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Mary Whiton Calkins Essay Research Paper INTRODUCTIONMary

Mary Whiton Calkins Essay Research Paper INTRODUCTIONMary

Mary Whiton Calkins Essay, Research Paper

Mary Whiton Calkins, is best known for two things: becoming the first woman president of The American Psychological Association and being denied her doctorate from Harvard. However, these two aspects only make up a small portion of what she accomplished in her life. Her entire life was dedicated to her work, especially the development of her Psychology of selves. She founded an early psychology laboratory and invented the paired-associate technique. She passionately dove into the new field of Psychology but also was highly active in the field of Philosophy. She was not deterred by being a woman and used her struggles to gain a voice to speak out against women’s oppression. (5)

Mary Whiton Calkins was born on March 30, 1863 in Buffalo, New York. Her father was Wolcott Calkins and a Presbyterian minister. She was from a close knit family, especially to her mother, and the eldest of five children. In 1880, when she was seventeen, she moved to Newton, Massachusetts where her family built a home that she lived in the rest of her life. Her father, knowing the education that women received, decided to design and supervise Mary’s education. This enabled her to enter Smith College in 1882 with advanced standing as a sophomore. However, in 1893, an experience that permanently influenced her thinking and character, was the death of her sister, Maude. The following academic year she stayed home and took private lessons. She reentered Smith College in the fall of 1884 as a senior and graduated with a concentration in classics and philosophy (7).

In 1886 her family went to Europe for sixteen months. This is where she broadened her knowledge of the classics. Upon returning to Massachusetts her father arranged an interview for Mary with the President of Wellesley College, a liberal arts college for women that was a few miles from their home. She was offered a position there as a tutor in Greek and began teaching in the fall of 1887. Mary remained in the Greek Department for three years. However, a professor in the Department of Philosophy noticed her talent of teaching. He discussed with Mary the position needed to teach the new field of Psychology, which was still a sub-discipline of Philosophy. Due to the scarcity of women in that area, it made it realistic to see her potential and offer her the position.

The only requirement that the professor had, was that Calkins study for one year in a Psychology program. However, she faced two problems meeting this condition. The first, being that there were few psychology departments in 1890. Secondly, getting admitted to these places that did offer the program was highly unlikely since she was a woman. Her first consideration was to study abroad. An instructor at Smith told her that her best chance was to try obtaining “private instruction in psychology and philosophy at any of the German universities outside of Zurich” (6).

However, another instructor told her that would be a good idea “if ladies had been allowed the same privileges as men” (6). Calkins formally dismissed going to Germany when she received a letter from a woman student attending the University of Gottingen which stated, “I wish I might encourage you; but past experience has proved to me the utter uselessness of trying to enlighten the authorities, at least, in our generation.”

Once Calkins started looking at the United States, she discovered that the University of Michigan, where she would be studying under John Dewey, and Yale, where she would be studying under G.T. Ladd, were promising. However, she received a letter from another woman student that dissuaded her. The letter stated, “Personally, I should be immensely glad if you would come. We might be able to get some delightful work together…By the way Prof. Ladd thinks you ought to have some lady with you at the lectures. If there were only one or two other girls who would come to join us, we could get a tremendous amount…”(4). She decided against both universities, most likely because they were further away from home that she would like and they did not have a psychological laboratory.

However, one of the few universities that did have a laboratory was Harvard. Two professors there, William James and Josiah Royce, had sent Calkins letters inviting her to “sit-in” on their lectures on a strictly informal basis. When Calkins requested that she be allowed to sit-in on these lectures, President Eliot refused stating that her presence at these lectures would receive an angry reaction from the governing body at Harvard. However, Calkins’ father wrote a petition to Harvard requesting that his daughter be granted admission to these lectures. In addition, the President of Wellesley College wrote a letter stating that Calkins was a member of their faculty and that this program suited her needs.

On October 1, 1890 Harvard approved the petition. Calkins was permitted to attend the seminars of James and Royce; however, it was noted in the university records “that by accepting this privilege Miss Calkins does not become a student of the University entitled to registration” (4). Calkins began attending her first lecture with James that fall. When she arrived to her lecture she was fortunate enough to be the only person left in the class, therefore giving her a private tutoring session of sorts. In addition to taking classes with James and Royce, Calkins began studying experimental psychology under Dr. Edmund Sanford of Clark University.

