Pharmacology Notes

Do You Know What is Phagocytosis?

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Phagocytosis What & How

 

Phagocytosis:

White blood cells internalize multimolecular particles such as bacteria or old red blood cells by extending pseudopods that wrap around and seal in the targeted material.

A lysosome fuses with and degrades the vesicle contents.

During phagocytosis is also known as “cell eating”.  Large multimolecular particles are internalized. Most body cells perform pinocytosis, many carry out receptor-mediated endocytosis, but only a few specialized cells are capable of phagocytosis, the most notable being certain types of white blood cells that play an important role in the body’s defense mechanisms. When a white blood cell encounters a large particle, such as a bacterium or tissue debris, it extends surface projections known as pseudopods (“false feet”) that surround or engulf the particle and trap it within an internalized vesicle . A lysosome fuses with the membrane of the phagocytic vesicle and releases its hydrolytic enzymes into the vesicle, where they safely attack the bacterium or other trapped material without damaging the remainder of the cell. Th e enzymes largely breakdown the engulfed material into raw ingredients, such as amino acids, glucose, and fatty acids, that the cell can use.

Phagocytosis Mechanism or Steps in Diagram

Role and Function of Phagocytosis in a Fun Learning Way:

Phagocytosis is a tale of drama, deception, and deadly dinner parties, that’s happening right inside your body!

Imagine, if you will, a game of ‘Pac-Man’ – but in this version, Pac-Man is a white blood cell, and the ghosts are pesky pathogens. Just like in the game, our white blood cell, Mr. Pac-Man, can’t just cruise around ignoring all the invaders in his path. He’s got to face them, gobble them up, and do some cellular spring cleaning.

You see, phagocytosis is just like a microscopic version of Pac-Man. When Pac-Cell, our hero, encounters a shady-looking bacterium, he doesn’t just shake his nucleus at it and walk away. Oh no. He goes full glutton mode and engulfs the whole thing – gulp! It’s like the world’s most deadly dinner party, where the guests are the meals! Canapes, anyone?

Once inside, the bacterium isn’t left to just roam about freely. This isn’t a vacation inside a cushy, plush cell, after all. It’s prison! There, the bacterium is greeted by a ruthless welcoming committee – lysosomes. They are filled with digestive enzymes that start breaking the bacterium down. These enzymes are like the cell’s personal chefs – but they’re not cooking up something delicious, they’re cooking up death for the bacteria. It’s the cellular equivalent of putting a virus through a meat grinder – not a pleasant experience!

In the end, the bacterium’s components are digested and recycled by the cell. And Pac-Cell? He’s ready for his next round of the game, always hungry, always hunting. So, next time you’re feeling a bit under the weather, remember – you’ve got an army of miniature Pac-Men inside you, gobbling up invaders and keeping you safe. Game on! What do you say?

That’s all about Phagocytosis. Comment us your doubts.

Structure Physiology Anatomy of EYE

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The eye is a specialized sensory organ of photoreception. The eye is an easily accessible organ for local or systemic drug delivery.

Clinically, the eye can be considered to be composed of two segments:

1. Anterior segment – all structures from (and including) the lens forward.
2. Posterior segment – all structures posterior to the lens.

 

  • The anatomical and physiological characteristics of the eye are described are outlined in this section.
  • Structure of the eye; The eye can be divided into two compartments: the anterior and posterior segments.
  • An internal cross section of an eye is shown in Fig.1
  • physiology of eye - structure of eye
  • Anterior segment; Externally, the anterior segment of eye is made up of cornea, conjunctiva, and sclera.
  • Internally, it consists of anterior chamber, iris/pupil, posterior chamber, and ciliary body.
  • The cornea, an optically transparent tissue that aids in refraction of light to the eye for focusing, is 1 mm thick at the periphery and 0.5 to 0.6 mm thick in the centre.
  • It is composed of squamous and basal columnar epithelium, Bowman’s membrane, substantia propria (stroma), limiting lamina, and the endothelium.
  •  The conjunctiva is a thin, transparent, vascularised mucous membrane with an area of 18 cm2 covering the eye globe and the inner eyelids.
  • It maintains the precorneal tear film and protects the eye. It produces mucus and lubricates the surface of the eye.
  • It is made up of stratified columnar epithelium and lamina propria. The conjunctiva epithelium is divided into bulbar (covering the eyeball), fornix (covering the cornea), and palpebral (covering the eyelid) conjunctivae.
  •  The sclera, the white outer coat of the eyeball, provides structural integrity, size, and shape to the eye.
  • There are three layers in the sclera, the anterior episclera, the middle scleral stroma, and the posterior lamina fusca.
  • The sclera is composed of gel like mucopolysaccharides, elastic fibers, bundles of dense collagen fibrils, and fibroblasts.
  • The iris is a diaphragm around the pupil (lens) and controls the amount of light entering the inner eye.
  • The ciliary body is made up of ciliary muscles, which aid in accommodation.
  • The anterior surface of the eye is constantly rinsed by tear fluid secreted at a flow rate of about 1 μL/min by the main lachrymal gland of the lachrymal apparatus.
  • Tears eventually drain into the nasal cavity through the nasolachrymal ducts.
  • Tear fluid contains mucin, lysozyme, lactoferrin, prealbumin, and serum proteins.
  • It functions as an antibacterial lubricant and aids in draining out foreign substances.
  • The normal volume of tear fluid is 5 to 10 μL.65

