NEET MDS Shorts
75369
Pathology
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.
81312
Pathology
Head and Neck: The head and neck region includes various structures such as
the oral cavity, nasal cavity, pharynx, larynx, and the salivary glands. This
region is highly susceptible to carcinomas due to the presence of mucosal
surfaces exposed to potential carcinogens. Common types of head and neck
carcinomas include:
- Oral Squamous Cell Carcinoma: This is the most common form of head and neck
cancer, typically occurring on the tongue, lips, oral cavity, and oropharynx.
Risk factors include tobacco use (smoking and smokeless), alcohol consumption,
and human papillomavirus (HPV) infection.
- Nasopharyngeal Carcinoma: This cancer arises from the nasopharynx and is often
associated with environmental factors such as the Epstein-Barr virus (EBV)
infection and dietary habits.
- Laryngeal Carcinoma: Cancer of the larynx (voice box) is often linked to
smoking and excessive alcohol intake.
51229
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.
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.
49048
PathologyAll of the listed conditions (leukoplakia, solar keratosis, and margins of long-standing draining sinuses) are known precursors to squamous cell carcinoma.
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.
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.
92926
Pathology
1. Noduloulcerative Basal Cell Carcinoma: This is the most common subtype of
BCC, making up about 60-70% of all cases. It typically appears as a slowly
growing, round to oval, pearly or translucent nodule with a central ulceration
that may bleed or ooze. The borders of the lesion are often not well-defined and
may have a rolled, pearly edge with telangiectasias (small, dilated blood
vessels).
2. Cystic Basal Cell Carcinoma: This subtype presents as a round, dome-shaped
lesion with a cystic or fluid-filled center. It is less common than the
noduloulcerative type, and it may be mistaken for a benign cyst or epidermoid
cyst.
3. Morphoeic Basal Cell Carcinoma: Also known as sclerosing or morpheaform BCC,
this type is characterized by a slowly growing, ill-defined, firm, plaque-like
lesion that can infiltrate deeply into the skin. It may have a whitish, waxy
appearance with a scar-like texture. Morphoeic BCC tends to be more aggressive
and can be challenging to diagnose due to its subtlety.
4. Pigmented Basal Cell Carcinoma: This is a less common variant of BCC,
accounting for approximately 6-15% of cases. It presents with pigmentation in
the lesion, which can be brown, blue, or black. The presence of pigment can make
it look similar to melanoma, another type of skin cancer, so a biopsy is often
necessary to confirm the diagnosis.
61993
Pathology
Opsonins 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.
61858
PathologyTumour 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.