NEET MDS Synopsis
Velopharyngeal Insufficiency (VPI)
Oral and Maxillofacial SurgeryVelopharyngeal Insufficiency (VPI)
Velopharyngeal insufficiency (VPI) is
characterized by inadequate closure of the nasopharyngeal airway during speech
production, leading to speech disorders such as hypernasality and nasal
regurgitation. This condition is particularly relevant in patients who have
undergone cleft palate repair, as the surgical success does not always guarantee
proper function of the velopharyngeal mechanism.
Etiology of VPI
The etiology of VPI following cleft palate repair is multifactorial and can
include:
Inadequate Surgical Repair: Insufficient repair of the
musculature involved in velopharyngeal closure can lead to persistent VPI.
This may occur if the muscles are not properly repositioned or if there is
inadequate tension in the repaired tissue.
Anatomical Variations: Variations in the anatomy of the
soft palate, pharynx, and surrounding structures can contribute to VPI.
These variations may not be fully addressed during initial surgical repair.
Neuromuscular Factors: Impaired neuromuscular function
of the muscles involved in velopharyngeal closure can also lead to VPI,
which may not be correctable through surgical means alone.
Surgical Management of VPI
Pharyngoplasty: One of the surgical options for managing VPI
is pharyngoplasty, which aims to improve the closure of the nasopharyngeal port
during speech.
Historical Background: The procedure was first
described by Hynes in 1951 and has since been modified by various authors to
enhance its effectiveness and reduce complications.
Operative Procedure
Flap Creation: The procedure involves the creation of
two superiorly based myomucosal flaps from each posterior tonsillar pillar.
Care is taken to include as much of the palatopharyngeal muscle as possible
in the flaps.
Flap Elevation: The flaps are elevated carefully to
preserve their vascular supply and muscular integrity.
Flap Insetting: The flaps are then attached and inset
within a horizontal incision made high on the posterior pharyngeal wall.
This technique aims to create a single nasopharyngeal port rather than the
two ports typically created with a superiorly based pharyngeal flap.
Contractile Ridge Formation: The goal of the procedure
is to establish a contractile ridge posteriorly, which enhances the function
of the velopharyngeal valve, thereby improving closure during speech.
Advantages of Sphincter Pharyngoplasty
Lower Complication Rate: One of the main advantages of
sphincter pharyngoplasty over the traditional superiorly based flap
technique is the lower incidence of complications related to nasal airway
obstruction. This is particularly important for patient comfort and quality
of life post-surgery.
Improved Speech Outcomes: By creating a more effective
velopharyngeal mechanism, patients often experience improved speech
outcomes, including reduced hypernasality and better articulation.
Surgical Considerations for the Submandibular and Parotid Glands
Oral and Maxillofacial SurgerySurgical Considerations for the Submandibular and Parotid Glands
When performing surgery on the submandibular and parotid glands, it is
crucial to be aware of the anatomical structures and nerves at risk to minimize
complications. Below is an overview of the key nerves and anatomical landmarks
relevant to these surgical procedures.
Major Nerves at Risk During Submandibular Gland Surgery
Hypoglossal Nerve (CN XII):
This nerve is responsible for motor innervation to the muscles of
the tongue. It lies deep to the submandibular gland and is at risk
during surgical manipulation in this area.
Marginal Mandibular Nerve:
A branch of the facial nerve (CN VII), the marginal mandibular nerve
innervates the muscles of the lower lip and chin. It runs just deep to
the superficial layer of the deep cervical fascia, below the platysma
muscle, making it vulnerable during submandibular gland surgery.
Lingual Nerve:
The lingual nerve provides sensory innervation to the anterior
two-thirds of the tongue and carries parasympathetic fibers to the
submandibular gland via the submandibular ganglion. It is located in
close proximity to the submandibular gland and is at risk during
dissection.
Anatomical Considerations for Parotid Gland Surgery
Parotid Fascia:
The parotid gland is encased in a capsule of parotid fascia, which
provides a protective layer during surgical procedures.
Facial Nerve (CN VII):
The facial nerve is a critical structure to identify during parotid
gland surgery to prevent injury. Key landmarks for locating the facial
nerve include:
Tympanomastoid Suture Line: This is a reliable
landmark for identifying the main trunk of the facial nerve, which
lies just deep and medial to this suture.
Tragal Pointer: The nerve is located about 1 cm
deep and inferior to the tragal pointer, although this landmark is
less reliable.
Posterior Belly of the Digastric Muscle: This
muscle provides a reference for the approximate depth of the facial
nerve.
Peripheral Buccal Branches: While following
these branches can help identify the nerve, this should not be the
standard approach due to the risk of injury.
Submandibular Gland Anatomy
Location:
The submandibular gland is situated in the submandibular triangle of
the neck, which is bordered by the mandible and the digastric muscles.
Mylohyoid Muscle:
The gland wraps around the mylohyoid muscle, which is typically
retracted anteriorly during surgery to provide better exposure of the
gland.
CN XII:
The hypoglossal nerve lies deep to the submandibular gland, making
it important to identify and protect during surgical procedures.