 

Posterior segment:

  • Externally, the posterior segment consists of the optic nerve and associated vasculature, and internally, it consists of the lens, vitreous, and rear ocular tissues. Vitreous is a colorless medium
  • Internal structure of the eye consisting of about 99 percent water, dissolved type II collagen, sodium hyaluronate, and proteoglycans.
  • The retina is the inner nervous layer of the eye responsible for the sensory function of sight.
  • The choroid is a dark brown vascular layer attached to the sclera and is believed to provide nourishment to the retina.

Basic Structure of the Eye

The eye has three layers or coats, three compartments and contains three fluids

1. The three coats of the eye are as follows:

(a) Outer fibrous layer:
• cornea
• sclera
• lamina cribrosa.
(b) Middle vascular layer (“uveal tract”):
• iris
• ciliary body – consisting of the pars
plicata and pars plana
• choroids.
(c) Inner nervous layer:
• pigment epithelium of the retina
• retinal photoreceptors
• retinal neurons.

2. The three compartments of the eye are as follows:

(a) Anterior chamber – the space between the cornea and the iris diaphragm.
(b) Posterior chamber – the triangular space between the iris anteriorly, the lens and zonule posteriorly, and the ciliary body.
(c) Vitreous chamber – the space behind the lens and zonule.

3. The three intraocular fluids are as follows:

(a) Aqueous humour – a watery, optically clear solution of water and electrolytes similar to tissue fluids except that aqueous humour has a low protein content normally.
(b) Vitreous humour – a transparent gel consisting of a three-dimensional network of collagen fibres with the interspaces filled with polymerised hyaluronic acid molecules and water. It fills the space between the posterior surface of the lens, ciliary body and retina.
(c) Blood – in addition to its usual functions, blood contributes to the maintenance of intraocular pressure. Most of the blood within the eye is in the choroid. The choroidal blood flow represents the largest blood flow per unit tissue in the body. The degree of desaturation of efferent choroidal blood is relatively small and indicates that the choroidal vasculature has functions beyond retinal nutrition. It might be that the choroid serves as a heat exchanger for the retina, which absorbs energy as light strikes the retinal pigment epithelium.

 

D Pharmacy 1st Year Notes PDF Download -ADME -Pharmacology

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D Pharmacy 1st Year Notes PDF Download -ADME -Pharmacology

ADME DEFINITION:

Absorption, distribution, metabolism, and excretion are sometimes referred to collectively as ADME processes. These processes determine when the drug appears in the blood stream and for how long it remains in the blood stream to give noticeable action.

  • Absorption, distribution, metabolism, and excretion

  • When & how long the drug appears in the blood stream

  • therapeutic response is dependent upon the ADME processes

In order for a drug to cause a therapeutic response, it must reach adequate concentrations in the blood so that it can reach and interact with drug receptors in adequate numbers to trigger a noticeable action. The course of drug action is, therefore, directly correlated with the concentration of the drug in the blood stream, and is dependent upon the ADME processes.

ABSORPTION:

Absorption is the transfer of a drug from its site of administration to the bloodstream. The rate and extent of absorption depends on the route of administration, the formulation and chemical properties of the drug, and physiologic factors that can impact the site of absorption.