In the fall of 1891, Calkins returned to Wellesley College as an Instructor of Psychology in the Department of Philosophy. In that same year she established a psychological laboratory at the college (7). At this time she was already planning on furthering her studies in Psychology and asked James, Royce and Sanford where they felt she should look into attending. Dr. Sanford made it clear in his correspondence that neither Clark nor John Hopkins University were not prepared to offer fellowships for graduate education to a woman. William James wrote that Calkins’ “best opportunity would be served learning under Hugo Munsterberg at the University of Freiburg who had had a woman student a year ago” (6). He informed her a month later, that Munsterberg would be coming to Harvard the following year. Once again another petition was submitted, by Calkins, asking for permission to attend Professor Munsterberg’s laboratory. In 1892, President Eliot of Harvard wrote, once again, that she would be permitted in his laboratory as a guest; but not as a registered student of the university.

During this period Calkins had been writing and conducting several experiments within the field of psychology. At this time she invented the paired-associate technique. This was a suggested classification of cases of associations. In her research Calkins originated a technical method for studying memory, later referred to as the method of paired associates. G.E. Muller refined the technique, and later Titchener included it in his Student’s Manual, taking full credit for it. She continued to conduct research under Professor Munsterberg until October of 1894. At this time Munsterberg wrote to the President and Fellows at Harvard requesting that Calkins be admitted as a candidate for the Ph.D. On October 29, 1894, Harvard considered Munsterberg’s request and refused (1).

In the spring of 1895, Calkins presented her thesis, An experimental research on the association of ideas. “At the examination, held May 28, 1895, before Professors Palmer, James, Royce, Munsterberg, Harris and Dr. Santayana, it was unanimously voted that Miss Calkins satisfied all customary requirements for the degree” (6). In Harvard’s records this communication was noted but not considered.


In 1895, Calkins returned to Wellesley College where she was made an Associate Professor of Psychology and Philosophy and was promoted to Professor in 1898. She wrote hundreds of papers divided between the two disciplines. Calkins’ writings encompass more than a hundred papers in professional journals of psychology and philosophy. She wrote four books, including, An Introduction to Psychology (1901); The Persistent Problems of Philosophy (1907), which went through five editions; and The Good Man and the Good (1918).

Throughout this period Calkins did work in both the fields of psychology and philosophy. For example, in the same year she published an analytic and experimental essay on association, she also published an article on the religiousness of children. Three years later her contribution to research on the attributes of sensation was published, along with a philosophical treatment of time as related to causality and to space. Her most influential work in philosophy, The Persistent Problems of Philosophy, appeared at the same time as some of her important psychological articles on the self (3).

After 1900, Calkins’ major contribution to psychology was the development of a system of self-psychology (2). Her own work in the field dealt primarily with such topics as space and time consciousness, emotion, association, color theory and dreams. Her theory held, in contrast to behaviorist views then in the ascendant, that the conscious self is the central fact of psychology. In the field of philosophy she acknowledged Royce’s idealism as the chief influence leading her to her own system of “personalistic absolutism.”

In 1905, Calkins was elected president of the American Psychological Association and the president of the American Philosophical Association in 1918. Her achievements brought her a number of honors in addition to the presidencies. In a 1908 list of leading psychologists in the United States, Calkins was ranked twelfth of the list (2). Columbia University bestowed a Doctor of Letters degree on her in 1909 and Smith College a Doctor of Laws degree in 1910. Both Columbia and Smith also offered her positions on their faculty, which she declined, partly because of the responsibility she felt to remain with and look after the welfare of her parents (2).

In 1929, after a teaching career spanning forty-two years, Calkins retired from Wellesley College with the title of Research Professor. She planned on devoting her retirement to writing and enjoying the companionship of her mother, but less than one year later she was dead, the victim of inoperable cancer (2).

Two underlying forms of psychology in vogue at the time were “atomistic psychology” and the “science of selves.” Calkins was the first to “discover” the psychology of selves. She called it reconciliation between structural and functional psychology. Her first basic definition of her psychology is as follows:

“All sciences deal with facts, and there are two great classes of facts-Selves and Facts-for-the-Selves. But the second of these great groups, the Facts-for-the-Selves, is again capable of an important division into internal and external facts. To the first class belong percepts, images, memories, thoughts, emotions and volitions, inner events as we may call them; to the second class belong the things and the events of the outside world, the physical facts, as we may name them… The physical sciences study these common and apparently independent or external facts; psychology as distinguished from them is the science of consciousness, the study of selves and the inner facts-for-selves (3).

