Friday, November 9, 2007
Epilepsy is a common disease because of what
Under the age of common diseases and because the table below. Physicians need special vigilance and prompt treatment of reversible factor is the low blood sugar and hypoxemia (secondary to narcotic overdose). Therefore, at the beginning, to use blood glucose test paper check blood sugar, but, based on experience, naloxone is the indication. Attention young and elderly patients, the cause of epilepsy similarity. Epilepsy reasons: Child care: Production injury (hypoxia, brain trauma), infection (brain abscess, meningitis), electrolyte imbalance (hyponatremia, low calcium, low magnesium), congenital malformations (intracranial cysts, hydrocephalus), and hereditary diseases (congenital metabolic disorders, vitamin B6 deficiency) Children: Heat epilepsy, primary epilepsy, trauma, infection (meningitis) Youth: Trauma, the original attack, drugs or alcohol (acute poisoning or stop medication), arteriovenous malformations Middle-aged: trauma, alcohol (acute poisoning or stop medication), brain tumor. Old age: Brain tumors, stroke, cerebral hemorrhage, alcoholism, abnormal metabolism (hyponatremia, hypernatremia, hypocalcemia, low blood sugar, uremia, hepatic failure)
Toxic common diseases due to epilepsy
Clinical external or internal biomass poisoning can cause epilepsy attack. Endogenous substances poisoning: If renal failure caused by metabolic acidosis can reduce seizure threshold; addition, the patients with phenylketonuria, because of their intimate phenylalanine into tyrosine obstacles in the process, affected some inhibitory neurotransmitter (ammonia cool acid) synthesis, increased excitability of nerve, which occurred epilepsy. Exogenous material poisoning: If acute alcoholism, excessive use of strychnine, camphor, nicorandil brake meters, PTZ and other central stimulants, or large-scale use of chlorpromazine,Trifluoperazine, and other anti - psychosis drugs and imipramine, and other antidepressant drugs.
Common characteristics of the frontal lobe epilepsy
Frontal lobe epilepsy some of the characteristics of simple, complex partial, secondary systemic attack or seizure of these mixed attack. Several attacks usually on the 1st and often occur during sleep. Sometimes part of the frontal lobe seizures and mental factors can cause the onset of confusion. Status epilepticus is their common complications. The diagnosis suggested that the general features are: ① usually attack shorter; ② usually start in the frontal part of the complex attack, after the attack with minor or no sense of chaos; ③ quickly from secondary systemic attack; ④ ankylosing or postural campaign prominent symptoms; ⑤ when the incidence of common complex gestures automatically disease; ⑥ when the discharge of the bilateral often falls. Supplementary motor area of the attack for more than posture, Focal ankylosis, with pronunciation, speech suspended and fencing posture. Cingulate attack for the type of complex partial seizures with onset at the complex movement of automatic gesture, and common autonomic disease, such as changes in mood and emotion. Attack forehead in the form of the polar regions of thinking including forced sexual contact or initial loss, as well as head and eyes to the movement, with possible opposition, the axis of clonic spasm, and autonomic of fall. Orbital for the district in the form of attack is a complex partial seizures, with the initiation of movement and gesture of automatic, and olfactory hallucinations of illusion and autonomic neuropathy. The Department of attack dorsal lateral forms may be ankylosing or less see the clonic, with a rotating head and eyes and stop words. Island Attack covered the characteristics including chewing, salivation, swallowing and throat symptoms, speech stopped, upper abdominal threatened, fear and autonomic symptoms and taste hallucinations particularly common in this area. Motor cortex is the main characteristics of seizures simple partial seizure, as well as different sides in different parts of the clinical manifestations vary.
Temporal lobe epilepsy characteristics of the Attack
Temporal lobe epilepsy is characterized by simple partial seizure, and the onset is usually part of secondary systemic attack or mixed these attacks, a common history and family history of febrile seizures, memory defect may occur. In metabolic imaging studies (such as PET), often observed that the low regional metabolism, often in the EEG showed unilateral or bilateral temporal lobe spikes. The diagnosis suggested that the general features are: ① simply part of the attack is a typical feature of the autonomic and (or) some of the spirit and feeling symptoms (such as olfactory and auditory) phenomena (including illusion,), the most common is abdominal (mostly rising) feeling. ② complex partial seizures often stop to campaign began, and then typically arise mouth? Silkworm? Automatic disease, often in the ensuing other automated. The duration of seizures in one minute more, it frequently was confusion after the attack, after the attack forgotten. Seizures can be intermittent period scalp EEG normal background activity can be expressed as mild or significant asymmetry, but also manifested as unilateral or bilateral, synchronous or asynchronous the temporal lobe spikes, a sharp wave and (or) slow wave. Hippocampus attack is the most common form of attack and the characteristics of the rise of upper abdominal discomfort, nausea, autonomic symptoms and signs, such as, navel and looking pale, facial Expanding redness, breathing stopped, expanding pupil , fear, terror and olfactory hallucinations. Simple lateral temporal lobe seizures to listen to the characteristics of illusion or hallucination or sleeping state, as well as visual barriers to know sexy. If involved advantage hemisphere, a language barrier, if the medial temporal lobe involvement or temporal lobe, or complex partial seizures for evolution.
Henoch - Schonlein purpura syndrome
[Outlined]
Henoch - Schonlein purpura syndrome (Allergic Purpura Syndrome), also known as Schonlein-Henoch purpura, capillary poisoning hemorrhagic disease (Hemorrhagic Capillary Toxicosis) is the result of microvascular caused by the abnormal bleeding systemic disease, involving the skin, joints, there gastrointestinal and kidney corresponding symptoms. The disease was particularly prevalent in children and adolescents.
[Diagnosis]
According to the upper respiratory tract infection, a skin purpura, and joints, abdomen and kidney involvement at the same time the performance of a recurrent feature of this disease should consider the possibility. It should be noted, and thrombocytopenic purpura, acute abdomen, glomerulonephritis, rheumatoid arthritis were identified.
[Treatment]
1. Removal causes: including anti-infection, remove感染灶to remove intestinal parasites, avoid application of the food and drug allergies. 2. Antihistamine drugs: the choice of chlorpheniramine, promethazine, diphenhydramine, such as drug Astemizole oral or intramuscular injection. Also Applications 10% glucose intravenous calcium 10 ml per day 1-2 times.
3. Glucocorticoid: acute phase and applied to the abdomen, joint pain obviously, can quickly ease the symptoms. Oral prednisone may be given, if necessary, hydrocortisone infusion. Short-term treatment (3-5) can ease the symptoms of withdrawal, but use a longer time after the reductions should gradually stop.
4. Other: the acute phase should bed rest, gastrointestinal symptoms should fasting. High-dose intravenous vitamin C (3 to 5 g / day). Abdominal pain can be intense intramuscular injection of atropine 0.5 to 1 mg. There are bleeding tendency may choose to use drugs to stop bleeding. Have kidney damage.
【Etiology:
The disease of unknown, and may be related to various factors, ① infection, the disease often in acute infection, the incubation period and after a certain incidence, mostly acute upper respiratory infection, hemolytic streptococcus pathogens to mainly, but also for gold Staphylococcus aureus, viral, and parasitic infections, ② food allergy, such as fish, prawns, crabs, and other allograft milk protein allergy can be induced by the disease, ③ drugs, such as Green streptomycin, sulfonamides, salicylic acid such formulations. It was also possible with the cold, insect bites, such as pollen dust exposure factors. All these factors have on the human small arteries, veins and capillaries small wall of inflammatory changes, increased vascular permeability caused subcutaneous tissue, and organ mucosal vascular hemorrhage of exudative edema, and a corresponding clinical manifestations.
【Pathological changes:
Blood and skin around the infiltration of lymphocytes and plasma cells, dermal capillary layer was inflammatory changes, exudative, edema, hemorrhage, and cause skin purpura. Intestinal mucosal layer edema, exudative, and bleeding caused abdominal pain, and so is the reason. Joint pain and peripheral edema due mainly to joints, the joint cavity caused by leakage. Renal involvement Visibility glomerular cell proliferation, necrotic foci with capillary thrombosis, renal tubular epithelial cells also visible swelling, degeneration, fibrosis.
Clinical manifestations】 【
Onset before 1 ~ 3 weeks are often the history of upper respiratory infection, the slow onset, duration protracted, often attack with ease in turn, according to the lesion site of different violations, and have different clinical manifestations:
1. Skin performance: most of the skin purpura as the first symptom. Often seen in the distal limb extensor side of hip back, face and torso rare Purpura showed symmetric distribution, in batches, sizes, and integration into films, or even hemorrhagic herpes and haemorrhagic necrosis. Purpura general a few days to be dissipated. A few may be accompanied by eyelids, lips, the hand-foot-site vascular edema or urticaria.
2. Gastrointestinal change: multi purpura for skin after abdominal symptoms, but also in gastrointestinal symptoms as the first persons. Mainly for paroxysmal or continuing in or lower abdomen, accompanied by nausea and vomiting, weight, there hematochezia, hematemesis, intussusception and intestinal perforation. Investigations have tenderness in the abdomen, without the muscle tension and anti-. If abdominal symptoms as the main performance, known as abdominal anaphylactoid purpura (Henoch Purpura).
3. Joint performance: the performance of joint swelling limbs pain to the knee, ankle, elbow, wrist, and so common, and often migrans, a few days dissipated, can be repeated attack, attack often accompanied by low heat. A joint symptoms for outstanding performance, known as joint - anaphylactoid purpura (Schonlein Purpura).
