NEET MDS Synopsis
Glycolysis Pathway
Biochemistry
Glycolysis Pathway
The reactions of Glycolysis take place in the cytosol of cells.
Glucose enters the Glycolysis pathway by conversion to glucose-6-phosphate. Initially, there is energy input corresponding to cleavage of two ~P bonds of ATP.
1. Hexokinase catalyzes: glucose + ATP → glucose-6-phosphate + ADP
ATP binds to the enzyme as a complex with Mg++.
The reaction catalyzed by Hexokinase is highly spontaneous
2. Phosphoglucose Isomerase catalyzes:
glucose-6-phosphate (aldose) → fructose-6-phosphate (ketose)
The Phosphoglucose Isomerase mechanism involves acid/base catalysis, with ring opening, isomerization via an enediolate intermediate, and then ring closure .
3. Phosphofructokinase catalyzes:
fructose-6-phosphate + ATP → fructose-1,6-bisphosphate + ADP
The Phosphofructokinase reaction is the rate-limiting step of Glycolysis. The enzyme is highly regulated.
4. Aldolase catalyzes:
fructose-1,6-bisphosphate → dihydroxyacetone phosphate + glyceraldehyde-3-phosphate
The Aldolase reaction is an aldol cleavage, the reverse of an aldol condensation.
5. Triose Phosphate Isomerase (TIM) catalyzes
dihydroxyacetone phosphate (ketose) → glyceraldehyde-3-phosphate (aldose)
Glycolysis continues from glyceraldehydes-3-phosphate
The equilibrium constant (Keq) for the TIM reaction favors dihydroxyacetone phosphate, but removal of glyceraldehyde-3-phosphate by a subsequent spontaneous reaction allows throughput.
6. Glyceraldehyde-3-phosphate Dehydrogenase catalyzes:
glyceraldehyde-3-phosphate + NAD+ + Pi → 1,3,bisphosphoglycerate + NADH + H+
This is the only step in Glycolysis in which NAD+ is reduced to NADH
A cysteine thiol at the active site of Glyceraldehyde-3-phosphate Dehydrogenase has a role in catalysis .
7. Phosphoglycerate Kinase catalyzes:
1,3-bisphosphoglycerate + ADP → 3-phosphoglycerate + ATP
This transfer of phosphate to ADP, from the carboxyl group on 1,3-bisphosphoglycerate, is reversible
8. Phosphoglycerate Mutase catalyzes: 3-phosphoglycerate → 2-phosphoglycerate
Phosphate is shifted from the hydroxyl on C3 of 3-phosphoglycerate to the hydroxyl on C2.
9. Enolase catalyzes: 2-phosphoglycerate → phosphoenolpyruvate + H2O
This Mg++-dependent dehydration reaction is inhibited by fluoride. Fluorophosphate forms a complex with Mg++ at the active site .
10. Pyruvate Kinase catalyzes: phosphoenolpyruvate + ADP → pyruvate + ATP
This transfer of phosphate from PEP to ADP is spontaneous.
Balance sheet for high energy bonds of ATP:
2 ATP expended
4 ATP produced (2 from each of two 3C fragments from glucose)
Net Production of 2~ P bonds of ATP per glucose
Window of Infectivity
Conservative DentistryWindow of Infectivity
The concept of the "window of infectivity" was introduced by Caufield in 1993
to describe critical periods in early childhood when the oral cavity is
particularly susceptible to colonization by Streptococcus mutans, a key
bacterium associated with dental caries. Understanding these windows is
essential for implementing preventive measures against caries in children.
Window of Infectivity: This term refers to specific
time periods during which the acquisition of Streptococcus mutans occurs,
leading to an increased risk of dental caries. These windows are
characterized by the eruption of teeth, which creates opportunities for
bacterial colonization.
First Window of Infectivity
A. Timing
Age Range: The first window of infectivity is observed
between 19 to 23 months of age, coinciding with the
eruption of primary teeth.
B. Mechanism
Eruption of Primary Teeth: As primary teeth erupt, they
provide a "virgin habitat" for S. mutans to colonize the oral
cavity. This is significant because:
Reduced Competition: The newly erupted teeth have
not yet been colonized by other indigenous bacteria, allowing S.
mutans to establish itself without competition.
Increased Risk of Caries: The presence of S.
mutans in the oral cavity during this period can lead to an
increased risk of developing dental caries, especially if dietary habits
include frequent sugar consumption.
Second Window of Infectivity
A. Timing
Age Range: The second window of infectivity occurs
between 6 to 12 years of age, coinciding with the eruption
of permanent teeth.
B. Mechanism
Eruption of Permanent Dentition: As permanent teeth
emerge, they again provide opportunities for S. mutans to colonize
the oral cavity. This window is characterized by:
Increased Susceptibility: The transition from
primary to permanent dentition can lead to changes in oral flora and an
increased risk of caries if preventive measures are not taken.
