NEET MDS Synopsis
Pernicious anaemia
General Pathology
Pernicious anaemia
The special features are:
Due to intrinsic factor deficiency
Gastric atrophy with histamine fast achlorhydria
Genetic basis (racial distribution and blood group A).
Seen with auto immune disorders.
Antibodies to parietal cells and to intrinsic factors are seen
Acute suppurative osteomyelitis
Oral Pathology
Acute suppurative osteomyelitis
Serious sequela of periapical infection.
Leads to spread of pus through the medullary cavities of bone.
Depending upon the main site of involvement of bone, can be of two types-
Acute intramedullary
Acute subperiosteal
Acute Intramedullary Osteomyelitis
CLINICAL FEATURES:
Patient experiences dull , continuous pain , indurated swelling forms over the affected region of jaw involving the cheek , febrile.
When mandible involved, loss of sensation occurs on lower lip on affected side due to involvement of inferior alveolar nerve.
Teeth become loose later along with tender on percussion
Pus discharge , trismus , foul smell , regional lymphadenopathy , weakness
RADIOGRAPHIC FEATURES
Earliest radiographic change is that trabeculae in involved area are thin, of poor density & slightly blurred.
Subsequently multiple radiolucencies appear which become apparent on radiograph.
In some cases there is saucer shaped area of destruction with irregular margins.
Loss of continuity of lamina dura, seen in more than one tooth.
HISTOLOGIC FEATURES:
Dense infiltration of marrow by polymorphonuclear leukocytes.
Bone trabeculae in involved site (sequestrum) are devoid of cells in the lacunae.
separation of considerable portions of devitalized bone.
Acute Subperiosteal Osteomyelitis
CLINICAL FEATURES
Pain , febrile condition , i/o and e/o swelling , parasthesia
Bone involvement limited to localized areas of cortex.
Pus ruptures rapidly through the overlying cortex, tracks along the surface of mandible under the periosteal sheath.
Elevation of periosteum from cortex is followed eventually by minute cortical sequestration.
IRON
Biochemistry
IRON
The normal limit for iron consumption is 20 mg/day for adults, 20-30 mg/day for children and 40 mg/day for pregnant women.
Milk is considered as a poor source of iron.
Factors influencing absorption of iron Iron is absorbed by upper part of duodenum and is affected by various factors
(a) Only reduced form of iron (ferrous) is absorbed and ferric form are not absorbed
(b) Ascorbic acid (Vitamin C) increases the absorption of iron (c) The interfering substances such as phytic acid and oxalic acid decreases absorption of iron
Regulation of absorption of Iron
Absorption of iron is regulated by three main mechanisms, which includes
(a) Mucosal Regulation
(b) Storer regulation
(c) Erythropoietic regulation
In mucosal regulation absorption of iron requires DM-1 and ferroportin. Both the proteins are down regulated by hepcidin secreted by liver. The above regulation occurs when the body irons reserves are adequate. When the body iron content gets felled, storer regulation takes place. In storer regulation the mucosal is signaled for increase in iron absorption. The erythropoietic regulation occurs in response to anemia. Here the erythroid cells will signal the mucosa to increase the iron absorption.
Iron transport in blood
The transport form of iron in blood is transferin. Transferin are glycoprotein secreted by liver. In blood, the ceruloplasmin is the ferroxidase which oxidizes ferrous to ferric state.
Storage form of iron is ferritin. Almost no iron is excreted through urine.
Anemia
Anemia is the most common nutritional deficiency disease. The microscopic appearance of anemia is characterized by microcytic hypochromic anemia
The abnormal gene responsible for hemosiderosis is located on the short arm of chromosome No.6.
