NEET MDS Synopsis
IONIZATION OF WATER, WEAK ACIDS AND WEAK BASES
Biochemistry
IONIZATION OF WATER, WEAK ACIDS AND WEAK BASES
The ionization of water can be described by an equilibrium constant. When weak acids or weak bases are dissolved in water, they can contribute H+ by ionizing (if acids) or consume H+ by being protonated (if bases). These processes are also governed by equilibrium constants
Water molecules have a slight tendency to undergo reversible ionization to yield a hydrogen ion and a hydroxide ion :
H2O = H+ + OH−
The position of equilibrium of any chemical reaction is given by its equilibrium constant. For the general reaction,
A+B = C + D
Chronic hepatitis
General Pathology
Chronic hepatitis
Chronic hepatitis occurs in 5%-10% of HBV infections and in well over 50% of HCV; it does not occur in HAV. Most chronic disease is due to chronic persistent hepatitis. The chronic form is more likely to occur in the very old or very young, in males, in immunocompromised hosts, in Down's syndrome, and in dialysis patients.
a. Chronic persistent hepatitis is a benign, self-limited disease with a prolonged recovery. Patients are asymptomatic except for elevated transaminases.
b. Chronic active hepatitis features chronic inflammation with hepatocyte destruction, resulting in cirrhosis and liver failure.
(1) Etiology. HBV, HCV, HDV, drug toxicity, Wilson's disease, alcohol, a,-antitrypsin deficiency, and autoimmune hepatitis are common etiologies.
(2) Clinical features may include fatigue, fever, malaise, anorexia, and elevated liver function tests.
(3) Diagnosis is made by liver biopsy.
8. Carrier state for HBV and HCV may be either asymptomatic or with liver disease; in the latter case, the patient has elevate transaminases.
a. Incidence is most common in immunodeficient, drug addicted, Down's syndrome, and dialysis patients.
b. Pathology of asymptomatic carriers shows "ground-glass"" hepatocytes with finely granular eosinophilic cytoplasm.
Stainless Steel Crowns
PedodonticsStainless Steel Crowns
Stainless steel crowns (SSCs) are a common restorative option for primary
teeth, particularly in pediatric dentistry. They are especially useful for teeth
with extensive carious lesions or structural damage, providing durability and
protection for the underlying tooth structure.
Indications for Stainless Steel Crowns
Primary Incisors or Canines:
SSCs are indicated for primary incisors or canines that have
extensive proximal lesions, especially when the incisal portion of the
tooth is involved.
They are particularly beneficial in cases where traditional
restorative materials (like amalgam or composite) may not provide
adequate strength or longevity.
Crown Selection and Preparation
Crown Selection:
An appropriate size of stainless steel crown is selected based on
the dimensions of the tooth being restored.
Contouring:
The crown is contoured at the cervical margin to ensure a proper fit
and to minimize the risk of gingival irritation.
Polishing:
The crown is polished to enhance its surface finish, which can help
reduce plaque accumulation and improve esthetics.
Cementation:
The crown is cemented into place using a suitable dental cement,
ensuring a secure fit even on teeth that have undergone significant
carious structure removal.
Advantages of Stainless Steel Crowns
Retention:
SSCs provide excellent retention and can remain in place even when
extensive portions of carious tooth structure have been removed.
Durability:
They are highly durable and can withstand the forces of mastication,
making them ideal for primary teeth that are subject to wear and tear.
Esthetic Considerations
Esthetic Limitations:
One of the drawbacks of stainless steel crowns is their metallic
appearance, which may not meet the esthetic requirements of some
children and their parents.
Open-Face Stainless Steel Crowns:
To address esthetic concerns, a technique known as the open-face
stainless steel crown can be employed.
In this technique, most of the labial metal of the crown is cut
away, creating a labial "window."
This window is then restored with composite resin, allowing for a
more natural appearance while still providing the strength and
durability of the stainless steel crown.
Platelets
PhysiologyPlatelets
Platelets are cell fragments produced from megakaryocytes.
Blood normally contains 150,000 to 350,000 per microliter (µl). If this value should drop much below 50,000/µl, there is a danger of uncontrolled bleeding. This is because of the essential role that platelets have in blood clotting.
