How to use nebulized medicine?💫💫💫

One of the important ways of treating respiratory diseases is aerosol inhalation therapy. One of the important means of treating respiratory diseases is aerosol inhalation therapy. Therefore, it is very important to understand the correct usage of nebulized drugs.

The process of inhaling a drug in the body.

Compared with administration methods such as injection or oral administration, the biggest advantage of aerosol inhalation administration is that the drug can be directly sent to the airway or lungs for local treatment. This advantage can make the drug less systemic adverse effects. The particle size of the aerosol inhalation drug is preferably 1 to 5 μm. If the particle size is larger than 5 μm, most of the drug will stay in the oropharynx and be swallowed into the body. If the particle size is less than 0.5 μm, although the drug can enter the alveoli and bronchioles, most of the drug will be excreted by exhalation.

Medication treatment of nebulized drugs.

Commonly used nebulized inhaled drugs are short-acting β-agonists (such as albuterol), short-acting anticholinergic drugs (such as ipratropium bromide), inhaled glucocorticoids (such as budesonide) and expectorants (such as ambroxol). 

Disease	Short-acting β-agonists	Short-acting anticholinergic drugs	Inhaled glucocorticoids	Expectorants
Acute exacerbation of bronchial asthma.	✔	Use when necessary.	✔	✖
Long-term control of bronchial asthma.	Use when necessary.	✖	✔	✖
Cough variant asthma.	✖	✖	✔	✖
Variant cough.	✖	✖	✔	✖
Eosinophilic bronchitis.	✖	✖	✔	Use when necessary.
Asthmatic bronchitis.	✔	Use when necessary.	✔	✖
Acute laryngotracheobronchitis.	✖	✖	✔	✖
Bronchiolitis obliterans.	Use when necessary.	Use when necessary.	✔	✔
Bronchiolitis.	✔	Use when necessary.	✔	✖
Pneumonia.	Use when necessary.	Use when necessary.	✖	✔
Acute epiglottitis.	✖	✖	✔	✖
Pertussis or pertussis-like syndrome.	Use when necessary.	Use when necessary.	✔	✖
Bronchopulmonary dysplasia.	✖	✔	✔	✖
Bronchiectasis.	Use when necessary.	Use when necessary.	✔	✔
Endotracheal intubation or throat surgery.	✖	✖	✔	✖
Cough after infection.	Use when necessary.	✖	✔	✖

 Commonly used nebulized drugs and their adverse reactions.

The nebulized drugs stay on the surface of the airway mucosa for a short time and have a short half-life in the blood, but have a long residence time in the local tissue.

1. Short-acting β-agonists: Commonly used drugs are salbutamol and terbutaline. Their common adverse reactions were headache, tremor and tachycardia.
2. Short-acting anticholinergic drugs: Commonly used drugs are ipratropium. Its common adverse reactions are headache, dizziness, dry mouth and vomiting.
3. Inhaled glucocorticoids: Commonly used drugs are beclomethasone dipropionate, fluticasone propionate and budesonide. Their common adverse reactions are pharyngitis, hoarseness and oropharyngeal candidiasis.
4. Expectorants: Commonly used drugs are acetylcysteine and ambroxol. Their common adverse reactions are stomatitis, oral numbness (ambroxol), disturbance of taste, nausea and vomiting.

What is the difference between inhaled glucocorticoids?

Commonly used drugs are beclomethasone dipropionate, fluticasone propionate and budesonide. Inhaled glucocorticoids have two mechanisms of action. The first is the genetic pathway. Their lipid solubility allows them to enter cells, where they bind to cytoplasmic receptors and then enter the nucleus. Once in the nucleus, they initiate gene transcription. It promotes anti-inflammatory protein synthesis and inhibits pro-inflammatory protein synthesis. They develop an anti-inflammatory effect after about a few hours. The second is the non-genetic pathway. They bind to hormone receptors on cell membranes. Cell energy metabolism and lysosomes are affected by it. They act as anti-inflammatory within minutes.

