Storage Temperature on Label – Freeze Cold Cool Dry Label Storage Temperature

Storage Temperature on Label - Freeze Cold Cool Dry Label Storage Temperature

Hello buddies. here with another amazing and most important article “Storage Temperature on Label – Freeze Cold Cool Dry Label Storage Temperature” for all the pharma students pharmacists and any one who is into pharmaceutical field. This article not only helps pharma people but also the general public as we see these terms daily on all the pharmaceutical products we use. Specifically today we are talking about storage temperature on the label. These temperatures and definitions will also help you in many competitive and entrance examinations like GPAT Pharmacist exam, Drug Inspector examination. Then why delay just jump into the points straight away. 

Storage Temperature and Humidity

Specific directions are stated in some monographs with respect to the temperatures and humidity at which official articles shall be stored and distributed (including the shipment of articles to the consumer) when stability data indicate that storage and distribution at a lower or a higher temperature and a higher humidity produce undesirable results. Such directions apply except where the label on an article states a different storage temperature on the basis of stability studies of that particular formulation. Where no specific storage directions or limitations are provided in the individual monograph, but the label of an article states a storage temperature that is based on stability studies of that particular formulation, such labeled storage directions apply. ) The conditions are defined by the following terms.


“Freezer” indicates a place in which the temperature is maintained thermostatically between −25° and −10° (−13° and 14°F).


Any temperature not exceeding 8° (46°F) is “cold.” A “refrigerator” is a cold place in which the temperature is maintained thermostatically between 2° and 8° (36° and 46°F).


Any temperature between 8° and 15° (46° and 59°F) is “cool.” An article for which storage in a cool place is directed may, alternatively, be stored and distributed in a refrigerator, unless otherwise specified by
the individual monograph.

 Controlled Cold Temperature

Storage Temperature on Label - Freeze Cold Cool Dry Label Storage Temperature

“Controlled cold temperature” is defined as temperature maintained thermostatically between 2° and 8° (36° and 46°F), that allows for excursions in temperature between 0° and 15° (32° and 59°F) that may be experienced during storage, shipping, and distribution such that the allowable calculated mean kinetic temperature is not more than 8° (46°F). Transient spikes up to 25° (77°F) may be permitted if the manufacturer so instructs and provided that such spikes do not exceed 24 hours unless supported by stability data or the manufacturer instructs otherwise.

Room Temperature

“Room temperature” indicates the temperature prevailing in a working area.

Controlled Room Temperature

“Controlled room temperature” indicates a temperature maintained thermostatically that encompasses the usual and customary working environment of 20° to 25° (68° to 77°F); that results in a mean kinetic temperature calculated to be not more than 25°; and that allows for excursions between 15° and 30° (59° and 86°F) that are experienced in pharmacies, hospitals, and warehouses. Provided the mean kinetic temperature remains in the allowed range, transient spikes up to 40° are permitted as long as they do not exceed 24 hours. Spikes above 40° may be permitted if the manufacturer so instructs. Articles may be labeled for storage at “controlled room temperature” or at “up to 25°”, or USP Pharmacists’ Pharmacopeia

General Notices other wording based on the same mean kinetic temperature. The mean kinetic temperature is a calculated value that may be used as an isothermal storage temperature that simulates the nonisothermal effects of storage temperature variations.  An article for which storage at controlled room temperature is directed may, alternatively, be stored and distributed in a cool place, unless otherwise specified in the individual monograph or on the label.


Any temperature between 30° and 40° (86° and 104°F) is “warm.”

 Excessive Heat

“Excessive heat” means any temperature above 40° (104°F).

Protection From Freezing

Where, in addition to the risk of breakage of the container, freezing subjects an article to loss of strength or potency, or to destructive alteration of its characteristics, the container label bears an appropriate instruction to protect the article from freezing.

