NEET MDS Synopsis
Aminoglycoside
Pharmacology
Aminoglycoside
Aminoglycosides are a group of antibiotics that are effective against certain types of bacteria. They include amikacin, gentamicin, kanamycin, neomycin, netilmicin, paromomycin, streptomycin, and tobramycin. Those which are derived from Streptomyces species
Aminoglycosides work by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth.
Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. Streptomycin was the first effective drug in the treatment of tuberculosis, though the role of aminoglycosides such as streptomycin and amikacin have been eclipsed (because of their toxicity and inconvenient route of administration) except for multiple drug resistant strains.
Infections caused by Gram-positive bacteria can also be treated with aminoglycosides, but other types of antibiotics are more potent and less damaging to the host. In the past the aminoglycosides have been used in conjunction with penicillin-related antibiotics in streptococcal infections for their synergistic effects, particularly in endocarditis.
Because of their potential for ototoxicity and renal toxicity, aminoglycosides are administered in doses based on body weight. Blood drug levels and creatinine are monitored during the course of therapy.
There is no oral form of these antibiotics: they are generally administered intravenously, though some are used in topical preparations used on wounds.
Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses.
Blastomycosis (North American Blastomycosis; Gilchrist's Disease)
General Pathology
Blastomycosis (North American Blastomycosis; Gilchrist's Disease)
A disease caused by inhalation of mold conidia (spores) of Blastomyces dermatitidis, which convert to yeasts and invade the lungs, occasionally spreading hematogenously to the skin or focal sites in other tissues.
Pulmonary blastomycosis tends to occur as individual cases of progressive infection
Symptoms are nonspecific and may include a productive or dry hacking cough, chest pain, dyspnea, fever, chills, and drenching sweats. Pleural effusion occurs occasionally. Some patients have rapidly progressive infections, and adult respiratory distress syndrome may develop.
CLASSIFICATION OF LIPIDS
Biochemistry
CLASSIFICATION OF LIPIDS
Lipids are classified as follows:
1. Simple lipids: Esters of fatty acids with various alcohols.
(a) Fats: Esters of fatty acids with glycerol. Oils are fats in the liquid state. A long-chain carboxylic acid; those in animal fats and vegetable oils often have 12–22 carbon atoms.
(b) Waxes: Esters of fatty acids with higher molecular weight monohydric alcohols. Waxes are carboxylic acid esters, RCOOR’ ,with long, straight hydrocarbon chains in both R groups
2. Complex lipids: Esters of fatty acids containing groups in addition to an alcohol and a fatty acid.
(a) Phospholipids: Lipids containing, in addition to fatty acids and an alcohol, a phosphoric acid residue. They frequently have nitrogen containing bases and other substituents,
Eg glycerophospholipids the alcohol is glycerol
sphingophospholipids the alcohol is sphingosine.
(b) Glycolipids (glycosphingolipids): Lipids containing a fatty acid, sphingosine, and carbohydrate. These lipids contain a fatty acid, carbohydrate and nitrogenous base. The alcohol is sphingosine, hence they are also called as glycosphingolipids. Clycerol and phosphate are absent
e.g., cerebrosides, gangliosides.
(c) Other complex lipids: Lipids such as sulfolipids and aminolipids. Lipoproteins may also be placed in this category.
3. Precursor and derived lipids: These include fatty acids, glycerol, steroids, other alcohols, fatty aldehydes, and ketone bodies, hydrocarbons, lipid soluble vitamins, and hormones. Because they are uncharged, acylglycerols (glycerides), cholesterol, and cholesteryl esters are termed neutral lipids
4. Miscellaneous lipids: These include a large number of compounds possessing the characteristics of lipids e.g., carotenoids, squalene, hydrocarbons such as pentacosane (in bees wax), terpenes etc.
NEUTRAL LIPIDS: The lipids which are uncharged are referred to as neutral lipids. These are mono-, di-, and triacylglycerols, cholesterol and cholesteryl esters.
