NEET MDS Synopsis
Ether (diethylether)
Pharmacology
Ether (diethylether)
Ether (diethylether) MAC 2.0%, Blood/gas solubility ratio 15
- Ether is generally mixed with 3% ethanol to retard oxidation. Peroxides form on exposure to air and can enhance the danger of an explosion.
- Slow rate of induction and recovery due to its high blood/gas solubility ratio.
- Produces profound muscular relaxation.
- Both the rate and the minute volume of ventilation tend to be elevated during the inhalation of ether.
- Ether maintains good circulatory stability and does not sensitize the heart to the arrhythmogenic action of catecholamines.
- More than 90% of the absorbed ether can be recovered unchanged in the expired air. Metabolism is not extensive and the metabolites are not hepatotoxic.
- Ether is a versatile anesthetic of unexcelled safety, but it is flammable and irritating to breathe. Secretions can be blocked with anticholinergics.
Drugs Used in Diabetes -Insulin
Pharmacology
Insulin
Insulin is only given parenterally (subcutaneous or IV) Various preparations have different durations of action
Preparation
Onset (hrs)
Peak (hrs)
Duration (hrs)
Lispro (rapid-acting)
15 min
0.5-1.5
3-4
Regular (short-acting)
0.5-1
2-4
5-7
NPH (intermediate)
1-2
6-12
18-24
Glargine (long-acting)
1
None
>24
Mechanism
bind transmembrane insulin receptor
activate tyrosine kinase
phosphorylate specific substrates in each tissue type
liver
↑ glycogenesis
store glucose as glycogen
muscle
↑ glycogen and protein synthesis
↑ K+ uptake
fat
increase triglyceride storage
Clinical use
type I DM
type II DM
life-threatening hyperkalemia
increases intracellular K+
stress-induced hyperglycemia
Toxicity
hypoglycemia
hypersensitivity reaction (very rare)
Insulin Synthesis
first generated as preproinsulin with an A chain and B chain connected by a C peptide.
c-peptide is cleaved from proinsulin after packaging into vesicles leaving behind the A and B chains
Bacteria Classification
General Microbiology
Classification:
Neutrophiles (pH = 7.0)
- P. aeruginosaqo
- Clostridium sporogenes
- Proteus species
Acidophiles (pH < 7.0)
- Thiobacillus thiooxidans
- Sulfollobus acidocaldaarius
- Bacillus acidocaldarius
Alkaliphiles (pH > 7.0)
- Nitrobacter species
- Streptococcus pneumoniae
Emergency conditions in Dental Clinics p2
Oral Medicine
Emergency conditions in Dental Clinics
Hypoadrenalism - Usually the patient is known to have Addison's disease or to be taking steroids long term and has forgotten to take the tablets.
Signs and symptoms
• Pallor
• Confusion
• Rapid weak pulse.
Treatment:
Give oxygen
Give 200 mg hydrocortisone sodium succinate by slow i.v. injection.
Give steroid replacement
Determining and managing underlying cause once the crisis over.
If required:
• Transfer to Emergeny hostpital
• Fluids and further hydrocortisone, both i.v.
Acute asthma - Exposure to antigen but precipitated by many factors including anxiety.
Signs and symptoms
• Persistent shortness of breath poorly relieved by bronchodilators
• Restlessness and exhaustion
• Tachycardia greater than 110 beats/min and low peak expiratory flow
• Respirations may be so shallow in severe cases that wheezing is absent.
Treatment
Excluded respiratory obstruction
Sit the patient up
Give oxygen
Salbutamol (Ventolin) via a nebuliser (2.5-5 mg of 1 mg/ml nebuliser solution) or via a large-volume spacer (two puffs of a metered dose inhaler 10-20 times: one puff every 30 seconds up to 10 puffs for a child)
Reassure and allow home if recovered.
• Bronchodilatation.
If Major Problem recommend to hospital Emergeny
• Hydrocortisone sodium succinate i.v.: adults 200 mg; child 100 mg
• Add ipratropium 0.5 mg to nebulised salbutamol
• Aminophylline slow i.v. injection of 250 mg in 10 ml over at least 20 minutes: monitor or keep finger on pulse during injection.
Caution in epilepsy: rapid injection of aminophylline may cause arrhythmias and convulsions.
Caution in patients already receiving theophylline: arrhythmias or convulsions may occur.
Anaphylactic shock
Signs and symptoms
• Paraesthesia, flushing and swelling of face, especially eyelids and lips (Fig. 13)
• generalised urticaria, especially hands and feet
• wheezing and difficulty in breathing
• rapid weak pulse.
These may develop over 15 to 30 minutes following the oral administration of a drug or rapidly over a few minutes following i.v. drug administration.
Treatment
Lay patient flat and raise feet
Give oxygen
Give 0.5 ml epinephrine (adrenaline) 1 mg/ml (1 in
1000) intramuscular
— 0.25 ml for 6-12 years
— 0.12 ml for 6 months to 6 years
repeated every 10 min until improvement.
