NEET MDS Synopsis
HAEMORRHAGIC DISORDERS
General Pathology
HAEMORRHAGIC DISORDERS
Normal homeostasis depends on
-Capillary integrity and tissue support.
- Platelets; number and function
(a) For integrity of capillary endothelium and platelet plug by adhesion and aggregation
(b) Vasoactive substances for vasoconstriction
(c) Platelet factor for coagulation.
(d) clot retraction.
- Fibrinolytic system(mainly Plasmin) : which keeps the coagulation system in check.
Coagulation disorders
These may be factors :
Deficiency .of factors
Genetic.
Vitamin K deficiency.
Liver disease.
Secondary to disseminated intravascular coagulation.or defibrinatian
Overactive fibrinolytic system.
Inhibitors of the factors (immune, acquired).
Anticoagulant therapy as in myocardial infarction.
Haemophilia. Genetic disease transmitted as X linked recessive trait. Common in Europe. Defect in fcatorVII Haemophilia A .or in fact .or IX-Haemaphilia B (rarer).
Features:
May manifest in infancy or later.
Severity depends on degree of deficiency.
Persistant wound bleeding.
Easy Bruising with Hematoma formation
Nose bleed , arthrosis, abdominal pain with fever and leukocytosis
Prognosis is good with prevention of trauma and-transfusion of Fresh blood or fTesh plasma except for danger of developing immune inhibitors.
Von Willebrand's disease. Capillary fragility and decreased factor VIII (due to deficient stimulatory factor). It is transmitted in an autosomal dominant manner both. Sexes affected equally
Vitamin K Deficiency. Vitamin K is needed for synthesis of factor II,VII,IX and X.
Deficiency maybe due to:
Obstructive jaundice.
Steatorrhoea.
Gut sterilisation by antibiotics.
Liver disease results in :
Deficient synthesis of factor I II, V, Vll, IX and X Incseased fibrinolysis (as liver is the site of detoxification of activators ).
Defibrination syndrome. occurs when factors are depleted due to disseminated .intravascular coagulation (DIC). It is initiated by endothelial damage or tissue factor entering the circulation.
Causes
Obstetric accidents, especially amniotic fluid embolism. Septicaemia. .
Hypersensitivity reactions.
Disseminated malignancy.
Snake bite.
Vascular defects : (Non thrombocytopenic purpura).
Acquired :
Simple purpura a seen in women. It is probably endocrinal
Senile parpura in old people due to reduced tissue support to vessels
Allergic or toxic damage to endothelium due to Infections like Typhoid Septicemia
Col!agen diseases.
Scurvy
Uraemia damage to endothelium (platelet defects).
Drugs like aspirin. tranquillisers, Streptomvcin pencillin etc.
Henoc schonlien purpura Widespeard vasculitis due to hypersensitivity to bacteria or foodstuff
It manifests as :
Pulrpurric rashes.
Arthralgia.
Abdominal pain.
Nephritis and haematuria.
Hereditary :
(a) Haemhoragic telangieclasia. Spider like tortous vessels which bleed easily. There are disseminated lesions in skin, mucosa and viscera.
(b) Hereditary capillary fragilily similar to the vascular component of von Willbrand’s disease
.(c) Ehler Danlos Syndrome which is a connective tissue defect with skin, vascular and joint manifestations.
Platelet defects
These may be :
(I) Qualitative thromboasthenia and thrombocytopathy.
(2) Thrombocytopenia :Reduction in number.
(a) Primary or idiopathic thrombocytopenic purpura.
(b) Secondary to :
(i) Drugs especially sedormid
(ii) Leukaemias
(iii) Aplastic-anaemia.
Idiopathic thrombocytopenic purpura (ITP). Commoner in young females.
Manifests as :
Acute self limiting type.
Chronic recurring type.
Features:
(i) Spontaneous bleeding and easy bruisability
(ii)Skin (petechiae), mucus membrane (epistaxis) lesions and sometimes visceral lesions involving any organ.
Thrombocytopenia with abnormal forms of platelets.
Marrow shows increased megakaryocytes with immature forms, vacuolation, and lack of platelet budding.
Pathogenesis:
hypersensitivity to infective agent in acute type.