  • Transfer of a drug from site to the blood

  • route of administration, Drug properties

  • IV route is fastest and effective for ABSORPTION

  • Highly water-soluble drugs absorb more readily than fat-soluble drugs

  • Drugs with smaller particle sizes ABSORB easily

When a drug is administered intravenously, absorption is not required because the drug is transferred from the administration device directly into the bloodstream. In the case of intravenous administration, the entire dose of the drug is available to move to the sites of drug action. Administration by other routes may result in less availability due to incomplete absorption. When this occurs, less of the drug is delivered by the bloodstream to the site of action. When a tablet or capsule is swallowed it must dissolve before it can be absorbed. The dissolving of a tablet or capsule is referred to as dissolution. Manufacturing processes and the water solubility of the drug affect dissolution rates. Highly water-soluble medications dissolve more readily in the gastrointestinal (GI) tract, while fat-soluble drugs dissolve more slowly. Drugs with smaller particle sizes go into solution more readily. The inert ingredients added to formulations can also affect their dissolution

DISTRIBUTION

Distribution is a process when a drug is absorbed into the bloodstream it can be carried throughout the body. This process specifically carrying is called distribution. It is a reversible process; while some molecules may be interacting with receptors on cell membranes or inside of cells, other molecules may move back into the bloodstream.

  • Process of distribution of a drug from the bloodstream to the site of absorption.

  • Factors influencing distribution are blood flow, capillary permeability, the degree of binding and its solubility.

  • Blood-brain barrier protects the brain from entering high concentrations of drugs to CNS central nervous system.

The delivery of a drug from the bloodstream to the site of drug action primarily depends on blood flow, capillary permeability, the degree of binding (attachment) of the drug to blood and tissue proteins, and the relative lipid-solubility of the drug molecule. Blood flow to different organs of the body is not equal. The most vitally important organs of the body receive the greatest supply of blood. These organs include the brain, liver, and kidneys. Skeletal muscle and bone receive less blood, and adipose tissue (fat) receives the least. If blood flow were the only factor affecting distribution, it would be reasonable to expect that high concentrations of administered medications would always appear in the brain and liver. In reality, few drugs exhibit good penetration of the central nervous system. The anatomical structure of the capillary network in the brain creates a significant barrier to the passage of many drugs and is commonly referred to as the blood-brain barrier. This barrier is an adaptation that for the most part protects brain tissue from invasion by foreign substances. To readily penetrate into the brain, drugs must be fairly small and lipidsoluble or must be picked up by the carrier-mediated transport mechanism in the central nervous system. This explains why the small and highly fat-soluble anesthetic gases quickly and easily penetrate the brain to cause anesthesia, while other larger and water soluble molecules like penicillin antibiotics penetrate the central nervous system to a much lesser degree.

METABOLISM

Drugs are eliminated from the body either unchanged through the kidneys and bile, or they may undergo chemical changes that allow them to be more easily excreted. The process of undergoing chemical changes is called biotransformation, or metabolism. As previously noted, anything absorbed through the GI tract goes directly into the portal circulaextracellular Outside of the cell or cells. interstitial Situated within or between parts of a particular organ or tissue. intracellular Existing or functioning inside a cell or cells. hydrophilic Having an affinity for, readily absorbing, or mixing with water. lipophilic Having an affinity for, or ability to absorb or dissolve in, fats. biotransformation Chemical alterations of a compound that occur within the body, as in drug metabolism. prodrug An inactive drug precursor that is converted in the body to the active drug form. Absorption  that feeds into the liver. The liver is adapted to clear toxins from the body and is the major site for drug metabolism, but specific drugs may undergo biotransformation in other tissues. The kidneys cannot efficiently excrete highly fat-soluble drugs that readily cross cell membranes because they are reabsorbed in the last stages of filtration. These compounds must first be metabolized in the liver to more water-soluble compounds and then removed. There are two types of metabolic processes drugs undergo in the liver. Most undergo one or both types of reactions. In the first type of reaction drugs are made more polar through oxidation-reduction reactions or hydrolysis. These reactions use metabolic enzymes, most often those of the cytochrome P450 enzyme system, to catalyze the biotransformation.

  • Metabolism is the process of undergoing chemical changes to get excreted easily is called metabolism

  • Biotransformation is also known as metabolism

  • Major site for drug metabolism is liver and Kidney

  • two types of metabolic processes

  • hydrolysis an enzyme-catalyzed reactions

  • conjugation reactions with glucuronic acid, sulfuric acid, acetic acid, or an amino acid like Glucuronidation.

