Oxytocin is a hormone, predominately belonging to mammalian family; it is secreted by the posterior pituitary gland. After its release in the blood stream it cannot re-enter the brain due to the presence of blood brain barrier .Oxytocin is a hormone that has both peripheral and central actions. y are synthesized in the magnocellular neurons present in the supra–optic and Para –ventricular nucleus present in the hypothalamus. The universally known functions would include its role at the time of labour and ejection of milk. The functions which remain partially unknown are in erectile responses, ejaculation, bonding, and feeling of love and maintenance of eye contact during a conversation.
Functions and roles of Oxytocin:
Oxytocin plays a key role in establishing trust , falling in love , parturition , milk ejection, mother – child bond , erection and ejaculatory response in males. Oxytocin insuffiency is leads to increased stress and sleep disturbances. The solution to the above mentioned problem lies in creating a drug which can mimic the functional properties of Oxytocin, which was achieved. Oxytocin has been widely used in the field of gynaecology to induce labour. It is also administered to patients i.e. mothers who are unable to produce milk after parturition. The invention of Oxytocin nasal sprays is not unknown. Recommended doses when administered to autism patients are proven to increase the sense of trust at the time of communication.
Mechanism of OXYTOCIN
Oxytocin is a naturally occurring nonapeptide hormone which acts through a G-protein coupled cell surface receptor to stimulate contractions of the uterus. A synthetic version of this hormone is used to induce contractions of the uterus which are indistinguishable from spontaneous labour.
Oxytocin is administered as a slow intravenous infusion (to induce or augment labour), or as a single intramuscular or intravenous injection to help prevent and treat uterine atony and postpartum haemorrhage. In pregnant women, oxytocin is metabolised very quickly in the maternal circulation by an aminopeptidase enzyme which cleaves the protein leaving it without biological function. This oxytocinase activity is also seen within the placenta and uterine tissue, and activity increases throughout pregnancy where at term the half -life of oxytocin is between 2 and 20 minutes.
The main side effects are related to overstimulation of the uterus which can compromise the placental blood supply and fetal well-being, and can also contribute to rupture of the uterus especially in women who have had a previous caesarean delivery. Oxytocin is similar in structure to Vasopressin which is also produced by the posterior pituitary, and prolonged administration with intravenous fluids may lead to fluid overload, pulmonary oedema and water intoxication.
Oxytocin Molecular Formula
It has a molecular formula of C43H66N12O12S 2.
Oxytocin is also known as Pitocin, Syntocinon, Ocytocin, Endopituitrina, Oxitocina, Oxytocine, Oxytocinum, Oxytocic hormone and Orasthin.
It has a molecular formula of C43H66N12O12S 2. They are commercially available as intravenous and intramuscular injections , nasal sprays and sublingual tablets .The commonly used Anirudha kabilan /J. Pharm. Sci. & Res. Vol. 6(4), 2014, 220-223 221 drug types are pitocin and syntocinon, the chemical resemblance to Oxytocin makes them an ideal drug of choice for various cases for example at time if parturition . Pitocin is composed of oxtocic acid/ml along with chlorobutanol , a chloroform derivative. However medical supervision is mandatory to rule out the onset of complications (20,31). The general uses of these Oxytocin drugs would include induction of labour .Under appropriate level , at the time delivery, Oxytocin binds to the receptors present in the myometrium , activates the pathway of hydrolysis of phoshotidyl inositol and diacyl glycerol, there by activating the same. This activation causes the release of intracellular Ca+ which causes contraction of the uterus .In conditions associated with low level of Oxytocin production this process is carried out by Oxytocin drugs (29, 27) Incase of people suffering from autism, administration of pitocin is said to reduce repetitive behaviour and also enhances speech. Few researches have proved the improvement of trust in people affected by autism when they were given pitocin nasal sprays. It also enhances eye to eye contact in these individuals. Pitcoin helps in social interaction in people who suffer from schizophrenia . So pitocin may not only combat hallucinogens and psychosis, but also make human interaction easier . Being a new field if research there is not enough evidence to prove the role pitocin in both autism and schizophrenia. Further, they are also used to cure problems in erectile responses, ejaculation, depression, anxiety, and stress management
Dosage of Oxytocin:
10 units by intravenous route or 20-40 mUnit/min by Intramuscular route are injected for post partum haemorrhage. 0.5-1 mUnit/min by intravenous route for the induction of labour.10-20 mUnit/min is administered along with other drugs for termination of pregnancy.
Uterine contractions are seen after 3-5 minutes and approx 1 minute of aministration through intramuscular and intravenous routes respectively. A steady state of the drug is reached after 40 mins of parenteral route of administration. It is distributed throughout extracellular fluid compartment of the mother; small amounts may cross the placental barrier and reach foetus. Metabolism takes place rapidly via the liver and plasma by the enzyme oxytocinase a few steps of metabolism also takes place via mammary gland. It has a half-life of 1-5 minute. Kidney and liver help in the elimination of Oxytocin drugs( 9) unchanged form of this drug is rarely excreted in urine (30). Overdose can cause titanic uterine contractions, impaired blood flow to the uterus, uterine ruptures, seizures and amniotic fluid embolism contractions, impaired blood flow to the uterus, uterine ruptures, seizures and amniotic fluid embolism.
Significant cephalopelvic disproportion Unfavourable foetal positions Obstetric emergencies which favours surgery Hyperactive or hypertonic uterus When vaginal delivery is contraindicated, Anaphylactic patients, Foetal distress Polyhydramnios Partial placenta pervia Elective labour induction
Nausea or vomiting Memory problems or confusion Runny nose, sore throat, or coughing severe headaches hallucinations vomiting confusion Seizures and severe hypertension
Clinical Scenario 1
Which of the following abnormalities of labor is associated with a significantly increased incidence of neonatal morbidity? a. Prolonged latent phase b. Protracted descent c. Secondary arrest of dilation d. Protracted active-phase dilation Answer: c (Secondary arrest of dilation) Explanation: Three significant advances in the treatment of uterine dysfunction have reduced the risk of perinatal morbidity (PNM) and mortality: (1) the avoidance of undue prolongation of labor, (2) the use of intravenous oxytocin in the treatment of some patterns of uterine dysfunction, and (3) the liberal use of cesarean section (rather than midforceps) to affect delivery when oxytocin fails.
Clinical Scenario 2
Management of obstructed labor includes all, except: [AIIMS May 2004] a. IV fluids b. Oxytocin use c. Antibiotics d. Cesarean section Answer: b (Oxytocin use) Explanation: Two main principles in management of obstructed labor are: 1. Never wait and watch. 2. Never use oxytocin. In patients of obstructed labor, the uterine contractions (power) are always adequate. There is a problem with the passage or the passenger. By increasing the power (by giving oxytocin) we are increasing the risk of rupture uterus. It is like flogging a dead horse. Uterus is already contracting, and there is no point in increasing the contractions further in a case of obstructed labor. The patient should be given IV fluids to correct the dehydration and ketoacidosis, which usually develops due to prolonged labor. Patient should be given antibiotics to prevent infection, and then steps should be taken to immediately relieve the obstruction either by instrumental deliver or by LSCS. LSCS may have to be done even if the baby is dead and if vaginal delivery is not possible, or else rupture uterus will occur. NOTE: In cases of prolonged labor where there are hypotonic uterine contractions, oxytocin is justified.
Today Pharmawiki is here with very important 40+ Pharmacology multiple choice questions along with answers. These are published especially for all our pharmacy students who are ready to take up different competitive exams like NEET PG GPAT PHARMACIST qualifying examinations. These questions are also very helpful to all the students and professionals of Nursing to take up different examinations for their career growth. This article specifically provides questions with answers pdf Book at the end for our readers convenience. You can click on the right side and download the entire copy to study easily.
