NEET MDS Synopsis
Dautrey Procedure
General SurgeryDautrey Procedure
The Dautrey procedure is a surgical intervention aimed at
preventing dislocation of the temporomandibular joint (TMJ) by creating a
mechanical obstacle that restricts abnormal forward translation of the condylar
head. This technique is particularly beneficial for patients who experience
recurrent TMJ dislocations or subluxations, especially when conservative
management strategies have proven ineffective.
Indications:
The Dautrey procedure is indicated for patients with a history of
recurrent TMJ dislocations. It is particularly useful when conservative
treatments, such as physical therapy or splint therapy, have failed to
provide adequate stabilization of the joint.
Surgical Technique:
Osteotomy of the Zygomatic Arch: The procedure
begins with an osteotomy, which involves surgically cutting the
zygomatic arch, the bony structure that forms the prominence of the
cheek.
Depressing the Zygomatic Arch: After the osteotomy,
the zygomatic arch is depressed in front of the condylar head. This
depression creates a physical barrier that acts as an obstacle to the
forward movement of the condylar head during jaw opening or excessive
movement.
Stabilization: The newly positioned zygomatic arch
limits the range of motion of the condylar head, thereby reducing the
risk of dislocation during functional activities such as chewing or
speaking.
Mechanism of Action:
By altering the position of the zygomatic arch, the Dautrey
procedure effectively changes the biomechanics of the TMJ. The new
position of the zygomatic arch prevents the condylar head from
translating too far forward, which is a common cause of dislocation.
Postoperative Care:
Following the procedure, patients may require a period of recovery
and rehabilitation. This may include:
Dietary Modifications: Soft diet to minimize
stress on the TMJ during the healing process.
Pain Management: Use of analgesics to manage
postoperative discomfort.
Physical Therapy: Exercises to restore normal
function and range of motion in the jaw.
Outcomes:
The Dautrey procedure has been shown to be effective in preventing
recurrent TMJ dislocations. Patients often experience improved joint
stability and a better quality of life following the surgery. Successful
outcomes can lead to reduced pain, improved jaw function, and enhanced
overall satisfaction with treatment.
Congenital heart defect
General Pathology
Congenital heart defect
Congenital heart defects can be broadly categorised into two groups,
o acyanotic heart defects ('pink' babies) :
An acyanotic heart defect is any heart defect of a group of structural congenital heart defects, approximately 75% of all congenital heart defects.
It can be subdivided into two groups depending on whether there is shunting of the blood from the left vasculature to the right (left to right shunt) or no shunting at all.
Left to right shunting heart defects include
- ventricular septal defect or VSD (30% of all congenital heart defects),
- persistent ductus arteriosus or PDA,
- atrial septal defect or ASD,
- atrioventricular septal defect or AVSD.
Acyanotic heart defects without shunting include
- pulmonary stenosis, a narrowing of the pulmonary valve,
- aortic stenosis
- coarctation of the aorta.
cyanotic heart defects ('blue' babies).
obstructive heart defects
cyanotic heart defect is a group-type of congenital heart defect. These defects account for about 25% of all congenital heart defects. The patient appears blue, or cyanotic, due to deoxygenated blood in the systemic circulation. This occurs due to either a right to left or a bidirectional shunt, allowing significant proportions of the blood to bypass the pulmonary vascular bed; or lack of normal shunting, preventing oxygenated blood from exiting the cardiac-pulmonary system (as with transposition of the great arteries).
Defects in this group include
hypoplastic left heart syndrome,
tetralogy of Fallot,
transposition of the great arteries,
tricuspid atresia,
pulmonary atresia,
persistent truncus arteriosus.
Nerves of the Palate
AnatomyNerves of the Palate
The sensory nerves of the palate, which are branches of the pterygopalatine ganglion, are the greater and lesser palatine nerves.
They accompany the arteries through the greater and lesser palatine foramina, respectively.
The greater palatine nerve supplies the gingivae, mucous membrane, and glands of the hard palate.
The lesser palatine nerve supplies the soft palate.
Another branch of the pterygopalatine ganglion, the nasopalatine nerve, emerges from the incisive foramen and supplies the mucous membrane of the anterior part of the hard palate.
