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NEET MDS Synopsis

Neck Dissection
Oral and Maxillofacial Surgery

1. Radical Neck Dissection

Complete removal of all ipsilateral
cervical lymph node groups (levels I-V) and three key non-lymphatic
structures:
Internal jugular vein
Sternocleidomastoid muscle
Spinal accessory nerve


Indication: Typically performed for extensive lymphatic
involvement.

2. Modified Radical Neck Dissection

Similar to radical neck dissection in terms
of lymph node removal (levels I-V) but with preservation of one or more of
the following structures:
Type I: Preserves the spinal accessory nerve.
Type II: Preserves the spinal accessory nerve and
the sternocleidomastoid muscle.
Type III: Preserves the spinal accessory nerve,
sternocleidomastoid muscle, and internal jugular vein.


Indication: Used when there is a need to reduce
morbidity while still addressing lymphatic involvement.

3. Selective Neck Dissection

Preservation of one or more lymph node
groups that are typically removed in a radical neck dissection.
Classification:
Originally had named dissections (e.g., supraomohyoid neck
dissection for levels I-III).
The 2001 modification proposed naming dissections based on the
cancer type and the specific node groups removed. For example, a
selective neck dissection for oral cavity cancer might be referred to as
a selective neck dissection (levels I-III).


Indication: Used when there is a lower risk of
lymphatic spread or when targeting specific areas.

4. Extended Neck Dissection

 Involves the removal of additional lymph
node groups or non-lymphatic structures beyond those included in a radical
neck dissection. This may include:
Mediastinal nodes
Non-lymphatic structures such as the carotid artery or hypoglossal
nerve.


Indication: Typically performed in cases of extensive
disease or when there is a need to address additional areas of concern.

The Scalp
Anatomy

The Scalp


The scalp consists of five layers of soft tissue.
It extends from the superior nuchal line on the posterior aspect of the skull of the supraorbital margins.
Laterally, the scalp extends into the temporal fossa to the level of the zygomatic arches.


 

Layers of the Scalp


The scalp proper is composed of three fused layers. It is separated from the pericranium by loose connective tissue.
Because of this potential areolar cleavage plane, the scalp is fairly mobile.
Each letter of the word "S C A L P" serves as a memory key for one of the layers of the scalp: Skin, Connective Tissue, Aponeurosis Epicranialis, Loose Areolar Tissue and Pericranium.


Layer 1: Skin


Hair covers the scalp in most people.
The skin of the scalp is thin, especially in elderly people, except in the occipital region.
The skin contains many sweat and sebaceous glands and hair follicles.
The skin of the scalp has an abundant arterial supply and good venous and lymphatic drainage systems.


Layer 2: Connective Tissue


This is a thick, subcutaneous layer of connective tissue and is richly vascularised and innervated.
It attaches the skin to the third layer of the scalp.
Fat is enclosed in lobules between the connective fibres.


Layer 3: Aponeurosis Epicranialis


This is a strong membranous sheet that covers the superior aspect of the cranium.
This aponeurosis is the membranous tendon of the fleshy bellies of the epicranius muscle.



The epicranius muscle consists of four parts: two occipital bellies, occipitalis and two frontal bellies, frontalis that are connected by the epicranial aponeurosis. 


Layer 4: Loose Areolar Tissue


This is a subaponeurotic layer or areolar or loose connective tissue.
It is somewhat like a sponge because it contains innumerable potential spaces that are capable of being distended by fluid.
It is this layer that allows free movement of the scalp proper, composed of layers 1-3.


Layer 5: Pericranium


This is a dense layer of specialised connective tissue.
The pericranium is firmly attached to the bones by connective tissue fibres called Sharpey’s fibres, however, they can be fairly easily stripped from the cranial bones of living persons, except where they are continuous with the fibrous tissues of the cranial sutures.

