NEET MDS Synopsis
Phenytoin-Induced Gingival Overgrowth
PedodonticsPhenytoin-Induced Gingival Overgrowth
Phenytoin (Dilantin):
An anticonvulsant medication primarily used in the treatment of
epilepsy.
First introduced in 1938 by Merrit and Putnam.
Gingival Hyperplasia
Gingival hyperplasia refers to the overgrowth of gum tissue, which
can lead to aesthetic concerns and functional issues, such as difficulty
in maintaining oral hygiene.
Historical Context:
The association between phenytoin therapy and gingival hyperplasia
was first reported by Kimball in 1939.
In his study, 57% of 119 patients taking phenytoin for seizure
control experienced some degree of gingival overgrowth.
Mechanism of Gingival Overgrowth
Fibroblast Activity:
Early research indicated an increase in the number of fibroblasts in
the gingival tissues of patients receiving phenytoin.
This led to the initial terminology of "Dilantin hyperplasia."
Current Understanding:
Subsequent studies, including those by Hassell and colleagues, have
shown that true hyperplasia does not exist in this condition.
Findings indicate:
There is no excessive collagen accumulation per unit of tissue.
Fibroblasts do not appear abnormal in number or size.
As a result, the term phenytoin-induced gingival overgrowth is
now preferred, as it more accurately reflects the condition.
Clinical Implications
Management:
Patients on phenytoin should be monitored for signs of gingival
overgrowth, especially if they have poor oral hygiene or other risk
factors.
Dental professionals should educate patients about maintaining good
oral hygiene practices to minimize the risk of gingival overgrowth.
In cases of significant overgrowth, treatment options may include:
Improved oral hygiene measures.
Professional dental cleanings.
Surgical intervention (gingivectomy) if necessary.
Patient Education:
It is important to inform patients about the potential side effects
of phenytoin, including gingival overgrowth, and the importance of
regular dental check-ups.
Alzheimer’s disease
General Pathology
Alzheimer’s disease
a. The most common cause of dementia in older people.
b. Characterized by degeneration of neurons in the cerebral cortex.
c. Histologic findings include amyloid plaques and neurofibrillary tangles.
d. Clinically, the disease takes years to develop and results in the loss of cognition, memory, and the ability to ommunicate. Motor problems, contractures, and paralysis are some of the symptoms at the terminal stage.
Nalidixic acid
Pharmacology
Nalidixic acid:
Nalidixic acid is the basis for quinolone antibiotics. It acts bacteriostatically (that is, it inhibits growth and reproduction) or bactericidally (it kills them) on both Gram positive and Gram negative bacteria, depending on the concentration. It is especially used in treating urinary tract infections, caused for example by Escherichia coli, Proteus, Enterobacter and Klebsiella.
Naber’s Probe and Furcation Involvement
Periodontology Naber’s Probe and Furcation Involvement
Furcation involvement is a critical aspect of periodontal disease that
affects the prognosis of teeth with multiple roots. Naber’s probe is a
specialized instrument designed to assess furcation areas, allowing clinicians
to determine the extent of periodontal attachment loss and the condition of the
furcation. This lecture will cover the use of Naber’s probe, the classification
of furcation involvement, and the clinical significance of these
classifications.
Naber’s Probe
Description: Naber’s probe is a curved, blunt-ended
instrument specifically designed for probing furcation areas. Its unique
shape allows for horizontal probing, which is essential for accurately
assessing the anatomy of multi-rooted teeth.
Usage: The probe is inserted horizontally into the
furcation area to evaluate the extent of periodontal involvement. The
clinician can feel the anatomical fluting between the roots, which aids in
determining the classification of furcation involvement.
Classification of Furcation Involvement
Furcation involvement is classified into four main classes using Naber’s
probe:
Class I:
Description: The furcation can be probed to a depth
of 3 mm.
Clinical Findings: The probe can feel the
anatomical fluting between the roots, but it cannot engage the roof of
the furcation.
Significance: Indicates early furcation involvement
with minimal attachment loss.
Class II:
Description: The furcation can be probed to a depth
greater than 3 mm, but not through and through.
Clinical Findings: This class represents a range
between Class I and Class III, where there is partial loss of attachment
but not complete penetration through the furcation.
