NEET MDS Synopsis
Mouth Breathing
OrthodonticsMouth Breathing
Mouth breathing is a condition where an individual breathes
primarily through the mouth instead of the nose. This habit can lead to various
dental, facial, and health issues, particularly in children. The etiology of
mouth breathing is often related to nasal obstruction, and it can have
significant clinical features and consequences.
Etiology
Nasal Obstruction: Approximately 85% of mouth breathers
suffer from some degree of nasal obstruction, which can be caused by:
Allergies: Allergic rhinitis can lead to
inflammation and blockage of the nasal passages.
Enlarged Adenoids: Hypertrophy of the adenoids can
obstruct airflow through the nasal passages.
Deviated Septum: A structural abnormality in the
nasal septum can impede airflow.
Chronic Sinusitis: Inflammation of the sinuses can
lead to nasal congestion and obstruction.
Clinical Features
Facial Characteristics:
Adenoid Facies: A characteristic appearance
associated with chronic mouth breathing, including:
Long, narrow face.
Narrow nose and nasal passage.
Short upper lip.
Nose tipped superiorly.
Expressionless or "flat" facial appearance.
Dental Effects (Intraoral):
Protrusion of Maxillary Incisors: The anterior
teeth may become protruded due to the altered position of the tongue and
lips.
High Palatal Vault: The shape of the palate may be
altered, leading to a high and narrow palatal vault.
Increased Incidence of Caries: Mouth breathers are
more prone to dental caries due to dry oral conditions and reduced
saliva flow.
Chronic Marginal Gingivitis: Inflammation of the
gums can occur due to poor oral hygiene and dry mouth.
Management
Symptomatic Treatment:
Gingival Health: The gingiva of mouth breathers
should be restored to normal health. Coating the gingiva with petroleum
jelly can help maintain moisture and protect the tissues.
Addressing Obstruction: If nasal or pharyngeal
obstruction has been diagnosed, surgical intervention may be necessary
to remove the cause (e.g., adenoidectomy, septoplasty).
Elimination of the Cause:
Identifying and treating the underlying cause of nasal obstruction
is crucial. This may involve medical management of allergies or surgical
correction of anatomical issues.
Interception of the Habit:
Physical Exercise: Encouraging physical activity
can help improve overall respiratory function and promote nasal
breathing.
Lip Exercises: Exercises to strengthen the lip
muscles can help encourage lip closure and discourage mouth breathing.
Oral Screen: An oral screen or similar appliance
can be used to promote nasal breathing by preventing the mouth from
remaining open.
The Walls of the Orbit
AnatomyThe Walls of the Orbit
Each orbit has four walls: superior (roof), medial, inferior (floor) and lateral.
The medial walls of the orbit are almost parallel with each other and with the superior part of the nasal cavities separating them.
The lateral walls are approximately at right angles to each other
Lipids
PhysiologyLipids:
about 40% of the dry mass of a typical cell
composed largely of carbon & hydrogen
generally insoluble in water
involved mainly with long-term energy storage; other functions are as structural components (as in the case of phospholipids that are the major building block in cell membranes) and as "messengers" (hormones) that play roles in communications within and between cells
Subclasses include:
Triglycerides - consist of one glycerol molecule + 3 fatty acids (e.g., stearic acid in the diagram below). Fatty acids typically consist of chains of 16 or 18 carbons (plus lots of hydrogens).
phospholipids - Composed of 2 fatty acids, glycerol, phosphate and polar groups , phosphate group (-PO4) substitutes for one fatty acid & these lipids are an important component of cell membranes
steroids - have 4 rings- cholesterol, some hormones, found in membranes include testosterone, estrogen, & cholesterol
Amino Acid Catabolism
Biochemistry
Amino Acid Catabolism
Glutamine/Glutamate and Asparagine/Aspartate Catabolism
Glutaminase is an important kidney tubule enzyme involved in converting glutamine (from liver and from other tissue) to glutamate and NH3+, with the NH3+ being excreted in the urine. Glutaminase activity is present in many other tissues as well, although its activity is not nearly as prominent as in the kidney. The glutamate produced from glutamine is converted to a-ketoglutarate, making glutamine a glucogenic amino acid.
