NEET MDS Synopsis
Nursing Bottle Caries
Conservative DentistryNursing Bottle Caries
Nursing bottle caries, also known as early childhood caries (ECC), is a
significant dental issue that affects infants and young children. Understanding
the etiological agents involved in this condition is crucial for prevention and
management. .
1. Pathogenic Microorganism
A. Streptococcus mutans
Role: Streptococcus mutans is the primary
microorganism responsible for the development of nursing bottle caries. It
colonizes the teeth after they erupt into the oral cavity.
Transmission: This bacterium is typically transmitted
to the infant’s mouth from the mother, often through saliva.
Virulence Factors:
Colonization: It effectively adheres to tooth
surfaces, establishing a foothold for caries development.
Acid Production: S. mutans produces large
amounts of acid as a byproduct of carbohydrate fermentation, leading to
demineralization of tooth enamel.
Extracellular Polysaccharides: It synthesizes
significant quantities of extracellular polysaccharides, which promote
plaque formation and enhance bacterial adherence to teeth.
2. Substrate (Fermentable Carbohydrates)
A. Sources of Fermentable Carbohydrates
Fermentable carbohydrates are utilized by S. mutans to form
dextrans, which facilitate bacterial adhesion to tooth surfaces and
contribute to acid production. Common sources include:
Bovine Milk or Milk Formulas: Often high in
lactose, which can be fermented by bacteria.
Human Milk: Breastfeeding on demand can expose
teeth to sugars.
Fruit Juices and Sweet Liquids: These are often
high in sugars and can contribute to caries.
Sweet Syrups: Such as those found in vitamin
preparations.
Pacifiers Dipped in Sugary Solutions: This practice
can introduce sugars directly to the oral cavity.
Chocolates and Other Sweets: These can provide a
continuous source of fermentable carbohydrates.
3. Host Factors
A. Tooth Structure
Host for Microorganisms: The tooth itself serves as the
host for S. mutans and other cariogenic bacteria.
Susceptibility Factors:
Hypomineralization or Hypoplasia: Defects in enamel
development can increase susceptibility to caries.
Thin Enamel and Developmental Grooves: These
anatomical features can create areas that are more prone to plaque
accumulation and caries.
4. Time
A. Duration of Exposure
Sleeping with a Bottle: The longer a child sleeps with
a bottle in their mouth, the higher the risk of developing caries. This is
due to:
Decreased Salivary Flow: Saliva plays a crucial
role in neutralizing acids and washing away food particles.
Prolonged Carbohydrate Accumulation: The swallowing
reflex is diminished during sleep, allowing carbohydrates to remain in
the mouth longer.
5. Other Predisposing Factors
Parental Overindulgence: Excessive use of sugary foods
and drinks can increase caries risk.
Sleep Patterns: Children who sleep less may have
increased exposure to cariogenic factors.
Malnutrition: Nutritional deficiencies can affect oral
health and increase susceptibility to caries.
Crowded Living Conditions: These may limit access to
dental care and hygiene practices.
Decreased Salivary Function: Conditions such as iron
deficiency and exposure to lead can impair salivary function, increasing
caries susceptibility.
Clinical Features of Nursing Bottle Caries
Intraoral Decay Pattern: The decay pattern associated
with nursing bottle caries is characteristic and pathognomonic, often
involving the maxillary incisors and molars.
Progression of Lesions: Lesions typically progress
rapidly, leading to extensive decay if not addressed promptly.
Management of Nursing Bottle Caries
First Visit
Lesion Management: Excavation and restoration of
carious lesions.
Abscess Drainage: If present, abscesses should be
drained.
Radiographs: Obtain necessary imaging to assess the
extent of caries.
Diet Chart: Provide a diet chart for parents to record
the child's diet for one week.
Parent Counseling: Educate parents on oral hygiene and
dietary practices.
Topical Fluoride: Administer topical fluoride to
strengthen enamel.
Second Visit
Diet Analysis: Review the diet chart with the parents.
Sugar Control: Identify and isolate sugar sources in
the diet and provide instructions to control sugar exposure.
Caries Activity Tests: Conduct tests to assess the
activity of carious lesions.
Third Visit
Endodontic Treatment: If necessary, perform root canal
treatment on affected teeth.
Extractions: Remove any non-restorable teeth, followed
by space maintenance if needed.
Crowns: Place crowns on teeth that require restoration.
Recall Schedule: Schedule follow-up visits every three
months to monitor progress and maintain oral health.
Intramembranous ossification
Anatomy
Intramembranous ossification
Flat bones develop in this way (bones of the skull)
This type of bone development takes place in mesenchymal tissue
Mesenchymal cells condense to form a primary ossification centre (blastema)
Some of the condensed mesenchymal cells change to osteoprogenitor cells
Osteoprogenitor cells change into osteoblasts which start to deposit bone
As the osteoblasts deposit bone some of them become trapped in lacunae in the bone and then change into osteocytes
Osteoblasts lie on the surface of the newly formed bone
As more and more bone is deposited more and more osteocytes are formed from mesenchymal cells
The bone that is formed is called a spicule
This process takes place in many places simultaneously
The spicules fuse to form trabeculae
Blood vessels grow into the spaces between the trabeculae
Mesenchymal cells in the spaces give rise to hemopoetic tissue
This type of bone development forms the first phase in endochondral development
It is also responsible for the growth of short bones and the thickening of long bones
Cardiovascular Effects of Sevoflurane, Halothane, and Isoflurane
General SurgeryCardiovascular Effects of Sevoflurane, Halothane, and Isoflurane
Sevoflurane:
Maintains cardiac index and heart rate effectively.
