NEET MDS Synopsis
Hyoid Bone
Anatomy
U-shaped bone
Body
Greater horn
Lesser horn
Suspended by ligaments from the styloid process
Infective osteomyelitis
Oral Pathology
Infective osteomyelitis
Tuberculous osteomyelitis
Syphilitic osteomyelitis
Actinomycotic osteomyelitis
Tuberculous osteomyelitis
Non healing sinus tract formation
Age group affected is around 15 – 40 years.
Commonly seen in phalanges and dorsal and lumbar vertebrae.
Usually occurs secondary to tuberculosis of lungs.
Cases have been reported where mandibular lesions were not associated with pulmonary disease.
Another common entrance is through a carious tooth via open pulp.
Usually affects long bones and rare in jaws.
Results when blood borne bacilli lodge in cancellous bone. Usually in ramus , body of mandible. may mimic parotid swelling or submassetric abscess.
Syphilitic osteomyelitis
Difficult to distinguish syphilitic osteomyelitis of the jaws from pyogenic osteomyelitis on clinical & radiographic examination.
Main features are progressive course & failure to improve with usual treatment for pyogenic osteomyelitis.
Massive sequestration may occur resulting in pathologic fracture.
If unchecked, eventually causes perforation of the cortex.
Actinomycotic Osteomyelitis
The organisms thrive in the oral cavity, especially tissues adjacent to mandible.
May enter the bone through a fresh wound, carious tooth or a periodontal pocket at the gingival margin of erupting tooth.
Soft or firm tissue masses on skin, which have purplish, dark red, oily areas with occasional zones of fluctuation.
Spontaneous drainage of serous fluid containing granular material.
Regional lymph nodes occasionally enlarged.
Mimics parotitis / parotid tumors
Langerhans cell granulomatosis
General Pathology
Langerhans cell granulomatosis (histocytosis X)
a. A group of diseases that are caused by the proliferation of Langerhans’ cells (previously known as histocytes).
b. Most commonly causes bone lesions; however, other tissues can be affected.
c. Histologic findings include Langerhans’ cells containing Birbeck granules and eosinophils.
d. Three types:
(1) Letterer-Siwe disease—an acute, disseminated form that is fatal in infants.
(2) Hand-Schüller-Christian disease—a chronic, disseminated form that has a better prognosis than LettererSiwe disease. It usually presents
before the age of 5 and is characterized by a triad of symptoms:
(a) Bone lesions—found in skull, mandible (loose teeth).
(b) Exophthalmos.
(c) Diabetes insipidus.
(3) Eosinophilic granuloma of bone—a localized, least severe form of the three. Lesions may heal without treatment.
(a) Most commonly occurs in young adults.
(b) Lesions in the mandible may cause loose teeth.
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.
Management and Treatment of Le Fort Fractures
Oral and Maxillofacial SurgeryManagement and Treatment of Le Fort Fractures
Le Fort fractures require careful assessment and management to restore facial
anatomy, function, and aesthetics. The treatment approach may vary depending on
the type and severity of the fracture.
Le Fort I Fracture
Initial Assessment:
Airway Management: Ensure the airway is patent,
especially if there is significant swelling or potential for airway
compromise.
Neurological Assessment: Evaluate for any signs of
neurological injury.
Treatment:
Non-Surgical Management:
Observation: In cases of non-displaced fractures,
close monitoring may be sufficient.
Pain Management: Analgesics to manage pain.
Surgical Management:
Open Reduction and Internal Fixation (ORIF):
Indicated for displaced fractures to restore occlusion and facial
symmetry.
Maxillomandibular Fixation (MMF): May be used
temporarily to stabilize the fracture during healing.
Postoperative Care:
Follow-Up: Regular follow-up to monitor healing and
occlusion.
Oral Hygiene: Emphasize the importance of
maintaining oral hygiene to prevent infection.
Le Fort II Fracture
Initial Assessment:
Airway Management: Critical due to potential airway
compromise.
Neurological Assessment: Evaluate for any signs of
neurological injury.
