What is the difference between apixaban, dabigatran, edoxaban and rivaroxaban?❓❓❓

For a long period of time in the past, warfarin was the only oral anticoagulant drug until the emergence of novel oral anticoagulant drugs. Although they are called "novel" oral anticoagulants, they are only relative to warfarin. New oral anticoagulants include factor Xa inhibitors (apixaban, edoxaban, and rivaroxaban) and direct thrombin factor IIa inhibitors (dabigatran). Learn more about these four new oral anticoagulants below.

1. Mechanism of action.

The anticoagulant effect of warfarin is produced through multiple targets. It exerts an anticoagulant effect by inhibiting the hepatic synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X.

Since new oral anticoagulants are anticoagulant drugs that act on a single target, their anticoagulant effects are easier to control. Apixaban, edoxaban, and rivaroxaban exert their anticoagulant effects by inhibiting coagulation factor Xa. Dabigatran exerts its anticoagulant effect by inhibiting coagulation factor IIa.

2. Risk of bleeding.

All of the novel oral anticoagulants were associated with a lower risk of intracranial hemorrhage than warfarin. Additionally, they do not increase the risk of fatal bleeding. Apixaban and edoxaban did not increase the risk of gastrointestinal bleeding compared with warfarin. However, dabigatran and rivaroxaban were associated with an increased risk of gastrointestinal bleeding compared with warfarin.

3. Indications.

a.) The difference between novel oral anticoagulants and warfarin: Atrial fibrillation can be divided into non-valvular atrial fibrillation and valvular atrial fibrillation (moderate to severe mitral stenosis, mechanical valve replacement surgery). Warfarin is recommended for valvular atrial fibrillation. Novel oral anticoagulants are recommended for nonvalvular atrial fibrillation.

b.) Differences between the novel oral anticoagulants:

• Apixaban is generally only used for anticoagulation after hip and knee surgery.
• Edoxaban and dabigatran can be used to prevent stroke in non-valvular atrial fibrillation. They can also be used to prevent deep vein thrombosis.
• Rivaroxaban can be used for more indications. It can be used to prevent non-valvular atrial fibrillation stroke, treat and prevent deep vein thrombosis and pulmonary embolism, anticoagulant therapy after hip and knee replacement, prevent coronary artery disease and peripheral artery disease.

4. Pharmacodynamics and pharmacokinetics.

The difference between novel oral anticoagulants and warfarin:

1. Novel oral anticoagulants reach peak blood concentrations more quickly after taking them, making them more effective. Their short half-life causes patients to lose their anticoagulant effect sooner after discontinuing the drug. It makes novel oral anticoagulants have good dose-response relationships. Activated coagulation factors II, VII, IX, and X are not affected by warfarin. Since the half-life of coagulation factor II is as long as 60 to 72 hours, it takes 2 to 7 days for warfarin to achieve its maximum effect.
2. Novel oral anticoagulants have few drug and food interactions.
3. Novel oral anticoagulants are rarely affected by disease or genetic factors. Patients have good medication compliance with them.
4. Andexanet is the specific reversal agent for apixaban, edoxaban and rivaroxaban. Idarucizumab is the specific reversal agent for dabigatran. If warfarin is overdose, vitamin K can be given intravenously.

5. Dosage of novel oral anticoagulants.

1. Apixaban: It is recommended to be taken at 2.5 mg twice daily. It is not affected by eating.
2. Edoxaban: It is recommended to take 60 mg once daily.
3. Dabigatran: It is recommended to be taken at 150 mg twice daily with meals. Dabigatran may damage the esophagus, so it is generally recommended to take it during or immediately after a meal and drink enough water (more than 100ml). Patients should remain in an upright or sitting position for more than 30 minutes after taking dabigatran.
4. Rivaroxaban: It is recommended to take 10mg once daily with or without food. However, rivaroxaban 15 mg or 20 mg tablets should be taken with food.

The frequency of administration is generally determined based on the half-life of drug efficacy and the half-life of plasma clearance. Patients should fix the time they take their medication every day. Novel oral anticoagulants generally do not require dose adjustment. However, in special circumstances (such as combined medication, the patient is underweight, old, or has liver and kidney problems), the dose may need to be reduced. 