The main causes of iron deficiency or anemia are
(a) Nutritional deficiency of iron (b) Lack of iron absorption (c) Hook worm infection (d) Repeated pregnancy (e) Chronic blood loss (f) Nephrosis (g) Lead poisoning
Dental Porcelain and PFM Porcelains
Dental Materials
Dental Porcelain and PFM Porcelains
Applications/Use
a. Porcelain inlays and jacket crowns
b. PFM crowns and bridges
c. Denture teeth
Terms
PFM-porcelain fused to metal
Fusing-adherence of porcelain particles into a single porcelain mass
Classification
Dental porcelain is manufactured as a powder. When it is heated to a very high temperature in a special oven, it fuses into a homogeneous mass. The heating process is called baking. Upon cooling, the mass is hard and dense. The material is made in a variety of shades to closely match most tooth colors. Baked porcelain has a translucency similar to that of dental enamel, so that porcelain crowns, pontics, and inlays of highly pleasing appearance can be made. Ingredients of porcelain include feldspar, kaolin, silica in the form of quartz, materials which act as fluxes to lower the fusion point, metallic oxide, and binders. Porcelains are classified into high-, medium-, and low-fusing groups, depending upon the temperature at which fusion takes place.
High-Fusing Porcelains. High-fusing porcelains fuse at 2,400o Fahrenheit or over. They are used for the fabrication of full porcelain crowns (jacket crowns).
Medium-Fusing Porcelains. Medium-fusing porcelains fuse between 2,000o and 2,400o Fahrenheit. They are used in the fabrication of inlays, crowns, facings, and pontics. A pontic is the portion of a fixed partial denture, which replaces a missing tooth.
Low-Fusing Porcelains. Low-fusing porcelains fuse between 1,600o and 2,000o Fahrenheit. They are used primarily to correct or modify the contours of previously baked high- or medium-fusing porcelain restorations. Eg for PFM restorations
Structure
Components
a. Large number of oxides but principally silicon oxide, aluminum oxide. and potassium oxide
b. Oxides are supplied by mixing clay, feldspar, and quartz.
Manipulation
Porcelain powders mixed with water and compacted into position for firing
Shrinkage is 30% on firing because of fusing and so must be made oversized and built up by several firing steps
Properties
1. Physical
a. Excellent electrical and thermal insulation
b. Low coefficient of thermal expansion and contraction
c. Good color and translucency; excellent aesthetics
2. Chemical
a. Not resistant to acids (and can be dissolved by contact with APF topical fluoride treatments)
b. Can be acid-etched with phosphoric acid or hydrofluoric acid for providing microll1echanical retention for cements
3. Mechanical
a. Harder than tooth structure and ,will cause opponent wear
b. Can be polished with aluminum oxide pastes
Hyperparathyroidism
General Pathology
Hyperparathyroidism
Hyperparathyroidism is defined as an elevated secretion of PTH, of which there are three main types:
1. Primary—hypersecretion of PTH by adenoma or hyperplasia of the gland.
2. Secondary—physiological increase in PTH secretions in response to hypocalcaemia of any cause.
3. Tertiary—supervention of an autonomous hypersecreting adenoma in long-standing secondary hyperparathyroidism.
Primary hyperparathyroidism
This is the most common of the parathyroid disorders, with a prevalence of about 1 per 800
It is an important cause of hypercalcaemia.
More than 90% of patients are over 50 years of age and the condition affects females more than males by nearly 3 : 1.
Aetiology
Adenoma 75% -> Orange−brown, well-encapsulated tumour of various size but seldom > 1 cm diameter Tumours are usually solitary, affecting only one of the parathyroids, the others often showing atrophy; they are deep seated and rarely palpable.
Primary hyperplasia 20% -> Diffuse enlargement of all the parathyroid glands
Parathyroid carcinoma 5% -> Usually resembles adenoma but is poorly encapsulated and invasive locally.
Effects of hyperparathyroidism
The clinical effects are the result of hypercalcaemia and bone resorption.
Effects of hypercalcaemia:
- Renal stones due to hypercalcuria.
- Excessive calcification of blood vessels.
- Corneal calcification.
- General muscle weakness and tiredness.
- Exacerbation of hypertension and potential shortening of the QT interval.
- Thirst and polyuria (may be dehydrated due to impaired concentrating ability of kidney).
- Anorexia and constipation
Effects of bone resorption:
- Osteitis fibrosa—increased bone resorption with fibrous replacement in the lacunae.
- ‘Brown tumours’—haemorrhagic and cystic tumour-like areas in the bone, containing large masses of giant osteoclastic cells.
- Osteitis fibrosa cystica (von Recklinghausen disease of bone)—multiple brown tumours combined with osteitis fibrosa.