Pharmacology MCQ for Anti Cancer Chemotherapy Drugs
ANTIVIRAL AGENTS. AGENTS FOR CHEMOTHERAPY OF CANCER
All of the following antiviral drugs are the analogs of nucleosides, EXCEPT:
Tick the drug, a derivative of adamantane:
Tick the drug, a derivative of pyrophosphate:
Tick the drug, inhibiting viral DNA synthesis:
Tick the drug, inhibiting uncoating of the viral RNA:
Tick the drug, inhibiting viral reverse transcriptase:
Tick the drug, inhibiting viral proteases:
Tick the drug of choice for herpes and cytomegalovirus infection treatment:
b) Interferon alfa
Tick the drug which belongs to nonnucleoside reverse transcriptase inhibitors:
All of the following antiviral drugs are antiretroviral agents, EXCEPT:
Tick the drug used for influenza A prevention:
Tick the drug used for HIV infection treatment, a derivative of nucleosides:
Tick the antiviral drug which belongs to endogenous proteins:
c) Interferon alfa
Tick the drug which belongs to nucleoside reverse transcriptase inhibitors:
All of the following antiviral drugs are anti-influenza agents, EXCEPT:
Tick the unwanted effects of zidovudine:
a) Hallucinations, dizziness
b) Anemia, neutropenia, nausea, insomnia
c) Hypertension, vomiting
d) Peripheral neuropathy
Tick the unwanted effects of intravenous acyclovir infusion:
a) Renal insufficiency, tremors, delerium
b) Rash, diarrhea, nausea
c) Neuropathy, abdominal pain
d) Anemia, neutropenia, nausea, insomnia
Tick the drug that can induce peripheral neuropathy and oral ulceration:
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Pharmacodynamics. We exactly know what pharmacodynamics is. It involves how the drugs act on target cells to alter cellular function. Let us discuss Dose Response relationship in this article. The exact relationship between the dose and the response depends on the biological object under observation and the drug employed is called Dose Response relationship.
Dose Response relationship
When a logarithm of dose as abscissa and responses as ordinate are constructed graphically, the “S” shaped or sigmoid type curve is obtained. The lowest concentration of a drug that elicits a response is minimal dose, and the largest concentration after which further increase in concentration will not change the response is the maximal dose.
1. Graded dose effect:
As the dose administered to a single subject or tissue increases, the pharmacological response also increases in graded fashion up to ceiling effect. – It is used for characterization of the action of drugs. The concentration that is required to produce 50 % of the maximum effect is termed as EC50 or ED50.
2. Quantal dose effect:
It is all or none response, the sensitive objects give response to small doses of a drug while some will be resistant and need very large doses. The quantal dose effect curve is often characterized by stating the median effective dose and the median lethal dose.
Median lethal dose or LD50:
This is the dose (mg/kg), which would be expected to kill one half of a population of the same species and strain.
Median effective dose or ED50:
This is the dose (mg/kg), which produces a desired response in 50 per cent of test population.
It is an approximate assessment of the safety of the drug. It is the ratio of the median lethal dose and the median effective dose. Also called as therapeutic window or safety. Herapeutic index (T. I) = The larger the therapeutic index, the safer is the drug.
Penicillin has a very high therapeutic index, while it is much smaller for the digitalis preparation.
D. Structural activity relationship The activity of a drug is intimately related to its chemical structure. Knowledge about the chemical structure of a drug is useful for: (i) Synthesis of new compounds with more specific actions and fewer adverse reactions (ii) Synthesis of competitive antagonist and (iii) Understanding the mechanism of drug action. Slight modification of structure of the compound can change the effect completely.
ROUTES OF DRUG ADMINISTRATION: The possible routes for drug entry into the body. Most drugs can be administered by a variety of routes. The choice of appropriate route in a given situation depends both on drug as well as patient related factors. Mostly common sense considerations, feasibility and convenience dictate the route to be used. Generally routes of drug administration refer to the right path or the required route through which a drug has to be administered into the body to obtain maximum benefit. Here is the list of 5, 10+ outes of drug administration.
Subcutaneous (under the skin)
Intramuscular (in a muscle)
Intravenous (in a vein)
Intrathecal (around the spinal cord
Factors governing choice of route
Physical and chemical properties of the drug (solid/ liquid/gas; solubility, stability, pH, irritancy).
Site of desired action—localized and approachable or generalized and not approachable.
Rate and extent of absorption of the drug from different routes.
Effect of digestive juices and first pass metabolism on the drug.
Rapidity with which the response is desired (routine treatment or emergency).
Accuracy of dosage required (i.v. and inhalational can provide fine tuning).
Condition of the patient (unconscious, vomiting).
Routes of Administration can be broadly divided into those for
(a) Local action and (b) Systemic action.
These routes can only be used for localized lesions at accessible sites and for drugs whose systemic absorption from these sites is minimal or absent. Thus, high concentrations are attained at the desired site without exposing the rest of the body. Systemic side effects or toxicity are consequently absent or minimal. For drugs (in suitable dosage forms) that are absorbed from these sites/routes, the same can serve as systemic route of administration, e.g. glyceryl trinitrate (GTN) applied on the skin as ointment or transdermal patch. The local routes are:
This refers to external application of the drug to the surface for localized action. It is often more convenient as well as encouraging to the patient. Drugs can be efficiently delivered to the localized lesions on skin, oropharyngeal/ nasal mucosa, eyes, ear canal, anal canal or vagina in the form of lotion, ointment, cream, powder, rinse, paints, drops, spray, lozengens, suppositories or pesseries. Nonabsorbable drugs given orally for action on g.i. mucosa (sucralfate, vancomycin), inhalation of drugs for action on bronchi (salbutamol, cromolyn sodium) and irrigating solutions/jellys (povidone iodine, lidocaine) applied to urethra are other forms of topical medication.
Certain deep areas can be approached by using a syringe and needle, but the drug should be in such a form that systemic absorption is slow, e.g. intra-articular injection (hydrocortisone acetate in knee joint), infiltration around a nerve or intrathecal injection (lidocaine), retrobulbar injection (hydrocortisone acetate behind the eyeball).
Close intra-arterial injection is used for contrast media in angiography; anticancer drugs can be infused in femoral or brachial artery to localise the effect for limb malignancies.
The drug administered through systemic routes is intended to be absorbed into the blood streamand distributed all over, including the site of action, through circulation
Oral ingestion is the oldest and commonest mode of drug administration. It is safer, more convenient, does not need assistance, noninvasive, often painless, the medicament need not be sterile and so is cheaper. Both solid dosage forms (powders, tablets, capsules, spansules, dragees, moulded tablets, gastrointestinal therapeutic systems— GITs) and liquid dosage forms (elixirs, syrups, emulsions, mixtures) can be given orally.
Limitations of oral route of administration
Action of drugs is slower and thus not suitable for emergencies.
Unpalatable drugs (chloramphenicol) are difficult to administer; drug may be filled in capsules to circumvent this.
May cause nausea and vomiting (emetine).
Cannot be used for uncooperative/unconscious/ vomiting patient.
Absorption of drugs may be variable and erratic; certain drugs are not absorbed (streptomycin).
Others are destroyed by digestive juices (penicillin G, insulin) or in liver (GTN, testosterone, lidocaine).
Sublingual (s.l.) or buccal
The tablet or pellet containing the drug is placed under the tongue or crushed in the mouth and spread over the buccal mucosa. Only lipid soluble and non-irritating drugs can be so administered. Absorption is relatively rapid—action can be produced in minutes. Though it is somewhat inconvenient, one can spit the drug after the desired effect has been obtained. The chief advantage is that liver is bypassed and drugs with high first pass metabolism can be absorbed directly into systemic circulation. Drugs given sublingually are—GTN, buprenorphine, desamino-oxytocin.
Certain irritant and unpleasant drugs can be put into rectum as suppositories or retention enema for systemic effect. This route can also be used when the patient is having recurrent vomiting or is unconscious. However, it is rather inconvenient and embarrassing; absorption is slower, irregular and often unpredictable, though diazepam solution and paracetamol suppository are rapidly and dependably absorbed from the rectum in children. Drug absorbed into external haemorrhoidal veins (about 50%) bypasses liver, but not that absorbed into internal haemorrhoidal veins. Rectal inflammation can result from irritant drugs. Diazepam, indomethacin, paracetamol, ergotamine and few other drugs are some times given rectally.
