NEET MDS Synopsis
Alzheimer’s disease
General Pathology
Alzheimer’s disease
a. The most common cause of dementia in older people.
b. Characterized by degeneration of neurons in the cerebral cortex.
c. Histologic findings include amyloid plaques and neurofibrillary tangles.
d. Clinically, the disease takes years to develop and results in the loss of cognition, memory, and the ability to ommunicate. Motor problems, contractures, and paralysis are some of the symptoms at the terminal stage.
Multiphase and Multistage random sampling
Public Health DentistryMultiphase and multistage random sampling are advanced
sampling techniques used in research, particularly in public health and social
sciences, to efficiently gather data from large and complex populations. Both
methods are designed to reduce costs and improve the feasibility of sampling
while maintaining the representativeness of the sample. Here’s a detailed
explanation of each method:
Multiphase Sampling
Description: Multiphase sampling involves conducting a
series of sampling phases, where each phase is used to refine the sample
further. This method is particularly useful when the population is large and
heterogeneous, and researchers want to focus on specific subgroups or
characteristics.
Process:
Initial Sampling: In the first phase, a large sample is
drawn from the entire population using a probability sampling method (e.g.,
simple random sampling or stratified sampling).
Subsequent Sampling: In the second phase, researchers
may apply additional criteria to select a smaller, more specific sample from
the initial sample. This could involve stratifying the sample based on
certain characteristics (e.g., age, health status) or conducting follow-up
surveys.
Data Collection: Data is collected from the final
sample, which is more targeted and relevant to the research question.
Applications:
Public Health Surveys: In a study assessing health
behaviors, researchers might first sample a broad population and then focus
on specific subgroups (e.g., smokers, individuals with chronic diseases) for
more detailed analysis.
Qualitative Research: Multiphase sampling can be used
to identify participants for in-depth interviews after an initial survey has
highlighted specific areas of interest.
Multistage Sampling
Description: Multistage sampling is a complex form of
sampling that involves selecting samples in multiple stages, often using a
combination of probability sampling methods. This technique is particularly
useful for large populations spread over wide geographic areas.
Process:
First Stage: The population is divided into clusters
(e.g., geographic areas, schools, or communities). A random sample of these
clusters is selected.
Second Stage: Within each selected cluster, a further
sampling method is applied to select individuals or smaller units. This
could involve simple random sampling, stratified sampling, or systematic
sampling.
Additional Stages: More stages can be added if
necessary, depending on the complexity of the population and the research
objectives.
Applications:
National Health Surveys: In a national health survey,
researchers might first randomly select states (clusters) and then randomly
select households within those states to gather health data.
Community Health Assessments: Multistage sampling can
be used to assess oral health in a large city by first selecting
neighborhoods and then sampling residents within those neighborhoods.
Key Differences
Structure:
Multiphase Sampling involves multiple phases of
sampling that refine the sample based on specific criteria, often
leading to a more focused subgroup.
Multistage Sampling involves multiple stages of
sampling, often starting with clusters and then selecting individuals
within those clusters.
Purpose:
Multiphase Sampling is typically used to narrow
down a broad sample to a more specific group for detailed study.
Multistage Sampling is used to manage large
populations and geographic diversity, making it easier to collect data
from a representative sample.
Local Anesthetic Toxicity and Dosing Guidelines
Oral and Maxillofacial SurgeryLocal Anesthetic (LA) Toxicity and Dosing Guidelines
Local anesthetics (LAs) are widely used in various medical and dental
procedures to provide pain relief. However, it is essential to understand their
effects on the cardiovascular system, potential toxicity, and appropriate dosing
guidelines to ensure patient safety.
Sensitivity of the Cardiovascular System
The cardiovascular system is generally less sensitive
to local anesthetics compared to the central nervous system (CNS).
However, toxicity can still lead to significant cardiovascular effects.
Effects of Local Anesthetic Toxicity
Mild Toxicity (5-10 μg/ml):
Myocardial Depression: Decreased contractility of
the heart muscle.
Decreased Cardiac Output: Reduced efficiency of the
heart in pumping blood.
Peripheral Vasodilation: Widening of blood vessels,
leading to decreased blood pressure.
Severe Toxicity (Above 10 μg/ml):
Intensification of Effects: The cardiovascular
effects become more pronounced, including:
Massive Vasodilation: Significant drop in blood
pressure.
Reduction in Myocardial Contractility: Further
decrease in the heart's ability to contract effectively.
Severe Bradycardia: Abnormally slow heart rate.
Possible Cardiac Arrest: Life-threatening
condition requiring immediate intervention.
Dosing Guidelines for Local Anesthetics
With Vasoconstrictor:
Maximum Recommended Dose:
7 mg/kg body weight
Should not exceed 500 mg total.
Without Vasoconstrictor:
Maximum Recommended Dose:
4 mg/kg body weight
Should not exceed 300 mg total.
Special Considerations for Dosing
The maximum calculated drug dose should always be decreased in
certain populations to minimize the risk of toxicity:
Medically Compromised Patients: Individuals with
underlying health conditions that may affect drug metabolism or
cardiovascular function.