BONES OF THE SKULL
Orthodontics
BONES OF THE SKULL
A) Bones of the cranial base:
A) Fontal (1)
B) Ethmoid (1)
C) Sphenoid (1)
D) Occipital (1)
B) Bones of the cranial vault:
1. Parietal (2)
2. Temporal (2)
C) Bones of the face:
Maxilla (2)
Mandible (1)
Nasal bone (2)
Lacrimal bone (2)
Zygomatic bone (2)
Palatine bone(2)
Infra nasal concha (2)
FUSION BETWEEN BONES
1. Syndesmosis: Membranous or ligamentus eg. Sutural point.
2. Synostosis: Bony union eg. symphysis menti.
3. Synchondrosis: Cartilaginous eg. sphenoccipital, spheno-ethmoidal.
GROWTH OF THE SKULL:
A) Cranium: 1. Base 2. Vault
B) Face: 1. Upper face 2.Lower face
CRANIAL BASE:
Cranial base grows at different cartilaginous suture. The cranial base may be divided into 3 areas.
1. The posterior part which extends from the occiput to the salatercica. The most important growth site spheno-occipital synchondrosis is situated here. It is active throughout the growing period and does not close until early adult life.
2. The middle portion extends from sella to foramen cecum and the sutural growth spheno-ethmoidal synchondrosis is situated here. The exact time of closing is not known but probably at the age of 7 years.
3. The anterior part is from foramen cecum and grows by surface deposition of bone in the frontal region and simultaneous development of frontal sinus.
CRANIAL VAULT:
The cranial vault grows as the brain grows. It is accelerated at infant. The growth is complete by 90% by the end of 5th year. At birth the sutures are wide sufficiently and become approximated during the 1st 2 years of life.
The development and extension of frontal sinus takes place particularly at the age of puberty and there is deposition of bone on the surfaces of cranial bone.
PULP
Dental Anatomy
PULP
Coronal
Occupies and resembles the crown,
Contains the pulp horns
It decreases in size with age
Radicular
Occupies roots
Contains the apical foramen
It decreases in size with age
Accessory apical canals
PULP FUNCTIONS
Inductive: The pulp anlage initiates tooth formation and probably induces the dental organ to become a particular type of tooth.
Formative: Pulp odontoblasts develop the organic matrix and function in its calcification.
Nutritive: Nourishment of dentin through the odontoblasts.
Protective: Sensory nerves in the tooth respond almost always with PAIN to all stimuli (heat, cold, pressure, operative procedures, chamical agents).
Defensive or reparative: It responds to irritation by producing reparative dentin. The response to stimuli is inflammation.
Histologically the pulp consists of delicate collagen fibers, blood vessels, lymphatics, nerves and cells. A histologic section of the pulp reveals four cellular zones:
Odontoblastic
Cell-free (Weil)
Cell-rich
Pulp core
Organic Nitrates
Pharmacology
Organic Nitrates
Relax smooth muscle in blood vessel
Produces vasodilatation
– Decreases venous pressure and venous return to the heart Which decreases the cardiac work load and oxygen demand.
– May have little effect on the coronary arteries CAD causes stiffening and lack of
– responsiveness in the coronary arteries
– Dilate arterioles, lowering peripheral vascular resistance Reducing the cardiac workload
Main effect related to drop in blood pressure by
– Vasodilation- pools blood in veins and capillaries, decreasing the volume of blood that the heart has to pump around (the preload)
– relaxation of the vessels which decreases the resistance the heart has to pump against (the afterload)
Indications
- Myocardial ischemia
– Prevention
– Treatment
Nitroglycerin (Nitro-Bid)
• Used
– To relive acute angina pectoris
– Prevent exercise induced angina
– Decrease frequency and severity of acute anginal episodes
Type
• Oral - rapidly metabolized in the liver only small amount reaches circulation
• Sublingual – Transmucosal tablets and sprays
• Transdermal – Ointment s
– Adhesive discs applied to the skin
• IV preparations
Sublingual Nitroglycerine
• Absorbed directly into the systemic circulation, Acts within 1-3 minutes , Lasts 30-60 min
Topical Nitroglycerine
• Absorbed directly into systemic circulation, Absorption at a slower rate. , Longer duration of action
Ointment - effective for 4-8 hours
Transdermal disc - effective for 18-24 hours
Isosorbide dinitrate
• Reduces frequency and severity of acute anginal episodes
• Sublingual or chewable acts in 2 min. effects last 2-3 hours
• Orally, systemic effects in about 30 minutes and last about 4 hours after oral administration
Tolerance to Long-Acting Nitrates
• Long-acting dosage forms of nitrates may develop tolerance
– Result in episodes of chest pain
– Short acting nitrates less effective
Prevention of Tolerance
• Use long-acting forms for approximately 12-16 hours daily during active periods and omit them during inactive periods or sleep
• Oral or topical should be given every 6 hours X 3 doses allowing a rest period of 6 hours
Isosorbide dinitrate (Isordil, Sorbitrate) is used to reduce the frequency and severity of acute anginal episodes.