Significance: Indicates moderate furcation
involvement that may require intervention.
Class III:
Description: The furcation can be completely probed
through and through.
Clinical Findings: The probe passes from one
furcation to the other, indicating significant loss of periodontal
support.
Significance: Represents advanced furcation
involvement, often associated with a poor prognosis for the affected
tooth.
Class III+:
Description: The probe can go halfway across the
tooth.
Clinical Findings: Similar to Class III, but with
partial obstruction or remaining tissue.
Significance: Indicates severe furcation
involvement with a significant loss of attachment.
Class IV:
Description: Clinically, the examiner can see
through the furcation.
Clinical Findings: There is complete loss of tissue
covering the furcation, making it visible upon examination.
Significance: Indicates the most severe form of
furcation involvement, often leading to tooth mobility and extraction.
Measurement Technique
Measurement Reference: Measurements are taken from an
imaginary tangent connecting the prominences of the root surfaces of both
roots. This provides a consistent reference point for assessing the depth of
furcation involvement.
Clinical Significance
Prognosis: The classification of furcation involvement
is crucial for determining the prognosis of multi-rooted teeth. Higher
classes of furcation involvement generally indicate a poorer prognosis and
may necessitate more aggressive treatment strategies.
Treatment Planning: Understanding the extent of
furcation involvement helps clinicians develop appropriate treatment plans,
which may include scaling and root planing, surgical intervention, or
extraction.
Monitoring: Regular assessment of furcation involvement
using Naber’s probe can help monitor disease progression and the
effectiveness of periodontal therapy.
Hepatitis D and E virus
General Pathology
Hepatitis D virus—can only infect cells previously infected with hepatitis B.
Delta hepatitis (HDV) is associated with a 35-nm RNA virus composed of a delta antigen-bearing core surrounded by HBV's Ag coat;
HDV requires HBV for replication.
Delta hepatitis can cause quiescent HBV states to suddenly worsened . Its transmission is the same as that of HBV.
Hepatitis E virus—a high mortality rate in infected pregnant women.
Hepatitis E (HEV) is caused by a single-stranded RNA virus. The disease is typically self-limited and does not evolve into chronic hepatitis; it may, however, be cholestatic.
Pregnant women may develop fulminant disease.
Transmission is by the fecal oral route.
HEV occurs mainly in India, Nepal, Pakistan, and Southeast Asia.
ADRENOCORTICAL TUMORS
General Pathology
ADRENOCORTICAL TUMORS
Functional adenomas are commonly associated with hyperaldosteronism and with Cushing syndrome, whereas a virilizing neoplasm is more likely to be a carcinoma. Determination of of the functional status of a tumor is based on clinical evaluation and measurement of the hormone or its metabolites. In other words, functional and nonfunctional adrenocortical neoplasms cannot be distinguished on the basis of morphologic features.
Patholgical features
Adrenocortical adenomas
- They are generally small, 1 to 2 cm in diameter.
- On cut surface, adenomas are usually yellow to yellow-brown due to presence of lipid within the neoplastic cells
- Microscopically, adenomas are composed of cells similar to those populating the normal adrenal cortex. The nuclei tend to be small, although some degree of pleomorphism may be encountered even in benign lesions ("endocrine atypia"). The cytoplasm ranges from eosinophilic to vacuolated, depending on their lipid content.
Adrenocortical carcinomas
These are rare and may occur at any age, including in childhood.
- Carcinomas are generally large, invasive lesions.
- The cut surface is typically variegated and poorly demarcated with areas of necrosis, hemorrhage, and cystic change.
- Microscopically, they are composed of well-differentiated cells resembling those of cortical adenomas or bizarre, pleomorphic cells, which may be difficult to distinguish from those of an undifferentiated carcinoma metastatic to the adrenal.
Induction of Local Anesthesia
Oral and Maxillofacial SurgeryInduction of Local Anesthesia
The induction of local anesthesia involves the administration of a local
anesthetic agent into the soft tissues surrounding a nerve, allowing for the
temporary loss of sensation in a specific area. Understanding the mechanisms of
diffusion, the organization of peripheral nerves, and the barriers to anesthetic
penetration is crucial for effective anesthesia management in clinical practice.
