NEET MDS Synopsis
COENZYMES
Biochemistry
COENZYMES
Enzymes may be simple proteins, or complex enzymes.
A complex enzyme contains a non-protein part, called as prosthetic group (co-enzymes).
Coenzymes are heat stable low molecular weight organic compound. The combined form of protein and the co-enzyme are called as holo-enzyme. The heat labile or unstable part of the holo-enzyme is called as apo-enzyme. The apo-enzyme gives necessary three dimensional structures required for the enzymatic chemical reaction.
Co-enzymes are very essential for the biological activities of the enzyme.
Co-enzymes combine loosely with apo-enzyme and are released easily by dialysis. Most of the co-enzymes are derivatives of vitamin B complex
Histology of the Periodontal Ligament (PDL)
Dental Anatomy
Histology of the Periodontal Ligament (PDL)
Embryogenesis of the periodontal ligament
The PDL forms from the dental follicle shortly after root development begins
The periodontal ligament is characterized by connective tissue. The thinnest portion is at the middle third of the root. Its width decreases with age. It is a tissue with a high turnover rate.
FUNCTIONS OF PERIODONTIUM
Tooth support
Shock absorber
Sensory (vibrations appreciated in the middle ear/reflex jaw opening)
The following cells can be identified in the periodontal ligament:
a) Osteoblasts and osteoclasts b) Fibroblasts, c) Epithelial cells
Rests of Malassez
d) Macrophages
e) Undifferentiated cells
f) Cementoblasts and cementoclasts (only in pathologic conditions)
The following types of fibers are found in the PDL
-Collagen fibers: groups of fibers
-Oxytalan fibers: variant of elastic fibers, perpendicular to teeth, adjacent to capillaries
-Eluanin: variant of elastic fibers
Ground substance
PERIODONTAL LIGAMENT FIBERS
Principal fibers
These fibers connect the cementum to the alveolar crest. These are:
a. Alveolar crest group: below CE junction, downward, outward
b. Horizontal group: apical to ACG, right angle
c. Oblique group: numerous, coronally to bone, oblique direction
d. Apical group: around the apex, base of socket
e. Interradicular group: multirooted teeth
Gingival ligament fibers
This group is not strictly related to periodontium. These fibers are:
a. Dentogingival: numerous, cervical cementum to f/a gingiva
b. Alveologingival: bone to f/a gingiva
c. Circular: around neck of teeth, free gingiva
d. Dentoperiosteal: cementum to alv. process or vestibule (muscle)
e. Transseptal: cementum between adjacent teeth, over the alveolar crest
Blood supply of the PDL
The PDL gets its blood supply from perforating arteries (from the cribriform plate of the bundle bone). The small capillaries derive from the superior & inferior alveolar arteries. The blood supply is rich because the PDL has a very high turnover as a tissue. The posterior supply is more prominent than the anterior. The mandibular is more prominent than the maxillary.
Nerve supply
The nerve supply originates from the inferior or the superior alveolar nerves. The fibers enter from the apical region and lateral socket walls. The apical region contains more nerve endings (except Upper Incisors)
Dentogingival junction
This area contains the gingival sulcus. The normal depth of the sulcus is 0.5 to 3.0 mm (mean: 1.8 mm). Depth > 3.0 mm is considered pathologic. The sulcus contains the crevicular fluid
The dentogingival junction is surfaced by:
1) Gingival epithelium: stratified squamous keratinized epithelium 2) Sulcular epithelium: stratified squamous non-keratinized epithelium The lack of keratinization is probably due to inflammation and due to high turnover of this epithelium.
3) Junctional epithelium: flattened epithelial cells with widened intercellular spaces. In the epithelium one identifies neutrophils and monocytes.
Connective tissue
The connective tissue of the dentogingival junction contains inflammatory cells, especially polymorphonuclear neutrophils. These cells migrate to the sulcular and junctional epithelium.
The connective tissue that supports the sulcular epithelium is also structurally and functionally different than the connective tissue that supports the junctional epithelium.
Histology of the Col (=depression)
The col is found in the interdental gingiva. It is surfaced by epithelium that is identical to junctional epithelium. It is an important area because of the accumulation of bacteria, food debris and plaque that can cause periodontal disease.
Blood supply: periosteal vessels
Nerve supply: periodontal nerve fibers, infraorbital, palatine, lingual, mental, buccal
SALIVARY GLANDS Embryonic development
Dental Anatomy
Embryonic development
The parotid derives from ectoderm
The sublingual-submandibular glands thought to derive from endoderm
Differentiation of the ectomesenchyme
Development of fibrous capsule
Formation of septa that divide the gland into lobes and lobules
The parotid develops around 4-6 weeks of embryonic lofe
The submandibular gland develops around the 6th week
The sublingual and the minor glands develop around the 8-12 week
Nevus
General Pathology
Nevus
1. Commonly known as moles.
2. A benign, pigmented tumor of melanocytes, found deep within connective tissue.
3. Types of skin nevi:
a. Junctional nevus—found in the epidermis.
It is the only type of nevus that may be considered to be premalignant.
b. Compound nevus—found in both the epidermis and underlying dermis.
c. Intraepidermal nevus—found in the dermis.
ECG FINDINGS
Physiology
1. Hypothermia → Elevation of the j-point — Osborne wave.
2. Hyperkalemia → peaking (tenting) of T-wave, ↓-P-wave amplitude, widening of the QRS interval, cardiac arrest with sine wave (in severe Hyper kalemia)
3. Hypokalemia → Prominent ‘U’-wave, prolongation of ‘QT’ interval.
4. Hypocalcemia → Prolong QT interval
5. Hyper calcemia — Short QT interval.
6. Digitalis toxicity — short QT interval with “scooping” of the ST-T wave comples (i.e. Depression of ST-T segment)
7. Sub arachnoid Hemorrhage→ “CVAT-wave” pattern → marked QT prolongation with deep wide T-wave inversions
8. M.I → T-wave inversion
Rofecoxib
Pharmacology
Rofecoxib
Inhibit prostacyclin(PGI2) in vascular endothelium , letting TXA2 act freely and promote platelet aggregation.
used in the treatment of osteoarthritis, acute pain conditions, and dysmenorrhea
Higher incidence of cardiovascular thrombotic events.
Not used due to increase risk of heart attack, stroke
COMPOSITE RESINS - Finishing and Polishing
Dental Materials
Finishing and Polishing
Remove oxygen-inhibited layer .Use stones or carbide burs for gross reduction.Use highly fluted carbide burs or special diamonds for fine reduction.Use aluminum oxide strips or disks for finishing. Use fine aluminum oxide finishing pastes. Microfills develop smoothest finish because of small size of filler particles
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.