5 bad habits that damage your health.💣💣💣

Good health is the wish of many people. But everyone's different ways of living and eating will have different effects on their health. In daily life, there are several common bad habits that may be causing harm to your health.

1. Taking medicine indiscriminately.

Modern people pay more and more attention to health. Many people, even if they are healthy, will take some herbal medicines and health care products that are good for their health. Although this idea is good, all medicines have certain side effects. The most common side effect is damage to the liver. The liver is the most important detoxification organ of the human body. It is the most important organ for drug concentration, transformation and metabolism. Most drugs are metabolized by the liver, and herbal medicines and health products are no exception. Once these drugs or their metabolites have a certain degree of toxicity, the liver will be the first to suffer damage. It can cause liver damage such as inflammation of liver tissue cells and cholestasis. Moreover, this kind of injury is often very complicated, including almost all types of liver disease. Once the liver is damaged, it will affect people's health. Therefore, you should not take medicine indiscriminately. If you feel unwell, you should go to the hospital as soon as possible. Don't deal with it by your own experience.

2. Smoking and drinking.

Smoking and drinking have a great impact on health. Heart health is one of them. For example, smoking can easily cause vasculitis, increase blood pressure, blood lipids, and even cause blood clots. Current research has also found that there are as many as 93 specific toxic substances contained in cigarettes and 78 specific carcinogens. In addition to the well-known lung cancer, cigarette-related cancers include bladder cancer, pancreatic cancer, colorectal cancer, and so on. Excessive drinking also has many health risks, including obesity, liver damage and even cardiovascular and cerebrovascular accidents. Ethanol in alcohol and its metabolite acetaldehyde are carcinogens, which can make cancer cells more aggressive and spread throughout the body. They are important causes of cancers such as liver cancer, oral cancer, esophageal cancer, and gastric cancer. Therefore, if you want to live healthier, it is better to quit smoking and quit bars.

3. Stay up late.

Many people think that staying up late is just a lack of energy, poor skin, and dark circles under the eyes. In fact, the harm of staying up late is far more than that. People who often stay up late are more likely to get cancer. There are proto-oncogenes and tumor suppressor genes in the human body. Proto-oncogenes are the type that may stimulate the potential of cells to become cancerous. Tumor suppressor gene is to suppress tumor production. When people have some bad habits, such as often staying up late, proto-oncogenes may be activated and tumor suppressor genes may become weaker. Cancer cells will appear. Studies have shown that women who have worked night shifts for more than 30 years are twice as likely to develop breast cancer.

4. Long sitting.

Modern people are busy at work. Many people go to work in the morning and sit for a day. If they have to sit long time, they will have problems with their bodies. The damage to people's health caused by long sitting can be whole body, such as stiffness of the cervical spine, damage to the normal physiological curvature of the spine, arched back or bone hyperplasia, increased risk of hemorrhoids and so on. 

For men, long sitting will cause venous blood to accumulate in the scrotum and increase the temperature of the testicles. This results in venous masses on the surface of the scrotum, which affects spermatogenesis. In severe cases, it may also lead to infertility.

For women, long sitting is more harmful than men. Studies have pointed out that as long as women sit for more than 6 hours a day, the risk of dying early from various diseases is 37% higher than that of people who sit less than 3 hours a day, while men are 18% more likely to die.

5. Be in bad mood for a long time.

Modern people are under pressure in life and busy at work. They often don't have time to relax. If they don't pay attention, they are easily trapped in bad emotions. The World Health Organization once pointed out: By the middle of the 21st century, no disaster will bring people as much pain as a psychological crisis. Clinical statistics show that psychosomatic diseases caused by psychological and emotional factors account for up to 80-90% of the total number of patients. It can be seen that the negative emotions and excessive emotions of human beings are the main factors that threaten the physical and mental health of human.

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When omeprazole is used in combination with drugs, pay attention to the interaction.👀

Omeprazole is a proton pump inhibitor (PPI) that can be converted into sulfenamide compounds by protonation in an acidic environment. This compound can specifically bind to the α subunit of H+/K+-ATPase and inhibit its acid secretion activity. It is currently one of the most commonly used drugs for the treatment of acid-related diseases in clinical practice.

Omeprazole

The sulfinyl group in the chemical structure of omeprazole can be decomposed in acidic solution to cause polymerization and discoloration. Its stability may be affected by various factors such as the pH value of the solution, light, and temperature. This leads to contraindications between omeprazole and a variety of drugs.

1. The influence of pH.

Omeprazole is a benzimidazole compound and a weakly alkaline substance. The effect of pH change on its stability is particularly obvious, which can lead to its discoloration and precipitation. The main reasons are:

• Causes chemical structure changes: Omeprazole is relatively stable when the pH is around 9.0. It is easy to decompose in acidic environment to produce sulfone compounds and sulfide compounds, which cause discoloration of the solution.
• Causes solubility changes: Omeprazole is insoluble in water. After it is made into sodium salt, the solubility is improved. The maximum concentration commonly used in clinic is 40mg omeprazole sodium dissolved in 100ml normal saline (concentration is 0.4mg/ml). When the pH value of the omeprazole sodium solution decreases, free omeprazole is formed, causing turbidity or precipitation.

Acidic drugs: 

Omeprazole sodium is weakly alkaline. It will react with acidic drugs to produce new compounds. Reactions such as precipitation and discoloration will occur, and at the same time will lead to a reduction of active ingredients. Such acidic drugs include sulfacetamide, penicillin sodium, cefotaxime, piperacillin, fructose diphosphate sodium, vitamin C, vitamin B6, aminophylline, cimetidine, gentamicin and so on.