Behavioral Factors: During this age range, children
may have increased exposure to sugary foods and beverages, further
enhancing the risk of S. mutans colonization and subsequent
caries development.
4. Clinical Implications
A. Preventive Strategies
Oral Hygiene Education: Parents and caregivers should
be educated about the importance of maintaining good oral hygiene practices
from an early age, especially during the windows of infectivity.
Dietary Counseling: Limiting sugary snacks and
beverages during these critical periods can help reduce the risk of S.
mutans colonization and caries development.
Regular Dental Visits: Early and regular dental
check-ups can help monitor the oral health of children and provide timely
interventions if necessary.
B. Targeted Interventions
Fluoride Treatments: Application of fluoride varnishes
or gels during these windows can help strengthen enamel and reduce the risk
of caries.
Sealants: Dental sealants can be applied to newly
erupted permanent molars to provide a protective barrier against caries.
Dental Plaque
PeriodontologyDental Plaque
Dental plaque is a biofilm that forms on the surfaces of teeth and is
composed of a diverse community of microorganisms. The development of dental
plaque occurs in stages, beginning with primary colonizers and progressing to
secondary colonization and plaque maturation.
Primary Colonizers
Timeframe:
Acquired within a few hours after tooth cleaning or exposure.
Characteristics:
Predominantly gram-positive facultative microbes.
Key Species:
Actinomyces viscosus
Streptococcus sanguis
Adhesion Mechanism:
Primary colonizers adhere to the tooth surface through specific
adhesins.
For example, A. viscosus possesses fimbriae that bind to
proline-rich proteins in the dental pellicle, facilitating initial
attachment.
Secondary Colonization and Plaque Maturation
Microbial Composition:
As plaque matures, it becomes predominantly populated by
gram-negative anaerobic microorganisms.
Key Species:
Prevotella intermedia
Prevotella loescheii
Capnocytophaga spp.
Fusobacterium nucleatum
Porphyromonas gingivalis
Coaggregation:
Coaggregation refers to the ability of different species and genera
of plaque microorganisms to adhere to one another.
This process occurs primarily through highly specific stereochemical
interactions of protein and carbohydrate molecules on cell surfaces,
along with hydrophobic, electrostatic, and van der Waals forces.
Plaque Hypotheses
Specific Plaque Hypothesis:
This hypothesis posits that only certain types of plaque are
pathogenic.
The pathogenicity of plaque depends on the presence or increase of
specific microorganisms.
It predicts that plaque harboring specific bacterial pathogens leads
to periodontal disease due to the production of substances that mediate
the destruction of host tissues.
Nonspecific Plaque Hypothesis:
This hypothesis maintains that periodontal disease results from the
overall activity of the entire plaque microflora.
It suggests that the elaboration of noxious products by the entire
microbial community contributes to periodontal disease, rather than
specific pathogens alone.
Uses of NSAIDs
Pharmacology
Uses of NSAIDs
NSAIDs are usually indicated for the treatment of acute or chronic conditions where pain and inflammation are present. Research continues into their potential for prevention of colorectal cancer, and treatment of other conditions, such as cancer and cardiovascular disease.
NSAIDs are generally indicated for the symptomatic relief of the following conditions.
rheumatoid arthritis, osteoarthritis, inflammatory arthropathies (e.g. ankylosing spondylitis, psoriatic arthritis, Reiter's syndrome), acute gout, dysmenorrhoea, metastatic bone pain ,headache and migraine, postoperative pain, mild-to-moderate pain due to inflammation and tissue injury, pyrexia, renal colic
Aspirin, the only NSAID able to irreversibly inhibit COX-1, is also indicated for inhibition of platelet aggregation; an indication useful in the management of arterial thrombosis and prevention of adverse cardiovascular events.
TEMPOROMANDIBULAR JOINT -ARTICULAR SURFACES COVERED BY FIBROUS TISSUE
Dental Anatomy
ARTICULAR SURFACES COVERED BY FIBROUS TISSUE
TMJ is an exception form other synovial joints. Two other joints, the acromio- and sternoclavicular joints are similar to the TMJ. Mandible & clavicle derive from intramembranous ossificiation.
Histologic
Fibrous layer: collagen type I, avascular (self-contained and replicating)
Proliferating zone that formes condylar cartilage
Condylar cartilage is fibrocartilage that does not play role in articulation nor has formal function
Capsule: dense collagenous tissue (includes the articular eminence)
Synovial membrane: lines capsule (does not cover disk except posterior region); contains folds (increase in pathologic conditions) and villi
Two layers: a cellular intima (synovial cells in fiber-free matrix) and a vascular subintima
Synovial cells: A (macrophage-like) syntesize hyaluronate
B (fibroblast-like) add protein in the fluid
Synovial fluid: plasma with mucin and proteins, cells
Liquid environment: lubrication, ?nutrition
Disk: separates the cavity into two comprartments, type I collagen
anterior and posterior portions
anetiorly it divides into two lamellae one towards the capsule, the other towards the condyle
vascular in the preiphery, avascular in the center
Ligaments: nonelastic collagenous structures. One ligament worth mentioning is the lateral or temporomandibular ligament. Also there are the spheno- and stylomandibular with debatable functional role.
