NEET MDS Synopsis
Basic Principles of Treatment of a Fracture
Oral and Maxillofacial SurgeryBasic Principles of Treatment of a Fracture
The treatment of fractures involves a systematic approach to restore the
normal anatomy and function of the affected bone. The basic principles of
fracture treatment can be summarized in three key steps: reduction, fixation,
and immobilization.
1. Reduction
Definition: Reduction is the process of restoring the
fractured bone fragments to their original anatomical position.
Methods of Reduction:
Closed Reduction: This technique involves
realigning the bone fragments without direct visualization of the
fracture line. It can be achieved through:
Reduction by Manipulation: The physician uses
manual techniques to manipulate the bone fragments into alignment.
Reduction by Traction: Gentle pulling forces
are applied to align the fragments, often used in conjunction with
other methods.
Open Reduction: In some cases, if closed reduction is
not successful or if the fracture is complex, an open reduction may be
necessary. This involves surgical exposure of the fracture site to directly
visualize and align the fragments.
2. Fixation
Definition: After reduction, fixation is the process of
stabilizing the fractured fragments in their normal anatomical relationship to
prevent displacement and ensure proper healing.
Types of Fixation:
Internal Fixation: This involves the use of devices
such as plates, screws, or intramedullary nails that are placed inside
the body to stabilize the fracture.
External Fixation: This method uses external
devices, such as pins or frames, that are attached to the bone through
the skin. External fixation is often used in cases of open fractures or
when internal fixation is not feasible.
Goals of Fixation: The primary goals are to maintain the
alignment of the bone fragments, prevent movement at the fracture site, and
facilitate healing.
3. Immobilization
Definition: Immobilization is the phase during which the
fixation device is retained to stabilize the reduced fragments until clinical
bony union occurs.
Duration of Immobilization: The length of the
immobilization period varies depending on the type of fracture and the bone
involved:
Maxillary Fractures: Typically require 3 to
4 weeks of immobilization.
Mandibular Fractures: Generally require 4
to 6 weeks of immobilization.
Condylar Fractures: Recommended immobilization
period is 2 to 3 weeks to prevent temporomandibular
joint (TMJ) ankylosis.
The Auditory Ossicles
AnatomyThe Auditory Ossicles
The Malleus
Its superior part, the head, lies in the epitympanic recess.
The head articulates with the incus.
The neck, lies against the flaccid part of the tympanic membrane.
The chorda tympani nerve crosses the medial surface of the neck of the malleus.
The handle of the malleus (L. hammer) is embedded in the tympanic membrane and moves with it.
The tendon of the tensor tympani muscle inserts into the handle.
The Incus
Its large body lies in the epitympanic recess where it articulates with the head of the malleus.
The long process of the incus (L. an anvil) articulates with the stapes.
The short process is connected by a ligament to the posterior wall of the tympanic cavity.
The Stapes
The base (footplate) of the stapes (L. a stirrup), the smallest ossicle, fits into the fenestra vestibuli or oval window on the medial wall of the tympanic cavity.
Functions of the Auditory Ossicles
The auditory ossicles increase the force but decrease the amplitude of the vibrations transmitted from the tympanic membrane.
Tubular secretion
Physiology
Tubular secretion:
Involves transfer of substances from peritubular capillaries into the tubular lumen. It involves transepithelial transport in a direction opposite to that of tubular absorption.
Renal tubules can selectively add some substances that have not been filtered to the substances that already have been filtered via tubular secretion.
Tubular secretion mostly function to eliminate foreign organic ions, hydrogen ions ( as a contribution to acid base balance ), potassium ions ( as a contribution to maintaining optimal plasma K+ level to assure normal proceeding of neural and muscular functions), and urea.
Here we will focus on K+ secretion and will later discuss H+ secretion in acid base balance, while urea secretion will be discussed in water balance.
K+ is filtered in glomerular capillaries and then reabsorbed in proximal convoluted tubules as well as in thick ascending limb of loop of Henley ( Na-2Cl-K symporter)
K+ secretion takes place in collecting tubules (distal nephron) . There are two types of cells in distal nephron:
- Principal cells that reabsorb sodium and secrete K+ .
