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NEET MDS Synopsis

Wedging Techniques
Conservative Dentistry

Wedging Techniques
Various wedging methods are employed to achieve optimal results,
especially in cases involving gingival recession or wide proximal boxes. Below
are descriptions of different wedging techniques, including "piggy back"
wedging, double wedging, and wedge wedging.

1. Piggy Back Wedging
A. Description

Technique: In piggy back wedging, a second smaller
wedge is placed on top of the first wedge.
Indication: This technique is particularly useful
in patients with gingival recession, where there is a risk of overhanging
restoration margins that could irritate the gingiva.

B. Purpose

Prevention of Gingival Overhang: The additional
wedge helps to ensure that the restoration does not extend beyond the tooth
surface into the gingival area, thereby preventing potential irritation and
maintaining periodontal health.


2. Double Wedging
A. Description

Technique: In double wedging, wedges are placed
from both the lingual and facial surfaces of the tooth.
Indication: This method is beneficial in cases
where the proximal box is wide, providing better adaptation of the matrix
band and ensuring a tighter seal.

B. Purpose

Enhanced Stability: By using wedges from both
sides, the matrix band is held securely in place, reducing the risk of
material leakage and improving the overall quality of the restoration.


3. Wedge Wedging
A. Description

Technique: In wedge wedging, a second wedge is
inserted between the first wedge and the matrix band, particularly in
specific anatomical situations.
Indication: This technique is commonly used in the
maxillary first premolar, where a mesial concavity may complicate the
placement of the matrix band.

B. Purpose

Improved Adaptation: The additional wedge helps to
fill the space created by the mesial concavity, ensuring that the matrix
band conforms closely to the tooth surface and providing a better seal for
the restorative material.

Classification
Pharmacology

Classification

1. Natural Alkaloids of Opium

Phenanthrenes -> morphine, codeine, thebaine

Benzylisoquinolines -> papaverine, noscapine

2. Semi-synthetic Derivatives

diacetylmorphine (heroin) hydromorphone, oxymorphone hydrocodone, oxycodone

3. Synthetic Derivatives

phenylpiperidines pethidine, fentanyl, alfentanyl, sufentnyl

benzmorphans pentazocine, phenazocine, cyclazocine

propionanilides methadone

morphinans levorphanol

The Walls of the Orbit
Anatomy

The Walls of the Orbit


Each orbit has four walls: superior (roof), medial, inferior (floor) and lateral.
The medial walls of the orbit are almost parallel with each other and with the superior part of the nasal cavities separating them.
The lateral walls are approximately at right angles to each other

Fermentation  
Biochemistry

Anaerobic organisms lack a respiratory chain. They must reoxidize NADH produced in Glycolysis through some other reaction, because NAD+ is needed for the Glyceraldehyde-3-phosphate Dehydrogenase reaction (see above). Usually NADH is reoxidized as pyruvate is converted to a more reduced compound, that may be excreted.

The complete pathway, including Glycolysis and the re-oxidation of NADH, is called fermentation.

For example, Lactate Dehydrogenase catalyzes reduction of the keto group in pyruvate to a hydroxyl, yielding lactate, as NADH is oxidized to NAD+.

Skeletal muscles ferment glucose to lactate during exercise, when aerobic metabolism cannot keep up with energy needs. Lactate released to the blood may be taken up by other tissues, or by muscle after exercise, and converted via the reversible Lactate Dehydrogenase back to pyruvate

Fermentation Pathway, from glucose to lactate (omitting H+):

   glucose + 2 ADP + 2 Pi → 2 lactate + 2 ATP

Anaerobic catabolism of glucose yields only 2 “high energy” bonds of ATP.

NITRIC OXIDE-DEPENDENT KILLING
General Microbiology

NITRIC OXIDE-DEPENDENT KILLING
Binding of bacteria to macrophages, particularly binding via Toll-like
receptors, results in the production of TNF-alpha, which acts in an autocrine
manner to induce the expression of the inducible nitric oxide synthetase gene (i-nos
) resulting in the production of nitric oxide (NO) . If the cell is also exposed
to interferon gamma (IFN-gamma) additional nitric oxide will be produced (figure
12). Nitric oxide released by the cell is toxic and can kill microorganism in
the vicinity of the macrophage.

Hyperpituitarism 
General Pathology

Hyperpituitarism 

Causes  
A. Pituitary; usually anterior lobe

1. Adenoma (the most common cause)
2. Hyperplasia  
3. Carcinoma  

B. Extra-pituitary causes 
1. Hormone producing extra-pituitary tumors (ectopic hormone production)
2. Certain hypothalamic disorders 

Pituitary adenomas are classified according to the hormone(s) produced by the neoplastic cells; these are detected by immunohistochemically-stained tissue sections. Pituitary adenomas can be functional (associated with hormone excess with their related clinical manifestations) or silent. 

