NEET MDS Synopsis
PHYSICAL AGENTS
General Microbiology
PHYSICAL AGENTS
Heat occupies the most important place as a physical agent.
Moist Heat : This is heating in the presence of water and can be employed in the following ways:
Temperature below 100°C: This includes holder method of Pasteurization where 60°C for 30 minutes is employed for sterilization and in its flash modification where in objects are subjected to a temperature of 71.1°C for 15 seconds. This method does not destroy spores.
Temperatures Around 100°C : Tyndallization is an example of this methodology in which steaming of the object is done for 30 minutes on each of three consecutive days. Spores which survive the heating process would germinate before the next thermal exposure and would then be killed.
Temperatures Above 100°C : Dry saturated steam acts as an excellent agent for sterilization. Autoclaves have been designed on the principles of moist heat.
Time-temperature relationship in heat sterilization
Moist heat (autoclaving)
121°C 15 minutes
126°C 10 minutes
134 C 3 minutes
Dry heat
>160°C >120 minutes
>170°C >60minutes
>180°C >30 minutes
Mechanism of microbial inactivation
The autoclaving is in use for the sterilization of many ophthalmic and parentral products. surgical dressings, rubber gloves, bacteriological media as well a of lab and hospital reusable goods.
Dry Heat: Less efficient, bacterial spores are most resistant. Spores may require a temperature of 140° C for three hours to get killed.
Dry heat sterilization is usually carried out by flaming as is done in microbiology laboratory to sterilize the inoculating loop and in hot air ovens in which a number of time-temperature combinations can be used. It is essential that hot air should circulate between the objects to be sterilized. Microbial inactivation by dry heat is primarily an oxidation process.
Dry heat is employed for sterilization of glassware glass syringes, oils and oily injections as well as metal instruments. -
Indicators of Sterilization:
These determine the efficacy of heat sterilization and can be in the form of spores of Bacillus stearothermophilus (killed at 121C in 12 minutes) or in the form of chemical indicators, autoclave tapes and thermocouples.
Ionizing Radiations
Ionizing radiations include X-rays, gamma rays and beta rays, and these induce defects in the microbial DNA synthesis is inhibited resulting in cell death. Spores are more resistant to ionizing radiations than nonsporulating bacteria.
The ionizing radiations are used for the sterilization of single use disposable medical items.
Mechanism of microbial inactivation by moist heat
Bacterial spores
• Denaturation of spore_epzymes
• Impairment of germination
• Damage to cell membrane
• Increased sensitivity to inhibitory agents
• Structural damage
• Damage to chromosome
Nonsporulating bacteria
• Damage to cytoplasmic membrane
• Breakdown of RNA
• Coagulation of proteins
• Damage to bacterial chromosome
Ultraviolet Radiations :
wave length 240-280 nm have been found to be most efficient in sterilizing. Bacterial spores are more resistant to U.V. rays than the vegetative forms. Even viruses are sometimes more resistant than vegetative bacteria.
Mechanism of Action :
Exposure to UV rays results in the formation of purine and pyrimidine diamers between adjacent molecules in the same strand of DNA. This results into noncoding lesions in DNA and bacterial death.
Used to disinfect drinking water, obtaining pyrogen free water, air disinfection (especially in safety laboratories, hospitals, operation theatres) and in places where dangerous microorganisms are being handled.
Filteration
Type of Filters
Various types of filters that are available are /
Unglazed ceramic filter (Chamberland and Doulton filters)
Asbestos filters (Seitz, Carlson and Sterimat filters)
Sintered glass filters
Membrane filters
Membrane filters are widely used now a days. Made up of cellulose ester and are most suitable for preparing_sterile solutions. The range of pore size in which these are available is 0.05-12 µm whereas the required pore size for sterlization is in range of 0.2-0.22 p.m.