Drugs that depend on the pH of the stomach for absorption: 

Iron agents are mainly absorbed in the form of ferrous ions, which depend on the presence of gastric acid. The non-absorbed ferric iron can be converted into the divalent iron that can be absorbed under the action of gastric acid. Omeprazole can inhibit gastric acid, affect the absorption of iron, and reduce the efficacy. When the pH in the stomach rises, the tetracycline drug easily becomes insoluble free tetracycline, the absorption is reduced, and the curative effect is reduced. The absorption of ketoconazole also depends on sufficient gastric acid secretion. The acid suppression effect of omeprazole can reduce the absorption of ketoconazole and the blood concentration. The low acid environment can also reduce the absorption of itraconazole, so if necessary, acidic beverages can be used to take its capsule preparation.

2. Drugs related to metabolic enzymes.

Omeprazole is mainly metabolized to 5-OH-omeprazole by CYP2C19, or metabolized to omeprazole sulfone by CYP3A4, the former being the main metabolic pathway. Omeprazole can delay the elimination of drugs metabolized by the liver cytochrome P450 system in the body. Therefore, when omeprazole is combined with drugs related to CYP2C19 metabolizing enzymes, interactions are likely to occur.

Clopidogrel (CYP2C19 substrate):

Clopidogrel is a prodrug. It can only exert its antiplatelet effect after it enters the body and is metabolized by CYP2C19. Omeprazole is also metabolized in the liver by CYP2C19. The simultaneous use of the two may produce competitive inhibition. Clopidogdar does not have the effect of anti-platelet aggregation, which increases the risk of patients with ischemic stroke, compound stroke and myocardial infarction.

Diazepam (CYP2C19 substrate):

Omeprazole can weaken the metabolism of diazepam and increase its efficacy by inhibiting liver cytochrome P450 enzymes. Therefore, when used in combination, it should be monitored for enhanced sedation. If necessary, reduce the dose of diazepam.

Warfarin:

Omeprazole delays the clearance of warfarin by acting on the CYP450 enzyme system. The increase in warfarin exposure increases the international normalized ratio (INR) and prolongs the prothrombin time, which may lead to abnormal bleeding and even death. INR and prothrombin time should be monitored when used in combination. If necessary, adjust the warfarin dose to ensure that the INR is within the target range.

CYP2C19 or CYP3A4 inhibitors (such as voriconazole) and inducers (such as rifampicin):

Voriconazole can increase the exposure of omeprazole, except that patients with Zollinger-Eye syndrome may need to adjust the dose of omeprazole, and other generally do not need to be adjusted. Rifampicin can reduce the blood concentration of omeprazole. The combination of the two should be avoided.

Cilostazol (CYP2C19 substrate):

Omeprazole can increase the exposure of the active metabolite of cilostazol (3,4-dihydro-cilostazol). The dosage of cilostazol should be reduced to 50 mg once, twice a day.

Citalopram (CYP2C19 substrate):

Omeprazole can increase the exposure of citalopram and increase the risk of Q-T interval prolongation. The maximum dose of citalopram when used in combination should be 20 mg per day.

3. Other.

Methotrexate:

Omeprazole can inhibit the H+/K+-ATPase of the kidney. This will inhibit the active secretion of methotrexate and increase its blood concentration and toxicity.

Bismuth agent, montmorillonite powder, hydrotalcite, etc.:

They have a certain adsorption effect on omeprazole and can reduce the efficacy of omeprazole. In addition, the bismuth agent can better form a film in an acidic environment, and play the best role in protecting the gastric mucosa. If it is in a low-acid environment, its efficacy is reduced.

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Briefly talk about the impact of hyperuricemia.(Part. 2)😎😎😎

Hyperuricemia (Part. 2)✌

1. Life management of patients with hyperuricemia.

Health education:

Patients should avoid high-purine diets, and avoid inducements such as fatigue, cold, and stress. Patients should also regularly monitor blood pressure, blood sugar and other risk factors. At the same time, the blood uric acid level should be monitored regularly and checked regularly to improve the treatment effect.

Patients try to avoid using drugs that raise uric acid. Such as low-dose aspirin, immunosuppressive agents (cyclosporine), anti-tuberculosis drugs, most chemotherapy drugs, etc. Many people have to use anti-tuberculosis drugs, chemotherapy drugs and other treatments because of certain diseases such as tuberculosis and cancer. After weighing the pros and cons, it is generally believed that the harm of patients with hyperuricemia is not enough to make them give up those treatments.

Patients should quit smoking and carry out weight management. Target BMI <20 kg/m^2, male waist circumference <90 cm, female waist circumference <80 cm. The patient should have proper aerobic exercise.

Diet:

Patients should eat more fresh vegetables, a low-sugar and low-fat diet, and limit the intake of red meat, fish, and foods containing fructose and sucrose. Patients should also avoid the intake of animal offal, crustaceans, thick soups and broths. The daily purine content of the patient's diet is controlled below 200 mg.

The patient should consume 300 mL of skimmed or low-fat dairy products, 1 egg, and maintain a water intake of more than 2L per day. Patients can drink water, tea or unsweetened coffee.

Patients should strictly control drinking alcohol, especially beer and hard alcohol. The total amount of alcohol consumed daily should not exceed 28 grams for men (650 mL of beer, 280 mL of wine, or 50 mL of liquor), and 14 grams for women.

2. Drug treatment of hyperuricemia.

National guidelines have different recommendations on whether patients with asymptomatic hyperuricemia need medication.