1. Beclomethasone dipropionate: It is the only prodrug of the three glucocorticoids. Its elimination half-life is approximately 0.5 hours. It has the highest rates of oropharyngeal candida infections and pharyngitis of the three.
2. Fluticasone propionate: It has better receptor affinity. Its stagnation time in the lungs is the shortest of the three. Its elimination half-life is approximately 8 hours. In addition, its inhibitory effect on the adrenal cortex is the strongest of the three.
3. Budesonide: It has the best hydrophilicity. Its stagnation time in the lungs is the longest of the three. Its elimination half-life is approximately 3 hours.

What is the combined use of nebulized drugs?

Short-acting β-agonist and inhaled glucocorticoid act synergistically, so they are the most commonly used combination. Short-acting β-agonist and short-acting anticholinergic drug are also more commonly used in combination.

1. Dual therapy: Short-acting β-agonist + short-acting anticholinergic drug, inhaled glucocorticoid + short-acting anticholinergic drug, acetylcysteine + short-acting β-agonist/short-acting anticholinergic drug/inhaled glucocorticoid.
2. Triple therapy: Short-acting β-agonist + short-acting anticholinergic drug + inhaled glucocorticoid, short-acting β-agonist/short-acting anticholinergic drug + inhaled glucocorticoid + acetylcysteine.
3. Quadruple Therapy: Short-acting β-agonist + short-acting anticholinergic drug + inhaled glucocorticoid + acetylcysteine.

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What is the difference between piperacillin combined with tazobactam and cefoperazone combined with sulbactam?📣📣📣

Due to the extensive use of antibiotics, bacterial resistance to antibiotics continues to rise. The most common pathogens of bacterial infectious diseases are caused by Gram-negative bacteria. The mechanism of resistance in Gram-negative bacteria is mainly the generation of different β-lactamases, such as penicillinase, cephalosporinase, carbapenemase and extended-spectrum β-lactamases (ESBLs). Most β-lactamases produced by bacteria are inactivated by binding to β-lactamase inhibitors. β-lactamase inhibitors can prevent the β-lactam ring in antibiotics from being hydrolyzed, thereby protecting the antibacterial effect of β-lactam antibiotics. In the combination of β-lactamase inhibitor and antibiotics, piperacillin combined with tazobactam and cefoperazone combined with sulbactam are drugs with high clinical use and good efficacy. However, what are the differences between them and how should choose them?

Comparison of antibacterial spectrum of piperacillin combined with tazobactam and cefoperazone combined with sulbactam.

	Piperacillin/tazobactam	Cefoperazone/sulbactamzxad
Acinetobacter	+	+++
Enterobacter	++	+++
Enterococcus	+	-
Escherichia coli	++++	++++
Haemophilus influenzae	+++	+++
Klebsiella	+++	++++
Methicillin-sensitive Staphylococcus aureus	+	+
Moraxella catarrhalis	+	+
Pseudomonas aeruginosa	++++	+++
Stenotrophomonas maltophilia	-	+++
Streptococcus	+	+
"-" means no effect. "+" means it works. The more "+" the table has, the stronger the effect.

Can they treat gram-positive infections?

In general, piperacillin combined with tazobactam and cefoperazone combined with sulbactam will not be used to treat pure gram-positive infections. Although cefoperazone combined with sulbactam may be effective against enterococci (eg, Streptococcus faecalis), cefoperazone combined with sulbactam is generally considered to be ineffective against enterococci. Ampicillin in combination with sulbactam and amoxicillin in combination with clavulanic acid are commonly used drugs for the treatment of gram-positive infections. They have a certain antibacterial ability against methicillin-sensitive staphylococcus aureus, enterococcus and streptococcus.

How effective are they in the treatment of bacterial infections that produce extended-spectrum β-lactamases?