Calkins felt that her psychology could relate, if not directly but indirectly, within other current models of psychology. As Sigmund Freud’s theory of psychoanalysis gained notoriety, she felt that self-psychology could interpret all the facts discovered by him. She wrote, “Self-psychology is finally at the core of every one of the psychoanalytic systems. Not only does the conscious ego play a role, if only a minor role, on the psychoanalytic stage, but even the unconscious closely studied turns out to resemble nothing so much as a dissociated self” (3).

As psychological views moved on, Calkins theory became dissolved and rather dated. However, in

1937, Gordon Allport wrote Personality: A Psychological Interpretation. In this book he gave considerable credit and notoriety to Calkins’ ideas and self-psychology. However, in the third revision of his book, he dropped all references to Calkins. Since then most of Calkins’ ideas and much of her work has been “swept under the rug.”

At the time in which Calkins was struggling to get her education, she faced many setbacks because she was a woman. These experiences shaped many of her views on women’s rights and cultivated her into somewhat of an advocate. In the 1890s, for example, she challenged the work of a colleague, Joseph Jastrow. In his study, he asked college students, both male and female, to write down one hundred words as fast as possible. He found “that women repeat one another’s words more than men” and “there is less variety among women than among men” (2). After analyzing these lists he concluded, “that the feminine traits revealed…are an attention to the immediate surroundings, to the finished product, to the ornamental, the individual, and the concrete; while the masculine preference is for the more remote, the constructive, the useful, the general, and the abstract” (2).

Calkins was infuriated by his findings and responded that “if sufficiently extended, establish characteristic differences in the interests of men and women.” However, she maintained that it was “futile and impossible to attempt a distinction between masculine and feminine intellect per-se…because of our entire inability to eliminate the effect of the environment” (6).

Another area that she opposed differentiation was the right to vote. In an address to a National Suffrage Convention at Baltimore, she maintained that: “the student trained to reach decisions in the light of logic and of history will be disposed to recognize that, in a democratic country, governed as this is by the suffrage of its citizens, and given over as this is to the principle and practice of educating women, a distinction based on difference of sex is artificial and illogical” (2).

The most profound action against sexist attitudes that she rejected was her refusal to accept the offer of a Radcliffe Ph.D. In 1902, she and three other women who had done graduate work at Harvard, but were not eligible for a Harvard degree on account of their sex were recommended by Radcliffe and approved by Harvard as candidates for the degree of Ph.D. from Radcliffe College. Although she was urged by several colleagues to take the degree, she declined. She writes,

“I sincerely admire the scholarship of the three women to whom it is to be given and I should be very glad to be classed with them. I furthermore think it highly probably that the Radcliffe degree will be regarded, generally, as the practical equivalent of the Harvard degree. Finally, I should be glad to hold the Ph.D. degree for I occasionally find the lack of it an inconvenience; and now that the Radcliffe degree is offered, I doubt whether the Harvard degree will ever be open to women. On the other hand, I still believe that the best ideals of education would be better served if Radcliffe College refused to confer the doctor’s degree. You will be quick to see that, holding this conviction, I cannot rightly take the easier course of accepting the degree” (2).

To this day Harvard has not issued any degree in honor of Mary Whiton Calkins and feels that there is “no reason to” award the degree


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To cite this page: Myers, P. R. Espinosa, C. S. Parr, T. Jones, G. S. Hammond, and T. A. Dewey. 2016. The Animal Diversity Web (online). Accessed at http://animaldiversity.org.

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Hytone Effects, Reviews, Images, Ingredients and Information

Hytone Hytone Description

Each gram of Hytone ® (hydrocortisone) Cream 2½% contains 25 mg of hydrocortisone in a water-washable base of purified water, propylene glycol, glyceryl monostearate SE, cholesterol and related sterols, isopropyl myristate, polysorbate 60, cetyl alcohol, sorbitan monostearate, polyoxyl 40 stearate and sorbic acid.

Each mL of Hytone (hydrocortisone) Lotion 2½% contains 25 mg of hydrocortisone in a vehicle consisting of carbomer 940, propylene glycol, polysorbate 40, propylene glycol stearate, cholesterol and related sterols, isopropyl myristate, sorbitan palmitate, cetyl alcohol, triethanolamine, sorbic acid, simethicone, and purified water.

