Granulocyte-macrophage colony-stimulating factor
Granulocyte-macrophage colony-stimulating factor known as colony-stimulating factor 2, is a monomeric glycoprotein secreted by macrophages, T cells, mast cells, natural killer cells, endothelial cells and fibroblasts that functions as a cytokine. The pharmaceutical analogs of occurring GM-CSF are called sargramostim and molgramostim. Unlike granulocyte colony-stimulating factor, which promotes neutrophil proliferation and maturation, GM-CSF affects more cell types macrophages and eosinophils. GM-CSF is a monomeric glycoprotein that functions as a cytokine — it is a white blood cell growth factor. GM-CSF stimulates stem cells to produce monocytes. Monocytes exit the circulation and migrate into tissue, whereupon they mature into macrophages and dendritic cells. Thus, it is part of the immune/inflammatory cascade, by which activation of a small number of macrophages can lead to an increase in their numbers, a process crucial for fighting infection. GM-CSF has some effects on mature cells of the immune system.
These include, for example, inhibiting neutrophil migration and causing an alteration of the receptors expressed on the cells surface. GM-CSF signals via signal transducer and activator of transcription, STAT5. In macrophages, it has been shown to signal via STAT3; the cytokine activates macrophages to inhibit fungal survival. It induces deprivation in intracellular free zinc and increases production of reactive oxygen species that culminate in fungal zinc starvation and toxicity. Thus, GM-CSF promotes defense against infections. GM-CSF plays a role in embryonic development by functioning as an embryokine produced by reproductive tract; the human gene has been localized in close proximity to the interleukin 3 gene within a T helper type 2-associated cytokine gene cluster at chromosome region 5q31, known to be associated with interstitial deletions in the 5q- syndrome and acute myelogenous leukemia. GM-CSF and IL-3 are separated by an insulator element and thus independently regulated. Other genes in the cluster include those encoding interleukins 4, 5, 13.
Human granulocyte-macrophage colony-stimulating factor is glycosylated in its mature form. GM-CSF was first cloned in 1985, soon afterwards three potential drug products were being made using recombinant DNA technology: molgramostim was made in Escherichia coli and is not glycosylated, sargramostim was made in yeast, has a leucine instead of proline at position 23 and is somewhat glyocylated, regramostim was made in Chinese hamster ovary cells and has more glycosylation than sargramostim; the amount of glycosylation affects how the body interacts with the drug and how the drug interacts with the body. At that time, Genetics Institute, Inc. was working on molgramostim, Immunex was working on sargramostim, Sandoz was working on regramostim. Molgramostim was co-developed and co-marketed by Novartis and Schering-Plough under the trade name Leucomax for use in helping white blood cell levels recover following chemotherapy, in 2002 Novartis sold its rights to Schering-Plough. Sargramostim was approved by the US FDA in 1991 to accelerate white blood cell recovery following autologous bone marrow transplantation under the trade name Leukine, passed through several hands, ending up with Genzyme which subsequently was acquired by Sanofi.
Leukine is now owned by Partner Therapeutics. GM-CSF is found in high levels in joints with rheumatoid arthritis and blocking GM-CSF as a biological target may reduce the inflammation or damage; some drugs are being developed to block GM-CSF. In critically ill patients GM-CSF has been trialled as a therapy for the immunosuppression of critical illness, has shown promise restoring monocyte and neutrophil function, although the impact on patient outcomes is unclear and awaits larger studies. CFU-GM Granulocyte-macrophage colony-stimulating factor receptor Filgrastim Pegfilgrastim Official gentaur web site Official Leukine web site Granulocyte-Macrophage+Colony-Stimulating+Factor at the US National Library of Medicine Medical Subject Headings
Metabolism is the set of life-sustaining chemical reactions in organisms. The three main purposes of metabolism are: the conversion of food to energy to run cellular processes; these enzyme-catalyzed reactions allow organisms to grow and reproduce, maintain their structures, respond to their environments.. Metabolic reactions may be categorized as catabolic - the breaking down of compounds. Catabolism releases energy, anabolism consumes energy; the chemical reactions of metabolism are organized into metabolic pathways, in which one chemical is transformed through a series of steps into another chemical, each step being facilitated by a specific enzyme. Enzymes are crucial to metabolism because they allow organisms to drive desirable reactions that require energy that will not occur by themselves, by coupling them to spontaneous reactions that release energy. Enzymes act as catalysts - they allow a reaction to proceed more - and they allow the regulation of the rate of a metabolic reaction, for example in response to changes in the cell's environment or to signals from other cells.