In the in vitro drug susceptibility test, their sensitivity were over 80% to the ESBLs-producing strains. For patients with mild to moderate infection without secondary severe sepsis or septic shock, one of them can be selected according to the results of drug susceptibility testing. However, they are not the first choice for patients with severe infections. Carbapenems are the most effective and reliable drugs for the treatment of various infections caused by enterobacteriaceae that produce extended-spectrum β-lactamases. Studies have shown that the high-dose extended infusion regimen of piperacillin/tazobactam can achieve the best pharmacodynamics, but any regimen of cefoperazone/sulbactam can not achieve the desired pharmacodynamics . Therefore, piperacillin combined with tazobactam is more suitable for the empirical treatment of extended-spectrum β-lactamase-producing bacterial infections.

How effective are they in the treatment of stenotrophomonas maltophilia infections?

Patients with more severe infections generally require combination therapy. Usually, sulfamethoxazole-trimethoprim or tigecycline or quinolones are used as the basic drugs in combination with sensitive β-lactamase inhibitor complexes, usually cefoperazone/sulbactam is more commonly used.

How effective are they in the treatment of acinetobacter baumannii infections?

Piperacillin combined with tazobactam and cefoperazone combined with sulbactam both have potential antimicrobial activity. According to drug susceptibility testing, they can be used to treat acinetobacter baumannii infection. However, sulbactam has strong antibacterial activity against Acinetobacter spp. The combination of cefoperazone and it has synergistic antibacterial activity, and their susceptibility is higher than that of piperacillin/tazobactam. 

How effective are they in the treatment of pseudomonas aeruginosa infections?

Although they have antibacterial activity, some studies indicate that piperacillin/tazobactam is slightly more sensitive than cefoperazone/sulbactam. Although they have antibacterial activity, some studies indicate that piperacillin/tazobactam is slightly more sensitive than cefoperazone/sulbactam. Both of them can be used to treat patients with non-multidrug-resistant pseudomonas aeruginosa infections or with milder disease. Patients with multidrug-resistant pseudomonas aeruginosa infection or severe disease require combination with fluoroquinolone or aminoglycoside antibiotics.

How effective are they in the treatment of anaerobic bacteria infections?

Piperacillin/tazobactam is effective against most anaerobic infections. Cefoperazone/sulbactam is effective against infections such as Preobacterium melanogenum, Peptococcus, Peptococcus, Clostridium, Fusobacterium, Bacteroides, Eubacterium, and Lactobacillus.

What are their clinical applications?

Pneumonia:

• Community-acquired pneumonia: Patients who are hospitalized and have underlying diseases or are older than 65 years old, have high risk factors for Pseudomonas aeruginosa infection, or need to be admitted to the ICU can choose piperacillin/tazobactam or cefoperazone//sulbactam.
• Hospital-acquired pneumonia: They are not the first choice for patients with mild to moderate disease and no risk factors for drug resistance. As long as there are risk factors for multidrug resistance, patients with mild to moderate or severe disease need to be combined with other antibiotics.
• Structural lung disease: For patients with high risk factors for Pseudomonas aeruginosa infection, choose one of them. Depending on the patient's condition, monotherapy or in combination with other antibiotics may be used.
• Aspiration pneumonia: Neither of them would be the drug of choice for patients without high-risk factors for drug-resistant bacteria. Patients with community-acquired pneumonia and with inhalation factors should be treated according to the principles of hospital-acquired pneumonia and need to be covered with anaerobic bacteria.

Blood Infections:

For neutropenic, immunocompromised, and severe systemic infections, treatment should be empirical coverage of multidrug-resistant Gram-negative bacilli. β-lactamase inhibitor complexes are the preferred treatment option, and then the treatment can be adjusted based on the test results.

Abdominal infection:

Patients with mild or moderate infection: Combination of third-generation cephalosporins with metronidazole or β-lactamase inhibitor.

Severe infection in patients: β-lactamase inhibitor combination preparations or carbapenems are recommended as the drugs of choice.

Urinary tract infection:

Hospitalized and Severely Infected: When a patient has a pseudomonas aeruginosa infection, they can use either one and usually require a combination of other medications.