Highly lipid soluble drugs can be applied over the skin for slow and prolonged absorption. The liver is also bypassed. The drug can be incorporated in an ointment and applied over specified area of skin. Absorption of the drug can be enhanced by rubbing the preparation, by using an oily base and by an occlusive dressing.
Transdermal therapeutic systems (TTS)
These are devices in the form of adhesive patches of various shapes and sizes (5–20 cm2) which deliver the contained drug at a constant rate into systemic circulation via the stratum corneum (Fig. 1.2). The drug (in solution or bound to a polymer) is held in a reservoir between an occlusive backing film and a rate controlling micropore membrane, the under surface of which is smeared with an adhesive impregnated with priming dose of the drug. The adhesive layer is protected by another film that is to be peeled off just before application. The drug is delivered at the skin surface by diffusion for percutaneous absorption into circulation. The micropore membrane is such that rate of drug delivery to skin surface is less than the slowest rate of absorption from the skin. This offsets any variation in the rate of absorption according to the properties of different sites. As such, the drug is delivered at a constant and predictable rate irrespective of site of application. Usually chest, abdomen, upper arm, lower back, buttock or mastoid region are utilized. Transdermal patches of GTN, fentanyl, nicotine and estradiol are available in India, while those of isosorbide dinitrate, hyoscine, and clonidine are marketed elsewhere. For different drugs, TTS have been designed to last for 1–3 days. Though more expensive, they provide smooth plasma concentrations of the drug without fluctuations; minimize interindividual variations (drug is subjected to little first pass metabolism) and side effects. They are also more convenient— many patients prefer transdermal patches to oral tablets of the same drug; patient compliance is better. Local irritation and erythema occurs in some, but is generally mild; can be minimized by changing the site of application each time by rotation. Discontinuation has been necessary in 2–7% cases.
Volatile liquids and gases are given by inhalation for systemic action, e.g. general anaesthetics. Absorption takes place from the vast surface of alveoli—action is very rapid. When administration is discontinued the drug diffuses back and is rapidly eliminated in expired air. Thus, controlled administration is possible with moment to moment adjustment. Irritant vapours (ether) cause inflammation of respiratory tract and increase secretion.
The mucous membrane of the nose can readily absorb many drugs; digestive juices and liver are bypassed. However, only certain drugs like GnRH agonists and desmopressin applied as a spray or nebulized solution have been used by this route. This route is being tried for some other peptide drugs like insulin, as well as to bypass the bloodbrain barrier.
Conventionally, parenteral refers to administration by injection which takes the drug directly into the tissue fluid or blood without having to cross the enteral mucosa. The limitations of oral administration are circumvented. Drug action is faster and surer (valuable in emergencies). Gastric irritation and vomiting are not provoked. Parenteral routes can be employed even in unconscious, uncooperative or vomiting patient. There are no chances of interference by food or digestive juices. Liver is bypassed. Disadvantages of parenteral routes are—the preparation has to be sterilized and is costlier, the technique is invasive and painful, assistance of another person is mostly needed (though self injection is possible, e.g. insulin by diabetics), there are chances of local tissue injury and, in general, parenteral route is more risky than oral.
The important parenteral routes are:
(i) Subcutaneous (s.c.)
The drug is deposited in the loose subcutaneous tissue which is richly supplied by nerves (irritant drugs cannot be injected) but is less vascular (absorption is slower than intramuscular). Only small volumes can be injected s.c. Self-injection is possible because deep penetration is not needed. This route should be avoided in shock patients who are vasoconstricted— absorption will be delayed. Repository (depot) preparations that are aqueous suspensions can be injected for prolonged action. Some special forms of this route are:
In this method needle is not used; a high velocity jet of drug solution is projected from a microfine orifice using a gun like implement. The solution passes through the superficial layers and gets deposited in the subcutaneous tissue. It is essentially painless and suited for mass inoculations.
(b) Pellet implantation
The drug in the form of a solid pellet is introduced with a trochar and cannula. This provides sustained release of the drug over weeks and months, e.g. DOCA, testosterone.
(c) Sialistic (nonbiodegradable) and biodegradable implants
Crystalline drug is packed in tubes or capsules made of suitable materials and implanted under the skin. Slow and uniform leaching of the drug occurs over months providing constant blood levels. The nonbiodegradable implant has to be removed later on but not the biodegradable one. This has been tried for hormones and contraceptives (e.g. NORPLANT).
(ii) Intramuscular (i.m.)
The drug is injected in one of the large skeletal muscles—deltoid, triceps, gluteus maximus, rectus femoris, etc. Muscle is less richly supplied with sensory nerves (mild irritants can be injected) and is more vascular (absorption of drugs in aqueous solution is faster). It is less painful, but self injection is often impracticable because deep penetration is needed. Depot preparations (oily solutions, aqueous suspensions) can be injected by this route. Intramuscular injections should be avoided in anticoagulant treated patients, because it can produce local haematoma.
(iii) Intravenous (i.v
.) The drug is injected as a bolus (Greek: bolos–lump) or infused slowly over hours in one of the superficial veins. The drug reaches directly into the blood stream and effects are produced immediately (great value in emergency). The intima of veins is insensitive and drug gets diluted with blood, therefore, even highly irritant drugs can be injected i.v., but hazards are—thrombophlebitis of the injected vein and necrosis of adjoining tissues if extravasation occurs. These complications can be minimized by diluting the drug or injecting it into a running i.v. line. Only aqueous solutions (not suspensions, because drug particles can cause embolism) are to be injected i.v. and there are no depot preparations for this route. Chances of causing air embolism is another risk. The dose of the drug required is smallest (bioavailability is 100%) and even large volumes can be infused. One big advantage with this route is—in case response is accurately measurable (e.g. BP) and the drug short acting (e.g. sodium nitroprusside), titration of the dose with the response is possible. However, this is the most risky route—vital organs like heart, brain, etc. get exposed to high concentrations of the drug.
The drug is injected into the skin raising a bleb (e.g. BCG vaccine, sensitivity testing) or scarring/multiple puncture of the epidermis through a drop of the drug is done. This route is employed for specific purposes only.
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Pharmacodynamics the branch of pharmacology concerned with the effects of drugs and the mechanism of their action.
“Pharmacodynamics involves how the drugs act on target cells to alter cellular function.”
A. Receptor and non-receptor mechanisms: Most of the drugs act by interacting with a cellular component called receptor. Some drugs act through simple physical or chemical reactions without interacting with any receptor.
• Receptors are protein molecules present either on the cell surface or with in the cell e.g. adrenergic receptors, cholinoceptors, insulin receptors, etc. • The endogenous neurotransmitters, hormones, autacoids and most of the drugs produce their effects by binding with their specific receptors. • Aluminium hydroxide and magnesium trisilicate, which are used in the treatment of peptic ulcer disease act by non-receptor mechanism by neutralizing the gastric acid.
Many drugs are similar to or have similar chemical groups to the naturally occurring chemical and have the ability to bind onto a receptor where one of two things can happen- either the receptor will respond or it will be blocked. A drug, which is able to fit onto a receptor, is said to have affinity for that receptor. Efficacy is the ability of a drug to produce an effect at a receptor. An agonist has both an affinity and efficacy whereas antagonist has affinity but not efficacy or intrinsic activity. When a drug is able to stimulate a receptor, it is known as an agonist and therefore mimics the endogenous transmitter. When the drug blocks a receptor, it is known as antagonist and therefore blocks the action of the endogenous transmitter (i.e. it will prevent the natural chemical from acting on the receptor). However, as most drug binding is reversible, there will be competition between the drug and the natural stimulus to the receptor.
Covalent bond is the strongest bond and the drug-receptor complex is usually irreversible. K1 K3 DR Biological effect D+R K2 Where D = Drug, R= receptor DR= Drug receptor complex (affinity) K1 = association constant K2 = dissociation constant K3 = intrinsic activity When first messengers like neurotransmitters, hormones, autacoids and most of drugs bind with their specific receptors, the drug receptor complex is formed which subsequently causes the synthesis and release of another intracellular regulatory molecule termed as second messengers e.g. cyclic AMP, calcium, cyclic GMP, inositol triphosphate (IP3), diacylglycerol and calmodulin which in turn produce subcellular or molecular mechanism of drug action.