Dry Place

The term “dry place” denotes a place that does not exceed 40% average relative humidity at Controlled Room Temperature or the equivalent water vapor pressure at other temperatures. The determination may be made by direct measurement at the place or may be based on reported climatic conditions. Determination is based on not less than 12 equally spaced measurements that encompass either a season, a year, or, where recorded data demonstrate, the storage period of the article. There may be values of up to 45% relative humidity provided that the average value is 40% relative humidity. Storage in a container validated to protect the article from moisture vapor, including storage in bulk, is considered storage in a dry place.

I hope this Storage Temperature on Label – Freeze Cold Cool Dry Label Storage Temperature article helped you. You need to know the definitions of these exactly to know where to store your medicines.

What is DRX RPH Meaning Definition RX Full Form ?

What is DRX RPH Meaning Definition RX Full Form ?

RX DRX-and-RPH: There are thousand of short abbreviations that are being used on a regular basis when we speak about pharmaceutical applications and in relation to taking drugs.  The medical dictionary has thousands of medical abbreviations that basically denote something in a shorter form which the physicians or those in relation to this trade are aware of but which most of us, the common masses or those who are not related to this field are aware of.  Each one of them has a specific meaning and denotes a specific action when speaking about the pharmaceutical products and is in accordance with treatment.  While the physicians prescribe drugs, generally they provide these short abbreviations in the prescriptions for us to know how and when to take them.  Today we are going to look at the meaning of DRx and RPh, its full form and use in brief here and consider its application and go through what they really means.

What is DRX RPH Meaning Definition RX Full Form ?

The meaning Rx and RPh

Rx and RPh are two of the most common abbreviations that are being used.  Firstly the “Rx” has derived from a Latin word which means “recipe”.  It basically means the action of taking something or receiving something or the fact of it being received.  This symbol basically has originated in the medieval manuscripts and denotes abbreviation of the late Latin verb “recipere”.  Here it denotes that the way how the things (which here is medicine) needs to be taken by the patient.  It basically denotes the direction by which the prescribed medicine needs to be taken by the patient in plain and simple words.  This is a symbol that is commonly found at the head of the prescription provided by the physician to us when means “take, thou”.

Thus accordingly when a pharmacist get the prescription and sees “Rx” written over it they get a clear idea about what the drugs have been prescribed to the patient and thus provides them in accordance to the order they are being prescribed.

What is “RPh”

Now speaking about “RPh” another most common term that is being used in the medical terminology and found common in the prescription, we get to know that it indicates the individual is registered under the State Board of Pharmacy (acknowledged by the Medical Board) and is eligible to prescribe drugs when in need.  He or she has been certified by the Government to prescribe medicines and drugs to patients.  The term “Rph” stands for “Registered Pharmacist”.  Now someone who is willing to complete and get registration must need to complete a tertiary degree in Pharmacy like that of a Bachelor or Master of Pharmacy.  Once the individual is graduated, he or she needs to go through a registration procedure with affiliated board of that particular country and complete internship which takes approximately a year or two (according to the rules laid by the medical bord of that particular country) and finally obtain a registered pharmacist degree.

Now in order to avoid any discrepancies the physicians use these types of short form which not only indicates how to take it but also denotes when to take.  It often helps them to write in short and to fully express what they intend to mean in the way of taking each and every drug as per the requirement.  Though these types of short abbreviations are quite impossible to understand for the common mass who have less knowledge about them, the druggist or the pharmacist who regularly handle medical cases are very much aware of the terms and understands the meaning perfectly.  This helps them to provide drugs to the patient in accordance.



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.

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 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.

HPLC Detectors – Types Comparison Principles {PDF PPT}*

HPLC Detectors - Types Comparison Principles {PDF PPT}*

Here in this article we provide HPLC Detectors – Types Comparison Principles {PDF PPT}*.Different types of HPLC Detectors are given here for you for educational purpose. The HPLC detectors are used to detect the solute present in the eluent comes from the HPLC column. Different HPLC detectors are used in analysis of different types of samples to detect solute having different chemical nature.