Chemically, hydrocortisone is [Pregn-4-ene-3,20-dione, 11,17,21-trihydroxy-, (11?)-] with the molecular formula (C21 H30 O5 ) and is represented by the following structural formula:

Its molecular weight is 362.47 and its CAS Registry Number is 50-23-7. The topical corticosteroids, including hydrocortisone, constitute a class of primarily synthetic steroids used as anti-inflammatory and antipruritic agents.

Hytone Drug Information, Indications - Other Medicaments on

Hytone Drug Information Hytone forms, composition and dosages:
  • Cream; Topical; Hydrocortisone 1%
  • Cream; Topical; Hydrocortisone 2.5%
  • Lotion; Topical; Hydrocortisone 1%
  • Lotion; Topical; Hydrocortisone 2.5%
  • Ointment; Topical; Hydrocortisone 1%
  • Ointment; Topical; Hydrocortisone 2.5%
Indications, usages and classification codes:

There is an additional general information about this medication active ingredient hydrocortisone:

Pharmacological action

Glucocorticosteroid. Inhibits the function of leukocytes and tissue macrophages. The migration of leukocytes in the area of inflammation. Impair the capacity of macrophages to phagocytosis and the formation of interleukin-1. Contributes to the stabilization of lysosomal membranes, thereby reducing the concentration of proteolytic enzymes in the field of inflammation. Decreases capillary permeability due to histamine release. Inhibits activity of fibroblasts and collagen formation.
Inhibits the activity of phospholipase A2 which leads to suppression of the synthesis of prostaglandins and leukotrienes. Suppresses the release of COX (mainly COX-2), which also helps to reduce production of prostaglandins.
Reduces the number of circulating lymphocytes (T-and B-cells), monocytes, eosinophils and basophils as a result of their displacement from the vascular bed to lymphoid tissue, suppresses the formation of antibodies.
hydrocortisone suppresses the release of pituitary ACTH and beta-lipotropin but does not reduce the level of circulating beta-endorphin. Inhibits the secretion of TSH and FSH.
With direct application of the receptacles has a vasoconstrictor effect.
hydrocortisone has a pronounced dose-dependent effect on the metabolism of carbohydrates, proteins and fats. Stimulates gluconeogenesis, promotes the capture of amino acids by the liver and kidneys and increases the activity of enzymes of gluconeogenesis. In the liver of hydrocortisone increases glycogen deposition by stimulating the activity of glycogen synthase and synthesis of glucose from the products of protein metabolism. Increased blood glucose activates the secretion of insulin.
hydrocortisone suppresses the seizure of glucose by fat cells that leads to activation of lipolysis. However, due to increased secretion of insulin is stimulation of lipogenesis which leads to the accumulation of fat.
This medication has catabolic effect in lymphoid and connective tissue, muscle, adipose tissue, skin, bone tissue; to a lesser extent than the mineralocorticoid affects the processes of water and electrolyte metabolism: promotes the excretion of potassium ions and calcium, delay in the body of sodium and water. Osteoporosis and Itsenko-Cushing's syndrome are the main factors limiting the long-term therapy of GCS. As a result of catabolic actions may suppress growth in children.
In high doses hydrocortisone may increase the excitability of brain tissue and contributes to lowering the threshold of convulsive readiness. It stimulates the excessive production of hydrochloric acid and pepsin in the stomach that promotes the development of peptic ulcers.
For systems use therapeutic activity of hydrocortisone caused by anti-inflammatory, anti-allergic, immunosuppressive and antiproliferative action. When external and local application the therapeutic activity of hydrocortisone is due to anti-inflammatory, anti-allergic and antiexudative (due to vasoconstrictor effect) action. For anti-inflammatory activity this medicine is 4 times weaker than prednisolone, at mineralocorticoid activity is superior to other GCS.


Binding to plasma proteins - 40-90%. Metabolised mainly in the liver. T1/2 is 80-120 min. It is withdrawed by the kidneys mainly as metabolites.

Why is Hytone prescribed?