Reflexes
PhysiologyReflexes
A reflex is a direct connection between stimulus and response, which does not require conscious thought. There are voluntary and involuntary reflexes.
The Stretch Reflex:
The stretch reflex in its simplest form involves only 2 neurons, and is therefore sometimes called a 2-neuron reflex. The two neurons are a sensory and a motor neuron. The sensory neuron is stimulated by stretch (extension) of a muscle. Stretch of a muscle normally happens when its antagonist contracts, or artificially when its tendon is stretched, as in the knee jerk reflex. Muscles contain receptors called muscle spindles. These receptors respond to the muscles's stretch. They send stimuli back to the spinal cord through a sensory neuron which connects directly to a motor neuron serving the same muscle. This causes the muscle to contract, reversing the stretch. The stretch reflex is important in helping to coordinate normal movements in which antagonistic muscles are contracted and relaxed in sequence, and in keeping the muscle from overstretching.
Since at the time of the muscle stretch its antagonist was contracting, in order to avoid damage it must be inhibited or tuned off in the reflex. So an additional connection through an interneuron sends an inhibitory pathway to the antagonist of the stretched muscle - this is called reciprocal inhibition.
The Deep Tendon Reflex:
Tendon receptors respond to the contraction of a muscle. Their function, like that of stretch reflexes, is the coordination of muscles and body movements. The deep tendon reflex involves sensory neurons, interneurons, and motor neurons. The response reverses the original stimulus therefore causing relaxation of the muscle stimulated. In order to facilitate that the reflex sends excitatory stimuli to the antagonists causing them to contract - reciprocal activation.
The stretch and tendon reflexes complement one another. When one muscle is stretching and stimulating the stretch reflex, its antagonist is contracting and stimulating the tendon reflex. The two reflexes cause the same responses thus enhancing one another.
The Crossed Extensor Reflex -
The crossed extensor reflex is just a withdrawal reflex on one side with the addition of inhibitory pathways needed to maintain balance and coordination. For example, you step on a nail with your right foot as you are walking along. This will initiate a withdrawal of your right leg. Since your quadriceps muscles, the extensors, were contracting to place your foot forward, they will now be inhibited and the flexors, the hamstrings will now be excited on your right leg. But in order to maintain your balance and not fall down your left leg, which was flexing, will now be extended to plant your left foot (e.g. crossed extensor). So on the left leg the flexor muscles which were contracting will be inhibited, and the extensor muscles will be excited
Direct Pulp Capping
EndodonticsDirect pulp capping is a minimally invasive endodontic procedure used to
preserve the vitality of the tooth's pulp when it is exposed due to caries or
trauma. The goal is to induce a biological response that leads to the formation
of dentin-bridge to seal the pulp and prevent further infection.
Indications:
- Cariously exposed pulp that is asymptomatic and has no evidence of
irreversible pulpitis.
- Recent traumatic exposure of the pulp with no signs of necrosis or infection.
- Presence of a thin layer of residual dentin over the pulp.
Contraindications:
- Signs of irreversible pulpitis or pulpal necrosis.
- Presence of a deep carious lesion that may lead to pulpal exposure during
restoration.
- Large pulp exposures or when the pulp is exposed for an extended period.
- Immunocompromised patients or those with poor oral hygiene.
Procedure:
1. Local anesthesia: Numb the tooth and surrounding tissue to ensure patient
comfort.
2. Caries removal: Carefully remove caries and any infected dentin using a
high-speed handpiece with water spray to prevent pulp exposure.
3. Hemostasis: Apply a mild hemostatic agent if necessary to control bleeding.
4. Pulp conditioning: Apply a calcium hydroxide paste or a bioactive material to
the exposed pulp for a brief period.
5. Application of the capping material: Place a bioactive material, such as
mineral trioxide aggregate (MTA), calcium silicate, or a glass ionomer cement,
directly over the pulp.
6. Restoration: Seal the tooth with a temporary restoration material and place a
final restoration (usually a composite resin) to protect the pulp from further
trauma.
7. Follow-up: Monitor the tooth for signs of pain, swelling, or discoloration.
If these symptoms occur, a root canal treatment may be necessary.
Advantages:
- Preservation of pulp vitality.
- Reduced need for root canal treatment.
- Faster healing and less post-operative sensitivity.
- Conservative approach, maintaining more natural tooth structure.
Disadvantages:
- Limited success in deep or prolonged exposures.
- Higher risk of failure in certain cases, such as extensive caries or pulp
exposure.
- Requires careful technique to avoid further pulp damage.