Vessels of the Palate
The palate has a rich blood supply from branches of the maxillary artery.
EMBOLISM
General Pathology
EMBOLISM
An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin
99% due to dislodged thrombus
Types:
1. Thrombo-embolism
2. Fat embolism
3. Air embolism
4. Nitrogen embolism
Emboli result in partial or complete vascular occlusion.
The consequences of thromboembolism include ischemic necrosis (infarction) of downstream tissue
PULMONARY THROMBOEMBOLISM
- 95% originate from deep veins of L.L
Special variants: - Saddle embolus: at bifurcation of Pulmonary artery
Paradoxical embolus: Passage of an embolus from venous to systemic circulation through IAD, IVD
CLINICAL CONSEQUENCE OF PULMONARY THROMBOEMBOLISM :
Most pulmonary emboli (60% to 80%) are clinically silent because they are small
a. Organization: 60 – 80 %
b. Sudden death, Right ventricle failure, CV collapse when more than 60 % of pulmonary vessels are obstructed.
c. Pulmonary hemorrhage: obstruction of medium sized arteries.
d. Pulmonary Hypertension and right ventricular failure due to multiple emboli over a long time.
Systemic thromboembolism
Emboli traveling within the arterial circulation
80% due to intracardiac mural thrombi
2/3 Lt. ventricular failure
The major targets are:
1. Lower limbs 75%
2. Brain 10%
3. Intestines
4. Kidneys
5. Spleen
Fat embolism
Causes
1. Skeletal injury (fractures of long bones )
2. Adipose tissue Injury
Mechanical obstruction is exacerbated by free fatty acid release from the fat globules, causing local toxic injury to endothelium. - In skeletal injury, fat embolism occurs in 90% of cases, but only 10% or less have clinical findings
Fat embolism syndrome is characterized by
A. Pulmonary Insufficiency
B. Neurologic symptoms
C. Anemia
D. Thrombocytopenia
E. Death in 10% of the case
Symptoms appears 1-3 days after injury
Tachypnea, Dyspnea, Tachycardia and Neurological symptoms
Air Embolism
causes: 1. Obstetric procedures
2. Chest wall injury
3. Decompression sickness: in Scuba and deep-sea divers ((nitrogen ))
More then 100ml of air is required to produce clinical effect.
Clinical consequence
1. Painful joints: due to rapid formation of gas bubbles within Sk. Muscles and supporting tissues.
2. Focal ischemia in brain and heart
3. Lung edema, Hemorrhage, atelectasis, emphysema, which all lead to Respiratory distress. (chokes)
4. caisson disease: gas emboli in the bones leads to multiple foci of ischemic necrosis, usually the heads of the femurs, tibias, and humeri
Amniotic fluid embolism
- Mortality Rate = 20%-40%
- Very rare complication of labor
- due to infusion of amniotic fluid into maternal circulation via tears in placental membranes and rupture of uterine veins.
- sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures, DIC and coma
- Findings: Squamous cells, languo hair, fat, mucin …..etc within the pulmonary microcirculation
Enophthalmos
Oral and Maxillofacial SurgeryEnophthalmos
Enophthalmos is a condition characterized by the inward
sinking of the eye into the orbit (the bony socket that holds the eye). It is
often a troublesome consequence of fractures involving the zygomatic complex
(the cheekbone area).
Causes of Enophthalmos
Enophthalmos can occur due to several factors following an injury:
Loss of Orbital Volume:
There may be a decrease in the volume of the contents within the
orbit, which can happen if soft tissues herniate into the maxillary
sinus or through the medial wall of the orbit.
Fractures of the Orbital Walls:
Fractures in the walls of the orbit can increase the volume of the
bony orbit. This can occur with lateral and inferior displacement of the
zygoma or disruption of the inferior and lateral orbital walls. A
quantitative CT scan can help visualize these changes.
Loss of Ligament Support:
The ligaments that support the eye may be damaged, contributing to
the sinking of the eye.
Post-Traumatic Changes:
After an injury, fibrosis (the formation of excess fibrous
connective tissue), scar contraction, and fat atrophy (loss of fat in
the orbit) can occur, leading to enophthalmos.