Complicated urinary tract infection: Hospitalization is required in patients with severe infection and/or suspected bacteremia. Piperacillin/tazobactam can be used for empirical antimicrobial therapy. Aminoglycosides can be combined if necessary, and treatment can then be adjusted based on bacterial susceptibility testing.

Fever with agranulocytosis:

High-risk patients should be treated with broad-spectrum antibiotics that cover Pseudomonas aeruginosa and other Gram-negative bacteria. Piperacillin combined with tazobactam and cefoperazone combined with sulbactam are both optional.

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What is diabetic ketoacidosis❓❓❓

One of the most common acute complications of diabetes is diabetic
ketoacidosis. The fatality rate of diabetic ketoacidosis in elderly patients with diabetes is as high as 5 to 16%. Therefore, we should master the diagnosis and treatment of diabetic ketoacidosis.

What are ketone bodies?

Fats are broken down into glycerol and fatty acids. Fatty acids are oxidatively broken down in the liver to form acetone, β-hydroxybutyric acid and acetoacetic acid. These three intermediate products are collectively referred to as ketone bodies. Since both acetoacetic acid and beta-hydroxybutyric acid are acidic substances, they can cause acidosis when they accumulate in large amounts in the body. In the blood, acetone accounts for only about 2% of the total ketone bodies, acetoacetic acid accounts for 28% and β-hydroxybutyric acid accounts for 70%. The blood concentration of β-hydroxybutyrate can directly reflect the ketone bodies in the body. However, the urine ketone measurement method can only measure acetone and acetoacetic acid, but not β-hydroxybutyric acid. 

What are the main causes of diabetic ketoacidosis?

Infection is the most common cause of diabetic ketoacidosis. Inappropriate dose reduction or interruption of insulin therapy is also a common cause of it. Insulin promotes the synthesis of fatty acids and glycerol into fat. When a patient's insulin is acutely deficient, it accelerates the breakdown of fat and increases the concentration of free fatty acids. Increased free fatty acid concentrations are oxidatively broken down in the liver to generate large amounts of ketone bodies. It will cause ketoacidosis.

How can a patient be diagnosed with diabetic ketoacidosis?

A lack of insulin in diabetics can increase blood sugar and accelerate fat breakdown. Hyperglycemia can cause osmotic diuresis. It causes dehydration and electrolyte loss in patients. Accelerated lipolysis increases free fatty acids in the patient's body. The oxidation and decomposition of fatty acids into ketone bodies will also increase. It can cause acidosis in patients.

Laboratory tests:

Blood sugar > 13.9 mmol/L.

Blood ketone ≥ 3 mmol/L or urine ketone(++).

Blood pH < 7.3 and/or HCO₃- < 18 mmol/L.

Diabetic ketoacidosis can be diagnosed with the above test results. The normal blood ketone value is 0.03 to 0.5 mmol/L. Plasma pH is normal 7.35 to 7.45. Serum HCO₃^- normal value is 22 to 27mmol/L. The clinical manifestations of diabetic ketoacidosis are lethargy, headache, abdominal pain, nausea, vomiting and rapid breathing (the exhaled breath will smell like rotten apples with acetone). Severe cases can cause dehydration, varying degrees of disturbance of consciousness and even coma.

What is the treatment for diabetic ketoacidosis?

Rehydration therapy: It is the primary treatment for patients with diabetic ketoacidosis. 0.9% Sodium Chloride Injection is the recommended treatment of choice. In principle, the rehydration treatment should be fast first and then slow. 1.0 to 1.5 L of normal saline should be infused during the first hour, and pre-estimated fluid losses should be replenished within the first 24 hours.

Insulin therapy: Insulin doesn't just lower a patient's blood sugar. It also reduces fat breakdown and inhibits the production of ketone bodies. Insulin is recommended as a continuous intravenous infusion of 0.1 U/kg/h. Insulin will generally correct ketosis more slowly than hyperglycemia. Therefore, when the patient's blood glucose was lowered to 11.1 mmol/L, the insulin input needed to be reduced and the patient started to be given 5% dextrose. It can maintain the patient's blood sugar at 8.3 to 11.1 mmol/L until the diabetic ketoacidosis is relieved.

