Inflammatory intestinal diseases of bacterial, viral (rotovirus), parasitic (giardiasis) etiology; for example, rotovirus penetrates mature microvilli cells of the mucosa of the small intestine, destroys and rejects them, the mucosa cells stop forming the enzyme lactase, dysentery bacillus, entering the intestine, produces toxins, causes inflammation throughout the small intestine, intensively multiplies in the ileum and then passes to the large intestine; giardia live in the upper small intestine, attach to the villi of the mucosa, multiply, affect the intestinal wall deep down, disrupt parietal (membrane digestion) by disrupting enzyme production.
chronic diseases of the stomach, biliary tract, pancreas,
operations on the organs of the gastrointestinal tract,
endocrine disorders (diabetes, hyperparathyroidism),
Whipple’s disease is a rare disease of the small intestine;
Gluten enteropathy (celiac disease), in celiac disease the synthesis of all enzymes, including lactase, is disrupted and lactase deficiency occurs, whose manifestations are greatly reduced by following an agluten diet;
Crohn’s disease is granulomatous enteritis, which affects the entire wall of the small intestine in any part of it. Inflammation develops, then scar tissue, and enzyme synthesis stops; autoimmune mechanisms underlie mucosal damage;
food allergy – damage to enterocytes (cells of the small intestine mucosa), it is called allergoenteropathy, which is based on immunoallergic antigen-antibody complexes, the antigen is the food, and the body produces antibodies; antigen-antibody complex in cells causes inflammation, release of neurotransmitters, which leads to enterocyte damage, their ability to secret lactase is compromised;
excessive bacterial growth in the small intestine;
lymphoma of the small intestine.
Сongestal – Analgesic in cases of flu and upper respiratory tract infections and symptoms For relief of flu symptoms, Influenza, hay fever or other symptoms of upper respiratory tract allergy such as nasal congestion, coryzea, snizzing, fever, headache and mild pain.
Some medicines and this medicine may interfere with eachother.
These include: warfarin, a medicine used to
prevent blood clots
* medicines used to treat high
* medicines used to treat heart
* quinidine, a medicine used to
treat abnormal or irregular heart
CONGESTAL SIDE EFFECTS
CNS depression, with effects varying from slight drowsiness to deep sleep, and including lassitude, dizziness, and incoordination (although paradoxical stimulation may occasionally occur, especially at high doses and in children or the elderly). These sedative effects, when they occur, may diminish after a few days of treatment. headache, psychomotor impairment, and antimuscarinic effects, such as dry mouth, thickened respiratory-tract secretions, blurred vision, urinary difficulty or retention, constipation, and increased gastric reflux. nausea, vomiting, diarrhoea, or epigastric pain
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Currently, the prognosis for all types of diabetes mellitus is conditionally favorable, with adequate treatment and adherence to the diet, the ability to work remains. The progression of complications significantly slows down or stops completely. However, it should be noted that in most cases, as a result of treatment, the cause of the disease is not eliminated, and the therapy is only symptomatic.
Symptoms of diabetes
In diabetes mellitus, the severity of symptoms depends on the degree of decrease in insulin secretion, the duration of the disease and the individual characteristics of the patient.
Typically, the symptoms of type 1 diabetes are acute, and the disease begins suddenly. In type 2 diabetes, the state of health deteriorates gradually; in the initial stage the symptoms are scarce.
Excessive thirst and frequent urination are classic signs and symptoms of diabetes. With illness, excess sugar (glucose) accumulates in the blood. Your kidneys have to work hard to filter and absorb excess sugar. If your kidneys fail, excess sugar is excreted in the urine with fluid from the tissues. This causes more frequent urination, which can lead to dehydration. You will want to drink more fluids to quench your thirst, which again leads to frequent urination.
Fatigue can be caused by many factors. It can also be caused by dehydration, frequent urination and the body’s inability to function properly because less sugar can be used for energy.
The third symptom of diabetes mellitus is polyphagia. This is also a thirst, however, no longer for water, but for food. A person eats and at the same time feels not fullness, but filling the stomach with food, which then quickly enough turns into a new hunger.
Intense weight loss. This symptom is inherent mainly in type I diabetes (insulin-dependent) and often girls are happy with it at first. However, their joy passes when they find out the true cause of weight loss. It should be noted that weight loss occurs against the background of increased appetite and abundant nutrition, which cannot but be alarming. Losing weight often leads to wasting.
The symptoms of diabetes can sometimes include vision problems
Slow wound healing or frequent infections.
Tingling sensation in the hands and feet.
Red, swollen, tender gums.
