NEET MDS Synopsis
Chronic hepatitis
General Pathology
Chronic hepatitis
Chronic hepatitis occurs in 5%-10% of HBV infections and in well over 50% of HCV; it does not occur in HAV. Most chronic disease is due to chronic persistent hepatitis. The chronic form is more likely to occur in the very old or very young, in males, in immunocompromised hosts, in Down's syndrome, and in dialysis patients.
a. Chronic persistent hepatitis is a benign, self-limited disease with a prolonged recovery. Patients are asymptomatic except for elevated transaminases.
b. Chronic active hepatitis features chronic inflammation with hepatocyte destruction, resulting in cirrhosis and liver failure.
(1) Etiology. HBV, HCV, HDV, drug toxicity, Wilson's disease, alcohol, a,-antitrypsin deficiency, and autoimmune hepatitis are common etiologies.
(2) Clinical features may include fatigue, fever, malaise, anorexia, and elevated liver function tests.
(3) Diagnosis is made by liver biopsy.
8. Carrier state for HBV and HCV may be either asymptomatic or with liver disease; in the latter case, the patient has elevate transaminases.
a. Incidence is most common in immunodeficient, drug addicted, Down's syndrome, and dialysis patients.
b. Pathology of asymptomatic carriers shows "ground-glass"" hepatocytes with finely granular eosinophilic cytoplasm.
Dental Practice Considerations
Conservative DentistryImplications for Dental Practice
A. Health and Safety Considerations
Mercury Exposure: Understanding the amounts of mercury
released during these procedures is crucial for assessing potential health
risks to dental professionals and patients.
Regulatory Guidelines: Dental practices should adhere
to guidelines and regulations regarding mercury handling and exposure limits
to ensure a safe working environment.
B. Best Practices
Use of Wet Polishing: Whenever possible, wet polishing
should be preferred over dry polishing to minimize mercury release.
Proper Ventilation: Ensuring adequate ventilation in
the dental operatory can help reduce the concentration of mercury vapor in
the air.
Personal Protective Equipment (PPE): Dental
professionals should use appropriate PPE, such as masks and gloves, to
minimize exposure during amalgam handling.
C. Patient Safety
Informed Consent: Patients should be informed about the
materials used in their restorations, including the presence of mercury in
amalgam, and the associated risks.
Monitoring: Regular monitoring of dental practices for
mercury exposure levels can help maintain a safe environment for both staff
and patients.
1. Noise Levels of Turbine Handpieces
Turbine Handpieces
Ball Bearings: Turbine handpieces equipped with ball
bearings can operate efficiently at air pressures of around 30 pounds.
Noise Levels: At high frequencies, these handpieces may
produce noise levels ranging from 70 to 94 dB.
Hearing Damage Risk: Exposure to noise levels exceeding
75 dB, particularly in the frequency range of 1000 to 8000 cycles per second
(cps), can pose a risk of hearing damage for dental professionals.
Implications for Practice
Hearing Protection: Dental professionals should
consider using hearing protection, especially during prolonged use of
high-speed handpieces, to mitigate the risk of noise-induced hearing loss.
Workplace Safety: Implementing noise-reduction
strategies in the dental operatory can enhance the comfort and safety of
both staff and patients.
2. Post-Carve Burnishing
Technique
Post-Carve Burnishing: This technique involves lightly
rubbing the carved surface of an amalgam restoration with a burnisher of
suitable size and shape.
Purpose: The goal is to improve the smoothness of the
restoration and produce a satin finish rather than a shiny appearance.
Benefits
Enhanced Aesthetics: A satin finish can improve the
aesthetic integration of the restoration with the surrounding tooth
structure.
Surface Integrity: Burnishing can help to compact the
surface of the amalgam, potentially enhancing its resistance to wear and
marginal integrity.
3. Preparing Mandibular First Premolars for MOD Amalgam Restorations
Considerations for Tooth Preparation
Conservation of Tooth Structure: When preparing a
mesio-occluso-distal (MOD) amalgam restoration for a mandibular first
premolar, it is important to conserve the support of the small lingual cusp.
Occlusal Step Preparation: The occlusal step should
be prepared more facially than lingually, which helps to maintain the
integrity of the lingual cusp.
Bur Positioning: The bur should be tilted slightly
lingually to establish the correct direction for the pulpal wall.