When blood vessels are damaged, fibrils of collagen are exposed.
von Willebrand factor links the collagen to platelets forming a plug of platelets there.
The bound platelets release ADP and thromboxane A2 which recruit and activate still more platelets circulating in the blood.
(This role of thromboxane accounts for the beneficial effect of low doses of aspirin a cyclooxygenase inhibitor in avoiding heart attacks.)
ReoPro is a monoclonal antibody directed against platelet receptors. It inhibits platelet aggregation and appears to reduce the risk that "reamed out" coronary arteries (after coronary angioplasty) will plug up again.
Pancreas
Physiology
The bulk of the pancreas is an exocrine gland secreting pancreatic fluid into the duodenum after a meal. However, scattered through the pancreas are several hundred thousand clusters of cells called islets of Langerhans. The islets are endocrine tissue containing four types of cells. In order of abundance, they are the:
beta cells, which secrete insulin and amylin;
alpha cells, which secrete glucagon;
delta cells, which secrete somatostatin, and
gamma cells, which secrete a polypeptide of unknown function.
Beta Cells
Beta cells secrete insulin in response to a rising level of blood sugar
Insulin affects many organs. It
stimulates skeletal muscle fibers to
take up glucose and convert it into glycogen;
take up amino acids from the blood and convert them into protein.
acts on liver cells
stimulating them to take up glucose from the blood and convert it into glycogen while
inhibiting production of the enzymes involved in breaking glycogen back down (glycogenolysis) and
inhibiting gluconeogenesis; that is, the conversion of fats and proteins into glucose.
acts on fat (adipose) cells to stimulate the uptake of glucose and the synthesis of fat.
acts on cells in the hypothalamus to reduce appetite.
Diabetes Mellitus
Diabetes mellitus is an endocrine disorder characterized by many signs and symptoms. Primary among these are:
a failure of the kidney to retain glucose .
a resulting increase in the volume of urine because of the osmotic effect of this glucose (it reduces the return of water to the blood).
There are three categories of diabetes mellitus:
Insulin-Dependent Diabetes Mellitus (IDDM) (Type 1) and
Non Insulin-Dependent Diabetes Mellitus (NIDDM)(Type 2)
Inherited Forms of Diabetes Mellitus
Insulin-Dependent Diabetes Mellitus (IDDM)
IDDM ( Type 1 diabetes)
is characterized by little or no circulating insulin;
most commonly appears in childhood.
It results from destruction of the beta cells of the islets.
The destruction results from a cell-mediated autoimmune attack against the beta cells.
What triggers this attack is still a mystery, although a prior viral infection may be the culprit.
Non Insulin-Dependent Diabetes Mellitus (NIDDM)
Many people develop diabetes mellitus without an accompanying drop in insulin levels In many cases, the problem appears to be a failure to express a sufficient number of glucose transporters in the plasma membrane (and T-system) of their skeletal muscles. Normally when insulin binds to its receptor on the cell surface, it initiates a chain of events that leads to the insertion in the plasma membrane of increased numbers of a transmembrane glucose transporter. This transporter forms a channel that permits the facilitated diffusion of glucose into the cell. Skeletal muscle is the major "sink" for removing excess glucose from the blood (and converting it into glycogen). In NIDDM, the patient's ability to remove glucose from the blood and convert it into glycogen is reduced. This is called insulin resistance. NIDDM (also called Type 2 diabetes mellitus) usually occurs in adults and, particularly often, in overweight people.
Alpha Cells
The alpha cells of the islets secrete glucagon, a polypeptide of 29 amino acids. Glucagon acts principally on the liver where it stimulates the conversion of glycogen into glucose (glycogenolysis) which is deposited in the blood.
Glucagon secretion is
stimulated by low levels of glucose in the blood;
inhibited by high levels, and
inhibited by amylin.
The physiological significance of this is that glucagon functions to maintain a steady level of blood sugar level between meals.
Delta Cells
The delta cells secrete somatostatin. Somatostatin has a variety of functions. Taken together, they work to reduce the rate at which food is absorbed from the contents of the intestine. Somatostatin is also secreted by the hypothalamus and by the intestine.
