Knowledge of calcium channel blockers.📓📓📓

Calcium channel blockers are one of the most commonly used
antihypertensive drugs in clinical practice. It has been used for many years. Its efficacy and safety have been proven. It plays an important role in the clinical treatment of cardiovascular disease. Therefore, for calcium channel blockers, you should have the following knowledge.

Mechanism of action of calcium channel blockers.

There are two types of calcium channel blockers: dihydropyridines and non-dihydropyridines. The pharmacological effects of both of them are to inhibit the influx of calcium ions into vascular smooth muscle cells by selectively blocking voltage-dependent calcium ion channels. This relaxes the smooth muscle of the blood vessels, which dilates the blood vessels. Peripheral vascular resistance will therefore decrease, to achieve a blood pressure lowering effect. They mainly dilate the arteries, especially the coronary arteries.

• Dihydropyridine calcium channel blockers have better vascular selectivity. It generally does not affect atrioventricular conduction, sinoatrial node function, and myocardial contractility at therapeutic doses.
• Non-dihydropyridine calcium channel blockers have poor vascular selectivity. It has a negative inotropic effect and negative conduction on the heart. Therefore, it not only lowers blood pressure but also lowers heart rate.

Calcium channel blockers commonly used in clinical practice.

Dihydropyridine calcium channel blockers:

Drug	Drug standard (mg)	Dosage (initial dose to full dose, mg/d)	Times of taking medicine (times/d)
Amlodipine	5、10	5 to 10	1
Barnidipine	5、10、15	5 to 15	1
Benidipine	2	4 to 8	1
Cilnidipine	5、10	5 to 10	1
Felodipine	2.5、5	2.5 to 10	2
Lacidipine	4	4 to 8	1
Lercanidipine	10	10 to 20	1
Levamlodipine	2.5、5	2.5 to 5	1
Manidipine	5	5 to 20	1
Nicardipine	20	40 to 80	2 to 3
Nifedipine	5、10	10 to 30	2 to 3
Nifedipine (Sustained Release)	20、30	10 to 80	2
Nifedipine (Controlled Release)	30	30 to 60	1
Nitrendipine	10	20 to 60	2 to 3

Non-dihydropyridine calcium channel blockers:

Drug	Drug standard (mg)	Dosage (initial dose to full dose, mg/d)	Times of taking medicine (times/d)
Diltiazem	30	90 to 360	1 to 2
Diltiazem (Sustained release)	200	200	1
Verapamil	40	80 to 480	2 to 3
Verapamil (Sustained release)	240	120 to 480	1 to 2

Characteristics of calcium channel blockers.

Their pharmacodynamics are dose-dependent and have a good antihypertensive effect. Single-agent therapy generally achieves the desired effect. Mild to moderate hypertension can generally be controlled by it. They are the first-line treatment in many national hypertension guidelines.

Stroke risk in hypertensive patients is significantly reduced by calcium channel blockers.

Many clinical studies have shown that calcium channel blockers can change the physiological activities related to calcium ions to affect atherosclerosis. They can slow the progression of atherosclerosis

Calcium channel blockers do not alter sugar and lipid metabolism. Therefore, it can be used by patients with diabetes and metabolic syndrome. In addition, levamlodipine besylate can dilate the bulbar arterioles and afferent arterioles. It reduces the resistance of the renal blood vessels without increasing the intra-glomerular pressure. These factors make it beneficial for hypertensive patients with diabetes mellitus and patients with parenchymal renal disease.

Calcium channel blockers have the effect of increasing sodium excretion. If the patient has salt-sensitive hypertension, its antihypertensive effect will be better. Its antihypertensive effect is not affected by a high-salt diet, so it is also suitable for people on a high-salt diet.

Calcium channel blockers have a good effect on volume hypertension such as isolated systolic hypertension and elderly hypertension.

Medium- and long-acting calcium channel blockers have a good safety profile, fewer side effects, and a lower incidence of hypotension. Their effects are gentle and long-lasting. Most only need to take 1 or 2 pills a day. This can improve patient compliance with medication and the efficacy of treatment.