- Changes may present clinically as bone pain, fracture or deformity.
about 50% of patients with biochemical evidence of primary hyperparathyroidism are asymptomatic.
Investigations are:
- Biochemical—increased PTH and Ca2+ , and decreased PO43- .
- Radiological—90% normal; 10% show evidence of bone resorption, particularly phalangeal erosions.
Management is by rehydration, medical reduction in plasma calcium using bisphosphonates and eventual surgical removal of abnormal parathyroid glands.
Secondary hyperparathyroidism
This is compensatory hyperplasia of the parathyroid glands, occurring in response to diseases of chronic low serum calcium or increased serum phosphate.
Its causes are:
- Chronic renal failure and some renal tubular disorders (most common cause).
- Steatorrhoea and other malabsorption syndromes.
- Osteomalacia and rickets.
- Pregnancy and lactation.
Morphological changes of the parathyroid glands are:
- Hyperplastic enlargement of all parathyroid glands, but to a lesser degree than in primary hyperplasia.
- Increase in ‘water clear’ cells and chief cells of the parathyroid glands, with loss of stromal fat cells.
Clinical manifestations—symptoms of bone resorption are dominant.
Renal osteodystrophy
Skeletal abnormalities, arising as a result of raised PTH secondary to chronic renal disease, are known as renal osteodystrophy.
Pathogenesis
renal Disease + ↓ vit. D activation , ↓ Ca 2+ reabsorption → ↓ serum Ca 2+ → ↑ PTH → ↓ bone absorption
Abnormalities vary widely according to the nature of the renal lesion, its duration and the age of the patient, but include:
- Osteitis fibrosa .
- Rickets or osteomalacia due to reduced activation of vitamin D.
- Osteosclerosis—increased radiodensity of certain bones, particularly the parts of vertebrae adjacent to the intervertebral discs.
The investigations are both biochemical (raised PTH and normal or lowered Ca 2+ ) and radiological (bone changes).
Management is by treatment of the underlying disease and oral calcium supplements to correct hypocalcaemia.
Tertiary hyperparathyroidism
This condition, resulting from chronic overstimulation of the parathyroid glands in renal failure, causes one or more of the glands to become an autonomous hypersecreting adenoma with resultant hypercalcaemia.
Physiologic anatomy of the respiratory system
PhysiologyRespiration occurs in three steps :
1- Mechanical ventilation : inhaling and exhaling of air between lungs and atmosphere.
2- Gas exchange : between pulmonary alveoli and pulmonary capillaries.
3- Transport of gases from the lung to the peripheral tissues , and from the peripheral tissues back to blood .
These steps are well regulated by neural and chemical regulation.
Respiratory tract is subdivided into upper and lower respiratory tract. The upper respiratory tract involves , nose , oropharynx and nasopharynx , while the lower respiratory tract involves larynx , trachea , bronchi ,and lungs .
Nose fulfills three important functions which are :
1. warming of inhaled air .
b. filtration of air .
c. humidification of air .
Pharynx is a muscular tube , which forms a passageway for air and food .During swallowing the epiglottis closes the larynx and the bolus of food falls in the esophagus .
Larynx is a respiratory organ that connects pharynx with trachea . It is composed of many cartilages and muscles and
vocal cords . Its role in respiration is limited to being a conductive passageway for air .
Trachea is a tube composed of C shaped cartilage rings from anterior side, and of muscle (trachealis muscle ) from its posterior side.The rings prevent trachea from collapsing during the inspiration.
From the trachea the bronchi are branched into right and left bronchus ( primary bronchi) , which enter the lung .Then they repeatedly branch into secondary and tertiary bronchi and then into terminal and respiratory broncholes.There are about 23 branching levels from the right and left bronchi to the respiratory bronchioles , the first upper 17 branching are considered as a part of the conductive zones , while the lower 6 are considered to be respiratory zone.
The cartilaginous component decreases gradually from the trachea to the bronchioles . Bronchioles are totally composed of smooth muscles ( no cartilage) . With each branching the diameter of bronchi get smaller , the smallest diameter of respiratory passageways is that of respiratory bronchiole.
Lungs are evolved by pleura . Pleura is composed of two layers : visceral and parietal .
Between the two layers of pleura , there is a pleural cavity , filled with a fluid that decrease the friction between the visceral and parietal pleura.