HPLC Detectors – Types:

  1. 1. Ultraviolet/visible spectroscopic detectors{UV Detector/ VIS Detector}

    – Fixed Wavelength Detector
    – Variable Wavelength Detector
    – Diode array Detector
    PDA Detector

  2. 2. Refractive-Index Detector

    -Deflection Detector
    -Refractive Detector (Fresnel refractometer)

  3. 3. Evaporative Light Scattering Detector

  4. 4. Multi-Angle Light Scattering Detector

  5. 5. Mass Spectrometer

  6. 6. Conductivity Detector

  7. 7. Fluorescence Detector

  8. 8. Chemiluminescence Detector

  9. 9. Optical Rotation Detector

  10. 10. Electro Chemical Detector

HPLC Detectors Comparision – Best Detectors properties:

Regardless of the principle of operation, an ideal LC detector should have the following properties:
Low drift and noise level (particularly crucial in trace analysis).
High sensitivity.
Fast response.
Wide linear dynamic range (this simplifies quantitation).
Low dead volume (minimal peak broadening).
Cell design which eliminates remixing of the separated bands.
Insensitivity to changes in type of solvent, flow rate, and temperature.
Operational simplicity and reliability.
It should be tuneable so that detection can be optimized for different compounds.
It should be non-destructive.

HPLC Detectors Uses:

Most common Detectors of HPLC:

Refractive index
Fixed wavelength (no longer used)
Variable wavelength
Diode array

Less common, but important Detectors:

Mass-spectrometric (LC/MS)
Evaporative light scattering

HPLC Detectors - Types Comparison Principles {PDF PPT}*

HPLC Detectors – Types Comparison Principles {PDF PPT}*:

Variable-wavelength UV detectors:

Detectors which allow the selection of the operating wavelength called variable wavelength detectors and they are are particularly useful in three cases:
offer best sensitivity for any absorptive component by selecting an appropriate wavelength;
individual sample components have high absorptivity at different wavelengths and thus, operation at a single wavelength would reduce the system’s sensitivity;

Depending on the sophistication of the detector, wavelength change is done manually or programmed on a time basis into the memory of the system.

Any chemical compound could interact with the electromagnetic field. Beam of the electromagnetic radiation passed through the detector flow-cell will experience some change in its intensity due to this interaction. Measurement of this changes is the basis of the most optical HPLC detectors.
Radiation absorbance depends on the radiation wavelength and the functional groups of the chemical compound. Electromagnetic field depending on its energy (frequency) can interact with electrons causing their excitation and transfer onto the higher energetical level, or it can excite molecular bonds causing their vibration or rotation of the functional group. The intensity of the beam which energy corresponds to the possible transitions will decrease while it is passing through the flow-cell. According to the Lambert-Bear law absorbance of the radiation is proportional to the compound concentration in the cell and the length of the cell.

HPLC Detectors – Types Comparison Principles Power point {PDF PPT}

Multi-Angle Light Scattering Detector:

For the SEC analysis, MW of analyte is estimated from the calibration curve drown using a set of known standards. However, by using a MALS, MW can be determined directly without the need of calibration curve. Also MALS can provide an absolute MW of the analyte with very low detection limit.

Refractive index detectors:

These bulk property detectors are based on the change of refractive index of the eluant from the column with respect to pure mobile phase. Although they are widely used, the refractive index detectors suffer from several disadvantages – lack of high sensitivity, lack of suitability for gradient elution, and the need for strict temperature control (±0.001 °C) to operate at their highest sensitivity. A pulseless pump, or a reciprocating pump equipped with a pulse dampener, must also be employed. The effect of these limitations may to some extent be overcome by the use of differential systems in which the column eluant is compared with a reference flow of pure mobile phase. The two chief types of RI detector are as follows.

Deflection refractometer:

The deflection refractometer, which measures the deflection of a beam of monochromatic light by a double prism in which the reference and sample cells are separated by a diagonal glass divide. When both cells contain solvent of the same composition, no deflection of the light beam occurs; if, however, the composition of the column mobile phase is changed because of the presence of a solute, then the altered refractive index causes the beam to be deflected. The magnitude of this deflection is dependent on the concentration of the solute in the mobile phase.