- Intercalated cells that reabsorb K+ in exchange with H+.
Mechanism of secretion of K+ in principal cells : Two steps
- K+ enters tubular cells by Na/K ATPase on the basolateral membrane.
- K+ leaves the tubular cells via K+ channels in apical membrane.
Aldosterone is a necessary regulatory factor.
If there is increased level of K+ in plasma,excessive K+ is secreted , some of which is reabsorbed back to the plasma in exchange with H+ via the intercalated cells.
Anti-Parkinson Drugs
Pharmacology
Anti-Parkinson Drugs
The disease involves degeneration of dopaminergic neurons in the nigral-striatal pathway in the basal ganglia. The cause is usually unknown. Sometimes it is associated with hypoxia, toxic chemicals, or cerebral infections.
Strategy
1. Increase dopamine in basal ganglia.
2. Block muscarinic receptors in the basal ganglia, since cholinergic function opposes the action of dopamine in the basal ganglia.
3. Newer therapies, such as the use of β-adrenergic receptor blockers.
Drugs
a. L-dopa plus carbidopa (Sinemet).
b. Bromocriptine, pergolide, pramipexole, ropinirole.
c. Benztropine, trihexyphenidyl, biperiden, procyclidine.
d. Diphenhydramine.
e. Amantadine.
f. Tolcapone and entacapone.
g. Selegiline.
Mechanisms of action of three drugs affecting DOPA
1. L-dopa plus carbidopa:
L-dopa is able to penetrate the blood–brain barrier and is then converted into dopamine. Carbidopa inhibits dopa decarboxylase, which catalyzes the formation of dopamine.
Carbidopa does not penetrate the blood–brain barrier; it therefore prevents the conversion of L-dopa to dopamine outside the CNS but allows
the conversion of L-dopa to dopamine inside the CNS.
2. Bromocriptine, pergolide, pramipexole, and ropinirole are direct dopamine receptor agonists.
3. Benztropine, trihexyphenidyl, biperiden, and procyclidine are antimuscarinic drugs.
4. Diphenhydramine is an antihistamine that has antimuscarinic action.
5. Amantadine releases dopamine and inhibits neuronal uptake of dopamine.
6. Selegiline is an irreversible inhibitor of monoamine oxidase B (MAO-B), which metabolizes dopamine. Selegiline therefore increases the level of dopamine.
7. Tolcapone is an inhibitor of catechol-O-methyl transferase (COMT), another enzyme that metabolizes dopamine.
8. Entacapone is another COMT inhibitor.
Dopamine and acetylcholine.
Loss of dopaminergic neurons in Parkinsonism leads to unopposed action by cholinergic neurons. Inhibiting muscarinic receptors can help alleviate symptoms of Parkinsonism
Adverse effects
1. L-dopa
- The therapeutic effects of the drug decrease with time.
- Oscillating levels of clinical efficacy of the drug (“on-off” effect).
- Mental changes—psychosis.
- Tachycardia and orthostatic hypotension.
- Nausea.
- Abnormal muscle movements (dyskinesias).
2. Tolcapone, entacapone (similar to L-dopa).
3. Direct dopamine receptor agonists (similar to L-dopa).
4. Antimuscarinic drugs
- Typical antimuscarinic adverse effects such as dry mouth.
b. Sedation.
5. Diphenhydramine (see antimuscarinic drugs).
6. Amantadine
- Nausea.
- Dizziness.
- Edema.
- Sweating.
7. Selegiline
- Nausea.
- Dry mouth.
- Dizziness.
- Insomnia.
- Although selegiline is selective for MAO-B, it still can cause excessive toxicity in the presence of tricyclic antidepressants, SSRIs, and meperidine.
Indications
Parkinson’s disease is the obvious major use of the above drugs. Parkinson-like symptoms can occur with many antipsychotic drugs. These symptoms are often treated with antimuscarinic drugs or diphenhydramine.