Drugs that inhibit the synthesis of uric acid: 

They reduce the synthesis of uric acid by inhibiting the activity of xanthine oxidase.

1. Allopurinol: It is recommended that the initial dose of 50 mg for adults is 1-2 times a day, and thereafter it is increased by 50-100 mg each time. The general dose is 200-300 mg/d, divided into two to three doses. The maximum daily dose is 600 mg. Patients with renal insufficiency must reduce the dose. When eGFR is less than 10 mL/min or for dialysis patients, it is contraindicated. Use the lowest effective dose to maintain blood uric acid below the target level.
2. Febuxostat: The recommended initial dose is 20-40 mg, once a day, with an increase of 20 mg each time, and the maximum daily dose is generally 80 mg. After the blood uric acid level reaches the target, maintain the lowest effective dose. It should be noted that the FDA black box warns that febuxostat may increase the risk of cardiovascular death in patients. Febuxostat should be considered only when the patient does not respond to or cannot tolerate allopurinol treatment, and the specialist must fully assess the patient's condition and the risk of cardiovascular events before taking the drug.

Uric acid excretion drugs: 

They promote uric acid excretion by inhibiting renal tubular uric acid-anion transporter 1 (URAT1) and inhibiting renal tubular uric acid reabsorption.

1. Probenecid: Urinary stones and renal insufficiency are relatively contraindicated. For patients with renal insufficiency with eGFR> 30 mL/min, the recommended starting dose for adults is 25 mg/d, and the maximum dose is 75-100 mg/d. Drink more water during the administration to increase urine output.

Allopurinol, probenecid and febuxostat are all first-line drugs for lowering uric acid treatment. Patients with asymptomatic hyperuricemia can choose the first two categories, and patients with gout can choose the above. For patients with chronic kidney disease, the above all three types of drugs can be used, but febuxostat is the first choice when renal function is severely impaired.

Alkalized urine:

Urine pH <6 is an important factor in the formation of uric acid kidney stones. For patients with hyperuricemia and gout, the optimal morning urine pH is recommended to be 6.2 to 6.9. When the urine pH is <6, alkaline drugs, such as sodium bicarbonate, citric acid preparations, etc., can be used to alkalize urine according to the drug's indications, contraindications, and the individual characteristics of the patient.

Treatment of acute episodes:

When hyperuricemia develops into an acute attack of gout, it is recommended to use anti-inflammatory analgesia as soon as possible to improve the pain. Patients can use small doses of colchicine or adequate, short-term non-steroidal anti-inflammatory drugs, or systemic glucocorticoids. For patients with more serious conditions (such as acute gout involving multiple joints, large joints, or combined systemic symptoms), systemic glucocorticoid therapy is recommended. When the patient has severe pain, polyarthritis, or cumulative seizures of ≥ 2 large joints, a combination of two or more analgesic drugs can be used. During an acute attack, there is no need to adjust the dose of uric acid-lowering drugs that have been used.

Choice of drugs when there are comorbidities:

The principle of medication for each disease should be considered for comprehensive treatment. Try to choose drugs that lower uric acid and avoid drugs that raise uric acid.

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Briefly talk about the impact of hyperuricemia.(Part. 1)😎😎😎

Uric acid is a catabolite of purine nucleotides in the human body. It is a weakorganic acid. 80% of purine nucleotides are produced by human cell metabolism and 20% are obtained from food. The main cause of the increase in uric acid is excessive uric acid production and decreased uric acid excretion. 90% of hyperuricemia is related to decreased renal uric acid excretion.

1. Uric acid metabolism.

Synthesis:

The catabolism of purine nucleotides in the body is mainly carried out in the liver, small intestine and kidney. The abnormality of various key enzymes in the metabolic process will lead to an increase in uric acid synthesis, which accounts for about 10%.

Excretion:

Uric acid is mainly excreted through the kidneys and intestines. Normally, the amount of uric acid excreted into the intestinal cavity through the liver every day is about 1/4 to 1/3 of that produced, and then it is decomposed by bacteria in the intestinal cavity and then excreted from the body. The remaining 3/4 to 2/3 are excreted in urine by the kidneys. The abnormality of uric acid transporter located in the glomerulus and renal tubules and intestinal tract can affect the excretion of uric acid.

2. Causes of hyperuricemia.

Hyperuricemia is a metabolic syndrome caused by a disorder of purine metabolism. At a body temperature of 37 ℃, the saturated solubility of monosodium urate (MSU) in serum is 404.5 umol/L (6.8 mg/dL). It is usually defined as hyperuricemia when the serum uric acid level is> 420 umol/L (about 7 mg/dL). According to the cause, hyperuricemia is mainly divided into two categories: primary and secondary.

Primary hyperuricemia is mainly caused by abnormal enzyme activity during purine metabolism.

Secondary urinary hyperuricemia is characterized by defects in enzyme structure, excessive purine intake, alcohol consumption, enhanced nucleic acid metabolism (such as leukemia, anemic hemolysis, and malignant tumors) and accelerated purine decomposition (such as type I glycogen accumulation disease, hypoglycemia, hunger or exercise). The main causes of secondary hyperuricemia are: blood system disease, kidney disease, drug-induced, and excessive production of organic acids.

3. The effect of hyperuricemia on the body.

When uric acid or urate exceeds the normal solubility limit in body fluids, it will form crystals and deposit in any soft tissues except nerve tissues, which will cause different pathological changes.