4. Kidney performance: changes in the kidney followed often Purpura showed proteinuria, hematuria, and urinary tube type, and some patients can be accompanied by swelling, oliguria and hypertension. Under normal circumstances the kidney damage of the disease better resume, leaving sequels, a few may be turned into a chronic nephritis, or uremia. Should occasional attention to the main renal lesions were not obvious and Purpura performance.
Exudative other vascular hemorrhage and edema can also involving the nervous system, respiratory tract, and other emerging corresponding symptoms.
【Auxiliary inspection --
Bleeding time, the clotting time, platelet count and function normal, normal or mildly ESR can be increased fast. Some patients capillary fragility test (beam-arm test) positive. Renal involvement can have proteinuria, hematuria, possession of urine.
Henoch - Schonlein purpura syndrome (Allergic Purpura Syndrome), also known as Schonlein-Henoch purpura, capillary poisoning hemorrhagic disease (Hemorrhagic Capillary Toxicosis) is the result of microvascular caused by the abnormal bleeding systemic disease, involving the skin, joints, there gastrointestinal and kidney corresponding symptoms. The disease was particularly prevalent in children and adolescents.
[Diagnosis]
According to the upper respiratory tract infection, a skin purpura, and joints, abdomen and kidney involvement at the same time the performance of a recurrent feature of this disease should consider the possibility. It should be noted, and thrombocytopenic purpura, acute abdomen, glomerulonephritis, rheumatoid arthritis were identified.
[Treatment]
1. Removal causes: including anti-infection, remove感染灶to remove intestinal parasites, avoid application of the food and drug allergies. 2. Antihistamine drugs: the choice of chlorpheniramine, promethazine, diphenhydramine, such as drug Astemizole oral or intramuscular injection. Also Applications 10% glucose intravenous calcium 10 ml per day 1-2 times.
3. Glucocorticoid: acute phase and applied to the abdomen, joint pain obviously, can quickly ease the symptoms. Oral prednisone may be given, if necessary, hydrocortisone infusion. Short-term treatment (3-5) can ease the symptoms of withdrawal, but use a longer time after the reductions should gradually stop.
4. Other: the acute phase should bed rest, gastrointestinal symptoms should fasting. High-dose intravenous vitamin C (3 to 5 g / day). Abdominal pain can be intense intramuscular injection of atropine 0.5 to 1 mg. There are bleeding tendency may choose to use drugs to stop bleeding. Have kidney damage.
【Etiology:
The disease of unknown, and may be related to various factors, ① infection, the disease often in acute infection, the incubation period and after a certain incidence, mostly acute upper respiratory infection, hemolytic streptococcus pathogens to mainly, but also for gold Staphylococcus aureus, viral, and parasitic infections, ② food allergy, such as fish, prawns, crabs, and other allograft milk protein allergy can be induced by the disease, ③ drugs, such as Green streptomycin, sulfonamides, salicylic acid such formulations. It was also possible with the cold, insect bites, such as pollen dust exposure factors. All these factors have on the human small arteries, veins and capillaries small wall of inflammatory changes, increased vascular permeability caused subcutaneous tissue, and organ mucosal vascular hemorrhage of exudative edema, and a corresponding clinical manifestations.
【Pathological changes:
Blood and skin around the infiltration of lymphocytes and plasma cells, dermal capillary layer was inflammatory changes, exudative, edema, hemorrhage, and cause skin purpura. Intestinal mucosal layer edema, exudative, and bleeding caused abdominal pain, and so is the reason. Joint pain and peripheral edema due mainly to joints, the joint cavity caused by leakage. Renal involvement Visibility glomerular cell proliferation, necrotic foci with capillary thrombosis, renal tubular epithelial cells also visible swelling, degeneration, fibrosis.
Clinical manifestations】 【
Onset before 1 ~ 3 weeks are often the history of upper respiratory infection, the slow onset, duration protracted, often attack with ease in turn, according to the lesion site of different violations, and have different clinical manifestations:
1. Skin performance: most of the skin purpura as the first symptom. Often seen in the distal limb extensor side of hip back, face and torso rare Purpura showed symmetric distribution, in batches, sizes, and integration into films, or even hemorrhagic herpes and haemorrhagic necrosis. Purpura general a few days to be dissipated. A few may be accompanied by eyelids, lips, the hand-foot-site vascular edema or urticaria.
2. Gastrointestinal change: multi purpura for skin after abdominal symptoms, but also in gastrointestinal symptoms as the first persons. Mainly for paroxysmal or continuing in or lower abdomen, accompanied by nausea and vomiting, weight, there hematochezia, hematemesis, intussusception and intestinal perforation. Investigations have tenderness in the abdomen, without the muscle tension and anti-. If abdominal symptoms as the main performance, known as abdominal anaphylactoid purpura (Henoch Purpura).
3. Joint performance: the performance of joint swelling limbs pain to the knee, ankle, elbow, wrist, and so common, and often migrans, a few days dissipated, can be repeated attack, attack often accompanied by low heat. A joint symptoms for outstanding performance, known as joint - anaphylactoid purpura (Schonlein Purpura).
4. Kidney performance: changes in the kidney followed often Purpura showed proteinuria, hematuria, and urinary tube type, and some patients can be accompanied by swelling, oliguria and hypertension. Under normal circumstances the kidney damage of the disease better resume, leaving sequels, a few may be turned into a chronic nephritis, or uremia. Should occasional attention to the main renal lesions were not obvious and Purpura performance.
Exudative other vascular hemorrhage and edema can also involving the nervous system, respiratory tract, and other emerging corresponding symptoms.
【Auxiliary inspection --
Bleeding time, the clotting time, platelet count and function normal, normal or mildly ESR can be increased fast. Some patients capillary fragility test (beam-arm test) positive. Renal involvement can have proteinuria, hematuria, possession of urine.
Children with idiopathic thrombocytopenic purpura
[Outlined]
Idiopathic thrombocytopenic purpura (ITP) is common in children of hemorrhagic disease. After 40 years of research proves that this disease and immune-related, are considered to be an autoimmune disease. Clinical to skin, mucous membrane characterized spontaneous bleeding, infection prevalence before history, as indicated respiratory tract infection (cold). The acute and chronic disease divided into two types, mostly children with acute idiopathic thrombocytopenic purpura, acute phase may all ages ITP incidence, but common to infants period, the incidence of the spring high. The disease in children with acute type in about 80 ￣ 90% in the six months rehabilitation, 10 ￣ 25% to chronic. Chronic cases was particularly prevalent in school-aged children, course in more than six months, about 1 / 3 ￣ 1 / 2 to five years resumed. Individual cases of acute severe bleeding may occur (especially intracranial hemorrhage) and leading to death
[Symptoms of the disease]
1. Disease before 1 ￣ six weeks virus infection, as indicated respiratory infections, measles, chicken pox, etc.. 2. Sudden onset, severe bleeding, skin, mucous membrane bleeding spontaneously mainly for common skin, oral mucosa, gums and eye conjunctiva, nasal cavity and trauma site. Gastrointestinal tract, urinary tract bleeding rare, occasionally intracranial hemorrhage. 3. See needle point-like skin bleeding, bruising, a few cases of mild hepatosplenomegaly.
[Diagnosis]
1. Repeatedly laboratory examination platelet count decrease. 2. Spleen does not increase or slightly increase. 3. Bone marrow examination megakaryocyte cells increased or normal, mature obstacles. 4. Below 5:00 in which two points should be: (1) prednisone therapy effective. (2) the splenectomy treatment effective. (3) PAIg increased. (4) PAC3 increased. (5) determination of platelet shortened life expectancy. 5. Exclusion of secondary thrombocytopenia.
[Treatment principle]
1. Bed rest and avoid injury. 2. Prevent and control infection. 3. Positive control bleeding. 4. Necessary, surgical treatment.
[Evaluation]
1. Cure: no bleeding, platelet count> 100 × 1000000000 / L, sustained more than three months. No recurrence. 2. Turn for the better: hemorrhage disappeared or improved platelet rose to 20 ￣ 50 × 1000000000 / L, but did not reach 100 × 1000000000 / L, continuous inspection three or observation two weeks more. 3. Surprised me: bleeding symptoms did not improve or worsen, and platelet count were not improved standards.
[The expert suggested that]
Pediatric if epistaxis, bleeding gums, skin bleeding, should immediately to the hospital for an examination. Once a patient thrombocytopenia best system further examination and treatment. Outpatient treatment of patients must be advised by doctors to do so as not to endanger children with serious bleeding lives, we must pay attention to the following points: (1) to restrict the activities of the best bed rest and avoid injury; (2) eat easily digested food, dry , uncompromising, and a sting Do not eat food, so as not to cause injury mucosal bleeding, (3) avoid application of aspirin, dipyridamole, and other drugs, (4) attention to the prevention of infection (such as the flu), so as not to add to improve the condition again .