Blood Transfusions
Physiology

Blood Transfusions


Some of these units ("whole blood") were transfused directly into patients (e.g., to replace blood lost by trauma or during surgery).
Most were further fractionated into components, including:

RBCs. When refrigerated these can be used for up to 42 days.
platelets. These must be stored at room temperature and thus can be saved for only 5 days.
plasma. This can be frozen and stored for up to a year.




safety of donated blood

A variety of infectious agents can be present in blood.


viruses (e.g., HIV-1, hepatitis B and C, HTLV, West Nile virus
bacteria like the spirochete of syphilis
protozoans like the agents of malaria and babesiosis
prions (e.g., the agent of variant Crueutzfeldt-Jakob disease)


and could be transmitted to recipients. To minimize these risks,


donors are questioned about their possible exposure to these agents;
each unit of blood is tested for a variety of infectious agents.


Most of these tests are performed with enzyme immunoassays (EIA) and detect antibodies against the agents. blood is now also checked for the presence of the RNA of these RNA viruses:


HIV-1
hepatitis C
West Nile virus



by the so-called nucleic acid-amplification test (NAT).

Antiemetics
Pharmacology

Antiemetics

 Antiemetic drugs are generally more effective in prophylaxis than treatment. Most antiemetic agents relieve nausea and vomiting by acting on the vomiting centre, dopamine receptors, chemoreceptors trigger zone (CTZ), cerebral cortex, vestibular apparatus, or a combination of these.
 
 Drugs used in the treatment of nausea and vomiting belong to several different groups. These include:
 
1. Phenothiazines, such as chlorpromazine, act on CTZ and vomiting centre, block dopamine receptors, are effective in preventing or treating nausea and vomiting induced by drugs, radiation therapy, surgery and most other stimuli (e.g. pregnancy).
They are generally ineffective in motion sickness.
Droperidol had been used most often for sedation in endoscopy and surgery, usually in combination with opioids or benzodiazepines

2. Antihistamines such as promethazine and Dimenhyrinate are especially effective in prevention and treatment of motion.

3. Metoclopramide has both central and peripheral antiemetic effects. Centrally, it antagonizes the action of dopamine. Peripherally metoclopramide stimulates the release of acetylcholine, which in turn, increases the rate of gastric. It has similar indications to those of chlorpromazine.

4. Scopolamine, an anticholinergic drug, is very effective in reliving nausea & vomiting associated with motion sickness.

5. Ondansetron, a serotonin antagonist, is effective in controlling chemical-induced vomiting and nausea such those induced by anticancer drugs. 

6. Benzodiazepines: The antiemetic potency of lorazepam and alprazolam is low. Their beneficial effects may be due to their sedative, anxiolytic, and amnesic properties

MAXILLARY FIRST MOLAR
Dental Anatomy

MAXILLARY FIRST MOLAR

The first molars are also known as 6-year molars, because they erupt when a child is about 6 years

Facial Surface:-The facial surface has a facial groove that continues over from the occlusal surface, and runs down to the middle third of the facial surface.

Lingual Surface:-In a great many instances, there is a cusp on the lingual surface of the mesiolingual cusp. This is a fifth cusp called the cusp of Carabelli, which is in addition to the four cusps on the occlusal surface.

Proximal: In mesial perspective the mesiolingual cusp, mesial marginal ridge, and mesiobuccal cusp comprise the occlusal outline. In its distal aspect, the two distal cusps are clearly seen; however, the distal marginal ridge is somewhat shorter than the mesial one.

Occlusal Surface:- The tooth outline is somewhat rhomboidal with four distinct cusps. The cusp order according to size is: mesiolingual, mesiobuccal, distobuccal, and distolingual. The tips of the mesiolingual, mesiobuccal, and distobuccal cusps form the trigon, Cusp of Carabelli located on the mesiolingual cusp.

Contact Points; The mesial contact is above, but close to, the mesial marginal ridge. It is somewhat buccal to the center of the crown mesiodistally. The distal contact is similarly above the distal marginal ridge but is centered buccolingually.

 

Roots:-The maxillary first molar has three roots, which are named according to their locations mesiofacial, distofacial, and lingual (or palatal root). The lingual root is the largest.

Muscles
Physiology

There are three types of muscle tissue, all of which share some common properties:


Excitability or responsiveness - muscle tissue can be stimulated by electrical, physical, or chemical means.
contractility - the response of muscle tissue to stimulation is contraction, or shortening.
elasticity or recoil - muscles have elastic elements (later we will call these their series elastic elements) which cause them to recoil to their original size.
stretchability or extensibility - muscles can also stretch and extend to a longer-than-resting length.