The metabolic system of a particular organism determines which substances it will find nutritious and which poisonous. For example, some prokaryotes use hydrogen sulfide as a nutrient, yet this gas is poisonous to animals; the basal metabolic rate of an organism is the measure of the amount of energy consumed by all of these chemical reactions. A striking feature of metabolism is the similarity of the basic metabolic pathways among vastly different species. For example, the set of carboxylic acids that are best known as the intermediates in the citric acid cycle are present in all known organisms, being found in species as diverse as the unicellular bacterium Escherichia coli and huge multicellular organisms like elephants; these similarities in metabolic pathways are due to their early appearance in evolutionary history, their retention because of their efficacy. Most of the structures that make up animals and microbes are made from three basic classes of molecule: amino acids and lipids; as these molecules are vital for life, metabolic reactions either focus on making these molecules during the construction of cells and tissues, or by breaking them down and using them as a source of energy, by their digestion.
These biochemicals can be joined together to make polymers such as DNA and proteins, essential macromolecules of life. Proteins are made of amino acids arranged in a linear chain joined together by peptide bonds. Many proteins are enzymes. Other proteins have structural or mechanical functions, such as those that form the cytoskeleton, a system of scaffolding that maintains the cell shape. Proteins are important in cell signaling, immune responses, cell adhesion, active transport across membranes, the cell cycle. Amino acids contribute to cellular energy metabolism by providing a carbon source for entry into the citric acid cycle when a primary source of energy, such as glucose, is scarce, or when cells undergo metabolic stress. Lipids are the most diverse group of biochemicals, their main structural uses are as part of biological membranes both internal and external, such as the cell membrane, or as a source of energy. Lipids are defined as hydrophobic or amphipathic biological molecules but will dissolve in organic solvents such as benzene or chloroform.
The fats are a large group of compounds that contain fatty glycerol. Several variations on this basic structure exist, including alternate backbones such as sphingosine in the sphingolipids, hydrophilic groups such as phosphate as in phospholipids. Steroids such as cholesterol are another major class of lipids. Carbohydrates are aldehydes or ketones, with many hydroxyl groups attached, that can exist as straight chains or rings. Carbohydrates are the most abundant biological molecules, fill numerous roles, such as the storage and transport of energy and structural components; the basic carbohydrate units are called monosaccharides and include galactose and most glucose. Monosaccharides can be linked together to form polysaccharides in limitless ways; the two nucleic acids, DNA and RNA, are polymers of nucleotides. Each nucleotide is composed of a phosphate attached to a ribose or deoxyribose sugar group, attached to a nitrogenous base. Nucleic acids are critical for the storage and use of genetic information, its interpretation through the processes of transcription and protein biosynthesis.
This information is propagated through DNA replication. Many viruses have an RNA genome, such as HIV, which uses reverse transcription to create a DNA template from its viral RNA genome. RNA in ribozymes such as spliceosomes and ribosomes is similar to enzymes as it can catalyze chemical reactions. Individual nucleosides are made
Anti-obesity medication or weight loss drugs are pharmacological agents that reduce or control weight. These drugs alter one of the fundamental processes of the human body, weight regulation, by altering either appetite, or absorption of calories; the main treatment modalities for overweight and obese individuals remain dieting and physical exercise. In the United States orlistat is approved by the FDA for long-term use, it reduces intestinal fat absorption by inhibiting pancreatic lipase. Rimonabant, a second drug, works via a specific blockade of the endocannabinoid system, it has been developed from the knowledge that cannabis smokers experience hunger, referred to as "the munchies". It had been approved in Europe for the treatment of obesity but has not received approval in the United States or Canada due to safety concerns; the European Medicines Agency in October 2008 recommended the suspension of the sale of rimonabant as the risks seem to be greater than the benefits. Sibutramine, which acts in the brain to inhibit deactivation of the neurotransmitters, thereby decreasing appetite was withdrawn from the United States and Canadian markets in October 2010 due to cardiovascular concerns.