Plasma thrombocytopenic factor ( Antibody in nature) in chronic type
The developing tooth bud
Dental Anatomy
Tooth development is commonly divided into the following stages: the bud stage, the cap, the bell, and finally maturation. The staging of tooth development is an attempt to categorize changes that take place along a continuum; frequently it is difficult to decide what stage should be assigned to a particular developing tooth. This determination is further complicated by the varying appearance of different histological sections of the same developing tooth, which can appear to be different stages.
Bud stage
The bud stage is characterized by the appearance of a tooth bud without a clear arrangement of cells. The stage technically begins once epithelial cells proliferate into the ectomesenchyme of the jaw. The tooth bud itself is the group of cells at the end of the dental lamina.
FORMATION OF THE PERMANENT DENTITION
Dental Anatomy
FORMATION OF THE PERMANENT DENTITION
Twenty deciduous tooth buds are formed initially.
Proliferative activity of the dental lamina during the bell stage that leads to formation of permanent tooth buds (cap stage) lingual of each deciduous tooth germ.
Molars have no predecessors; they are formed by posterior proliferation of the dental lamina.
HARD TISSUE FORMATION
Hard tissue formation starts at the late stages of the bell stage.
Differentiatioin of cells into odontoblasts and ameloblasts.
The cells of the inner dental epithelium will become ameloblasts.
The cells of the dental papilla opposite to the inner dental epithelium will become odontoblasts.
Dentin is formed before enamel.
Dentin initiates the formation of enamel.
ROOT FORMATION
The root of the tooth is composed by dentin and cementum.
Dentinogenesis is initiated by the odontoblasts.
Odontoblasts are formed as epithelial cells continue to proliferate from the cervical loop as a double layer of cells known as Hertwig's root sheath.
TOOTH SHAPE
The shape of the crowns results from the interaction of inner dental epithelium and the dental papilla.
The cells of the inner dental epithelium have a programmed proliferation.
This internal program determines the tooth form.
The fate of the dental lamina
Rests of Serres
The rest of Serres are rests of the dental lamina identified in the gingival soft tissues.
They are round to ovoid aggregates of epithelial cells that have clear cytoplasm (glucogen rich).
They result from early breakup of the dental lamina during bell stage.
Rests of Malassez
The rests of Malassez result from breakup of the Hertwig's root sheath during root formation.
They can be identified in the periodontal ligament and are responsible for the development of radicular cysts.
Primary Retention Form
Conservative DentistryPrimary Retention Form in Dental Restorations
Primary retention form refers to the geometric shape or design of a prepared
cavity that helps resist the displacement or removal of a restoration due to
tipping or lifting forces. Understanding the primary retention form is crucial
for ensuring the longevity and stability of various types of dental
restorations. Below is an overview of primary retention forms for different
types of restorations.
1. Amalgam Restorations
A. Class I & II Restorations
Primary Retention Form:
Occlusally Converging External Walls: The walls of
the cavity preparation converge towards the occlusal surface, which
helps resist displacement.
Occlusal Dovetail: In Class II restorations, an
occlusal dovetail is often included to enhance retention by providing
additional resistance to displacement.
B. Class III & V Restorations
Primary Retention Form:
Diverging External Walls: The external walls
diverge outward, which can reduce retention.
Retention Grooves or Coves: These features are
added to enhance retention by providing mechanical interlocking and
resistance to displacement.
2. Composite Restorations
A. Primary Retention Form
Mechanical Bond:
Acid Etching: The enamel and dentin surfaces are
etched to create a roughened surface that enhances mechanical retention.
Dentin Bonding Agents: These agents infiltrate the
demineralized dentin and create a hybrid layer, providing a strong bond
between the composite material and the tooth structure.
3. Cast Metal Inlays
A. Primary Retention Form
Parallel Longitudinal Walls: The cavity preparation
features parallel walls that help resist displacement.
Small Angle of Divergence: A divergence of 2-5 degrees
may be used to facilitate the seating of the inlay while still providing
adequate retention.
4. Additional Considerations
A. Occlusal Dovetail and Secondary Retention Grooves
Function: These features aid in preventing the proximal
displacement of restorations by occlusal forces, enhancing the overall
retention of the restoration.