Idiopathic thrombocytopenic purpura (ITP) is common in children of hemorrhagic disease. After 40 years of research proves that this disease and immune-related, are considered to be an autoimmune disease. Clinical to skin, mucous membrane characterized spontaneous bleeding, infection prevalence before history, as indicated respiratory tract infection (cold). The acute and chronic disease divided into two types, mostly children with acute idiopathic thrombocytopenic purpura, acute phase may all ages ITP incidence, but common to infants period, the incidence of the spring high. The disease in children with acute type in about 80 ￣ 90% in the six months rehabilitation, 10 ￣ 25% to chronic. Chronic cases was particularly prevalent in school-aged children, course in more than six months, about 1 / 3 ￣ 1 / 2 to five years resumed. Individual cases of acute severe bleeding may occur (especially intracranial hemorrhage) and leading to death
[Symptoms of the disease]
1. Disease before 1 ￣ six weeks virus infection, as indicated respiratory infections, measles, chicken pox, etc.. 2. Sudden onset, severe bleeding, skin, mucous membrane bleeding spontaneously mainly for common skin, oral mucosa, gums and eye conjunctiva, nasal cavity and trauma site. Gastrointestinal tract, urinary tract bleeding rare, occasionally intracranial hemorrhage. 3. See needle point-like skin bleeding, bruising, a few cases of mild hepatosplenomegaly.
[Diagnosis]
1. Repeatedly laboratory examination platelet count decrease. 2. Spleen does not increase or slightly increase. 3. Bone marrow examination megakaryocyte cells increased or normal, mature obstacles. 4. Below 5:00 in which two points should be: (1) prednisone therapy effective. (2) the splenectomy treatment effective. (3) PAIg increased. (4) PAC3 increased. (5) determination of platelet shortened life expectancy. 5. Exclusion of secondary thrombocytopenia.
[Treatment principle]
1. Bed rest and avoid injury. 2. Prevent and control infection. 3. Positive control bleeding. 4. Necessary, surgical treatment.
[Evaluation]
1. Cure: no bleeding, platelet count> 100 × 1000000000 / L, sustained more than three months. No recurrence. 2. Turn for the better: hemorrhage disappeared or improved platelet rose to 20 ￣ 50 × 1000000000 / L, but did not reach 100 × 1000000000 / L, continuous inspection three or observation two weeks more. 3. Surprised me: bleeding symptoms did not improve or worsen, and platelet count were not improved standards.
[The expert suggested that]
Pediatric if epistaxis, bleeding gums, skin bleeding, should immediately to the hospital for an examination. Once a patient thrombocytopenia best system further examination and treatment. Outpatient treatment of patients must be advised by doctors to do so as not to endanger children with serious bleeding lives, we must pay attention to the following points: (1) to restrict the activities of the best bed rest and avoid injury; (2) eat easily digested food, dry , uncompromising, and a sting Do not eat food, so as not to cause injury mucosal bleeding, (3) avoid application of aspirin, dipyridamole, and other drugs, (4) attention to the prevention of infection (such as the flu), so as not to add to improve the condition again .
Thrombotic thrombocytopenic purpura disease
For an uncommon micro-hemolytic disease of the micro-vascular disease and thrombosis. Cause unknown, a small number of patients may be related to infection, pregnancy, collagen vascular disease, cancer, and genetic and other related drugs. Various causes damage microvascular endothelial cells, resulting in collagen and basement membrane exposure caused platelets and fibrin deposition. Certain patients plasma existence of one or more platelet aggregation factor (PAF), or lack of normal plasma in the PAF inhibitor, induced platelet aggregation. Some people in TTP in patients with isolated VWF giant polymer, in vitro platelet aggregation that VWF metabolic abnormalities may also be related to the incidence and TTP. Peripheral artery disease and mainly involved capillaries, microvascular obstruction caused multiple organ failure. The disease onset of intense, rapid progress, a small number can be slow and recurrent. Clinical to 30 ~ 40-year-old female common, mainly manifested as bleeding, microvascular of hemolytic anemia, neurological symptoms, fever and kidney damage, called TTP five of the levy. Neuropsychiatric symptoms often intermittent or volatility. Laboratory tests: platelets decreased significantly, to severe anemia, reticulocyte increased blood platelet great film that, nucleated red blood cells and red blood cell debris, and bone marrow megakaryocyte erythroid of compensatory hyperplasia, normal coagulation checks. The skin, muscle, gums and bone marrow biopsy in capillary endothelial classes, small muscular arteries within the cortex and between glass-like deposits, with vascular endothelial proliferation and luminal obstruction. Except for a small number of chronic-disease sustainable few months to a few years, 80% of patients in three months killed. Plasma exchange and plasma infusion will enable 64% to 80% of patients eased, large dose PGI2 infusion or intravenous vincristine could ease a few cases, splenectomy only to improve the symptoms of some patients short period of time, the joint anti-platelet drugs glucocorticoid the plasma exchange can be used as adjuvant therapy.
Thursday, November 8, 2007
Systemic lupus erythematosus liver damage
Systemic lupus erythematosus (SLE) is an autoimmune disease, liver damage in the combined clinical more common, caused by different reasons. Briefly as follows: 1, the major clinical manifestations Systemic lupus erythematosus induced liver injury is mainly expressed in hepatomegaly, jaundice, and abnormal liver function may exist in a variety of serum autoantibodies, etc.. Among them, hepatomegaly or about 10% -32% more than in 2-3 cm, a small number of significantly enlarged. Lupus erythematosus cause jaundice various reasons, mainly hemolytic anemia, the merger viral hepatitis, biliary obstruction and acute pancreatitis, and so on. About 30% -60% of the SLE patients have abnormal liver function tests, mainly manifested as elevated aminotransferase levels, lower levels of serum albumin, globulin levels and increased levels of blood lipids, such as. Lupus Erythematosus liver damage often mild to moderate liver dysfunction, severe liver damage are rare. Systemic lupus erythematosus can be complicated with type I autoimmune hepatitis (hepatitis lupus), will occur in younger women, can be manifested as clinical weakness, joint pain, fever, hepatosplenomegaly, jaundice, and so on. 2, identifying the reasons for liver damage Systemic lupus erythematosus patients with liver damage, we should pay attention to identifying the reasons for the cause liver damage. Some of the patients with abnormal liver function itself is not a direct result of induced lupus erythematosus. SLE with lupus itself and hepatitis can cause liver damage, but to rule out viral hepatitis, excessive drinking and liver toxicity of drugs, such as biliary tract disease. In addition, congestive heart failure, primary biliary cirrhosis, also can cause abnormal liver function. First, my viral hepatitis, particularly hepatitis B and its related diseases caused by the higher incidence rates, so patients must check the viral markers and remove viral hepatitis; Also, as caused by excessive drinking of alcoholic hepatitis are becoming increasingly more; Third, the drug hepatitis patients with SLE is also common cause of liver damage, especially because of the process used in the treatment of lupus erythematosus drug caused, including certain anti-inflammatory analgesic drugs, methotrexate (MTX) and cyclophosphamide (CTX); In addition, we should also exclude other abnormal liver function caused the disease, including biliary and pancreatic diseases. 3, pay attention to the correct treatment and monitoring Against cause liver damage in patients with SLE of different reasons, we should adopt different treatment measures. Incorrect and unscientific treatment of the disease may add to, or even after the differential diagnosis and treatment lead to greater difficulties. Currently glucocorticoid treatment of systemic lupus erythematosus is still caused by the hepatitis major lupus drug. Against Drug-induced hepatitis, if early identification, after stopping lesions often reversible. Therefore, in the course of treatment the event of abnormal liver function or jaundice, should immediately stop using the drug or suspicious, and again to avoid the same or similar chemical structure of the drug, should be in accordance with the nature of drug detoxification agent. SLE patients in each treatment period, attention should be paid to monitoring of disease activity and treatment response, in particular attention should be paid to various toxic reactions, the periodic determination of blood, urine, liver function and other relevant inspection. In short, systemic lupus erythematosus combined liver damage is very common in clinical practice, the reasons for the cause of liver damage is not the same as clinical attention should identify and timely processing.
Primary chronic adrenal hypofunction Diagnosis
Clinical manifestations: 1. Skin pigmentation, weak weakness, anorexia, weight loss, low blood pressure, vertical syncope, cardiac narrowing, women and pubic hair scarce or exfoliated;
2. Tuberculosis may have fever, night sweats, pulmonary tuberculosis and adrenal calcification imaging;
3. Stress (trauma, infection, etc.) or abrupt discontinuation of hormone replacement therapy can be induced adrenal crisis, there may be nausea, vomiting, syncope, shock, coma.
Diagnosis: 1. Skin pigmentation, general weakness, dizziness, anorexia, weight loss, low blood pressure, vertical syncope, cardiac narrowing, women and pubic hair scarce or falling out of tuberculosis may have low heat, night sweats;
2. Blood eosinophils, lymphocytes increased pigment is mild anemia, a small number of merger pernicious anemia, reduced neutrophil;
3. Hyponatremia, hyperkalemia, low blood glucose, glucose tolerance test was curve;
4. Plasma cortisol and 24-hour urinary free cortisol lower;
5.24 hour urine 17 hydroxybutyrate corticosteroid, 17 ketones reduce steroid content;
6. Increased plasma ACTH, ACTH stimulation test no obvious reaction;
7. Chest and abdominal X-ray film can be found signs of TB, positive tuberculin test;
8. Adrenal CT and MRI lesion can be found.
2. Tuberculosis may have fever, night sweats, pulmonary tuberculosis and adrenal calcification imaging;
3. Stress (trauma, infection, etc.) or abrupt discontinuation of hormone replacement therapy can be induced adrenal crisis, there may be nausea, vomiting, syncope, shock, coma.