Exhibits less hypotensive and negative inotropic effects compared to
halothane.
Cardiac output is greater than that observed with halothane.
Recovery from sevoflurane anesthesia is smooth and comparable to
isoflurane, with a shorter time to standing than halothane.
Halothane:
Causes significant decreases in mean arterial pressure, ejection
fraction, and cardiac index.
Heart rate remains at baseline levels, but overall cardiovascular
function is depressed.
Recovery from halothane is less favorable compared to sevoflurane and
isoflurane.
Isoflurane:
Preserves cardiac index and ejection fraction better than halothane.
Increases heart rate while having less suppression of mean arterial
pressure compared to halothane.
Cardiac output during isoflurane anesthesia is similar to that of
sevoflurane, indicating a favorable cardiovascular profile.
Glomerulonephritis
General Pathology
Glomerulonephritis
Characterized by inflammation of the glomerulus.
Clinical manifestations:
Nephrotic syndrome (nephrosis) → Most often caused by glomerulonephritis.
Laboratory findings:
(i) Proteinuria (albuminuria) and lipiduria—proteins and lipids are present in urine.
(ii) Hypoalbuminemia—decreased serum albumin due to albuminuria.
(iii) Hyperlipidemia—especially an increase in plasma levels of low-density lipoproteins and cholesterol.
Symptoms
severe edema, resulting from a decrease in colloid osmotic pressure due to a decrease in serum albumin.
Biosynthesis Of Pyrimidine and Purines Nucleotides
Biochemistry
Purines synthesis and metabolism
Purines are biologically synthesized as nucleotides and in particular as ribotides, i.e. bases attached to ribose 5-phosphate. Both adenine and guanine are derived from the nucleotide inosine monophosphate (IMP), which is the first compound in the pathway to have a completely formed purine ring system
The major site of purine synthesis is in the liver. Synthesis of the purine nucleotides begins with PRPP and leads to the first fully formed nucleotide, inosine 5'-monophosphate (IMP). This pathway is diagrammed below. The purine base without the attached ribose moiety is hypoxanthine.
Biosynthesis of purine and pyrimidine nucleotides requires carbon dioxide and the amide nitrogen of glutamine. Both use an amino acid nucleus – glycine in purine biosynthesis and aspartate in pyrimidine biosynthesis. Both use PRPP as the source of ribose 1-phosphate.
The end product of purine catabolism in man is uric acid.
Biosynthesis Of Pyrimidine Nucleotides
CO2 reacts with N of glutamine to form carbamoyl phosphate, which fuses with aspartate to form carbamoyl aspartate.
Carbamoyl aspartate on ring closure forms the first pyrimidine ring named OROTATE.
Orotate combines with PRPP to form OMP which is the first pyrimidine nucleotide.
OMP forms UMP which can be converted to CMP or dTMP
Stylohyoid Muscle
AnatomyStylohyoid Muscle
Origin: Posterior border of the styloid process of the
temporal bone.
Insertion: Body of the hyoid bone at the junction with
the greater horn.
Nerve Supply: Facial nerve (CN VII).
Arterial Supply: Muscular branches of the facial artery
and muscular branches of the occipital artery.
Action: Elevates the hyoid bone and base of the tongue.
Vital Capacity
PhysiologyVital Capacity: The vital capacity (VC) is the maximum volume which can be ventilated in a single breath. VC= IRV+TV+ERV. VC varies with gender, age, and body build. Measuring VC gives a device for diagnosis of respiratory disorder, and a benchmark for judging the effectiveness of treatment. (4600 ml)
Vital Capacity is reduced in restrictive disorders, but not in disorders which are purely obstructive.
The FEV1 is the % of the vital capacity which is expelled in the first second. It should be at least 75%. The FEV1 is reduced in obstructive disorders.
Both VC and the FEV1 are reduced in disorders which are both restrictive and obstructive
Oxygen is present at nearly 21% of ambient air. Multiplying .21 times 760 mmHg (standard pressure at sea level) yields a pO2 of about 160. Carbon dioxide is .04% of air and its partial pressure, pCO2, is .3.
With alveolar air having a pO2 of 104 and a pCO2 of 40. So oxygen diffuses into the alveoli from inspired air and carbon dioxide diffuses from the alveoli into air which will be expired. This causes the levels of oxygen and carbon dioxide to be intermediate in expired air when compared to inspired air and alveolar air. Some oxygen has been lost to the alveolus, lowering its level to 120, carbon dioxide has been gained from the alveolus raising its level to 27.
Likewise a concentration gradient causes oxygen to diffuse into the blood from the alveoli and carbon dioxide to leave the blood. This produces the levels seen in oxygenated blood in the body. When this blood reaches the systemic tissues the reverse process occurs restoring levels seen in deoxygenated blood.
Blood
PhysiologyBlood is a liquid tissue. Suspended in the watery plasma are seven types of cells and cell fragments.
red blood cells (RBCs) or erythrocytes
platelets or thrombocytes
five kinds of white blood cells (WBCs) or leukocytes
Three kinds of granulocytes
neutrophils
eosinophils
basophils
Two kinds of leukocytes without granules in their cytoplasm
lymphocytes
monocytes