6. How should novel oral anticoagulants replace other anticoagulants? 

Replacement of warfarin with novel oral anticoagulants: Check INR after discontinuing warfarin. Novel oral anticoagulants can be used when INR <2.0.

Substitution between novel oral anticoagulants: Patients should take the new novel oral anticoagulant directly with their next dose. Delayed dosing may be required in patients with renal impairment. 

Replacement of heparins with novel oral anticoagulants: The patient takes novel oral anticoagulants with the next injection of LMWH. The patient can take novel oral anticoagulant directly after stopping UFH.

Replacement of novel oral anticoagulants with injectable anticoagulants: The patient can switch to injectable anticoagulants when taking the next medication. Delayed dosing may be required in patients with renal impairment.

Replacing antiplatelet drugs with novel oral anticoagulants: Patients can take novel oral anticoagulants after they stop taking aspirin or clopidogrel.

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What antihypertensive drugs should be used in patients with diastolic hypertension?💓💓💓

Isolated diastolic hypertension (IDH) refers to patients with systolic blood
pressure < 140 mmHg and diastolic blood pressure ≥ 90 mmHg. Isolated diastolic hypertension is common in people younger than 65 and is often accompanied by a rapid heart rate.

What is arterial compliance? What is Peripheral Resistance?

Arterial compliance is arterial elasticity. When the heart contracts, blood rushes into the aorta putting pressure on it, known as systolic pressure. If the arterial elasticity of the patient is poor, the degree of dilation of the large arteries decreases and the volume of the blood vessels decreases, resulting in an increase in systolic blood pressure.

Peripheral resistance refers to resistance to blood flow by arterioles. when the heart is in diastole, the large arteries elastically recoil as they expand, pushing blood into the arterioles. When the heart is at the end of diastole, there will still be a certain amount of blood remaining in the aorta, which will exert pressure on it and that is the diastolic pressure. If the patient's arteriolar resistance increases, blood will flow into the arteriole less. As a result, more blood will remain in the aorta and diastolic blood pressure will increase. In addition, the increased heart rate of the patient will shorten the diastolic period of the heart. Blood flow into arterioles will also be reduced. The aorta will also retain more blood and increase the diastolic pressure. There is usually no obvious abnormality in the elasticity of the large arteries in young and middle-aged people. However, a significant increase in peripheral resistance is often accompanied by an increase in heart rate. Therefore, they are prone to isolated elevated diastolic blood pressure.

What is the mechanism of action of commonly used antihypertensive drugs?

Antihypertensive drugs commonly used in clinical practice include angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), β-blockers, dihydropyridine calcium channel blockers and thiazides diuretics.

1. Angiotensin-converting enzyme inhibitor (ACEI): It inhibits angiotensin-converting enzyme and blocks the production of the renin angiotensin II. It has no effect on heart rate but increases blood potassium levels. It can inhibit the synthesis of angiotensin II and reduce the level of angiotensin II. 
2. Angiotensin Receptor Blocker (ARB): It inhibits the angiotensin II receptor (AT1 type). It does not affect the patient's heart rate but increases his potassium levels. It inhibits the action of angiotensin II.
3. β-blockers: It suppresses sympathetic nerve activity and cardiac contractility and slows the heart rate. It also raises the level of blood potassium. It reduces renin secretion and lowers the level of angiotensin II.
4. Calcium channel blockers: It dilates blood vessels by inhibiting calcium channels on vascular smooth muscle cells. It reflexively activates the sympathetic nerves to increase the heart rate.
5. Diuretics: These decrease volume overload by increasing urination. It does not affect the patient's heart rate but lowers blood potassium levels. It decreases the secretion of renin and the level of angiotensin II.

What are the pathophysiological characteristics of hypertensive patients in young and middle-aged patients?

Activation of the sympathetic nervous system: The biological marker of sympathetic nervous activation is increased heart rate, hypertensive patients in young and middle-aged are often accompanied by increased heart rate.

