NEET MDS Synopsis
Digestive System
PhysiologyIngestion: Food taken in the mouth is
ground into finer particles by the teeth,
moistened and lubricated by saliva (secreted by three pairs of salivary glands)
small amounts of starch are digested by the amylase present in saliva
the resulting bolus of food is swallowed into the esophagus and
carried by peristalsis to the stomach.
MANDIBULAR CENTRAL INCISORS
Dental Anatomy
MANDIBULAR CENTRAL INCISORS
These are the first permanent teeth to erupt, replacing deciduous teeth, and are the smallest teeth in either arch
Facial Surfaces:-The facial surface of the mandibular central incisor is widest at the incisal edge. Both the mesial and the distal surfaces join the incisal surface at almost a 90° angle. Although these two surfaces are nearly parallel at the incisal edge, they converge toward the cervical margin. The developmental grooves may or may not be present. When present, they appear as very faint furrows.
Lingual: The lingual surface has no definite marginal ridges. The surface is concave and the cingulum is minimal in size.
Proximal: Both mesial and distal surfaces present a triangular outline.
Incisal: The incisal edge is at right angles to a line passing labiolingually through the tooth reflecting its bilateral symmetry.
Root Surface:-The root is slender and extremely flattened on its mesial and distal surfaces.
Rheumatic Fever - Major and Minor Criteria
Medicine
Rheumatic fever occurs after a streptococcal infection (usually caused by Group A Beta-Hemolytic Strep (GABHS)).
It is an inflammatory condition that affects the joints, skin, heart and brain.
Major criteria are referred to as Jones criteria
J – Joint involvement which is usually migratory and inflammatory joint involvement that starts in the lower joints and ascends to upper joints
O – (“O” Looks like heart shape) – indicating that patients can develop myocarditis or inflammation of the heart
N – Nodules that are subcutaneous
E – Erythema marginatum which is a rash of ring-like lesions that can start in the trunk or arms. When joined with other rings, it can create a snake-like appearance
S – Sydenham chorea is a late feature which is characterized by jerky, uncontrollable, and purposeless movements resembling twitches
Minor criteria include
C – CRP Increased
A – Arthralgia
F – Fever
E – Elevated ESR
P – Prolonged PR Interval
A – Anamesis
L – Leukocytosis
Diagnosis of rheumatic fever is made after a strep infection (indicated by either throat cultures growing GABHS OR elevated anti-streptolysin O titers in the blood) and:
Two major criteria OR
One major criterion and two minor criteria
The Bicarbonate Buffer System
Biochemistry
The Bicarbonate Buffer System
This is the main extracellular buffer system which (also) provides a means for the necessary removal of the CO2 produced by tissue metabolism. The bicarbonate buffer system is the main buffer in blood plasma and consists of carbonic acid as proton donor and bicarbonate as proton acceptor :
H2CO3 = H+ + HCO3–
If there is a change in the ratio in favour of H2CO3, acidosis results.
This change can result from a decrease in [HCO3 − ] or from an increase in [H2CO3 ]
Most common forms of acidosis are metabolic or respiratory
Metabolic acidosis is caused by a decrease in [HCO3 − ] and occurs, for example, in uncontrolled diabetes with ketosis or as a result of starvation.
Respiratory acidosis is brought about when there is an obstruction to respiration (emphysema, asthma or pneumonia) or depression of respiration (toxic doses of morphine or other respiratory depressants)
Alkalosis results when [HCO3 − ] becomes favoured in the bicarbonate/carbonic acid ratio
Metabolic alkalosis occurs when the HCO3 − fraction increases with little or no concomitant change in H2CO3
Severe vomiting (loss of H+ as HCl) or ingestion of excessive amounts of sodium bicarbonate (bicarbonate of soda) can produce this condition
Respiratory alkalosis is induced by hyperventilation because an excessive removal of CO2 from the blood results in a decrease in [H2CO3 ]
Alkalosis can produce convulsive seizures in children and tetany, hysteria, prolonged hot baths or lack of O2 as high altitudes.