For parenteral use: acute adrenal insufficiency, allergic reactions of immediate type, asthmatic status, prevention and treatment of shock, myocardial infarction complicated by cardiogenic shock, thyrotoxic crisis, thyroiditis, congenital adrenal hyperplasia, hypercalcemia due to tumor disease, short or additional therapy in acute rheumatic diseases, collagen diseases, pemphigus, bullous Dermatitis herpetiformis (Duhring disease), polymorphic bullous erythema, exfoliative dermatitis, granulosarcoid, severe forms of psoriasis and seborrheic dermatitis, severe acute and chronic allergic and inflammatory processes with eyes involvement, symptomatic sarcoidosis, Loeffler syndrome if not amenable to other forms of therapy, berylliosis, focal or disseminated form of tuberculosis during anti tuberculosis chemotherapy, aspiration pneumonitis, adult idiopathic thrombocytopenic purpura (only IV), adult secondary thrombocytopenia, acquired (autoimmune) hemolytic anemia, erythroblastopenia, congenital (erythroid) anemotrophy, palliative therapy in leukemia and lymphoma adults with acute leukemia in children, to enhance diuresis and to reduce proteinuria in nephrotic syndrome without uremia, with nephrotic syndrome of idiopathic type or lupus erythematosus, in a critical stage of ulcerative colitis, and regional enteritis (as a systemic treatment), tuberculous meningitis with subarachnoid block or the development of its stake (in conjunction with antituberculosis chemotherapy), trichinosis with nervous system or myocardium, bronchial asthma, diseases of the joints.
For local use: inflammation of the anterior eyeball in intact epithelium of the cornea and after injury and surgery on the eyeball.
For external use: allergic dermatitis, seborrhea, various forms of eczema, atopic dermatitis, psoriasis, pruritus, red flat verrucous zoster.

Dosage and administration

For parenteral use. Dosage and administration is individual. Applied IV as jet, IV as drip, rarely - IM. For emergency treatment is recommended IV injections. The initial dose is 100 mg (to be entered for 30 seconds) - 500 mg (to be entered for 10 min), then repeat every 2-6 hours, depending on the clinical situation. High doses should be used only to stabilize the patient's condition, but usually not more than 48-72 hours, because possible development of hypernatraemia. For children - not less than 25 mg / kg / day. In the form of depot-entry form intra or periarticular in a dose of 5-50 mg single with an interval of 1-3 weeks. IM - 125-250 mg / day.
In ophthalmology apply 2-3 times / day.
Topically - 1-3 times / day.

Hytone side effects

Endocrine system: reduction of glucose tolerance, diabetes mellitus, steroid or manifestation of latent diabetes mellitus, adrenal suppression, Itsenko-Cushing's syndrome (including moon face, obesity, pituitary type, hirsutism, increased blood pressure, dysmenorrhea, amenorrhea, myasthenia gravis, striae), delayed sexual development in children.
Metabolism: increased excretion of calcium, hypocalcemia, increased body weight, negative nitrogen balance (increased breakdown of proteins), increased sweating, fluid retention and sodium ions (peripheral edema), hypernatremia, kaliopenia syndrome (including hypokalemia, arrhythmia, myalgia or muscle spasm, unusual weakness, and fatigue).
CNS: delirium, disorientation, euphoria, hallucinations, manic-depressive psychosis, depression, paranoia, increased intracranial pressure, nervousness or anxiety, insomnia, dizziness, vertigo, pseudotumor cerebellum, headache, convulsions.
Cardiovascular system: arrhythmia, bradycardia (up to heart failure), development (in predisposed patients) or increased severity of chronic heart failure, ECG changes typical for hypokalemia, increased blood pressure, hypercoagulation, thrombosis. In patients with acute and subacute myocardial infarction - the spread foci of necrosis, slowing the formation of scar tissue that may lead to rupture of the heart muscle, with intracranial introduction - nosebleeds.
Digestive system: nausea, vomiting, pancreatitis, steroid ulcer and duodenal ulcers, erosive esophagitis, bleeding and perforation of the gastrointestinal tract, increased or decreased appetite, flatulence, hiccups, rarely - increased activity of hepatic transaminases and alkaline phosphatase.
Senses: a sudden loss of view (for parenteral administration in the head, neck, nasal turbinate, the scalp may be the deposition of crystals of the drug in the vessels of eyes), posterior subcapsular cataracts, increased intraocular pressure with possible damage to the optic nerve, the propensity to develop secondary bacterial, fungal or viral eye infections, trophic changes of the cornea, exophthalmos.
Musculoskeletal system: slowing growth and ossification processes in children (premature closure of epiphyseal growth zones), osteoporosis (very rarely - pathological fractures, aseptic necrosis of head of humerus and femur), rupture of tendons of muscles, steroid myopathy, reduced muscle mass (atrophy); with intraarticular injection - increased pain in the joint.
Dermatological reactions: delayed wound healing, petechiae, ecchymosis, skin thinning, hyper- or hypopigmentation, steroid acne, striae, susceptibility to the development of pyoderma and candidiasis.
Allergic reactions: generalized (including skin rash, itching skin, anaphylactic shock), local allergic reaction.
Effects due to the immunosuppressive effect: the development or exacerbation of infection (the appearance of this side effect contribute jointly used immunosuppressive drugs and vaccination).
Local reactions: with a parenteral - burning, numbness, pain, paresthesia, and infection at the injection site, rarely - necrosis of surrounding tissue, scarring at the injection site, with i / m administration (particularly in the deltoid muscle) - atrophy of the skin and subcutaneous tissue.
Other: pyuria, withdrawal syndrome.
For IV administration - arrhythmias, rush of blood to the face, convulsions.
For exterior use: rarely - itching, hyperemia, burning, dryness, folliculitis, acne, hypopigmentation, perioral dermatitis, allergic dermatitis, maceration of the skin, secondary infection, skin atrophy, striae, miliaria. With prolonged use or application on large areas of skin may develop systemic side effects characteristic of SCS.