B. Site of drug action:
– A drug may act: (i) Extracellularly e.g: osmotic diuretics, plasma expanders. (ii) On the cell surface e.g.: digitalis, penicillin, catecholamines (iii) Inside the cell e.g.: anti-cancer drugs, steroid hormones. C. Dose Response relationship The exact relationship between the dose and the response depends on the biological object under observation and the drug employed. When a logarithm of dose as abscissa and responses as ordinate are constructed graphically, the “S” shaped or sigmoid type curve is obtained. The lowest concentration of a drug that elicits a response is minimal dose, and the largest concentration after which further increase in concentration will not change the response is the maximal dose. 1. Graded dose effect: As the dose administered to a single subject or tissue increases, the pharmacological response also increases in graded fashion up to ceiling effect. – It is used for characterization of the action of drugs. The concentration that is required to produce 50 % of the maximum effect is termed as EC50 or ED50.50
2. Quantal dose effect: It is all or none response, the sensitive objects give response to small doses of a drug while some will be resistant and need very large doses. The quantal dose effect curve is often characterized by stating the median effective dose and the median lethal dose. Median lethal dose or LD50: This is the dose (mg/kg), which would be expected to kill one half of a population of the same species and strain. Median effective dose or ED50: This is the dose (mg/kg), which produces a desired response in 50 per cent of test population. Therapeutic index: It is an approximate assessment of the safety of the drug. It is the ratio of the median lethal dose and the median effective dose. Also called as therapeutic window or safety.
The larger the therapeutic index, the safer is the drug. Penicillin has a very high therapeutic index, while it is much smaller for the digitalis preparation.
D. Structural activity relationship
The activity of a drug is intimately related to its chemical structure. Knowledge about the chemical structure of a drug is useful for: (i) Synthesis of new compounds with more specific actions and fewer adverse reactions (ii) Synthesis of competitive antagonist and (iii) Understanding the mechanism of drug action. Slight modification of structure of the compound can change the effect completely.
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Pharmacodynamics of atropine:
Atropine, a naturally occurring belladonna alkaloid, is a racemic mixture of equal parts of d- and l-hyoscyamine, whose activity is due almost entirely to the levo isomer of the drug. Atropine is commonly classified as an anticholinergic or antiparasympathetic (parasympatholytic) drug. More precisely, however, it is termed an antimuscarinic agent since it antagonizes the muscarine-like actions of acetylcholine and other choline esters. Adequate doses of atropine abolish various types of reflex vagal cardiac slowing or asystole. The drug also prevents or abolishes bradycardia or asystole produced by injection of choline esters, anticholinesterase agents or other parasympathomimetic drugs, and cardiac arrest produced by stimulation of the vagus. Atropine may also lessen the degree of partial heart block when vagal activity is an etiologic factor. Atropine in clinical doses counteracts the peripheral dilatation and abrupt decrease in blood pressure produced by choline esters. However, when given by itself, atropine does not exert a striking or uniform effect on blood vessels or blood pressure.
Pharmacodynamics of Furosemide
Furosemide, a sulfonamide-type loop diuretic structurally related to bumetanide, is used to manage hypertension and edema associated with congestive heart failure, cirrhosis, and renal disease, including the nephrotic syndrome.
Furosemide, a loop diuretic, inhibits water reabsorption in the nephron by blocking the sodium-potassium-chloride cotransporter (NKCC2) in the thick ascending limb of the loop of Henle. This is achieved through competitive inhibition at the chloride binding site on the cotransporter, thus preventing the transport of sodium from the lumen of the loop of Henle into the basolateral interstitium. Consequently, the lumen becomes more hypertonic while the interstitium becomes less hypertonic, which in turn diminishes the osmotic gradient for water reabsorption throughout the nephron. Because the thick ascending limb is responsible for 25% of sodium reabsorption in the nephron, furosemide is a very potent diuretic.
Pharmacodynamics of Heparin
Unfractionated heparin is a highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from 3000 to 30,000 daltons. Heparin is obtained from liver, lung, mast cells, and other cells of vertebrates. Heparin is a well-known and commonly used anticoagulant which has antithrombotic properties. Heparin inhibits reactions that lead to the clotting of blood and the formation of fibrin clots both in vitro and in vivo. Small amounts of heparin in combination with antithrombin III, a heparin cofactor,) can inhibit thrombosis by inactivating Factor Xa and thrombin. Once active thrombosis has developed, larger amounts of heparin can inhibit further coagulation by inactivating thrombin and preventing the conversion of fibrinogen to fibrin. Heparin also prevents the formation of a stable fibrin clot by inhibiting the activation of the fibrin stabilizing factor. Heparin prolongs several coagulation tests. Of all the coagulation tests, activated partial prothrombin time (aPTT) is the most clinically important value.
Mechanism of action
Under normal circumstances, antithrombin III (ATIII) inactivates thrombin (factor IIa) and factor Xa. This process occurs at a slow rate. Administered heparin binds reversibly to ATIII and leads to almost instantaneous inactivation of factors IIa and Xa The heparin-ATIII complex can also inactivate factors IX, XI, XII and plasmin. The mechanism of action of heparin is ATIII-dependent. It acts mainly by accelerating the rate of the neutralization of certain activated coagulation factors by antithrombin, but other mechanisms may also be involved. The antithrombotic effect of heparin is well correlated to the inhibition of factor Xa. Heparin is not a thrombolytic or fibrinolytic. It prevents progression of existing clots by inhibiting further clotting. The lysis of existing clots relies on endogenous thrombolytics.
Pharmacodynamics of paracetamol Pharmacodynamics of Acetaminophen
Acetaminophen (USAN) or Paracetamol (INN) is a widely used analgesic and antipyretic drug that is used for the relief of fever, headaches, and other minor aches and pains. It is a major ingredient in numerous cold and flu medications and many prescription analgesics. It is extremely safe in standard doses, but because of its wide availability, deliberate or accidental overdoses are not uncommon. Acetaminophen, unlike other common analgesics such as aspirin and ibuprofen, has no anti-inflammatory properties or effects on platelet function, and it is not a member of the class of drugs known as non-steroidal anti-inflammatory drugs or NSAIDs. At therapeutic doses acetaminophen does not irritate the lining of the stomach nor affect blood coagulation, kidney function, or the fetal ductus arteriosus (as NSAIDs can). Like NSAIDs and unlike opioid analgesics, acetaminophen does not cause euphoria or alter mood in any way. Acetaminophen and NSAIDs have the benefit of being completely free of problems with addiction, dependence, tolerance and withdrawal. Acetaminophen is used on its own or in combination with pseudoephedrine, dextromethorphan, chlorpheniramine, diphenhydramine, doxylamine, codeine, hydrocodone, or oxycodone.
Mechanism of action:
Acetaminophen is thought to act primarily in the CNS, increasing the pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1, COX-2, and COX-3 enzymes involved in prostaglandin (PG) synthesis. Unlike NSAIDs, acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, thus, has no peripheral anti-inflammatory affects. While aspirin acts as an irreversible inhibitor of COX and directly blocks the enzyme’s active site, studies have found that acetaminophen indirectly blocks COX, and that this blockade is ineffective in the presence of peroxides. This might explain why acetaminophen is effective in the central nervous system and in endothelial cells but not in platelets and immune cells which have high levels of peroxides. Studies also report data suggesting that acetaminophen selectively blocks a variant of the COX enzyme that is different from the known variants COX-1 and COX-2. This enzyme is now referred to as COX-3. Its exact mechanism of action is still poorly understood, but future research may provide further insight into how it works. The antipyretic properties of acetaminophen are likely due to direct effects on the heat-regulating centres of the hypothalamus resulting in peripheral vasodilation, sweating and hence heat dissipation.
Pharmacodynamics of salbutamol
Salbutamol (INN) or albuterol (USAN), a moderately selective beta(2)-receptor agonist similar in structure to terbutaline, is widely used as a bronchodilator to manage asthma and other chronic obstructive airway diseases. The R-isomer, levalbuterol, is responsible for bronchodilation while the S-isomer increases bronchial reactivity. The R-enantiomer is sold in its pure form as Levalbuterol. The manufacturer of levalbuterol, Sepracor, has implied (although not directly claimed) that the presence of only the R-enantiomer produces fewer side-effects.