Antihypertensives drugs -RENIN-ANGIOTENSIN SYSTEM INHIBITORS
Pharmacology
RENIN-ANGIOTENSIN SYSTEM INHIBITORS
The actions of Angiotensin II include an increase in blood pressure and a stimulation of the secretion of aldosterone (a hormone from the adrenal cortex) that promotes sodium retention. By preventing the formation of angiotensin II, blood pressure will be reduced. This is the strategy for development of inhibitors. Useful inhibitors of the renin-angiotensin system are the Angiotensin Converting Enzyme Inhibitors
First line treatment for: Hypertension , Congestive heart failure [CHF]
ACE-Inhibitor’s MOA (Angiotensin Converting Enzyme Inhibitors)
Renin-Angiotensin Aldosterone System:
. Renin & Angiotensin = vasoconstrictor
. constricts blood vessels & increases BP
. increases SVR or afterload
. ACE Inhibitors blocks these effects decreasing SVR & afterload
. Aldosterone = secreted from adrenal glands
. cause sodium & water reabsorption
. increase blood volume
. increase preload
. ACE I blocks this and decreases preload
Types
Class I: captopril
Class II (prodrug) : e.g., ramipril, enalapril, perindopril
Class III ( water soluble) : lisinopril.
Mechanism of Action
Inhibition of circulating and tissue angiotensin- converting enzyme.
Increased formation of bradykinin and vasodilatory prostaglandins.
Decreased secretion of aldosterone; help sodium excretion.
Advantages
- Reduction of cardiovascular morbidity and mortality in patients with atherosclerotic vascular disease, diabetes, and heart failure.
- Favorable metabolic profile.
- Improvement in glucose tolerance and insulin resistance.
- Renal glomerular protection effect especially in diabetes mellitus.
- Do not adversely affect quality of life.
Indications
- Diabetes mellitus, particularly with nephropathy.
- Congestive heart failure.
- Following myocardial infraction.
Side Effects
- Cough (10 - 30%): a dry irritant cough with tickling sensation in the throat.
- Skin rash (6%).
- Postural hypotension in salt depleted or blood volume depleted patients.
- Angioedema (0.2%) : life threatening.
- Renal failure: rare, high risk with bilateral renal artery stenosis.
- Hyperkalaemia
- Teratogenicity.
Considerations
- Contraindications include bilateral renal artery stenosis, pregnancy, known allergy, and hyperkalaemia.
- High serum creatinine (> 3 mg/dl) is an indication for careful monitoring of renal function, and potassium. Benefits can still be obtained in spite of renal insufficiency.
- A slight stable increase in serum creatinine after the introduction of ACE inhibitors does not limit use.
- ACE-I are more effective when combined with diuretics and moderate salt restriction.
ACE inhibitors drugs
Captopril 50-150 mg
Enalapril 2.5-40 mg
Lisinopril 10-40 mg
Ramipril 2.5-20 mg
Perindopril 2-8 mg
Angiotensin Receptor Blocker
Losartan 25-100 mg
Candesartan 4-32 mg
Telmisartan 20-80 mg
Mechanism of action
They act by blocking type I angiotensin II receptors generally, producing more blockade of the renin -angiotensin - aldosterone axis.
Advantages
• Similar metabolic profile to that of ACE-I.
• Renal protection.
• They do not produce cough.
Indications
Patients with a compelling indication for ACE-I and who can not tolerate them because of cough or allergic reactions.
Alcohols as Antiseptics
Oral and Maxillofacial SurgeryAlcohols as Antiseptics
Ethanol and isopropyl alcohol are commonly
used as antiseptics in various healthcare settings. They possess antibacterial
properties and are effective against a range of microorganisms, although they
have limitations in their effectiveness against certain pathogens.
Mechanism of Action
Antibacterial Activity: Alcohols exhibit antibacterial
activity against both gram-positive and gram-negative bacteria,
including Mycobacterium tuberculosis.
Protein Denaturation: The primary mechanism by which
alcohols exert their antimicrobial effects is through the denaturation
of proteins. This disrupts cellular structures and functions,
leading to cell death.
Effectiveness and Recommendations
Contact Time:
According to Spaulding (1939), for alcohol to achieve maximum
effectiveness, it must remain in contact with the microorganisms for at
least 10 minutes. This extended contact time is crucial
for ensuring adequate antimicrobial action.
Concentration:
Solutions of 70% alcohol are more effective than
higher concentrations (e.g., 90% or 100%). The presence of water in the
70% solution enhances the denaturation process of proteins, as reported
by Lawrence and Block (1968). Water acts as a co-solvent, allowing for
better penetration and interaction with microbial cells.
Opiate Antagonists
Pharmacology
Opiate Antagonists
Opiate antagonists have no agonist properties. They are utilized to reverse opiate induced respiratory depression and to prevent drug abuse.
A. Naloxone
Pure opiate antagonist , Short duration of action, Only 1/50th as potent orally as parenterally
B. Naltrexone
Pure opiate antagonist, Long duration of action, Better oral efficacy
Pemphigoid
General Pathology
Pemphigoid
1. Ulcerative lesions on the skin and oral mucosa.
2. An autoimmune disease in which patients have autoantibodies against basal cells (desmosome attachment to the basement membrane).
3. Histologically, the entire epithelium appears to separate from the connective tissue. There is no acantholysis.
4. A positive Nikolsky sign is observed.
5. Complications include blindness, due to ocular lesions present in some patients.
6. Treatment: corticosteroids.