Because of potential side effects, limited evidence of small benefits in weight reduction in obese children and adolescents, it is recommended that anti-obesity drugs only be prescribed for obesity where it is hoped that the benefits of the treatment outweigh its risks. Current and potential anti-obesity drugs may operate through one or more of the following mechanisms: Catecholamine releasing agents such as amphetamine and related substituted amphetamines which act as appetite suppressants are the main tools used for the treatment of obesity. Increase of the body's metabolism. Interference with the body's ability to absorb specific nutrients in food. For example, Orlistat thereby prevents fat absorption; the OTC fiber supplements glucomannan and guar gum have been used for the purpose of inhibiting digestion and lowering caloric absorptionAnorectics are intended to suppress the appetite, but most of the drugs in this class act as stimulants, patients have abused drugs "off label" to suppress appetite.
The first described attempts at producing weight loss are those of Soranus of Ephesus, a Greek physician, in the second century AD. He prescribed elixirs of laxatives and purgatives, as well as heat and exercise; this remained the mainstay of treatment for well over a thousand years. It was not until the 1930s that new treatments began to appear. Based on its effectiveness for hypothyroidism, thyroid hormone became a popular treatment for obesity in euthyroid people, it had a modest effect but produced the symptoms of hyperthyroidism as a side effect, such as palpitations and difficulty sleeping. 2,4-Dinitrophenol was introduced in 1933. The most significant side effect was a sensation of warmth with sweating. Overdose, although rare, lead to a rise in body temperature and fatal hyperthermia. By the end of 1938 DNP had fallen out of use because the FDA had become empowered to put pressure on manufacturers, who voluntarily withdrew it from the market. Amphetamines became popular for weight loss during the late 1930s.
They worked by suppressing appetite, had other beneficial effects such as increased alertness. Use of amphetamines increased over the subsequent decades, including Obetrol and culminating in the "rainbow diet pill" regime; this was a combination of multiple pills, all thought to help with weight loss, taken throughout the day. Typical regimens included stimulants, such as amphetamines, as well as thyroid hormone, digitalis, a barbiturate to suppress the side effects of the stimulants. In 1967/1968 a number of deaths attributed to diet pills triggered a Senate investigation and the gradual implementation of greater restrictions on the market. While rainbow diet pills were banned in the US in the late 1960s, they reappeared in South America and Europe in the 1980s. Rainbow diet pills were re-introduced into the US by the 2000s and led to additional adverse health effects. Meanwhile, phentermine had been FDA approved in 1959 and fenfluramine in 1973; the two were no more popular than other drugs until in 1992 a researcher reported that when combined the two caused a 10% weight loss, maintained for more than two years.