Potassium supplementation therapy: If the patient's serum potassium is less than 3.3mmol/L, potassium supplementation therapy should be given priority to the patient. Insulin therapy should be started when the patient's serum potassium rises to 3.3 mmol/L. Cell membrane Na+-K⁺-ATPase is activated by insulin. It increases the intracellular potassium concentration, thereby reducing the blood potassium concentration. If the patient has normal urine output but serum potassium is less than 5.2 mmol/L after starting rehydration therapy and insulin, the patient should receive intravenous potassium supplementation. In general, 1.5 to 3.0 g of potassium chloride is added to each liter of infusion solution to maintain the patient's serum potassium level between 4 and 5 mmol/L.

Correction of acidosis: lipolysis is inhibited by insulin. It reduces the production of ketone bodies so that the acidosis is corrected. If the patient's circulation is not depleted, they generally do not need additional alkaline supplements. Generally, the use of 5% sodium bicarbonate solution for alkaline supplementation is only considered in the case of patients whose pH is less than or equal to 6.9.

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New findings on metformin.👀👀👀

Every once in a while, new benefits of metformin are discovered. Earlier this
year, a large cohort study conducted by researchers from the University of Southern Denmark in Denmark and Stanford University in the United States also found new findings on metformin. The study noted that men took metformin in the three months before conception (during sperm development). His male offspring will be more prone to reproductive organ defects at birth. The incidence of severe defects of the genitals or urinary tract was 3.39 times that of the control group. They also found that a man taking metformin for a year before or after the 90 days window period for sperm production did not affect his male offspring. However, it is worth noting that the findings of this study are only preliminary and observational and require further confirmation. Men who are taking metformin do not need to stop taking metformin before trying to conceive. In fact, many reasons for miscarriage are due to problems with men's sperm. It takes about 90 days for sperm to develop, form and finally mature in the epididymis. Therefore, men should also prepare for pregnancy three months in advance to improve the quantity and quality of sperm.

Mechanism of action of metformin.

Metformin reduces postprandial blood glucose levels by delaying intestinal absorption of glucose, increasing GLP-1 levels, reducing peripheral insulin resistance, and increasing muscle tissue uptake and utilization of glucose. It also reduces fasting blood glucose levels by reducing hepatic insulin resistance and reducing hepatic glucose output. The reduction in postprandial blood glucose and fasting blood glucose results in a reduction in HbA1c.

Common adverse reactions of metformin.

Common adverse reactions to metformin are headache, nausea, vomiting, bloating, indigestion, abdominal discomfort, diarrhea and fatigue. Most patients experience adverse reactions within the first 10 weeks of treatment. These adverse reactions generally will be gradually tolerated or disappear with the extension of treatment time. 

Therapeutic dose of metformin.

The minimum recommended dose of metformin is 500 mg per day and the optimal effective dose is 2000 mg per day. The maximum dose for adults in ordinary tablets is 2550 mg per day and the maximum recommended dose in extended-release formulations is 2000 mg per day. Switching to metformin sustained-release preparations, starting with small doses and gradually increasing the dose are all effective ways to reduce the occurrence of adverse reactions. In addition, long-term use of metformin may affect the absorption of vitamin B12, resulting in a decrease in vitamin B12 levels in the patient's body.

Other effects of metformin.

Cardiovascular protection.

Insulin resistance in diabetic and non-diabetic patients is improved by metformin. This reduces basal and post-load insulin levels, which directly and indirectly protects the cardiovascular system.

Improve blood lipid levels.

Fat synthesis and metabolism are improved by metformin. Studies have shown that metformin can significantly reduce triglyceride, LDL-cholesterol and total cholesterol levels in patients with type 2 diabetes, but it did not significantly alter the effect of HDL-cholesterol.

Improve the effect of non-alcoholic fatty liver.