B. Converging Axial Walls
Function: Converging axial walls help prevent occlusal
displacement of the restoration, ensuring that the restoration remains
securely in place during function.
HAEMORRHAGIC DISORDERS
General Pathology
HAEMORRHAGIC DISORDERS
Normal homeostasis depends on
-Capillary integrity and tissue support.
- Platelets; number and function
(a) For integrity of capillary endothelium and platelet plug by adhesion and aggregation
(b) Vasoactive substances for vasoconstriction
(c) Platelet factor for coagulation.
(d) clot retraction.
- Fibrinolytic system(mainly Plasmin) : which keeps the coagulatian system in check.
Coagulation disorders
These may be factors :
Deficiency .of factors
Genetic.
Vitamin K deficiency.
Liver disease.
Secondary to disseminated intravascular coagulation.or defibrinatian
Overactive fibrinolytic system.
Inhibitors of the factars (immune, acquired).
Anticoagulant therapy as in myocardial infarctian.
Haemophilia. Genetic disease transmitted as X linked recessive trait. Comman in Europe. Defect in fcatorVII Haemophilia A .or in fact .or IX-Haemaphilia B (rarer).
Features:
May manifest in infancy or later.
Severity depends on degree of deficiency.
Persistant woundbleeding.
Easy Bruising with Haemotoma formation
Nose bleed , arthrosis, abdominal pain with fever and leucocytosis
Prognosis is good with prevention of trauma and-transfusion of Fresh blood or fTesh plasma except for danger of developing immune inhibitors.
Von Willebrand's disease. Capillary fragility and decreased factor VIII (due to deficient stimulatory factor). It is transmitted in an autosomal dominant manner both. Sexes affected equally
Vitamin K Deficiency. Vitamin K is needed for synthesis of factor II,VII,IX and X.
Deficiency maybe due to:
Obstructive jaundice.
Steatorrhoea.
Gut sterilisation by antibiotics.
Liver disease results in :
Deficient synthesis of factor I II, V, Vll, IX and X Incseased fibrinolysis (as liver is the site of detoxification of activators ).
Defibrination syndrome. occurs when factors are depleted due to disseminated .intravascular coagulation (DIC). It is initiated by endothelial damage or tissue factor entering the circulation.
Causes
Obstetric accidents, especially amniotic fluid embolism. Septicaemia. .
Hypersensitivity reactions.
Disseminated malignancy.
Snake bite.
Vascular defects :
(Non thrombocytopenic purpura).
Acquired :
Simple purpura a seen in women. It is probably endocrinal
Senile parpura in old people due to reduced tissue support to vessels
Allergic or toxic damage to endothelium due to Infections like Typhoid Septicemia
Col!agen diseases.
Scurvy
Uraemia damage to endothelium (platelet defects).
Drugs like aspirin. tranquillisers, Streptomvcin pencillin etc.
Henoc schonlien purpura Widespeard vasculitis due to hypersensitivity to bacteria or foodstuff
It manifests as :
Pulrpurric rashes.
Arthralgia.
Abdominal pain.
Nephritis and haematuria.
Hereditary :
(a) Haemhoragic telangieclasia. Spider like tortous vessels which bleed easily. There are disseminated lesions in skin, mucosa and viscera.
(b) Hereditary capillary fragilily similar to the vascular component of von Willbrand’s disease
.(c) Ehler Danlos Syndrome which is a connective tissue defect with skin, vascular and joint manifestations.
Platelet defects
These may be :
(I) Qualitative thromboasthenia and thrombocytopathy.
(2) Thrombocytopenia :Reduction in number.
(a) Primary or idiopathic thrombocytopenic purpura.
(b) Secondary to :
(i) Drugs especially sedormid
(ii) Leukaemias
(iii) Aplastic-anaemia.
Idiopathic thrombocytopenic purpura (ITP). Commoner in young females.
Manifests as :
Acute self limiting type.
Chronic recurring type.
Features:
(i) Spontaneous bleeding and easy bruisability
(ii)Skin (petechiae), mucus membrane (epistaxis) lesions and sometimes visceral lesions involving any organ.
Thrombocytopenia with abnormal forms of platelets.
Marrow shows increased megakaryocytes with immature forms,
vacuolation, and lack of platelet budding.