Respiratory muscles : There are two group of respiratory muscles:
1. Inspiratory muscles : diaphragm and external intercostal muscle ( contract during quiet breathing ) , and accessory inspiratory muscles : scaleni , sternocleidomastoid , internal pectoral muscle , and others( contract during forceful inspiration).
2. Expiratory muscles : internal intercostal muscles , and abdominal muscles ( contract during forceful expiration)
Theories Regarding the Mineralization of Dental Calculus
PeriodontologyTheories Regarding the Mineralization of Dental Calculus
Dental calculus, or tartar, is a hard deposit that forms on teeth due to the
mineralization of dental plaque. Understanding the mechanisms by which plaque
becomes mineralized is essential for dental professionals in managing
periodontal health. The theories regarding the mineralization of calculus can be
categorized into two main mechanisms: mineral precipitation and the role of
seeding agents.
1. Mineral Precipitation
Mineral precipitation involves the local rise in the saturation of calcium
and phosphate ions, leading to the formation of calcium phosphate salts. This
process can occur through several mechanisms:
A. Rise in pH
Mechanism: An increase in the pH of saliva can lead to
the precipitation of calcium phosphate salts by lowering the precipitation
constant.
Causes:
Loss of Carbon Dioxide: Bacterial activity in
dental plaque can lead to the loss of CO2, resulting in an increase in
pH.
Formation of Ammonia: The degradation of proteins
by plaque bacteria can produce ammonia, further elevating the pH.
B. Colloidal Proteins
Mechanism: Colloidal proteins in saliva bind calcium
and phosphate ions, maintaining a supersaturated solution with respect to
calcium phosphate salts.
Process:
When saliva stagnates, these colloids can settle out, disrupting the
supersaturated state and leading to the precipitation of calcium
phosphate salts.
C. Enzymatic Activity
Phosphatase:
This enzyme, released from dental plaque, desquamated epithelial
cells, or bacteria, hydrolyzes organic phosphates in saliva, increasing
the concentration of free phosphate ions and promoting mineralization.
Esterase:
Present in cocci, filamentous organisms, leukocytes, macrophages,
and desquamated epithelial cells, esterase can hydrolyze fatty esters
into free fatty acids.
These fatty acids can form soaps with calcium and magnesium, which
are subsequently converted into less-soluble calcium phosphate salts,
facilitating calcification.
2. Seeding Agents and Heterogeneous Nucleation
The second theory posits that seeding agents induce small foci of
calcification that enlarge and coalesce to form a calcified mass. This concept
is often referred to as the epitactic concept or heterogeneous
nucleation.
A. Role of Seeding Agents
Unknown Agents: The specific seeding agents involved in
calculus formation are not fully understood, but it is believed that the
intercellular matrix of plaque plays a significant role.
Carbohydrate-Protein Complexes:
These complexes may initiate calcification by chelating calcium from
saliva and binding it to form nuclei that promote the deposition of
minerals.
Clinical Implications
Understanding Calculus Formation:
Knowledge of the mechanisms behind calculus mineralization can help
dental professionals develop effective strategies for preventing and
managing calculus formation.
Preventive Measures:
Maintaining good oral hygiene practices can help reduce plaque
accumulation and the conditions that favor mineralization, such as
stagnation of saliva and elevated pH.
Treatment Approaches:
Understanding the role of enzymes and proteins in calculus formation
may lead to the development of therapeutic agents that inhibit
mineralization or promote the dissolution of existing calculus.
Research Directions:
Further research into the specific seeding agents and the
biochemical processes involved in calculus formation may provide new
insights into preventing and treating periodontal disease.
COMPOSITE RESINS
Dental Materials
COMPOSITE RESINS
Applications / Use
Anterior restorations for aesthetics (class III, IV, V, cervical erosion abrasion lesions)
Low-stress posterior restorations (small class I, II)
Veneers
Cores for cast restorations
Cements for porcelain restorations
Cements for acid-etched Maryland bridges
Repair systems for composites or porcelains
Polymerization--reaction of small molecules (monomers) into very large molecules (polymers)
Cross-linking-tying together of polymer molecules by chemical reaction between the molecules to produce a continuous three-dimensional network