Diagnosis: 1. Skin pigmentation, general weakness, dizziness, anorexia, weight loss, low blood pressure, vertical syncope, cardiac narrowing, women and pubic hair scarce or falling out of tuberculosis may have low heat, night sweats;
2. Blood eosinophils, lymphocytes increased pigment is mild anemia, a small number of merger pernicious anemia, reduced neutrophil;
3. Hyponatremia, hyperkalemia, low blood glucose, glucose tolerance test was curve;
4. Plasma cortisol and 24-hour urinary free cortisol lower;
5.24 hour urine 17 hydroxybutyrate corticosteroid, 17 ketones reduce steroid content;
6. Increased plasma ACTH, ACTH stimulation test no obvious reaction;
7. Chest and abdominal X-ray film can be found signs of TB, positive tuberculin test;
8. Adrenal CT and MRI lesion can be found.
Primary chronic adrenal hypofunction
Primary chronic adrenal hypofunction also known as Adison. Damage due to bilateral adrenal cortex, adrenal glucocorticoid (cortisol) and salt cortex hormone (aldosterone) lack of secretion caused. Adrenal cortical atrophy is the main reason (with autoimmune related), and adrenal tuberculosis, as other bilateral adrenalectomy, fungal infections, leukemia cell invasion and metastasis, such as those caused rare. The incidence rate of 4 / 100,000, was particularly prevalent in adults. Onset slow, early performance easily tired, fatigue, memory decline, gradually appearing skin pigmentation, general weakness, weight loss, low blood sugar, low blood pressure, vertical syncope, cardiac narrowing, women and scarce or pubic hair off. The stress (trauma, infection, etc.) easily lead to adrenal crisis. Blood biochemistry, adrenal reserve function tests, positioning checks may clear diagnosis. Treatment for hormone replacement therapy for the treatment and.
Chronic adrenal hypofunction
Bilateral adrenal when most of the damage, there are all sorts of glucocorticoid inadequate performance, saying adrenal hypofunction. There are primary and secondary. Primary chronic adrenal hypofunction also known as Addison disease, relatively rare; secondary Visibility hypothalamus - patients with pituitary dysfunction, as CRF or inadequate secretion of ACTH, which adrenal atrophy.
Etiology:
First, adrenal tuberculosis only bilateral adrenal tuberculosis, the majority of adrenal tissue damaged before clinical symptoms arise. With more than lung, bone or other parts of TB lesions. During the 1950s about chronic adrenal hypofunction in half in recent years, with the control of TB is diminishing. Second, autoimmune disorder idiopathic autoimmune reaction caused adrenal atrophy as the most common reason for the present, can often be measured in serum anti-adrenal tissue antibodies to. The main transgression and fascicular zone cells, antigen mainly in microsomes and mitochondria within. Many of the disease associated with other autoimmune disorders. If multiple endocrine gland dysfunction syndrome (Schmidt syndrome), may include, for example adrenal dysfunction, hypothyroidism, hypoparathyroidism, gonadal failure, diabetes, pituitary dysfunction, gastric parietal cell antibody positive, pernicious anemia, thyroid Gong can hyperthyroidism, colon tumor, myasthenia gravis, solitary red cell aplasia, and so on. Three other adrenal cancer metastasis, or tumor metastasis in patients with 10% of the bilateral adrenal metastasis to lung cancer and breast cancer as common. Can also be found in bilateral adrenal after resection, systemic fungal infection, such as adrenal amyloidosis.
Etiology:
First, adrenal tuberculosis only bilateral adrenal tuberculosis, the majority of adrenal tissue damaged before clinical symptoms arise. With more than lung, bone or other parts of TB lesions. During the 1950s about chronic adrenal hypofunction in half in recent years, with the control of TB is diminishing. Second, autoimmune disorder idiopathic autoimmune reaction caused adrenal atrophy as the most common reason for the present, can often be measured in serum anti-adrenal tissue antibodies to. The main transgression and fascicular zone cells, antigen mainly in microsomes and mitochondria within. Many of the disease associated with other autoimmune disorders. If multiple endocrine gland dysfunction syndrome (Schmidt syndrome), may include, for example adrenal dysfunction, hypothyroidism, hypoparathyroidism, gonadal failure, diabetes, pituitary dysfunction, gastric parietal cell antibody positive, pernicious anemia, thyroid Gong can hyperthyroidism, colon tumor, myasthenia gravis, solitary red cell aplasia, and so on. Three other adrenal cancer metastasis, or tumor metastasis in patients with 10% of the bilateral adrenal metastasis to lung cancer and breast cancer as common. Can also be found in bilateral adrenal after resection, systemic fungal infection, such as adrenal amyloidosis.
What is non-functional pituitary tumor
Pituitary tumors are more common brain tumor, brain tumor about the five percent of a 10 percent. In the past, the classification of pituitary tumors more staining inspection to determine, in accordance with different staining divided into oncocytoma, basophilic tumor and chromophobe cell tumor. Recently a variety of inspection methods of establishment and constant improvement of tumor cells can secrete hormones whether the capacity is divided into two categories: functional and non-functional pituitary tumor of the pituitary tumor. Functional hormone secreting pituitary tumor according to the type of tumor into growth hormone, prolactin tumor, ACTH tumor, tumor and thyroid stimulating hormone gonadotropin of the latter two kinds of rare. Function of pituitary tumor may also be mixed exist, such as growth hormone prolactin tumor of 10. Thought about pituitary tumors 80% of the chromophobe cell tumor secreting hormones do not have the capacity now discovered that many chromophobe cell tumor is functional pituitary tumor, which in about 30 percent of a 70 percent prolactin tumor. Therefore, the non-functioning of the pituitary tumor in the pituitary tumor in the percentage has been greatly decreased, or about pituitary tumors 25% a 30%.
Cushing's syndrome caused by a number of factors which?
Special bushy hair, hair low, in the forehead,side also has some careful long hair, often are hand ringworm and tinea pedis. These people had to be called a "Cushing syndrome" disease.
Cushing disease called Cushing's syndrome is the result of in vivo glucocorticoid caused by the excessive, clinical mainly concentric obesity, one month after face, buffalo back, and more blood quality, and more hair, acne, etc., in addition, in patients with abdominal and thigh also found generally longitudinal distribution of a wide diamond-shaped purple red stripes, called purple stripes, menstrual disorders, hypertension, osteoporosis is rare, a small number can be associated with androgen, salt glucocorticoid, PRL, ACTH (a sugar Stone promote secretion of the hormone hormone) too many points汔performance, such as masculine, electrolyte imbalance,pigmentation, etc..
Glucocorticoid secreted by the adrenal gland, the adrenal and pituitary function of this regulation, often from Cushing of adrenal tumors and pituitary adenomas (or cancer) caused by. Long a pituitary adenoma, increased secretion of ACTH, making adrenal hyperplasia, excessive secretion of hormones. Adrenocortical adenoma and carcinoma may also result in increased glucocorticoid. Other less See also the cause of ectopic ACTH points汔syndrome and long-term use of glucocorticoids caused by a large number of drug-Cushing's syndrome.
Cushing disease called Cushing's syndrome is the result of in vivo glucocorticoid caused by the excessive, clinical mainly concentric obesity, one month after face, buffalo back, and more blood quality, and more hair, acne, etc., in addition, in patients with abdominal and thigh also found generally longitudinal distribution of a wide diamond-shaped purple red stripes, called purple stripes, menstrual disorders, hypertension, osteoporosis is rare, a small number can be associated with androgen, salt glucocorticoid, PRL, ACTH (a sugar Stone promote secretion of the hormone hormone) too many points汔performance, such as masculine, electrolyte imbalance,pigmentation, etc..
Glucocorticoid secreted by the adrenal gland, the adrenal and pituitary function of this regulation, often from Cushing of adrenal tumors and pituitary adenomas (or cancer) caused by. Long a pituitary adenoma, increased secretion of ACTH, making adrenal hyperplasia, excessive secretion of hormones. Adrenocortical adenoma and carcinoma may also result in increased glucocorticoid. Other less See also the cause of ectopic ACTH points汔syndrome and long-term use of glucocorticoids caused by a large number of drug-Cushing's syndrome.
What the attention of gouty arthritis
(1) should be acute bed rest, Chigaohuanshi to alleviate pain.
(2) dietary restraint to prevent obesity, avoid eating high - purine foods such as heart, liver, kidney, eggs, dried, sardines, salt pork, Herring, condensed gravy, anchovies, salmon, Goose,such as food fermentation. Temperance, bogey spicy food. Avoid over exertion and tension, and stimulate the damp cold, avoid the use of the drug suppression uric acid excretion. More drinking water daily, urine output not less than 2000 ml for the benefit of uric acid discharge.
(3) If the concurrent cardiovascular, kidney and other diseases, such as hypertension, coronary heart disease, kidney stones, urinary tract infection, renal failure, and other diseases, should go to a local hospital symptomatic treatment.
(4) Patients should actively medication, oral pure Chinese medicine preparations "quick-impact rheumatoid Ling", "quick-impact Qufeng casual" disease control mitigation, it should further consolidate 1-2 courses until thoroughly, it is not appropriate without stopping.
(2) dietary restraint to prevent obesity, avoid eating high - purine foods such as heart, liver, kidney, eggs, dried, sardines, salt pork, Herring, condensed gravy, anchovies, salmon, Goose,such as food fermentation. Temperance, bogey spicy food. Avoid over exertion and tension, and stimulate the damp cold, avoid the use of the drug suppression uric acid excretion. More drinking water daily, urine output not less than 2000 ml for the benefit of uric acid discharge.
