NEET MDS Synopsis
COMPOSITE RESINS -Bonding Agents
Dental Materials
Bonding Agents
Applications-composites, resin-modified gIass ionomers, ceramic bonded to enamel restorations, veneers, orthodontic brackets, and desensitizing dentin by covering exposed tubules (Maryland bridges, composite and ceramic repair systems, amalgams and amalgam repair, and pinned amalgams)
Definitions;-
Smear layer - Layer of compacted debris on enamel and/or dentin from the cavity preparation process that is weakly held to the surface (6 to 7 MPa) , and that limits bonding agent strength if not removed
Etching (or, conditioning)- smear layer removal and production of microspaces for micromechanical bonding by dissolving –minor amounts of surface hydroxyapatite crystals
Priming..- micromechanical (and chemical) bonding to the microspaces created by conditioning step.
Conditioning/priming agent-agent that accomplishes both actions
Bonding- formation of resin layer that connect the primed surface to the overlying restoration (e.g., composite) .. –
Enamel bonding System-for bonding to enamel (although dentin bonding may be a Second step)
Dentin bonding system for bonding to dentin (although enamel bonding may have been a first step)
• First-generation dentin bonding system for bonding to smear layer
• New-generation dentin bonding system- for removing smear layer and etching intertubular dentin to allow primer and/or bonding agent to diffuse into spaces between collagen and form hybrid zone
Enamel and dentin bonding system-for bonding to enamel and dentin surfaces with the same procedures
Amalgam bonding system for bonding to enamel, dentin, and amalgam, dentin and amalgam during an amalgam placement procedure or for amalgam repair
Universal bonding system-for bonding to enamel, dentin, amalgam, porcelain , or any other substrate intraorally that may be necessary for a restorative procedure using the same set of procedures and materials
Types
Enamel bonding systems
Dentin bonding systems
Amalgam bonding systems
Universal bonding systems
Structure
o Components of bonding systems
o Conditioning agent-mineral or organic acid
Enamel only 37% phosphoric acid
Dentin only or enamel and .dentin---37% phosphoric acid, citric acid, maleic acid, or nitric acid
o Priming agent
Hydrophobic-solvent-soluble, light cured monomer system
Hydrophilic-water-soluble, light-cured monomer system
Bonding agent
BIS-GMA-type monomer system
UDMA-type monomer system
Reaction
Bonding occurs primarily by intimate micromechanical retention with the relief created by the conditioning step
Chemical bonding is possible but is not recognized as contributing significantly to the overall bond strength
Manipulation-follow manufacturer's directions
Properties
Physical-thermal expansion and contraction may create fatigue stresses that debond the interface and permit micro leakage
Chemical-water absorption into the bonding agent may chemically alter the bonding
Mechanical-mechanical stresses may produce fatigue that debonds the interface and permits microleakage
Enamel bonding-adhesion occurs by macrotags (between enamel prisms) and microtags (into enamel prisms) to produce micromechanical retention
Dentin bonding-adhesion occurs by penetration of smear layer and formation of microtags into intertubular dentin to produce a hybrid zone (interpenetration zone or diffusion zone) that microscopically intertwines collagen bundles and bonding agent polymer
Biologic
Conditioning agents may be locally irritating if they come into contact with soft tissue
Priming agents (uncured), particularly those based on HEMA, may be skin sensitizers after several contacts with dental personnel
Protect skin on hands and face from inadvertent contact with unset materials and/ or their vapors
HEMA and other priming monomers may penetrate through rubber gloves in relatively short times (60 to 90 seconds)
Pulmonary edema
General Pathology
Pulmonary edema
Pulmonary edema is swelling and/or fluid accumulation in the lungs. It leads to impaired gas exchange and may cause respiratory failure.
Signs and symptoms
Symptoms of pulmonary edema include difficulty breathing, coughing up blood, excessive sweating, anxiety and pale skin. If left untreated, it can lead to death, generally due to its main complication of acute respiratory distress syndrome.
Diagnosis
physical examination: end-inspiratory crackles during auscultation (listening to the breathing through a stethoscope) can be due to pulmonary edema. The diagnosis is confirmed on X-ray of the lungs, which shows increased vascular filling and fluid in the alveolar walls.