Pathogenesis
Guanine nucleotide-binding protein (G-protein) mutations are the best characterized molecular abnormalities. Such mutations eventuate in a persistent increase in intracellular cAMP, which is a potent mitogenic stimulus promoting cellular proliferation and hormone synthesis and secretion. In the setting of MEN-1 syndrome there are mutations in the MEN-1 (menin) gene. 

Gross features

• Adenomas are usually soft & well-circumscribed   
• Larger lesions extend superiorly through the sellar diaphragm compressing the optic chiasm and adjacent structures .  
• Invasive adenomas refer to nonencapsulated tumors that infiltrate adjacent bone, dura, and even brain.

Microscopic features.  

• Adenomas are composed of monomorphic, polygonal cells displayed in sheets, cords, or papillae. Their nuclei may be uniform or pleomorphic but the mitotic activity is scanty. The cytoplasm of the constituent cells may be acidophilic, basophilic, or chromophobic. 
• The connective tissue is scanty that is why many lesions are soft & even gelatinous in consistency.  

Prolactinomas are the most common type of hyperfunctioning pituitary adenoma.
Hyperprolactinemia causes amenorrhea, galactorrhea, loss of libido, and infertility. 

Growth Hormone-Producing Adenomas (somatotroph cell adenomas) are the second most common type of functional pituitary adenoma. Because the clinical manifestations of excessive growth hormone may be subtle, the tumor may be quite large by the time they come to clinical attention. If such tumors occur before closure of epiphyses (prepubertal children), excessive levels of growth hormone result in gigantism. If elevated levels persist, or present after closure of the epiphyses, individuals develop acromegaly. 

Corticotroph Cell Adenomas are mostly small (microadenomas) at the time of diagnosis. They may be clinically silent or cause hypercortisolism referred to as Cushing disease 

Other Anterior Pituitary Neoplasms 
• Gonadotroph adenomas (luteinizing hormone [LH]-producing and follicle-stimulating hormone [FSH]producing)
• Thyrotroph (thyroid-stimulating hormone [TSH]-producing) adenomas 
• Nonfunctioning pituitary adenomas (hormone-negative (null cell) adenomas) Nonfunctioning adenomas constitute approximately 25% of all pituitary tumors; they typically present through their mass effects. 

ATROPHY
General Pathology

ATROPHY
It is the acquired decrease in the size of an organ due to decrease in the size and/or number of its constituent cells.
Causes:
(1) Physiological

- Foetal involution.
    o    Branchial clefts.
    o    Ductus arterious.
- Involution of thymus and other lymphoid organs in childhood and adolescence.
- In adults:
    o    Post-partum uterus.
    o    Post-menopausal ovaries and uterus
    o    Post-lactational breast
    o    Thymus.
(2) Pathological:
- Generalised as in

    o    Ageing.
    o    Severe starvation and cachexia
- Localised :
    o    Disuse atropy of bone and muscle.
    o    Ischaemic atrophy as in arteriosclerotic kidney. .
    o    Pressure atrophy due  to tumours and of kidney in hydronephrosis.
    o    Lack of trophic stimulus to endocrines and gonads.
 

Beta - Adrenergic Blocking Agents
Pharmacology

 Beta - Adrenergic Blocking Agents 
 
 Mechanisms of Action  
 
- Initial decrease in cardiac output, followed by reduction in peripheral vascular resistance. 
- Other actions include decrease plasma renin activity, resetting of baroreceptors,  release of vasodilator prostaglandins, and blockade of prejunctional beta-receptors.  

Advantages 

- Documented reduction in cardiovascular morbidity and mortality. 
- Cardioprotection: primary and secondary prevention against coronary artery events (i.e. ischemia, infarction, arrhythmias, death). 
- Relatively not expensive. 

Considerations 

- Beta blockers are used with caution in patients with bronchospasm. 
- Contraindicated in more than grade I AV, heart block. 
- Do not discontinue abruptly. 

 Side Effects
- Bronchospasm and obstructive airway disease. 
- Bradycardia  
- Metabolic effects (raise triglyerides levels and decrease HDL cholesterol; may worsen insulin sensitivity and cause glucose intolerance). Increased incidence of diabetes mellitus.  
- Coldness of extremities.  
- Fatigue. 
- Mask symptoms of hypoglycemia. 
- Impotence. 

Indications 

- First line treatment for hypertension as an alternative to diuretics. 
- Hypertension associated with coronary artery disease.
- Hyperkinetic circulation and high cardiac output hypertension (e.g., young hypertensives). 
- Hypertension associated with supraventricular tachycardia, migraine, essential tremors, or hypertrophic cardiomyopathy. 

Beta adrenergic blocker Drugs

Atenolol 25-100
Metoprolol 50-200 
Bisoprolol 2.5-10 

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