Activation of the renin-angiotensin system: hypertensive patients in young and middle-aged , especially those with risk factors such as abdominal obesity, dyslipidemia, and smoking, have higher plasma renin activity and angiotensin II levels than the elderly.

What antihypertensive drug should be preferred in patients with isolated elevated diastolic blood pressure?

ACEI and ARB inhibit the renin-angiotensin system. β-blockers inhibit the sympathetic nervous system. 

If the patient's heart rate is >80 beats/min, β-blockers such as bisoprolol, carvedilol, and metoprolol are preferred.

If the heart rate of the patient is ≤80 beats/min, ACEIs (such as enalapril, perindopril) or ARBs (such as losartan, valsartan) are preferred.

Calcium channel blockers reflexively activate the sympathetic nerves. Diuretics can increase renin secretion and thereby promote the synthesis of angiotensin I and II. They are ineffective in the treatment of isolated diastolic hypertension.

In addition, studies have pointed out that about 200 patients who use β-blockers for 1 year will suffer from erectile dysfunction. ACEIs and ARBs are generally considered to have no adverse effects on sexual function, and some studies even suggest that they can improve.

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What are the normal values of blood pressure, blood sugar, blood lipids and uric acid for people of different ages?👀👀👀

Blood pressure, blood sugar, blood lipids and uric acid are the four basic
indicators for evaluating the health of the human body. However, the values of these indicators are not fixed and it will change with age. Therefore, some people will mistakenly think that they are unhealthy when they find that the value of the index is different from the standard value after the physical examination.

What is the normal blood pressure value?

A person's blood pressure should neither be too high nor too low. Excessive blood pressure can damage organs or tissues such as the cardiovascular system and kidneys. It also increases the risk of stroke. Low blood pressure prevents sufficient delivery of oxygen and blood to all parts of the body. It can cause fatigue, weakness, dizziness, and even fainting. Low blood pressure also increases the risk of stroke. However, in fact, people's blood pressure is not always stable. A person's blood pressure can vary at different times of the day and in different physical conditions. The following is the reference value of normal blood pressure for people of various ages:

Age	Systolic blood pressure (Male)	Diastolic blood pressure (Male)	Systolic blood pressure (Female)	Diastolic blood pressure (Female)
16-20 y/o	115	73	110	70
21-25 y/o	115	73	110	71
26-30 y/o	115	75	112	73
31-35 y/o	117	76	114	74
36-40 y/o	120	80	116	77
41-45 y/o	124	81	122	78
46-50 y/o	128	82	128	79
51-55 y/o	134	84	134	80
56-60 y/o	137	84	139	82
61-65 y/o	148	86	145	83

The following table will indicate the blood pressure status represented by each blood pressure range:

Type	Systolic blood pressure	Diastolic blood pressure
Hypotension	Below 90	Below 60
Ideal blood pressure	About 120	About 80
Normal blood pressure	Below 130	Below 85
Normal hypertension	130-139	85-89
Borderline hypertension	140-149	90-94
Mild hypertension	140-159	90-99
Simple systolic hypertension	Over140	Below 90
Moderately hypertension	160-179	100-109
Highly hypertension	Over 180	Over110

However, many factors such as mood, exercise and temperature can affect blood pressure values. Therefore, a single blood pressure measurement cannot be used as a diagnostic result.

What is the normal blood glucose value?

Similarly, too high or too low blood sugar will also have adverse effects on the human body. Excessive blood glucose can cause disease in the patient's large blood vessels. These lesions include atherosclerosis in the basilar arteries, coronary arteries, aorta, renal arteries, and peripheral arteries. These patients tend to have severe atherosclerosis and high mortality. About 70 to 80% of diabetic patients die of diabetic macrovascular disease. In addition, hypoglycemia will also damage the patient's health. Hypoglycemia may lead to memory loss, slow reaction time, dementia, coma, and even death. Hypoglycemia may also induce arrhythmia and myocardial infarction in patients. People's blood glucose levels change as they eat, digest and absorb food. Therefore, fasting blood glucose and postprandial blood glucose are generally used as reference values. 