Calcium channel blockers dilate the coronary arteries, thereby reducing coronary resistance and improving the ability of the heart muscle to supply blood. It can treat coronary heart disease, angina pectoris, hypertrophic cardiomyopathy and peripheral vascular disease, especially for variant angina pectoris caused by coronary spasm.

Non-dihydropyridine calcium channel blockers can also slow the heart rate and improve blood supply to the coronary arteries. It can prevent and treat coronary heart disease, arrhythmias such as premature atrial beats, and supraventricular tachycardia.

Indications for calcium channel blockers.

Calcium channel blockers are used for various types of high blood pressure. It is the first-line treatment for high blood pressure.

Dihydropyridine calcium channel blockers:

• Hypertension with atherosclerosis: Peripheral vascular disease, coronary atherosclerosis, carotid atherosclerosis or stable angina with hypertension.
• Volumetric hypertension: Hypertension with low sympathetic or low renin activity, isolated systolic hypertension and elderly hypertension.

Non-dihydropyridine calcium channel blockers:

• Angina pectoris, supraventricular tachycardia, carotid atherosclerosis with hypertension.

Combination medication.

Diuretics: The risk of stroke in hypertensive patients can be reduced by combining calcium channel blockers with diuretics. However, the hypotensive effect of calcium channel blockers reflexively activates sympathetic nerves. Diuretics also activate sympathetic nerves after reducing blood volume. Their side effects may be aggravated by this.

Angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists: They dilate arteries and veins. Calcium channel blockers can directly dilate the arteries. Therefore, their combined use will have a synergistic effect. Angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists can partially inhibit the side effects of increased heart rate and increased reflex sympathetic tone caused by calcium channel blockers. Ankle edema is a common side effect of dihydropyridine calcium channel blockers, which can be eliminated or alleviated by angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists.

β-blockers: It can inhibit the blood volume mechanism and sympathetic nerve, and achieve a significant antihypertensive effect. The reflex sympathetic excitation caused by vasodilation by calcium channel blockers is inhibited by β-blockers. The increase in peripheral arterial resistance caused by long-term use of β-blockers is also inhibited by calcium channel blockers. They are suitable for patients with angina pectoris, heart failure, tachycardia, myocardial infarction with hypertension.

Side effects of calcium channel blockers.

Edema: It is a common side effect of calcium channel blockers. Edema of the face, lower extremity pretibial, lower extremity pretibial edema may occur. It will improve after stopping the drug. Alternatively, it may try to replace the patient with other calcium channel blockers. The incidence of side effects with levamlodipine is relatively low.

Gingival hyperplasia: It may occur in patients taking calcium channel blockers for a long time. Among them, nifedipine caused the highest incidence of gingival hyperplasia.

Hypotension: Some calcium channel blockers, especially short-acting calcium channel blockers, may lower blood pressure too quickly and cause hypotension. Therefore, it recommends the use of long-acting calcium channel blockers (eg, amlodipine) to lower blood pressure. The patient's blood pressure should also be monitored after taking the drug.

Atrioventricular block: Non-dihydropyridine calcium channel blockers have negative effects on the heart. It inhibits sinus node and myocardial contraction. The main clinical manifestation is atrioventricular block. Therefore, patients with sick sinus syndrome and 2nd degree or higher atrioventricular block are contraindicated.

Heart failure: Calcium channel blockers dilate systemic blood vessels, reduce cardiac load and protect ischemic myocardium. However, the degree of heart failure can be aggravated, so it should be used with caution in patients with heart failure.

Tachycardia: Calcium channel blockers reflexively activate the sympathetic nervous system. It increases the heart rate. When necessary, calcium channel blockers should be combined with β-blockers to alleviate this adverse effect.

Headache and flushing: The dilation of blood vessels caused by calcium channel blockers may cause headaches and flushing. If the patient cannot tolerate it, other antihypertensive drugs should be used.

Constipation: Intestinal smooth muscle calcium transport may also be affected, resulting in constipation. If the constipation is more severe, it may consider changing the dressing or adding a laxative.

Caution with calcium channel blockers.

