NEET MDS Synopsis
Maxillary First Deciduous Molar
Dental Anatomy
Maxillary First Deciduous Molar.
-The notation is B or I.
-It looks a bit like an upper 1st premolar.
-There are three roots.
-It has a strong bulbous enamel bulge that protrudes buccally at the mesial.
-It is the smallest of the deciduous molars in crown height and in the mesiodistal dimension.
Graves disease
General Pathology
Graves disease
Graves disease is an organ-specific autoimmune disorder that results in thyrotoxicosis due to overstimulation of the thyroid gland by autoantibodies.
- It is the most common form of thyrotoxicosis, females being affected more than males by 8: 1.
- It is usually associated with a diffuse enlargement of the thyroid.
Pathogenesis
IgG-type immunoglobulins bind to TSH membrane receptors and cause prolonged stimulation of the thyroid, lasting for as long as 12 hours
(cf. 1 hour for TSH). The autoantibody binds at a site different to the hormone-binding locus and is termed the TSH-receptor autoantibody (TRAb); 95% of Graves’ disease patients are positive for TRAbs
Gross features
- The thyroid gland is diffusely and moderately enlarged
- It is usually smooth, soft, and congested
Histologically
- the gland shows diffuse hypertrophy and hyperplasia of acinar epithelium, reduction of stored colloid and local accumulations of lymphocytes with lymphoid follicle formation.
Clinical features
- Exophthalmos (protrusion of the eyeballs in their sockets)—due to the infiltration of orbital tissues by fat, mucopolysaccharides and lymphocytes. May cause compression of the optic nerve, hence blindness. However, only about 5% of Graves’ patients show signs of exophthalmos.
- Thyroid acropachy—enlargement of fingernails.
- Pretibial myxoedema—accumulation of mucoproteins in the deep dermis of the skin.
Treatment is as for thyrotoxicosis.
Pharmacology NEET MDS MCQ Discussion Part 1
NEET MDS
COMPOSITE RESINS -Pit-and-Fissure Dental Sealants
Dental Materials
Pit-and-Fissure Dental Sealants
Applications/Use
Occlusal surfaces of newly erupted posterior teeth
Labial surfaces of anterior teeth with fissures
Occlusal surfaces of teeth in older patients with reduced saliva flow (because low saliva increases the susceptibility to caries)
Types
Polymerization method
Self-curing (amine accelerated)
Light curing (light accelerated)
Filler content
Unfilled-most systems are unfilled because filler tends to interfere with wear away from self-cleaning occlusal areas(sealants are designed to wear away, except where there is no self-cleaning action a common misconception is that sealants should be wear resistant)
Components
Monomer-BIS-GMA with TEGDM diluent to facilitate flow into pits and fissures prior to cure
Initiator-benzoyl peroxide (in self-cured) and diketone (in light cured)
Accelerator-amine (In light cured)
Opaque filler-I % titanium dioxide. or other colorant to make the material detectable on tooth surfaces
Reinforcing filler-generally not added because wear resistance is not required within pits and fissures
Reaction-free radical reaction
Manipulation
Preparation
Clean pits and fissures of organic debris. Do not apply fluoride before etching because it will tend to make enamel more acid resistant. Etch occlusal surfaces, pits, and fissures for 30 seconds (gel) or 60 seconds (liquid) with 37% phosphoric acid . Wash occlusal surfaces for 20 seconds. Dry etched area for 20 seconds with clean air spray. Apply sealant and polymerize
Mixing or dispensing
Self-cured-mix equal amounts of liquids in Dappen dish for 5 seconds with brush applicator. Light cured-dispense from syringe tips
Placement
-pits, fissures, and occlusal surfaces --> Allow 60 seconds for self-cured materials to set.
Finishing
Remove unpolymerized and excess material .Examine hardness of sealant. Make occlusal adjustments where necessary in sealant; some sealant materials are self-adjusting
Properties
Physical
Wetting-low-viscosity sealants wet acid etched tooth structure the best
Mechanical
Wear resistance should not be too great because sealant should be able to wear off of self-cleaning areas of tooth
Be careful to protect sealants during polishing procedures with air abrading units to prevent sealant loss
Clinical efficacy
Effectiveness is 100% if retained in pits and fissures .Requires routine clinical evaluation for resealing of areas of sealant loss attributable to poor retention .