	Venous (whole blood)	Capillary	Venous (plasma)
Normal value - fasting	3.9 – 6.1
Normal values – 2hrs after meals	Below 7.8
Diabetics - fasting	Over 6.1	Over 6.1	Over 7.0
Diabetics - 2hrs after meals	Over 10	Over 11.1	Over 11.1
Impaired glucose tolerance - fasting	Below 6.1	Below 6.1	Below 7.0
Impaired glucose tolerance - 2hrs after meals	6.7 – 10.0	7.8 – 11.1	7.8 – 11.1
Impaired fasting glucose - fasting	5.6 – 6.1	5.6 – 6.1	6.1 – 7.0
Impaired fasting glucose - 2hrs after meals	Below 6.7	Below 7.8	Below 7.8

What is the normal blood lipid value?

Patients with hyperlipidemia will make the blood thicken. Blood becomes prone to deposits on the walls of blood vessels, gradually forming plaques. These plaques can gradually build up and grow and clog blood vessels. It slows or even blocks blood flow. However, blood lipid levels are not as low as possible. Some studies have pointed out that when the cholesterol level of the elderly over 70 years old is lower than 4.16mmol/L, their risk of acute cardiovascular and cerebrovascular events is similar to that of the elderly whose cholesterol level is higher than 6.24 mmol/L. The normal reference values of blood lipids are as follows:

Types	Normal values
Total Cholesterol	2.8 – 5.17 mmol/L
Triglycerides	0.56 – 1.7 mmol/L
High Density Lipoprotein (Male)	0.96 – 1.15 mmol/L
High Density Lipoprotein (Female)	0.90 – 1.55 mmol/L
Low Density Lipoprotein	0 – 3.1 mmol/L

What is the normal uric acid value?

Under a normal diet, hyperuricemia is clinically diagnosed when the blood uric acid value of males exceeds 420 μmol/L and that of females exceeds 360 μmol/L in two tests on different days. 

	The range of normal blood uric acid level
Male	237.9 – 420 μmol/L
Female	178.4 – 360 μmol/L

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How should patients take Ambroxol?😷😷😷

Ambroxol is a very commonly used expectorant in clinical practice. Recently, more and more people pay attention to other pharmacological effects of ambroxol. The following relevant knowledge can help us use ambroxol rationally.

1. Chemical structure of Ambroxol.

Ambroxol is the active product produced by the metabolism of bromhexine. Due to its local anesthetic properties, it is given as a lozenge to soothe sore throats. Ambroxol is broken down by light, so it needs to be stored away from light. Its granule form needs to be dissolved in room temperature water. The injection form of ambroxol will produce free base precipitation of ambroxol due to the increase of the pH value of the solution, so it should not be mixed with an alkaline solution with a pH>6.3.

2. The expectorant effect of ambroxol.

The main components of sputum secreted by humans are a small amount of acidic glycoprotein and a large amount of water. When inflammation occurs in the respiratory tract, there will also be a small amount of residual DNA from damaged inflammatory cells in the sputum. There are disulfide bonds (-S-S-) in the acid glycoprotein molecular structure, so the sputum has a certain viscosity. It is also the main component in white sputum. Ambroxol can reduce the production of acidic mucopolysaccharides in the trachea, bronchial glands and goblet cells to reduce the viscosity of sputum. In addition, it can also promote the movement of cilia on the trachea and increase the expectoration of sputum. Ambroxol is suitable for patients with white and sticky sputum that is not easy to cough up.

3. Common dosage forms and dosages of ambroxol.

Ambroxol is generally administered 2 to 3 times a day. Its half-life is about 10 hours. If ambroxol is in the form of injection, its dosage is about half that of oral administration. Inhaled dosage forms will have smaller doses. 

1. Ambroxol Hydrochloride Tablets: Adults take orally three times a day, 30 to 60 mg each time, after meals.
2. Ambroxol hydrochloride oral solution: 1 to 2 years old, twice a day, 15mg each time. From 2 to 6 years old, three times a day, 15mg each time. 6 to 12 years old, two to three times a day, 30mg each time. Over 12 years old and adults, twice a day, 60mg each time.
3. Ambroxol Hydrochloride Injection: Children under 2 years old twice a day, 7.5mg each time. From 2 to 6 years old, three times a day, 7.5mg each time. 6 to 12 years old, two to three times a day, 15mg each time. Over 12 years old and adults, two to three times a day, 15 to 30mg each time.
4. Ambroxol hydrochloride solution for inhalation: children from 6 months to 2 years old inhale once or twice a day, 7.5mg each time. From 2 to 12 years old, inhale once or twice a day, 15mg each time. Over 12 years old and adults inhale once or twice a day, 15 to 22.5mg each time.