 

The three types of muscle: skeletal, cardiac, and visceral (smooth) muscle.

Skeletal muscle

It is found attached to the bones for movement.

cells are long multi-nucleated cylinders.

 The cells may be many inches long but vary in diameter, averaging between 100 and 150 microns.

 All the cells innervated by branches from the same neuron will contract at the same time and are referred to as a motor unit.

 Skeletal muscle is voluntary because the neurons which innervate it come from the somatic or voluntary branch of the nervous system.

That means you have willful control over your skeletal muscles.

 Skeletal muscles have distinct stripes or striations which identify them and are related to the organization of protein myofilaments inside the cell.

 

Cardiac muscle

This muscle found in the heart.

 It is composed of much shorter cells than skeletal muscle which branch to connect to one another.

 These connections are by means of gap junctions called intercalated disks which allow an electrochemical impulse to pass to all the connected cells.

 This causes the cells to form a functional network called a syncytium in which the cells work as a unit. Many cardiac muscle cells are myogenic which means that the impulse arises from the muscle, not from the nervous system. This causes the heart muscle and the heart itself to beat with its own natural rhythm.

But the autonomic nervous system controls the rate of the heart and allows it to respond to stress and other demands. As such the heart is said to be involuntary.

 

Visceral muscle is found in the body's internal organs and blood vessels.

 It is usually called smooth muscle because it has no striations and is therefore smooth in appearance. It is found as layers in the mucous membranes of the respiratory and digestive systems.

It is found as distinct bands in the walls of blood vessels and as sphincter muscles.

Single unit smooth muscle is also connected into a syncytium similar to cardiac muscle and is also partly myogenic. As such it causes continual rhythmic contractions in the stomach and intestine. There and in blood vessels smooth muscle also forms multiunit muscle which is stimulated by the autonomic nervous system. So smooth muscle is involuntary as well

Histamine
Pharmacology

Histamine: 

Involved in inflammatory and anaphylactic reactions 
Local application causes swelling redness, and edema, mimicking a mild inflammatory reaction.

Large systemic doses leads to profound vascular changes similar to those seen after shock or anaphylactic origin.

Storage: widely distributed; in tissues, primarily in mast cells; in blood- in basophils, platelets; non-mast cell sites (epidermis, CNS, regenerating cells)

Histamine Stored in complex with:
Heparin
Chondroitin Sulfate
Eosinophilic Chemotactic Factor
Neutrophilic Chemotactic Factor
Proteases

Release: during type I (IgE-mediated) immediate hypersensitivity rxns, tissue injury, in response to some drugs
a.    Process: Fcε receptor on mast cell or basophil binds IgE, when Ag binds → ↑ PLC activity → histamine

Symptoms: bronchoconstriction, ↓ Pa, ↑ capillary permeability, edema

Action

H1 receptors are located mainly on smooth muscle cells in blood vessels and the respiratory and GI tracts. When histamine binds with these receptors producing the following effects.

-Contraction of smooth muscle in the bronchi and bronchioles producing bronchoconstraction.

-stimulation of vagus nerve endings to produce reflex bronchoconstraction and cough.

-Increased permeability of veins and capillaries, which allows fluid to flow into subcutaneous tissues and form edema (little lower blood pressure).

-Increased secretion of mucous glands. Mucosal edema and increased nasal mucus produce the nasal congestion characteristic of allergic rhinitis and the common cold.

-Stimulation of sensory peripheral nerve endings to cause pain and pruritus.

Histamine promotes vasodilation by causing vascular endothelium to release nitric oxide. This chemical signal diffuses to the vascular smooth muscle, where it stimulates cyclic guanosine monophosphate production, causing vasodilation.


H2-receptors present mostly in gastric glands and smooth muscle of some blood vessels. When receptors are stimulated, the main effects are increased secretion of gastric acid and pepsin, increased rate and force of myocardial contraction.