Gout:

Hyperuricemia is the main risk factor for gout. Uric acid crystals deposit on joints and cause gout attacks. It causes bone and joint damage. Studies have shown that about 5% to 12% of hyperuricemia eventually develops into gout.

Hypertension:

Hyperuricemia can activate the renin-angiotensin system. It reduces the synthesis of nitric oxide in vascular endothelial cells and stimulates the proliferation of vascular smooth muscle. This can lead to increased blood pressure through various mechanisms such as vascular remodeling. In addition, long-term hypertension also affects uric acid metabolism through glomerular arteriosclerosis and other pathways, thereby aggravating hyperuricemia.

Abnormal blood lipid metabolism:

There is a mutual influence between uric acid metabolism and fat metabolism. Hyperuricemia and blood lipids can cause a decrease in lipoproteinase activity. At the same time, hyperlipidemia will also increase the rise of uric acid. In addition, hyperuricemia and hyperlipidemia are risk factors for arteriosclerosis and hypertension.

Diabetes:

Hyperuricemia can directly damage the function of pancreatic β-cells, thereby affecting insulin secretion and leading to diabetes. It can also aggravate metabolic disorders and insulin resistance in diabetic patients. It promotes the occurrence of macrovascular and microvascular complications in diabetic patients. At the same time, diabetic nephropathy and insulin resistance can also lead to aggravation of hyperuricemia.

Arteriosclerosis:

Uric acid crystals stimulate the blood vessel wall and induce an inflammatory response that damages vascular endothelial cells. In addition, hyperuricemia can also promote the formation of atherosclerosis together with hypertension, hyperlipidemia and hyperglycemia.

Heart failure:

Most cardiovascular diseases eventually lead to heart failure. Hyperuricemia is a risk factor for heart failure. This is closely related to its occurrence, development and prognosis.

Kidney damage:

Uric acid crystals are deposited in the kidneys. It causes uric acid nephropathy, increases the incidence of kidney stones and the risk of kidney failure.

Androgenetic alopecia:

Studies have shown that there is a significant correlation between hyperuricemia and androgenic alopecia, especially in patients with early-onset androgenic alopecia (< 30 years).

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The difference between empagliflozin, dapagliflozin, canagliflozin and ertugliflozin. 😵😵😵

Nowadays, the pros and cons of hypoglycemic drugs are no longer based on the hypoglycemic value as an evaluation criterion, but whether they have heart and kidney protection while reducing blood glucose as the evaluation criterion. SGLT2 inhibitors are a new type of oral hypoglycemic drugs that have received great attention in recent years. In addition to the treatment of type 2 diabetes, it is also used for the treatment of chronic heart failure and chronic kidney disease. Empagliflozin, dapagliflozin, canagliflozin and ertugliflozin are very commonly used SGLT2 inhibitors. What is the difference between them?

1. Hypoglycemic mechanism.

The full name of SGLT2 inhibitors is sodium-glucose cotransporter 2 inhibitor. Normally, the glucose filtered through the glomerulus per day is about 180g/d, but all glucose will be reabsorbed by the sodium-glucose cotransporter (SGLT1, SGLT2) on the renal tubules. SGLT2 inhibitors reduce the reabsorption of glucose and sodium by the kidneys by inhibiting SGLT2. It can excrete 70~80g/d glucose from the urine, thereby exerting a hypoglycemic effect, and has a certain hypotensive effect. 

2. Other effects.

SGLT2 inhibitors can reduce glycosylated hemoglobin (HbA1c) 0.5-1.2%, weight 0.6-3.0kg, systolic blood pressure 3-5mmHg, and blood uric acid about 50μmol/L. They are all good for heart failure. SGLT2 inhibitors have shown cardiovascular and renal benefits in a series of large cardiovascular and renal outcomes studies. Among them, only empagliflozin and canagliflozin are beneficial to atherosclerotic vascular disease. Empagliflozin, canagliflozin and dapagliflozin are beneficial for delaying chronic kidney disease.

3. Clinical application.

The 2022 edition of "ADA Diabetes Medical Diagnosis and Treatment Standards" recommends:

For patients with atherosclerotic vascular disease, heart failure and/or diabetic kidney disease, it is recommended to use GLP-1 receptor agonists or SGLT-2 inhibitors as the initial treatment. According to the patient's blood sugar status, metformin is combined or not combined.

ASCVD/high-risk factors: It is recommended to use GLP-1 receptor agonist or SGLT2 inhibitor. Choose GLP-1 receptor agonists that have proven cardiovascular benefits: dulaglutide, liraglutide and semaglutide. Choose SGLT2 inhibitors that have proven cardiovascular benefits: empagliflozin and canagliflozin.

Heart failure: It is recommended to choose SGLT2 inhibitors that have been proven to be beneficial for heart failure: empagliflozin, canagliflozin, dapagliflozin and ertugliflozin.

Chronic kidney disease: 

Patients with chronic kidney disease and proteinuria should first choose SGLT2 inhibitors that can delay the progression of chronic kidney disease: canagliflozin, empagliflozin and dapagliflozin. If SGLT2 inhibitors are contraindicated/intolerant, choose GLP1 receptor agonists with cardiovascular benefits: dulaglutide, liraglutide and semaglutide. 

Patients with chronic kidney disease who do not have proteinuria should choose GLP-1 receptor agonists or SGLT2 inhibitors that have cardiovascular benefits.

4. Dosage.

SGLT2 inhibitor has diuretic effect. To avoid excessive nocturia, it is recommended to take it in the morning. They are not affected by meals.

Empagliflozin: It has a peak time of 1.5 hours and a half-life of 12.4 hours. Its recommended dosage is 10 mg once a day. The maximum dose is 25 mg once a day.