Generally, patients with nonalcoholic fatty liver disease can safely take metformin. Unless the patient has significant hepatic impairment (such as serum transaminases greater than three times the upper limit of normal), hepatic insufficiency, or decompensated cirrhosis.

Treatment of polycystic ovary syndrome.

Polycystic ovary syndrome is a heterogeneous disorder characterized by polycystic ovary morphology, ovarian dysfunction, and hyperandrogenism. Its pathogenesis is unclear. Patients usually have varying degrees of hyperinsulinemia. There is medical evidence that metformin reduces androgen levels, plasma insulin levels and increases estradiol levels. It can improve menstrual regularity, improve hirsutism and induce ovulation in polycystic ovary syndrome patients.

Antitumor effect.

Diabetes may be a risk factor for a variety of tumors, including breast, pancreatic, colorectal, and endometrial cancers. Several studies have shown that metformin inhibits tumor initiation and progression. It reduces the risk of breast, lung, rectal, prostate and other cancers.

Other potential effects of metformin.

Alter gut flora.

A study found that the gut microbiome of patients with type 2 diabetes was favorably changed by metformin.

Reduce the risk of Parkinson's disease in patients with type 2 diabetes.

Metformin promotes the growth of new neurons and repairs damage to the nervous system.

Reversal of left ventricular hypertrophy in non-diabetic patients.

Studies have shown that metformin can improve vascular endothelial cell function, delay myocardial cell apoptosis, inhibit ventricular remodeling, and reduce patient weight. These effects may reverse left ventricular hypertrophy in non-diabetic patients.

Prevent age-related macular degeneration.

A study found that people with type 2 diabetes who took metformin had a significantly lower incidence of age-related macular degeneration. This may be related to the antioxidant and anti-inflammatory functions of metformin.

Reversal of pulmonary fibrosis.

Studies have shown that the use of metformin can re-sensitize myofibroblasts to apoptosis. And in mouse models, metformin can speed up the ablation of already fibrotic tissue.

Promote hair growth.

Studies have found that metformin can stimulate telogen hair follicles to enter the growth phase and promote hair growth in mice.

Reduce the risk of blood clots caused by haze.

There are animal studies showing that inflammation caused by smog is prevented by metformin. It inhibits the formation of arterial blood clots, thereby reducing the risk of cardiovascular disease.

Reduce adverse effects of glucocorticoid therapy.

Some studies have shown that patients treated with glucocorticoids and metformin have the possibility of reversing the adverse effects of glucocorticoids.

Finally, metformin can cause fatal lactic acidosis. Therefore, metformin should be used under the guidance of a doctor or pharmacist. Although new effects of metformin are frequently discovered recently, few of them are certified by medical guidelines.

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What should patients pay attention to when taking aspirin for a long time?📝📝📝

Aspirin is a classic and commonly used antithrombotic drug. In clinical, its application is very extensive. It can be used to prevent and treat cerebral thrombosis, cardiopulmonary infarction, angina pectoris, ischemic heart disease, etc. It plays an important role in the prevention of primary and secondary cardiovascular disease. Therefore, aspirin needs to be taken by many patients for a long time. The best results for these patients can only be achieved by taking aspirin correctly. The following will tell about the correct way to take aspirin.

When is it better to take aspirin?

Is it better for patients to take aspirin in the morning, noon, or evening? Some experts pointed out that there is controversy about the time of taking aspirin in the current research. Studies have shown that platelet activity increases in the morning. Therefore, from six o'clock to twelve o'clock in the morning is the high incidence time of cardiovascular events, so patients are advised to take aspirin in the morning. However, other studies have suggested that patients take aspirin at night to lower their blood pressure better, so they are advised to take it at night. In fact, the mechanism of action of aspirin is that the peak blood levels of the drug are not reached until several hours after taking the drug. Its antiplatelet effect can also last for several days after repeated administration. Therefore, whether aspirin is taken in the morning or in the evening, its antiplatelet effect persists after repeated doses. Therefore, it is generally more important to recommend that patients take aspirin regularly for a long time.