Mechanism of action:
Salbutamol is a beta(2)-adrenergic agonist and thus it stimulates beta(2)-adrenergic receptors. Binding of albuterol to beta(2)-receptors in the lungs results in relaxation of bronchial smooth muscles. It is believed that salbutamol increases cAMP production by activating adenylate cyclase, and the actions of salbutamol are mediated by cAMP. Increased intracellular cyclic AMP increases the activity of cAMP-dependent protein kinase A, which inhibits the phosphorylation of myosin and lowers intracellular calcium concentrations. A lowered intracellular calcium concentration leads to a smooth muscle relaxation and bronchodilation. In addition to bronchodilation, salbutamol inhibits the release of bronchoconstricting agents from mast cells, inhibits microvascular leakage, and enhances mucociliary clearance.
Pharmacodynamics of vamana
The overall Pharmacodynamic of Vamanopaga dasemāni drugs is based on guna concept. Most of the drugs (90%) are having property of Laghu and Ruksa guna. These are based on Vāyu, Agni and Ākasa mahābhaūtik (one of the five elements of the universe) composition. Ācarya Caraka has mentioned only the role of gunas in the Pharmacodynamic of Vamana karma (Bhadanta Nāgārjunā, Rasavaisesika, 2010). In fact guna is the thing which represents a drug. So, the selection of a drug should be on the basis of gunas for Vamana karma. Ācarya has mentioned predominance of Vāyu and Agni mahābhūta drugs for Vamana karma. Rasas (taste) of vamana dravyas are chiefly katu and kasāya rasa which are composition of the same mahābhūtas. Most of drugs are katu Vipāka having similar bhaūtic constitution. Other drugs are supportive to the therapy or to avoid complications during Vamana karma. As an example; honey which is mentioned in Vamanopaga dasemāni is added to Vamana kalpa (prepared medicine) for increasing the palatability and giving soothing effect. Āyurveda says it is a good kapha chedaka (expectorant), helps in better expulsion of malarūpī kapha by vamana karma. Likewise Saindhava (salt) should be added to Vamana kalpa for Vilāyana (Agnivesa, Caraka Samhita, 2001) (liquefying) of sticky Kaphadosa in channels. Effect of both the drugs is to help in a comfortable and irritation less procedure. added to Vamana kalpa for Vilāyana (Agnivesa, Caraka Samhita, 2001) (liquefying) of sticky Kaphadosa in channels. Effect of both the drugs is to help in a comfortable and irritation less procedure.
Pharmacodynamics of basti
Basti is chief Panchakama procedure used in Ayurveda. The pharmacodynamics of systemic effect of Basti may be understood through absorption mechanism, concept of system biology, neural stimulation mechanism, and excretory mechanism. As Basti is homogenous emulsion mixture of Honey, Saindhava,Sneha Dravya, Kalka, and decoction of crude drugs and Prakshepa Dravya, which is given through rectum, is absorbed, hence Basti is used as route of drug administration. Through rectal route large quantity of drugs can be delivered for systemic circulation and act accordingly. Concept of system biology opines that a change at cellular level of a system can bring changes in tissue, organ and system and in another system consequently & finally in whole body. As per recent advancement intestine not only is highly vascular but also highly innervated organ which forms ‘Enteric Nervous System’ (ENS).ENS may works in synergism with Central Nervous System of body. The cleansing action of Basti is related with the facilitation of excretion of morbid substances responsible for the disease process into the colon, from where it is evacuated.
Basti being the most widely used and highly effective treatment modality in the Ayurveda, it is the prime subject of interest for modern scientific community. With this background the basic question which comes forward regarding Basti is, “do active principles of drugs used in Basti get absorbed in systemic circulation. Triphaladi decoction Basti containing biomarker gallic acid and after Basti they traced it in the circulation. The rectum has rich blood and lymph supply and drugs can cross the rectal mucosa like other lipid membrane. Thus unionised and lipid soluble substances are readily absorbed from the rectal mucosa. Small quantity of short chain fatty acid fatty acids, such as those from butterfat are absorbed directly into portal blood rather than being converted into triglycerides. This is because short chain fatty acids are more water soluble and allow direct diffusion from the epithelial cells into capillary blood of villi. However decoction Basti gets a very little time maximum 48 minutes to absorb from colon and rectum how so ever these areas have very large surface area and highly vascular needed for absorption. Retention time for Anuvashana Basti is relatively more so probability of absorption also increases. Anuvasana Basti after reaching in the rectum and colon causes secretion of bile from gall bladder which leads to the formation of conjugate micelles which is absorbed through passive diffusion. Especially short chain fatty acid present in Sneha of Anuvasana Basti may absorb from colon and large intestine part of gastrointestinal tract and break the pathology of disease. In Basti Karma, a homogenous emulsion
2) By System Biology Concept of Honey, Saindhava, Sneha Dravya, Kalka, and decoction mixed in remarkable combination after proper churning (break the large and middle chain fatty acid into small chain fatty acids) is given which facilitates absorption better then a single drug per rectum. In Ayurveda classics, various Basti Dravya are mentioned in diverse proportion in different diseases, it again confirms pharmacodynamics of Basti through absorption mechanism
Pharmacodynamics of phenytoin
Phenytoin is an antiepileptic drug which can be useful in the treatment of epilepsy. The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited. Phenytoin reduces the maximal activity of brain stem centers responsible for the tonic phase of tonic-clonic (grand mal) seizures. Phenytoin acts to dampen the unwanted, runaway brain activity seen in seizure by reducing electrical conductance among brain cells. It lacks the sedation effects associated with phenobarbital. There are some indications that phenytoin has other effects, including anxiety control and mood stabilization, although it has never been approved for those purposes by the FDA. Phenytoin is primarily metabolized by CYP2C9.
Mechanism of action
Phenytoin acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. By promoting sodium efflux from neurons, phenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. This includes the reduction of post-tetanic potentiation at synapses. Loss of post-tetanic potentiation prevents cortical seizure foci from detonating adjacent cortical areas.
Pharmacodynamics of Aspirin
Acetylsalicylic acid is an analgesic, antipyretic, antirheumatic, and anti-inflammatory agent. Acetylsalicylic acid’s mode of action as an antiinflammatory and antirheumatic agent may be due to inhibition of synthesis and release of prostaglandins. Acetylsalicylic acid appears to produce analgesia by virtue of both a peripheral and CNS effect. Peripherally, acetylsalicylic acid acts by inhibiting the synthesis and release of prostaglandins. Acting centrally, it would appear to produce analgesia at a hypothalamic site in the brain, although the mode of action is not known. Acetylsalicylic acid also acts on the hypothalamus to produce antipyresis; heat dissipation is increased as a result of vasodilation and increased peripheral blood flow. Acetylsalicylic acid’s antipyretic activity may also be related to inhibition of synthesis and release of prostaglandins.
Mechanism of action:
The analgesic, antipyretic, and anti-inflammatory effects of acetylsalicylic acid are due to actions by both the acetyl and the salicylate portions of the intact molecule as well as by the active salicylate metabolite. Acetylsalicylic acid directly and irreversibly inhibits the activity of both types of cyclooxygenase (COX-1 and COX-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. This makes acetylsalicylic acid different from other NSAIDS (such as diclofenac and ibuprofen) which are reversible inhibitors. Salicylate may competitively inhibit prostaglandin formation. Acetylsalicylic acid’s antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms; the therapeutic effects are not due to pituitary-adrenal stimulation. The platelet aggregation-inhibiting effect of acetylsalicylic acid specifically involves the compound’s ability to act as an acetyl donor to cyclooxygenase; the nonacetylated salicylates have no clinically significant effect on platelet aggregation. Irreversible acetylation renders cyclooxygenase inactive, thereby preventing the formation of the aggregating agent thromboxane A2 in platelets. Since platelets lack the ability to synthesize new proteins, the effects persist for the life of the exposed platelets (7-10 days). Acetylsalicylic acid may also inhibit production of the platelet aggregation inhibitor, prostacyclin (prostaglandin I2), by blood vessel endothelial cells; however, inhibition prostacyclin production is not permanent as endothelial cells can produce more cyclooxygenase to replace the non-functional enzyme.