Fen-phen was born and became the most prescribed diet medication. Dexfenfluramine was developed in the mid-1990s as an alternative to fenfluramine with fewer side-effects, received regulatory approval in 1996. However, this coincided with mounting evidence that the combination could cause valvular heart disease in up to 30% of those who had taken it, leading to withdrawal of Fen-phen and dexfenfluramine from the market in September 1997. Ephedra was removed from the US market in 2004 over concerns that it raises blood pressure and could lead to strokes and death; some patients find that exercise is not a viable option. Some prescription weight loss drugs are stimulants, which are recommended only for short-term use, thus are of limited usefulness for obese patients, who may need to reduce weight over months or years. Orlistat reduces intestinal fat absorption by inhibiting pancreatic lipase; some side-effects of using Orlistat include frequent, oily bowel movements
Pharmacology is the branch of biology concerned with the study of drug action, where a drug can be broadly defined as any man-made, natural, or endogenous molecule which exerts a biochemical or physiological effect on the cell, organ, or organism. More it is the study of the interactions that occur between a living organism and chemicals that affect normal or abnormal biochemical function. If substances have medicinal properties, they are considered pharmaceuticals; the field encompasses drug composition and properties and drug design and cellular mechanisms, organ/systems mechanisms, signal transduction/cellular communication, molecular diagnostics, toxicology, chemical biology and medical applications and antipathogenic capabilities. The two main areas of pharmacology are pharmacokinetics. Pharmacodynamics studies the effects of a drug on biological systems, Pharmacokinetics studies the effects of biological systems on a drug. In broad terms, pharmacodynamics discusses the chemicals with biological receptors, pharmacokinetics discusses the absorption, distribution and excretion of chemicals from the biological systems.
Pharmacology is not synonymous with pharmacy and the two terms are confused. Pharmacology, a biomedical science, deals with the research and characterization of chemicals which show biological effects and the elucidation of cellular and organismal function in relation to these chemicals. In contrast, pharmacy, a health services profession, is concerned with application of the principles learned from pharmacology in its clinical settings. In either field, the primary contrast between the two are their distinctions between direct-patient care, for pharmacy practice, the science-oriented research field, driven by pharmacology; the origins of clinical pharmacology date back to the Middle Ages in Avicenna's The Canon of Medicine, Peter of Spain's Commentary on Isaac, John of St Amand's Commentary on the Antedotary of Nicholas. Clinical pharmacology owes much of its foundation to the work of William Withering. Pharmacology as a scientific discipline did not further advance until the mid-19th century amid the great biomedical resurgence of that period.
Before the second half of the nineteenth century, the remarkable potency and specificity of the actions of drugs such as morphine and digitalis were explained vaguely and with reference to extraordinary chemical powers and affinities to certain organs or tissues. The first pharmacology department was set up by Rudolf Buchheim in 1847, in recognition of the need to understand how therapeutic drugs and poisons produced their effects. Early pharmacologists focused on natural substances plant extracts. Pharmacology developed in the 19th century as a biomedical science that applied the principles of scientific experimentation to therapeutic contexts. Today pharmacologists use genetics, molecular biology and other advanced tools to transform information about molecular mechanisms and targets into therapies directed against disease, defects or pathogens, create methods for preventative care and personalized medicine; the word "pharmacology" is derived from Greek φάρμακον, pharmakon, "drug, spell" and -λογία, -logia "study of", "knowledge of".
The discipline of pharmacology can be divided into many sub disciplines each with a specific focus. Clinical pharmacology is the basic science of pharmacology with an added focus on the application of pharmacological principles and methods in the medical clinic and towards patient care and outcomes. Neuropharmacology is the study of the effects of medication on central and peripheral nervous system functioning. Psychopharmacology known as behavioral pharmacology, is the study of the effects of medication on the psyche, observing changed behaviors of the body and mind, how molecular events are manifest in a measurable behavioral form. Psychopharmacology is an interdisciplinary field which studies behavioral effects of psychoactive drugs, it incorporates approaches and techniques from neuropharmacology, animal behavior and behavioral neuroscience, is interested in the behavioral and neurobiological mechanisms of action of psychoactive drugs. Another goal of behavioral pharmacology is to develop animal behavioral models to screen chemical compounds with therapeutic potentials.
People in this field use small animals to study psychotherapeutic drugs such as antipsychotics and anxiolytics, drugs of abuse such as nicotine and methamphetamine. Ethopharmacology is a term, in use since the 1960s and derives from the Greek word ἦθος ethos meaning character and "pharmacology" the study of drug actions and mechanism. Cardiovascular pharmacology is the study of the effects of drugs on the entire cardiovascular system, including the heart and blood vessels. Pharmacogenetics is clinical testing of genetic variation that gives rise to differing response to drugs. Pharmacogenomics is the application of genomic technologies to drug discovery and further characterization of older drugs. Pharmacoepidemiology is the study of the effects of drugs in large numbers of people. Safety pharmacology specialises in detecting and investigating potential undesirable pharmacodynamic effects of new chemical entities on physiological functions in relation to exposure in the therapeutic range and above.