Requires prompt energetic treatment of
• laryngeal oedema
• bronchospasm
• hypotension.
• Chlorphenamine (chlorpheniramine) 10 mg in 1 ml intramuscular or slow i.v. injection
• Hydrocortisone sodium succinate 200 mg by slow i.v. injection: valuable as action persists after that of adrenaline has worn off
• Fluids i.v. (colloids) infused rapidly if shock not responding quickly to adrenaline.
Stroke - Stroke results from either cerebral haemorrhage or cerebral ischaemia.
Signs and symptoms
• Confusion followed by signs and symptoms of focal brain damage
• Hemiplegia or quadriplegia
• Sensory loss
• Dysphasia
• Locked-in syndrome (aware, but unable to respond).
Treatment
Maintain and transfer for further investigation.
Benzodiazepine overdose - Overdose can result from a large or a fast dose of benzodiazepine or can occur in a sensitive patient.
Signs and symptoms
• Deeply sedated
• Severe respiratory depression.
Treatment
Flumazenil (Annexate) 200 mg over 15 seconds as 100 mg/ml i.v. followed by 100 mg every 1 minute up to maximum of 1 mg Maintain airway with head tilt/chin lift
Give oxygen.
Treatment
The action of the benzodiazepine is reversed with the specific antagonist.
Angina and myocardial infarction
Signs and symptoms
• Sudden onset of severe crushing pain across front of chest, which may radiate towards the shoulder and down the left arm or into the neck and jaw; pain from angina usually radiates down left arm
Skin pale and clammy
Shallow respirations
Nausea
Weak pulse and hypotension
If the pain not relieved by glyceryl trinitrate (GTN) then cause is myocardial infarction rather than angina.
First-line treatment of angina and myocardial infarction
Allow patient to rest in position that feels most comfortable:
• in presence of breathlessness this is likely to be the sitting position, whereas syncopal patients will want to lie flat
• often an intermediate position will be most appropriate.
Angina -
Angina results from reduced coronary artery lumen diameter because of atheromatous plaques
Myocardial infarction is usually the result of thrombosis in a coronary artery.
Angina is relieved by rest and nitrates:
• Glyceryl trinitrate spray 400 mg metered dose (sprayed on oral mucosa or under tongue and mouth then closed)
• Give oxygen
• Allow home if attack is mild and the patient recovers rapidly.
Myocardial infarction
If a myocardial infarction is suspected:
• give oxygen
• aspirin tablet 300 mg chewed.
• Pain control
• Vasodilatation of blood vessels to reduce load on heart.
Further management for severe angina or myocardial infarction
• Transfer to Emergency
• Diamorphine 5 mg (2.5 mg in older people) by slow i.v. injection (1 mg/min)
• Early thrombolytic therapy reduces mortality.
Cardiac arrest
• Most cardiac arrests result from arrhythmias associated with acute myocardial infarction or chronic ischaemic heart disease
• The heart arrests in one of three rhythms
— VF (ventricular fibrillation) or pulseless VT (ventricular tachycardia)
— asystole
— PEA (pulseless electrical activity) or EMD (electromechanical dissociation).
Signs and symptoms
• Unconscious
• No breathing
• Absent carotid pulse.
Treatment
• Circulation failure for 4 minutes, or less if the patient is already hypoxaemic, will lead to irreversible brain damage
• Institute early basic life support as holding procedure until early advanced life support is available.
• Transfer to Emergency
• Advanced life support.
Advanced life support for cardiac arrest
Advanced airway management techniques and specific treatment of the underlying cause of cardiac arrest constitute advanced life support (ALS).
Factors to Design a Spring for Appliances
OrthodonticsFactors to Consider in Designing a Spring for Orthodontic Appliances
In orthodontics, the design of springs is critical for achieving effective
tooth movement while ensuring patient comfort. Several factors must be
considered when designing a spring to optimize its performance and
functionality. Below, we will discuss these factors in detail.
1. Diameter of Wire
Flexibility: The diameter of the wire used in the
spring significantly influences its flexibility. A thinner wire will yield a
more flexible spring, allowing for greater movement and adaptability.
Force Delivery: The relationship between wire diameter
and force delivery is crucial. A thicker wire will produce a stiffer spring,
which may be necessary for certain applications but can limit flexibility.
2. Force Delivered by the Spring
Formula: The force (F) delivered by a spring can be
expressed by the formula: [ $$F \propto \frac{d^4}{l^3} $$] Where:
( F ) = force applied by the spring
( d ) = diameter of the wire
( l ) = length of the wire
Implications: This formula indicates that the force
exerted by the spring is directly proportional to the fourth power of the
diameter of the wire and inversely proportional to the cube of the length of
the wire. Therefore, small changes in wire diameter can lead to significant
changes in force delivery.
3. Length of Wire
Flexibility and Force: Increasing the length of the
wire decreases the force exerted by the spring. Longer springs are generally
more flexible and can remain active for extended periods.
