NEET MDS Synopsis
Wedging Techniques
Conservative DentistryWedging Techniques
Various wedging methods are employed to achieve optimal results,
especially in cases involving gingival recession or wide proximal boxes. Below
are descriptions of different wedging techniques, including "piggy back"
wedging, double wedging, and wedge wedging.
1. Piggy Back Wedging
A. Description
Technique: In piggy back wedging, a second smaller
wedge is placed on top of the first wedge.
Indication: This technique is particularly useful
in patients with gingival recession, where there is a risk of overhanging
restoration margins that could irritate the gingiva.
B. Purpose
Prevention of Gingival Overhang: The additional
wedge helps to ensure that the restoration does not extend beyond the tooth
surface into the gingival area, thereby preventing potential irritation and
maintaining periodontal health.
2. Double Wedging
A. Description
Technique: In double wedging, wedges are placed
from both the lingual and facial surfaces of the tooth.
Indication: This method is beneficial in cases
where the proximal box is wide, providing better adaptation of the matrix
band and ensuring a tighter seal.
B. Purpose
Enhanced Stability: By using wedges from both
sides, the matrix band is held securely in place, reducing the risk of
material leakage and improving the overall quality of the restoration.
3. Wedge Wedging
A. Description
Technique: In wedge wedging, a second wedge is
inserted between the first wedge and the matrix band, particularly in
specific anatomical situations.
Indication: This technique is commonly used in the
maxillary first premolar, where a mesial concavity may complicate the
placement of the matrix band.
B. Purpose
Improved Adaptation: The additional wedge helps to
fill the space created by the mesial concavity, ensuring that the matrix
band conforms closely to the tooth surface and providing a better seal for
the restorative material.
Neurogenic Shock
Oral and Maxillofacial SurgeryNeurogenic Shock
Neurogenic shock is a type of distributive shock that occurs
due to the loss of vasomotor tone, leading to widespread vasodilation and a
significant decrease in systemic vascular resistance. This condition can occur
without any loss of blood volume, resulting in inadequate filling of the
circulatory system despite normal blood volume. Below is a detailed overview of
neurogenic shock, its causes, symptoms, and management.
Mechanism of Neurogenic Shock
Loss of Vasomotor Tone: Neurogenic shock is primarily
caused by the disruption of sympathetic nervous system activity, which leads
to a loss of vasomotor tone. This results in massive dilation of blood
vessels, particularly veins, causing a significant increase in vascular
capacity.
Decreased Systemic Vascular Resistance: The dilated
blood vessels cannot effectively maintain blood pressure, leading to
inadequate perfusion of vital organs, including the brain.
Causes
Spinal Cord Injury: Damage to the spinal cord,
particularly at the cervical or upper thoracic levels, can disrupt
sympathetic outflow and lead to neurogenic shock.
Severe Head Injury: Traumatic brain injury can also
affect autonomic regulation and result in neurogenic shock.
Vasovagal Syncope: A common form of neurogenic shock,
often triggered by emotional stress, pain, or prolonged standing, leading to
a sudden drop in heart rate and blood pressure.
Symptoms
Early Signs:
Pale or Ashen Gray Skin: Due to peripheral vasodilation
and reduced blood flow to the skin.
Heavy Perspiration: Increased sweating as a response to
stress or pain.
Nausea: Gastrointestinal distress may occur.
Tachycardia: Increased heart rate as the body attempts
to compensate for low blood pressure.
Feeling of Warmth: Particularly in the neck or face due
to vasodilation.
Late Symptoms:
Coldness in Hands and Feet: Peripheral vasoconstriction
may occur as the body prioritizes blood flow to vital organs.
Hypotension: Significantly low blood pressure due to
vasodilation.
Bradycardia: Decreased heart rate, particularly in
cases of vasovagal syncope.
Dizziness and Visual Disturbance: Due to decreased
cerebral perfusion.
Papillary Dilation: As a response to low light levels
in the eyes.
Hyperpnea: Increased respiratory rate as the body
attempts to compensate for low oxygen delivery.
Loss of Consciousness: Resulting from critically low
cerebral blood flow.
Duration of Syncope
Brief Duration: The duration of syncope in neurogenic
shock is typically very brief. Patients often regain consciousness almost
immediately upon being placed in a supine position.
Supine Positioning: This position is crucial as it
helps increase venous return to the heart and improves cerebral perfusion,
aiding in recovery.
Management
Positioning: The first and most important step in
managing neurogenic shock is to place the patient in a supine position. This
helps facilitate blood flow to the brain.
Fluid Resuscitation: While neurogenic shock does not
typically involve blood loss, intravenous fluids may be administered to help
restore vascular volume and improve blood pressure.
Vasopressors: In cases where hypotension persists
despite fluid resuscitation, vasopressor medications may be used to
constrict blood vessels and increase blood pressure.
Monitoring: Continuous monitoring of vital signs,
including blood pressure, heart rate, and oxygen saturation, is essential to
assess the patient's response to treatment.