The developing tooth bud -Bell stage
Dental Anatomy
Bell stage
The bell stage is known for the histodifferentiation and morphodifferentiation that takes place. The dental organ is bell-shaped during this stage, and the majority of its cells are called stellate reticulum because of their star-shaped appearance. Cells on the periphery of the enamel organ separate into three important layers. Cuboidal cells on the periphery of the dental organ are known as outer enamel epithelium.The cells of the enamel organ adjacent to the dental papilla are known as inner enamel epithelium. The cells between the inner enamel epithelium and the stellate reticulum form a layer known as the stratum intermedium. The rim of the dental organ where the outer and inner enamel epithelium join is called the cervical loop
Other events occur during the bell stage. The dental lamina disintegrates, leaving the developing teeth completely separated from the epithelium of the oral cavity; the two will not join again until the final eruption of the tooth into the mouth
The crown of the tooth, which is influenced by the shape of the internal enamel epithelium, also takes shape during this stage. Throughout the mouth, all teeth undergo this same process; it is still uncertain why teeth form various crown shapes—for instance, incisors versus canines. There are two dominant hypotheses. The "field model" proposes there are components for each type of tooth shape found in the ectomesenchyme during tooth development. The components for particular types of teeth, such as incisors, are localized in one area and dissipate rapidly in different parts of the mouth. Thus, for example, the "incisor field" has factors that develop teeth into incisor shape, and this field is concentrated in the central incisor area, but decreases rapidly in the canine area. The other dominant hypothesis, the "clone model", proposes that the epithelium programs a group of ectomesenchymal cells to generate teeth of particular shapes. This group of cells, called a clone, coaxes the dental lamina into tooth development, causing a tooth bud to form. Growth of the dental lamina continues in an area called the "progress zone". Once the progress zone travels a certain distance from the first tooth bud, a second tooth bud will start to develop. These two models are not necessarily mutually exclusive, nor does widely accepted dental science consider them to be so: it is postulated that both models influence tooth development at different times.Other structures that may appear in a developing tooth in this stage are enamel knots, enamel cords, and enamel niche.
Neurogenic Shock
Oral and Maxillofacial SurgeryNeurogenic Shock
Neurogenic shock is a type of distributive shock that occurs
due to the loss of vasomotor tone, leading to widespread vasodilation and a
significant decrease in systemic vascular resistance. This condition can occur
without any loss of blood volume, resulting in inadequate filling of the
circulatory system despite normal blood volume. Below is a detailed overview of
neurogenic shock, its causes, symptoms, and management.
Mechanism of Neurogenic Shock
Loss of Vasomotor Tone: Neurogenic shock is primarily
caused by the disruption of sympathetic nervous system activity, which leads
to a loss of vasomotor tone. This results in massive dilation of blood
vessels, particularly veins, causing a significant increase in vascular
capacity.
Decreased Systemic Vascular Resistance: The dilated
blood vessels cannot effectively maintain blood pressure, leading to
inadequate perfusion of vital organs, including the brain.
Causes
Spinal Cord Injury: Damage to the spinal cord,
particularly at the cervical or upper thoracic levels, can disrupt
sympathetic outflow and lead to neurogenic shock.
Severe Head Injury: Traumatic brain injury can also
affect autonomic regulation and result in neurogenic shock.
Vasovagal Syncope: A common form of neurogenic shock,
often triggered by emotional stress, pain, or prolonged standing, leading to
a sudden drop in heart rate and blood pressure.
Symptoms
Early Signs:
Pale or Ashen Gray Skin: Due to peripheral vasodilation
and reduced blood flow to the skin.
Heavy Perspiration: Increased sweating as a response to
stress or pain.
Nausea: Gastrointestinal distress may occur.
Tachycardia: Increased heart rate as the body attempts
to compensate for low blood pressure.
Feeling of Warmth: Particularly in the neck or face due
to vasodilation.
Late Symptoms:
Coldness in Hands and Feet: Peripheral vasoconstriction
may occur as the body prioritizes blood flow to vital organs.
Hypotension: Significantly low blood pressure due to
vasodilation.
Bradycardia: Decreased heart rate, particularly in
cases of vasovagal syncope.
Dizziness and Visual Disturbance: Due to decreased
cerebral perfusion.
Papillary Dilation: As a response to low light levels
in the eyes.
Hyperpnea: Increased respiratory rate as the body
attempts to compensate for low oxygen delivery.
Loss of Consciousness: Resulting from critically low
cerebral blood flow.
Duration of Syncope
Brief Duration: The duration of syncope in neurogenic
shock is typically very brief. Patients often regain consciousness almost
immediately upon being placed in a supine position.
Supine Positioning: This position is crucial as it
helps increase venous return to the heart and improves cerebral perfusion,
aiding in recovery.
Management
Positioning: The first and most important step in
managing neurogenic shock is to place the patient in a supine position. This
helps facilitate blood flow to the brain.
Fluid Resuscitation: While neurogenic shock does not
typically involve blood loss, intravenous fluids may be administered to help
restore vascular volume and improve blood pressure.
Vasopressors: In cases where hypotension persists
despite fluid resuscitation, vasopressor medications may be used to
constrict blood vessels and increase blood pressure.
Monitoring: Continuous monitoring of vital signs,
including blood pressure, heart rate, and oxygen saturation, is essential to
assess the patient's response to treatment.
