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NEETMDS- Pathology short notes

NEET MDS Shorts

520701
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.

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.

734447
Pathology


The first vascular reaction in inflammation is Vasodilation.

Explanation:

Inflammation is the body's protective response to tissue injury or infection. It
is characterized by the classical signs of redness (rubor), heat (calor),
swelling (tumor), pain (dolor), and loss of function (functio laesa). The
initial vascular changes in the inflammatory process include:

1. Vasoconstriction: This is a temporary response that occurs immediately after
injury to minimize blood loss. However, it is quickly followed by the more
significant and prolonged phase of vasodilation.

2. Vasodilation: This is the first major vascular reaction in the inflammatory
response. Vasodilation occurs due to the release of substances such as
histamine, bradykinins, and prostaglandins from the damaged tissue cells and
mast cells. These substances are known as vasodilators and they cause the smooth
muscles surrounding the blood vessels to relax, leading to an increase in the
diameter of the blood vessels. This results in increased blood flow to the
injured area, which is essential for delivering white blood cells, nutrients,
and oxygen to the site of inflammation. The increased blood flow is what causes
the characteristic redness and heat of an inflamed area.

3. Increased vascular permeability: Although it is not the first vascular
reaction, increased vascular permeability is a critical component of the
inflammatory process. After vasodilation, the endothelial cells that line the
blood vessels become more permeable, allowing plasma and proteins to leak out of
the vessels into the surrounding tissue. This leads to the formation of an
exudate, which is the accumulation of fluid and proteins that makes up the
swelling (edema) seen in inflammation.

4. Marginisation or Pavementing: This is the process where neutrophils (a type
of white blood cell) move along the walls of blood vessels towards the site of
inflammation. It occurs later in the inflammatory response after the initial
vasodilation and increased vascular permeability. These cells then migrate
through the vessel walls into the tissue to combat pathogens and debris.

748440
Pathology

Diapedesis is a critical process in the body's immune response, particularly in the context of inflammation.

757861
Pathology

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.

406416
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

135863
Pathology

Mcroscopic picture of red blood cells (RBCs) in thalassemia, the following
characteristics are typically observed:

Microcytic: The RBCs are smaller than normal (microcytic)
due to the reduced hemoglobin content.
Hypochromic: The RBCs have a lower concentration of
hemoglobin, leading to a paler appearance (hypochromic).
Target cells: These are RBCs that have a bullseye
appearance due to an abnormal distribution of hemoglobin within the cell.
Target cells are often seen in thalassemia due to the imbalance of globin
chains and the resultant membrane changes.

616900
Pathology

Leptospirosis, Malaria, Viral Hepatitis A can produce febrile jaundice

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