Short-acting nifedipine: It may drop blood pressure too quickly and cause low blood pressure. It will also increase the heart rate reflex reflex, blood pressure fluctuations and other problems. Therefore, it is mainly used in the clinical treatment of coronary heart disease and angina pectoris, and it can be sucked in the first aid.

Pay attention to the method of administration: Sustained-release or controlled-release tablets should be swallowed whole.

Avoid grapefruit or grapefruit juice: The activity of the CYP3A4 enzyme can be inhibited by grapefruit. In addition to no obvious effect on amlodipine, other metabolic rates will be reduced, thereby enhancing drug efficacy and the occurrence of adverse reactions.

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How can kidney stones be prevented and treated?💎💎💎

Kidney stones are formed by the deposition of mineral crystals in the urine in the kidneys. It is one of the more common types of urinary system diseases. It is a type of urinary tract stone. In addition to kidney stones, other urinary tract stones include ureteral stones, bladder stones, and urethral stones, depending on where the stones are deposited.

Clinical manifestations of kidney stones.

Severe lower back or abdominal pain is one of the symptoms of kidney stones. Kidney stones can move within the calyces, renal pelvis, and ureter. It causes the smooth muscle of the kidneys to contract, spasm and block. Severe pain occurs in the corresponding area of the kidney. If the stone moves to the ureter, it can block the ureter. As a result, urine cannot be excreted normally. Urine accumulates in the renal pelvis. This can cause hydronephrosis. Symptoms of kidney stones include difficulty urinating, frequent urination, urgency, blood in the urine, nausea and vomiting.

People who are prone to kidney stones.

Male: Men are more likely to have kidney stones than women. This is because the urinary system of men is different from that of women. Men's urethra is longer than women's, which makes it easier for crystals to deposit in the urine, so they are more likely to have stones.

Drink too little water: If people drink too little water, their urine will be concentrated from too little water. It can make people more likely to have kidney stones.

Foods high in salt, fat, purines, and calcium: People who eat these foods regularly and drink alcohol are more likely to develop kidney stones.

Diseases: Patients with hyperthyroidism, diabetes, hyperuricemia, gout, obesity, urinary tract obstruction and urinary tract infection are more likely to have kidney stones.

Others: People who often hold their urine and sit for long periods of time are also more likely to have kidney stones.

How to prevent different types of kidney stones.

Common types of kidney stones include calcium oxalate stones, calcium phosphate stones, uric acid stones, cystine stones, magnesium ammonium phosphate stones, and mixed stones. Among them, calcium oxalate stones are the most common.

Calcium oxalate stones: Patients with these stones should limit their intake of high salt, sugar, fat, protein, and high doses of vitamin C. Foods high in oxalate such as spinach, celery, soybeans, black beans, peanuts, kiwi, grapes and mutton should also be eaten less.

Calcium oxalate stone

Calcium phosphate stones: Patients should avoid monosodium glutamate and carbonated beverages. Foods high in phosphorus such as red meat, bran, and whole milk powder should be avoided. They should eat more vegetables and fruits. When people consume too much phosphorus, it increases their calcium loss and increases the pH of the urine. If they don't drink enough water, calcium phosphate stones can easily form.

Calcium phosphate stone

Uric acid stones: Patients should limit their consumption of high-purine foods such as meat, seafood, and coffee. Drugs that increase the pH of the urine, such as sodium potassium citrate and sodium bicarbonate, can alkalize the urine and increase the excretion of uric acid.

Uric acid stone

Cystine stones: Meat, eggs, fish and other foods rich in methionine should be limited. Salt intake should also be reduced. Alkalizing urine reduces the risk of cystine stone formation.

Cystine stone

Magnesium ammonium phosphate stones: Because it mainly occurs after urinary tract infection, it is also called infectious stone. Prevention and treatment of bacterial infections are the main methods of prevention of magnesium ammonium phosphate stones. Patients over the age of 60 are at high risk of developing magnesium ammonium phosphate stones, and they are more common in women. Its texture is usually brittle, so when it is located in the renal pelvis or upper ureter, it can be crushed with extracorporeal shock wave lithotripsy.