Asparaginase is also widely distributed within the body, where it converts asparagine into ammonia and aspartate. Aspartate transaminates to oxaloacetate, which follows the gluconeogenic pathway to glucose.
Glutamate and aspartate are important in collecting and eliminating amino nitrogen via glutamine synthetase and the urea cycle, respectively. The catabolic path of the carbon skeletons involves simple 1-step aminotransferase reactions that directly produce net quantities of a TCA cycle intermediate. The glutamate dehydrogenase reaction operating in the direction of a-ketoglutarate production provides a second avenue leading from glutamate to gluconeogenesis.
Alanine Catabolism
Alanine is also important in intertissue nitrogen transport as part of the glucose-alanine cycle. Alanine's catabolic pathway involves a simple aminotransferase reaction that directly produces pyruvate. Generally pyruvate produced by this pathway will result in the formation of oxaloacetate, although when the energy charge of a cell is low the pyruvate will be oxidized to CO2 and H2O via the PDH complex and the TCA cycle. This makes alanine a glucogenic amino acid.
Arginine, Ornithine and Proline Catabolism
The catabolism of arginine begins within the context of the urea cycle. It is hydrolyzed to urea and ornithine by arginase.
Ornithine, in excess of urea cycle needs, is transaminated to form glutamate semialdehyde. Glutamate semialdehyde can serve as the precursor for proline biosynthesis as described above or it can be converted to glutamate.
Proline catabolism is a reversal of its synthesis process.
The glutamate semialdehyde generated from ornithine and proline catabolism is oxidized to glutamate by an ATP-independent glutamate semialdehyde dehydrogenase. The glutamate can then be converted to α-ketoglutarate in a transamination reaction. Thus arginine, ornithine and proline, are glucogenic.
Methionine Catabolism
The principal fates of the essential amino acid methionine are incorporation into polypeptide chains, and use in the production of α -ketobutyrate and cysteine via SAM as described above. The transulfuration reactions that produce cysteine from homocysteine and serine also produce α -ketobutyrate, the latter being converted to succinyl-CoA.
Regulation of the methionine metabolic pathway is based on the availability of methionine and cysteine
Phenylalanine and Tyrosine Catabolism
Phenylalanine normally has only two fates: incorporation into polypeptide chains, and production of tyrosine via the tetrahydrobiopterin-requiring phenylalanine hydroxylase. Thus, phenylalanine catabolism always follows the pathway of tyrosine catabolism. The main pathway for tyrosine degradation involves conversion to fumarate and acetoacetate, allowing phenylalanine and tyrosine to be classified as both glucogenic and ketogenic.
Tyrosine is equally important for protein biosynthesis as well as an intermediate in the biosynthesis of several physiologically important metabolites e.g. dopamine, norepinephrine and epinephrine
Fixation of Condylar Fractures
Oral and Maxillofacial SurgeryFixation of Condylar Fractures
Condylar fractures of the mandible can be challenging to manage due to their
location and the functional demands placed on the condylar region. Various
fixation techniques have been developed to achieve stable fixation and promote
healing. Below is an overview of the different methods of fixation for condylar
fractures, including their advantages, disadvantages, and indications.
1. Miniplate Osteosynthesis
Overview:
Miniplate osteosynthesis involves the use of condylar plates and
screw systems designed to withstand biochemical forces, minimizing
micromotion at the fracture site.
Primary Bone Healing:
Under optimal conditions of stability and fracture reduction,
primary bone healing can occur, allowing new bone to form along the
fracture surface without the formation of fibrous tissue.
Plate Placement:
High condylar fractures may accommodate only one plate with two
screws above and below the fracture line, parallel to the posterior
border, providing adequate stability in most cases.
For low condylar fractures, two plates may be required. The
posterior plate should parallel the posterior ascending ramus, while the
anterior plate can be angulated across the fracture line.
Mechanical Advantage:
The use of two miniplates at the anterior and posterior borders of
the condylar neck restores tension and compression trajectories,
neutralizing functional stresses in the condylar neck.
Research Findings:
Studies have shown that the double mini plate method is the only
system able to withstand normal loading forces in cadaver mandibles.