The pH of blood is maintained at 7.4 when the buffer ratio [HCO3 − ] / [ H2CO3] becomes 20
Mouthguards
PedodonticsClassification of Mouthguards
Mouthguards are essential dental appliances used primarily in sports to
protect the teeth, gums, and jaw from injury. The American Society for Testing
and Materials (ASTM) has established a classification system for athletic
mouthguards, which categorizes them into three types based on their design, fit,
and level of customization.
Classification of Mouthguards
ASTM Designation: F697-80 (Reapproved 1986)
Type I: Stock Mouthguards
Description: These are pre-manufactured mouthguards
that come in standard sizes and shapes.
Characteristics:
Readily available and inexpensive.
No customization for individual fit.
Typically made from a single layer of material.
May not provide optimal protection or comfort due to their
generic fit.
Usage: Suitable for recreational sports or
activities where the risk of dental injury is low.
Type II: Mouth-Formed Mouthguards
Description: Also known as "boil-and-bite"
mouthguards, these are made from thermoplastic materials that can be
softened in hot water and then molded to the shape of the wearer�s
teeth.
Characteristics:
Offers a better fit than stock mouthguards.
Provides moderate protection and comfort.
Can be remolded if necessary, allowing for some customization.
Usage: Commonly used in youth sports and activities
where a higher risk of dental injury exists.
Type III: Custom-Fabricated Mouthguards
Description: These mouthguards are custom-made by
dental professionals using a dental cast of the individual�s teeth.
Characteristics:
Provides the best fit, comfort, and protection.
Made from high-quality materials, often with multiple layers for
enhanced shock absorption.
Tailored to the specific dental anatomy of the wearer, ensuring
optimal retention and stability.
Usage: Recommended for athletes participating in
contact sports or those at high risk for dental injuries.
Summary of Preference
The classification system is based on an ascending order of preference:
Type I (Stock Mouthguards): Least preferred due to
lack of customization and fit.
Type II (Mouth-Formed Mouthguards): Moderate
preference, offering better fit than stock options.
Type III (Custom-Fabricated Mouthguards): Most
preferred for their superior fit, comfort, and protection.
Glass Ionomer Cements
Conservative Dentistry
Glass ionomer cement is a tooth coloured material
Material was based on reaction between silicate glass powder & polyacrylicacid.
They bond chemically to tooth structure & release fluoride for relatively long period
CLASSIFICATION
Type I. For luting
Type II. For restoration
Type II.1 Restorative esthetic
Type II.2 Restorative reinforced
Type III. For liner & bases
Type IV. Fissure & sealent
Type V. As Orthodontic cement
Type VI. For core build up
Physical Properties
1. Low solubility
2. Coefficient of thermal expansion similar to dentin
3. Fluoride release and fluoride recharge
4. High compressive strengths
5. Bonds to tooth structure
6. Low flexural strength
7. Low shear strength
8. Dimensional change (slight expansion) (shrinks on setting, expands with water sorption)
9. Brittle
10.Lacks translucency
11.Rough surface texture
Indications for use of Type II glass ionomer cements
1) non-stress bearing areas
2) class III and V restorations in adults
3) class I and II restorations in primary dentition
4) temporary or “caries control” restorations
5) crown margin repairs
6) cement base under amalgam, resin, ceramics, direct and indirect gold
7) core buildups when at least 3 walls of tooth are remaining (after crown preparation)
Contraindications
1) high stress applications I. class IV and class II restorations II. cusp replacement III. core build-ups with less than 3 sound walls remaining
Composition
Factors affecting the rate or setting
1. Glass composition:Higher Alumina – Silica ratio, faster set and shorter working time.
2. Particle Size: finer the powder, faster the set.
3. Addition of Tartaric Acid:-Sharpens set without shortening the working time.
4. Relative proportions of the constituents: Greater the proportion of glass and lower the proportion of water, the faster the set.