Magnesium ammonium phosphate stone

How should kidney stone patients be treated?

If the patient's kidney stones are not too large, they can be tested regularly. They should drink plenty of water and do moderate exercise such as skipping rope. Kidney stones may pass out of the body on their own. Terazosin and tamsulosin are the most commonly used drugs for kidney stones. They can facilitate the passage of kidney stones. If the patient's kidney stone is too large, appropriate lithotripsy should be performed clinically according to the actual situation of the patient.

How to prevent kidney stone recurrence?

1. Drink more water and less beverages. 
2. Beverages high in sugar, strong tea, coffee and beer should be avoided or avoided as much as possible.
3. Do appropriate exercise.
4. According to the type of kidney stone, adjust the patient's eating habits.

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What is the difference between unfractionated heparin, low molecular weight heparin and fondaparinux❓❓❓

Heparins are one type of the most commonly used anticoagulant drugs in clinical practice. Unfractionated heparin, low molecular weight heparin and fondaparinux are very commonly used heparins. Thrombosis or embolic diseases such as myocardial infarction, vascular embolism and pulmonary embolism can be prevented and treated with these drugs. They have similar therapeutic uses and belong to the same type of drug, so what is the difference between them?

Thrombotic disease.

Thrombotic disorders can be divided into venous thromboembolism and arterial thromboembolism. Common venous thromboembolisms include deep vein thrombosis and pulmonary embolism. Common arterial thromboembolisms include myocardial infarction and acute cerebral infarction.

Mechanisms of heparin anticoagulants.

The liver can synthesize antithrombin which is a natural anticoagulant. Its anticoagulant effect is by binding to coagulation factors Xa and IIa and inhibiting their activity. However, heparin has no direct anticoagulant ability. Its anticoagulant effect is through binding to antithrombin, thereby enhancing the inhibitory ability of antithrombin on coagulation factors Xa and IIa. 

Unfractionated heparin has a longer molecular chain. The molecular weight range is about 3000 to 30000KD. Heparin with a molecular weight greater than 5400KD can be combined with thrombin and antithrombin. It inhibits coagulation factors Xa and IIa.

Enoxaparin, nadroparin and dalteparin are commonly used low molecular weight heparins. Their molecular weight is less than 8000KD. They mainly inhibit coagulation factor Xa. They inhibit coagulation factor Xa and IIa in a ratio of (2 to 4):1.

The molecular chain of fondaparinux is very short. Its molecular weight is 1728. It only inhibits coagulation factor Xa.

Pharmacokinetics of unfractionated heparin, low molecular weight heparin and fondaparinux.

The smaller the molecular weight of heparins, the longer their half-life.

• Unfractionated heparin: Only a small amount of unfractionated heparin is excreted by the kidneys, so patients with creatinine clearance less than 30ml/min can also use it. It can be administered by intravenous or subcutaneous injection, but the bioavailability of subcutaneous injection is only 30% and the intravenous administration has immediate effect. Its half-life is about 1 to 2 hours.
• Low molecular weight heparin: Because it is excreted by the kidneys, it should be used with caution in patients with renal insufficiency. It can be administered intravenously or subcutaneously, but subcutaneous injection has better bioavailability (about 90%). It works 3 to 4 hours after subcutaneous injection. Its half-life is about 5 to 7 hours.
• Fondaparinux: The kidneys are its main route of excretion. In patients with creatinine clearance of 30 to 50 ml/min, the dose should be halved. It is contraindicated in patients with creatinine clearance less than 30. It can be given by intravenous or subcutaneous injection. The bioavailability of subcutaneous injection can reach 100%. It works 2 to 3 hours after subcutaneous injection. It has a half-life of 17 to 21 hours, so only one subcutaneous injection per day is required.

They can be administered intravenously or subcutaneously, but intramuscular injection is prohibited. They cannot penetrate the placenta, so they do not cause teratogenicity. Protamine can completely eliminate the anticoagulant effect of unfractionated heparin with larger molecular weight. However, it can only eliminate part of the anticoagulant effect of low molecular weight heparin and is ineffective against fondaparinux.