2. Dynamic Compression Plating
Overview:
Dynamic compression plating is generally not recommended for
condylar fractures due to the oblique nature of the fractures, which can
lead to overlap of fragment ends and loss of ramus height.
Current Practice:
The consensus is that treatment is adequate with miniplates placed
in a neutral mode, avoiding the complications associated with dynamic
compression plating.
3. Lag Screw Osteosynthesis
Overview:
First described for condylar fractures by Wackerbauer in 1962, lag
screws provide a biomechanically advantageous method of fixation.
Mechanism:
A true lag screw has threads only on the distal end, allowing for
compression when tightened against the near cortex. This central
placement of the screw enhances stability.
Advantages:
Rapid application of rigid fixation and close approximation of
fractured parts due to significant compression generated.
Less traumatic than miniplates, as there is no need to open the
joint capsule.
Disadvantages:
Risk of lateralization and rotation of the condylar head if the
screw is not placed centrally.
Requires a steep learning curve for proper application.
Contraindications:
Not suitable for cases with loss of bone in the fracture gap or
comminution that could lead to displacement when compression is applied.
Popular Options:
The Eckelt screw is one of the most widely used lag screws in
current practice.
4. Pin Fixation
Overview:
Pin fixation involves the use of 1.3 mm Kirschner wires (K-wires)
placed into the condyle under direct vision.
Technique:
This method requires an open approach to the condylar head and
traction applied to the lower border of the mandible. A minimum of three
convergent K-wires is typically needed to ensure stability.
5. Resorbable Pins and Plates
Overview:
Resorbable fixation devices may take more than two years to fully
resorb. Materials used include self-reinforced poly-L-lactide screws
(SR-PLLA), polyglycolide pins, and absorbable alpha-hydroxy polyesters.
Indications:
These materials are particularly useful in pediatric patients or in
situations where permanent hardware may not be desirable.
Surface Tension
PhysiologySurface Tension
1. Maintains stability of alveolus, preventing collapse
2. Surfactant (Type II pneumocytes) = dipalmityl lecithin
3. Type II pneumocyte appears at 24 weeks of gestation;
1. Surfactant production, 28-32 weeks;
2. Surfactant in amniotic fluid, 35 weeks.
3. Laplace equation for thin walled spheres P = 2T
a. P = alveolar internal pressure r
b. T = tension in the walls r = radius of alveolus
4. During normal tidal respiration
1. Some alveoli do collapse (Tidal pressure can't open)
2. Higher than normal pressure needed (Coughing)
3. Deep breaths & sighs promote re-expansion
4. After surgery/Other conditions, Coughing, deep breathing, sustained maximal respiration
Glycogen Storage Diseases
Biochemistry
A glycogen storage disease (GSD, also glycogenosis and dextrinosis) is a metabolic disorder caused by enzyme deficiencies affecting either glycogen synthesis, glycogen breakdown or glycolysis (glucose breakdown), typically in muscles and/or liver cells. GSD has two classes of cause: genetic and acquired.
Mnemonic:VP CAM HT.– Very Poor Carbohydrate Affects Muscle and Hepatic Target.
Type I – Von Gierke’s disease
Type II – Pompe’s disease
Type III – Cori’s disease
Type IV – Anderson’s disease
Type V – McArdle’s disease
Type VI – Her’s disease
Type VII – Tauri’s disease
Type 0 (Glycogen synthase deficiency)
There is hypoglycemia; hyperketonemia and early death.
Type I (Glucose-6-phosphatase deficiency)-Von Gierke’s disease
- most common autosomal recessive disease.
- characterized by severe hypoglycemia that coincides with metabolic acidosis,
- ketonemia and elevated lactate (due to excess glycolysis) and alanine
Type II (Lysosomal α1->4 and α1->6 Glucosidase deficiency)- Pompes disease
- It affects predominantly the heart and skeletal muscle, producing muscle weakness and cardiomegaly. Liver function is normal and patients do not have hypoglycemia. Two forms identified;
(1) infantile (pompes disease) that develop in first few months of life with weakness and respiratory difficulties and
(2) juvenile that is present in second or third decade of life with difficulty in walking.