Gamma Cells
The gamma cells of the islets secrete pancreatic polypeptide. No function has yet been found for this peptide of 36 amino acids.
Pneumoconioses
General Pathology
Pneumoconioses—are environmentally related lung diseases that result from chronic inhalation of various substances.
1. Silicosis (stone mason’s disease)
a. Inhalant: silica dust.
b. Associated with extensive fibrosis of the lungs.
c. Patients have a higher susceptibility to tuberculosis infections.
2. Asbestosis
a. Inhalant: asbestos fibers.
b. Associated with the presence of pleural plaques.
c. Consequences include:
(1) Mesothelioma (malignant mesothelial tumor).
(2) Bronchogenic carcinoma.
3. Anthracosis
a. Inhalant: carbon dust.
b. Usually not as harmful as silicosis or asbestosis.
c. Associated with the presence of macrophages containing carbon.
Antimicrobial Agents
Conservative DentistryAntimicrobial Agents in Dental Care
Antimicrobial agents play a crucial role in preventing dental caries and
managing oral health. Various agents are available, each with specific
mechanisms of action, antibacterial activity, persistence in the mouth, and
potential side effects. This guide provides an overview of key antimicrobial
agents used in dentistry, their properties, and their applications.
1. Overview of Antimicrobial Agents
A. General Use
Antimicrobial agents are utilized to prevent caries and manage oral
microbial populations. While antibiotics may be considered in rare cases,
their systemic effects must be carefully evaluated.
Fluoride: Known for its antimicrobial effects, fluoride
helps reduce the incidence of caries.
Chlorhexidine: This agent has been widely used for its
beneficial results in oral health, particularly in periodontal therapy and
caries prevention.
2. Chlorhexidine
A. Properties and Use
Initial Availability: Chlorhexidine was first
introduced in the United States as a rinse for periodontal therapy,
typically prescribed as a 0.12% rinse for high-risk patients for short-term
use.
Varnish Application: In other countries, chlorhexidine
is used as a varnish, with professional application being the most effective
mode. Chlorhexidine varnish enhances remineralization and decreases the
presence of mutans streptococci (MS).
B. Mechanism of Action
Antiseptic Properties: Chlorhexidine acts as an
antiseptic, preventing bacterial adherence and reducing microbial counts.
C. Application and Efficacy
Home Use: Chlorhexidine is prescribed for home use at
bedtime as a 30-second rinse. This timing allows for better interaction with
MS organisms due to decreased salivary flow.
Duration of Use: Typically used for about 2 weeks,
chlorhexidine can reduce MS counts to below caries-potential levels, with
sustained effects lasting 12 to 26 weeks.
Professional Application: It can also be applied
professionally once a week for several weeks, with monitoring of microbial
counts to assess effectiveness.
D. Combination with Other Measures
Chlorhexidine may be used in conjunction with other preventive measures
for high-risk patients.
Antimicrobial Agents
A.
Antibiotics
These agents inhibit bacterial growth or kill
bacteria by targeting specific cellular processes.
Agent
Mechanism of Action
Spectrum of Activity
Persistence in Mouth
Side Effects
Vancomycin
Blocks cell-wall synthesis
Narrow (mainly Gram-positive)
Short
Can increase gram-negative bacterial flora
Kanamycin
Blocks protein synthesis
Broad
Short
Not specified
Actinobolin
Blocks protein synthesis
Targets Streptococci
Long
Not specified
B.
Bis-Biguanides
These are
antiseptics that prevent
bacterial adherence and reduce plaque formation.
Agent
Mechanism of Action
Spectrum of Activity
Persistence in Mouth
Side Effects
Alexidine
Antiseptic; prevents bacterial adherence
Broad
Long
Bitter taste; stains teeth and tongue brown; mucosal irritation
Chlorhexidine
Antiseptic; prevents bacterial adherence
Broad
Long
Bitter taste; stains teeth and tongue brown; mucosal irritation
C. Halogens
Halogen-based compounds work as
bactericidal agents by
disrupting microbial cell function.