Combination of Factors:
Often, enophthalmos results from a combination of the above factors.
Diagnosis
Acute Cases: In the early stages after an injury,
diagnosing enophthalmos can be challenging. This is because swelling (edema)
of the surrounding soft tissues can create a false appearance of
enophthalmos, making it seem like the eye is more sunken than it actually
is.
Bleeding Disorders
PhysiologyBleeding Disorders
A deficiency of a clotting factor can lead to uncontrolled bleeding.
The deficiency may arise because
not enough of the factor is produced or
a mutant version of the factor fails to perform properly.
Examples:
von Willebrand disease (the most common)
hemophilia A for factor 8 deficiency
hemophilia B for factor 9 deficiency.
hemophilia C for factor 11 deficiency
In some cases of von Willebrand disease, either a deficient level or a mutant version of the factor eliminates its protective effect on factor 8. The resulting low level of factor 8 mimics hemophilia A.
Window of Infectivity
Conservative DentistryWindow of Infectivity
The concept of the "window of infectivity" was introduced by Caufield in 1993
to describe critical periods in early childhood when the oral cavity is
particularly susceptible to colonization by Streptococcus mutans, a key
bacterium associated with dental caries. Understanding these windows is
essential for implementing preventive measures against caries in children.
Window of Infectivity: This term refers to specific
time periods during which the acquisition of Streptococcus mutans occurs,
leading to an increased risk of dental caries. These windows are
characterized by the eruption of teeth, which creates opportunities for
bacterial colonization.
First Window of Infectivity
A. Timing
Age Range: The first window of infectivity is observed
between 19 to 23 months of age, coinciding with the
eruption of primary teeth.
B. Mechanism
Eruption of Primary Teeth: As primary teeth erupt, they
provide a "virgin habitat" for S. mutans to colonize the oral
cavity. This is significant because:
Reduced Competition: The newly erupted teeth have
not yet been colonized by other indigenous bacteria, allowing S.
mutans to establish itself without competition.
Increased Risk of Caries: The presence of S.
mutans in the oral cavity during this period can lead to an
increased risk of developing dental caries, especially if dietary habits
include frequent sugar consumption.
Second Window of Infectivity
A. Timing
Age Range: The second window of infectivity occurs
between 6 to 12 years of age, coinciding with the eruption
of permanent teeth.
B. Mechanism
Eruption of Permanent Dentition: As permanent teeth
emerge, they again provide opportunities for S. mutans to colonize
the oral cavity. This window is characterized by:
Increased Susceptibility: The transition from
primary to permanent dentition can lead to changes in oral flora and an
increased risk of caries if preventive measures are not taken.
Behavioral Factors: During this age range, children
may have increased exposure to sugary foods and beverages, further
enhancing the risk of S. mutans colonization and subsequent
caries development.
4. Clinical Implications
A. Preventive Strategies
Oral Hygiene Education: Parents and caregivers should
be educated about the importance of maintaining good oral hygiene practices
from an early age, especially during the windows of infectivity.
Dietary Counseling: Limiting sugary snacks and
beverages during these critical periods can help reduce the risk of S.
mutans colonization and caries development.
Regular Dental Visits: Early and regular dental
check-ups can help monitor the oral health of children and provide timely
interventions if necessary.
B. Targeted Interventions
Fluoride Treatments: Application of fluoride varnishes
or gels during these windows can help strengthen enamel and reduce the risk
of caries.
Sealants: Dental sealants can be applied to newly
erupted permanent molars to provide a protective barrier against caries.
Periodontal ligament development
Dental Anatomy
Periodontal ligament development
Cells from the dental follicle give rise to the periodontal ligaments (PDL).
Formation of the periodontal ligaments begins with ligament fibroblasts from the dental follicle. These fibroblasts secrete collagen, which interacts with fibers on the surfaces of adjacent bone and cementum. This interaction leads to an attachment that develops as the tooth erupts into the mouth. The occlusion, which is the arrangement of teeth and how teeth in opposite arches come in contact with one another, continually affects the formation of periodontal ligaments. This perpetual creation of periodontal ligaments leads to the formation of groups of fibers in different orientations, such as horizontal and oblique fibers.