NEET MDS Synopsis
Introduction
Dental Materials
Introduction
The science of dental materials involves a study of the composition and properties of materials and the way in which they interact with the environment in which they are placed
Selection of Dental materials
The process of materials selection should ideally follow a logical sequence involving
(1) analysis of the problem,
(2) consideration of requirements,
(3) consideration of available materials and their properties, leading to
(4) choice of material.
Evaluation of the success or failure of a material may be used to influence future decisions on materials selection.
Fourth Generation:
Pharmacology
Fourth Generation:
These are extended spectrum antibiotics. They are resistant to beta lactamases.
Cefipime
Multiple Endocrine Neoplasia Syndromes
General Pathology
Multiple Endocrine Neoplasia Syndromes (MEN)
The MEN syndromes are a group of inherited diseases resulting in proliferative lesions (hyperplasias, adenomas, and carcinomas) of multiple endocrine organs. Even in one organ, the tumors are often multifocal. These tumors are usually more aggressive and recur in a higher proportion of cases than similar but sporadic endocrine tumors.
Multiple Endocrine Neoplasia Type 1 (MEN1) is inherited in an autosomal dominant pattern. The gene (MEN1) is a tumor suppressor gene; thus, inactivation of both alleles of the gene is believed to be the basis of tumorigenesis. Organs commonly involved include the parathyroid, pancreas, and pituitary (the 3 Ps). Parathyroid hyperplasia is the most consistent feature of MEN-1 but endocrine tumors of the pancreas are the leading cause of death because such tumors are usually aggressive and present with metastatic disease.
Zollinger-Ellison syndrome, associated with gastrinomas, and hypoglycemia, related to insulinomas, are common endocrine manifestations. Prolactin-secreting macroadenoma is the most frequent pituitary tumor in MEN-1 patients.
Multiple Endocrine Neoplasia Type 2 (MEN2)
MEN type 2 is actually two distinct groups of disorders that are unified by the occurrence of activating mutations of the RET protooncogene. Both are inherited in an autosomal dominant pattern.
MEN 2A
Organs commonly involved include:
Medullary carcinoma of the thyroid develops in virtually all cases, and the tumors usually occur in the first 2 decades of life. The tumors are commonly multifocal, and foci of C-cell hyperplasia can be found in the adjacent thyroid. Adrenal pheochromocytomas develop in 50% of patients; fortunately, no more than 10% are malignant. Parathyroid gland hyperplasia with primary hyperparathyroidism occurs in a third of patients.
Multiple Endocrine Neoplasia, Type 2B
Organs commonly involved include the thyroid and adrenal medulla. The spectrum of thyroid and adrenal medullary disease is similar to that in MEN-2A. However, unlike MEN-2A, patients with MEN-2B:
1. Do not develop primary hyperparathyroidism
2. Develop extraendocrine manifestations: ganglioneuromas of mucosal sites (gastrointestinal tract, lips, tongue) and marfanoid habitus
Ossification
Anatomy
Ossification
Intramembranous-found in the flat bones of the face
Mesenchymal cells cluster and form strands
Strands are cemented in a uniform network. Which is known as osteoid
Calcium salts are deposited; osteoid is converted to bone
Trabeculae are formed and make cancellous bone with open spaces known as marrow cavities
Periosteum forms on the inner and outer surfaces of the ossification centers
Surface bone becomes compact bone
Endochondral-primary type of ossification In the human
Nerves of the Tongue
Anatomy
Anterior 2/3 of tongue
Posterior 1/3 of tongue
Motor Innervation
All muscles by hypoglossal nerve (CN XII) except palatoglossus muscle (by the pharyngeal plexus)
General Sensory Innervation
Lingual nerve (branch of mandibular nerve CN V3)
Glossopharyngeal nerve (CN IX)
Special Sensory Innervation
Chorda tympani nerve (branch of facial nerve)
Glossopharyngeal nerve (CN IX)
AMYLOIDOSIS
General Pathology
AMYLOIDOSIS
Definition. Extra cellular deposition of an eosinophilic hyaline homogenous material in Various organs, occurring in a variety of clinical states.