  • Metabolism converts the prodrug to the active form. Example: Fosphenytoin is a prodrug of phenytoin,

 

In enzyme-catalyzed reactions, the rate of the reaction is accelerated by the presence of enzymes. A limited amount of enzyme is present at any given time in the liver. Since the rate of enzyme-catalyzed drug metabolism is limited by the quantity of available enzyme, metabolism in these cases is considered a saturable process. This means that the rate of conversion will only continue at the normal pace until the available supply of enzyme is used. At that point, metabolism is slowed until enzyme becomes available again. For the usual doses of most drugs, these reactions never reach saturation. There are a few drugs where doses may reach the saturation point of the enzymes. Once enzymes become saturated, blood levels increase exponentially toward toxicity. Examples include metabolism of alcohol and phenytoin. The second type of metabolism involves conjugation reactions. In this type of reaction the drug undergoing change is joined with another substance, such as glucuronic acid, sulfuric acid, acetic acid, or an amino acid. Glucuronidation is the most common conjugation reaction. The result of conjugation is a more water-soluble compound that is easier for the kidneys to excrete. These metabolites are most often therapeutically inactive. Some agents are initially administered as an inactive compound (prodrug) in order to improve availability or reduce side effects. Metabolism converts the prodrug to the active form. Fosphenytoin, for example, is a prodrug of phenytoin, a drug used for seizure disorders. Fosphenytoin is more completely and quickly absorbed when given by IM injection than phenytoin and can be used in critical situations with greater ease because it dose not require insertion of an intravenous catheter.

EXCRETION

When a drug is taken into and distributed throughout the body, it must be subsequently removed, or concentrations of the drug would continue to rise with each successive dose. The complete removal of the drug from the body is referred to as elimination. Elimination of the drug encompasses both the metabolism of the drug, and excretion of the drug through the kidneys, and to a much lesser degree into the bile. Excretion into the urine is one of the most important mechanisms of drug removal. The kidneys act as a filter for the blood and create urine as a vehicle for removal of waste. Blood enters the kidney through renal arteries and then is filtered by the glomerulus.

  • The complete removal of the drug from the body is referred to as elimination.

  • Excretion of the drug through the kidneys into the urine is one of the most important mechanisms of drug removal aside of liver.

  • the amount being taken in by the patient is equal to the amount being removed by the liver and kidneys. This state of equilibrium is called steady state

The glomerular filtrate becomes concentrated and substances are removed as it passes through the renal tubule and eventually becomes urine. Drug molecules in the bloodstream that are not bound to albumin are also filtered out into the glomerular filtrate. When drugs have not been converted to water soluble compounds in the liver, they are likely to be reabsorbed back into the bloodstream at the end of the filtration process, and will cycle through the body again. If they are water soluble, they will end up in the urine and be excreted. When a medication is given repeatedly, as most are in real patients, the total amount of drug in the body will increase up to a point and then stabilize. At this point, the amount being taken in by the patient is equal to the amount being removed by the liver and kidneys (Fig. 3.7). This state of equilibrium is called steady state, and drug levels will remain fairly constant unless there is a dose change, an interruption in treatment, or failure of the organs of elimination. The therapeutic effects of many drugs are closely correlated to a specific range of steady state serum drug levels, and physicians or clinical pharmacists will monitor these levels and adjust doses when necessary so that patients obtain the appropriate drug response.

Oxytocin: Functions Drugs Side Effects Contraindications Pharmacokinetics Dynamics

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Oxytocin: Functions Drugs Side Effects Contraindications Pharmacokinetics Dynamics

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.

Pharmacokinetics

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.

Oxytocin: Functions Drugs Side Effects Contraindications Pharmacokinetics Dynamics

Adverse effects

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 drugs:

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.

Pharmacodynamics

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.

Contraindications:

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

Side effects

 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.