Pharmacodynamics of pantaprazole
Pantoprazole is a substituted benzimidazole indicated for the short-term treatment (up to 16 weeks) in the healing and symptomatic relief of erosive esophagitis. Pantoprazole is a proton pump inhibitor (PPI) that suppresses the final step in gastric acid production.
Mechanism of action:
Pantoprazole is a proton pump inhibitor (PPI) that suppresses the final step in gastric acid production by forming a covalent bond to two sites of the (H+,K+ )- ATPase enzyme system at the secretory surface of the gastric parietal cell. This effect is dose- related and leads to inhibition of both basal and stimulated gastric acid secretion irrespective of the stimulus.
Hello readers in this article “List of Pharmacology & Toxicology Books” we provide Top 10 best rated Pharmacology Books along with Author Name which are bestselling Pharmacology textbooks in the current market. We provide Best Pharmacology Books Every Student Should Know to understand the subject in a proper and interactive way.
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What is Pharmacology:
Pharmacology is the study of interaction of drugs with living organisms. It also includes history, source, physicochemical properties, dosage forms, methods of administration, absorption, distribution mechanism of action, biotransformation, excretion, clinical uses and adverse effects of drugs. Pharmacology is both a basic and an applied science. It forms the backbone of rational therapeutics.Whereas the medical student and the prescribing physician are primarily concerned with the applied aspects, correct and skillful application of drugs is impossible without a proper understanding of their basic pharmacology. Medical pharmacology, therefore, must include both fundamental background and clinical pharmacological information. Objective and quantitative data on the use of drugs in man, i.e., relationship between plasma concentration and intensity of therapeutic/toxic actions, plasma half lives, relative efficacy of different medications and incidence of adverse effects etc., are being obtained with the aim of optimising drug therapy. The concepts regarding mechanism of action of drugs are changing. In addition, new drugs are being introduced in different countries at an explosive pace. A plethora of information thus appears to be important.
Here is a overview of General Pharmacology Text Books:
Section 1 General Pharmacological Principles 1. Introduction, Routes of Drug Administration 2. Pharmacokinetics: Membrane Transport, Absorption and Distribution of Drugs 3. Pharmacokinetics: Metabolism and Excretion of Drugs, Kinetics of Elimination 4. Pharmacodynamics: Mechanism of Drug Action; Receptor Pharmacology 5. Aspects of Pharmacotherapy, Clinical Pharmacology and Drug Development 6. Adverse Drug Effects 82 Section 2 Drugs Acting on Autonomic Nervous System 7a. Autonomic Nervous System: General Considerations 7b. Cholinergic System and Drugs 99 8. Anticholinergic Drugs and Drugs Acting on Autonomic Ganglia 9. Adrenergic System and Drugs 10. Antiadrenergic Drugs (Adrenergic Receptor Antagonists) and Drugs for Glaucoma
Section 3 Autacoids and Related Drugs 11. Histamine and Antihistaminics 2. 5-Hydroxytryptamine, its Antagonists and Drug Therapy of Migraine 13. Prostaglandins, Leukotrienes (Eicosanoids) and Platelet Activating Factor 14. Nonsteroidal Antiinflammatory Drugs and Antipyretic-Analgesics 15. Antirheumatoid and Antigout Drugs Section 4 Respiratory System Drugs 16. Drugs for Cough and Bronchial Asthma Section 5 Hormones and Related Drugs 17a. Introduction 17b. Anterior Pituitary Hormones 18. Thyroid Hormone and Thyroid Inhibitors 19. Insulin, Oral Hypoglycaemic Drugs and Glucagon 20. Corticosteroids 282 21. Androgens and Drugs for Erectile Dysfunction 22. Estrogens, Progestins and Contraceptives 23. Oxytocin and Other Drugs Acting on Uterus 24. Drugs Affecting Calcium Balance Section 6 Drugs Acting on Peripheral (Somatic) Nervous System 25. Skeletal Muscle Relaxants 26. Local Anaesthetics Section 7 Drugs Acting on Central Nervous System 27. General Anaesthetics 28. Ethyl and Methyl Alcohols 29. Sedative-Hypnotics 30. Antiepileptic Drugs 31. Antiparkinsonian Drugs 32. Drugs Used in Mental Illness: Antipsychotic and Antimanic Drugs 33. Drugs Used in Mental Illness: Antidepressant and Antianxiety Drugs 454 34. Opioid Analgesics and Antagonists 469 35. CNS Stimulants and Cognition Enhancers 486
Section 8 Cardiovascular Drugs 36a. Cardiac Electrophysiological Considerations 36b. Drugs Affecting Renin-Angiotensin System and Plasma Kinins 37. Cardiac Glycosides and Drugs for Heart Failure 512 38. Antiarrhythmic Drugs 526 39. Antianginal and Other Anti-ischaemic Drugs 40. Antihypertensive Drugs 558 Section 9 Drugs Acting on Kidney 41a. Relevant Physiology of Urine Formation 41b. Diuretics 579 42. Antidiuretics 593 Section 10 Drugs Affecting Blood and Blood Formation 43. Haematinics and Erythropoietin 599 44. Drugs Affecting Coagulation, Bleeding and Thrombosis 45. Hypolipidaemic Drugs and Plasma Expanders 634 Section 11 Gastrointestinal Drugs 46. Drugs for Peptic Ulcer and Gastroesophageal Reflux Disease 47. Antiemetic, Prokinetic and Digestant Drugs 48. Drugs for Constipation and Diarrhoea 672 Section 12 Antimicrobial Drugs 49. Antimicrobial Drugs: General Considerations 50. Sulfonamides, Cotrimoxazole and Quinolones 51. Beta-Lactam Antibiotics 716
52. Tetracyclines and Chloramphenicol (Broad-Spectrum Antibiotics) 53. Aminoglycoside Antibiotics 743 54. Macrolide, Lincosamide, Glycopeptide and Other Antibacterial Antibiotics; Urinary Antiseptics 752 55. Antitubercular Drugs 56. Antileprotic Drugs 57. Antifungal Drugs 58. Antiviral Drugs 59. Antimalarial Drugs 60. Antiamoebic and Other Antiprotozoal Drugs 61. Anthelmintic Drugs 849 Section 13 Chemotherapy of Neoplastic Diseases 62. Anticancer Drugs 857 Section 14 Miscellaneous Drugs 63. Immunosuppressant Drugs 64. Drugs Acting on Skin and Mucous Membranes 65. Antiseptics, Disinfectants and Ectoparasiticides 66. Chelating Agents 905 67. Vitamins 909 68. Vaccines and Sera 69. Drug Interactions
Top 10 best rated Pharmacology Books List of Pharmacology & Toxicology Books AuthorName Top 6 Best Pharmacology Books Every Student Should Know bestselling textbook What are some good popular pharmacology books? Which book for pharmacology is the best for a beginner MBBS What are some good reference books for pharmacy students? Which books are best for second year MBBS? What are some good books on medical pharmacology, Buy pharmacy-pharmacology Text books online, 2016 discounts sales … best books for pharmacology Basic And Clinical Pharmacology Basic And Clinical Pharmacology Essentials of Medical Pharmacology Essentials of Medical Pharmacology Goodman & Gilman’s The Phar… Rang & Dale’s Pharmacology Rang & Dale’s Pharmacology Pharmacology: Examination & Board Review Pharmacology: Examination & Board… Pharmacology and Pharmacotherapeutics Pharmacology and Pharmacotherapeutics Lippincott’s Illustrated Reviews Martindale: The Complete… British National Formulary Ansel’s Pharmaceutical Dosage Forms and Drug Delivery Systems Pharmacology Text Books Lists pharmacology books indian authors pharmacology books for medical students pharmacology books for pharmacy students pharmacology books pdf free download top 10 pharmacology books best pharmacology book for pharmacy students pharmacology and toxicology book pdf list of 2016 pharmacology books Textbook Of Pharmacology For Nurses And Allied Health Sciences 1st Edition Pharmacology Best Books Tom Corbo Color Kinetics Whichauthor Is The Best For Pharmacology To Study Dpharmacy Students D’pharmacy 2nd Year Text Books With Best References Text Of Pharmacology Pharmacology Books List Of Pharmacy Books Top 10 Pharmacology Books D Pharmacy 1st Year Books Name Pharmacology All Writers Name Of The Pharmocolgy Books D Pharmacy Some Books Names Pharmacology Book Uesawa Yoshihiro “TOPICS ON DRUG METABOLISM” List Of Pharmacology & Toxicology Books Pharmacology & Toxicology Books Pharmacology Text Books Pharmacology Text Books For B Pharmacy Pharmacology Text Books For M Pharmacy Pharmacology Text Books For D Pharmacy Pharmacology Text Books For Pharmd Pharmacology Text Books For Medicos Pharmacology Text Books For Medical Students
General Pharmacology Textbooks will help B Pharm M Pharm D Pharm and medical students to:
1. Define various terminologies used in Pharmacology. 2. Know about nature and sources of drugs. 3. Understand pharmacodynamics like mechanism of drug action, dose relation ship and pharmacokinetics like absorption, distribution, metabolism and excretion (ADME) of drugs. 4. Understand theoritical pharmacokinetics like half-life, order of kinetics, steady state plasma concentration. 5. Understand drug safety and effectiveness like factors affecting drug action and adverse drug reactions. 6. Understand new drug development and evaluation
The main clinical use of skeletal muscle relaxant is it acts an adjuvant in surgical anesthesia to obtain relaxation of skeletal muscles à this minimizes the risk of respiratory & cardiovascular depression
These drugs block the post-synaptic actions of ACh at motor end plate
On the basis of their site & mechanism of action…these are classified as
Peripherally acting muscle relaxants[These act peripherally at neuromuscular junction]
a) Non-Depolarizing Blockers (Competitive Blockers)
Basis:These drugs prevent the access of ACh to NM receptor of motor end plate à prevent its depolarization
Long Acting: d-Tubocurarine (d-TC), Metocurine, Doxacurium, pancuronium, pipecuronium, gallamine
d-Tubocurarine: – Not clinical used do to its histaminic effects. • Succinylcholine: – SCh is the most commonly used muscle relaxant for passing tracheal tube. It induces rapid, complete and predictable paralysis with spontaneous recovery in ~5 min. – Occasionally SCh is used by continuous i.v. infusion for producing controlled muscle relaxation of longer duration. – It should be avoided in younger children unless absolutely necessary, because risk of hyperkalaemia and cardiac arrhythmia is higher
Pancuronium: – It is a synthetic steroidal compound, ~5 times more potent and longer acting than d-TC. – Because of longer duration of action, needing reversal, its use is now restricted to prolonged operations, especially neurosurgery. • Pipecuronium: – Muscle relaxant with a slow onset and long duration of action; steroidal in nature; recommended for prolonged surgeries. Nondepolarizing blockers – Individual compounds
Vecuronium: – It is a most commonly used muscle relaxant for routine surgery and in intensive care units.. • Atracurium: – Four times less potent than pancuronium and shorter acting. • Rocuronium: – Muscle relaxant with a rapid onset and intermediate duration of action which can be used as alternative to SCh for tracheal intubation without the disadvantages of depolarizing block and cardiovascular changes. Nondepolarizing blockers – Individual compounds
iii.Short Acting: Mivacurine, Rapacuronium
b) Depolarizing Blockers (persistent depolarizers)
Basis:They produce an excessive depolarization which persists for longer duration at NMJ à because they are resistant to hydrolysis by true AChE present in synaptic cleft
Centrally Acting Muscle Relaxants
Basis:These drugs reduce skeletal muscle tone à by selective action in the cerebrospinal axis without altering consciousness
Cancer cells have lost the normal regulatory mechanisms that control cell growth and multiplication.
What is Cancer?
• Cancer cell have lost their ability to differentiate (that means to specialize). Cancer refers to any one of a large number of diseases characterized by the development of abnormal cells that divide uncontrollably and have the ability to infiltrate and destroy normal body tissue. Cancer often has the ability to spread throughout your body.
Types of Cancer?
• Benign cancer cell stay at the same place Malignant cancer cells invade new tissues to set up secondary tumors, a process known as metastasis
Causes of cancer
Common Causes of Cancer:
Smoking and Tobacco. Diet and Physical Activity. Sun and Other Types of Radiation. Viruses and Other Infections
• Chemicals causing cancer are called mutagens • Cancer can be caused by chemicals, life style (smoking), and viruses
A gene mutation can instruct a healthy cell to Allow rapid growth or Fail to stop uncontrolled cell growth or cells lose the controls (tumor suppressor genes) or even Make mistakes when repairing DNA errors
Definitions of cancer
genes that are related to cause cancer are called oncogenes. Genes that become onogenic upon mutation are called protooncogenes.
General signs and symptoms of cancer
Unexplained weight loss Fever Fatigue Pain Skin changes Darker looking skin (hyperpigmentation) Yellowish skin and eyes (jaundice) Reddened skin (erythema) Itching (pruritis) Excessive hair growth Change in bowel habits or bladder function Long-term constipation, diarrhea, Sores that do not heal White patches inside the mouth or white spots on the tongue Unusual bleeding or discharge Thickening or lump in the breast or other parts of the body Indigestion or trouble swallowing Recent change in a wart or mole or any new skin change Nagging cough or hoarseness
Anticancer drugs pharmacology pdf anticancer drugs list pdf classification of anticancer drugs wikipedia anticancer drugs classification ppt classification of anticancer drugs with mechanism of action classification of anticancer agents anticancer drugs classification mnemonics top 10 anti cancer drugs.
Homology modelling allows users to safely use rapidly generated in silico protein models in all the contexts where today only experimental structures provide a solid basis: structure-based drug design, analysis of protein function, interactions, antigenic behavior, and rational design of proteins with increased stability or novel functions. In addition, protein modeling is the only way to obtain structural information if experimental techniques fail. Many proteins are simply too large for NMR analysis and cannot be crystallized for X-ray diffraction.
Among the major approaches to three-dimensional (3D) structure prediction, homology modeling is the easiest one. In the Homology Modelling, structure of a protein is uniquely determined by its amino acid sequence (Epstain, Goldberger, and Anfinsen, 1963). Knowing the sequence should, at least in theory, suffice to obtain the structure. 2. During evolution, the structure is more stable and changes much slower than the associated sequence, so that similar sequences adopt practically identical structures, and distantly related sequences still fold into similar structures. This relationship was first identified by Chothia and Lesk (1986) and later quantified by Sander and Schneider (1991). Thanks to the exponential growth of the Protein Data Bank (PDB), Rost (1999) could recently derive a precise limit for this rule. As long as the length of two sequences and the percentage of identical residues fall in the region marked as “safe,” the two sequences are practically guaranteed to adopt a similar structure.
Homology Modelling or Protein Modelling Example
Imagine that we want to know the structure of sequence A (150 amino acids long,). We compare sequence A to all the sequences of known structures stored in the PDB (using, for example, BLAST), and luckily find a sequence B (300 amino acids long) containing a region of 150 amino acids that match sequence A with 50% identical residues. As this match (alignment) clearly falls in the safe zone (Fig. 25.1), we can simply take the known structure of sequence B (the template), cut out the fragment corresponding to the aligned region, mutate those amino acids that differ between sequences A and B, and finally arrive at our model for structure A. Structure A is called the target and is of course not known at the time of modeling.
In practice, homology modeling is a multistep process that can be summarized in seven steps: 1. Template recognition and initial alignment 2. Alignment correction 3. Backbone generation 4. Loop modeling 5. Side-chain modeling 6. Model optimization 7. Model validation
At almost all the steps choices have to be made. The modeler can never be sure to make the best ones, and thus a large part of the modeling process consists of serious thought about how to gamble between multiple seemingly similar choices. A lot of research has been spent on teaching the computer how to make these decisions, so that homology models can be built fully automatically. Currently, this allows modelers to construct models for about 25% of the amino acids in a genome, thereby supplementing the efforts of structural genomics projects.