Addressing Underlying Causes: If neurogenic shock is due
to a specific cause, such as spinal cord injury or vasovagal syncope,
appropriate interventions should be initiated to address the underlying
issue.
Modified Widman Flap
PeriodontologyModified Widman Flap Procedure
The modified Widman flap procedure is a surgical technique used in
periodontal therapy to treat periodontal pockets while preserving the
surrounding tissues and promoting healing. This lecture will discuss the
advantages and disadvantages of the modified Widman flap, its indications, and
the procedural steps involved.
Advantages of the Modified Widman Flap Procedure
Intimate Postoperative Adaptation:
The main advantage of the modified Widman flap procedure is the
ability to establish a close adaptation of healthy collagenous
connective tissues and normal epithelium to all tooth surfaces. This
promotes better healing and integration of tissues post-surgery
Feasibility for Bone Implantation:
The modified Widman flap procedure is advantageous over curettage,
particularly when the implantation of bone and other substances is
planned. This allows for better access and preparation of the surgical
site for grafting .
Conservation of Bone and Optimal Coverage:
Compared to conventional reverse bevel flap surgery, the modified
Widman flap conserves bone and provides optimal coverage of root
surfaces by soft tissues. This results in:
A more aesthetically pleasing outcome.
A favorable environment for oral hygiene.
Potentially less root sensitivity and reduced risk of root
caries.
More effective pocket closure compared to pocket elimination
procedures .
Minimized Gingival Recession:
When reattachment or minimal gingival recession is desired, the
modified Widman flap is preferred over subgingival curettage, making it
a suitable choice for treating deeper pockets (greater than 5 mm) and
other complex periodontal conditions.
Disadvantages of the Modified Widman Flap Procedure
Interproximal Architecture:
One apparent disadvantage is the potential for flat or concave
interproximal architecture immediately following the removal of the
surgical dressing, particularly in areas with interproximal bony
craters. This can affect the aesthetic outcome and may require further
management .
Indications for the Modified Widman Flap Procedure
Deep Pockets: Pockets greater than 5 mm, especially in
the anterior and buccal maxillary posterior regions.
Intrabony Pockets and Craters: Effective for treating
pockets with vertical bone loss.
Furcation Involvement: Suitable for managing
periodontal disease in multi-rooted teeth.
Bone Grafts: Facilitates the placement of bone grafts
during surgery.
Severe Root Sensitivity: Indicated when root
sensitivity is a significant concern.
Procedure Overview
Incisions and Flap Reflection:
Vertical Incisions: Made to access the periodontal
pocket.
Crevicular Incision: A horizontal incision along
the gingival margin.
Horizontal Incision: Undermines and removes the
collar of tissue around the teeth.
Conservative Debridement:
Flap is reflected just beyond the alveolar crest.
Careful removal of all plaque and calculus while preserving the root
surface.
Frequent sterile saline irrigation is used to maintain a clean
surgical field.
Preservation of Proximal Bone Surface:
The proximal bone surface is preserved and not curetted, allowing
for better healing and adaptation of the flap.
Exact flap adaptation is achieved with full coverage of the bone.
Suturing:
Suturing is aimed at achieving primary union of the proximal flap
projections, ensuring proper healing and tissue integration.
Postoperative Care
Antibiotic Ointment and Periodontal Dressing:
Traditionally, antibiotic ointment was applied over sutures, and a
periodontal dressing was placed. However, these practices are often omitted
today.
Current Recommendations: Patients are advised not to
disturb the surgical area and to use a chlorhexidine mouth rinse every 12
hours for effective plaque control and to promote healing.
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Neutrophil Disorders Associated with Periodontal Diseases
Neutrophils play a crucial role in the immune response, particularly in
combating infections, including those associated with periodontal diseases.
Various neutrophil disorders can significantly impact periodontal health,
leading to increased susceptibility to periodontal diseases. This lecture will
explore the relationship between neutrophil disorders and specific periodontal
diseases.
Neutrophil Disorders
Diabetes Mellitus
Description: A metabolic disorder characterized by
high blood sugar levels due to insulin resistance or deficiency.
Impact on Neutrophils: Diabetes can impair
neutrophil function, including chemotaxis, phagocytosis, and the
oxidative burst, leading to an increased risk of periodontal infections.
Papillon-Lefevre Syndrome
Description: A rare genetic disorder characterized
by palmoplantar keratoderma and severe periodontitis.
Impact on Neutrophils: Patients exhibit neutrophil
dysfunction, leading to early onset and rapid progression of periodontal
disease.
Down’s Syndrome
Description: A genetic disorder caused by the
presence of an extra chromosome 21, leading to various developmental and
health issues.