Fresnel refractometer:

The Fresnel refractometer which measures the change in the fractions of reflected and transmitted light at a glass-liquid interface as the refractive index of the liquid changes. In this detector both the column mobile phase and a reference flow of solvent are passed through small cells on the back surface of a prism. When the two liquids are identical there is no difference between the two beams reaching the photocell, but when the mobile phase containing solute passes through the cell there is a change in the amount of light transmitted to the photocell, and a signal is produced. The smaller cell volume (about 3 ilL) in this detector makes it more suitable for high-efficiency columns but, for sensitive operation, the cell windows must be kept scrupulously clean.

HPLC Detectors – Types Comparison Principles PDF word document {PDF PPT}

Mass Spectrometer:

The analytes are detected based on their MW. The obtained information is especially useful for compound structure identification. However, its use is not limited to structure identification and can be used to quantify very low detection limit of elemental and molecular components.

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Friabilator Operation Cleaning {Friability Test Apparatus Procedure of Tablets}

Friabilator Operation Cleaning

Friabilator – Operation & Cleaning:

Friabilator Operation Cleaning {Friability Test Apparatus Procedure of Tablets}


Friabilator Operation


Connect power cord to an
appropriate electrical outlet

Unscrew locking nut to release drum

Brush any loose dust from tablets

Accurately weigh tablets

Load tablets into drum

Place plastic cover over drum

Hold cover firmly in place and

slide drum onto the shaft

Place locking nut onto the end of the shaft

Tighten locking nut into position

Turn timer to the desired

number of rotations

Wait until drum returns
to stationary position

Remove locking nut

Carefully remove drum from shaft

Remove tablets and brush away
any loose powder

Any cracked, cleaved
or broken tablets

Tablets sample has failed the friability test

Reweigh tablets

Calculate the percentage weight loss using
the following formula:

% Weight Loss = (Initial weight – Final
weight) /

This Standard Operating Procedure (SOP) applies to the staff and students using the Friability Tester in the laboratories of the Pharmacy Department

Standard Operating Procedure SOP FOR OPERATION AND CLEANING

Friabilator Operation Cleaning

To provide a written procedure for operation and cleaning of the Automated Friabilator EF-2 (USP) .

2.0 SCOPE:
Applicable to determine Friability of tablets in Manufacturing.

Executive Manufacturing,Executive QA and Assistant Manager QA.

Manager Quality Assurance

Tablet friability can be used to measure efficiency of tabletting equipment or as an indicator of formulation suitability as well as routine QC functions. It can also be thought of as measuring “dusting”. Tablets are rotated in a plastic drum for a specified period of time.  A gravimetric determination is then made to quantitate the amount of surface material that has worn off.





Check cleanliness of the equipment.

6.1.2 Switch ON the instrument, drum will initialize itself to the loading position, the display will now show START.

6.1.3 Weigh and record the weight of the tablets.

A. For the tablets having individual weight up to 0.650 g take 20 tablets.
B. For the tablets having individual weight above 0.650 g take 10 tablets.

6.1.4 Adjust the counts to 100 by pressing the COUNT key followed by ‘1’, ‘0’, ‘0’ keys. (Count range 1 to 99999).

6.1.5 Press ENTER to confirm the reading.

6.1.6 To see and confirm the number of counts press COUNT key.

6.1.7 On confirming the number of counts press RUN/HALT key to start, the display shows the elapsed count.

6.1.8 NOTE: Test can be performed by adjusting ‘TIME’ similarly as ‘COUNT’.

6.1.9 When test is over drum rotates in reverse direction discharging the tablets in the tray.

6.1.10 The test over is indicated by an audible beep and display shows END

6.1.11 The drum initializes itself to loading position and display shows START indicating the instrument is ready for the next run.