Type III (Amylo-1,6-Glucosidase deficiency)-Forbe’s or Cori’s disease
- Deficiency of glycogen debranching enzyme results in storage of an abnormal form of glycogen (limit dextrinosis).
- Both liver and muscle are affected (type IIIA), producing hepatomegaly and muscle weakness. About 15% have only liver involvement (Type IIIB).
Differentiation from type I is by hyperglycemic response to galactose, low concentration of urate and lactate in blood, and elevated serum transaminases and creatinine kinase activities
Type IV (Branching Enzyme deficiency)-Andersons disease of Amylopectinosis
- production of an abnormal form of unbranched glycogen in all tissue.
- Patients exhibit hepatospleenomegaly with ascites and liver failure.
- There is death from heart or liver failure before 5 years of age.
Type V (Muscle Phosphorylase deficiency)-McArdle’s disease
- Increased plasma creatine kinase activity at rest,
- failure of ischemic exercise to increase serum lactate concentrations while producing an exaggerated increase in ammonia,
- myoglobinuria and diminished activity of muscle phosphorylase establish the diagnosis.
TYPE VI (LIVER PHOSPHORYLASE DEFICIENCY)- HERS’ DISEASE
- It manifest as hepatomegaly caused by increased deposits of normal glycogen in liver or in red or white blood cells.
Type VII (Muscle and erythrocyte phosphofructokinase deficiency)-Taruis’ disease
- Abnormal glycogen in muscle.
- Exercise intolerance, unresponsiveness to glucose administration, and hemolysis (caused by decreased glycolysis in RBC) are noted clinically,
- hyperbilirubinemia, pigmenturia and reticulocytosis.
Insulin
Biochemistry
Insulin
Insulin is a polypeptide hormone synthesized in the pancreas by β-cells, which construct a single chain molecule called proinsulin.
Insulin, secreted by the β-cells of the pancreas in response to rising blood glucose levels, is a signal that glucose is abundant.
Insulin binds to a specific receptor on the cell surface and exerts its metabolic effect by a signaling pathway that involves a receptor tyrosine kinase phosphorylation cascade.
The pancreas secretes insulin or glucagon in response to changes in blood glucose.
Each cell type of the islets produces a single hormone: α-cells produce glucagon; β-cells, insulin; and δ-cells, somatostatin.
Insulin secretion
When blood glucose rises, GLUT2 transporters carry glucose into the b-cells, where it is immediately converted to glucose 6-phosphate by hexokinase IV (glucokinase) and enters glycolysis. The increased rate of glucose catabolism raises [ATP], causing the closing of ATP-gated K+ channels in the plasma membrane. Reduced efflux of K+ depolarizes the membrane, thereby opening voltage-sensitive Ca2+ channels in the plasma membrane. The resulting influx of Ca2+ triggers the release of insulin by exocytosis.
Insulin lowers blood glucose by stimulating glucose uptake by the tissues; the reduced blood glucose is detected by the β-cell as a diminished flux through the hexokinase reaction; this slows or stops the release of insulin. This feedback regulation holds blood glucose concentration nearly constant despite large fluctuations in dietary intake.
Insulin counters high blood glucose
Insulin stimulates glucose uptake by muscle and adipose tissue, where the glucose is converted to glucose 6-phosphate. In the liver, insulin also activates glycogen synthase and inactivates glycogen phosphorylase, so that much of the glucose 6-phosphate is channelled into glycogen.
Diabetes mellitus, caused by a deficiency in the secretion or action of insulin, is a relatively common disease. There are two major clinical classes of diabetes mellitus: type I diabetes, or insulin-dependent diabetes mellitus (IDDM), and type II diabetes, or non-insulin-dependent diabetes mellitus (NIDDM), also called insulin-resistant diabetes. In type I diabetes, the disease begins early in life and quickly becomes severe. IDDM requires insulin therapy and careful, lifelong control of the balance between dietary intake and insulin dose.
Characteristic symptoms of type I (and type II) diabetes are excessive thirst and frequent urination (polyuria), leading to the intake of large volumes of water (polydipsia)
Type II diabetes is slow to develop (typically in older, obese individuals), and the symptoms are milder.