(3) If the concurrent cardiovascular, kidney and other diseases, such as hypertension, coronary heart disease, kidney stones, urinary tract infection, renal failure, and other diseases, should go to a local hospital symptomatic treatment.
(4) Patients should actively medication, oral pure Chinese medicine preparations "quick-impact rheumatoid Ling", "quick-impact Qufeng casual" disease control mitigation, it should further consolidate 1-2 courses until thoroughly, it is not appropriate without stopping.
Gout complications
Most patients with gout have one or more complications, common complications include hypertension, hyperlipidemia, diabetes, obesity, atherosclerosis, coronary heart disease, cerebral vascular disease.
First, Hypertension
Gout Patients often accompanied hypertension, I Branch information for 58.8 percent. Some scholars believe that hyperuricemia and hypertension may have relevance, and that Hyperuricemia is a risk factor for hypertension, hyperuricemia are susceptible to hypertension. The reason is not clear, is the quality of the response gout, and hyperinsulinemia may be related.
Hyperuricemia the impact of hypertension: hypertensive patients such as occurred hyperuricemia, hematuria Acid Hydrolysis normal renal hemodynamic and related reflect hypertension renal vascular damage caused by the degree of renal sclerosis and serve as a hemodynamic parameters. The longer the duration, the higher the uric acid, the more severe the disease, renal blood flow more heavy damage. Its mechanism is not clear, probably by direct crystallization of uric acid deposition in sodium small artery wall and caused damage artery arteriosclerosis increase endometrial hypertension.
Hypertension on the impact of hyperuricemia: If gout patients with hypertension, can affect uric acid excretion, hyperuricemia more obvious. Hypertension is the mechanism itself may have decreased renal function caused the trend, thereby affecting the function of renal excretion of uric acid. Including: ① hypertensive renal disease can cause arteriosclerosis; ② angiotensin hypertension, elevated catecholamine concentrations, renal blood flow reduction, tubular hypoxia increased lactate formation, the latter on uric acid excretion competitive inhibition to reduce uric acid secretion, the effects of renal excretion of uric acid, making into uric acid retention; ③ long-term use of certain patients with hypertension such as Thiazide diuretics, triamterene Pteridine, but also the impact of tubular excretion of uric acid, uric acid emission reduction.
In short, hypertension and gout may mutually some reason, mutual promotion, hyperuricemia and hypertension at the same time caused by the existence of different levels of atherosclerosis and renal sclerosis common renal blood flow leading to the reduction and deterioration, thereby increasing the development of the illness. But its exact relationship to be further studied.
Second, hyperlipidemia
Homoharringtonine hyperlipidemia or triglyceride (TG) and hyperlipidemia significantly increased serum uric acid related. According to the information I Branch, gout patients with 75% to 80% with hyperlipidemia. While patients with hyperlipidemia 60 percent to 80 percent with hyperuricemia. Serum uric acid and triglyceride numerical significant positive correlation. Some scholars believe that the third year triglycerides decreased renal excretion of uric acid is one of the reasons for gout.
Third, diabetes
Gout patients is often associated with Iridium chain spectrum N dobsons persimmon deck Yun Jing? Gout with diabetes - 8.6 percent. Gout and diabetic there are many common factors, such as age, obesity, and so on. Like human blood glucose values as uric acid, with the increase of age have increased tendencies. Some scholars believe that the excessive concentration of serum uric acid can directly damage the pancreas J3 cells, and induced diabetes. Even some patients with gout increased insulin antibody diabetes.
Conversely, patients with diabetes easily generate hyperuricemia. Decomposition of purine metabolism and increased uric acid production increase is diabetic characteristics. Diabetic patients in hyperuricemia can be divided into three types: type metabolism, kidney-type, mixed. Metabotropic features have increased uric acid in the body, kidney type is characterized by lower renal excretion of uric acid, mixed type is characterized by the formation increased uric acid excretion and reduce both. Hyperuricemia in the formation of kidney factors often is of great significance. Hyperuricemia almost all the diabetic patients have chronic renal insufficiency, and the characteristics of renal excretion of uric acid damage. In type 1 diabetes incidence hyperuricemia, kidney damage play a major role. Type 2 diabetes hyperuricemia composite factor is the occurrence of the decision, that is, kidney damage and function of increased uric acid formation.
4, obesity
Gout was particularly prevalent in the obese. Obesity is defined as artificial, the majority of the current standard weight as the basis. The standard weight (kg) = height (cm) -105, or height (cm) -100 later by the 0.9 (male) or 85 (women). Weight exceeded the standard body weight 20 percent for obesity, and in 10% ~ 20% for overweight.
Obesity may cause hyperuricemia and endocrine system disorders or in vivo - generated inhibit excessive uric acid excretion related. Obesity energy intake increased, purine metabolism can also lead to accelerated serum uric acid concentrations increased. Some studies show that overweight or obese Mean serum uric acid and hyperuricemia detection rate were significantly higher than those of normal weight or low. Overweight or obese than those of normal weight or below the standard weight, easy existence of sugar, fat and protein substances such as metabolic disorders, the risk of gout, hypertension, hyperlipidemia, and diabetes and other diseases. Thus the prevention and treatment of overweight and obesity in these substances to improve metabolic abnormalities useful so that they could reduce gout, hypertension, hyperlipidemia, and diabetes prevalence rate. Total weight loss also invaded blast torsion chuiwan high plane trip Т practicing ┲? One?
5, coronary heart disease
According to the information I Branch, gout patients with coronary artery disease for 15.6 percent.
Some scholars will hyperuricemia as one of the risk factors of coronary heart disease. Some even call it "gout" heart disease. But whether hyperuricemia can be used as the risk factors of coronary heart disease is still controversial, uric acid and other scholars believe that the occurrence of coronary heart disease, cardiovascular disease mortality was no causal relationship.
Conversely, patients with coronary artery disease may exist uric acid metabolic disorders, and often associated with higher serum uric acid. The reason is not clear, some academics have found blood insulin resistance in patients with coronary heart disease although the index was higher, but the insulin resistance index and not obvious correlation between serum uric acid, showed that insulin resistance may not be the main reason for uric acid metabolic disorders.
6. Cerebral infarction
Gout with cerebral infarction rare, accounting for only 2.1 percent.
In short, because of gout was particularly prevalent in the elderly, and is often associated with obesity, hypertension, hyperlipidemia, diabetes, atherosclerosis, coronary heart disease, cerebral vascular disease, and so on. The above several diseases associated with hyperuricemia of strong, but all of these factors will combine perfect is difficult, hyperuricemia these diseases may not be an independent risk factor, and multiple factors. Like hypertension affect the renal excretion of uric acid, uric acid intake obesity more acidic metabolites competitive inhibition of tubular excretion of uric acid, diabetes increased catabolism of purine and uric acid production increase. The pathogenesis,
Hyperuricemia often associated with these risk factors more or less together, the incidence of gout and progress plays a synergy. It that the above factors may be common, casual, constitute incidence trend. But hyperuricemia and obesity, hypertension, hyperlipidemia, diabetes, atherosclerosis, coronary heart disease, cerebral vascular disease, bringing together the pathological basis of what this phenomenon will be gathered, what are intrinsically linked? Family of genetic factors on the number of such contacts from the role? These mutual the precise relationship is not yet clear, it is worth further exploration.
In the treatment of primary gout was found along with the decline in the level of serum uric acid and gout symptoms eased, with the incidence of certain symptoms such as angina, chest tightness, lightheadedness, heart palpitations, headache, and so obviously improved. Some unused hypolipidemic drugs in patients with high blood lipids, blood uric acid level with the effective control lipids decreased significantly. Some refractory diabetes, blood glucose also decreased significantly. Therefore, as purine metabolism disorder is the primary gout coronary heart disease, hypertension, diabetes, hyperlipidemia deterioration factors, the timely control gout, with the incidence of their control is also very useful. Therefore, I believe that the primary diagnosis for patients with gout should conduct routine blood lipids, blood sugar, ECG, X-ray and other inspection, with early detection of disease. As for the above patients with the disease need to repeatedly check serum uric acid and urinary uric acid, timely treatment of hyperuricemia.
First, Hypertension
Gout Patients often accompanied hypertension, I Branch information for 58.8 percent. Some scholars believe that hyperuricemia and hypertension may have relevance, and that Hyperuricemia is a risk factor for hypertension, hyperuricemia are susceptible to hypertension. The reason is not clear, is the quality of the response gout, and hyperinsulinemia may be related.
Hyperuricemia the impact of hypertension: hypertensive patients such as occurred hyperuricemia, hematuria Acid Hydrolysis normal renal hemodynamic and related reflect hypertension renal vascular damage caused by the degree of renal sclerosis and serve as a hemodynamic parameters. The longer the duration, the higher the uric acid, the more severe the disease, renal blood flow more heavy damage. Its mechanism is not clear, probably by direct crystallization of uric acid deposition in sodium small artery wall and caused damage artery arteriosclerosis increase endometrial hypertension.
