NEET MDS Synopsis
Actinic keratosis
General Pathology
Actinic keratosis
1. Dry, scaly plaques with an erythematous base.
2. Similar to actinic cheilosis, which occurs along the vermilion border of the lower lip.
3. Caused by sun damage to the skin.
4. Dysplastic lesion, may be premalignant.
APPLICATIONS OF LASERS IN ENDODONTICS
Endodontics
I. VASCULAR VITALITY ASSESSMENT OF PULP
Traditional vitality assessment methods such as heat, cold, and electric pulp testers assess neural vitality and often cause false-positive
errors. As the histological assessment of pulpal status is not feasible clinically, a tool to assess the vascular flow of the pulp would be
very useful.
Laser Doppler flowmetry (LDF) is an accurate method to assess the blood flow in a microvascular
system
II. PULP CAPPING AND PULPOTOMY
Pulp capping and pulpotomy constitute a more conservative form of pulp therapy in comparison to pulpectomy. Although the outcome
of pulp capping procedure is variable ranging from 44 to 97%, the procedure is recommended when the exposure is 1.0 mm or less
and especially when the patient is young. Pulpotomy is recommended in immature permanent teeth, where pulpectomy is not advised.
The most commonly used agents for both the procedures are calcium hydroxide and MTA (mineral trioxide aggregate). The use of a
laser in these procedures leads to a potentially bloodless field as the laser has the ability to coagulate and seal small blood vessels. The
laser-tissue interactions make the treated wound surface sterile and also improve the prognosis of the procedure.
III. DISINFECTION OF ROOT CANALS
The ability of bacterial pathogens to persist after shaping and cleaning is one of the main reasons for endodontic failures. This is
attributed to the complex nature of the root canal system, the presence of a smear layer, and the fact that large areas (over 35%) of the
canal surface area remain unchanged following instrumentation with various Ni-Ti techniques.
IV. OBTURATION
Thermoplasticized gutta-percha obturation systems are one of the most efficient methods is achieving a fluid-impervious seal.
Softening of the gutta-percha has been attempted with various lasers. These include argon, CO
, Nd:YAG, and Er:YAG.
V.APICAL SURGERY
Apical surgery including apical resection is indicated when the previously performed root canal therapy fails and nonsurgical means
are inadequate to ensure the complete removal of the pathological process.
The potential for using lasers is on the basis of the following observations:
• Ability of lasers to coagulate and seal small blood vessels, thereby enabling a bloodless surgical field
• Sterilization of the surgical site
• Potential of lasers (Er:YAG) to cut hard dental tissues without causing elaborate thermal damage to the adjoining tissues .
Keratoses (Horny Growth)
General Pathology
Keratoses (Horny Growth)
1. Seborrheic keratosis is a common benign epidermal tumor composed of basaloid (basal cell-like) cells with increased pigmentation that produce a raised, pigmented, "stuck-on" appearance on the skin of middle-aged individuals.
- they can easily be scraped from the skin's surface.
- frequently enlarge of multiply following hormonal therapy.
- sudden appearance of large numbers of Seborrheic keratosis is a possible indication of a malignancy of the gastrointestinal tract (Leser-Trelat sign).
2. An actinic keratosis is a pre-malignant skin lesion induced by ultraviolet light damage.
- sun exposed areas.
- parakeratosis and atypia (dysplasia) of the keratinocytes.
- solar damage to underlying elastic and collagen tissue (solar elastosis).
- may progress to squamous carcinoma in situ (Bowen's disease) or invasive cancer.
3. A keratoacanthoma is characterized by the rapid growth of a crateriform lesion in 3 to 6
weeks usually on the face or upper extremity.
- it eventually regresses and involutes with scarring.
- commonly confused with a well-differentiated squamous cell carcinoma.