Debilitated Patients: Those who are physically
weakened or have reduced physiological reserve.
Elderly Persons: Older adults may have altered
pharmacokinetics and increased sensitivity to medications.
Strep viridans
General Pathology
Strep viridans
Mixed species, all causing α-hemolysis. All are protective normal flora which block adherence of other pathogens. Low virulence, but can cause some diseases:
Sub-acute endocarditis can damage heart valves.
Abscesses can form which are necrotizing. This is the primary cause of liver abscesses.
Dental caries are caused by Str. mutans. High virulence due to lactic acid production from glucose fermentation. This is why eating sugar rots teeth. Also have surface enzymes which deposit plaque.
Thrombosis
General Pathology
Thrombosis
Definition-The formation from constituents of the blood, of a mass within the venous or arterial vasculature of a living animal. Natural defense of the body to acute vascular injury.
Pathologic thrombosis includes deep venous thrombosis (DVT), pulmonary embolism (PE), coronary artery thrombosis leading to myocardial infarct and cerebrovascular thrombosis leading to stroke.
Coagulated blood- clots formed
Clot – formation of solid mass of blood components formed outside the vascular tree
Thrombosis with resulting embolic phenomena is important cause of morbidity and mortality.
Haemostatic system allows blood to remain in fluid form under normal conditions and causes the development of temporary thrombus at site of vascular injury.
Components of haemostatic system:
1. Platelets
2. Vascular endothelium
3. Procoagulant plasma protein clotting factors
4. Natural anticoagulants
5. Fibrinolytic proteins
6. Antifibrinolytic proteins
Normal haemostasis:
1. Primary haemostasis-platelet plug formation
2. Secondary haemostasis-stable plug or thrombus
3. Natural anticoagulants-confines thrombus site and size to maintain blood flow
4. Fibrinolysis-degrades fibrin , limits thrombus size and dissolves thrombus once vessel injury is repaired
Changes in any of these factors may result in pathologic thrombosis.
Pathophysiology of thrombosis:
Virchow’s Triad-Thrombosis results from a) decreased blood flow b) vascular endothelial injury and c) alterations in the components of blood.
Vessel wall:
EC (intima), smooth muscle cells (media) and the connective tissue (adventitia).Vascular endothelium is thromboresistant. EC injury leads to TF expression and thrombosis.
Vessel wall has antiplatelet, anticoagulant and fibrinolytic activities which make it thromboresistant.
Antiplatelet activities:
1. Prostacyclin synthesized by EC in response to thrombin. Inhibits platelet adhesion as well as causes vasodilation
2. NO regulates vascular tone as well as functioning as inhibitor of platelet adhesion. Constitutive expression as well as induced expression by EC in response to cytokines
3. Ectozymes which metabolize ADP and ATP to AMP and adenosine. Adenosine inhibits platelet function, ADP is platelet agonist
Anticoagulant activities:
1. Synthesis of heparin like GAG which inactivate activated clotting factors
2. Protein C and S and thrombomodulin-Thrombin generated binds to thrombomodulin which activates protein C which then binds to Protein S and this inhibits coagulation by its proteolytic effect on Factors Va and VIIIa
3. TFPI is synthesized by EC and regulates TF-VIIa activation of Factor X. Also inhibits vascular cell proliferation
Fibrinolytic activities:
1. Secretion and synthesis of plasminogen activators TPA in response to thrombin and vasoactive stimulants such as vasopressin and histamine
2. Synthesis of urokinase in response to inflammatory cytokines
3. FDP’s generated have antiplatelet and antithrombin activity
4. Secretion of PAI
Prothrombotic properties of vascular endothelium promote coagulation with appropriates stimuli.
EC exposure to stimuli such as trauma, cytokines, atherogenic stimuli, endotoxins and immune complexes result in increased TF expression, reduced Protein C activation and reduced fibrinolysis so converting an antithrombotic surface to a prothrombotic surface.
Inherited conditions which result in abnormalities of EC derived or regulated proteins will cause thrombosis.
Arterial thrombosis:
1. Abnormal vessel wall due to atherosclerotic plaque rupture, arterial outflow obstruction, vessel dissection EC injury promote platelet adhesion and activation
2. Release of contents of platelet granules cause recruitment and activation of additional platelets
3. Thromboxane synthesis induces platelet aggregation
4. Thrombin generation due to presence of PL
Platelets are pathogenetically more important in arterial thrombi thus antiplatelet agents are very important in arterial thrombosis management.
Venous thrombosis:
1. Vessel wall is usually normal except if there is direct vessel trauma, extrinsic venous compression or damage due to drugs like chemotherapy
2. Reduction in venous tone is important in pathophysiology
Venous thrombi can be of two types.