For short-term use according to the life - hypersensitivity to hydrocortisone. For intraarticular administration and injection directly into the lesion: previous arthroplasty, abnormal bleeding (endogenous or caused by the use of anticoagulants), intra-articular fracture, infection (septic) inflammatory process in joints and periarticular infections (including history), and also general infectious disease marked juxta-articular osteoporosis, lack of signs of inflammation in the joint ("dry" joint, such as osteoarthrosis without synovitis), marked bone destruction and deformity of joints (sharp narrowing of joint space, ankylosis), instability of the joint as a result of arthritis, aseptic necrosis of the epiphyses of bones forming the joint.
For external use: bacterial, viral, fungal skin diseases, tuberculosis, skin, cutaneous manifestations of syphilis, tumors of the skin, post-vaccination period, violation of the integrity of the skin (ulcers, wounds), children's age (up to 2 years, with itching in the anal area - up to 12 years), rosacea, acne vulgaris, perioral dermatitis.
For use in ophthalmology: bacterial, viral, fungal eye diseases, tuberculosis eye disease, trachoma, violation of the integrity of the eye epithelium.

Using during pregnancy and breastfeeding

Application of pregnancy is only possible when the intended benefits to the mother outweighs the potential risk to the fetus, it is recommended to use the minimum dose and short-term therapy. Children whose mothers during pregnancy were receiving hydrocortisone are subject to careful monitoring for signs of adrenal insufficiency.
If necessary, use during lactation should decide on the termination of breastfeeding.
In experimental studies have shown that GCS can cause malformations of the fetus. Currently there is no clear evidence of these data in humans.

Special instructions

With caution use in parasitic and infectious diseases of viral, fungal or bacterial origin (currently or recently transferred, including the recent contact with a patient) - herpes simplex, herpes zoster (viremic phase), chickenpox, measles, amoebiasis, strongyloidiasis (set or suspected), systemic mycosis, active and latent tuberculosis. Application for serious infectious diseases is permissible only against the background of specific therapy.
Precautions to apply for 8 weeks before and 2 weeks after vaccination, with lymphadenitis after BCG, with immunodeficiency (including AIDS or HIV infection).
Precautions to apply for gastrointestinal diseases: gastric ulcer and duodenal ulcer, esophagitis, gastritis, acute or latent peptic ulcer, the newly formed anastomosis of the intestine, ulcerative colitis with perforation or abscess formation threat, diverticulitis.
With caution used in diseases of the cardiovascular system, including after recent myocardial infarction (in patients with acute and subacute myocardial necrosis may spread the fire, slowing the formation of scar tissue and therefore break the heart muscle), with decompensated chronic heart failure, hypertension, hyperlipidemia) and endocrine diseases - diabetes mellitus (including breach of tolerance to carbohydrates), thyrotoxicosis, hypothyroidism, Itsenko-Cushing disease, with severe chronic renal and / or hepatic failure, nefrourolitiaze, with hypoalbuminemia and conditions that predispose to its occurrence, with systemic osteoporosis, myasthenia gravis, acute psychosis, obesity (III-IV degree), and polio (except bulbar form of encephalitis), open-and angle-closure glaucoma, pregnancy, lactation.
If necessary of intraarticular injection use with caution to patients with severe general condition, failure (or brevity) of the 2 previous injections (based on the individual properties used GCS).
For lack of effectiveness of hydrocortisone in 48-72 hours and the need for more long-term therapy should be replaced by hydrocortisone at different glucocorticoid preparation does not cause sodium retention in the body. During treatment with hydrocortisone should appoint a diet with restriction of sodium and high potassium content. hydrocortisone caused a relative adrenal insufficiency may persist for several months after its cancellation. Given this under stressful situations that arise during the period, hormone therapy resume with simultaneous appointment of salts and / or mineral corticoids.
Patients with active tuberculosis hydrocortisone should be used in conjunction with the appropriate anti tuberculosis therapy. In latent tuberculosis or during superelevation tuberculin tests should carefully monitor the status of the patient, and if necessary to chemoprophylaxis.