Different dosage forms of aspirin have different doses.

Different dosage forms of aspirin have different effects when taken before or after meals. If a patient is taking aspirin as a regular tablet, this dosage form causes it to be broken down in the stomach. Therefore, this form of aspirin should be taken after meals to reduce its damage to the gastric mucosa. If a patient is taking aspirin as an enteric-coated tablet, it will only dissolve in alkaline intestinal fluids and not in acidic gastric fluids. Taking this form of aspirin after meals can delay its absorption. Moreover, the alkaline content of food may cause the enteric-coated tablet to dissolve in the stomach and cause damage to the gastric mucosa. Therefore, it recommends that enteric-coated tablets should be taken 30 to 60 minutes before meals.

Patients should avoid missing to take aspirin.

Missed doses occasionally occur in patients taking long-term medication. What are the effects of missing an aspirin? Although the activity of existing platelets can be effectively inhibited by a single low-dose aspirin, the human body generates 10-15% of platelets every day. Therefore, patients need to take regular daily aspirin to keep these new platelets suppressed. If the patient occasionally misses an aspirin, it has little effect on the antithrombotic effect. However, frequent missed doses increase the risk of blood clots. It is recommended to take the medicine at a fixed time each day to avoid missed doses. If the patient misses a dose and is close to the next dose, there is no need to make up the dose and do not double the dose to avoid increasing adverse reactions. If the patient misses a dose and it is long before the next dose, make up the dose immediately.

Do not drink alcohol while taking aspirin.

First, the activity of an alcohol metabolizing enzyme (alcohol dehydrogenase) is inhibited by aspirin. It slows the metabolism of alcohol and causes more alcohol to accumulate in the body. Alcohol intoxication can become more likely. In addition, alcohol also increases the risk of gastric mucosa and liver damage. Therefore, alcohol should be avoided while taking aspirin. If the patient must drink alcohol, the patient should separate the medication time and alcohol consumption to reduce the interaction between the two.

Who is more likely to experience gastrointestinal adverse reactions when taking aspirin?

The patient's medication compliance is often affected by the adverse reactions of the medication. If a patient develops stomach pain after taking aspirin, it is easy for them to stop taking the drug. Digestive tract adverse reactions are more likely to occur in patients with a history of smoking and drinking, taking high-dose aspirin, taking anticoagulants at the same time, age > 65 years, or previous history of gastrointestinal diseases. These patients may need to take stomach-protecting drugs to reduce the occurrence of gastrointestinal adverse reactions.

Patients who develop aspirin resistance should be reassessed and adjusted their medication.

Aspirin resistance refers to the inability of patients to prevent blood clots after taking aspirin. When this occurs, the patient needs to be reassessed and assessed for factors that affect the efficacy of aspirin. Such as blood pressure, blood sugar, blood lipids are not effectively controlled. Does the patient take medication regularly? Are there any interactions between other drugs (such as NSAIDs) and aspirin? If the patient does not have the above factors, consider increasing the aspirin dose or switching to other antiplatelet drugs.

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What is the difference between alogliptin, linagliptin, saxagliptin, sitagliptin and vildagliptin?📊📊📊

Dipeptidyl peptidase-4 (DPP-4) inhibitor is a new type of oral hypoglycemic drug with the fastest growing clinical use recently. Alogliptin, linagliptin, saxagliptin, sitagliptin and vildagliptin all belong to this class of drugs, but what exactly is the difference between them?

What is the mechanism of action of DPP-4 inhibitors?

Intestinal cells are stimulated by food (especially carbohydrates) to secrete hormones (such as GIP and GLP-1) that increase insulin secretion. And 70 to 80% of the incretin activity is produced by GLP-1.