A. Phlebo thrombosis
This is thrombus formation in an uninflammed vein usually due to stasis or changes in coagulability of blood. This occurs mostly in deep calf veins and varicose veins in the legs originating near valve pockets. They may propagate to extend to popliteal ,femoral and iliac-veins. These are a common source of massive emboli ‘Phlegmasia alba dolens’ (painful white leg) is a condition seen in late pregnancy and puerperium. In this condition, in addition to iliofemoral thrombosis , there is arterial spasm
B Thrombophlebitis:
In this condition venous wall is inflamed and initiates thrombosis. This is more firmly attached to the vessel wall and also there is much less tendency for propagation Hence there is little chance or embolism.
Cardiac Thrombosis
Intra cardiac thrombus formation can be at 3 sites
• Valvular: as in endocarditis
• Atrial : as in atrial fibrilation ('ball valve thrombus") over MacCallum’s patch is Rheumatic Fever.
• Ventricular mural thrombus over site of MI
Fate of Thrombus
- Resolution : if small, the thrombus is rapidly covered by endothelial cells. Then it can Resolved by a combination of retraction, phgocytosis , platelet autolysis, and fibrinolysis
- Organisation: there is in growth of vascular granulation tissue. This can result in
a. recanalisation
b. collagenisation and-scarring
- Detachment resulting in thromboembolism
Monosaccharides
Biochemistry
Monosaccharides: Aldoses (e.g., glucose) have an aldehyde at one end
They are classified acc to the number of carbon atoms present
Trioses, tetroses, pentose ( ribose, deoxyribose), hexoses (glucose, galactose, fructose) Heptoses (sedoheptulose)
Glyceraldehyde simplest aldose
Ketoses (e.g., fructose) have a keto group, usually at C 2.
Dihydroxyacetone simplest Ketoses
The higher sugar exists in ring form rather than chain form
Furan : 4 carbons and 1 oxygen
Pyrans : 5 carban and 1 oxygen
These result from formation of hemiacital linkage b/w carbonyl and an alcohol group
CASTING
Dental Materials
CASTING
Melting & Casting Technique Melting & Casting requires Heat source to melt the alloy Casting force, to drive the alloy into the mould
Casting Torch Selection Two type of torch tips: Multi-orifice Single-orifice Multi-orifice tip is widely used for metal ceramic alloys. Main advantage is distribution of heat over wide area for uniform heating of the alloy. Single-orifice tip concentrate more heat in one area.Three fuel sources are used for Casting Torch; Acetylene ,Natural Gas ,Propane
CASTING CRUCIBLES
Four types are available ;
1) Clay .
2) Carbon .
3) Quartz .
4) Zirconia –Alumina .
Casting Machines
It is a device which uses heat source to melt the alloy casting force .
Heat sources can be :
1) Reducing flame of a torch .( conventional alloys & metal ceramic alloys )
2) Electricity .(Base metal alloys )
Advantages of electric heating :
-heating is evenly controlled .
-minimal undesirable changes in the alloy composition .
- Appropriate for large labs .
Disadvantage :
Expensive .
Casting machines use :
1) Air pressure .
2) Centrifugal force .
3) Evacuation technique .
Alloys can be melted by :
1) Alloy is melted in a separate crucible by a torch flame & is cast into the mold by centrifugal force .(centrifugal C M )
2) Alloy is melted by resistance heating or by induction furnace & then cast centrifugally by motor or spring action (springwound CM electrical resistance )
3) Alloy is melted by induction heating cast into mold centrifugally by motor or spring action .(Induction CM )
4) Alloy is vacum melted by an argon atmosphere
Torch melting / Centrifugal casting machine
Electrical resistance /Heated casting machine
Melting of the alloy should be done in a graphite or ceramic crucible .
Advantage :
-Oxidation of metal ceramic restorations on
overheating is prevented .
-Help in solidification from tip of the casting to the button surface .
Induction casting machine
Commonly used for melting base metal alloys.
Advantage :
- Highly efficient .
- Compact machine withlow power consumption
-No pre heating needed ,
- safe & reliable.
Direct current arc melting machine
A direct current arc is produced between two electrodes :
The alloy & the water cooled tungsten electrode .Temp used is 4000 degrees .
Disadvanage :
High risk of overheating the alloy .
Vacuum or pressure assisted casting machine
Molten alloy is drawn into the evacuated mold by gravity or vacuum & subjected to aditional pressure
For Titanium & its alloys vacuum heated argon pressure casting machines are used .
Accelerated casting method
This method reduces the time of both bench set of the investment & burnout .
Uses phosphate bonded investments which uses 15 mnts for bench set & 15mnts for burnout by placing in a pre – heated furnace to 815 degrees .
Effect of burnout on gypsum bonded investments
Rate of heating has influence on smoothness & on overall dimensions of the investment
Rapid heating causes cracking & flaking which can cause fins or spines .
Avoid heating gypsum bonded investment above 700 degrees .Complete the wax elimination below that temp .
Effect of burnout on phosphate bonded investments
Usual burnout temp is 750 -1030 degrees.
Although they are strong they are brittle too .
Since the entire process takes a long time two stage burnout & plastic ring can be used .
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.