Pathogenesis:
hypersensitivity to infective agent in acute type.
Plasma thrombocytopenic factor ( Antibody in nature) in chronic type
Classification of Early Childhood Caries
Pedodontics
Classification of Early Childhood Caries (ECC)
Type 1 ECC (Mild to Moderate)
Affects molars and incisors
Typically seen in children aged 2-5 years
Type 2 ECC (Moderate to Severe)
Characterized by labiolingual caries affecting maxillary incisors,
with or without molar involvement
Usually observed soon after the first tooth erupts
Mandibular incisors remain unaffected
Often caused by inappropriate bottle feeding
Type 3 ECC (Severe)
Involves all primary teeth
Commonly seen in children aged 3-5 years
Monoamine oxidase inhibitors
Pharmacology
Monoamine oxidase inhibitors (MAOIs)
e.g. phenelzine, tranylcypromine, moclobemide
- Belong to first generation antidepressants with TCAs
- Most MAOIs irreversibly inhibit the intraneuronal catabolism of norepinephrine and serotonin by MAO-A and MAO-B
- increase brain levels of noradrenaline and 5-HT
- Moclobemide causes selective, reversible inhibition of MAO-A
DRUG INTERACTIONS
Hypertensive crises similar to cheese reaction with OTC cough/cold preparations containing indirect-sympathomimetics
e.g. ephedrine
- Other antidepressants should not be started at least 2 weeks after stopping MAOIs and vice versa due to risk of serotonin syndrome
- Similar interaction with pethidine
ADVERSE DRUG REACTIONS
- Antimuscarinic side effects (e.g. dry mouth, blurred vision, urinary retention)vision, urinary retention)
- Excessive central stimulation causes tremors, excitement and insomnia
- Postural hypotension
- Increased appetite with weight gain
COMPOSITE RESINS -Pit-and-Fissure Dental Sealants
Dental Materials
Pit-and-Fissure Dental Sealants
Applications/Use
Occlusal surfaces of newly erupted posterior teeth
Labial surfaces of anterior teeth with fissures
Occlusal surfaces of teeth in older patients with reduced saliva flow (because low saliva increases the susceptibility to caries)
Types
Polymerization method
Self-curing (amine accelerated)
Light curing (light accelerated)
Filler content
Unfilled-most systems are unfilled because filler tends to interfere with wear away from self-cleaning occlusal areas(sealants are designed to wear away, except where there is no self-cleaning action a common misconception is that sealants should be wear resistant)
Components
Monomer-BIS-GMA with TEGDM diluent to facilitate flow into pits and fissures prior to cure
Initiator-benzoyl peroxide (in self-cured) and diketone (in light cured)
Accelerator-amine (In light cured)
Opaque filler-I % titanium dioxide. or other colorant to make the material detectable on tooth surfaces
Reinforcing filler-generally not added because wear resistance is not required within pits and fissures
Reaction-free radical reaction
Manipulation
Preparation
Clean pits and fissures of organic debris. Do not apply fluoride before etching because it will tend to make enamel more acid resistant. Etch occlusal surfaces, pits, and fissures for 30 seconds (gel) or 60 seconds (liquid) with 37% phosphoric acid . Wash occlusal surfaces for 20 seconds. Dry etched area for 20 seconds with clean air spray. Apply sealant and polymerize
Mixing or dispensing
Self-cured-mix equal amounts of liquids in Dappen dish for 5 seconds with brush applicator. Light cured-dispense from syringe tips
Placement
-pits, fissures, and occlusal surfaces --> Allow 60 seconds for self-cured materials to set.
Finishing
Remove unpolymerized and excess material .Examine hardness of sealant. Make occlusal adjustments where necessary in sealant; some sealant materials are self-adjusting
Properties
Physical
Wetting-low-viscosity sealants wet acid etched tooth structure the best
Mechanical
Wear resistance should not be too great because sealant should be able to wear off of self-cleaning areas of tooth
Be careful to protect sealants during polishing procedures with air abrading units to prevent sealant loss
Clinical efficacy
Effectiveness is 100% if retained in pits and fissures .Requires routine clinical evaluation for resealing of areas of sealant loss attributable to poor retention .
Sealants resist effects of topical fluorides