Low oxygen saturation and disturbed arterial blood gas readings may strengthen the diagnosis
Causes
Cardiogenic causes:
Heart failure
Tachy- or bradyarrhythmias
Severe heart attack
Hypertensive crisis
Excess body fluids, e.g. from kidney failure
Pericardial effusion with tamponade
Non-cardiogenic causes, or ARDS (acute respiratory distress syndrome):
Inhalation of toxic gases
Multiple blood transfusions
Severe infection
Pulmonary contusion, i.e. high-energy trauma
Multitrauma, i.e. severe car accident
Neurogenic, i.e. cerebrovascular accident (CVA)
Aspiration, i.e. gastric fluid or in case of drowning
Certain types of medication
Upper airway obstruction
Reexpansion, i.e. postpneumonectomy or large volume thoracentesis
Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation
Lack of proper altitude acclimatization.
Treatment
When circulatory causes have led to pulmonary edema, treatment with loop diuretics, such as furosemide or bumetanide, is the mainstay of therapy. Secondly, one can start with noninvasive ventilation. Other useful treatments include glyceryl trinitrate, CPAP and oxygen.
Autopsy
General Pathology
Autopsy
Autopsy is examination of the dead body to identify the cause of death. This can be for forensic or clinical purposes.
Ketorolac
Pharmacology
Ketorolac
Mechanism of action
primary action responsible for its anti-inflammatory/antipyretic/analgesic effects is inhibition of prostaglandin synthesis through inhibition of the enzyme cyclooxygenase (COX). Ketorolac is not a selective inhibitor of COX enzymes
Indications: short-term management of pain
Contraindications
hypersensitivity to ketorolac, and against patients with the complete or partial syndrome of nasal polyps, angioedema, bronchospastic reactivity or other allergic manifestations to aspirin or other non-steroidal anti-inflammatory drugs (due to possibility of severe anaphylaxis).
Connective Tissue of the Gingiva
PeriodontologyConnective Tissue of the Gingiva and Related Cellular Components
The connective tissue of the gingiva, known as the lamina propria,
plays a crucial role in supporting the gingival epithelium and maintaining
periodontal health. This lecture will cover the structure of the lamina propria,
the types of connective tissue fibers present, the role of Langerhans cells, and
the changes observed in the periodontal ligament (PDL) with aging.
Structure of the Lamina Propria
Layers of the Lamina Propria:
The lamina propria consists of two distinct layers:
Papillary Layer:
The upper layer that interdigitates with the epithelium,
containing finger-like projections that increase the surface
area for exchange of nutrients and waste.
Reticular Layer:
The deeper layer that provides structural support and
contains larger blood vessels and nerves.
Types of Connective Tissue Fibers:
The lamina propria contains three main types of connective tissue
fibers:
Collagen Fibers:
Type I Collagen: Forms the bulk of the
lamina propria and provides tensile strength to the gingival
fibers, essential for maintaining the integrity of the gingiva.
Reticular Fibers:
These fibers provide a supportive network within the
connective tissue.
Elastic Fibers:
Contribute to the elasticity and flexibility of the gingival
tissue.
Type IV Collagen:
Found branching between the Type I collagen bundles, it is
continuous with the fibers of the basement membrane and the walls of
blood vessels.
Langerhans Cells
Description:
Langerhans cells are dendritic cells located among keratinocytes at
all suprabasal levels of the gingival epithelium.
They belong to the mononuclear phagocyte system and play a critical
role in immune responses.
Function:
Act as antigen-presenting cells for lymphocytes, facilitating the
immune reaction.
Contain specific granules known as Birbeck’s granules and
exhibit marked ATP activity.
Location:
Found in the oral epithelium of normal gingiva and in small amounts
in the sulcular epithelium.
Absent from the junctional epithelium of normal gingiva.
Changes in the Periodontal Ligament (PDL) with Aging
Aging Effects:
With aging, several changes have been reported in the periodontal
ligament:
Decreased Numbers of Fibroblasts: This
reduction can lead to impaired healing and regeneration of the PDL.
Irregular Structure: The PDL may exhibit a more
irregular structure, paralleling changes in the gingival connective
tissues.
Decreased Organic Matrix Production: This can
affect the overall health and function of the PDL.
Epithelial Cell Rests: There may be a decrease
in the number of epithelial cell rests, which are remnants of the
Hertwig's epithelial root sheath.
Increased Amounts of Elastic Fibers: This
change may contribute to the altered mechanical properties of the
PDL.