DPP-4 in the human body can easily degrade GLP-1. It results in a half-life of GLP-1 in plasma of less than two minutes. Concentrations of endogenous GLP-1 are elevated two to threefold by the efficacy of DPP-4 inhibitors in inhibiting DPP-4. The effects of promoting insulin secretion and inhibiting glucagon secretion of GLP-1 are glucose concentration-dependent. Therefore, DPP-4 inhibitors do not increase the risk of hypoglycemia and are therefore suitable for use in the elderly.

What is the difference in chemical structure between DPP-4 inhibitors?

Alogliptin

Linagliptin

Saxagliptin

Sitagliptin

Vildagliptin

What is the difference between the dosage of DPP-4 inhibitors?

1. Alogliptin: It is a DPP-4 competitive inhibitor. It binds non-covalently to the active site of DPP-4. Therefore, its half-life is relatively long, up to 21 hours. Alogliptin is taken once a day, 25 mg each time.
2. Linagliptin: It is a DPP-4 competitive inhibitor. It binds non-covalently to the active site of DPP-4. Therefore, its half-life is 12 hours. Linagliptin is taken once a day, 5 mg each time.
3. Saxagliptin: It binds covalently to the active site of DPP-4. Therefore, its dissociation and association will be slower. This makes its half-life only 2.5 hours, but its hypoglycemic effect lasts longer. Saxagliptin is taken once a day, 5 mg each time.
4. Sitagliptin: It is a DPP-4 competitive inhibitor. It binds non-covalently to the active site of DPP-4. Therefore, its half-life is about 12 hours. Sitagliptin is taken once a day, 100 mg each time.
5. Vildagliptin: It is also covalently bound to the active site of DPP-4. Its half-life is 3 hours. Vildagliptin is taken twice a day, 50 mg each time.

Food does not affect the absorption of the above DPP-4 inhibitors.

Precautions for use in patients with renal insufficiency.

1. Alogliptin: It is rarely metabolized in the body and its metabolites are also active. Its bioavailability can reach 100%. It rarely interacts with other medicines. About 76% of alogliptin is excreted through the kidneys. Therefore, its dosage should be adjusted when it is used in patients with renal insufficiency.
2. Linagliptin: It is rarely metabolized in the body. Its metabolites are inactive. Its bioavailability is about 30%. It rarely interacts with other medicines. Less than 5% of the administered dose of linagliptin is excreted by the kidneys. Therefore, it does not require dose adjustment when used in patients with renal insufficiency.
3. Saxagliptin: It is metabolized by CYP3A4/5. Its metabolites are active. Its bioavailability is about 67%. It rarely interacts with other medicines. Its usual dose is 5 mg once a day. However, when it is co-administered with potent CYP3A4/5 drugs such as itraconazole, clarithromycin and atazanavir, the dose of saxagliptin should not exceed 2.5 mg per day. About 75% of saxagliptin is excreted through the kidneys. Therefore, its dosage should be adjusted when it is used in patients with renal insufficiency.
4. Sitagliptin: It is rarely metabolized in the body. Its metabolites are inactive. Its bioavailability is about 87%. It rarely interacts with other medicines. About 79% of sitagliptin is excreted by the kidneys. Therefore, its dosage should be adjusted when it is used in patients with renal insufficiency.
5. Vildagliptin: It is not metabolized by CYP enzymes, but inactivated by hydrolysis. Its bioavailability is about 85%. It is less likely to interact with other drugs. About 85% of vildagliptin is excreted through the kidneys. Therefore, its dosage should be adjusted when it is used in patients with renal insufficiency.

What are the common adverse reactions of DPP-4 inhibitors?

It is possible that DPP-4 inhibitors increase GLP-1 levels. This can be associated with delayed gastric emptying and appetite suppression. Therefore, DPP-4 inhibitors can cause stomach upset. Their main adverse reactions are upper respiratory tract infection, nasopharyngitis and headache. Less common adverse reactions are hypersensitivity reactions and angioedema. 

In addition, alogliptin and saxagliptin have the potential to increase the risk of heart failure hospitalization events. Therefore, when a patient has risk factors for heart failure, the patient should be observed for symptoms and signs of heart failure during treatment.

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