Sealants resist effects of topical fluorides
Azithromycin
Pharmacology
Azithromycin
Azithromycin is the first macrolide antibiotic belonging to the azalide group. Azithromycin is derived from erythromycin by adding a nitrogen atom into the lactone ring of erythromycin A, thus making lactone ring 15-membered.
Azithromycin has similar antimicrobial spectrum as erythromycin, but is more effective against certain gram-negative bacteria, particularly Hemophilus influenzae.
azithromycin is acid-stable and can therefore be taken orally without being protected from gastric acids.
Main elimination route is through excretion in to the biliary fluid, and some can also be eliminated through urinary excretion
Endodontics Root Canal Anatomy -MDS Lecture
Endodontics
Classification of Local anesthetics
Pharmacology
Classification
I) Esters
1. Formed from an aromatic acid and an amino alcohol.
2. Examples of ester type local anesthetics:
Procaine
Chloroprocaine
Tetracaine
Cocaine
Benzocaine- topical applications only
2) Amides
1. Formed from an aromatic amine and an amino acid.
2. Examples of amide type local anesthetics:
Articaine
Mepivacaine
Bupivacaine
Prilocaine
Etidocaine
Ropivacaine
Lidocaine
EMBOLISM
General Pathology
EMBOLISM
An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin
99% due to dislodged thrombus
Types:
1. Thrombo-embolism
2. Fat embolism
3. Air embolism
4. Nitrogen embolism
Emboli result in partial or complete vascular occlusion.
The consequences of thromboembolism include ischemic necrosis (infarction) of downstream tissue
PULMONARY THROMBOEMBOLISM
- 95% originate from deep veins of L.L
Special variants: - Saddle embolus: at bifurcation of Pulmonary artery
Paradoxical embolus: Passage of an embolus from venous to systemic circulation through IAD, IVD
CLINICAL CONSEQUENCE OF PULMONARY THROMBOEMBOLISM :
Most pulmonary emboli (60% to 80%) are clinically silent because they are small
a. Organization: 60 – 80 %
b. Sudden death, Right ventricle failure, CV collapse when more than 60 % of pulmonary vessels are obstructed.
c. Pulmonary hemorrhage: obstruction of medium sized arteries.
d. Pulmonary Hypertension and right ventricular failure due to multiple emboli over a long time.
Systemic thromboembolism
Emboli traveling within the arterial circulation
80% due to intracardiac mural thrombi
2/3 Lt. ventricular failure
The major targets are:
1. Lower limbs 75%
2. Brain 10%
3. Intestines
4. Kidneys
5. Spleen
Fat embolism
Causes
1. Skeletal injury (fractures of long bones )
2. Adipose tissue Injury
Mechanical obstruction is exacerbated by free fatty acid release from the fat globules, causing local toxic injury to endothelium. - In skeletal injury, fat embolism occurs in 90% of cases, but only 10% or less have clinical findings
Fat embolism syndrome is characterized by
A. Pulmonary Insufficiency
B. Neurologic symptoms
C. Anemia
D. Thrombocytopenia
E. Death in 10% of the case
Symptoms appears 1-3 days after injury
Tachypnea, Dyspnea, Tachycardia and Neurological symptoms
Air Embolism
causes: 1. Obstetric procedures
2. Chest wall injury
3. Decompression sickness: in Scuba and deep-sea divers ((nitrogen ))
More then 100ml of air is required to produce clinical effect.
Clinical consequence
1. Painful joints: due to rapid formation of gas bubbles within Sk. Muscles and supporting tissues.
2. Focal ischemia in brain and heart
3. Lung edema, Hemorrhage, atelectasis, emphysema, which all lead to Respiratory distress. (chokes)
4. caisson disease: gas emboli in the bones leads to multiple foci of ischemic necrosis, usually the heads of the femurs, tibias, and humeri
Amniotic fluid embolism
- Mortality Rate = 20%-40%
- Very rare complication of labor
- due to infusion of amniotic fluid into maternal circulation via tears in placental membranes and rupture of uterine veins.
- sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures, DIC and coma
- Findings: Squamous cells, languo hair, fat, mucin …..etc within the pulmonary microcirculation