6.1.12 Remove the tablets from the tray.

6.1.13 De- dust and weigh the tablets and note down the weight of the tablets.

Calculate the percentage loss in the weight by using the formula

Percentage Loss =Initial Wt – Final Wt/Initial Wt X 100

Notes :
• Do not hold the drums while rotating.
• After testing destroy the tablets.

6.2 CLEANING: Friabilator

6.2.1 Remove the knob on the shaft by pressing the button.

6.2.2 Pull the outside drum out from the shaft carefully. Similarly remove the inside drum by pulling it outside.

6.2.3 Remove the detachable disc from the drum by pulling it outside of both the drums.

6.2.4 Clean both the drums with clean cloth.

6.2.5 Remove both the trays.

6.2.6 Clean the trays with clean cloth.

6.2.7 After cleaning, put the drums and trays back on its position.



British Pharmacopoeia 2009 Vol 4. London: The Stationary Office; 2009. P. A438-A439.

Chourasia A, Mishra BJ, Mishra R, Kannojia P. Comparative in vitro Evaluation of Government Hospital Supplied and Commercial Brands of Paracetamol Tablets. The Pharmacist 2007; 2 (2): 37-39.

Huynh-Ba K, editor. Handbook of Stability Testing in Pharmaceutical Development. New York: Springer; 2009. p. 215-216.

Salman AD, Ghadiri M, Hounslow MJ editors. Volume 12 Particle Breakage. The Netherlands: Elsevier; 2007. p. 960-962.

Varian. Friability Tester Operator’s Manual. North Carolina: Varian Inc;

Handling of friabilator appratus
8.0 6. Precautions

6.1. Do not open the electical compartment due to the risk of shock and allow only trained personnel to do so.

6.2. When tightening the locking nut, ensure that it is not overtightened since this can cause damage to the drum.

6.3. Do not use cleaning compounds containing ammonia or abrasive cleaners to clean the plastic drum since such compounds may damage plastic, causing it to crack and fracture.

6.4. For tablets with a unit mass equal to or less than 650mg, a sample of tablets corresponding as near as possible to 6.5g is to be used whilst for tablets with a unit mass greater than 650mg, a sample of 10 whole tablets is to be used.

6.5. According to the British Pharmacopoeia, 100 rotations are considered to be the standard number of rotations to be used for each test.

6.6. According to the British Pharmacopoeia, a maximum loss of mass not greater than 1.0 per cent is considered acceptable for most types of tablets.

9.1 Wt: Weight.
Tablet friability can be used to measure efficiency of tabletting equipment or as an indicator of formulation suitability as well as routine QC functions. It can also be thought of as measuring “dusting”. Tablets are rotated in a plastic drum for a specified period of time. A gravimetric determination is then made to quantitate the amount of surface material that has worn off.

Friabilator Operation Cleaning {Friability Test Apparatus Procedure of Tablets}

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|Humidity|- Absolute, Relative and Specific.


Humidity is a term for water vapor in the air, and can refer to any one of several measurements of humidity.

Absolute humidity

Absolute humidity is an amount of water vapor, usually discussed per unit volume. The mass of water vapor,  m_w , per unit volume of total moist air,  V_{net} , can be expressed as follows:

 AH = {m_w \over V_{net}}.

Absolute humidity in air ranges from zero to roughly 30 grams per cubic meter when the air is saturated at 30 °C.


Relative humidity

Relative humidity is a term used to describe the amount of water vapor in a mixture of air and water vapor. It is defined as the ratio of the partial pressure of water vapor in the air-water mixture to the saturated vapor pressure of a flat sheet of pure water at those conditions. The relative humidity of air depends not only on temperature but also on the pressure of the system of interest.

Relative humidity is normally expressed as a percentage and is calculated by using the following equation, it is defined as the ratio of thepartial pressure of water vapor (H2O)  \left({e_w}\right)  in the mixture to the saturated vapor pressure of water  \left({{e^*}_w}\right)  at a prescribed temperature.

 \phi = {{e_w} \over {{e^*}_w}} \times 100%

Relative humidity is often used instead of absolute humidity in situations where the rate of water evaporation is important, as it takes into account the variation in saturated vapor pressure.


