NEET MDS Synopsis
Edgewise Technique
OrthodonticsEdgewise Technique
The Edgewise Technique is based on the use of brackets that have a slot
(or edge) into which an archwire is placed. This design allows for precise
control of tooth movement in multiple dimensions (buccal-lingual,
mesial-distal, and vertical).
Mechanics:
The technique utilizes a combination of archwires, brackets, and
ligatures to apply forces to the teeth. The archwire is engaged in the
bracket slots, and adjustments to the wire can be made to achieve
desired tooth movements.
Components of the Edgewise Technique
Brackets:
Edgewise Brackets: These brackets have a vertical
slot that allows the archwire to be positioned at different angles,
providing control over the movement of the teeth. They can be made of
metal or ceramic materials.
Slot Size: Common slot sizes include 0.022 inches
and 0.018 inches, with the choice depending on the specific treatment
goals.
Archwires:
Archwires are made from various materials (stainless steel,
nickel-titanium, etc.) and come in different shapes and sizes. They
provide the primary force for tooth movement and can be adjusted
throughout treatment to achieve desired results.
Ligatures:
Ligatures are used to hold the archwire in place within the bracket
slots. They can be elastic or metal, and their selection can affect the
friction and force applied to the teeth.
Auxiliary Components:
Additional components such as springs, elastics, and separators may
be used to enhance the mechanics of the Edgewise system and facilitate
specific tooth movements.
Advantages of the Edgewise Technique
Precision:
The Edgewise Technique allows for precise control of tooth movement
in all three dimensions, making it suitable for complex cases.
Versatility:
It can be used to treat a wide range of malocclusions, including
crowding, spacing, overbites, underbites, and crossbites.
Effective Force Application:
The design of the brackets and the use of archwires enable the
application of light, continuous forces, which are more effective and
comfortable for patients.
Predictable Outcomes:
The technique is based on established principles of biomechanics,
leading to predictable and consistent treatment outcomes.
Applications of the Edgewise Technique
Comprehensive Orthodontic Treatment: The Edgewise
Technique is commonly used for full orthodontic treatment in both children
and adults.
Complex Malocclusions: It is particularly effective for
treating complex cases that require detailed tooth movement and alignment.
Retention: After active treatment, the Edgewise system
can be used in conjunction with retainers to maintain the corrected
positions of the teeth.
Clotrimazole
Pharmacology
Clotrimazole: Clotrimazole is a potent, specific inhibitor of p450 enzymes.
It is used in some antifungal medications, and in the treatment of yeast infections.
A dermatofibroma
General Pathology
A dermatofibroma is a benign tumor of the dermis, MC located on the lower extremity, where it has a nodular, pigmented appearance.
- composed of benign histiocytes.
Gingiva
Dental Anatomy
Gingiva
The connection between the gingiva and the tooth is called the dentogingival junction. This junction has three epithelial types: gingival, sulcular, and junctional epithelium. These three types form from a mass of epithelial cells known as the epithelial cuff between the tooth and the mouth.
Much about gingival formation is not fully understood, but it is known that hemidesmosomes form between the gingival epithelium and the tooth and are responsible for the primary epithelial attachment. Hemidesmosomes provide anchorage between cells through small filament-like structures provided by the remnants of ameloblasts. Once this occurs, junctional epithelium forms from reduced enamel epithelium, one of the products of the enamel organ, and divides rapidly. This results in the perpetually increasing size of the junctional epithelial layer and the isolation of the remenants of ameloblasts from any source of nutrition. As the ameloblasts degenerate, a gingival sulcus is created.
Bile
PhysiologyBile contains:
bile acids. These amphiphilic steroids emulsify ingested fat. The hydrophobic portion of the steroid dissolves in the fat while the negatively-charged side chain interacts with water molecules. The mutual repulsion of these negatively-charged droplets keeps them from coalescing. Thus large globules of fat (liquid at body temperature) are emulsified into tiny droplets (about 1 µm in diameter) that can be more easily digested and absorbed.
bile pigments. These are the products of the breakdown of hemoglobin removed by the liver from old red blood cells. The brownish color of the bile pigments imparts the characteristic brown color of the feces.
Glycogen storage diseases (glycogenoses)
General Pathology
Glycogen storage diseases (glycogenoses)
1. Genetic transmission: autosomal recessive.
2. This group of diseases is characterized by a deficiency of a particular enzyme involved in either glycogen production or degradative pathways.