Impact on Neutrophils: Individuals with Down’s
syndrome often have impaired neutrophil function, which contributes to
an increased prevalence of periodontal disease.
Chediak-Higashi Syndrome
Description: A rare genetic disorder characterized
by immunodeficiency, partial oculocutaneous albinism, and neurological
problems.
Impact on Neutrophils: This syndrome results in
defective neutrophil chemotaxis and phagocytosis, leading to increased
susceptibility to infections, including periodontal diseases.
Drug-Induced Agranulocytosis
Description: A condition characterized by a
dangerously low level of neutrophils due to certain medications.
Impact on Neutrophils: The reduction in neutrophil
count compromises the immune response, increasing the risk of
periodontal infections.
Cyclic Neutropenia
Description: A rare genetic disorder characterized
by recurrent episodes of neutropenia (low neutrophil count) occurring
every 21 days.
Impact on Neutrophils: During neutropenic episodes,
patients are at a heightened risk for infections, including periodontal
disease.
SALIVARY GLANDS -Structure
Dental Anatomy
Structure
There are 3 pairs
The functional unit is the adenomere.
The adenomere consists of secreting units and an intercalated duct, which opens, in a striated duct.
An secreting unit can be:
- mucous secreting
- serous secreting
THE SECRETING UNIT
THE CELLS
Serous cells
(seromucus cells=secrete also polysaccharides), They have all the features of a cell specialized for the synthesis, storage, and secretion of protein
Pyramidal, Nuclei are rounded and more centrally placed, In the basal 1/3 there is an accumulation of Granular EPR, In the apex there are proteinaceous secretory granules, Cells stain well with H & E (red), Between cells are intercellular secretory capillaries
Rough endoplasmic reticulum (ribosomal sites-->cisternae)
Prominent Golgi-->carbohydrate moieties are added
Secretory granules-->exocytosis
The secretory process is continuous but cyclic
There are complex foldings of cytoplasmic membrane
The junctional complex consists of: 1) tight junctions (zonula occludens)-->fusion of outer cell layer, 2) intermediate junction (zonula adherens)-->intercellular communication, 3)desmosomes-->firm adhesion
Mucus cells
Pyramidal, Nuclei are flattened and near the base, Have big clear secretory granules
Cells do not stain well with H & E (white)
Production, storage, and secretion of proteinaceous material; smaller enzymatic component
-more carbohydrates-->mucins=more prominent Golgi
-less prominent (conspicuous) rough endoplasmic reticulum, mitochondria
-less interdigitations
Myoepithelial cells
Star-shaped, Centrally located nucleus, Long cytoplasmic arms - bound to the secretory cells by desmosomes, Have fibrils like smooth muscle, Squeeze the secretory cell
One, two or even three myoepithelial cells in each salivary and piece body, four to eight processes
Desmosomes between myoepithelial cells and secretory cells myofilaments frequently aggregated to form dark bodies along the course of the process. The myoepithelial cells of the intercalated ducts are more spindled-shaped and fewer processes
Ultrastructure very similar to that of smooth muscle cells (myofilaments, desmosomal attachments)
Functions of myoepithelial cells
-Support secretory cells
-Contract and widen the diameter of the intercalated ducts
-Contraction may aid in the rupture of acinar cells of epithelial origin
Ductal system
Three classes of ducts:
Intercalated ducts
They have small diameter; lined by small cuboidal cells; nucleus located in the center. They have a well-developed RER, Golgi apparatus, occasionally secretory granules, few microvilli. Myoepithelial cells are also present. Intercalated ducts are prominent in salivary glands having a watery secretion (parotid).
Striated ducts
They have columnar cells, a centrally located nucleus, eosinophilic cytoplasm. Prominenty striations that refer to indentations of the cytoplasmic membrane with many mitochondria present between the folds. Some RER and some Golgi. The cells have short microvilli.
The cells of the striated ducts modify the secretion (hypotonic solution=low sodium and chloride and high potassium). There is also presence of few basal cells.
Terminal excretory ducts
Near the striated ducts they have the same histology as the striated ducts. As the duct reaches the oral mucosa the lining becomes stratified. In the terminal ducts one can find goblet cells, basal cells, clear cells. The terminal ducts alter the electrolyte concentration and add mucoid substance.
Connective tissue
Presence of fibroblasts, inflammatory cells, mast cells, adipose cells
Extracellular matrix (glycoproteins and proteoglycans)
Collagen and oxytalan fibers
Nerve supply
The innervation of salivary glands is very complicated. There is no direct inhibitory innervation. There are parasympathetic and sympathetic impulses, the parasympathetic are more prevalent.