Specific humidity

Specific humidity is the ratio of water vapor to dry air in a particular mass, and is sometimes referred to as humidity ratio. Specific humidity ratio is expressed as a ratio of mass of water vapor,  m_v , per unit mass of dry air  m_a  .

That ratio is defined as:

 SH = {m_v \over m_a}.



Dissolution is the process by which a solid, liquid or gas forms a solution in a solvent. For the dissolution of solids, the process of dissolution can be explained as the breakdown of the crystal lattice into individual ions, atoms or molecules and their transport into the solvent

The rate of dissolution quantifies the speed of the dissolution process.

The rate of dissolution depends on:

  • nature of the solvent and solute

  • temperature (and to a small degree pressure)

  • degree of undersaturation

  • presence of mixing

  • interfacial surface area

  • presence of inhibitors (e.g., a substance adsorbed on the surface).

The rate of dissolution can be often expressed by the Noyes-Whitney Equation or the Nernst and Brunner equation[1] of the form:

\frac {dm} {dt} = A \frac {D} {d} (C_s-C_b)


m – amount of dissolved material, kg

t – time, seconds

A – surface area of the interface between the dissolving substance and the solvent, m2

D – diffusion coefficient, m2/s

d – thickness of the boundary layer of the solvent at the surface of the dissolving substance, m

Cs – concentration of the substance on the surface, kg/m3

Cb – concentration of the substance in the bulk of the solvent, kg/m3

For dissolution limited by diffusion, Cs is equal to the solubility of the substance.

When the dissolution rate of a pure substance is normalized to the surface area of the solid (which usually changes with time during the dissolution process), then it is expressed in kg/m2s and referred to as “intrinsic dissolution rate”. The intrinsic dissolution rate is defined by the United States Pharmacopeia.

Dissolution rates vary by orders of magnitude between different systems. Typically, very low dissolution rates parallel low solubilities, and substances with high solubilities exhibit high dissolution rates, as suggested by the Noyes-Whitney equation. However, this is not a rule.


Diffusion describes the spread of particles through random motion from regions of higherconcentration to regions of lower concentration. The time dependence of the statistical distribution in space is given by the diffusion equation. The concept of diffusion is tied to that of mass transferdriven by a concentration gradient. Diffusion is invoked in the social sciences to describe the spread of ideas.

Fick’s laws of diffusion describe diffusion and can be used to solve for the diffusion coefficient, D. They were derived by Adolf Fick in the year 1855.

Fick’s first law relates the diffusive flux to the concentration under the assumption of steady state. It postulates that the flux goes from regions of high concentration to regions of low concentration, with a magnitude that is proportional to the concentration gradient (spatial derivative). In one (spatial) dimension, the law is

\bigg. J = - D \frac{\partial \phi}{\partial x} \bigg.


  •  J is the “diffusion flux” [(amount of substance) per unit area per unit time], example (\tfrac{\mathrm{mol}}{ \mathrm m^2\cdot \mathrm s}) J measures the amount of substance that will flow through a small area during a small time interval.

  • \, D is the diffusion coefficient or diffusivity in dimensions of [length2 time−1], example (\tfrac{\mathrm m^2}{\mathrm s})

  • \, \phi (for ideal mixtures) is the concentration in dimensions of [(amount of substance) length−3], example (\tfrac\mathrm{mol}{\mathrm m^3})

  • \, x is the position [length], example \,\mathrm m

Fick’s second law predicts how diffusion causes the concentration to change with time:

\frac{\partial \phi}{\partial t} = D\,\frac{\partial^2 \phi}{\partial x^2}\,\!


  • \,\phi is the concentration in dimensions of [(amount of substance) length−3], example (\tfrac\mathrm{mol}{m^3})

  • \, t is time [s]

  • \, D is the diffusion coefficient in dimensions of [length2 time−1], example (\tfrac{m^2}{s})

  • \, x is the position [length], example \,m