When given sublingually or in chewable tablets, it acts in about 2 minutes, and its effects last 2 to 3 hours. When higher doses are given orally, more drug escapes metabolism in the liver and produces systemic effects in approximately 30 minutes. Therapeutic effects last about 4 hours after oral administration
Isosorbide mononitrate (Ismo, Imdur) is the metabolite and active component of isosorbide dinitrate. It is well absorbed after oral administration and almost 100% bioavailable. Unlike other oral nitrates, this drug is not subject to first-pass hepatic metabolism. Onset of action occurs within 1 hour, peak effects occur between 1 and 4 hours, and the elimination half-life is approximately 5 hours. It is used only for prophylaxis of angina; it does not act rapidly enough to relieve acute attacks.
Oral Surgery NEET MDS Discussion part 1
NEET MDS
Amino Acid Catabolism
Biochemistry
Amino Acid Catabolism
Glutamine/Glutamate and Asparagine/Aspartate Catabolism
Glutaminase is an important kidney tubule enzyme involved in converting glutamine (from liver and from other tissue) to glutamate and NH3+, with the NH3+ being excreted in the urine. Glutaminase activity is present in many other tissues as well, although its activity is not nearly as prominent as in the kidney. The glutamate produced from glutamine is converted to a-ketoglutarate, making glutamine a glucogenic amino acid.
Asparaginase is also widely distributed within the body, where it converts asparagine into ammonia and aspartate. Aspartate transaminates to oxaloacetate, which follows the gluconeogenic pathway to glucose.
Glutamate and aspartate are important in collecting and eliminating amino nitrogen via glutamine synthetase and the urea cycle, respectively. The catabolic path of the carbon skeletons involves simple 1-step aminotransferase reactions that directly produce net quantities of a TCA cycle intermediate. The glutamate dehydrogenase reaction operating in the direction of a-ketoglutarate production provides a second avenue leading from glutamate to gluconeogenesis.
Alanine Catabolism
Alanine is also important in intertissue nitrogen transport as part of the glucose-alanine cycle. Alanine's catabolic pathway involves a simple aminotransferase reaction that directly produces pyruvate. Generally pyruvate produced by this pathway will result in the formation of oxaloacetate, although when the energy charge of a cell is low the pyruvate will be oxidized to CO2 and H2O via the PDH complex and the TCA cycle. This makes alanine a glucogenic amino acid.
Arginine, Ornithine and Proline Catabolism
The catabolism of arginine begins within the context of the urea cycle. It is hydrolyzed to urea and ornithine by arginase.
Ornithine, in excess of urea cycle needs, is transaminated to form glutamate semialdehyde. Glutamate semialdehyde can serve as the precursor for proline biosynthesis as described above or it can be converted to glutamate.
Proline catabolism is a reversal of its synthesis process.
The glutamate semialdehyde generated from ornithine and proline catabolism is oxidized to glutamate by an ATP-independent glutamate semialdehyde dehydrogenase. The glutamate can then be converted to α-ketoglutarate in a transamination reaction. Thus arginine, ornithine and proline, are glucogenic.
Methionine Catabolism
The principal fates of the essential amino acid methionine are incorporation into polypeptide chains, and use in the production of α -ketobutyrate and cysteine via SAM as described above. The transulfuration reactions that produce cysteine from homocysteine and serine also produce α -ketobutyrate, the latter being converted to succinyl-CoA.
Regulation of the methionine metabolic pathway is based on the availability of methionine and cysteine
Phenylalanine and Tyrosine Catabolism
Phenylalanine normally has only two fates: incorporation into polypeptide chains, and production of tyrosine via the tetrahydrobiopterin-requiring phenylalanine hydroxylase. Thus, phenylalanine catabolism always follows the pathway of tyrosine catabolism. The main pathway for tyrosine degradation involves conversion to fumarate and acetoacetate, allowing phenylalanine and tyrosine to be classified as both glucogenic and ketogenic.
Tyrosine is equally important for protein biosynthesis as well as an intermediate in the biosynthesis of several physiologically important metabolites e.g. dopamine, norepinephrine and epinephrine