Systems pharmacology is
The immune system is a host defense system comprising many biological structures and processes within an organism that protects against disease. To function properly, an immune system must detect a wide variety of agents, known as pathogens, from viruses to parasitic worms, distinguish them from the organism's own healthy tissue. In many species, the immune system can be classified into subsystems, such as the innate immune system versus the adaptive immune system, or humoral immunity versus cell-mediated immunity. In humans, the blood–brain barrier, blood–cerebrospinal fluid barrier, similar fluid–brain barriers separate the peripheral immune system from the neuroimmune system, which protects the brain. Pathogens can evolve and adapt, thereby avoid detection and neutralization by the immune system. Simple unicellular organisms such as bacteria possess a rudimentary immune system in the form of enzymes that protect against bacteriophage infections. Other basic immune mechanisms evolved in ancient eukaryotes and remain in their modern descendants, such as plants and invertebrates.
These mechanisms include phagocytosis, antimicrobial peptides called defensins, the complement system. Jawed vertebrates, including humans, have more sophisticated defense mechanisms, including the ability to adapt over time to recognize specific pathogens more efficiently. Adaptive immunity creates immunological memory after an initial response to a specific pathogen, leading to an enhanced response to subsequent encounters with that same pathogen; this process of acquired immunity is the basis of vaccination. Disorders of the immune system can result in inflammatory diseases and cancer. Immunodeficiency occurs when the immune system is less active than normal, resulting in recurring and life-threatening infections. In humans, immunodeficiency can either be the result of a genetic disease such as severe combined immunodeficiency, acquired conditions such as HIV/AIDS, or the use of immunosuppressive medication. In contrast, autoimmunity results from a hyperactive immune system attacking normal tissues as if they were foreign organisms.
Common autoimmune diseases include Hashimoto's thyroiditis, rheumatoid arthritis, diabetes mellitus type 1, systemic lupus erythematosus. Immunology covers the study of all aspects of the immune system; the immune system protects organisms from infection with layered defenses of increasing specificity. In simple terms, physical barriers prevent pathogens such as bacteria and viruses from entering the organism. If a pathogen breaches these barriers, the innate immune system provides an immediate, but non-specific response. Innate immune systems are found in all animals. If pathogens evade the innate response, vertebrates possess a second layer of protection, the adaptive immune system, activated by the innate response. Here, the immune system adapts its response during an infection to improve its recognition of the pathogen; this improved response is retained after the pathogen has been eliminated, in the form of an immunological memory, allows the adaptive immune system to mount faster and stronger attacks each time this pathogen is encountered.
Both innate and adaptive immunity depend on the ability of the immune system to distinguish between self and non-self molecules. In immunology, self molecules are those components of an organism's body that can be distinguished from foreign substances by the immune system. Conversely, non-self molecules are those recognized as foreign molecules. One class of non-self molecules are called antigens and are defined as substances that bind to specific immune receptors and elicit an immune response. Newborn infants have no prior exposure to microbes and are vulnerable to infection. Several layers of passive protection are provided by the mother. During pregnancy, a particular type of antibody, called IgG, is transported from mother to baby directly through the placenta, so human babies have high levels of antibodies at birth, with the same range of antigen specificities as their mother. Breast milk or colostrum contains antibodies that are transferred to the gut of the infant and protect against bacterial infections until the newborn can synthesize its own antibodies.