Innervations
Ruffini
Posture
Dynamic and static balance
Pacini
Dynamic mechanoreception
Movement accelerator
Golgi
Static mechanoreception
Protection (ligament)
Free
Pain
Protection joint
Classification of Cerebral Palsy
PedodonticsClassification of Cerebral Palsy
Cerebral palsy (CP) is a group of neurological disorders that affect
movement, muscle tone, and motor skills. The classification of cerebral palsy is
primarily based on the type of neuromuscular dysfunction observed in affected
individuals. Below is an outline of the main types of cerebral palsy, along with
their basic characteristics.
1. Spastic Cerebral Palsy (Approximately 70% of Cases)
Definition: Characterized by hypertonicity (increased
muscle tone) and exaggerated reflexes.
Characteristics:
A. Hyperirritability of Muscles: Involved muscles
exhibit exaggerated contractions when stimulated.
B. Tense, Contracted Muscles:
Example: Spastic Hemiplegia affects one side of
the body, with the affected hand and arm flexed against the trunk.
The leg may be flexed and internally rotated, leading to a limping
gait with circumduction of the affected leg.
C. Limited Neck Control: Difficulty controlling
neck muscles results in head rolling.
D. Trunk Muscle Control: Lack of control in trunk
muscles leads to difficulties in maintaining an upright posture.
E. Coordination Issues: Impaired coordination of
intraoral, perioral, and masticatory muscles can result in:
Impaired chewing and swallowing
Excessive drooling
Persistent spastic tongue thrust
Speech impairments
2. Dyskinetic Cerebral Palsy (Athetosis and Choreoathetosis) (Approximately
15% of Cases)
Definition: Characterized by constant and uncontrolled
movements.
Characteristics:
A. Uncontrolled Motion: Involved muscles exhibit
constant, uncontrolled movements.
B. Athetoid Movements: Slow, twisting, or writhing
involuntary movements (athetosis) or quick, jerky movements
(choreoathetosis).
C. Neck Muscle Involvement: Excessive head movement
due to hypertonicity of neck muscles, which may cause the head to be
held back, with the mouth open and tongue protruded.
D. Jaw Involvement: Frequent uncontrolled jaw
movements or severe bruxism (teeth grinding).
E. Hypotonicity of Perioral Musculature:
Symptoms include mouth breathing, tongue protrusion, and
excessive drooling.
F. Facial Grimacing: Involuntary facial expressions
may occur.
G. Chewing and Swallowing Difficulties: Challenges
in these areas are common.
H. Speech Problems: Communication difficulties may
arise.
3. Ataxic Cerebral Palsy (Approximately 5% of Cases)
Definition: Characterized by poor coordination and
balance.
Characteristics:
A. Incomplete Muscle Contraction: Involved muscles
do not contract completely, leading to partial voluntary movements.
B. Poor Balance and Coordination: Individuals may
exhibit a staggering or stumbling gait and difficulty grasping objects.
C. Tremors: Possible tremors or uncontrollable
trembling when attempting voluntary tasks.
4. Mixed Cerebral Palsy (Approximately 10% of Cases)
Definition: A combination of characteristics from more
than one type of cerebral palsy.
Example: Mixed spastic-athetoid quadriplegia, where
features of both spastic and dyskinetic types are present.
Varicose Veins
General Pathology
Varicose Veins
- are abnormally dilated, tortuous veins produced by prolonged increase in intraluminal pressure and loss of vessel wall support.
- The superficial veins of the leg are typically involved
-venous pressures in these sites can be markedly elevated -> venous stasis and pedal edema (simple orthostatic edema)
-Some 10% to 20% of adult males and 25% to 33% of adult females develop lower extremity varicose veins
RISK FACTORS
-> obesity
-> Female gender
-> pregnancy.
-> familial tendency (premature varicosities results from imperfect venous wall development)
Morphology
- wall thinning
- intimal fibrosis in adjacent segments
- spotty medial calcifications (phlebosclerosis)
- Focal intraluminal thrombosis
- venous valve deformities (rolling and shortening)
COMPLICATIONS
- stasis, congestion, edema, pain, and thrombosis
- chronic varicose ulcers
- embolism is very rare.
Structure of gypsum products
Dental Materials
Structure of gypsum products
Components
a. Powder (calcium sulfate hemihydrate = CaSO4½H2O)
b. Water (for reaction with powder and dispersing powder)