Microscopic structure
Anatomy
Cartilage model is covered with perichondrium that is converted to periosteum
Diaphysis-central shaft
Epiphysis-located at either end of the diaphysis
Growth in length of the bone is provided by the emetaphyseal plate located between the epiphyseal cartilage and the diaphysis
Blood capillaries and the mesenchymal cells infiltrate the spaces left by the destroyed chondrocytes
Osteoblasts are derived from the undifferentiated cells; form an osseous matrix in the cartilage
Bone appears at the site where there was cartilage
Microscopic structure
Compact bone is found on the exterior of all bones; canceIlous bone is found in the interior
Surface of compact bone is covered by periosteum that is attached by Sharpey's fibers
Blood vessels enter the periosteum via Volkmann's canals and then enter the haversian canals that are formed by the canaliculi and lacunae
Marrow
FiIls spaces of spongy bone
Contains blood vessels and blood ceIls in various stages of development
Types
Red bone marrow
Formation of red blood ceIls (RBCs) and some white blood cells (WBCs) in this location
Predominate type of marrow in newborn
Found in spongy bone of adults (sternum, ribs, vertebrae, and proximal epiphyses of long bones)
Yellow bone marrow
Fatty marrow
Generally replaces red bone marrow in the adult, except in areas mentioned above
Ossification is completed as the proximal epiphysis joins with the diaphysis between the twentieth and twenty-fifth year
DIABETES MELLITUS
General Pathology
DIABETES MELLITUS
a group of metabolic disorders sharing the common underlying characteristic of hyperglycemia.
Diabetes is an important disease because
1. It is common (affects 7% of the population).
2. It increases the risk of atherosclerotic coronary artery and cerebrovascular diseases.
3. It is a leading cause of
a. Chronic renal failure
b. Adult-onset blindness
c. Non traumatic lower extremity amputations (due to gangrene)
Classification
Diabetes is divided into two broad classes:
1. Type1 diabetes (10%): characterized by an absolute deficiency of insulin secretion caused by pancreatic βcell destruction, usually as a result of an autoimmune attack.
2. Type2 diabetes (80%): caused by a combination of peripheral resistance to insulin action and an inadequate secretion of insulin from the pancreatic β cells in response to elevated blood glucose levels.
The long-term complications in kidneys, eyes, nerves, and blood vessels are the same in both types.
Pathogenesis
Type 1 diabetes is an autoimmune disease and as in all such diseases, genetic susceptibility and environmental influences play important roles in the pathogenesis. The islet destruction is caused primarily by T lymphocytes reacting against immunologic epitopes on the insulin hormone located within β-cell; this results in a reduction of β-cell mass. The reactive T cells include CD4+ T cells of the TH1 subset, which cause tissue injury by activating macrophages, and CD8+ cytotoxic T lymphocytes; these directly kill β cells and also secrete cytokines that activate further macrophages. The islets show cellular necrosis and lymphocytic infiltration (insulitis). Autoantibodies against a variety of β-cell antigens, including insulin are also detected in the blood and may also contribute to islet damage.
Type 2 Diabetes Mellitus: the pathogenesis remains unsettled. Environmental influences, such as inactive life style and dietary habits that eventuates in obesity, clearly have a role. Nevertheless, genetic factors are even more important than in type 1 diabetes. Among first-degree relatives with type 2 diabetes the risk of developing the disease is 20% to 40%, as compared with 5% in the general population.
The two metabolic defects that characterize type 2 diabetes are 1. A decreased ability of peripheral tissues to respond to insulin (insulin resistance) and 2. β-cell dysfunction manifested as inadequate insulin secretion in the face of hyperglycemia. In most cases, insulin resistance is the primary event and is followed by increasing degrees of β-cell dysfunction.
Morphology of Diabetes and Its Late Complications
The important morphologic changes are related to the many late systemic complications of diabetes and thus are likely to be found in arteries (macrovascular disease), basement membranes of small vessels (microangiopathy), kidneys (diabetic nephropathy), retina (retinopathy), and nerves (neuropathy). These changes are seen in both type 1 and type 2 diabetes.
The changes are divided into pancreatic & extrapancreatic
A. Pancreatic changes are inconstant and are more commonly associated with type 1 than with type 2 diabetes.
One or more of the following alterations may be present.