This is passive immunity because the fetus does not make any memory cells or antibodies—it only borrows them. This passive immunity is short-term, lasting from a few days up to several months. In medicine, protective passive immunity can be transferred artificially from one individual to another via antibody-rich serum. Microorganisms or toxins that enter an organism encounter the cells and mechanisms of the innate immune system; the innate response is triggered when microbes are identified by pattern recognition receptors, which recognize components that are conserved among broad groups of microorganisms, or when damaged, injured or stressed cells send out alarm signals, many of which are recognized by the same receptors as those that recognize pathogens. Innate immune defenses are non-specific, meaning these systems respond to pathogens in a generic way; this system does not confer long-lasting immunity against a pathogen. The innate immune system is the dominant system of host defense in most organisms.
Cells in innate immune system recognizes use pattern recognition receptors to recognize molecular structures that are produced by microbial pathogens. PRRs are germline-encoded host sensors, they are proteins expressed by cells of the innate immune system, such as dendritic cells, macrophages, m
H2 antagonists, sometimes referred to as H2RA and called H2 blockers, are a class of medications that block the action of histamine at the histamine H2 receptors of the parietal cells in the stomach. This decreases the production of stomach acid. H2 antagonists can be used in the treatment of dyspepsia, peptic ulcers and gastroesophageal reflux disease, they have been surpassed by proton pump inhibitors. H2 antagonists are a type of antihistamine, although in common use the term "antihistamine" is reserved for H1 antagonists, which relieve allergic reactions. Like the H1 antagonists, some H2 antagonists function as inverse agonists rather than receptor antagonists, due to the constitutive activity of these receptors; the prototypical H2 antagonist, called cimetidine, was developed by Sir James Black at Smith, Kline & French – now GlaxoSmithKline – in the mid-to-late 1960s. It was first marketed in 1976 and sold under the trade name Tagamet, which became the first blockbuster drug; the use of quantitative structure-activity relationships led to the development of other agents – starting with ranitidine, first sold as Zantac, which has fewer adverse effects and drug interactions and is more potent.
Cimetidine ranitidine famotidine nizatidine roxatidine lafutidine Cimetidine was the prototypical histamine H2-receptor antagonist from which drugs were developed. Cimetidine was the culmination of a project at Smith, Kline & French by James W. Black, C. Robin Ganellin, others to develop a histamine receptor antagonist that would suppress stomach acid secretion. In 1964, it was known that histamine stimulated the secretion of stomach acid, that traditional antihistamines had no effect on acid production. From these facts the SK&F scientists postulated the existence of two different types of histamine receptors, they designated the one acted upon by the traditional antihistamines as H1, the one acted upon by histamine to stimulate the secretion of stomach acid as H2. The SK&F team used a classical design process starting from the structure of histamine. Hundreds of modified compounds were synthesised in an effort to develop a model of the then-unknown H2 receptor; the first breakthrough was Nα-guanylhistamine, a partial H2-receptor antagonist.
From this lead, the receptor model was further refined, which led to the development of burimamide, a specific competitive antagonist at the H2 receptor. Burimamide is 100 times more potent than Nα-guanylhistamine, proving its efficacy on the H2 receptor; the potency of burimamide was still too low for oral administration. And efforts on further improvement of the structure, based on the structure modification in the stomach due to the acid dissociation constant of the compound, led to the development of metiamide. Metiamide was an effective agent, it was proposed that the toxicity arose from the thiourea group, similar guanidine analogues were investigated until the discovery of cimetidine, which would become the first clinically successful H2 antagonist. Ranitidine was developed by Glaxo, in an effort to match the success of Smith, Kline & French with cimetidine. Ranitidine was the result of a rational drug design process utilising the by-then-fairly-refined model of the histamine H2 receptor and quantitative structure-activity relationships.