Cusp Reduction
Lingual Cusp Consideration: If the lingual margin of
the occlusal step extends more than two-thirds the distance from the central
fissure to the cuspal eminence, the lingual cusp may need to be reduced to
ensure proper occlusal function and stability of the restoration.
4. Universal Matrix System
Overview
Tofflemire Matrix System: Designed by B.R. Tofflemire,
the Universal matrix system is a commonly used tool in restorative
dentistry.
Indications: This system is ideally indicated when
three surfaces (mesial, occlusal, distal) of a posterior tooth have been
prepared for restoration.
Benefits
Retention and Contour: The matrix system helps in
achieving proper contour and retention of the restorative material, ensuring
a well-adapted restoration.
Ease of Use: The design allows for easy placement and
adjustment, facilitating efficient restorative procedures.
5. Angle Former Excavator
Functionality
Angle Former: A special type of excavator used
primarily for sharpening line angles and creating retentive features in
dentin, particularly in preparations for gold restorations.
Beveling Enamel Margins: The angle former can also be
used to place a bevel on enamel margins, enhancing the retention of
restorative materials.
Clinical Applications
Preparation for Gold Restorations: The angle former is
particularly useful in preparations where precise line angles and retention
are critical for the success of gold restorations.
Versatility: Its ability to create retentive features
makes it a valuable tool in various restorative procedures.
Movements of the Temporomandibular Joint
AnatomyMovements of the Temporomandibular Joint
The two movements that occur at this joint are anterior gliding and a hinge-like rotation.
When the mandible is depressed during opening of the mouth, the head of the mandible and articular disc move anteriorly on the articular surface until the head lies inferior to the articular tubercle.
As this anterior gliding occurs, the head of the mandible rotates on the inferior surface of the articular disc.
This permits simple chewing or grinding movements over a small range.
Movements that are seen in this joint are: depression, elevation, protrusion, retraction and grinding
Infectious Mononucleosis
General Pathology
Infectious Mononucleosis
It is an Epstein Barr virus infection in children and young adults.
Features
-Constitutional symptoms.
-Sore throat.
-Lymphnode enlargement.
-Skin rashes
-Jaundice.
-Rarely pneumonia, meningitis and encephalitis.
Blood Picture
- Total count of I0,000. 20,000 /cu.mm.
- Lymphocytosis (50-90%) with atypical forms. They are larger with more cytoplasm which may be vacuolated or basophilic. Nucleus may be indented. with nucleoli (Downy type I to III).
- Platelets may be reduced.
- Paul Bunell test (for heterophil antibody against sheep RBC) is positive
THYROIDITIS
General Pathology
THYROIDITIS
The more common and clinically significant thyroidites are:
1. Hashimoto thyroiditis
2. Subacute granulomatous thyroiditis
3. Subacute lymphocytic thyroiditis
Hashimoto thyroiditis
Hashimoto thyroiditis (Chronic Lymphocytic Thyroiditis) is the most common cause of hypothyroidism. It results from gradual autoimmune destruction of the thyroid gland. There is striking female predominance (10: 1 to 20:1), and is most prevalent around a mean age of 50 years.
Pathogenesis
• The dominant feature is progressive destruction of thyroid follicular epithelial cells with gradual replacement by mononuclear cell infiltration and fibrosis.
• Sensitization of CD4+ T-helper cells to thyroid antigens seems to be the initiating event.
• The reaction of CD4+ T cells with thyroid antigens produces interferon γ which promote inflammation and activate macrophages. Injury to the thyroid results from the toxic products of these inflammatory cells.
• CD8+ cytotoxic T cells also contribute to epithelial cells killing as are natural killer cells.
• There is a significant genetic component to disease pathogenesis. This is supported by
1. The increased frequency of the disease in first-degree relatives,
2. Unaffected family members often have circulating thyroid autoantibodies.
Gross features
• The thyroid shows moderate, diffuse, and symmetric enlargement.
• The cut surface is pale, gray-tan, firm, nodular and somewhat friable.
• Eventually there is thyroid atrophy
Microscopic features
• There is widespread, diffuse infiltration of the parenchyma by small lymphocytes, plasma cells. The lymphocytes are also form follicles some with well-developed germinal centers
• The thyroid follicles are atrophic and lined by epithelial cells having abundant eosinophilic, granular cytoplasm (Hurthle cells). This is a metaplastic response to the ongoing injury; ultrastructurally the Hurthle cells are stuffed by numerous mitochondria.