Dapagliflozin: It has a peak time of 2 hours and a half-life of 12.9 hours. Its recommended dosage is 5 mg once a day. The maximum dose is 10 mg once a day.

Canagliflozin: It has a peak time of 1-2 hours and a half-life of 10.6-13.1 hours. Its recommended dosage is 100 mg once a day. The maximum dose is 300 mg once a day.

Ertugliflozin: It has a peak time of 1 hours and a half-life of 16.6 hours. Its recommended dosage is 5 mg once a day.

5. Adverse effects.

Urinary and reproductive tract infections: SGLT2 inhibitors play a hypoglycemic effect mainly by promoting urinary glucose excretion. Due to the increased concentration of glucose in urine, SGLT2 inhibitors can significantly increase the risk of urinary tract infections and genital fungal infections. During the medication, you should increase the amount of drinking water and keep the vulva clean. If urinary tract infections and reproductive tract infections occur, symptomatic treatments such as antibacterial drugs (including antifungal drugs) are required.

Hypovolemia: SGLT2 inhibitors have an osmotic diuretic effect, which can lead to a decrease in blood volume. Elderly patients or those taking loop diuretics (such as furosemide) are at increased risk of hypovolemia. The main manifestations of hypovolemia are dehydration, orthostatic hypotension or hypotension.

Fracture risk: Patients with type 2 diabetes are more likely to fracture than the general population. The main fracture sites are the hip, foot and proximal femur. SGLT inhibitors can inhibit the reabsorption of sodium in the renal tubules and increase the reabsorption of phosphorus. This leads to increased blood phosphorus levels, stimulates parathyroid hormone secretion, and increases bone resorption. Canagliflozin can increase the risk of fractures.

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Summarize the diabetes medical diagnosis and treatment standards issued by the American Diabetes Association in 2022.👀

Recently, the American Diabetes Association released the Diabetes Medical Diagnosis and Treatment Standards for 2022. With regard to the treatment of type 2 diabetes, the new version of the guidelines has made many updates, weakening the status of metformin as the first-line medication.

1. Recommendations for the treatment of type 2 diabetes.

Initial treatment: Metformin is generally used. For patients with atherosclerotic cardiovascular disease (ASCVD)/high-risk factors, heart failure and/or chronic kidney disease, GLP-1 receptor agonist or SGLT2 inhibitor is recommended as the initial treatment. According to the patient's blood sugar status, metformin is combined or not combined. Unless the patient is contraindicated or intolerant, metformin should be continued after the initial insulin therapy to continuously improve blood sugar and metabolism. 

• Compared with insulin monotherapy, metformin combined with insulin can further reduce HbA1c, reduce insulin dosage, weight gain and the risk of hypoglycemia.

For some patients, early combination therapy can be considered when starting treatment to prolong the time of treatment failure. 

When choosing hypoglycemic drugs, cardiovascular complications, the efficacy of hypoglycemic drugs, the risk of hypoglycemia, the impact on weight, cost, availability, side effects and patient wishes should be considered.

Regardless of whether the HbA1c level is up to standard, if the patient has ASCVD/high-risk factors, kidney disease or heart failure, it is recommended to use SGLT2 inhibitors and/or GLP-1 receptor agonists that have proven cardiovascular benefits.

For patients with type 2 diabetes, GLP-1 receptor agonists are better than insulin.

If insulin is used, it is recommended to combine therapy with GLP-1 receptor agonists to improve the efficacy and durability of the therapeutic effect.

Patients with type 2 diabetes who are not up to the standard should be intensively treated as soon as possible.

The treatment plan should be re-evaluated every 3-6 months, and adjusted according to needs and new influencing factors.

Clinicians should be alert to insulin overtreatment. The following conditions may indicate that there may be excessive insulin consumption. Including the basic dose of more than 0.5IU/kg, the great difference in blood glucose between bedtime and fasting or before and after meals, hypoglycemia (symptomatic or asymptomatic), and high variability. When insulin overtreatment occurs, the next step of individualized treatment should be redesigned.

2. The choice of hypoglycemic drugs for patients with ASCVD, heart failure and chronic kidney disease.

ASCVD/high-risk factors: It is recommended to use GLP-1 receptor agonist or SGLT2 inhibitor. Choose GLP-1 receptor agonists that have proven cardiovascular benefits: dulaglutide, liraglutide and semaglutide. Choose SGLT2 inhibitors that have proven cardiovascular benefits: empagliflozin and canagliflozin.

Heart failure: It is recommended to choose SGLT2 inhibitors that have been proven to be beneficial for heart failure: empagliflozin, canagliflozin, dapagliflozin and ertugliflozin.

Chronic kidney disease: 

• Patients with chronic kidney disease and proteinuria should first choose SGLT2 inhibitors that can delay the progression of chronic kidney disease: canagliflozin, empagliflozin and dapagliflozin. If SGLT2 inhibitors are contraindicated/intolerant, choose GLP1 receptor agonists with cardiovascular benefits: dulaglutide, liraglutide and semaglutide. 
• Patients with chronic kidney disease who do not have proteinuria should choose GLP-1 receptor agonists or SGLT2 inhibitors that have cardiovascular benefits.

3. The main features of hypoglycemic drugs.

Metformin: It has a higher efficacy, no risk of hypoglycemia, and does not have much effect on body weight. There are potential benefits for cardiovascular, but no obvious benefits for the progression of kidney disease and heart failure.