4. What is Neonatal Respiratory Distress Syndrome?

The site of gas exchange in the lungs is the alveoli. Oxygen in the alveoli will diffuse into the blood through the liquid membrane on the inner surface of the alveoli, the epithelial cells of the alveoli, the interstitium between the epithelium of the alveoli and the endothelium of the pulmonary capillaries, the endothelial cells of the capillaries, and then enter the blood. Alveolar epithelial cells are classified into type I and type II. Type II alveolar epithelial cells are inlaid between type I alveolar epithelial cells. It can synthesize and secrete alveolar surfactant. The main component of this surface active substance is phospholipid protein. It reduces the surface tension of the alveoli, preventing the alveoli from collapsing or overinflating. Neonatal respiratory distress syndrome refers to symptoms such as progressive dyspnea and respiratory failure in newborns. Its main cause is a series of symptoms caused by alveolar atrophy due to the lack of alveolar surfactant. Because ambroxol can increase the synthesis and secretion of alveolar surfactant, it has been approved for the treatment of respiratory distress syndrome in premature infants and neonatal infants. The dosage is 30mg/kg as the total daily dosage, divided into 4 doses. It should be administered with a syringe pump and administered intravenously over at least 5 minutes. In addition, when amoxicillin, cefuroxime, erythromycin, doxycycline and other antibiotics are taken together with ambroxol, the concentration of antibiotics in lung tissue can be increased.

5. Off-label use of ambroxol.

Taking large doses of ambroxol has the effects of anti-inflammation, anti-oxidation and scavenging free radicals in the body. It also increases alveolar surfactant. This has a protective and therapeutic effect on lung damage. It is used off-label to prevent postoperative atelectasis in patients with chronic obstructive airway disease. It is used continuously for six days from the third day before the patient's lung surgery to the second day after the operation, with a daily dose of 1000mg. Ambroxol can cause adverse reactions such as nausea, stomach discomfort, and loss of appetite, so it is recommended to take ambroxol oral preparations after meals. Ambroxol may also cause severe skin reactions such as toxic epidermal necrolysis. If patient develops symptoms of progressive rash, discontinue use ambroxol and seek medical attention immediately.

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What are the common problems of gout?🔍🔍🔍

Gout is a very common metabolic disease clinically. Here are some practical facts and frequently asked questions about gout.

1. What is the difference between hyperuricemia and gout?

Hyperuricemia refers to the blood uric acid levels of both men and women are higher than 420 μmol/L twice on different days. In patients with hyperuricemia, urate crystallizes and deposits in the body. It can cause patients to develop gouty arthritis, uric acid nephropathy, and kidney stones called gout. Some researchers now refer to gouty arthritis as gout. In addition, some patients with hyperuricemia have no obvious symptoms such as arthritis for life, which is called asymptomatic hyperuricemia. Subclinical gout can be diagnosed in patients with asymptomatic hyperuricemia if sodium urate crystal deposition and/or gouty bone erosions are found on examination.

2. Are Gout and Hyperuricemia Inherited to Offspring?

The probability of blood uric acid level being inherited is approximately 27 to 41% and the probability of gout being inherited is about 30%. About 20% of gout patients have a family history of it. Environmental factors such as alcohol consumption, overeating and weather are closely related to the occurrence of gout. Environmental factors such as alcohol consumption, overeating and weather are closely related to the occurrence of gout. Acute gouty arthritis has the characteristics of rapid onset. Within hours, patients experience redness, swelling, heat, pain, and dysfunction in affected joints. Midnight or early morning is the more common time of onset. In addition, due to the poor blood supply, low skin temperature, low interstitial fluid pH and high pressure of the foot, the first metatarsophalangeal joint is the first joint of most gout.