Agent
Mechanism of Action
Spectrum of Activity
Persistence in Mouth
Side Effects
Iodine
Bactericidal (kills bacteria)
Broad
Short
Metallic taste
D. Fluoride
Fluoride compounds help prevent dental
caries by inhibiting bacterial metabolism and strengthening enamel.
Concentration
Mechanism of Action
Spectrum of Activity
Persistence in Mouth
Side Effects
1–10 ppm
Reduces acid production in bacteria
Broad
Long
Increases enamel resistance to caries attack; fluorosis with
chronic high doses in developing teeth
250 ppm
Bacteriostatic (inhibits bacterial growth)
Broad
Long
Not specified
1000 ppm
Bactericidal (kills bacteria)
Broad
Long
Not specified
Summary & Key Takeaways:
Antibiotics target
specific bacterial processes but may lead to resistance or unwanted
microbial shifts.
Bis-Biguanides (e.g.,
Chlorhexidine) are
effective but cause staining and taste disturbances.
Halogens (e.g.,
Iodine) are
broad-spectrum but may have unpleasant taste.
Fluoride plays a
dual role: it
reduces bacterial acid production
and strengthens enamel.
Antimicrobial agents in operative dentistry include a variety of substances
used to prevent infections and enhance oral health. Key agents include:
Chlorhexidine: A broad-spectrum antiseptic that prevents
bacterial adherence and is effective in reducing mutans streptococci. It can
be used as a rinse or varnish.
Fluoride: Offers antimicrobial effects at various
concentrations, enhancing enamel resistance to caries and reducing acid
production.
Antibiotics: Such as amoxicillin and metronidazole, are
used in specific cases to control infections, with careful consideration of
systemic effects.
Bis Biguanides: Agents like alexidine and chlorhexidine,
which have long-lasting effects and can cause staining and irritation.
Halogens: Iodine is bactericidal but has a short
persistence in the mouth and may cause a metallic taste.
These agents are crucial for managing oral health, particularly in high-risk
patients. ## Other Antimicrobial Agents in Operative Dentistry
In addition to the commonly known antimicrobial agents, several other
substances are utilized in operative dentistry to prevent infections and promote
oral health. Here’s a detailed overview of these agents:
1. Antiseptic Agents
Triclosan:
Mechanism of Action: A chlorinated bisphenol that
disrupts bacterial cell membranes and inhibits fatty acid synthesis.
Applications: Often found in toothpaste and
mouthwashes, it is effective in reducing plaque and gingivitis.
Persistence: Moderate substantivity, allowing for
prolonged antibacterial effects.
Essential Oils:
Components: Includes thymol, menthol, and
eucalyptol.
Mechanism of Action: Disrupts bacterial cell
membranes and has anti-inflammatory properties.
Applications: Commonly used in mouthwashes, they
can reduce plaque and gingivitis effectively.
2. Enzymatic Agents
Enzymes:
Mechanism of Action: Certain enzymes can activate
salivary antibacterial mechanisms, aiding in the breakdown of biofilms.
Applications: Enzymatic toothpastes are designed to
enhance the natural antibacterial properties of saliva.
3. Chemical Plaque Control Agents
Zinc Compounds:
Zinc Citrate:
Mechanism of Action: Exhibits antibacterial
properties and inhibits plaque formation.
Applications: Often combined with other agents
like triclosan in toothpaste formulations.
Sanguinarine:
Source: A plant extract with antimicrobial
properties.
Applications: Available in some toothpaste and
mouthwash formulations, it helps in reducing plaque and gingivitis.
4. Irrigation Solutions
Povidone Iodine:
Mechanism of Action: A broad-spectrum antiseptic
that kills bacteria, viruses, and fungi.
Applications: Used for irrigation during surgical
procedures to reduce the risk of infection.
Hexetidine:
Mechanism of Action: An antiseptic that disrupts
bacterial cell membranes.
Applications: Found in mouthwashes, it has minimal
effects on plaque but can help in managing oral infections.
5. Photodynamic Therapy (PDT)
Mechanism of Action: Involves the use of
light-activated compounds that produce reactive oxygen species to kill
bacteria.