Treatment:
Non-Surgical Management:
Observation: For non-displaced fractures, close
monitoring may be sufficient.
Pain Management: Analgesics to manage pain.
Surgical Management:
Open Reduction and Internal Fixation (ORIF):
Required for displaced fractures to restore occlusion and facial
symmetry.
Maxillomandibular Fixation (MMF): May be used to
stabilize the fracture during healing.
Postoperative Care:
Follow-Up: Regular follow-up to monitor healing and
occlusion.
Oral Hygiene: Emphasize the importance of
maintaining oral hygiene to prevent infection.
Le Fort III Fracture
Initial Assessment:
Airway Management: Critical due to potential airway
compromise and significant facial swelling.
Neurological Assessment: Evaluate for any signs of
neurological injury.
Treatment:
Non-Surgical Management:
Observation: In cases of non-displaced fractures,
close monitoring may be sufficient.
Pain Management: Analgesics to manage pain.
Surgical Management:
Open Reduction and Internal Fixation (ORIF):
Essential for restoring facial anatomy and occlusion. This may involve
complex reconstruction of the midface.
Maxillomandibular Fixation (MMF): Often used to
stabilize the fracture during healing.
Craniofacial Reconstruction: In cases of severe
displacement or associated injuries, additional reconstructive
procedures may be necessary.
Postoperative Care:
Follow-Up: Regular follow-up to monitor healing,
occlusion, and any complications.
Oral Hygiene: Emphasize the importance of
maintaining oral hygiene to prevent infection.
Physical Therapy: May be necessary to restore
function and mobility.
General Considerations for All Le Fort Fractures
Antibiotic Prophylaxis: Consideration for prophylactic
antibiotics to prevent infection, especially in open fractures.
Nutritional Support: Ensure adequate nutrition,
especially if oral intake is compromised.
Psychological Support: Address any psychological impact
of facial injuries, especially in pediatric patients.
The Hemoglobin Buffer Systems
Biochemistry
The Hemoglobin Buffer Systems
These buffer systems are involved in buffering CO2 inside erythrocytes. The buffering capacity of hemoglobin depends on its oxygenation and deoxygenation. Inside the erythrocytes, CO2 combines with H2O to form carbonic acid (H2CO3) under the action of carbonic anhydrase.
At the blood pH 7.4, H2CO3 dissociates into H+ and HCO3 − and needs immediate buffering.
Hepatic failure
General Pathology
Hepatic failure
Etiology. Chronic hepatic disease (e.g., chronic active hepatitis or alcoholic cirrhosis) is the most common cause of hepatic failure although acute liver disease may also be responsible.
- Widespread liver necrosis may be seen with carbon tetrachloride and acetaminophen toxicity. Widespread steatosis is seen in Reye's syndrome, a cause of acute liver failure most often seen in children with a recent history of aspirin ingestion for an unrelated viral illness.
- Massive necrosis may also be seen in acute viral hepatitis, after certain anesthetic agents, and in shock from any cause.
Clinical features. Hepatic failure causes jaundice, musty odor of breath and urine, encephalopathy, renal failure (either by simultaneous toxicity to the liver and kidneys or the hepatorerial syndrome), palmar erythema, spider angiomas, gynecomastia , testicular atrophy
Classification of Dental amalgam
Dental Materials
Classification of Dental amalgam
1. By powder particle shape .
Irregular (comminuted, filing, or lathecut)
Spherical (spherodized)
Blends (e.g., irregular-irregular, irregularspherical, or spherical-spherical)
2. By total amount of copper
Low-copper alloys (e.g., conventional, traditional); <5% copper
High-copper alloys (e,g. corrosion resistant); 12% to 28% copper
3.By presence of zinc
Examples
Low-copper, irregular-particle alloy-silver (70%)-tin (26%)-copper (4%)
High-copper, blended-particles alloy-irregular particles, silver (70%) –tin (26%) -Copper (4%); spherical particles, silver (72%)-copper (28%)
High-copper, spherical-particles alloy-silver (60%) - tin (27%)-copper (13%)