Diseases include:
on Gierke disease (type I)
(a) Deficient enzyme: glucose-6-phosphatase.
(b) Major organ affected by the buildup of glycogen: liver.
Pompe disease (type II)
(1) Deficient enzyme: α-glucosidase(acid maltase).
(2) Major organ affected by the buildup of glycogen: heart.
Cori disease (type III)
(1) Deficient enzyme: debranching enzyme (amylo-1,6-glucosidase).
(2) Organs affected by the buildup of glycogen: varies between the heart, liver, or skeletal muscle.
Brancher glycogenosis (type IV)
(1) Deficient enzyme: branching enzyme.
(2) Organs affected by the buildup of glycogen: liver, heart, skeletal muscle, and brain.
McArdle syndrome (type V)
(1) Deficient enzyme: muscle phosphorylase.
(2) Major organ affected by the buildup of glycogen: skeletal muscle.
Autoimmune Diseases
General Pathology
Autoimmune Diseases
These are a group of disease where antibodies (or CMI) are produced against self antigens, causing disease process.
Normally one's immune competent cells do not react against one's own tissues.
This is due to self tolerance acquired during embryogenesis. Any antigen encountered at
that stage is recognized as self and the clone of cells capable of forming the corresponding antibody is suppressed.
Mechanism of autoimmunity
(1) Alteration of antigen
-Physicochemical denaturation by UV light, drugs etc. e.g. SLE.
- Native protein may turn antigenic when a foreign hapten combines with it, e.g. Haemolytic anemia with Alpha methyl dopa.
(2) Cross reaction: Antibody produced against foreign antigen may cross react with native protein because of partial similarity e.g. Rheumatic fever.
(3) Exposure of sequestered antigens: Antigens not normally exposed to immune competent cells are not accepted as self as tolerance has not been developed to them. e.g. thyroglobulin, lens protein, sperms.
(4) Breakdown of tolerance :
- Emergence of forbidden clones (due to neoplasia of immune system as in lymphomas and lymphocytic leukaemia)
- Loss of suppressor T cells as in old age and CMI defects
Autoimmunity may be
- Organ specific.
- Non organ specific (multisystemic)
I. Organ specific.
(I) Hemolytic anaemia:
- Warm or cold antibodies (active at 37° C or at colder temperature)
- They may lyse the RBC by complement activation or coat them and make them vulnerable to phagocytosis
(ii) Hashimoto's thyroiditis:
- Antibodies to thyroglobulin and microsomal antigens.
- Cell mediated immunity.
- Leads to chronic. destructive thyroiditis.
(3) Pernicious anemia
Antibodies to gastric parietal cells and to intrinsic factor.
2. Non organ specific.
Lesions are seen in more than one system but principally affect blood vessels and connective tissue (collagen diseases).
(I) Systemic lupus erythematosus (SLE). Antibodies to varied antigens are seen. Hence it is possible that there is abnormal reactivity of the immune system in self recognition.
Antibodies have been demonstrated against:
- Nuclear material (antinuclear I antibodies) including DNA. nucleoprotein etc. Anti nuclear antibodies are demonstrated by LE cell test.
- Cytoplasmic organelles- mitochondria, rib osomes, Iysosomes.
- Blood constituents like RBC, WBC. platelets, coagulation factors.
Mechanism. Immune complexes of body proteins and auto antibodies deposit in various organs and cause damage as in type III hypersensitivity
Organs involved
- Skin- basal dissolution and collagen degeneration with fibrinoid vasculitis.
- Heart- pancarditis.
- Kidneys- glomerulonephritis of focal, diffuse or membranous type
- Joints- arthritis.
- Spleen- perisplenitis and vascular thickening (onion skin).
- Lymph nodes- focal necrosis and follicular hyperplasia.
- Vasculitis in other organs like liver, central or peripheral nervous system etc,
2. Polyarteritis nodosa. Remittant .disseminated necrotising vasculitis of small and medium sized arteries
Mechanism :- Not definitely known. Proposed immune reaction to exogenous or auto antigens
Lesion : Focal panarteritis- a segment of vessel is involved. There is fibrinoid necrosis with initially acute and later chronic inflammatory cells. This may result in haemorrhage and aneurysm.