Dental implications of anti-Parkinson drugs
1. Dyskinesia caused by drugs can present a challenge for dental treatment.
2. Orthostatic hypotension poses a risk when changing from a reclining to a standing position.
3. The dentist should schedule appointments at a time of day at which the best control of the disease occurs.
4. Dry mouth occurs with several of the drugs.
Tooth Deformation Under Load
Conservative DentistryTooth Deformation Under Load
Biomechanical Properties of Teeth
Deformation (Strain): Teeth are not rigid structures;
they undergo deformation (strain) during normal loading. This deformation is
a natural response to the forces applied during chewing and other functional
activities.
Intraoral Loads: The loads experienced by teeth can
vary widely, with reported forces ranging from 10 to 431 N (1 N = 0.225 lb
of force). A functional load of approximately 70 N is considered clinically
normal.
Factors Influencing Load Distribution
Number of Teeth: The total number of teeth in the arch
affects how forces are distributed. More teeth can share the load, reducing
the stress on individual teeth.
Type of Occlusion: The occlusal relationship (how the
upper and lower teeth come together) influences how forces are transmitted
through the dental arch.
Occlusal Habits: Habits such as bruxism (teeth
grinding) can significantly increase the forces applied to individual teeth,
leading to greater strain and potential damage.
Clinical Implications
Restorative Considerations: Understanding the
biomechanical behavior of teeth under load is essential for designing
restorations that can withstand functional forces without failure.
Patient Management: Awareness of occlusal habits, such
as bruxism, can guide clinicians in developing appropriate treatment plans,
including the use of occlusal splints or other interventions to protect
teeth from excessive forces.
DAMAGE TO THE SPINAL NERVES AND SPINAL CORD
Physiology
Damage to Spinal Nerves and Spinal Cord
Damage
Possible cause of damage
Symptoms associated with innervated area
Peripheral nerve
Mechanical injury
Loss of muscle tone. Loss of reflexes. Flaccid paralysis. Denervation atrophy. Loss of sensation
Posterior root
Tabes dorsalis
Paresthesia. Intermittent sharp pains. Decreased sensitivity to pain. Loss of reflexes. Loss of sensation. Positive Romberg sign. High stepping and slapping of feet.
Anterior Horn
Poliomyelitis
Loss of muscle tone. Loss of reflexes. Flaccid paralysis. Denervation atrophy
Lamina X (gray matter)
Syringomyelia
Bilateral loss of pain and temperature sense only at afflicted cord level. Sensory dissociation. No sensory impairment below afflicted level
Anterior horn and lateral corticospinal tract
Amyotrophic lateral sclerosis
Muscle weakness. Muscle atrophy. Fasciculations of hand and arm muscles. Spastic paralysis
Posterior and lateral funiculi
Subacute combined degeneration
Loss of position sense. Loss of vibratory sense. Positive Romberg sign. Muscle weakness. Spasticity. Hyperactive tendon reflexes. Positive Babinski sign.
Hemisection of the spinal cord
Mechanical injury
Brown-Sequard syndrome
Below cord level on injured side
Flaccid paralysis. Hyperactive tendon reflexes. Loss of position sense. Loss of vibratory sense. Tactile impairment
Below cord level on opposite side beginning one or two segments below injury
Loss of pain and temperature
Anterior bite plate
OrthodonticsAnterior bite plate is an orthodontic appliance used
primarily to manage various dental issues, particularly those related to
occlusion and alignment of the anterior teeth. It is a removable appliance that
is placed in the mouth to help correct bite discrepancies, improve dental
function, and protect the teeth from wear.
Indications for Use
Anterior Crossbite:
An anterior bite plate can help correct an anterior crossbite by
repositioning the maxillary incisors in relation to the mandibular
incisors.
Open Bite:
It can be used to help close an anterior open bite by providing a
surface for the anterior teeth to occlude against, encouraging proper
alignment.