5. Temperature
Setting Time
Type 1 - 4-5 min
type II - 7 min
PROPERTIES
Adhesion :
- Glass ionomer cement bonds chemically to the tooth structure->reaction occur between carboxyl group of poly acid & calcium of hydroxyl apatite.
- Bonding with enamel is higher than that of dentin ,due to greater inorganic content.
Esthetics :
-GIC is tooth coloured material & available in different shades.
Inferior to composites.
They lack translucency & rough surface texture.
Potential for discolouration & staining.
Biocompatibilty :
- Pulpal response to glass ionomer cement is favorable.
- Pulpal response is mild due to
- High buffering capacity of hydroxy apatite.
- Large molecular weight of the polyacrylic acid ,which prevents entry into dentinal tubules.
a) Pulp reaction – ZOE < Glass Ionomer < Zinc Phosphate
b) Powder:liquid ratio influences acidity
c) Solubility & Disintegration:-Initial solubility is high due to leaching of intermediate products.The complete setting reaction takes place in 24 hrs, cement should be protected from saliva during this period.
Anticariogenic properties :
- Fluoride is released from glass ionomer at the time of mixing & lies with in matrix.
Fluoride can be released out without affecting the physical properties of cement.
ADVANTAGE DISADVANTAGE
Jaundice
General Pathology
Jaundice, or icterus
a. Characterized by yellowness of tissues, including skin, eyes, and mucous membranes.
b. Caused by excess conjugated and/or unconjugated serum bilirubin. (increased levels of bilirubin in the blood)
lcterus is visible when the serum bilirubin exceeds 2 mg/dl. In unconjugated hyperbilirubinemia, bilirubin is not excreted into the urine because of tight protein binding in serum. In conjugated hyperbilirubinemia, small amounts of bilirubin are excreted in the urine because
it is less tightly protein bound.
NOTE: Concentration of bilirubin in blood plasma does not normally exceed 1 mg/dL (>17µmol/L). A concentration higher than 1.8 mg/dL (>30µmol/L) leads to jaundice.
The conjunctiva of the eye are one of the first tissues to change color as bilirubin levels rise in jaundice. This is sometimes referred to as scleral icterus.
c. Types and causes include:
(1) Hepatocellular jaundice—caused by liver diseases such as cirrhosis and hepatitis.
(2) Hemolytic jaundice—caused by hemolytic anemias.
(3) Obstructive jaundice—caused by blockage of the common bile duct either by gallstones (cholelithiasis) or carcinomas involving the head of
the pancreas.
Differential diagnosis
Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:
Pre-hepatic → The pathology is occurring prior to the liver.
Hepatic → The pathology is located within the liver.
Post-Hepatic → The pathology is located after the conjugation of bilirubin in the liver.
Pre-hepatic
Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells).
Certain genetic diseases, such as sickle cell anemia, spherocytosis, thalassemia and glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice.
Commonly, diseases of the kidney, such as hemolytic uremic syndrome, can also lead to coloration. Defects in bilirubin metabolism also
present as jaundice, as in Gilbert's syndrome (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population) and Crigler-Najjar syndrome.
In jaundice secondary to hemolysis, the increased production of bilirubin, leads to the increased production of urine-urobilinogen. Bilirubin is not usually found in the urine because unconjugated bilirubin is not water-soluble, so, the combination of increased urine-urobilinogen with no bilirubin (since, unconjugated) in urine is suggestive of hemolytic jaundice.
Laboratory findings include:
• Urine: no bilirubin present, urobilinogen > 2 units (i.e., hemolytic anemia causes increased heme metabolism; exception: infants where gut flora has not developed).
• Serum: increased unconjugated bilirubin.
• Kernicterus is associated with increased unconjugated bilirubin.
Hepatocellular
Hepatocellular (hepatic) jaundice can be caused by acute or chronic hepatitis, hepatotoxicity, cirrhosis, drug induced hepatitis and alcoholic liver disease. Cell necrosis reduces the liver's ability to metabolize and excrete bilirubin leading to a buildup of unconjugated bilirubin in the blood.
Laboratory findings depend on the cause of jaundice.