Pharmacology MCQ for NEET PG GPAT PHARMACIST Nursing Questions with Answers pdf Book

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Pharmacology MCQ for NEET PG GPAT PHARMACIST Nursing Questions with Answers pdf Book

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:

a) Acyclovir

b) Zidovudine

c) Saquinavir

d) Didanozine

Tick the drug, a derivative of adamantane:

a) Didanozine

b) Rimantadine

c) Gancyclovir

d) Foscarnet

Tick the drug, a derivative of pyrophosphate:

a) Foscarnet

b) Zidovudine

c) Vidarabine

d) Acyclovir

Tick the drug, inhibiting viral DNA synthesis:

a) Interferon

b) Saquinavir

c) Amantadine

d) Acyclovir

Tick the drug, inhibiting uncoating of the viral RNA:

a) Vidarabine

b) Rimantadine

c) Acyclovir

d) Didanozine

Tick the drug, inhibiting viral reverse transcriptase:

a) Zidovudine

b) Vidarabine

c) Rimantadine

d) Gancyclovir

Tick the drug, inhibiting viral proteases:

a) Rimantadine

b) Acyclovir

c) Saquinavir

d) Zalcitabine

Tick the drug of choice for herpes and cytomegalovirus infection treatment:

a) Saquinavir

b) Interferon alfa

c) Didanozine

d) Acyclovir

136

Tick the drug which belongs to nonnucleoside reverse transcriptase inhibitors:

a) Zidovudine

b) Vidarabine

c) Nevirapine

d) Gancyclovir

All of the following antiviral drugs are antiretroviral agents, EXCEPT:

a) Acyclovir

b) Zidovudine

c) Zalcitabine

d) Didanozine

Tick the drug used for influenza A prevention:

a) Acyclovir

b) Rimantadine

c) Saquinavir

d) Foscarnet

Tick the drug used for HIV infection treatment, a derivative of nucleosides:

a) Acyclovir

b) Zidovudine

c) Gancyclovir

d) Trifluridine

Tick the antiviral drug which belongs to endogenous proteins:

a) Amantadine

b) Saquinavir

c) Interferon alfa

d) Pencyclovir

Tick the drug which belongs to nucleoside reverse transcriptase inhibitors:

a) Didanosine

b) Gancyclovir

c) Nevirapine

d) Vidarabine

All of the following antiviral drugs are anti-influenza agents, EXCEPT:

a) Acyclovir

b) Amantadine

c) Interferons

d) Rimantadine

Pharmacology MCQ for NEET PG GPAT PHARMACIST Nursing Questions with Answers pdf Book

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:

a) Acyclovire

b) Zalcitabine

c) Zidovudine

d) Saquinavir

Tick the unwanted effects of didanozine:

a) Hallucinations, dizziness, insomnia

b) Anemia, neutropenia, nausea

c) Hypertension, vomiting, diarrhea

d) Peripheral neuropathy, pancreatitis, diarrhea, hyperuricemia

Tick the unwanted effects of indinavir:

a) Hypotension, vomiting, dizziness

b) Nephrolithiasis, nausea, hepatotoxicity

c) Peripheral neuropathy, pancreatitis, hyperuricemia

d) Anemia, neutropenia, nausea

Tick the drug that can induce nausea, diarrhea, abdominal pain and rhinitis:

137

a) Acyclovire

b) Zalcitabine

c) Zidovudine

d) Saquinavir

All of the following effects are disadvantages of anticancer drugs, EXCEPT:

a) Low selectivity to cancer cells

b) Depression of bone marrow

c) Depression of angiogenesis

d) Depression of immune system

Rational combination of anticancer drugs is used to:

a) Provide synergism resulting from the use of anticancer drugs with different mechanisms combination

b) Provide synergism resulting from the use of anticancer drugs with the same mechanisms combination

c) Provide stimulation of immune system

d) Provide stimulation of cell proliferation

Tick the anticancer alkylating drug, a derivative of chloroethylamine:

a) Methotrexate

b) Cisplatin

c) Cyclophosphamide

d) Carmustine

Tick the anticancer alkylating drug, a derivative of ethylenimine:

a) Mercaptopurine

b) Thiotepa

c) Chlorambucil

d) Procarbazine

Tick the group of hormonal drugs used for cancer treatment:

a) Mineralocorticoids and glucocorticoids

b) Glucocorticoids and gonadal hormones

c) Gonadal hormones and somatotropin

d) Insulin

Tick the anticancer alkylating drug, a derivative of alkylsulfonate:

a) Fluorouracil

b) Carboplatin

c) Vinblastine

d) Busulfan

Tick the anticancer drug of plant origin:

a) Dactinomycin

b) Vincristine

c) Methotrexate

d) Procarbazine

Action mechanism of alkylating agents is:

a) Producing carbonium ions altering protein structure

b) Producing carbonium ions altering DNA structure

c) Structural antagonism against purine and pyrimidine

d) Inhibition of DNA-dependent RNA synthesis

Tick the anticancer drug, a pyrimidine antagonist:

a) Fluorouracil

b) Mercaptopurine

c) Thioguanine

d) Methotrexate

Methotrexate is:

a) A purine antagonist

b) A folic acid antagonist

c) An antibiotic

d) An alkylating agent

Tick the antibiotic for cancer chemotherapy:

a) Cytarabine

b) Doxorubicin

c) Gentamycin

d) Etoposide

Fluorouracil belongs to:

a) Antibiotics

b) Antimetabolites

c) Plant alkaloids

d) Bone marrow growth factor

Tick the action mechanism of anticancer drugs belonging to plant alkaloids:

a) Inhibition of DNA-dependent RNA synthesis

b) Cross-linking of DNA

c) Mitotic arrest at a metaphase

d) Nonselective inhibition of aromatases

ANTIVIRAL AGENTS. AGENTS FOR CHEMOTHERAPY OF CANCER

General contraindications for anticancer drugs are:

a) Depression of bone marrow

b) Acute infections

c) Severe hepatic and/or renal insufficiency

d) All of the above

Action mechanism of methotrexate is:

a) Inhibition of dihydrofolate reductase

b) Activation of cell differentiation

c) Catabolic depletion of serum asparagine

d) All of the above

Tick the anticancer drug belonging to inorganic metal complexes:

a) Dacarbazine

b) Cisplatin

c) Methotrexate

d) Vincristine

Tick the indication for estrogens in oncological practice:

a) Leukemia

b) Cancer of prostate

c) Endometrial cancer

d) Brain tumors

Enzyme drug used for acute leukemia treatment:

a) Dihydrofolate reductase

b) Asparaginase

c) Aromatase

d) DNA gyrase

All of the following drugs are derivatives of nitrosoureas, EXCEPT:

a) Carmustine

b) Vincristine

c) Lomustine

d) Semustine

Tick the group of drugs used as subsidiary medicines in cancer treatment:

a) Cytoprotectors

b) Bone marrow growth factors

c) Antimetastatic agents

d) All of the above

Tick the estrogen inhibitor:

a) Leuprolide

b) Tamoxifen

c) Flutamide

d) Anastrozole

Tick the antiandrogen drug:

a) Flutamide

b) Aminoglutethimide

c) Tamoxifen

d) Testosterone

Tick the drug belonging to aromatase inhibitors:

a) Octreotide

b) Anastrozole

c) Flutamide

d) Tamoxifen

Tick the drug belonging to gonadotropin-releasing hormone agonists:

a) Leuprolide

b) Tamoxifen

c) Flutamide

d) Anastrozole

Pharmacology MCQ for Anti Cancer Chemotherapy Drugs

Pharmacology MCQ for Anti Cancer Chemotherapy Drugs

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Pharmacodynamics – Dose Response relationship- Terms Definitions PDF

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Pharmacodynamics - Dose Response relationship- Terms Definitions PDF

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.

Pharmacodynamics - Dose Response relationship- Terms Definitions PDF

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.
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.

Download the pdf of this article here to read:

Pharmacodynamics – Dose Response relationship- Terms Definitions PDF

These are few very important terms you need to understand in pharmacodynamics.

 

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ROUTES OF DRUG ADMINISTRATION PPT PDF 10 Routes of Drug Administration

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Which drug administration route is fastest?,

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.

  1. oral
  2. sublingual
  3. rectal
  4. nasal
  5. ocular
  6. otic
  7. inhalation
  8. nebulization
  9. transdermal
  10. Subcutaneous (under the skin)
  11. Intramuscular (in a muscle)
  12. Intravenous (in a vein)
  13. Intrathecal (around the spinal cord

Factors governing choice of route

  1. Physical and chemical properties of the drug (solid/ liquid/gas; solubility, stability, pH, irritancy).
  2. Site of desired action—localized and approachable or generalized and not approachable.
  3. Rate and extent of absorption of the drug from different routes.
  4. Effect of digestive juices and first pass metabolism on the drug.
  5. Rapidity with which the response is desired (routine treatment or emergency).
  6. Accuracy of dosage required (i.v. and inhalational can provide fine tuning).
  7. Condition of the patient (unconscious, vomiting).

Routes of Administration can be broadly divided into those for

(a) Local action and (b) Systemic action.