SGLT2 inhibitor: It has a moderate effect, has no risk of hypoglycemia, and can reduce weight. Empagliflozin and canagliflozin have cardiovascular benefits. Empagliflozin, canagliflozin, dapagliflozin and ertugliflozin are beneficial for heart failure. Canagliflozin, dapagliflozin and empagliflozin are beneficial to the progression of kidney disease.

GLP-1 receptor agonist: It has higher efficacy, no risk of hypoglycemia, and can reduce weight. Dulaglutide, liraglutide, and semaglutide have cardiovascular benefits. Neutral to heart failure. Dulaglutide, liraglutide and semaglutide are beneficial for renal endpoints.

DPP-4 inhibitor: It has moderate efficacy, no risk of hypoglycemia, and does not affect body weight. There is no benefit to cardiovascular and the progression of kidney disease. In addition, saxagliptin has a potential risk of heart failure.

Thiazolidinedione: It has a higher efficacy, no risk of hypoglycemia, and will increase weight. Pioglitazone has potential cardiovascular benefits. Thiazolidinediones increase the risk of heart failure and are not beneficial to the progression of kidney disease.

Sulfonylureas: It has a higher efficacy. It has a risk of hypoglycemia and can increase weight. It has no effect on cardiovascular, heart failure and the progression of kidney disease.

Insulin: It has a higher efficacy. It has a risk of hypoglycemia and can increase weight. It has no effect on cardiovascular, heart failure and the progression of kidney disease.

4. Adverse reactions and precautions.

Metformin: Common gastrointestinal reactions (diarrhea, nausea). It may cause vitamin B12 deficiency.

SGLT2 inhibitor: SGLT2 inhibitors need to be stopped before any elective surgery to avoid the risk of DKA (diabetic ketoacidosis). Common side effects include genitourinary system infection, hypovolemia, risk of hypotension, elevated LDL-C, and Fournier gangrene. Canagliflozin has a risk of fracture.

GLP-1 receptor agonist: Common side effects are gastrointestinal reactions (nausea, vomiting, diarrhea). FDA black box warning: risk of thyroid C-cell tumors in rodent studies. However, the relevance to humans is not clear (liraglutide, dulaglutide, exenatide sustained-release agent, semaglutide).

DPP-4 inhibitor: Clinical trials have reported pancreatitis, but the causality has not yet been clarified. If pancreatitis is suspected, the drug should be discontinued. Joint pain is also a common side effect.

Thiazolidinedione: Common side effects include water and sodium retention (edema, heart failure) and the risk of fractures. Pioglitazone and rosiglitazone are at risk of congestive heart failure. Pioglitazone has a risk of bladder cancer. Rosiglitazone may increase LDL-C.

Sulfonylureas: The first generation of sulfonylureas (tolbutamide) has an increased risk of cardiovascular death.

Insulin: Risk of hypoglycemia: human insulin> human insulin analogues.

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Some lifestyle habits that can help you prevent cancer.📆📆📆

Even though medical technology is becoming more and more advanced
nowadays, cancer is still one of the diseases that everyone is afraid of. There are more and more people suffering from cancer. Every minute around the world, many people are diagnosed with cancer or die of cancer. In addition to genetics that affect cancer, daily living habits can also affect cancer. Some bad habits can make people more prone to cancer. Here are some lifestyle habits that can help you prevent cancer.

1. Eating habits.

Many families are accustomed to a high-salt, high-sugar, and high-oil diet, which makes it easy to suffer from various chronic diseases, such as high blood pressure, diabetes, gout, and high blood lipids. At the same time, it will be more prone to cancer. Therefore, the usual diet should do the following:

1. Try to have a light diet, eat less high-fat, high-salt and pickled foods. It is best to consume no more than 6 grams of salt per day.
2. Eat moderate amounts of meat, each person consumes 50-75g of livestock and poultry meat and 50-100g of fish and shrimp every day. Appropriately reduce the intake of red meat (such as beef, pig and mutton), and eat less processed meat products (such as sausage and ham).
3. Drink less sugary drinks and eat less high-energy-density foods, such as desserts and high-fat meats.
4. Drink less alcohol. If you cannot avoid drinking, men should limit their drinking to less than 2 alcohol units per day, and women should limit their drinking to 1 alcohol unit per day (1 alcohol unit is 10 ml of pure alcohol, which is approximately equivalent to 360 ml of beer and 150 ml of wine or 45ml of white wine).
5. Eat more vegetables, fruits, whole grains and legumes, which should account for more than 2/3 of your daily diet. The more types, the better.
6. To maintain good eating habits. Eat regularly every day, eat slowly and avoid overeating.

2. Exercise.

Proper exercise can enhance physical fitness, improve immunity and enhance the body's resistance. Studies have shown that exercise can significantly reduce the incidence of 13 types of cancer. Lack of necessary exercise can reduce a person's life span by 3-5 years. This also increases the probability of cancer, heart disease and stroke by 25-50%. 

Suggestion:

• Perform aerobic exercises 3 times or more a week, such as jogging, swimming, skipping rope, and cycling for at least 30 minutes each time. Pay attention to warming up and stretching before and after exercise. After adapting to this exercise intensity, gradually increase the amount of exercise according to personal circumstances.

3. Sleeping.

Studies have shown that long-term lack of sleep increases the risk of cancers such as colorectal cancer, thyroid cancer and lung cancer. Studies have investigated more than 1000 cancer patients between the ages of 30 and 50 from all over the world. It was found that 99.3% of them would not rest until after the early hours of the morning for a long time. 