Hypertension on the impact of hyperuricemia: If gout patients with hypertension, can affect uric acid excretion, hyperuricemia more obvious. Hypertension is the mechanism itself may have decreased renal function caused the trend, thereby affecting the function of renal excretion of uric acid. Including: ① hypertensive renal disease can cause arteriosclerosis; ② angiotensin hypertension, elevated catecholamine concentrations, renal blood flow reduction, tubular hypoxia increased lactate formation, the latter on uric acid excretion competitive inhibition to reduce uric acid secretion, the effects of renal excretion of uric acid, making into uric acid retention; ③ long-term use of certain patients with hypertension such as Thiazide diuretics, triamterene Pteridine, but also the impact of tubular excretion of uric acid, uric acid emission reduction.
In short, hypertension and gout may mutually some reason, mutual promotion, hyperuricemia and hypertension at the same time caused by the existence of different levels of atherosclerosis and renal sclerosis common renal blood flow leading to the reduction and deterioration, thereby increasing the development of the illness. But its exact relationship to be further studied.
Second, hyperlipidemia
Homoharringtonine hyperlipidemia or triglyceride (TG) and hyperlipidemia significantly increased serum uric acid related. According to the information I Branch, gout patients with 75% to 80% with hyperlipidemia. While patients with hyperlipidemia 60 percent to 80 percent with hyperuricemia. Serum uric acid and triglyceride numerical significant positive correlation. Some scholars believe that the third year triglycerides decreased renal excretion of uric acid is one of the reasons for gout.
Third, diabetes
Gout patients is often associated with Iridium chain spectrum N dobsons persimmon deck Yun Jing? Gout with diabetes - 8.6 percent. Gout and diabetic there are many common factors, such as age, obesity, and so on. Like human blood glucose values as uric acid, with the increase of age have increased tendencies. Some scholars believe that the excessive concentration of serum uric acid can directly damage the pancreas J3 cells, and induced diabetes. Even some patients with gout increased insulin antibody diabetes.
Conversely, patients with diabetes easily generate hyperuricemia. Decomposition of purine metabolism and increased uric acid production increase is diabetic characteristics. Diabetic patients in hyperuricemia can be divided into three types: type metabolism, kidney-type, mixed. Metabotropic features have increased uric acid in the body, kidney type is characterized by lower renal excretion of uric acid, mixed type is characterized by the formation increased uric acid excretion and reduce both. Hyperuricemia in the formation of kidney factors often is of great significance. Hyperuricemia almost all the diabetic patients have chronic renal insufficiency, and the characteristics of renal excretion of uric acid damage. In type 1 diabetes incidence hyperuricemia, kidney damage play a major role. Type 2 diabetes hyperuricemia composite factor is the occurrence of the decision, that is, kidney damage and function of increased uric acid formation.
4, obesity
Gout was particularly prevalent in the obese. Obesity is defined as artificial, the majority of the current standard weight as the basis. The standard weight (kg) = height (cm) -105, or height (cm) -100 later by the 0.9 (male) or 85 (women). Weight exceeded the standard body weight 20 percent for obesity, and in 10% ~ 20% for overweight.
Obesity may cause hyperuricemia and endocrine system disorders or in vivo - generated inhibit excessive uric acid excretion related. Obesity energy intake increased, purine metabolism can also lead to accelerated serum uric acid concentrations increased. Some studies show that overweight or obese Mean serum uric acid and hyperuricemia detection rate were significantly higher than those of normal weight or low. Overweight or obese than those of normal weight or below the standard weight, easy existence of sugar, fat and protein substances such as metabolic disorders, the risk of gout, hypertension, hyperlipidemia, and diabetes and other diseases. Thus the prevention and treatment of overweight and obesity in these substances to improve metabolic abnormalities useful so that they could reduce gout, hypertension, hyperlipidemia, and diabetes prevalence rate. Total weight loss also invaded blast torsion chuiwan high plane trip Т practicing ┲? One?
5, coronary heart disease
According to the information I Branch, gout patients with coronary artery disease for 15.6 percent.
Some scholars will hyperuricemia as one of the risk factors of coronary heart disease. Some even call it "gout" heart disease. But whether hyperuricemia can be used as the risk factors of coronary heart disease is still controversial, uric acid and other scholars believe that the occurrence of coronary heart disease, cardiovascular disease mortality was no causal relationship.
Conversely, patients with coronary artery disease may exist uric acid metabolic disorders, and often associated with higher serum uric acid. The reason is not clear, some academics have found blood insulin resistance in patients with coronary heart disease although the index was higher, but the insulin resistance index and not obvious correlation between serum uric acid, showed that insulin resistance may not be the main reason for uric acid metabolic disorders.
6. Cerebral infarction
Gout with cerebral infarction rare, accounting for only 2.1 percent.
In short, because of gout was particularly prevalent in the elderly, and is often associated with obesity, hypertension, hyperlipidemia, diabetes, atherosclerosis, coronary heart disease, cerebral vascular disease, and so on. The above several diseases associated with hyperuricemia of strong, but all of these factors will combine perfect is difficult, hyperuricemia these diseases may not be an independent risk factor, and multiple factors. Like hypertension affect the renal excretion of uric acid, uric acid intake obesity more acidic metabolites competitive inhibition of tubular excretion of uric acid, diabetes increased catabolism of purine and uric acid production increase. The pathogenesis,
Hyperuricemia often associated with these risk factors more or less together, the incidence of gout and progress plays a synergy. It that the above factors may be common, casual, constitute incidence trend. But hyperuricemia and obesity, hypertension, hyperlipidemia, diabetes, atherosclerosis, coronary heart disease, cerebral vascular disease, bringing together the pathological basis of what this phenomenon will be gathered, what are intrinsically linked? Family of genetic factors on the number of such contacts from the role? These mutual the precise relationship is not yet clear, it is worth further exploration.
In the treatment of primary gout was found along with the decline in the level of serum uric acid and gout symptoms eased, with the incidence of certain symptoms such as angina, chest tightness, lightheadedness, heart palpitations, headache, and so obviously improved. Some unused hypolipidemic drugs in patients with high blood lipids, blood uric acid level with the effective control lipids decreased significantly. Some refractory diabetes, blood glucose also decreased significantly. Therefore, as purine metabolism disorder is the primary gout coronary heart disease, hypertension, diabetes, hyperlipidemia deterioration factors, the timely control gout, with the incidence of their control is also very useful. Therefore, I believe that the primary diagnosis for patients with gout should conduct routine blood lipids, blood sugar, ECG, X-ray and other inspection, with early detection of disease. As for the above patients with the disease need to repeatedly check serum uric acid and urinary uric acid, timely treatment of hyperuricemia.
Gout and Hyperuricemia What is the difference
Hyperuricemia refers to blood uric acid than normal scope of a state. Many factors can cause blood uric acid salt content increased, and gout is one of the most common causes. Gout refers to the long-term hyperuricemia circumstances, lead to human organs and tissues in lesions. The main result gouty arthritis, gout and kidney disease, gout and kidney stones, gout and heart disease, gout and hypertension, and other serious complications. Hyperuricemia can also say is a prelude to gout, but not necessarily able to evolve into gout disease, gout patients have hyperuricemia.
What factors can cause acute gouty arthritis
Apart from the joint local damp, cold, there are factors which can cause acute gouty arthritis? Many factors may cause acute gouty arthritis attack. Clinical data from the statistics, about 40% -50% of patients can be found that lead to acute arthritis incentives. Fatigue and high - purine diet is the most common incentives. Clinically, some overtime work in the border, or long-distance travel, or circumstances, such as the relocation of new homes due to fatigue and excessive incidence, but some are in the eat three square meals a large fish, meat food after onset. Other common incentives include alcohol, a cold, the local strain or sprain joints, excessive movement (such as long-distance running, swimming, playing soccer, etc.), mental stress, respiratory tract infections. A small number of patients have excessive induced arthritis and acute attack. Peacetime drugs can effectively control serum uric acid attack for a long time without the sick man of arthritis in hand to stop medication may also cause acute arthritis. Some patients can often be found two or more incentives exist, such as drinking and eating of fish, meat, fatigue and cold; mental stimulation and drinking; campaign excessive strain or sprain joints and such. There are also a large number of acute gouty arthritis attack patients can not find the incentive.
Gout can cause kidney damage?
Gout kidney damage can occur. According to statistics, gout patients 20% -25% of uric acid nephropathy, and the autopsy confirmed the kidney lesions were almost 100%. It includes gouty nephropathy, acute obstructive nephropathy and urolithiasis. (1) gouty nephropathy sustainability of hyperuricemia, 20% in clinical nephropathy on the performance, after several years or more may have a glomerular and tubular damage to a small number of developing uremia. Uric acid salt nephropathy after the incidence of gout of joint damage, and close relationship with the course and treatment. Studies show that uric acid salt nephropathy and gouty arthritis unrelated to the severity of that mild arthritis patients may have nephropathy, and serious kidney arthritis patients is not necessarily abnormal. Early mild unilateral or bilateral flank pain, swelling and later appeared mild to moderate hypertension. Urine was acidic, intermittent or persistent proteinuria, generally no more than + +. Renal tubular function has concentrated almost fell, a nocturnal enuresis, polyuria, urine relatively low density. About 5-10 years after nephropathy increase, in turn developed into uremia, about 17% -25% died of renal failure. (2) urinary calculi gout patients were acidic urine, thus urinary uric acid concentrations increase, the smaller stones from the urine, but often without feeling, urine sediments shows that the small brown sand; larger obstructive ureteral stones can be caused hematuria and renal colic due to a urinary infection secondary to renal impeded glenoid nephritis. Huge stones can cause renal calyceal deformed pelvis, hydronephrosis. Uric acid stones X line simply does not contrast, when uric acid, sodium and calcium X Online Visibility stone shadow. (3) acute obstructive nephropathy found in serum uric acid and uric acid in urine increased significantly, it is because of the influx extensive crystallization of uric acid caused by tubular obstruction. Gout often and hypertension, hyperlipidemia, atherosclerosis, coronary heart disease and type 2 diabetes. In older people Gout causes of death, cardiovascular factors far more than renal insufficiency. But between gout and cardiovascular disease there is no direct causal link, but both obesity, dietary factors are related.