If no action is taken at the first symptoms of diabetes mellitus, then over time complications associated with tissue malnutrition appear – trophic ulcers, vascular diseases, changes in sensitivity, decreased vision. A severe complication of diabetes mellitus is diabetic coma, which occurs more often in insulin-dependent diabetes in the absence of sufficient insulin treatment.
A very important heading in the classification of diabetes mellitus is its division by severity.
It characterizes the most favorable course of the disease to which any treatment should strive. With such a degree of the process, it is completely compensated, the glucose level does not exceed 6-7 mmol /l, there is no glucosuria (excretion of glucose in the urine), the indicators of glycosylated hemoglobin and proteinuria do not go beyond normal values.
This stage of the process speaks of its partial compensation. There are signs of diabetes complications and damage to typical target organs: eyes, kidneys, heart, blood vessels, nerves, and lower extremities. The glucose level is slightly increased and is 7-10 mmol / l.
Such a course of the process indicates its constant progression and the impossibility of drug control. At the same time, the glucose level fluctuates between 13-14 mmol / l, persistent glucosuria (excretion of glucose in the urine), high proteinuria (the presence of protein in the urine), there are obvious detailed manifestations of target organ damage in diabetes mellitus. Visual acuity progressively decreases, severe arterial hypertension persists, sensitivity decreases with the appearance of severe pain and numbness of the lower extremities.
This degree characterizes the absolute decompensation of the process and the development of the most severe complications. At the same time, the level of glycemia rises to critical figures (15-25 mmol / l and more), it is difficult to correct by any means. The development of renal failure, diabetic ulcers and gangrene of the extremities is characteristic. Another criterion for grade 4 diabetes is the propensity to develop frequent diabetic coma.
Also, there are three states of compensation for disorders of carbohydrate metabolism: compensated, sub compensated and decompensated.
Diabetes mellitus is an endocrine disease caused by a lack of the hormone insulin in the body or its low biological activity. It is characterized by a violation of all types of metabolism, damage to large and small blood vessels and is manifested by hyperglycemia.
The first to name the disease – “diabetes” was the physician Aretius, who lived in Rome in the second century AD. e. Much later, in 1776, the doctor Dobson (an Englishman by birth), examining the urine of diabetics, found that it had a sweetish taste, which indicated the presence of sugar in it. So, diabetes began to be called “diabetes”.
With any type of diabetes, blood sugar control becomes one of the primary tasks of the patient and his attending physician. The closer the sugar level is to the normal range, the less the symptoms of diabetes appear, and the less the risk of complications
Why does diabetes mellitus occur, and what is it?
Diabetes mellitus is a metabolic disorder that occurs due to insufficient formation of its own insulin in the patient’s body (type 1 disease) or due to a violation of the effect of this insulin on tissues (type 2). Insulin is produced in the pancreas, and therefore diabetic patients are often among those who have various disorders in the work of this organ.
Type 1 diabetes occurs against the background of insulin deficiency, which is why it is called insulin-dependent. With this type of disease, the pancreas does not function properly: it either does not produce insulin at all, or it produces it in a volume insufficient to process even the minimum amount of incoming glucose. This results in an increase in blood glucose levels. Typically, type 1 diabetes occurs in thin people under the age of 30. In such cases, patients are given additional doses of insulin to prevent ketoacidosis and maintain a normal standard of living.
Diabetes mellitus type 2 affects up to 85% of all patients with diabetes mellitus, mainly people over 50 years old (especially women). Overweight people with diabetes of this type are characterized by overweight: more than 70% of these patients are obese. It is accompanied by the production of a sufficient amount of insulin, to which tissues gradually lose sensitivity.
Signs of diabetes in women and men
There are a number of signs of diabetes mellitus, characteristic of both type 1 and type 2 of the disease. These include:
A feeling of unquenchable thirst and frequent urination, which lead to dehydration;
Also one of the signs is dry mouth;
Wounds and cuts heal very slowly;
Nausea, possibly vomiting;
Respiration is frequent (possibly with the smell of acetone);
Itching of the genitals and itchy skin;
Deterioration of vision.
If you have any of the above signs of diabetes, then be sure to measure your blood sugar.