Addressing Underlying Causes: If neurogenic shock is due
to a specific cause, such as spinal cord injury or vasovagal syncope,
appropriate interventions should be initiated to address the underlying
issue.
Parathyroid Hormone
Biochemistry
Parathyroid Hormone
Parathyroid hormone (PTH), parathormone or parathyrin, is secreted by the chief cells of the parathyroid glands.
It acts to increase the concentration of calcium (Ca2+) in the blood, whereas calcitonin (a hormone produced by the parafollicular cells of the thyroid gland) acts to decrease calcium concentration.
PTH acts to increase the concentration of calcium in the blood by acting upon the parathyroid hormone 1 receptor (high levels in bone and kidney) and the parathyroid hormone 2 receptor (high levels in the central nervous system, pancreas, testis, and placenta).
Effect of parathyroid hormone in regulation of serum calcium.
Bone -> PTH enhances the release of calcium from the large reservoir contained in the bones. Bone resorption is the normal destruction of bone by osteoclasts, which are indirectly stimulated by PTH forming new osteoclasts, which ultimately enhances bone resorption.
Kidney -> PTH enhances active reabsorption of calcium and magnesium from distal tubules of kidney. As bone is degraded, both calcium and phosphate are released. It also decreases the reabsorption of phosphate, with a net loss in plasma phosphate concentration. When the calcium:phosphate ratio increases, more calcium is free in the circulation.
Intestine -> PTH enhances the absorption of calcium in the intestine by increasing the production of activated vitamin D. Vitamin D activation occurs in the kidney. PTH converts vitamin D to its active form (1,25-dihydroxy vitamin D). This activated form of vitamin D increases the absorption of calcium (as Ca2+ ions) by the intestine via calbindin.
Posterior Pituitary Syndromes
General Pathology
Posterior Pituitary Syndromes
The posterior pituitary, or neurohypophysis, is composed of modified glial cells (termed pituicytes) and axonal processes extending from nerve cell bodies in the hypothalamus. The hypothalamic neurons produce two peptides: antidiuretic hormone (ADH) and oxytocin that are stored in axon terminals in the neurohypophysis.
The clinically important posterior pituitary syndromes involve ADH production and include
1. Diabetes insipidus and
2. Inappropriate secretion of high levels of ADH.
- ADH is released into the general circulation in response to increased plasma oncotic pressure & left atrial distention.
- It acts on the renal collecting tubules to increase the resorption of free water.
- ADH deficiency causes diabetes insipidus, a condition characterized by polyuria. If the cause is related to ADH Diabetes insipidus from - - ADH deficiency is designated as central, to differentiate it from nephrogenic diabetes insipidus due to renal tubular unresponsiveness to circulating ADH.
- The clinical manifestations of both diseases are similar and include the excretion of large volumes of dilute urine with low specific gravity. Serum sodium and osmolality are increased as a result of excessive renal loss of free water, resulting in thirst and polydipsia.
- ADH excess causes resorption of excessive amounts of free water, with resultant hyponatremia.
- The most common causes of the syndrome include the secretion of ectopic ADH by malignant neoplasms (particularly small-cell carcinomas of the lung), and local injury to the hypothalamus and/or neurohypophysis.
- The clinical manifestations are dominated by hyponatremia, cerebral edema, and resultant neurologic dysfunction.
Gross Features of the Tongue
AnatomyGross Features of the Tongue
The dorsum of the tongue is divided by a V-shaped sulcus terminalis into anterior oral (presulcal) and posterior pharyngeal (postsulcal) parts.
The apex of the V is posterior and the two limbs diverge anteriorly.
The oral part forms about 2/3 of the tongue and the pharyngeal part forms about 1/3.
Oral Part of the Tongue
This part is freely movable, but it is loosely attached to the floor of the mouth by the lingual frenulum.
On each side of the frenulum is a deep lingual vein, visible as a blue line.
It begins at the tip of the tongue and runs posteriorly.
All the veins on one side of the tongue unite at the posterior border of the hyoglossus muscle to form the lingual vein, which joins the facial vein or the internal jugular vein.
On the dorsum of the oral part of the tongue is a median groove.
This groove represents the site of fusion of the distal tongue buds during embryonic development.
The Lingual Papillae and Taste Buds
The filiform papillae (L. filum, thread) are numerous, rough, and thread-like.
They are arranged in rows parallel to the sulcus terminalis.
The fungiform papillae are small and mushroom-shaped.
They usually appear are pink or red spots.
The vallate (circumvallate) papillae are surrounded by a deep, circular trench (trough), the walls of which are studded with taste buds.
The foliate papillae are small lateral folds of lingual mucosa that are poorly formed in humans.
The vallate, foliate and most of the fungiform papillae contain taste receptors, which are located in the taste buds.
The Pharyngeal Part of the Tongue
This part lies posterior to the sulcus terminalis and palatoglossal arches.