Hytone drug interactions

With simultaneous use of hydrocortisone increases the toxicity of cardiac glycosides (because of the emerging hypokalemia increases the risk of arrhythmias); with acetylsalicylic acid - accelerates its excretion and reduces its concentration in blood plasma (with the abolition of hydrocortisone concentration of salicylates in the blood increases, and increases the risk of side effects); with paracetamol - increased risk of hepatotoxic action of paracetamol (induction of hepatic enzymes and formation of a toxic metabolite of paracetamol); with cyclosporine - increased side effects of hydrocortisone as a result of inhibition of its metabolism; with ketoconazole - increased side effects of hydrocortisone as a result of reduction of its clearance.
hydrocortisone reduces the effectiveness of hypoglycemic; intensifies the effect of indirect anticoagulants of coumarin derivatives.
hydrocortisone reduces the effect of vitamin D on the absorption of calcium ions into the lumen of the intestine. Ergocalciferol and parathyroid hormone hinder the development of osteopathy caused by GCS.
hydrocortisone increases the metabolism of isoniazid, meksiletina (especially in "fast acetylators"), which leads to a decrease in their plasma concentrations; increases (with prolonged therapy) the content of folic acid reduces the concentration of praziquantel in blood.
hydrocortisone in high doses reduces the effect somatropina.
Hypokalemia caused by GCS, may increase the severity and duration of muscle blockade on the background of muscle relaxants.
Antacids reduce the absorption of the GCS.
At simultaneous application with SCS thiazides, carbonic anhydrase inhibitors, other GCS, amphotericin B increase the risk of hypokalemia, drugs containing sodium ions - swelling and increase blood pressure.
NSAIDs and ethanol increases the risk of gastrointestinal ulcerations and bleeding, in combination with NSAIDs to treat arthritis may reduce the dose of GCS due to summation of therapeutic effect. Indomethacin displacing the SCS from its association with albumin, increases the risk of its side effects.
Amphotericin B and carbonic anhydrase inhibitors increase the risk of osteoporosis.
The therapeutic effect of GCS is reduced under the influence of inducers of microsomal liver enzymes (including phenytoin, barbiturates, ephedrine, theophylline, rifampin) due to increased rate of metabolism of these substances.
Inhibitors of the function of the adrenal cortex (including mitotan) may necessitate higher doses of GCS.
Clearance GCS increased against the background of preparations of thyroid hormones.
Immunosuppressants increase the risk of infection and lymphoma or other lymphoproliferative disorders associated with Epstein-Barr virus.
Estrogens (including oral contraceptives containing estrogen) reduce the clearance of GKS, lengthens T1/2 and their therapeutic and toxic effects. The appearance of hirsutism and acne promotes the simultaneous use of other steroid hormone funds - androgens, estrogens, anabolic steroids, oral contraceptives.
Tricyclic antidepressants may increase the severity of depression caused by GCS (not shown for the treatment of these side effects).
The risk of developing cataracts increases with the application against other GCS antipsychotic funds (neuroleptics), carbutamide and azathioprine. Simultaneous with the appointment of m-cholinoblockers, as well as with means having m-anticholinergic action (including antihistamines, tricyclic antidepressants), with nitrates improves the intraocular pressure.
With simultaneous application of SCS with live vaccines and antiviral compared to other types of immunization increases the risk of activation of viruses and development of infections.


Be sure to consult your doctor before taking any medication!