Staining reactions
Iodine :- Brown, turning blue on addition of H2SO4 (gross and microscopic Stain).
P.A.S. – Positive (Magenta pink).
Congo Red -Orange red which on polarisation gives green birefringence.
Von Geison's –Khaki colour.
Thioflavin T -Yellow fluorescence.
Amyloid is called typical if it given the above staining reactions Other wise it is termed atypical or para-amyloid.
Classification
1. Systemic amyloidosis associated with underlying disease (secondary),
(A) Chronic infections like
- Tuberculosis.
- Bronchiectasis.
- Lung abscess.
- Osteomyelitis.
- Syphilis.
(B) Chronic inflammations of varied etiology:
- Rheumatoid arthritis.
- Ulcerative colitis.
- Regional enteritis.
- Lupus erythematosus.
(C) Neoplastic proliferations:
- Of immune system – Multiple myeloma, Hodgkin’s disease.
- Cancers like Renal cell carcinoma etc.
II Systemic primary amyloidosis with no underlying cause.
III Heredofamilial types.
- Amyloidosis with mediterranean fever.
- Amyloid polyneuropathy.
- Amyloid nephrophathy
- Familial cardiac amyloidosis
- Familial cutaneous amyloid.
- Lattice corneal dystrophy
IV. Localised amyloidosis:
- Senile - in heart, brain, seminal vesicles.
- Amyloidoma of tongue, bronchial tree, skin.
- In islets of Langerhans in Diabetes mellitus.
- In medullary thyroid carcinoma.
Deposition sites
In relation to reticulin and collagen fibres and to basement, membranes especially
subendothelial.
Organs involved commonly are :
Secondary amyloidosis
- Liver.
- Spleen.
- Kidney
- Lymph nodes.
- Adrenals.
Primary amyloidosis
- Heart
- Tongue and gingiva.
- Gastro intestinal tract.
- Lung.
- Wall of small vessels.
Nature and pathogenesis of amyloid
It is primarily made up of protein arranged in two patterns
- There are filaments twisted together to from the fibrils. These chemically resemble light chains of immunoglobulins
- Rods composed of stacked rings. These are made up of alpha globulin components of plasma proteins (P-components)
- In addition to these, extracts of crude amyloid contain mucopolysacharides complement and gamma globulins.
- Origin of amyloid :- current concept is that it is a direct product of cells of the immune sustem with some abnormality in their immune response
The abnormality may be due to :
- A genetic enzyme defect.
- Prolonged antigenic challenge.
- Neoplastic transformation
- Supression of normal. Response as in induced tolerance.
Radiation Biology
Radiology
Radiation Biology
-X- and g -rays are called sparsely ionizing because along the tracks of the electrons set in motion, primary ionizing events are well separated in space.
Alpha-particles and neutrons are densely ionizing because the tracks consist of dense columns of ionization.
X-rays, gamma rays, electrons, and protons are all low LET forms of radiation in that their density of ionization is sparse. In general, they penetrate tissues deeply and result in less intracellular radiation injury.
High LET forms of radiation, such as heavy nuclear particles (e.g. fast neutrons), penetrate tissues less deeply and cause more radiation injury to biologic material.
Cells are most sensitive to Radiation when:
- they are actively proliferating.
- they are undifferentiated.
Exceptions to this Law:
- lymphocyte
- Oocyte
X-rays and gamma rays show latent injury that is residual tissue damage even after the initial radiation reaction is subsided.
Proteins tend to be more radiosensitive than carbohydrates and lipids.
Most radiosensitive tissue-small lymphocyte
Most radioresistant tissue- brain
Embryonic, immature or poorly differentiated tissues are more easily injured by radiation, but they also show greater recovery properties.
All cells show increased susceptibility to radiation at the time of mitotic division and if the cells are irradiated during the resting phase, mitosis is delayed or inhibited.