Glaxo refined the model further by replacing the imidazole-ring of cimetidine with a furan-ring with a nitrogen-containing substituent, in doing so developed ranitidine. Ranitidine was found to have a far-improved tolerability profile, longer-lasting action, ten times the activity of cimetidine. Ranitidine was introduced in 1981 and was the world's biggest-selling prescription drug by 1988; the H2-receptor antagonists have since been superseded by the more effective proton pump inhibitors, with omeprazole becoming the biggest-selling drug for many years. The H2 antagonists are competitive antagonists of histamine at the parietal cell's H2 receptor, they suppress the normal secretion of acid by parietal cells and the meal-stimulated secretion of acid. They accomplish this by two mechanisms: Histamine released by ECL cells in the stomach is blocked from binding on parietal cell H2 receptors, which stimulate acid secretion. H2-antagonists are used by clinicians in the treatment of acid-related gastrointestinal conditions, including: Peptic ulcer disease Gastroesophageal reflux disease Dyspepsia Prevention of stress ulcer Prevention of aspiration pneumonitis during surgery.
Oral H2-antagonists reduce gastric acidity and volume and have shown to reduce the frequency of aspiration pneumonitis. People who suffer from infrequent heartburn may take either antacids or H2-receptor antagonists for treatment; the H2-antagonists offer several advantages over antacids, including longer duration of action, greater efficacy, ability to be used prophylactically before meals to reduce the chance of heartburn occurring. Proton pump inhibitors, are the preferred treatment for erosive esophagitis since they have been shown to promote healing better than H2-antagonists. H2 antagonists are, in general, well-tolerated, except for cimetidine
An antihemorrhagic agent is a substance that promotes hemostasis. It may be known as a hemostatic agent. A styptic is a specific type of antihemorrhagic agent that works by contracting tissue to seal injured blood vessels. Styptic pencils contain astringents. Antihemorrhagic agents used in medicine have various mechanisms of action: Systemic drugs work by inhibiting fibrinolysis or promoting coagulation. Locally-acting hemostatic agents work by promoting platelet aggregation. Hemostatic agents are used during surgical procedures to achieve hemostasis and are categorized as hemostats and adhesives, they vary based on their mechanism of action, ease of application, adherence to tissue and cost. These agents permit rapid hemostasis, better visualization of the surgical area, shorter operative times, decreased requirement for transfusions, decreased wound healing time and overall improvement in patient recovery time. There are several classes of antihemorrhagic drugs used in medicine; these include antifibrinolytics, blood coagulation factors and vitamin K.
Topical hemostatic agents have been gaining popularity for use in emergency bleeding control in military medicine. They are available in two forms -- as a granular powder embedded in a dressing. Microfibrillar collagen hemostat is a topical agent composed of resorbable microfibrillar collagen, it attracts platelets and allows for the formation of a blood clot when it comes into contact with blood. Unlike the hemostatic clamp, no mechanical action is involved; the surgeon presses the MCH against a bleeding site, the collagen attracts and helps with the clotting process to stop bleeding. The practical application for MCH is different from that of the hemostatic clamp. Chitosan hemostats are topical agents composed of its salts. Chitosan bonds with platelets and red blood cells to form a gel-like clot which seals a bleeding vessel. Unlike other hemostat technologies its action does not require the normal hemostatic pathway and therefore continues to function when anticoagulants like heparin are present.
Chitosan is used in some emergency hemostats which are designed to stop traumatic life-threatening bleeding. Their use is well established in many trauma units. Kaolin and zeolite activate the coagulation cascade, have been used as the active component of hemostatic dressings. Styptics cause hemostasis by contracting blood vessels. A common delivery system for this is a hemostatic pencil; this is a short stick of medication. Anhydrous aluminium sulfate is the main ingredient and acts as a vasoconstrictor in order to disable blood flow; the stick is applied directly to the bleeding site. The high ionic strength promotes flocculation of the blood, the astringent chemical causes local vasoconstriction. Before safety razors were invented, it was a standard part of a shaving kit and was used to seal shaving cuts; some people continue to use styptic pencils for minor skin wounds from electric razors. Styptic powder is used in the veterinary trade to stop bleeding from nails that are clipped too closely.
This powder is used on animals, such as turtles, cats and rabbits, whose vein is found in the center of the nail. ATC code B02 – Antihemorrhagics Hemostatic clamp