Organs involved. No organ or tissue is exempt but commonly involved organs are :
- Kidneys.
- Heart.
- Spleen.
- GIT.
3. Rheumatoid arthritis. A disease primarily of females in young adult life.
Antibodies
- Rheumatoid factor (An IgM antibody to self IgG)
- Antinuclear antibodies in 20% patients.
Lesions
- Arthritis which may progress on to a crippling deformity.
- Arteritis in various organs- heart, GIT, muscles.
- Pleuritis and fibrosing alveolitis.
- Amyloidosis is an important complication.
4. Sjogren's Syndrome. This is constituted by
- Kerato conjunctivitis sicca
- Xerostomia
- Rheumatoid arthritis.
Antibodies
- Rheumatoid factor
- Antinuclear factors (70%).
- Other antibodies like antithyroid, complement fixing Ab etc
- Functional defects in lymphocytes. There is a higher incidence of lymphoma
5. Scleroderma (Progressive systemic sclerosis)
Inflammation and progressive sclerosis of connective tissue of skin and viscera.
Antibodies
- Antinuclear antibodies.
- Rheumatoid factor. .
- Defect is cell mediated.
lesions
- Skin- depigmentation, sclerotic atrophy followed by cakinosis-claw fingers and mask face.
- Joints-synovitis with fibrosis
- Muscles- myositis.
- GIT- diffuse fibrous replacement of muscularis resulting in hypomotility and malabsorption
- Kidneys changes as in SLE and necrotising vasculitis.
- Lungs – fibrosing alveolitis.
- Vasculitis in any organ or tissue.
6.Wegener’s granulomatosis. A complex of:
- Necrotising lesions in upper respiratory tract.
- Disseminated necrotising vasculitis.
- Focal or diffuse glomerulitis.
Mechanism. Not known. It is classed with autoimmune diseases because of the vasculitis resembling other immune based disorders.
SPECIAL SOMATIC AFFERENT (SSA) PATHWAYS
Physiology
SPECIAL SOMATIC AFFERENT (SSA) PATHWAYS
Hearing
The organ of Corti with its sound-sensitive hair cells and basilar membrane are important parts of the sound transducing system for hearing. Mechanical vibrations of the basilar membrane generate membrane potentials in the hair cells which produce impulse patterns in the cochlear portion of the vestibulocochlear nerve (VIII)
Special somatic nerve fibers of cranial nerve VIII relay impulses from the sound receptors (hair cells) in the cochlear nuclei of the brainstem
These are bipolar neurons with cell bodies located in the spiral ganglia of the cochlea.
Vestibular System
The vestibulocochlear nerve serves two quite different functions.
The cochlear portion, conducts sound information to the brain,
The vestibular portion conducts proprioceptive information.
It is the central neural pathways
Special somatic afferent fibers from the hair cells of the macula utriculi and macula sacculi conduct information into the vestibular nuclei on the ipsilateral side of the pons and medulla.
These are bipolar neurons with cell bodies located in the vestibular ganglion.
Some of the fibers project directly into the ipsilateral cerebellum to terminate in the uvula, flocculus, and nodulus, but most enter the vestibular nuclei and synapse there.
Vision
The visual system receptors are the rods and cones of the retina.
Special somatic afferent fibers of the optic nerve (II) conduct visual signals into the brain
Fibers from the lateral (temporal) retina of either eye terminate in the lateral geniculate body on the same side of the brain as that eye.
SSA II fibers from the medial (nasal) retina of each eye cross over in the optic chiasm to terminate in the contralateral lateral geniculate body.
Area 17 is the primary visual area, which receives initial visual signals.
Neurons from this area project into the adjacent occipital cortex (areas 18 and 19) which is known as the secondary visual area. It is here that the visual signal is fully evaluated.
The visual reflex pathway involving the pupillary light reflex - in which the pupils constrict when a light is shined into the eyes and dilate when the light is removed.
Some SSA II fibers leave the optic tract before reaching the lateral geniculates, terminating in the superior colliculi instead.
From here, short neurons project to the EdingerWestphal nucleus (an accessory nucleus of III) in the midbrain, which serves as the origin of the preganglionic parasympathetic fibers of the oculomotor nerve (GVE III).
The GVE III fibers in turn project to the ciliary ganglia, from which arise the postganglionic fibers to the sphincter muscles of the iris, which constrict the pupils.