3. What is the relationship between high blood pressure and hyperuricemia/gout?

It is generally believed that for every 60 μmol/L increase in blood uric acid in a patient, his relative risk of hypertension will increase by 1.4 times. Blood vessels and kidneys can be damaged by high blood pressure. It will reduce uric acid excretion and increase blood uric acid level. Angiotensin converting enzyme inhibitors (eg, captopril), angiotensin-receptor blockers (eg, irbesartan, except losartan.), β-blockers (eg, metoprolol), and thiazide diuretics (eg, hydrochlorothiazide and indapamide) significantly increase the risk of gout attacks. Patients with hypertension complicated with hyperuricemia or gout should preferably choose antihypertensive drugs that do not affect blood uric acid levels, such as amlodipine and losartan. Atorvastatin is the first choice for patients with hyperuricemia or gout combined with hypercholesterolemia, which can promote the excretion of uric acid by the kidneys. Fenofibrate is the first choice for patients with hyperuricemia or gout with hypertriglyceridemia, which can inhibit uric acid reabsorption.

4. Are people with hyperuricemia or gout more likely to develop diabetes?

For every 60 μmol/L increase in the blood uric acid level of a patient, the risk of new-onset diabetes increased by 17%. Uric acid-lowering treatment can reduce the incidence of diabetes in people with hyperuricemia. Their incidence of cardiovascular and renal complications will also be reduced. In addition, insulin can lead to elevated blood uric acid levels in patients. Therefore, hypoglycemic drugs such as α-glucosidase inhibitors, metformin, SGLT-2 inhibitors and thiazolidinediones will increase insulin levels in patients. Patients with gout who use hypoglycemic drugs should try to avoid using the above drugs.

5. Do patients with asymptomatic hyperuricemia need uric acid-lowering therapy?

Non-drug treatments such as diet adjustment and weight control will be the first choice for patients with asymptomatic hyperuricemia. Treatment guidelines in China and Japan suggest that patients with asymptomatic hyperuricemia should be treated with uric acid-lowering drugs when the blood uric acid level is ≥540 μmol/L. Treatment guidelines in Europe and the United States recommend that patients with asymptomatic hyperuricemia need to start uric acid-lowering drug therapy only when they have chronic kidney disease and cardiovascular risk factors. Among the urate-lowering drugs, allopurinol can cause fatal allergic reactions in patients, benzbromarone can seriously damage the liver function of patients and febuxostat can increase the risk of cardiovascular events in patients.

6. What value should the blood uric acid target value be reduced to in patients with gout?

Studies have pointed out that when the patient's blood uric acid is controlled at <360 μmol/L for a long time, it can dissolve the urate crystals in the patient's body, and reduce the number and volume of crystals. It also prevents the formation of new urate crystals in the body. It is recommended to control the blood uric acid level of all gout patients to <360 μmol/L, and the blood uric acid level of severe gout patients to be controlled to <300 μmol/L. However, it is not recommended to control the patient's blood uric acid level at <180 μmol/L for a long time.

7. Which uric acid-lowering drugs can be used in patients with gout?

Allopurinol, benzbromarone, and febuxostat are the first-line drugs for uric acid-lowering therapy in patients with gout. Allopurinol and febuxostat inhibit uric acid synthesis in patients. Benzbromarone stimulates the excretion of uric acid. Allopurinol and benzbromarone are the first-line uric acid-lowering drugs for patients with asymptomatic hyperuricemia. If the patient's blood uric acid still does not reach the target value after using a sufficient amount and a full course of monotherapy, two uric acid-lowering drugs with different mechanisms of action can be considered in combination.

8. What uric acid-lowering drugs should be used in patients with gout and chronic kidney disease?

For gout patients with chronic kidney disease, uric acid-lowering therapy can inhibit the progression of their chronic kidney disease. Uric acid synthesis inhibitors such as allopurinol and febuxostat will be given priority to gout patients with chronic kidney disease stage 3 or above (glomerular filtration rate <60ml/min).Since the fatality rate of hypersensitivity reaction to allopurinol is as high as 30% and is obviously related to the HLA-B*5801 gene, patients should be tested for their HLA-B*5801 gene before using it. Therefore, febuxostat is especially suitable for gout patients with chronic renal insufficiency.

