IgG is the most abundant and versatile class of
antibodies in the blood. It plays a pivotal role in the immune response by
binding to pathogens and facilitating their destruction through various
mechanisms, such as opsonization (enhancing phagocytosis), activation of the
complement system, and neutralization of toxins. IgG can interact with
macrophages via Fcγ receptors, which can lead to phagocytosis of
antigen-antibody complexes. However, IgG is not a direct stimulator of monocytes
in the same sense that IL-1 is. Monocytes are primarily activated by cytokines
and other signaling molecules released during inflammation and infection, rather
than by antibodies.
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.
451930
PathologyOpsonins 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.
757861
PathologyEnlarged 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.
616900
PathologyLeptospirosis, Malaria, Viral Hepatitis A can produce febrile jaundice