Mechanism of Action
Diffusion:
After the local anesthetic is injected, it begins to diffuse from
the site of deposition into the surrounding tissues. This process is
driven by the concentration gradient, where the anesthetic moves from an
area of higher concentration (the injection site) to areas of lower
concentration (toward the nerve).
Unhindered Migration: The local anesthetic
molecules migrate through the extracellular fluid, seeking to reach the
nerve fibers. This movement is termed diffusion, which is the passive
movement of molecules through a fluid medium.
Anatomic Barriers:
The penetration of local anesthetics can be hindered by anatomical
barriers, particularly the perineurium, which is the
most significant barrier to the diffusion of local anesthetics. The
perineurium surrounds each fascicle of nerve fibers and restricts the
free movement of molecules.
Perilemma: The innermost layer of the perineurium,
known as the perilemma, also contributes to the barrier effect, making
it challenging for local anesthetics to penetrate effectively.
Organization of a Peripheral Nerve
Understanding the structure of peripheral nerves is essential for
comprehending how local anesthetics work. Here’s a breakdown of the components:
Organization of a Peripheral Nerve
Structure
Description
Nerve fiber
Single nerve cell
Endoneurium
Covers each nerve fiber
Fasciculi
Bundles of 500 to 1000 nerve fibres
Perineurium
Covers fascicule
Perilemma
Innermost layer of perinuerium
Epineurium
Alveolar connective tissue supporting fasciculi andCarrying nutrient
vessels
Epineural sheath
Outer layer of epinuerium
Composition of Nerve Fibers and Bundles
In a large peripheral nerve, which contains numerous axons, the local
anesthetic must diffuse inward toward the nerve core from the extraneural site
of injection. Here’s how this process works:
Diffusion Toward the Nerve Core:
The local anesthetic solution must travel through the endoneurium
and perineurium to reach the nerve fibers. As it penetrates, the
anesthetic is subject to dilution due to tissue uptake and mixing with
interstitial fluid.
This dilution can lead to a concentration gradient where the outer
mantle fibers (those closest to the injection site) are blocked
effectively, while the inner core fibers (those deeper within the nerve)
may not be blocked immediately.
Concentration Gradient:
The outer fibers are exposed to a higher concentration of the local
anesthetic, leading to a more rapid onset of anesthesia in these areas.
In contrast, the inner core fibers receive a lower concentration and are
blocked later.
The delay in blocking the core fibers is influenced by factors such
as the mass of tissue that the anesthetic must penetrate and the
diffusivity of the local anesthetic agent.
Clinical Implications
Understanding the induction of local anesthesia and the barriers to diffusion
is crucial for clinicians to optimize anesthesia techniques. Here are some key
points:
Injection Technique: Proper technique and site
selection for local anesthetic injection can enhance the effectiveness of
the anesthetic by maximizing diffusion toward the nerve.
Choice of Anesthetic: The selection of local anesthetic
agents with favorable diffusion properties can improve the onset and
duration of anesthesia.
Monitoring: Clinicians should monitor the effectiveness
of anesthesia, especially in procedures involving larger nerves or areas
with significant anatomical barriers.
Pulmonary Hypertension
General Pathology
Pulmonary Hypertension
Sustained elevation of mean pulmonary arterial pressure.
Pathogenesis
Elevated pressure, through endothelial cell dysfunction, produces structural changes in the pulmonary vasculature. These changes ultimately decrease pulmonary blood flow and stress the heart to the point of failure. Based on etiology, pulmonary hypertension is divided into two categories.
Primary (idiopathic): The cause is unknown.
Secondary: The hypertension is secondary to a variety of conditions which increase pulmonary blood flow or increase resistance to blood flow. Example: Interstitial fibrosis.
Pathology
The changes involve large and small pulmonary blood vessels and range from mild to severe. The major changes include atherosclerosis, striking medial hypertrophy and intimal fibrosis of small arteries and arterioles, and plexogenic arteriopathy. Refer to Figure 15-7 in your textbook.
Pathophysiology
Dyspnea and fatigue eventually give way to irreversible respiratory insufficiency, cyanosis and cor pulmonale.