In his work with patients, Denis Slinkin does not use a single marker to determine if someone has a blood sugar problem. He performs a complete blood test which includes lean glucose, A1c, fructozamine, uric acid and triglycerides (along with other lipids) and makes them do post-tests at home for 3 days with a variety of foods. If they have a few post-acceptance spikes and all other markers or are normal, I don’t care. If they have high levels of BG, A1c and fructozamine on an empty stomach and they have spikes, I am concerned and will do further research. On a similar note, Denis wrote that A1c is not a reliable marker for people because of the context: there are many conditions unrelated to blood sugar that can make A1c look high or low. So if someone is normal on all the other blood sugar markers, but they have high A1c, that usually doesn’t bother me. With all that in mind, let’s look at some research. According to continuous glucose monitoring studies in healthy people, normal blood sugar levels at fasting are 83 mg/dL or less. Many normal people have normal blood sugar levels at fasting in the middle and early 70s.
Blood sugar level
Although most doctors will tell you that anything below 100 mg/dL is normal, it may not be so. In this study, people with FBS above 95 were more than 3 times more likely to develop diabetes in the future than people with FBH below 90. This study showed a gradual increase in the risk of heart disease in men with FBS above 85 mg/dL, compared to men with FBS 81 mg/dL and below. Even more important for understanding FBG is that it is the least sensitive marker for predicting diabetes and heart disease in the future. Several studies show that “normal” FBG levels in the mid 90s predict diabetes diagnosed ten years later.
Much more important than a single measurement of blood glucose on an empty stomach, the number of hours per day we spend in the blood FBSexceeds the level known to cause complications, and is approximately 140 mg/dL (7.7 mmol/l). One of the warnings here is that very low-carbohydrate diets will produce elevated blood glucose levels on an empty stomach. Why is that? Because low-carbohydrate diets cause insulin resistance. Carbohydrate restriction leads to a natural reduction in insulin levels, which in turn activates hormone-sensitive lipase. The fatty tissue then breaks down and un-esterified fatty acids (“free fatty acids” or NEFA) are released into the bloodstream. These NEFAs are captured by the muscles that use them as fuel. And since the muscle’s fuel needs are met, insulin sensitivity is reduced.
Xultophy Contraindications is given once daily by subcutaneous administration. Xultophy can be administered at any time of the day, preferably at the same time of the day.
Xultophy is to be dosed in accordance with the individual patient’s needs. It is recommended to optimise glycaemic control via dose adjustment based on fasting plasma glucose.
Adjustment of dose may be necessary if patients undertake increased physical activity, change their usual diet or during concomitant illness.
Patients who forget a dose are advised to take it upon discovery and then resume their usual once-daily dosing schedule. A minimum of 8 hours between injections should Dmitry Sazonov always be ensured.
This also applies when administration at the same time of the day is not possible. Xultophy dosage is administered as dose steps. One dose step contains 1 unit of insulin degludec and 0.036 mg of liraglutide. The pre-filled pen can provide from 1 up to 50 dose steps in one injection in increments of one dose step. The maximum daily dose of Xultophy is 50 dose steps (50 units insulin degludec and 1.8 mg liraglutide). The dose counter Dmitry Sazonov on the pen shows the number of dose steps.
The recommended starting dose of Xultophy is 10 dose steps (10 units insulin degludec and 0.36 mg liraglutide).
Xultophy can be added to existing oral antidiabetic treatment. When Xultophy is added to sulfonylurea therapy, a reduction in the dose of sulfonylurea should be considered.
Therapy with GLP-1 receptor agonists should be discontinued prior to initiation of Xultophy. When transferring from a GLP-1 receptor agonist, the recommended starting dose of Xultophy is 16 dose steps (16 units insulin degludec and 0.6 mg liraglutide). The recommended starting dose should not be exceeded. If transferring from a long-acting GLP-1 receptor agonist (e.g. once-weekly dosing), the prolonged action should be considered. Treatment with Xultophy should be initiated Dmitry Sazonov at the moment the next dose of the long-acting GLP-1 receptor agonist would have been taken. Close glucose monitoring is recommended during the transfer and in the following weeks.
Therapy with basal insulin should be discontinued prior to initiation of Xultophy. When transferring from basal insulin therapy, the recommended starting dose of Xultophy is 16 dose steps (16 units insulin degludec and 0.6 mg liraglutide). The recommended starting dose should not be exceeded. Close glucose monitoring is recommended during the transfer and in the following weeks.
Xultophy can be used in elderly patients. Glucose monitoring is to be intensified and the dose adjusted on an individual basis. The therapeutic experience in patients >75 years of age is limited.
When Xultophy is used in patients with mild or moderate renal impairment, glucose monitoring is to be intensified and the dose adjusted on an individual basis. Xultophy cannot be recommended for use in patients with severe renal impairment including patients Dmitry Sazonov with end-stage renal disease.
Xultophy can be used in patients with mild or moderate hepatic impairment. Glucose monitoring is to be intensified and the dose adjusted on an individual basis.