- In general, cells are most radiosensitive in late M and G2 phases and most resistant in late S.
- for cells with a longer cell cycle time and a significantly long G1 phase, there is a second peak of resistance late in G1
- the pattern of resistance and sensitivity correlates with the level of sulfhydryl compounds in the cell. Sulfhydryls are natural radioprotectors and tend to be at their highest levels in S and at their lowest near mitosis.
- To produce its effect. Oxygen must be present during the radiation exposure or at least during the lifetime of the free radicals (10-5 sec).
- Mandible is more ssceptible to radiation injury than maxilla due to the denser structure and poorer blood supply.
- Salivary glands though an organ with a low turnover rate, was unusually sensitive to radiation
- Liposarcoma tumors are the most radiosensitive soft tissue tumors
- Exophytic tumors are usually more easily controlled with radiation while infiltrative and ulcerative lesions are more radioresistant.
The infiltrative and ulcerative lesions are more likely to be larger than clinically apparent and contain a larger proportion of hypoxic cells.
Events in Muscle Contraction
PhysiologyEvents in Muscle Contraction - the sequence of events in crossbridge formation:
1) In response to Ca2+ release into the sarcoplasm, the troponin-tropomyosin complex removes its block from actin, and the myosin heads immediately bind to active sites.
2) The myosin heads then swivel, the Working Stroke, pulling the Z-lines closer together and shortening the sarcomeres. As this occurs the products of ATP hydrolysis, ADP and Pi, are released.
3) ATP is taken up by the myosin heads as the crossbridges detach. If ATP is unavailable at this point the crossbridges cannot detach and release. Such a condition occurs in rigor mortis, the tensing seen in muscles after death, and in extreme forms of contracture in which muscle metabolism can no longer provide ATP.
4) ATP is hydrolyzed and the energy transferred to the myosin heads as they cock and reset for the next stimulus.
Excitation-Contraction Coupling: the Neuromuscular Junction
Each muscle cell is stimulated by a motor neuron axon. The point where the axon terminus contacts the sarcolemma is at a synapse called the neuromuscular junction. The terminus of the axon at the sarcolemma is called the motor end plate. The sarcolemma is polarized, in part due to the unequal distribution of ions due to the Sodium/Potassium Pump.
1) Impulse arrives at the motor end plate (axon terminus) causing Ca2+ to enter the axon.
2) Ca2+ binds to ACh vesicles causing them to release the ACh (acetylcholine) into the synapse by exocytosis.
3) ACH diffuses across the synapse to bind to receptors on the sarcolemma. Binding of ACH to the receptors opens chemically-gated ion channels causing Na+ to enter the cell producing depolarization.
4) When threshold depolarization occurs, a new impulse (action potential) is produced that will move along the sarcolemma. (This occurs because voltage-gated ion channels open as a result of the depolarization -
5) The sarcolemma repolarizes:
a) K+ leaves cell (potassium channels open as sodium channels close) returning positive ions to the outside of the sarcolemma. (More K+ actually leaves than necessary and the membrane is hyperpolarized briefly. This causes the relative refractory period) (b) Na+/K+ pump eventually restores resting ion distribution. The Na+/K+ pump is very slow compared to the movement of ions through the ion gates. But a muscle can be stimulated thousands of times before the ion distribution is substantially affected.
6) ACH broken down by ACH-E (a.k.a. ACHase, cholinesterase). This permits the receptors to respond to another stimulus.
Excitation-Contraction Coupling:
1) The impulse (action potential) travels along the sarcolemma. At each point the voltaged-gated Na+ channels open to cause depolarization, and then the K+ channels open to produce repolarization.
2) The impulse enters the cell through the T-tublules, located at each Z-disk, and reach the sarcoplasmic reticulum (SR), stimulating it.
3) The SR releases Ca2+ into the sarcoplasm, triggering the muscle contraction as previously discussed.
4) Ca2+ is pumped out of the sarcoplasm by the SR and another stimulus will be required to continue the muscle contraction.