1. Reduction in the number and size of islets
2. Leukocytic infiltration of the islets (insulitis) principally byT lymphocytes.
3. Amyloid replacement of islets; which is seen in advanced stages
B. Extrapancreatic changes
1. Diabetic macrovascular disease is reflected as accelerated atherosclerosis affecting the aorta and other large and medium-sized arteries including the coronaries. Myocardial infarction is the most common cause of death in diabetics. Gangrene of the lower limbs due to advanced vascular disease, is about 100 times more common in diabetics than in the general population.
2. Hyaline arteriolosclerosis
is the vascular lesion associated with hypertension. It is both more prevalent and more severe in diabetics than in nondiabetics, but it is not specific for diabetes and may be seen in elderly nondiabetics without hypertension.
3. Diabetic microangiopathy
is one of the most consistent morphologic features of diabetes, which reflected morphologically as diffuse thickening of basement membranes. The thickening is most evident in the capillaries of the retina, renal glomeruli, and peripheral nerves. The thickened capillary basement membranes are associated with leakiness to plasma proteins. The microangiopathy underlies the development of diabetic nephropathy, retinopathy, and some forms of neuropathy.
4. Diabetic Nephropathy: renal failure is second only to myocardial infarction as a cause of death from diabetes.
Three lesions encountered are:
1. Glomerular lesions
2. Renal vascular lesions, principally arteriolosclerosis; and
3. Pyelonephritis, including necrotizing papillitis.
Glomerular lesions: these include
a. diffuse glomerular capillary basement membrane thickening
b. diffuse glomerular sclerosis : diffuse increase in mesangial matrix; always associated with the above.
c. nodular glomerulosclerosis (Kimmelstiel-Wilson lesion) refers to a rounded deposits of a laminated matrix situated in the periphery of the glomerulus
Pyelonephritis: both acute and chronic pyelonephritis are more common & more severe
Ocular Complications of Diabetes: Visual impairment up to total blindness may occur in long-standing diabetes. The ocular involvement may take the form of
a. retinopathy
b. cataract formation
c. glaucoma
In both forms of long-standing diabetes, cardiovascular events such as myocardial infarction, renal vascular insufficiency, and cerebrovascular accidents are the most common causes of mortality. Diabetic nephropathy is a leading cause of end-stage renal disease. By 20 years after diagnosis, more than 75% of type 1 diabetics and about 20% of type 2 diabetics with overt renal disease will develop end-stage renal disease, requiring dialysis or renal transplantation.
Diabetics are plagued by an enhanced susceptibility to infections of the skin, as well as to tuberculosis,
pneumonia, and pyelonephritis. Such infections cause the deaths of about 5% of diabetics.
The Protein Buffer Systems
Biochemistry
The Protein Buffer Systems
The protein buffers are very important in the plasma and the intracellular fluids but their concentration is very low in cerebrospinal fluid, lymph and interstitial fluids.
The proteins exist as anions serving as conjugate bases (Pr − ) at the blood pH 7.4 and form conjugate acids (HPr) accepting H+ . They have the capacity to buffer some H2CO3 in the blood.
PHARMACOLOGY OF LOCAL ANESTHETICS
Pharmacology
PHARMACOLOGY OF LOCAL ANESTHETICS
Characteristics
1. Block axon conduction (nerve impulse) when applied locally in appropriate concentrations.
2. Local anesthetic action must be completely reversible; however, the duration of the anesthetic block should be of sufficient length to allow completion of the planned treatment.
3. Produce minimal local toxic effects such as nerve and muscle damage as well as minimal systemic toxic effects of organ systems such as the cardiovascular and central nervous system.
The Muscles of Facial Expression
AnatomyThe Muscles of Facial Expression
These lie in the subcutaneous tissue and are attached to the skin of the face.
They enable us to move our skin and change our facial expression. They produce their effects by pulling on the skin but do not move the facial skeleton.
These muscles surround the facial orifices and act as sphincters and dilators.
All facial muscles receive their innervation from the branches of the facial nerve (CN VII)-temporal, zygomatic, buccal, marginal mandibular, cervical.