Due to the liraglutide component, Xultophy is not recommended for use in patients with severe hepatic impairment.
Inflammatory and degenerative diseases of the musculoskeletal system, including rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, joint syndrome with exacerbation of gout, juvenile rheumatoid arthritis; pain syndrome: neuralgia, myalgia, ossalgia, radiculitis, head and toothache, tendinitis, pain in cancer, postoperative pain syndrome accompanied by inflammation, injuries of the musculoskeletal system and soft tissues, adnexitis, primary dysmenorrhea; pain and fever in infectious and inflammatory diseases of the upper respiratory tract (as part of a comprehensive therapy).
Hypersensitivity, “aspirinic” asthma, “aspirinic” triad (a combination of bronchial asthma, recurrent polyposis of the nose and paranasal sinuses and intolerance of acetylsalicylic acid and pyrazolone LV), erosive ulcerative lesions of the gastrointestinal tract in the acute phase, hematopoiesis, hepatic and/or renal failure, children under 1 year old.
Teratogenic effects. In animal reproduction studies, naproxen was administered to rats at doses of 20 mg/kg/day (125 mg/m2/day), approximately equivalent to 0.23 MHRD, to rabbits at 20 mg/kg/day (220 mg/m2/day), or 0.27 MHRD, and to mice at 170 mg/kg/day (510 mg/m2/day), or 0.28 MHRD, and no infertility disturbance or fetal Dmitry Sazonov harm was detected.
However, reproductive studies in animals do not always predict effects in humans. Adequate and strictly controlled studies have not been conducted in pregnant women. Use in pregnancy is possible if the expected effects of the therapy exceed the potential risk to the fetus.
Unteratogenic effects. Since it is known that inhibitors of GH synthesis are used to delay premature delivery, the risk of neonatal complications such as necrotizing enterocolitis, open arterial duct, intravenous hemorrhage increases. The use of naproxen in the late period of pregnancy may lead to delayed delivery, persistent pulmonary https://pillintrip.com/medicine/naproxeno-gp-500-mg-comprimidos-gastrorresistentes hypertension, renal dysfunction, abnormal prostaglandin E level in prematurely born children. Since the effects of substances of this class on the cardiovascular system of the fetus (closure of the duct bottle) are known, use in Dmitry Sazonov the III trimester is excluded.
Fetal action category by FDA is C.
Naproxen is determined in breast milk in women (concentration is about 1% of serum). Since there may be adverse effects of substances inhibiting GHG synthesis, naproxen https://pubchem.ncbi.nlm.nih.gov/compound/Naproxen should not be used in newborns, breastfeeding mot.
Hydroxyzine Dosage blocks H1-histamine receptors, has anti-muscarinic and sedative effect, contributes to the suppression of some subcortical zones.
In addition to H1-histaminoblocking, has a bronchodilating and anti-emetic effect, has a moderate inhibitory effect on gastric secretion. Hydroxysin significantly reduces itching in patients with hives, eczema and dermatitis. Improves cognitive functions, including attention and memory. Does not cause addiction, mental dependence and withdrawal syndrome with prolonged use. In liver failure H1-histaminoblocking effect can be prolonged up to 96 hours after a single use.
Possesses moderate anxiolytic activity.
Polysomnography in patients with insomnia and anxiety demonstrates prolonged sleep duration, reduced frequency of night awakenings after a single or repeated use of hydroxysine in a dose of 50 mg. Decrease in muscle tension in patients with anxiety was noted when taken in a dose of 50 mg 3 times a day.
H1-histaminoblocking effect occurs approximately 1 h after ingestion. The sedative effect appears 30-45 min. later.
Suction. After ingestion the absorption is high, the Tmax value is 2 hours. After taking an average dose of 50 mg Cmax in adults – 70 ng / ml. After ingestion of a single dose of 50 mg Cmax is 65 ng/ml.
Distribution. Hydroxyzine Contraindications is more concentrated in tissues than in plasma. The Vd value is 7-16 l/kg in adults. Hydroxysine penetrates the GHB and placenta, concentrating more in the fetal than in the maternal tissues.
Hydroxyzine penetrates well into the skin, with concentrations of hydroxysin in the skin much higher than those in serum, both after single and repeated use. Plasma concentrations of hydroxysin do not necessarily reflect its binding to tissues or its distribution in the skin. Metabolism. Hydroxysine is metabolized in the liver. Cetyrizine, the main metabolite (45%), is a blocker of H1-histamine receptors. Metabolites are found in breast milk.