• Interstitial connective tissue is increased and may be abundant.
Hashimoto thyroiditis presents as painless symmetrical goiter, usually with some degree of hypothyroidism. In some cases there is an initial transient thyrotoxicosis caused by disruption of thyroid follicles, with secondary release of thyroid hormones ("hashitoxicosis"). As hypothyroidism supervenes T4 and T3 levels progressively fall & TSH levels are increased. Patients often have other autoimmune diseases and are at increased risk for the development of B-cell non-Hodgkin lymphomas.
Subacute Granulomatous (de Quervain) Thyroiditis
Subacute Granulomatous (de Quervain) Thyroiditis is much less common than Hashimoto disease.
- It is most common around the age of 40 years and occurs more frequently in women than in men.
- An upper respiratory infection just before the onset of thyroiditis. Thus, a viral infection is probably the cause.
- There is firm uni- or bilateral enlargement of the gland.
Microscopically, there is disruption of thyroid follicles, with extravasation of colloid. The extravasated colloid provokes a granulomatous reaction, with giant cells.
Thyroid function tests are those of thyrotoxicosis but with progression and gland destruction, a transient hypothyroid phase occurs. The condition is self-limited, with most patients returning to a euthyroid state within at most 2 months.
Subacute Lymphocytic Thyroiditis
Subacute Lymphocytic Thyroiditis may follow pregnancy (postpartum thyroiditis).
- It is most likely autoimmune in etiology, because circulating antithyroid antibodies are found in the majority of patients.
- It mostly affects middle-aged women and present as painless, mild, symmetric neck mass. Initially, there is thyrotoxicosis, followed by return to a euthyroid state within a few months. In a minority there is progression to hypothyroidism.
Microscopically, there is a lymphocytic infiltration and hyperplastic germinal center within the thyroid parenchyma; unlike Hashimoto thyroiditis, follicular atrophy or Hürthle cell metaplasia are not commonly seen.
Riedel thyroiditis
Riedel thyroiditis is a rare disorder of unknown etiology, characterized by extensive fibrosis involving the thyroid and the surrounding neck structures. The presence of a hard and fixed thyroid mass may be confused clinically with thyroid cancer. It may be associated with idiopathic fibrosis in other sites, such as the retroperitoneum. The presence of circulating antithyroid antibodies in most patients suggests an autoimmune etiology.
HEALING
General Pathology
HEALING
Definition. Replacement of damages tissue by healthy tissue. It is an attempt to restore the tissue to structural and functional normalcy.
Healing may be of 2 types
A. Regeneration.
B. Repair by granulation tissue.
A. Regeneration
Where the replacement is by proliferation of parenchymatous cells of type destroyed. This depends upon:
(1) Regenerative capacity of cells. Cells may be :
(a) Labile cells which are constantly proliferating to replace cells continuously shed off or destroyed
Epithelial cells of skin and lining surfaces.
Lymphoid and haemopoietic tissue.
(b) Stable cell. Cells mostly in resting-phase, but capable of dividing when necessary e.g.
Liver and other parenchymatous and glandular cells.
Connective tissue cells.
Muscle cells have a limited capacity to divide.
(c) Permanent cell. These cells, once differentiated are not capable. of dividing e.g.-nerve
(2) The extent of tissue loss. If there is extensive destruction including disruption of the framework, complete.regeneration is not possible. even with labile an stable cell
B. Repair by granulation tissue
Granulation tissue is formed by proliferation of surrounding connective tissue elements. which migrate into the site to be repaired.
Granulation tissue formation seen in :
Wound healing.
Organisation of exudates.
Thrombi.
Infarcts.
Haematomas.
The process of repair can be best studied in clean incised wounds, where there is .no or minimal tjssue loss or the_edges or the edges of the wound are approximated closely as in a surgical wound. This is called Primary union (healing by first intention).
1. The blood in the incised area clots and the fibrin binds the edges together.
2. During the first 24 hours, an acute inflammation sets in to .bring protein and phagocyte rich exudates to the site.
3. The superficial part of the clot get dry and dehydrated{scab). The surface epithelium proliferates just beyond the cut edges and the cells migrate-deep to dry scab. Epithelialisation is usually complete by 24- 48 hours.