Suggestion:

• Children 1-2 years old: It is recommended to sleep 11-14 hours a day, but it should not be less than 9 hours or more than 16 hours.
• Children 3-5 years old: It is recommended to sleep 10-13 hours a day, but it should not be less than 8 hours or more than 14 hours.
• Children 6-13 years old: It is recommended to sleep 9-11 hours a day, but it should not be less than 7 hours or more than 12 hours.
• Adolescents aged 14-17: It is recommended to sleep 8-10 hours a day, but it should not be less than 7 hours or more than 11 hours.
• Adults aged 18-64: It is recommended to sleep 7-9 hours a day, but should not be less than 6 hours or more than 11 hours.
• Elderly people over 65: It is recommended to sleep 7-9 hours a day, but it should not be less than 5 hours or more than 9 hours.

4. Emotion.

Studies have found that experimental mice live in a pleasant environment, and their tumors are getting smaller than those in the control group, and even disappear. Positive emotions have a positive impact on the immune system and can help prevent cancer.

5. Examination.

Cancer is a chronic development process. Therefore, if cancer is detected as early as possible, there is a greater chance of recovery. Lung cancer is the cancer with the highest morbidity and mortality. However, if it is detected and treated early, the 5-year survival rate can reach 90%. Regular examination can detect cancer early and improve the cure rate of patients. In addition, people with past medical or family history should undergo more targeted examinations.

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Knowledge about streptococcal infection.📜📜📜

Streptococcus has a wide variety of bacteria and is widely distributed. Some streptococci are normal human flora, while others are pathogenic bacteria of humans. 

1. What is streptococcus?

Streptococcus is a gram-positive cocci and the bacteria are purple after Gram staining. According to whether hemolysis occurs on blood agar, Streptococcus bacteria are divided into three categories: α-hemolytic streptococcus, β-hemolytic streptococcus and γ-streptococcus.

Medically important streptococci:

1. α-hemolytic streptococcus: Streptococcus pneumoniae, Streptococcus viridans.
2. β-hemolytic streptococcus: Group A Streptococcus (also call streptococcus pyogenes), group B, group C, group D and group G streptococcus.
3. γ-streptococcus: They are generally not causing disease.

2. Common streptococcus infections:

• Streptococcus pneumoniae: Streptococcus pneumoniae is distributed in the nasopharynx of 5-10% of adults and 20-40% of children. Most of the strains are not pathogenic and only a few strains are pathogenic. It is the main pathogen of bacterial pneumonia. It causes diseases such as acute bacterial otitis media, acute bacterial sinusitis, community-acquired pneumonia and lung abscess.
• Streptococcus viridans: It is mainly distributed in the oropharynx and gastrointestinal tract. It1 is a common pathogen causing dental caries, infective endocarditis and bacteremia.
• Streptococcus pyogenes: It is mainly distributed in the throat and is the most pathogenic bacteria among streptococci. It accounts for about 90% of streptococcal infections. It is the main pathogen of acute bacterial pharyngitis and tonsillitis. It can also cause lymphangitis, acute cellulitis, acute rheumatic fever, and glomerulonephritis.

3. Commonly used antibacterial drugs for streptococcal infections.

• Penicillin is the first choice for streptococcal infections. The antibacterial activity of the first and second generation cephalosporins against Streptococcus pneumoniae is less than penicillin. The drug resistance of streptococcus is caused by genetic mutations. Streptococcus pneumoniae is also less resistant to them. Streptococcus is not sensitive to penicillin. Amoxicillin, ceftriaxone and cefotaxime will have good antibacterial activity. 
• Penicillin-resistant Streptococcus pneumoniae is highly sensitive to vancomycin, linezolid and carbapenems.
• The resistance rate of macrolides and clindamycin is high.
• Aminoglycosides have no antibacterial activity against streptococci, but have synergistic effects with β-lactam antibiotics.

Acute bacterial pharyngitis and tonsillitis:

The common pathogen is group A hemolytic streptococcus. Penicillin is the first choice. Optional amoxicillin. Amoxicillin/clavulanic acid should not be used. This is mainly because hemolytic streptococcus does not produce β-lactamase, and clavulanic acid is useless at all. Since non-suppurative complications (acute rheumatic fever and glomerulonephritis) can occur after infection of group A hemolytic streptococcus, antibacterial treatment is aimed at removing bacteria and the course of treatment takes 10 days.

Acute bacterial otitis media and acute bacterial sinusitis:

The common pathogens are Streptococcus pneumoniae, Moraxella catarrhalis and Haemophilus influenzae. The first choice is amoxicillin or amoxicillin/clavulanic acid. 

Mainly reasons:

• Anti-Gram-positive bacteria activity (group A hemolytic streptococcus, streptococcus pneumoniae): amoxicillin ≈ penicillin.
• Anti-Gram-negative bacteria activity (Moraxella catarrhalis, Haemophilus influenzae): amoxicillin/clavulanic acid> amoxicillin> penicillin.