Bruxism:
The appliance can protect the anterior teeth from wear caused by
grinding or clenching, acting as a barrier between the upper and lower
teeth.
Space Maintenance:
In cases where anterior teeth have been lost or extracted, an
anterior bite plate can help maintain space for future dental work or
the eruption of permanent teeth.
Facilitation of Orthodontic Treatment:
It can be used as part of a comprehensive orthodontic treatment plan
to help achieve desired tooth movements and improve overall occlusion.
Design and Features
Material: Anterior bite plates are typically made from
acrylic or thermoplastic materials, which are durable and can be easily
adjusted.
Shape: The appliance is designed to cover the anterior
teeth, providing a flat occlusal surface for the upper and lower teeth to
meet.
Retention: The bite plate is custom-fitted to the
patient’s dental arch to ensure comfort and stability during use.
Mechanism of Action
Repositioning Teeth: The anterior bite plate can help
reposition the anterior teeth by providing a surface that encourages proper
occlusion and alignment.
Distributing Forces: It helps distribute occlusal
forces evenly across the anterior teeth, reducing the risk of localized wear
or damage.
Encouraging Proper Function: By providing a stable
occlusal surface, the bite plate encourages proper chewing and speaking
functions.
Management and Care
Patient Compliance: For the anterior bite plate to be
effective, patients must wear it as prescribed by their orthodontist. This
may involve wearing it during the day, at night, or both, depending on the
specific treatment goals.
Hygiene: Patients should maintain good oral hygiene and
clean the bite plate regularly to prevent plaque buildup and maintain oral
health.
Regular Check-Ups: Follow-up appointments with the
orthodontist are essential to monitor progress and make any necessary
adjustments to the appliance.
Salivary gland pathology
General Pathology
Salivary gland pathology
Inflammation
a. Sialolithiasis produces a secondary inflammatory reaction to obstruction and the resultant enlargement of ducts by stones. It may be complicated by actual infection with mouth flora.
b. Sialadenitis is a primary inflammatory reaction, but it is not always infectious. It may be part of an autoimmune disease (e.g., Sjogren's syndrome), or the result of bacterial or virals (e.g., mumps) infection.
Sjögren’s syndrome
a. An autoimmune disease of the salivary and lacrimal glands.
b. Autonuclear antibodies (ANAs) against salivary ducts may be seen.
c. Triad of symptoms include:
(1) Xerostomia—from decreased saliva production.
(2) Keratoconjunctivitis sicca (dry eyes)—from decreased tear production.
(3) Rheumatoid arthritis.
(4) Enlargement of the salivary or lacrimal glands, known as Mikulicz syndrome, may also be observed.
d. Histologically, a dense infiltration of the gland by lymphocytes is observed.
Tumors
The parotid gland accounts for more than three-quarters of these tumors, most of which are benign. Of the remainder, more occur in the submandibular gland than in the sublingual, and most of these are malignant. Many are surgically, cured, but local recurrence is common.
a. Pleomorphic adenoma is generally benign and accounts for approximately three-quarters of all salivary gland tumors. If is composed of multiple epithelial and mesenchymal cell types. Complications may arise due to involvement of cranial nerve VII.
(a) The most common salivary gland tumor.
(b) Is benign.
(c) Prognosis is good after proper surgical excision.
b. Warthin's tumor (adenolymphoma) is also benign, occuring almost exclusively in the parotid gland. It is grossly cystic.
Microscopic examination reveals cell types suggestive of branchial cleft origin embedded in a lymphoid matrix.
c. Mucoepidermoid tumors also occur primarily in the parotid and have a high rate of malignant transformation.The malignant component is usually squamous cell. Prognosis of tumor depends on grade and stage of disease.
d. Cylindroma (adenoid cysticc. Mucoepidermoid tumors carcinoma) is more common in the minor salivary glands found in the oral mucosa, and metastases are more common than in other tumors of the salivary glands. Facial nerve complications are frequent.
(1) Grossly, the tumor forms multiple lobules surrounded by a capsule.
(2) Microscopically, small cells form glands containin mucoid material