LOCAL ROUTES

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:

  1. Topical

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.

  1. Deeper tissues

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).

  1. Arterial supply

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.

SYSTEMIC ROUTES

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

  1. Oral

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).

  1. 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.

  1. Rectal

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.

  1. Cutaneous

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.

 

  1. Inhalation

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.

  1. Nasal

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.

  1. Parenteral

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:

 (a) Dermojet

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.

ROUTES OF DRUG ADMINISTRATION 10 Fastest routes

ROUTES OF DRUG ADMINISTRATION 10 Fastest routes PDF

routes of administration PPT

(iv) Intradermal injection

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.

Search Terms

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Pharmacodynamics Basic Notes – PDF PPT – ATROPINE FUROSIMIDE HEPARIN BASTI VAMANA

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Pharmacodynamics Basic Notes - PDF PPT - ATROPINE FUROSIMIDE HEPARIN BASTI VAMANA

Pharmacodynamics Definition:

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.

Pharmacodynamics Basics:

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.

Pharmacodynamics Basic Notes – PDF PPT – ATROPINE FUROSIMIDE HEPARIN BASTI VAMANA
The forces that attract the drug to its receptor are termed chemical bonds and they are

(a)hydrogen bond

(b) ionic bond

(c) covalent bond

(d) Vander waals force.

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 Examples:

Pharmacodynamics Basic Notes - PDF PPT - ATROPINE FUROSIMIDE HEPARIN BASTI VAMANA

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.

Pharmacology Text Books Lists: D Pharm B Pharm Medical Students Top 10 Pharmacology Books

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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.

If you have Following Questions in your mind Pls read the entire article and get to a great conclusion:

  • What are some good popular pharmacology books?
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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

List Of Pharmacology & Toxicology Books:

Pharmacology & Toxicology Books

List of Pharmacology Text Books Pharmacology Text Books For Pharmacy Medical Dentist Students
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

Pharmacology Text Books For B Pharmacy

Kd-Tripathi-Essentials-Of-Medical-Pharmacology

Rang & Dale’s Pharmacology- 7th Edition

Pharmacology: Lippincott’s Illustrated Reviews

Pharmacology Text Books For M Pharmacy:

Kd-Tripathi-Essentials-Of-Medical-Pharmacology

Rang & Dale’s Pharmacology- 7th Edition

Pharmacology: Lippincott’s Illustrated Reviews

Goodman & Gilman’s The Pharmacological Basis of Therapeutics

Pharmacology Text Books For D Pharmacy

Kd-Tripathi-Essentials-Of-Medical-Pharmacology

Rang & Dale’s Pharmacology- 7th Edition

Pharmacology: Lippincott’s Illustrated Reviews

Pharmacology Text Books For Pharmd

Kd-Tripathi-Essentials-Of-Medical-Pharmacology

Rang & Dale’s Pharmacology- 7th Edition

Pharmacology: Lippincott’s Illustrated Reviews

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Pharmacology Text Books For Medical Students

Kd-Tripathi-Essentials-Of-Medical-Pharmacology

) Pharmacology: Lippincott’s Illustrated Reviews

2) USMLE Road Map – Pharmacology

3) Katzung’s Pharmacology: Examination and Board Review

4) Kaplan Lecture Notes: Pharmacology

5) Pharmacology Brenner

6) Pharmacology: PreTest Self-Assessment and Review

7) Elsevier’s Integrated Pharmacology

8) Lecture Notes on Clinical Pharmacology

9) Pharmcards

10) Pharmacology – Oklahoma Notes

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Skeletal Muscle Relaxants Drugs Classification Uses Pharmacology PPT + PDF Mechanism of Action

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Skeletal muscle relaxant mechanism of Action 1

Skeletal Muscle Relaxants Drugs

Skeletal Muscle Relaxants

  • 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
  1. Peripherally acting muscle relaxants[These act peripherally at neuromuscular junction]
  2. 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
  1. Long Acting: d-Tubocurarine (d-TC), Metocurine, Doxacurium, pancuronium, pipecuronium, gallamine
  2. Intermediate acting: Atracurium, Cisatracurium, Vecuronium, Rcuronium

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

  1. 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
  • Succinyl Choline

  1. Centrally Acting Muscle Relaxants

  • Basis:These drugs reduce skeletal muscle tone à by selective action in the cerebrospinal axis without altering consciousness
  • Carisoprodol, Chlorzoxazone, Diazepam, Clonazepam, Baclofen, Tizanidine