Gout stones can occur in the bladder and ureter?
Gout occurs in the kidney stone mainly to two factors: (1) the blood uric acid excretion through the kidneys approximately 75% -80% of the uric acid from the kidneys, about 20 percent of uric acid through the bile duct into the gut, with the feces from. Other organs such as the lung, pancreas, and so almost zero urinary acid, uric acid deposition easy in the formation of kidney stones in the kidney. Especially high concentrations of serum uric acid excretion over the ability of the kidney, kidney stones more prone to gout. (2) uric acid deposition and local environmental organizations pH (the pH value). When local, that is, when the low value of HP sedimentary formation of uric acid stones easily when local partial base, that is, at high pH values, not in some uric acid deposition. Normal blood pH value of 7.35 ~ 7.45 (neutral). Liver, lung, heart, brain and other organizations of similar pH and blood, and uric acid secretion is not the place, so difficult sedimentary formation of uric acid stones. While urine is a kidney premises, the urine pH values in the 5.5 to 6 or so, was acidic, and uric acid in urine from the mainly by the, so easy in the deposition and formation of kidney stones. Sometimes in the deposition of ureter and bladder stone formation. In a few cases, gout may also large stone vessel wall, endocardial and biliary formed, but such cases are rarely seen.
Four dangerous complications of gout
Patients suffering from gout, the in vivo metabolism of sugar and fat will be significantly
reduced functional, it is relatively easy with various serious diseases:
[Diabetes]
Both diabetes and gout because abnormal metabolism in vivo caused by diseases easily
with the patients. Regulate blood glucose because diabetes is the lack of the hormone
insulin, resulting in a continuous state of high blood sugar; and uric acid value and great
correlation between blood glucose levels are usually high value of uric acid, glucose
values will be relatively high.
【Hypertension / high blood lipids --
Most patients with gout is more body fat, excessive accumulation of body fat tends to
cause arteriosclerosis and hypertension; and because gout patients daily intake of high fat
diet on the bias, high-calorie food, the neutral body fat content is very high, cholesterol
values usually exceeded normal standards, hyperlipidemia one of the good of the group.
【Myocardial infarction / angina pectoris:
Gout patients with atherosclerotic cardiovascular cases is high, resulting in blood
unable to fully serve the heart, blood circulation dysfunction caused angina pectoris or
myocardial infarction on the particularly high rate, especially on the original with
hyperlipidemia patients with gout is more susceptible to heart disease.
【Obstacles - Cerebrovascular
At the same arteriosclerosis is caused by the problem, the difference in the brain
occurred. Its symptoms include headache, dizziness, hands and feet or paralysis,
serious, the patients have lost consciousness of the danger, or even death, in addition to
attending patients with angiography, CT brain needs to be done, MRI.
reduced functional, it is relatively easy with various serious diseases:
[Diabetes]
Both diabetes and gout because abnormal metabolism in vivo caused by diseases easily
with the patients. Regulate blood glucose because diabetes is the lack of the hormone
insulin, resulting in a continuous state of high blood sugar; and uric acid value and great
correlation between blood glucose levels are usually high value of uric acid, glucose
values will be relatively high.
【Hypertension / high blood lipids --
Most patients with gout is more body fat, excessive accumulation of body fat tends to
cause arteriosclerosis and hypertension; and because gout patients daily intake of high fat
diet on the bias, high-calorie food, the neutral body fat content is very high, cholesterol
values usually exceeded normal standards, hyperlipidemia one of the good of the group.
【Myocardial infarction / angina pectoris:
Gout patients with atherosclerotic cardiovascular cases is high, resulting in blood
unable to fully serve the heart, blood circulation dysfunction caused angina pectoris or
myocardial infarction on the particularly high rate, especially on the original with
hyperlipidemia patients with gout is more susceptible to heart disease.
【Obstacles - Cerebrovascular
At the same arteriosclerosis is caused by the problem, the difference in the brain
occurred. Its symptoms include headache, dizziness, hands and feet or paralysis,
serious, the patients have lost consciousness of the danger, or even death, in addition to
attending patients with angiography, CT brain needs to be done, MRI.
What is gout? Gout at which several types?
Gout is a group of purine metabolism disorder chronic metabolic disorder caused by the
disease. The main clinical features are produced in excessive uric acid excretion of uric
acid kidney or decrease, caused elevated blood uric acid formed hyperuricemia and the
repeated attacks of acute gouty arthritis, gout stone deposition, gouty arthritis and
chronic joint deformities, etc.. Gout often involving caused chronic renal interstitial
nephritis and uric acid kidney stones. Gout Gout is divided into primary and secondary gout
two categories. Apart from a few primary gout due to genetic causes of certain defects in
the body, mostly unknown etiology, and accompanied obesity, hyperlipidemia, hypertension,
coronary heart disease, arteriosclerosis, diabetes and hyperthyroidism, and so on.
Secondary gout is secondary to white blood, lymphoma, multiple myeloma, hemolytic anemia,
polycythemia vera disease, cancer, chronic renal insufficiency, certain congenital
metabolic disorders such as type I glycogen accumulation of such. Certain drugs such as
furosemide, ethambutol, salicylic acid category (A Division District Forest, aminosalicylic
acid) and nicotinic acid, etc., can cause secondary pain. In addition, alcohol abuse, lead
poisoning, beryllium poisoning and acid poisoning also can be complicated by secondary
gout. Clinical work habits of the "primary" omitted, we usually refer to the "gout"
generally refers to the primary and gout.
disease. The main clinical features are produced in excessive uric acid excretion of uric
acid kidney or decrease, caused elevated blood uric acid formed hyperuricemia and the
repeated attacks of acute gouty arthritis, gout stone deposition, gouty arthritis and
chronic joint deformities, etc.. Gout often involving caused chronic renal interstitial
nephritis and uric acid kidney stones. Gout Gout is divided into primary and secondary gout
two categories. Apart from a few primary gout due to genetic causes of certain defects in
the body, mostly unknown etiology, and accompanied obesity, hyperlipidemia, hypertension,
coronary heart disease, arteriosclerosis, diabetes and hyperthyroidism, and so on.
Secondary gout is secondary to white blood, lymphoma, multiple myeloma, hemolytic anemia,
polycythemia vera disease, cancer, chronic renal insufficiency, certain congenital
metabolic disorders such as type I glycogen accumulation of such. Certain drugs such as
furosemide, ethambutol, salicylic acid category (A Division District Forest, aminosalicylic
acid) and nicotinic acid, etc., can cause secondary pain. In addition, alcohol abuse, lead
poisoning, beryllium poisoning and acid poisoning also can be complicated by secondary
gout. Clinical work habits of the "primary" omitted, we usually refer to the "gout"
generally refers to the primary and gout.
A gouty arthritis performance?
The first attack typical of gouty arthritis for more than single-arthritis, as the first
metatarsophalangeal joint and toe for the common, followed by the ankle, knee, elbow,
wrist, hand and foot other joints. Many acute phase of intense, often in the evening
sudden, the pain and can not sleep through the night and wake up. Recurrent disease may
develop more arthritis, or migratory arthritis. Joint involvement red, swelling, heat,
pain, activity limitation, the joint involvement often exudate. Can be accompanied by
fever, chills, fatigue, anorexia, headache, and other symptoms. Symptoms generally last for
1-2 weeks mitigation. Local reddish brown skin irritation to gradually return to normal.
Sometimes, there will be scaling and itching. Uric acid in the chronic stage of intra-
articular sodium calm gradually increased gradually frequent attack, intermittent
shortened, increased involvement joints, pain exacerbated, inflammation can not completely
dissipated, there tophi, tophi to see more joints and kidneys, the helix external ear,
metatarsophalangeal, interphalangeal and metacarpophalangeal joints and other places, will
be there tophi, with the constant wind sedimentary stone increased, leading to joint mast,
deformity, rigid and limited activities.
metatarsophalangeal joint and toe for the common, followed by the ankle, knee, elbow,
wrist, hand and foot other joints. Many acute phase of intense, often in the evening
sudden, the pain and can not sleep through the night and wake up. Recurrent disease may
develop more arthritis, or migratory arthritis. Joint involvement red, swelling, heat,
pain, activity limitation, the joint involvement often exudate. Can be accompanied by
fever, chills, fatigue, anorexia, headache, and other symptoms. Symptoms generally last for
1-2 weeks mitigation. Local reddish brown skin irritation to gradually return to normal.
Sometimes, there will be scaling and itching. Uric acid in the chronic stage of intra-
articular sodium calm gradually increased gradually frequent attack, intermittent
shortened, increased involvement joints, pain exacerbated, inflammation can not completely
dissipated, there tophi, tophi to see more joints and kidneys, the helix external ear,
metatarsophalangeal, interphalangeal and metacarpophalangeal joints and other places, will
be there tophi, with the constant wind sedimentary stone increased, leading to joint mast,
deformity, rigid and limited activities.