Sympatholytics And Alpha Adrenergic Blockers
Pharmacology
Sympatholytics And Alpha Adrenergic Blockers
Types
1. Alpha 1-receptor blockers: prazocin,doxazocin.
2. Centrally acting alpha 2- agonists: methyldopa, clonidine.
3. Peripherally acting adrenergic antagonists: reserpine.
4. Imidazoline receptor agonists: rilmenidine, moxonidine.
Advantages
- Alpha1- receptor blockers and imidazoline receptor agonists improve lipid profile and insulin sensitivity.
- Methyldopa: increases renal blood flow. Drug of choice during pregnancy.
- Reserpine: neutral metabolic effects and cheap.
Indications:
- Diabetes mellitus: alpha1- receptor blockers, imidazoline receptor agonists.
- Dyslipidemia: alpha 1- receptor blockers, imidazoline receptor agonists.
- Prostatic hypertrophy: alpha 1- receptor blockers.
- When there is a need for rapid reduction in blood pressure: clonidine.
Side Effects
- Prazocin: postural hypotension, diarrhea, occasional tachycardia, and tolerance (due to fluid retention).
- Methyldopa: sedation, hepatotoxicity, hemolytic anemia, and tolerance.
- Reserpine: depression, lethargy, weight loss, peptic ulcer, diarrhea, and impotence
- Clonidine: dry mouth, sedation, bradycardia, impotence, and rebound hypertension if stopped suddenly.
Considerations
- Prazocin, methyldopa, and reserpine should be combined with a diuretic because of fluid retention.
Direct Arterial Vasodilators
Types: hydralazine, diazoxide, nitroprusside, and minoxidil
Vitamin B6: Pyridoxine, Pyridoxal, Pyridoxamine
Biochemistry
Vitamin B6: Pyridoxine, Pyridoxal, Pyridoxamine
Aids in protein metabolism and red blood cell formation. It is also involved in the body’s production of chemicals such as insulin and hemoglobin.
Vitamin B6 Deficiency Deficiency symptoms include skin disorders, dermatitis, cracks at corners of mouth, anemia, kidney stones, and nausea. A vitamin B6 deficiency in infants can cause mental confusion.
Other lung diseases
General Pathology
Other lung diseases
1.Sarcoidosis
1. Sarcoidosis
a. More common in African-Americans.
b. Associated with the presence of noncaseating granulomas.
Sarcoidosis is an immune system disorder characterised by non-necrotising granulomas (small inflammatory nodules). Virtually any organ can be affected, however, granulomas most often appear in the lungs or the lymph nodes.
Signs and symptoms
Sarcoidosis is a systemic disease that can affect any organ. Common symptoms are vague, such as fatigue unchanged by sleep, lack of energy, aches and pains, dry eyes, blurry vision, shortness of breath, a dry hacking cough or skin lesions. The cutaneous symptoms are protean, and range from rashes and noduli (small bumps) to erythema nodosum or lupus pernio
Renal, liver, heart or brain involvement may cause further symptoms and altered functioning. Manifestations in the eye include uveitis and retinal inflammation
Sarcoidosis affecting the brain or nerves is known as neurosarcoidosis.
Hypercalcemia (high calcium levels) and its symptoms may be the result of excessive vitamin D production
Sarcoidosis most often manifests as a restrictive disease of the lungs, causing a decrease in lung volume and decreased compliance (the ability to stretch). The vital capacity (full breath in, to full breath out) is decreased, and most of this air can be blown out in the first second. This means the FEV1/FVC ratio is increased from the normal of about 80%, to 90%.
Treatment
Corticosteroids, most commonly prednisone
2. Cystic fibrosis
a. Transmission: caused by a genetic mutation (nucleotide deletion) on chromosome 7, resulting in abnormal chloride channels.
b. The most common hereditary disease in Caucasians.
c. Genetic transmission: autosomal recessive.
d. Affects all exocrine glands. Organs affected include lungs, pancreas, salivary glands, and intestines. Thick secretions or mucous plugs are
seen to obstruct the pulmonary airways and intestinal tracts.
e. Is ultimately fatal.
f. Diagnostic test: sweat test—sweat contains increased amounts of chloride.
3. Atelectasis
a. Characterized by collapse of the alveoli.
b. May be caused by a deficiency of surfactant and/or hypoventilation of alveoli.