	Common pathogens	Antibacterial drugs
Acute bacterial pharyngitis and tonsillitis	Group A hemolytic streptococcus	l   Penicillin, amoxicillin. l   Patients who are allergic to penicillin can choose tetracyclines or fluoroquinolones that are sensitive to hemolytic streptococci (such as levofloxacin, moxifloxacin).
Acute cellulitis and lymphangitis.	Group A hemolytic streptococcus	l   Penicillin, amoxicillin. l   Amoxicillin/clavulanic acid, ceftriaxone.
Acute bacterial otitis media.	Streptococcus pneumoniae, Moraxella catarrhalis and Haemophilus influenzae.	l   Amoxicillin. l   If Moraxella catarrhalis and Haemophilus influenzae which producing β-lactamase strains are common in the local area, amoxicillin/clavulanic acid should be used. l   If the patient has no effect after taking the medicine for 3 days, it should be considered as possible penicillin-resistant Streptococcus pneumoniae infection. Ceftriaxone should be used.
Acute bacterial sinusitis.	Streptococcus pneumoniae, Moraxella catarrhalis and Haemophilus influenzae.	l   Amoxicillin/clavulanic acid.
Infective endocarditis	Streptococcus viridans.	l   Penicillin is used in combination with gentamicin. l   Combine ceftriaxone or cefotaxime with gentamicin.
Purulent meningitis (age < 1 month)	Group B hemolytic streptococcus, Escherichia coli, Listeria and Klebsiella pneumoniae.	l   Combine ceftriaxone or cefotaxime with ampicillin. l   Gentamicin is combined with ampicillin.

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Have you ever used corticosteroids ointments❓❓❓

Topical glucocorticoid is a very commonly used topical drug. Some people think that it is a panacea that can cure skin diseases such as itching, redness and swelling. However, some people refuse to use it because it contains steroids. The following are some practical knowledge about topical glucocorticoids.

1. Classification and intensity.

According to the different types and concentrations of glucocorticoids, topical glucocorticoids can be divided into 4 categories: super strong, strong, medium and weak. The same glucocorticoid has different strengths at different concentrations.

Commonly used topical glucocorticoids
Super strong	Clobetasol propionate	0.02%	1.    It is suitable for severe and hypertrophic skin lesions. 2.      Not for use in children <12 years old. 3.    Do not use on soft skin area. 4.    Long-term use in a small area. 5.    Do not exceed 50g per week. 6.    Continuous medication should not exceed 2-3 weeks. 7.    * They can be used with caution in children.
	Betamethasone valerate	0.1%
	Halometasone	0.05%
	Halcinonide	0.1%
	Fluocinolone	0.2%
Strong	Beclomethasone dipropionate	0.025%
	Betamethasone valerate	0.05%
	Fluocinolone	0.025%
	*Fluticasone propionate	0.05%
	*Mometasone furoate	0.1%
Medium	Prednisolone acetate	0.5%	1.    Suitable for mild to moderate skin lesions. 2.    It should not be used for a long time in a large area. 3.    It can be applied continuously for 4-6 weeks. 4.    Children <12 years old try not to use it continuously for more than 2 weeks.
	Dexamethasone acetate	0.05%
	Clobetasone butyrate	0.05%
	Hydrocortisone butyrate	1%
	Triamcinolone acetonide	0.025%
	Fludrocortisone acetate	0.025%
	Fluocinolone acetonide	0.01%
Weak	Hydrocortisone acetate	1%	1.    Suitable for mild to moderate skin lesions. 2.    Apply to the soft skin areas. 3.    Suitable for children <12 years old. 4.    It can be used in a larger area in a short time. 5.    It can be used for a long time if necessary.
	Methylprednisolone acetate	0.025%
	Desonide	0.05%
	Fluocinolone acetonide	0.0025%

Although fluticasone propionate and mometasone furoate are both strong glucocorticoids, they are less absorbed throughout the body when used externally. They are suitable for use by the elderly, infants and in a large areas.

2. The choice of topical glucocorticoids in various populations.

Children and the elderly: It is advisable to choose weak glucocorticoids, and use strong and super strong types with caution.

Pregnant women: Glucocorticoids should be used with caution in pregnant women. Weak or medium types can be selected when they must be used.

Soft skin areas: The face, neck, armpits, groin, inner thighs, perineum and other soft skin areas have a high drug absorption rate, so strong glucocorticoids should not be used. When it must be used, desonide, mometasone furoate and hydrocortisone can be used.

Ointment: The ointment dosage form has an encapsulating effect, which enhances the drug penetration ability. Ointment is suitable for keratinized, hypertrophic and desquamative skin, especially palms and soles. It is not recommended for non-hypertrophic, keratinized skin lesions on soft skin areas such as the face. Ointment should not be used in skin areas where babies wear diapers.

Creams, gels and solutions: They are suitable for all kinds of skin lesions and are also suitable for thick hair areas.

3. Indications.

Dermatitis, eczema, papular urticaria, erythema scaly skin disease, autoimmune skin disease, etc.

4. Contraindications.

Impetigo (bacterial infection), tinea hand and foot (fungal infection), shingles (viral infection), rosacea, acne, skin ulcers, etc. It is also not suitable for acute urticaria. The redness and itching caused by acute urticaria should be relieved with appropriate antihistamines (such as cetirizine, loratadine).

5. Dosage:

The most commonly used method for estimating the amount is the "fingertip unit"(FTU).

FTU: It refers to the amount of ointment squeezed from the ointment tube (with a diameter of 5mm) to an adult's fingertip (from the end of the index finger to the horizontal line of the first knuckle joint). A fingertip unit is about 0.5g ointment.

Estimate the skin area with the palm of your hand, and then calculate the FTU based on the area. Use about 0.5 FTU per palm area.

6. Adverse reactions.

The correct use of topical glucocorticoids is relatively safe. Long-term or large amounts of topical glucocorticoids may induce or aggravate local infections, leading to skin atrophy, telangiectasia, hirsutism, pigment changes, hormone dependence and other adverse reactions.

Patients should actively monitor for adverse reactions: The strong and super strong types are once every 2 weeks, the medium types are once every 3-4 weeks, and the weak types are once every 4-6 weeks.

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