Indications.

In the thrombosis process of ST elevation myocardial infarction, coagulation factor IIa plays an important role. Unfractionated heparin has a strong inhibitory effect on coagulation factor IIa. It can effectively and rapidly inhibit coagulation and prevent the expansion of infarct size. Therefore, unfractionated heparin is an important basic treatment for the thrombolysis of ST elevation myocardial infarction and before percutaneous coronary intervention.

Unfractionated heparin: It can be used to prevent venous thromboembolic disease associated with surgery, treat established deep vein thrombosis, treat unstable angina pectoris and acute phase of non-Q-wave myocardial infarction, treat acute ST elevation myocardial infarction, combined use with thrombolytic agents or concurrent use with percutaneous coronary intervention, treatment of disseminated intravascular coagulation of various causes, prevention of clot formation in extracorporeal circulation during hemodialysis.

Low molecular weight heparin (nadroparin, enoxaparin, dalteparin): it can be used to prevent venous thromboembolic disease associated with surgery, treat established deep vein thrombosis, treat unstable angina and non-Q-wave myocardium In the acute phase of infarction, prevention of clot formation in cardiopulmonary bypass during hemodialysis. Only enoxaparin can be used to treat acute ST elevation myocardial infarction, in combination with thrombolytics, or concomitantly with percutaneous coronary intervention.

Fondaparinux: It is used to prevent venous thromboembolic events in patients undergoing major orthopedic surgery of the lower extremity, such as hip fractures, major knee surgery, or hip replacements. It treats unstable angina pectoris or non-ST elevation myocardial infarction for not indicated urgent (less than 120 minutes) percutaneous coronary intervention. It is used to treat patients with ST elevation myocardial infarction who are on thrombolytics or who are not initially receiving other forms of reperfusion therapy. It significantly increases the risk of catheter thrombosis, so it is not suitable for patients undergoing percutaneous coronary intervention.

Adverse effects.

Although they have similar side effects, they occur at different rates. In general, lower molecular weight heparins are safer.

Hyperkalemia: Heparin drugs inhibit the synthesis of aldosterone. Therefore, even in small doses, it may cause an increase in serum potassium.

Bleeding: The higher the molecular weight of heparin, the higher the risk of bleeding. Therefore, unfractionated heparin has the highest bleeding risk. Activated partial thrombin time should be monitored when using it.

Thrombocytopenia: Unfractionated heparin may cause fatal thrombocytopenia. Low molecular weight heparin has a low incidence of thrombocytopenia. Patients should have their platelet counts monitored when using both of them. Thrombocytopenia caused by fondaparinux is rare.

Osteoporosis: Patients receiving long-term (3 to 6 months) or high-dose (>20,000 units/day) unfractionated heparin are at risk for spontaneous vertebral fractures or osteoporosis. Low molecular weight heparin and fondaparinux are less risky.

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Several medicines that can cause coughing.😷😷😷

Cough is a very common symptom of respiratory disease. There are many
reasons for a cough. In addition to illness, drugs can also cause coughing. It's called a drug-induced cough. The following medicines can easily cause coughing.

Angiotensin-converting enzyme inhibitors.

Angiotensin-converting enzyme inhibitors such as captopril and enalapril increase prostaglandins. The increase in prostaglandins can make coughing easier. In addition, they increase the amount of bradykinin and cell fiber stimulators such as substance P in the lungs. These substances induce bronchoconstriction leading to a severe dry cough. Such dry coughs are generally irritating and persistent in character. No secretions are excreted when coughing. Sometimes it appears paroxysmal. Symptoms can be worsened by lying down and at night. This can affect the patient's sleep. Symptoms of dry cough usually appear within 3 to 7 days of taking an angiotensin-converting enzyme inhibitor. It will get worse over time. This cough cannot be cured with cough suppressants or antibiotics. It usually resolves gradually with discontinuation of the drug.

Antiarrhythmic drugs.

