NEET MDS Synopsis
Oxygen Carriage in Blood at High Altitude
PhysiologyOxygen Uptake in the Lungs is Increased About 70X by Hemoglobin in the Red Cells
In the lungs oxygen must enter the blood
A small amount of oxygen dissolves directly in the serum, but 98.5% of the oxygen is carried by hemoglobin
All of the hemoglobin is found within the red blood cells (RBCs or erythrocytes)
The hemoglobin content of the blood is about 15 gm/deciliter (deciliter = 100 mL)
Red cell count is about 5 million per microliter
Each Hemoglobin Can Bind Four O2 Molecules (100% Saturation)
Hemoglobin is a protein molecule with 4 protein sub-units (2 alphas and 2 betas)
Each of the 4 sub-units contains a heme group which gives the protein a red color
Each heme has an iron atom in the center which can bind an oxygen molecule (O2)
The 4 hemes in a hemoglobin can carry a maximum of 4 oxygen molecules
When hemoglobin is saturated with oxygen it has a bright red color; as it loses oxygen it becomes bluish (cyanosis)
The Normal Blood Hematocrit is Just Below 50%
Blood consists of cells suspended in serum
More than 99% of the cells in the blood are red blood cells designed to carry oxygen
25% of all the cells in the body are RBCs
The volume percentage of cells in the blood is called the hematocrit
Normal hematocrits are about 40% for women and 45% for men
At Sea Level the Partial Pressure of O2 is High Enough to Give Nearly 100% Saturation of Hemoglobin
As the partial pressure of oxygen in the alveoli increases the hemoglobin in the red cells passing through the lungs rises until the hemoglobin is 100% saturated with oxygen
At 100% saturation each hemoglobin carries 4 O2 molecules
This is equal to 1.33 mL O2 per gram of hemoglobin
A person with 15 gm Hb/deciliter can carry:
Max O2 carriage = 1.33 mL O2/gm X 15 gm/deciliter = 20 mL O2/deciliter
A plot of % saturation vs pO2 gives an S-shaped "hemoglobin dissociation curve"
At 100% saturation each hemoglobin binds 4 oxygen molecules
At High Altitudes Hemoglobin Saturation May be Well Below 100%
At the alveolar pO2 of 105 mm Hg at sea level the hemoglobin will be about 97% saturated, but the saturation will fall at high altitudes
At 12,000 feet altitude alveolar pO2 will be about 60 mm Hg and the hemoglobin will be 90% saturated
At 29,000 feet (Mt. Everest) alveolar pO2 is about 24 mm Hg and the hemoglobin will be only 42% saturated
At very high altitudes most climbers must breath pure oxygen from tanks
During acclimatization to high altitude the hematocrit can rise to about 60%- this increases the amount of oxygen that can be carried
Hematocrits above 60% are not useful because the blood viscosity will increase to the point where it impairs circulation
TEMPOROMANDIBULAR JOINT
Dental Anatomy
TEMPOROMANDIBULAR JOINT
There are three kind of joints:
· Fibrous
Two bones connected with fibrous tissue
Examples
suture (little or no movement)
gomphosis (tooth - PDL - bone)
syndesmosis (fibula & tibia, radius and ulna; interosseous ligament)
· Cartilagenous
Two subtypes:
2a) primary: bone<--->cartilage (costochondral joint)
2b) secondary: bone<-->cartilage<-->FT<-->cartilage<--> bone (pubic symphysis)
· Synovial
Two bones; each articular surface covered with hyaline cartilage in most cases
The bones are united with a capsule (joint cavity)
In the capsule there is presence of synovial fluid
The capsule is lined by a synovial membrane
In many synovial joints there maybe an articular disk
Synovial joints are characterized by the presence of ligaments
Synovial joints are classified according to the number of axes of bone movement: uniaxial, biaxial, multiaxial
the shapes of articulating surfaces: planar, ginglymoid (=hinged), pivot, condyloid
The movement of the joints is controlled by muscles
The temporomandibular joint is a synovial, sliding-ginglymoid joint (humans)
Embryology of the TMJ
Primary TMJ: Meckel's cartilage --> malleus & incal cartilage. It lasts for 4 months.