4 Granulation tissue, with actively growing fibroblasts and capillary buds invades the clot (stage of vascularisation). These fibroblasts 'posses contractile myofibrils & hence are termed as myofibroblasts'.
5. Simultaneously, demolition of the debris and clot components takes place.
6 The granulation tissue initially lays down a mucopolysacharide rich ground substance
7.Reticulin and later collagen fibrils are formed by the fibroblasts (with 5 days)
8 with progressive maturation of collagen, some of the capiliary buds develop into arterioles and venules and majority of them are obliterated (stage of devascularisation).
9. With time (weeks to months) the tensile strength of the scar increases and it shrinks.
Secondary union (excised wound-healing by secondary intention).
1. Coagulum forms and fills the gap.
2. Inflammatory reaction is seen as in primary union but is more intense, as a lot more debris has to be removed. .
3. Epithelial proliferation starts covering the surface from the periphery by proliferation beyond the edges and migration under scab.
4.Debridement starts and simultaneously granulation tissue grows into the coagulum from the sides and base of the wound. This is much more exuberant than in primary union. The surface now looks red and granular.
5. Wound contraction. This is early contraction (starts after 3 days and is complete in 2 weeks) and must be differentiated from contraction after scar formation Wounds can contract by up to 80% of original size of that the gap to be filled is much reduced, resulting in faster healing with a smaller scar.
Wound contraction is probably caused by:
Dehydration
Collagen contraction.
Granulation tissue contraction .(myofibroblasts).
The exact mechanism is not known.
6. Laying down of collagen.
7 Maturation to form a scar which later shrinks and devascularises.
Factors affecting wound healing
Wound healing is delayed by :
A. Local factors
1. Poor blood supply.
2. Adhesion to bony surfaces (e.g. over the tibia).
3. Persistent injurious agents (infective or particulate) results in chronicity of inflammation and ineffective healing. .
4. Constant movement (especially in fracture healing).
5. ionizing radiation (in contrast, ultraviolet rays hasten healing).
6. Neoplasia.
B. General factors
I. Nutritional deficiency, especially of.
(i) Protein
(ii) Ascorbic acid (Vitamin C).
(iii) Zinc
2. Corticoids adversely affect wound contraction and granulation tissue formation
(anabolic steroids have a favorable effect).
3. Low temperature.
4. Defects (qualitative or quantitative) in polymorphs and macrophages
.Complication of wound healing
1. Wound dehiscence
2. Infection
3. Epidermal inclusion (implantation) cysts.
4. Keloid formation
5. Cicatrisation resulting in contract Ires and obstruction(in hollow viscera).
6. Calcification and ossification.
7. Weak scar which could be a site for incisional hernia
8. Painful scar if it involves a nerve twig.
9. Rarely neoplasia (especially in burn scars).
RESPIRATORY DISORDERS - Acute Obstructive Disorders
Physiology Acute Obstructive Disorders
1. Heimlich maneuver
2. Bypass, tracheostomy w/catheter to suck up secretion
Cementum
Dental Anatomy
Cementum
Composition
a. Inorganic (50%)—calcium hydroxyapatite crystals.
b. Organic (50%)—water, proteins, and type I collagen.
c. Note: Compared to the other dental tissues, the composition of cementum is most similar to bone; however, unlike bone, cementum is avascular (i.e., no Haversian systems or other vessels are present).
Main function of cementum is to attach PDL fibers to the root surface.
Cementum is generally thickest at the root apex and in interradicular areas of multirooted
Types of cementum
a. Acellular (primary) cementum
(1) A thin layer of cementum that surrounds the root, adjacent to the dentin.
(2) May be covered by a layer of cellular cementum, which most often occurs in the middle and apical root.
(3) It does not contain any cells.
b. Cellular (secondary) cementum
(1) A thicker, less-mineralized layer of cementum that is most prevalent along the apical root and in interradicular (furcal) areas of multirooted teeth.
(2) Contains cementocytes.
(3) Lacunae and canaliculi:
(a) Cementocytes (cementoblasts that become trapped in the extracellular matrix during cementogenesis) are observed in their entrapped spaces, known as lacunae.
(b) The processes of cementocytes extend through narrow channels called canaliculi.
(4) Microscopically, the best way to differentiate between acellular and cellular cementum is the presence of lacunae in cellular cementum.