Anatomy and Physiology Of human respiratory system is a complicated organ system of very close structure– function relationships. The system consisted of two regions: the conducting airway and the respiratory region. The airway is further divided into many folds: nasal cavity and the associated sinuses, and the nasopharynx, oropharynx, larynx, trachea, bronchi, and bronchioles. The respiratory region consists of respiratory bronchioles, alveolar ducts, and alveolar sacs.
ANATOMY AND PHYSIOLOGY OF HUMAN RESPIRATORY TRACT:
The respiratory system works with the circulatory system to deliver oxygen from the lungs to the cells and remove carbon dioxide, and return it to the lungs to be exhaled. The exchange of oxygen and carbon dioxide between the air, blood and body tissues is known as respiration. Healthy lungs take in about 1 pint of air about 12–15 times each minute. All of the blood in the body is passed through the lungs every minute. The respiratory tract is divided into two main parts: the upper respiratory tract, consisting of the nose, nasal cavity and the pharynx; and the lower respiratory tract consisting of the larynx, trachea, bronchi and the lungs The trachea, which begins at the edge of the larynx, divides into two bronchi and continues into the lungs. The trachea allows air to pass from the larynx to the bronchi and then to the lungs. The bronchi divide into smaller bronchioles which branch in the lungs forming passageways for air. The terminal parts of the bronchi are the alveoli. The alveoli are the functional units of the lungs and they form the site of gaseous exchange
The blood barrier between the alveolar space and the pulmonary capillaries is very thin to allow for rapid gas exchange. During inspiration, oxygen diffuses through the alveoli walls and the interstitial space, into the blood. Carbon dioxide diffuses in the opposite direction during exhalation. Alveoli are small and there are approximately 300 million of them in each lung. Although alveoli are tiny structures, they have a very large surface area in total (~100 m2) for performing efficient gas exchange.
The alveoli form a honeycomb of cells around the spiral, cylindrical surface of the alveolar duct. The exposed alveolar surface is normally covered with a surface film of lipoprotein material.
There are several types of pulmonary alveolar cells. Type I (or small type A), are non-phagocytic, membranous pneumocytes. These surface-lining epithelial cells are approximately 5 μm in thickness and possess thin squamous cytoplasmic extensions that originate from a central nucleated portion. These portions do not have any organelles and hence they are metabolically dependent on the central portion of the cell. This reduces their ability to repair themselves if damaged. Attached to the basement membrane are the larger alveolar cells (Type II, type B or septal cells). These rounded, granular, epithelial pneumocytes are approximately 10 to 15 μm tick. There are 6 to 7 cells per alveolus and these cells possess great metabolic activity. They are believed to produce the surfactant material that lines the lung and to be essential for alveolar repair after damage from viruses or chemical agents.
Amongst, the important roles of the lungs, one can cite: (i) supply oxygen, (ii) remove wastes and toxins, and (iii) defend against hostile intruders. The lungs have three dozen distinct types of cells. Some of these cells scavenge foreign matter. Others have cilia that sweep the mucous membranes lining the smallest air passages. Some cells act on blood pressure control, while others spot infection invaders.
The respiratory system is susceptible to a number of diseases, and the lungs are prone to a wide range of disorders caused by genetic factors, infection and pollutants in the air. The most common problems of the respiratory system are:
Chronic obstructive pulmonary disease (COPD)
Cystic fibrosis (CF)
PRINCIPAL MECHANISMS OF RESPIRATORY DEPOSITION
The deposition of inhaled particles in the different regions of the respiratory system is very complex, and depends on many factors. Some of the factors influencing respiratory deposition include:
Mouth or nose breathing
Health of the individual
Bifurcations in the airways result in a constantly changing hydrodynamic flow field.
Depending on the particle size, airflow, and location in the respiratory system, particle deposition occurs via on of the following principal mechanisms:
Each time the airflow changes due to a bifurcation in the airways, the suspended particles tend to travel along their original path due to inertia and may impact on an airway surface. This mechanism is highly dependent on aerodynamic diameter, since the stopping distance for very small particles is quite low. Impaction occurs mostly in the case of larger particles that are very close to airway walls, near the first airway bifurcations. Therefore, deposition by impaction is greatest in the bronchial region. Impaction accounts for the majority of particle deposition on a mass basis.
Sedimentation is the settling out of particles in the smaller airways of the bronchioles and alveoli, where the air flow is low and airway dimensions are small. The rate of sedimentation is dependent on the terminal settling velocity of the particles, so sedimentation plays a greater role in the deposition of particles with larger aerodynamic diameters. Hygroscopic particles may grow in size as they pass through the warm, humid air passages, thus increasing the probability of deposition by sedimentation.
Interception occurs when a particle contacts an airway surface due to its physical size or shape. Unlike impaction, particles that are deposited by interception do not deviate from their air streamlines. Interception is most likely to occur in small airways or when the air streamline is close to an airway wall. Interception is most significant for fibers, which easily contact airway surfaces do to their length. Furthermore, fibers have small aerodynamic diameters relative to their size, so they can often reach the smallest airways.
Diffusion is the primary mechanism of deposition for particles less than 0.5 microns in diameter and is governed by geometric rather than aerodynamic size. Diffusion is the net transport of particles from a region of high concentration to a region of lower concentration due to Brownian motion. Brownian motion is the random wiggling motion of a particle due to the constant bombardment of air molecules. Diffusional deposition occurs mostly when the particles have just entered the nasopharynx, and is also most likely to occur in the smaller airways of the pulmonary (alveolar) region, where air flow is low.
Absorption – bioavailability of drugs
Although inhaled drugs have been used for over 50 years to treat airway disease and are in development or being considered for the treatment of many other lung diseases, insulin is at present time the only one representative inhaled drug on the market for systemic disease. Exubera® (insulin human [rDNA origin] inhalation powder is the first diabetes treatment which can be inhaled. Exubera® helps control high blood sugar, works in adults with type 1 diabetes and with type 2 diabetes as well This therapeutic success has lead a number of other companies to investigate and to advance clinical trials as inhaled formulations for systemic applications with a variety of large molecules (leuprolide, a luteinizing hormone-releasing hormone (LHRH) analogue, …). Recent advances in the development of particle technologies and devices now make it possible to formulate, stabilize, and accurately deliver almost any drug to the lungs.
The pulmonary membrane is naturally permeable to small molecule drugs and to many therapeutic peptides and proteins. The epithelium of the lung, the significant barrier to absorption of inhaled drugs, is thick (50–60 μm) in the trachea, but diminishes in thickness to an extremely thin 0.2 μm in the alveoli. The change in cell types and morphology going from trachea, bronchi, and bronchioles to alveoli is very dramatic. The lungs are for more permeable to macromolecules than any other portal of entry into the body. Some of the most promising therapeutic agents are peptides and proteins, which could be inhaled instead of injected, thereby improving compliance .Particularly, peptides that have been chemically altered to inhibit peptidase enzymes exhibit very high bioavailabilities by the pulmonary route .Indeed, natural mammalian peptides, les than 30 amino acids (somatostatin, vaso active intestinal peptide [VIP], and glucagons), are broken down in the lung by ubiquitous peptidases and have very poor bioavailabilities. Conversely, proteins with molecular weights between 6000 and 50,000 Da are relatively resistant to most peptidases and have good bioavailabilities following inhalation. For larger proteins, the bioavailabilities and absorption mechanisms are not well completely elucidated.
ADVANTAGES OF PULMONARY DRUG DELIVERY SYSTEM
The ability to nebulize viscous drug formulations for pulmonary delivery, thereby overcoming drug solubility issues with the ability to use lipid, water or lipid/water emulsions as drug carriers.
Ability to nebulize viscous liquids into droplets in the 2-5μm range regardless of the carrier composition solubility which would allow for a wide range of drug formulation options.
Increased drug delivery efficacy due to size-stable aerosol droplets with reduced
hygroscopic growth and evaporative shrinkage.
Liposomal drug formulations remain stable when nebulized.
Ability to nebulize protein-containing solutions.
For hand held inhaler applications, drug does not need to be emulsified in liquefied nebulizing gas to achieve aerosolization.