Its mucous membrane has no papillae.
The underlying nodules of lymphoid tissue give this part of the tongue a cobblestone appearance.
The lymphoid nodules (lingual follicles) are collectively known as the lingual tonsil.
Biological Functions are Extremely Sensitive to pH
PhysiologyBiological Functions are Extremely Sensitive to pH
H+ and OH- ions get special attention because they are very reactive
Substance which donates H+ ions to solution = acid
Substance which donates OH- ions to solution = base
Because we deal with H ions over a very wide range of concentration, physiologists have devised a logarithmic unit, pH, to deal with it
pH = - log [H+]
[H+] is the H ion concentration in moles/liter
Because of the way it is defined a high pH indicates low H ion and a low pH indicates high H ion- it takes a while to get used to the strange definition
Also because of the way it is defined, a change of 1 pH unit means a 10X change in the concentration of H ions
If pH changes by 2 units the H+ concentration changes by 10 X 10 = 100 times
Human blood pH is 7.4
Blood pH above 7.4 = alkalosis
Blood pH below 7.4 = acidosis
Body must get rid of ~15 moles of potential acid/day (mostly CO2)
CO2 reacts with water to form carbonic acid (H2CO3)
Done mostly by lungs & kidney
In neutralization H+ and OH- react to form water
If the pH changes charges on molecules also change, especially charges on proteins
This changes the reactivity of proteins such as enzymes
Large pH changes occur as food passes through the intestines.
Fatty acid activation:
Biochemistry
Acyl-CoA Synthases (Thiokinases), associated with endoplasmic reticulum membranes and the outer mitochondrial membrane, catalyze activation of long chain fatty acids, esterifying them to coenzyme A, as shown at right. This process is ATP-dependent, and occurs in 2 steps. There are different Acyl-CoA Synthases for fatty acids of different chain lengths.
Exergonic hydrolysis of PPi (P~P), catalyzed by Pyrophosphatase, makes the coupled reaction spontaneous. Overall, two ~P bonds of ATP are cleaved during fatty acid activation. The acyl-coenzyme A product includes one "high energy" thioester linkage.
Summary of fatty acid activation:
fatty acid + ATP → acyl-adenylate + PPi
PPi → Pi
acyladenylate + HS-CoA → acyl-CoA + AMP
Overall: fatty acid + ATP + HS-CoA → acyl-CoA + AMP + 2 Pi
For most steps of the b-Oxidation Pathway, there are multiple enzymes specific for particular fatty acid chain lengths.
Fatty acid b-oxidation is considered to occur in the mitochondrial matrix. Fatty acids must enter the matrix to be oxidized. However enzymes of the pathway specific for very long chain fatty acids are associated with the inner mitochondrial membrane (facing the matrix).
Fatty acyl-CoA formed outside the mitochondria can pass through the outer mitochondrial membrane, which contains large VDAC channels, but cannot penetrate the mitochondrial inner membrane.
Transfer of the fatty acid moiety across the inner mitochondrial membrane involves carnitine.
Carnitine Palmitoyl Transferases catalyze transfer of a fatty acid between the thiol of Coenzyme A and the hydroxyl on carnitine.
Carnitine-mediated transfer of the fatty acyl moiety into the mitochondrial matrix is a 3-step process, as presented below.
Carnitine Palmitoyl Transferase I, an enzyme associated with the cytosolic surface of the outer mitochondrial membrane, catalyzes transfer of a fatty acid from ester linkage with the thiol of coenzyme A to the hydroxyl on carnitine.
Carnitine Acyltransferase, an antiporter in the inner mitochondrial membrane, mediates transmembrane exchange of fatty acyl-carnitine for carnitine.
Within the mitochondrial matrix (or associated with the matrix surface of the inner mitochondrial membrane, Carnitine Palmitoyl Transferase II catalyzes transfer of the fatty acid from carnitine to coenzyme A. (Carnitine exits the matrix in step 2.) The fatty acid is now esterified to coenzyme A within the mitochondrial matrix
Control of fatty acid oxidation is exerted mainly at the step of fatty acid entry into mitochondria.
Malonyl-CoA inhibits Carnitine Palmitoyl Transferase I. (Malonyl-CoA is also a precursor for fatty acid synthesis). Malonyl-CoA is produced from acetyl-CoA by the enzyme Acetyl-CoA Carboxylase
AMP-Activated Kinase, a sensor of cellular energy levels, catalyzes phosphorylation of Acetyl-CoA Carboxylase under conditions of high AMP (when ATP is low). Phosphorylation inhibits Acetyl-CoA Carboxylase, thereby decreasing malonyl-CoA production.
The decrease in malonyl-CoA concentration releases Carnitine Palmitoyl Transferase I from inhibition. The resulting increase in fatty acid oxidation generates acetyl-CoA for entry into Krebs cycle, with associated production of ATP
Vessels of the Palate
Anatomy
The palate has a rich blood supply from branches of the maxillary artery.