The parasympathetic impulses may occur in isolation, evoke most of the fluid to be excreted, cause exocytosis, induce contraction of myoepithelial cells (sympathetic too) and cause vasodialtion. There are two types of innervation: epilemmal and hypolemmal. There are beta-adrenergic receptors that induce protein secretion and L-adrenergic and cholinergic receptors that induce water and electrolyte secretion.
Hormones can influence the function of the salivary glands. They modify the salivary content but cannot initiate salivary flow.
Age changes
Fibrosis and fatty degenerative changes
Presence of oncocytes (eosinophilic cells containing many mitochondria)
Clinical considerations
Role of drugs, systemic disorders, bacterial or viral infections, therapeutic radiation, obstruction, formation of plaque and calculus.
- Rich capillary networks surround the adenomeres.
Measles (rubeola)
General Pathology
Measles (rubeola)
-incubation period 7 to 14 days
-begins with fever (up to 40 degrees C), cough, conjunctivitis (photophobia is first sign), and coryza (excessive mucous production)Æfollowed by Koplik's spots (red with white center) in the mouth, posterior cervical Lymphadenopathy, and a generalized, blanching, maculopapular, brownish-pink rash (viral induced vasculitis) beginning at the hairline and extending down over the body which gradually resolves in 5 days with some desquamation.
CLINICAL SIGNIFICANCE OF ENZYMES
Biochemistry
CLINICAL SIGNIFICANCE OF ENZYMES
The measurement of enzymes level in serum is applied in diagnostic application
Pancreatic Enzymes
Acute pancreatitis is an inflammatory process where auto digestion of gland was noticed with activation of the certain pancreatic enzymes. Enzymes which involves in pancreatic destruction includes α-amylase, lipase etc.,
1. α-amylase (AMYs) are calcium dependent hydrolyase class of metaloenzyme that catalyzes the hydrolysis of 1, 4- α-glycosidic linkages in polysaccharides. The normal values of amylase is in range of 28-100 U/L. Marked increase of 5 to 10 times the upper reference limit (URL) in AMYs activity indicates acute pancreatitis and severe glomerular impairment.
2. Lipase is single chain glycoprotein. Bile salts and a cofactor called colipase are required for full catalytic activity of lipase. Colipase is secreted by pancreas. Increase in plasma lipase activity indicates acute pancreatitis and carcinoma of the pancreas.
Liver Enzymes
Markers of Hepatocellular Damage
1. Aspartate transaminase (AST) Aspartate transaminase is present in high concentrations in cells of cardiac and skeletal muscle, liver, kidney and erythrocytes. Damage to any of these tissues may increase plasma AST levels.
The normal value of AST for male is <35 U/ L and for female it is <31 U/L.
2. Alanine transaminase (ALT) Alanine transaminase is present at high concentrations in liver and to a lesser extent, in skeletal muscle, kidney and heart. Thus in case of liver damage increase in both AST and ALT were noticed. While in myocardial infarction AST is increased with little or no increase in ALT.
The normal value of ALT is <45 U/L and <34 U/L for male and female respectively
Markers of cholestasis
1. Alkaline phosphatases
Alkaline phosphatases are a group of enzymes that hydrolyse organic phosphates at high pH. They are present in osteoblasts of bone, the cells of the hepatobiliary tract, intestinal wall, renal tubules and placenta.
Gamma-glutamyl-transferase (GGT) Gamma-glutamyl-transferase catalyzes the transfere of the γ–glutamyl group from peptides. The activity of GGT is higher in men than in women. In male the normal value of GGT activity is <55 U/L and for female it is <38 U/L.
2. Glutamate dehydrogenase (GLD) Glutamate dehydrogenase is a mitochondrial enzyme found in liver, heart muscle and kidneys.
Muscle Enzymes
1. Creatine Kinase Creatine kinase (CK) is most abundant in cells of brain, cardiac and skeletal.
2. Lactate Dehydrogenase
Lactate dehydrogenase (LD) catalyses the reversible interconversion of lactate and pyruvate.
Hepatitis Summary
General Pathology
Summary
Hepatitis A → ssRNA → Picornavirus → Oral–anal
Hepatitis B → dsDNA → Hepadnavirus → Sexual contact , Blood (needles), Perinatal
Hepatitis C → ssRNA → Flavivirus → Sexual contact , Blood (needles)
Hepatitis D → ssRNA → Deltavirus → Sexual contact, Blood (needles)
Hepatitis E → ssRNA → Calicivirus → Oral–anal