Force Reduction: By doubling the length of the wire,
the force can be reduced by a factor of eight. This principle is essential
when designing springs for specific tooth movements that require gentler
forces.
4. Patient Comfort
Design Considerations: The design, shape, size, and
force generation of the spring must prioritize patient comfort. A
well-designed spring should not cause discomfort or irritation to the oral
tissues.
Customization: Springs may need to be customized to fit
the individual patient's anatomy and treatment needs, ensuring that they are
comfortable during use.
5. Direction of Tooth Movement
Point of Contact: The direction of tooth movement is
determined by the point of contact between the spring and the tooth. Proper
placement of the spring is essential for achieving the desired movement.
Placement Considerations:
Palatally Placed Springs: These are used for labial
(toward the lips) and mesio-distal (toward the midline) tooth movements.
Buccally Placed Springs: These are employed when
the tooth needs to be moved palatally and in a mesio-distal direction.
Classification
Pharmacology
Classification Based on
a. Chemical structure
I. Sulphonamidcs.and others - c.g.. sulphadiazine. etc.
2. Beta-lactum ring - e.g.. penicillin
3. Tetracycline - e.g.. Oxytetracycline,.doxycycline.etc.
b. Mechanism of action
1. Inhibits cell-wall synthesis - penicillin. cephalosporin..cycloserine. etc.
2. Cause leakage from cell-membrane – polypeptides (polymyxin, Bacitracin), polyenes (Nystatin)
3. Inhibit protein synthesis - tetracyclines. chloramphenicols. erythromycin.
4. Cause mis-reading of mRNA code - aminoglycosides
5. Interfere with DNA function - refampicin.. metronidazole
6. Interfere with intermediary metabolism - sulphonamides. ethambutole
c. Type of organism against which it is primarily activate
I. Antibacterial - penicillin.
2. Antifungal - nystatin.
d. Spectrum of activity
1. Broad spectrum - tetracylines .
2. Narrow spectrum - penicillin G (penG). streptomycin.erythromycin
e. Type of action
I. Bacteriostatic - sulphonamides, erythromycin.tertracyclines
2. Bacteriocidal - penicillin. aminoglycoside
f. Source
I. Fungi - penicillin. cephalosporins
2. Bacteria - Polymyxin B
Beta - Adrenoceptor blocking Agents
Pharmacology
Beta - Adrenoceptor blocking Agents
These are the agents which block the action of sympathetic nerve stimulation and circulating sympathomimetic amines on the beta adrenergic receptors.
At the cellular level, they inhibit the activity of the membrane cAMP. The main effect is to reduce cardiac activity by diminishing β1 receptor stimulation in the heart. This decreases the rate and force of myocardial contraction of the heart, and decreases the rate of conduction of impulses through the conduction system.
Beta blockers may further be classified on basis of their site of action into following two main classes namely
cardioselective beta blockers (selective beta 1 blockers)
non selective beta 1 + beta 2 blockers
Classification for beta adrenergic blocking agents.
A. Non-selective (β1+β2)
Propranolol Sotalol Nadolol Timolol Alprenolol Pindolol
With additional alpha blocking activity
Labetalol Carvedilol
B. β1 Selective (cardioselective)
Metoprolol Atenolol Bisoprolol Celiprolol
C. β2 Selective
Butoxamine
Mechanisms of Action of beta blocker
Beta adrenoceptor Blockers competitively antagonize the responses to catecholamines that are mediated by beta-receptors and other
adrenomimetics at β-receptors
Because the β-receptors of the heart are primarily of the β1 type and those in the pulmonary and vascular smooth muscle are β2 receptors, β1-selective antagonists are frequently referred to as cardioselective blockers.
β-adrenergic receptor blockers (β blockers)
1. Used more often than α blockers.
2. Some are partial agonists (have intrinsic sympathomimetic activity).
3. Propranolol is the prototype of nonselective β blockers.
4. β blocker effects: lower blood pressure, reduce angina, reduce risk after myocardial infarction, reduce heart rate and force, have antiarrhythmic effect, cause hypoglycemia in diabetics, lower intraocular pressure.
5. Carvedilol: a nonselective β blocker that also blocks α receptors; used for heart failure.
Cori Cycle
Biochemistry
Cori Cycle
The Cori Cycle operates during exercise, when aerobic metabolism in muscle cannot keep up with energy needs.
For a brief burst of ATP utilization, muscle cells utilize ~P stored as phosphocreatine. For more extended exercise, ATP is mainly provided by Glycolysis.
Lactate, produced from pyruvate, passes via the blood to the liver where it is converted to glucose. The glucose may travel back to the muscle to fuel Glycolysis.
The Cori Cycle costs 6 P in liver for every 2P made available in muscle. The net cost is 4 P Although costly in terms of "high energy" bonds, the Cori Cycle allows the organism to accommodate to large fluctuations in energy needs of skeletal muscle between rest and exercise.