III. Directly Acting Muscle Relaxants

  • Basis:These directly interfere with the contractile mechanisms of voluntary muscle
  • Dantrolene
  1. Misc Group
  • Quinine, Botulinum toxins A & B

Comparison of d-Tubocurarine & Succinylcholine

Parameters d-Tubocurarine Succinylcholine
1.Mechanism Competitive blockade at NM receptors Persistent depolarization of NM receptors followed by their desensitization
2.Potency ++ (Moderate) + (less)
3.Onset 4-5 min 1 min
4.Duration 30 – 50 min with no muscle sore 5 – 6 min followed by muscle sore
5.Type of Relaxation Progressive flaccid paralysis Initial fasciculations followed by flaccid paralysis
6.Effect of Neostigmine Reversal i.e antagonism Potentiation on effect
7.NM  blocking drugs Potentiation on effect No effect
8.Hypothermia Decreases effect Increased effect
9.Histamine release ++ (Moderate) Negligible
10.    BP Hypotension No effect
11.    Cardiac Muscarinic receptors No effect Stimulates. Bradycardia in low doses, tachycardia in large doses
12.    Respiratory effects Bronchospasm Nil
13.    GIT Effects Constipation Nausea, Vomitting
14.    Serum K+ levels No change Hyperkalaemia
15.    Intraocular pressure No change Raised
16.    Pharmacogenetic variation in metabolism Nil (it is excreted through kidney) Metabolized by pseudocholinesterase (exhibit prolonged apnoea)
17.    Other Nil Malignanat hyperthermia



Mechanism of Action of Skeletal Muscle Relaxants Drugs:

Skeletal muscle relaxant Drugs mechanism of Action PDF MOAPPT

Skeletal muscle relaxant mechanism of Action 1 Skeletal muscle relaxant mechanism of Action PPT



Baclofen

  • It is orally active GABA-mimetic drug àwhich acts as a GABA agonist at GABAB receptors
  • The GABABreceptors are G-protein coupled receptors à which hyperpolarize neurons by increasing K+ conductance & reduce Ca+2 conductance
  • Its actions àresults from an action at spinal level where it inhibits both monosynaptic & polysynaptic reflexes
  • Activation of GABAB recptors in the brain àresults in hyperpolarisation in the cord & brain à which interfere with the release of excitatory neurotransmitters
  • It also reduces pain associated with spastic conditions ßas it inhibits the release of substance-P in the spinal cord

Baclofen Therapeutic Uses

  • To relieve painful spasticity in multiple sclerosis
  • It is also used to relieve spasticity from spinal injuries but it is not very useful in cerebral palsy
  • It can also serve as an important substitute to treat trigeminal neuralgia & tardive dyskinesia
  • It imrves he quality f life of patients suffering with severe spasticity & pain

Baclofen Side Effects

  • Sedation, drowsiness, muscle weakness, ataxia
  • Sudden withdrawal may precipitate anxiety, tachycardia & Hallucinations
  • It is teratogenic & risk in pregnancy

Dantrolene

  • It is a phenytoin analogue àbut its site for antispastic action lies ouside the CNS
  • It acts directly at the contractile mechanisms of voluntary muscle by reducing depolarization induced Ca+2 release from the sarcoplasmic reticulum
  • The muscle fibers still respond to nerve stimulus àthe contractile responses are reduced but not absolutely abolished by dantrolene à the net result is muscle weakness rather than paralysis
  • It also facilitates GABA which results in the depression of brain stem reticular functions & efferent motor neuron activity àit produces sedation but no selective action on polysynaptic reflexes

Dantrolene Therapeutic Uses

  • It is used to treat spasticity resulting from upper motor neuron lesions such as spinal cord injury, multiple sclerosis & cerebral palsy
  • It is the drug of choice for the treatment of malignant hyperthermia
  • It is also used in the treatment of neurolept malignant syndrome
  • Orally it is poorly absorbed but absorption is consistent
  • Plasma half-life is 9-12 hrs
  • A/Es– generalized muscle weakness, sedation, diarrhea, hepatitis after prolonged use

References •

Tripathi KD. Essentials of Medical Pharmacology, 7th Ed, New Delhi: Jaypee Brothers Medical Publisher (P) Ltd, 2013.