9. Do patients with gout who taking benzbromarone need to also take sodium bicarbonate?

Although oral administration of sodium bicarbonate has a certain effect on reducing uric acid in patients with gout, the effect on reducing uric acid is limited. In addition, long-term use of sodium bicarbonate can cause water and sodium retention in patients, which can cause and aggravate high blood pressure and induce heart failure. Therefore, patients only need to take sodium bicarbonate if the pH of the morning urine is <6.0.

10. What is the correct way to use colchicine?

Compared with taking large doses of colchicum, the effect of small doses of gout is similar and the side effects will be significantly reduced. When the patient has an acute gout attack, the first dose of colchicine is 1 mg, and then an additional 0.5 mg is given every hour. Until 12 hours later, take 0.5mg once or twice a day. When patients start uric acid-lowering drug therapy, fluctuating blood uric acid levels can easily induce acute gout attacks. Therefore, patients can take colchicine for at least 3 to 6 months to prevent acute gout attacks. The dosage is 0.5 to 1 mg per day.

11. Why are obese people more prone to gout attacks?

Gout is a metabolic disease and many patients with gout will be accompanied by obesity. The daily caloric intake of obese patients will be greater than the daily consumption. Purine synthesis in the body will increase with the increase in calorie intake, and the production of uric acid will also increase. In addition, obesity, especially abdominal obesity, can cause insulin resistance in patients. Insulin resistance can increase blood uric acid levels in the body. Therefore, many gout treatment guidelines recommend that patients with gout control their weight. 

12. Why are patients prone to gout attacks after drinking alcohol?

Some studies have pointed out that liquor and beer can increase the risk of gout attacks in patients, but there is little evidence that red wine increases the risk of gout attacks. Some studies have pointed out that hard alcohol and beer can increase the risk of gout attacks in patients, but there is little evidence that red wine increases the risk of gout attacks. Metabolism of alcohol increases consumption of ATP. Serum lactic acid will increase due to alcohol, thereby reducing uric acid excretion. The purines in alcohol lead to increased uric acid production. These are the reasons why alcohol consumption can increase blood uric acid levels.

13. What vegetables and fruits should patients with gout eat?

Patients with gout should not eat foods with too much sugar. Therefore, fruits with too much sugar such as apples, oranges and grapefruit should not be eaten too much. Plant foods with high purine content such as mushrooms, seaweed and kelp should not be eaten too much. Patients with gout can eat watermelon, coconut, grapes, strawberries, plums and peaches in moderation. Lemons, cherries and olives have certain benefits for patients with gout. It is recommended to eat low-purine foods such as most melons, tubers, root and leafy vegetables.

14. What kind of meat should patients with gout eat?

White meat such as chicken and duck has lower purine content than red meat such as beef and pork. The purine content of animal offal is generally higher than that of meat. Patients with gout should not consume more than 100g of meat per day. Cured or smoked meats are high in purines and sodium, which interfere with the metabolism of uric acid. Patients with gout are not suitable for eating these foods.

15. How much and how should patients with gout drinking water?

Patients with gout but without contraindications such as kidney disease or heart failure are recommended to drink 2 to 3L of water per day. Patients should try to maintain a daily urine output of about 2 L and a urine pH of 6.3 to 6.8. In addition, lemon water can help lower uric acid. It can add 1 to 2 fresh lemon slices to 2 to 3L of water.

16. How can patients with gout exercise?

Vigorous exercise can increase sweating in patients with gout. It reduces blood volume, renal blood flow, and uric acid excretion. It can even induce gout attacks. Low-intensity aerobic exercise such as jogging can reduce gout attacks in patients. Low-intensity aerobic exercise such as jogging can reduce gout attacks in patients. It is recommended that patients perform low-intensity aerobic exercise 4 to 5 times a week, 0.5 to 1 hour each time. In addition, since low temperature can easily induce acute gout attacks in patients, patients should avoid taking cold baths after exercise.

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