• Urine: Conjugated bilirubin present, urobilirubin > 2 units but variable (except in children). Kernicterus is a condition not associated with increased conjugated bilirubin.
• Plasma protein show characteristic changes.
• Plasma albumin level is low but plasma globulins are raised due to an increased formation of antibodies.
Bilirubin transport across the hepatocyte may be impaired at any point between the uptake of unconjugated bilirubin into the cell and transport of conjugated bilirubin into biliary canaliculi.
Post-hepatic
Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of bile in the biliary system. The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as "liver flukes" can live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, cholangiocarcinoma, pancreatitis and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome.
Pathophysiology
When RBCs are damaged, their membranes become fragile and prone to rupture. As each RBC traverses through the reticuloendothelial system, its cell membrane ruptures when its membrane is fragile enough to allow this.
Hemoglobin, are released into the blood. The hemoglobin is phagocytosed by macrophages, and split into its heme and globin portions. The globin portion, a protein, is degraded into amino acids and plays no role in jaundice.
Two reactions then take place with the heme molecule.
The first oxidation reaction is catalyzed by the microsomal enzyme heme oxygenase and results in biliverdin (green color pigment), iron
and carbon monoxide.
The next step is the reduction of biliverdin to a yellow color tetrapyrol pigment called bilirubin by cytosolic enzyme biliverdin reductase.
This bilirubin is "unconjugated," "free" or "indirect" bilirubin. Approximately 4 mg of bilirubin per kg of blood is produced each day.[11] The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described.
However approximately 20 percent comes from other heme sources, including ineffective erythropoiesis, and the breakdown of other heme-containing proteins, such as muscle myoglobin and cytochromes.
Hepatic events
The unconjugated bilirubin then travels to the liver through the bloodstream. Because bilirubin is not soluble, however, it is transported through the blood bound to serum albumin.
In Liver, it is conjugated with glucuronic acid (to form bilirubin diglucuronide, or just "conjugated bilirubin") to become more water soluble.
The reaction is catalyzed by the enzyme UDP-glucuronyl transferase.
This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of bile. Intestinal bacteria convert the bilirubin into urobilinogen.
Urobilinogen can take two pathways. It can either be further converted into stercobilinogen, which is then oxidized to stercobilin and passed out in the feces, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and passed out in the urine as the oxidised product urobilin.
Stercobilin and urobilin are the products responsible for the coloration of feces and urine, respectively.
The Parotid Glands
AnatomyThe Parotid Glands
The parotid glands are the largest of the three pairs of salivary glands.
Each gland is wedged between the mandible and the sternocleidomastoid muscle and partly covers them.
The parotid gland is wrapped with a fibrous capsule (parotid fascia) that is continuous with the deep investing fascia of the neck.
Viewed superficially, the parotid gland is somewhat triangular in shape.
Its apex is posterior to the angle of the mandible and its base is along the zygomatic arch.
The parotid gland overlaps the posterior part of the masseter muscle.
The parotid duct (Stensen's duct) is about 5 cm long and 5 mm in diameter.
It passes horizontally from the anterior edge of the gland.
At the anterior border of the masseter muscle, the parotid duct turns medially and pierces the buccinator muscle.
It enters the oral cavity opposite the second maxillary molar.
Blood Vessels of the Parotid Gland
This gland is supplied by branches of the external carotid artery.
The veins from the parotid gland drains into the retromandibular vein, which enters the internal jugular vein.
Lymphatic Drainage of the Parotid Gland
The lymph vessels of this gland end in the superficial and deep cervical lymph nodes.
Nerves of the Parotid Gland
These nerves are derived from the auriculotemporal nerve and from the sympathetic and parasympathetic systems.
The parasympathetic fibres are derived from the glossopharyngeal nerve (CN IX) through the otic ganglion.
Stimulation of these fibres produces a thin watery (serous) saliva to flow from the parotid duct.
The sympathetic fibres are derived from the cervical ganglia through the external carotid plexus.
Stimulation of these fibres produces a thick mucous saliva.