Among the antiarrhythmic drugs that most commonly cause dry cough is amiodarone. It is mainly used to prevent or treat ventricular arrhythmia, atrial fibrillation, etc. Its most common side effect is pulmonary toxicity-related symptoms, occurring in approximately 1 to 17%. Generally, hypersensitivity pneumonitis or interstitial pneumonitis will occur after continuous use for 3 to 12 months. In patients with lung disease, excessive doses or prolonged courses of amiodarone are more likely to develop pulmonary toxicity. Its most common clinical manifestation is dry cough. Therefore, monitoring of lung function is recommended within 3 to 6 months of taking amiodarone. In addition, it is necessary to pay attention to the adjustment of the drug dosage when using it.

Diuretic drugs.

Diuretics such as hydrochlorothiazide can increase urine output and lower blood pressure. One of its common side effects is a dry cough. Most coughs are induced within a few hours of taking the medicine. In severe cases, it can even lead to asthma. The cough usually gets better after the drug is stopped.

Nitroimidazole antibiotics.

Among the nitroimidazole antibiotics, nitrofurantoin is the most likely to induce cough. Its most common side effect is acute pneumonia injury. If the patient has pneumonia or is allergic, it will be more likely to induce pneumonia damage. Its clinical manifestations are mainly dry cough. Most acute pneumonia injuries occur within 1 month of taking nitrofurantoin. If a dry cough develops after more than 6 months of use, it should be considered as possible pulmonary toxicity. Symptoms usually get better when the drug is stopped. If the symptoms do not improve after stopping the drug, oral antihistamines and glucocorticoids can be used to relieve the symptoms.

Antituberculosis drugs.

Among the anti-tuberculosis drugs, para-aminosalicylic acid is the most likely to cause dry cough. Most of the irritating coughs it causes appear within 3 weeks of taking the drug and usually get better when the drug is stopped.

Anti-cancer drugs.

Among the anticancer drugs, bleomycin is one of the drugs that is more likely to cause lung damage. It produces reactive oxidative products that cause direct damage to lung tissue. This results in massive infiltration of leukocytes, increased release of proteases, proliferation of fibroblasts, and pulmonary fibrosis. The common clinical symptom is dry cough. It occurs in about 2 to 4 percent. Lung damage can still occur weeks, months, or even years after the drug is stopped. If lung injury occurs while taking the drug, the drug should be discontinued immediately. If symptoms do not improve after stopping the drug, intravenous glucocorticoids should be administered to inhibit fibroblast activity. Patients can also supplement with oxygen to improve the symptoms of dyspnea.

Antibiotics.

Antibacterial drugs such as penicillins, cephalosporins, macrolides, etc. can cause cough. Patients with allergies are more likely to induce cough. Symptoms generally improve when the drug is stopped.

Anticoagulant drugs.

The most common adverse effect of anticoagulant drugs is bleeding. If the bleeding is in the chest cavity or lung parenchyma, it can damage lung tissue and cause coughing. Therefore, it is recommended to observe whether there is bleeding during taking the medicine, and adjust the dose in time. It is recommended to start with a low dose and then gradually increase the dose.

Sodium cromoglycate

Sodium cromoglycate can be used to prevent asthma attacks and the prevention and treatment of allergic symptoms. However, inhaled sodium cromoglycate tends to irritate the mucous membranes of the airways and cause coughing when used. Coughing may occur a few minutes after taking the medicine. Symptoms can be improved with dose reduction or discontinuation.

Aspirin.

Aspirin can increase the production of leukotrienes. It irritates the mucous membranes of the airways causing coughing. Cough usually occurs within 30 minutes of taking the medicine. Symptoms will gradually relief after the drug is discontinued.

Drug-induced cough usually improves when the drug is discontinued. If it does not improve, it should be promptly treated according to the patient's condition.

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Diagnosis and treatment of sarcopenia.🔬🔬🔬

As populations around the world tend to age, sarcopenia has gradually become a public health concern. Recent studies have shown that middle-aged and elderly people with sarcopenia have a higher incidence of cardiovascular disease than the general population. They had a 72% and 33% increase in the incidence of cardiovascular disease and the risk of cardiovascular events, respectively. 

What is sarcopenia?