Applications: Used in the treatment of periodontal
diseases and localized infections, PDT can effectively reduce bacterial load
without the use of traditional antibiotics.
6. Low-Level Laser Therapy (LLLT)
Mechanism of Action: Utilizes specific wavelengths of
light to promote healing and reduce inflammation.
Applications: Effective in managing pain and promoting
tissue repair in dental procedures, it can also help in controlling
infections.
Endodontic Microbiology
EndodonticsBacterial portals to pulp: caries (most common source), exposed dentinal tubules (tubule permeability ↓ by dentinal fluid, live odontoblastic processes, tertiary and peritubular dentin)
1. Vital pulp is very resistant to microbial invasion but necrotic pulps are rapidly colonized
2. Rarely does periodontal disease → pulp necrosis
3. Anachoresis: microbes carried in blood to area of inflammation where they establish infection
Caries → pulp disease: infecting bacteria are immobile, carried to pulp by binary fission, dentinal fluid movement
1. Smooth surface and pit and fissure caries: S. mutans (important in early caries) and S. sobrinus
2. Root caries: Actinomyces spp.
3. Mostly anaerobes in deep caries.
4. Once pulp exposed by caries, many opportunists enter (e.g., yeast, viruses) → polymicrobial infection
Pulp reaction to bacteria: non-specific inflammation and specific immunologic reactions
1. Initially inflammation is a chronic cellular response (lymphocytes, plasma cells, macrophages) → formation of peritubular dentin (↓ permeability of tubules) and often tertiary dentin (irregular, less tubular, barrier)
2. Carious pulp exposure → acute inflammation (PMN infiltration → abscess formation). Pulp may remain inflamed for a long time or become necrotic (depends on virulence, host response, circulation, drainage, etc.)
Endodontic infections: most commonly Prevotella nigrescens; also many Prevotella & Porphyromonas sp.
1. Actinomyces and Propionibacterium species can persist in periradicular tissues in presence of chronic inflammation; they respond to RCT but need surgery or abx to resolve infection
2. Streptococcus faecalis is commonly found in root canals requiring retreatment due to persistent inflammation
Root canal ecosystem: lack of circulation in pulp → compromised host defense
1. Favors growth of anaerobes that metabolize peptides and amino acids rather than carbohydrates
2. Bacteriocins: antibiotic-like proteins made by one species of bacteria that inhibit growth of another species
Virulence factors: fimbriae, capsules, enzymes (neutralize Ig and complement), polyamines (↑ # in infected canals)
1. LPS: G(-), → periradicular pathosis; when released from cell wall = endotoxin (can diffuse across dentin)
2. Extracellular vesicles: may → hemagglutination, hemolysis, bacterial adhesion, proteolysis
3. Short-chain fatty acids: affect PMN chemotaxis, degranulation, etc.; butyric acid → IL-1 production (→ bone resorption and periradicular pathosis)
Pathosis and treatment:
1. Acute apical periodontitis (AAP): pulpal inflammation extends to periradicular tissues; initial response
2. Chronic apical periodontitis (CAP): can be asymptomatic (controversial whether bacteria can colonize)
3. Acute apical abscess (AAA), phoenix abscesses (acute exacerbation of CAP), and suppurative apical periodontitis: all characterized by many PMNs, necrotic tissue, and bacteria
Treatment of endodontic infections: must remove reservoir of infection by thorough debridement
1. Debridement: removal of substrates that support microorganisms; use sodium hypochlorite (NaOCl) to irrigate canals (dissolves some organic debris in areas that can’t be reached by instruments); creates smear layer
2. Intracanal medication: recommend calcium hydroxide (greatest antimicrobial effect between appointments) inserted into pulp chamber then driven into canals (lentulo spiral, plugger, or counterclockwise rotation of files) and covered with sterile cotton pellet and temporary restoration (at least 3mm thick)
3. Drainage: for severe infections to ↓ pressure (improve circulation), release bacteria and products; consider abx
4. Culturing: rarely needed but if so, sterilize tissue with chlorhexidine and obtain submucosal sample via aspiration with a 16- to 20-gauge needle