The H3-receptor functions as a negative-feedback mechanism to inhibit histamine synthesis and release in many body tissues. Stimulation of H3 receptors opposes the effects produced by stimulation of H1 receptors.

The H4- receptor is expressed in only a few cell types, and their role in drug action is unclear.

Drugs cause release of histamine: 

Many drugs can cause release of histamine in the body.
-Intracutaneouse morphine injection in humans produced localized redness, localized edema and a diffuse redness. This is due to release of histamine.

-I.V. inj of curare may cause bronchial constriction due to release of histamine.

-codeine , papaverine, meperidine (pethedine), atropine, hydralizine and sympathomimetic amines, histamine releases by these drugs may not be significant unless they are administered I.V in large doses

Pharmacological effects

-  If injected I.V. (0.1 mg of histamine) causes a sharp decline in the blood pressure, flushing of the face and headache. 
- There is also stimulation of gastric acid secretion. 
- If this injection is given to an asthmatic individual, there will be a marked decrease in vital capacity and a sever attack of asthma. 

Circulatory effects of histamine:

The two factors involved in the circulatory action of histamine are:
Arteriolar dilatation and
Capillary permeability
So it leads to loss of plasma from circulation

Effect on gastric secretion:
Histamine is a potent stimulant of gastric Hcl secretion. 

Host Defense Mechanisms
Periodontology

Bacterial Properties Involved in Evasion of Host Defense Mechanisms
Bacteria have evolved various strategies to evade the host's immune defenses,
allowing them to persist and cause disease. Understanding these mechanisms is
crucial for developing effective treatments and preventive measures against
bacterial infections, particularly in the context of periodontal disease. This
lecture will explore the bacterial species involved, their properties, and the
biological effects of these properties on host defense mechanisms.

Host Defense Mechanisms and Bacterial Evasion Strategies


Specific Antibody Evasion

Bacterial Species:
Porphyromonas gingivalis
Prevotella intermedia
Prevotella melaninogenica
Capnocytophaga spp.


Bacterial Property:
IgA- and IgG-degrading proteases


Biologic Effect:
Degradation of specific antibodies, which impairs the host's
ability to mount an effective immune response against these
bacteria.





Evasion of Polymorphonuclear Leukocytes (PMNs)

Bacterial Species:
Aggregatibacter actinomycetemcomitans
Fusobacterium nucleatum
Porphyromonas gingivalis
Treponema denticola


Bacterial Properties:
Leukotoxin: A toxin that can induce apoptosis
in PMNs.
Heat-sensitive surface protein: May interfere
with immune recognition.
Capsule: A protective layer that inhibits
phagocytosis.
Inhibition of superoxide production: Reduces
the oxidative burst necessary for bacterial killing.


Biologic Effects:
Inhibition of PMN function, leading to decreased bacterial
killing.
Induction of apoptosis (programmed cell death) in PMNs, reducing
the number of immune cells available to fight infection.
Inhibition of phagocytosis, allowing bacteria to evade
clearance.





Evasion of Lymphocytes

Bacterial Species:
Aggregatibacter actinomycetemcomitans
Fusobacterium nucleatum
Tannerella forsythia
Prevotella intermedia


Bacterial Properties:
Leukotoxin: Induces apoptosis in lymphocytes.
Cytolethal distending toxin: Affects cell cycle
progression and induces cell death.
Heat-sensitive surface protein: May interfere
with immune recognition.
Cytotoxin: Directly damages immune cells.


Biologic Effects:
Killing of mature B and T cells, leading to a weakened adaptive
immune response.
Nonlethal suppression of lymphocyte activity, impairing the
immune response.
Impairment of lymphocyte function by arresting the cell cycle,
leading to decreased responses to antigens and mitogens.
Induction of apoptosis in mononuclear cells and lymphocytes,
further reducing immune capacity.





Inhibition of Interleukin-8 (IL-8) Production

Bacterial Species:
Porphyromonas gingivalis


Bacterial Property:
Inhibition of IL-8 production by epithelial cells.


Biologic Effect:
Impairment of PMN response to bacteria, leading to reduced
recruitment and activation of neutrophils at the site of infection.





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