In clinical practice, sarcopenia generally refers to the continuous decrease in the number, strength and function of skeletal muscle caused by aging. It can make the patient slow and unsteady. It also makes people prone to falls and fractures. Organ function may also be affected. It can lead to heart and lung failure, and even death. Its pathogenesis and etiology are complex. It is currently believed that sarcopenia is associated with the following pathological changes: Autophagy of skeletal muscle stem cells, excessive inflammatory state, oxidative stress, muscle mitochondrial dysfunction, protein breakdown and synthesis disorders, microvascular endothelial dysfunction and metabolic disorders, etc. Risk factors for sarcopenia include physical inactivity and malnutrition.

Diagnosis of sarcopenia.

Appendicular skeletal muscle mass index (ASMI) is a determining index. Appendicular skeletal muscle mass can be measured by dual-energy X-ray absorptiometry and divided by the square of height to calculate the index. The presence of sarcopenia was considered if it was less than 7.0 kg/m2 in men and 5.4 kg/m2 in women. The diagnostic process for sarcopenia is as follows:

If the patient is 65 years or older, perform a pace test.

If the pace is greater than 0.8m/s, measure the patient's grip strength. There is no sarcopenia if the grip strength is >25kg in men or >18kg in women. If the grip strength of men is ≤25kg or the grip strength of women is ≤18kg, ASMI should be measured. Sarcopenia was diagnosed if ASMI < 7.0 kg/m2 in men or ASMI < 5.4 kg/m2 in women.

If the pace is smaller than 0.8m/s, measure ASMI. Sarcopenia was diagnosed if < 7.0 kg/m2 in men or < 5.4 kg/m2 in women.

Nutritional interventions for sarcopenia.

Nutritional interventions for sarcopenia require adequate supplementation of these three.

Protein: Human skeletal muscle stores large amounts of various forms of protein. An important solution for the treatment of sarcopenia is to supplement high-quality protein. It improves muscle mass. Among them, leucine whey protein is widely believed to stimulate muscle protein synthesis, thereby it can maintain muscle mass. Therefore, foods rich in whey protein such as eggs, soy products and milk are recommended.

Vitamin D: Vitamin D plays a key role in the process of bone mineralization. It regulates the absorption of calcium and phosphorus in the body. Maintaining healthy bones and muscles depends on vitamin D. Therefore, vitamin D supplementation is great significance for improving and strengthening the muscle function of the elderly.

Omega-3 Fatty Acids: Studies have shown that both muscle mass and synthesis of muscle protein can be improved by omega-3 fatty acids. 

Exercise intervention for sarcopenia.

While muscle mass in older adults declines with age, exercise can slow or even reverse the decline in muscle function and mass. Since sarcopenia also increases the risk of cardiovascular disease, many patients with sarcopenia have cardiovascular disease. Moderate exercise can reduce the incidence of adverse cardiovascular events and help prevent cardiovascular disease. However, patients with cardiovascular disease also have certain risks when exercising. Their exercise should be done after evaluation and advice. 

• For healthy people: Get at least 150 minutes of moderate-intensity physical activity per week, or 75 minutes of vigorous-intensity physical activity per week, or a combination of the two. Studies have shown additional benefits of increasing moderate-intensity exercise to 300 minutes per week, or high-intensity exercise to 150 minutes per week. It is recommended to exercise several times a week, and daily exercise would be more recommended.
• For those with other medical conditions: Patients should be diagnosed and treated for their disease, as well as undergo a cardiopulmonary exercise test to assess exercise capacity. According to the patient's physical condition, cardiopulmonary capacity, disease, etc. to develop an individualized exercise program. The patient's Borg Scale of Perceived Exertion can be used to determine whether the intensity of exercise is appropriate.

Medical treatment of sarcopenia.

Medications for sarcopenia include hormones, omega-3 fatty acids, osteocalcin, stem cell transplantation, and more. They are of great help in the prevention and treatment of sarcopenia.

The basis of sarcopenia prevention and treatment lies in diet and exercise, and then combined with drug treatment depending on the patient's condition. A healthy diet and exercise can also reduce the risk of cardiovascular disease. Seniors and their families should pay more attention.

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