Secondary TMJ: Starts developing around the third month of gestation
Two blastemas (temporal and condylar); condylar grows toward the temporal (temporal appears and ossifies first)
Formation of two cavities: inferior and upper
Appearance of disk
Bones: glenoid fossa (temporal bone) and condyle (mandible)
Abnormalities of Salt, Water or pH
PhysiologyAbnormalities of Salt, Water or pH
Examples:
Hyperkalemia: caused by kidney disease & medical malpractice
High K+ in blood- can stop the heart in contraction (systole)
Dehydration: walking in desert- can lose 1-2 liters/hour through sweat
Blood becomes too viscous to circulate well -> loss of temperature regulation -> hyperthermia, death
Acidosis: many causes including diabetes mellitus and respiratory problems; can cause coma, death
Glycogen storage diseases (glycogenoses)
General Pathology
Glycogen storage diseases (glycogenoses)
1. Genetic transmission: autosomal recessive.
2. This group of diseases is characterized by a deficiency of a particular enzyme involved in either glycogen production or degradative pathways.
Diseases include:
on Gierke disease (type I)
(a) Deficient enzyme: glucose-6-phosphatase.
(b) Major organ affected by the buildup of glycogen: liver.
Pompe disease (type II)
(1) Deficient enzyme: α-glucosidase(acid maltase).
(2) Major organ affected by the buildup of glycogen: heart.
Cori disease (type III)
(1) Deficient enzyme: debranching enzyme (amylo-1,6-glucosidase).
(2) Organs affected by the buildup of glycogen: varies between the heart, liver, or skeletal muscle.
Brancher glycogenosis (type IV)
(1) Deficient enzyme: branching enzyme.
(2) Organs affected by the buildup of glycogen: liver, heart, skeletal muscle, and brain.
McArdle syndrome (type V)
(1) Deficient enzyme: muscle phosphorylase.
(2) Major organ affected by the buildup of glycogen: skeletal muscle.
Digital X-Ray
PedodonticsDigital X-Ray Systems in Pediatric Dentistry
Digital x-ray systems have revolutionized dental imaging, providing numerous
advantages over traditional film-based radiography. Understanding the technology
behind these systems, particularly in the context of pediatric patients, is
essential for dental professionals.
1. Digital X-Ray Technology
Solid State Detector Technology:
Digital x-ray systems utilize solid-state detector technology,
primarily through Charge-Coupled Devices (CCD) or Complementary
Metal Oxide Semiconductors (CMOS) for image acquisition.
These detectors convert x-ray photons into electronic signals, which
are then processed to create digital images.
2. Challenges with Wired Sensors in Young Children
Tolerability Issues:
Children under 4 or 5 years of age may have difficulty tolerating
wired sensors due to their limited understanding of the procedure.
The presence of electronic wires can lead to:
Fear or anxiety about the procedure.
Physical damage to the cables, as young children may "chew" on
them or pull at them during the imaging process.
Recommendation:
For these reasons, a phosphor-based digital x-ray system may
be more suitable for pediatric patients, as it minimizes the discomfort
and potential for damage associated with wired sensors.
3. Photostimulable Phosphors (PSPs)
Definition:
Photostimulable phosphors (PSPs), also known as storage phosphors,
are used in digital imaging for image acquisition.
Functionality:
Unlike traditional panoramic or cephalometric screen materials, PSPs
do not fluoresce instantly to produce light photons.
Instead, they store incoming x-ray photon information as a latent
image, similar to conventional film-based radiography.
Image Processing:
After exposure, the plates containing the stored image are scanned
by a laser beam in a drum scanner.
The laser excites the phosphor, releasing the stored energy as an
electronic signal.
This signal is then digitized, with various gray levels assigned to
points on the curve to create the final image.
4. Available Phosphor Imaging Systems
Several manufacturers provide phosphor imaging systems suitable for dental
practices:
Soredex: Digora
Air Techniques: Scan X
Gendex: Denoptix
Osteoporosis
General Pathology
Osteoporosis
is characterized by increased porosity of the skeleton resulting from reduced bone mass. The disorder may be localized to a certain bone (s), as in disuse osteoporosis of a limb, or generalized involving the entire skeleton. Generalized osteoporosis may be primary, or secondary
Primary generalized osteoporosis
• Postmenopausal
• Senile
Secondary generalized osteoporosis
A. Endocrine disorders
• Hyperparathyroidism
• Hypo or hyperthyroidism
• Others
B. Neoplasia
• Multiple myeloma
• Carcinomatosis
C. Gastrointestinal disorders
• Malnutrition & malabsorption
• Vit D & C deficiency
• Hepatic insufficiency
D. Drugs
• Corticosteroids
• Anticoagulants
• Chemotherapy
• Alcohol
E. Miscellaneous
• osteogenesis imperfecta
• immobilization
• pulmonary disease
Senile and postmenopausal osteoporosis are the most common forms. In the fourth decade in both sexes, bone resorption begins to overrun bone deposition. Such losses generally occur in areas containing abundant cancelloues bone such as the vertebrae & femoral neck. The postmenopausal state accelerates the rate of loss; that is why females are more susceptible to osteoporosis and its complications.
Gross features
• Because of bone loss, the bony trabeculae are thinner and more widely separated than usual. This leads to obvious porosity of otherwise spongy cancellous bones
Microscopic features
• There is thinning of the trabeculae and widening of Haversian canals.
• The mineral content of the thinned bone is normal, and thus there is no alteration in the ratio of minerals to protein matrix
Etiology & Pathogenesis
• Osteoporosis involves an imbalance of bone formation, bone resorption, & regulation of osteoclast activation. It occurs when the balance tilts in favor of resorption.
• Osteoclasts (as macrophages) bear receptors (called RANK receptors) that when stimulated activate the nuclear factor (NFκB) transcriptional pathway. RANK ligand synthesized by bone stromal cells and osteoblasts activates RANK. RANK activation converts macrophages into bone-crunching osteoclasts and is therefore a major stimulus for bone resorption.
• Osteoprotegerin (OPG) is a receptor secreted by osteoblasts and stromal cells, which can bind RANK ligand and by doing so makes the ligand unavailable to activate RANK, thus limiting osteoclast bone-resorbing activity.
• Dysregulation of RANK, RANK ligand, and OPG interactions seems to be a major contributor in the pathogenesis of osteoporosis. Such dysregulation can occur for a variety of reasons, including aging and estrogen deficiency.
• Influence of age: with increasing age, osteoblasts synthetic activity of bone matrix progressively diminished in the face of fully active osteoclasts.
• The hypoestrogenic effects: the decline in estrogen levels associated with menopause correlates with an annual decline of as much as 2% of cortical bone and 9% of cancellous bone. The hypoestrogenic effects are attributable in part to augmented cytokine production (especially interleukin-1 and TNF). These translate into increased RANK-RANK ligand activity and diminished OPG.
• Physical activity: reduced physical activity increases bone loss. This effect is obvious in an immobilized limb, but also occurs diffusely with decreased physical activity in older individuals.
• Genetic factors: these influence vitamin D receptors efficiency, calcium uptake, or PTH synthesis and responses.
• Calcium nutritional insufficiency: the majority of adolescent girls (but not boys) have insufficient dietary intake of calcium. As a result, they do not achieve the maximal peak bone mass, and are therefore likely to develop clinically significant osteoporosis at an earlier age.
• Secondary causes of osteoporosis: these include prolonged glucocorticoid therapy (increases bone resorption and reduce bone synthesis.)
The clinical outcome of osteoporosis depends on which bones are involved. Thoracic and lumbar vertebral fractures are extremely common, and produce loss of height and various deformities, including kyphoscoliosis that can compromise respiratory function. Pulmonary embolism and pneumonia are common complications of fractures of the femoral neck, pelvis, or spine.
Chloramphenicol
Pharmacology
Chloramphenicol
derived from the bacterium Streptomyces venezuelae
Chloramphenicol is effective against a wide variety of microorganisms, but due to serious side-effects (e.g., damage to the bone marrow, including aplastic anemia) in humans, it is usually reserved for the treatment of serious and life-threatening infections (e.g., typhoid fever). It is used in treatment of cholera, as it destroys the
vibrios and decreases the diarrhoea. It is effective against tetracycline-resistant vibrios.It is also used in eye drops or ointment to treat bacterial conjunctivitis.
Mechanism and Resistance Chloramphenicol stops bacterial growth by binding to the bacterial ribosome (blocking peptidyl transferase) and inhibiting protein synthesis.
Chloramphenicol irreversibly binds to a receptor site on the 50S subunit of the bacterial ribosome, inhibiting peptidyl transferase. This inhibition consequently results in the prevention of amino acid transfer to growing peptide chains, ultimately leading to inhibition of protein formation.
Spectrum of activity: Broad-spectrum
Effect on bacteria: Bacteriostatic
SELECTION OF SPRUE
Dental Materials
SELECTION OF SPRUE
1 . DIAMETER :
It should be approximately the same size of the thickest portion of the wax pattern .
Too small sprue diameter suck back porosity results .
2 . SPRUE FORMER ATTACHMENT :
Sprue should be attached to the thickest portion of the wax pattern .
It should be Flared for high density alloys & Restricted for low density alloys .
3 . SPRUE FORMER POSITION
Based on the
1. Individual judgement .
2. Shape & form of the wax pattern .
Patterns may be sprued directly or indirectly .
Indirect method is commonly used