Tophi with chronic gout arthritis
Stone suffering from gout arthritis and chronic gout patients more chronic in vivo
crystallization of uric acid deposition will be in the cartilage and synovial membrane, and
soft tissue, the formation of tophi, and the blood uric acid concentrations higher, the
sick, the longer the period, it may be deposition of the more tophi, and sometimes will
affect vascular with the kidney, causing serious renal failure, nephrotic more serious and
difficult to create a vicious cycle of uric acid excretion, tophi sedimentary the more.
Often the site of deposition tophi many, including the ears, hands, elbow, Achilles tendon,
ankle or toe, and sometimes even lead to partial ulcer and difficult healing, or even to
accept the latest addition to surgery. Serious patients and cause deformation or chronic
joint symptoms, severe deformation of the foot may cause the patient wears shoes when the
serious problem. Moreover, the risk of kidney stones occur with increased serum uric acid
concentrations increase, and they often cause nephropathy, renal failure may need to
receive hemodialysis, this is cause gout patients died one of the main causes of death.
crystallization of uric acid deposition will be in the cartilage and synovial membrane, and
soft tissue, the formation of tophi, and the blood uric acid concentrations higher, the
sick, the longer the period, it may be deposition of the more tophi, and sometimes will
affect vascular with the kidney, causing serious renal failure, nephrotic more serious and
difficult to create a vicious cycle of uric acid excretion, tophi sedimentary the more.
Often the site of deposition tophi many, including the ears, hands, elbow, Achilles tendon,
ankle or toe, and sometimes even lead to partial ulcer and difficult healing, or even to
accept the latest addition to surgery. Serious patients and cause deformation or chronic
joint symptoms, severe deformation of the foot may cause the patient wears shoes when the
serious problem. Moreover, the risk of kidney stones occur with increased serum uric acid
concentrations increase, and they often cause nephropathy, renal failure may need to
receive hemodialysis, this is cause gout patients died one of the main causes of death.
Gouty arthritis and gout What is the relationship between
Gout is pretty metabolic disorder and reduce the excretion of uric acid caused by a group
of diseases. Clinical performance: asymptomatic hyperuricemia, gout arthritis stone,
urinary stone disease and renal parenchyma. Gouty arthritis when uric acid salt in the articular cartilage or synovial deposition,
leading to surrounding tissue and articular synovial inflammation reaction. Hyperuricemia Gout is the most important biochemical basis, but is not synonymous with
gout. As living standards improve, changes in the structure of diet, and many affect uric
acid excretion drugs (diuretics) use, are now actually hyperuricemia in the incidence of
adult male is 5% -7%, the researchers statistics about 5% -12% of the high blood uric acid
patients eventually develop gout. When the blood uric acid level over 420 micro-Mount /
liter, arthritis and gout in uric acid kidney stones, or the danger of a significant
increase
of diseases. Clinical performance: asymptomatic hyperuricemia, gout arthritis stone,
urinary stone disease and renal parenchyma. Gouty arthritis when uric acid salt in the articular cartilage or synovial deposition,
leading to surrounding tissue and articular synovial inflammation reaction. Hyperuricemia Gout is the most important biochemical basis, but is not synonymous with
gout. As living standards improve, changes in the structure of diet, and many affect uric
acid excretion drugs (diuretics) use, are now actually hyperuricemia in the incidence of
adult male is 5% -7%, the researchers statistics about 5% -12% of the high blood uric acid
patients eventually develop gout. When the blood uric acid level over 420 micro-Mount /
liter, arthritis and gout in uric acid kidney stones, or the danger of a significant
increase
The coexistence of hypertension and hyperlipidemia how do the
The occurrence of hypertension and hyperlipidemia and development are closely related.
Numerous studies show that many patients with hypertension associated with lipid metabolism
disorders, blood cholesterol and triglyceride levels were significantly higher than normal,
while high-density lipoprotein cholesterol levels were lower. On the other hand, many of
hyperlipidemia also often associated with hypertension, a causal relationship between the
two, but what the reasons for the fruit, is not very clear. Hypertension and hyperlipidemia
are important risk factors for coronary heart disease, the two co-exist, the incidence of
coronary heart disease than a higher, therefore, the two co-exist, should actively
treatment.
Well, the coexistence of hypertension and hyperlipidemia, how do?
(1) In order to enhance living and diet management, control calorie intake, and
appropriately increase activity levels. Eating too many calories, the excess calories in
the form of fat stored in the body and blood lipid and blood pressure to rise, therefore,
should be to limit fat main staple food every day 200 to 250 grams, do not eat sweets, can
be appropriate to eat fish, soybean products, poultry, vegetables, etc., but not too many
meals, not overeating, dinner to eat less. Eat rich in calcium, potassium foods, such as
bananas, Laver, kelp, potato, mushroom, and other soybean products and to promote the
excretion of sodium in vivo, cells adjust the ratio of sodium and calcium, reducing
vascular tension and maintain normal systolic and diastolic arterial responses to the
protection of the heart.
Moderate exercise can effectively increase endogenous pyrogen quality, increase body
heat, accelerating body fat, sugar and protein decomposition, to scour the vascular wall
sediment, and can accelerate the decomposition of lipids, thereby preventing hypertension,
hyperlipidemia, retard the aging organs, therefore, training should persist, but the
elderly should be walking, jogging, mainly lot of shadow boxing, not strenuous exercise.
(2) patients should be adequate. According to reports, some academics found that the
salt-sensitive hypertension and some who have salt-sensitive sodium pump gene mutation,
which was dominant genetic mutation, which reveals the world studied more than 100 years of
on many areas hypertension, and some people more incidence of the answers is not,
therefore, salt sensitivity in patients with hypertension, reduce salt is very important,
not salt-sensitive hypertensive patients, excessive salt can be affected by sugar and fat
metabolism, master general of the daily salt in 5g following, the two do not have a
significant effect on induced.
(3) on tobacco and alcohol are hypertension and hyperlipidemia promoting factors, the
patient should be categorically quit smoking for good wine to drink.
(4) the use of antihypertensive agents, it is necessary to consider the impact on lipid
metabolism. Clinical research shows that some antihypertensive drugs on lipid metabolism
may produce adverse effects and thus become a catalyst for atherosclerosis, such as
diuretic antihypertensive agents, beta-blockers have that role. Angiotensin-converting
enzyme inhibitors, calcium antagonists on lipid metabolism have influenced it. The
coexistence of hypertension and hyperlipidemia patients, which were the best drug is of
Doxazosin, urapidil took a1-blockers, they can buck, and it helps lipid metabolism.
(5) the buck in treating hyperlipidemia showed no sign of improvement, but there
coronary heart disease risk factors, should Application Compatibility anti-hyperlipidemia
drugs.
Numerous studies show that many patients with hypertension associated with lipid metabolism
disorders, blood cholesterol and triglyceride levels were significantly higher than normal,
while high-density lipoprotein cholesterol levels were lower. On the other hand, many of
hyperlipidemia also often associated with hypertension, a causal relationship between the
two, but what the reasons for the fruit, is not very clear. Hypertension and hyperlipidemia
are important risk factors for coronary heart disease, the two co-exist, the incidence of
coronary heart disease than a higher, therefore, the two co-exist, should actively
treatment.
Well, the coexistence of hypertension and hyperlipidemia, how do?
(1) In order to enhance living and diet management, control calorie intake, and
appropriately increase activity levels. Eating too many calories, the excess calories in
the form of fat stored in the body and blood lipid and blood pressure to rise, therefore,
should be to limit fat main staple food every day 200 to 250 grams, do not eat sweets, can
be appropriate to eat fish, soybean products, poultry, vegetables, etc., but not too many
meals, not overeating, dinner to eat less. Eat rich in calcium, potassium foods, such as
bananas, Laver, kelp, potato, mushroom, and other soybean products and to promote the
excretion of sodium in vivo, cells adjust the ratio of sodium and calcium, reducing
vascular tension and maintain normal systolic and diastolic arterial responses to the
protection of the heart.
Moderate exercise can effectively increase endogenous pyrogen quality, increase body
heat, accelerating body fat, sugar and protein decomposition, to scour the vascular wall
sediment, and can accelerate the decomposition of lipids, thereby preventing hypertension,
hyperlipidemia, retard the aging organs, therefore, training should persist, but the
elderly should be walking, jogging, mainly lot of shadow boxing, not strenuous exercise.
(2) patients should be adequate. According to reports, some academics found that the
salt-sensitive hypertension and some who have salt-sensitive sodium pump gene mutation,
which was dominant genetic mutation, which reveals the world studied more than 100 years of
on many areas hypertension, and some people more incidence of the answers is not,
therefore, salt sensitivity in patients with hypertension, reduce salt is very important,
not salt-sensitive hypertensive patients, excessive salt can be affected by sugar and fat
metabolism, master general of the daily salt in 5g following, the two do not have a
significant effect on induced.
(3) on tobacco and alcohol are hypertension and hyperlipidemia promoting factors, the
patient should be categorically quit smoking for good wine to drink.
(4) the use of antihypertensive agents, it is necessary to consider the impact on lipid
metabolism. Clinical research shows that some antihypertensive drugs on lipid metabolism
may produce adverse effects and thus become a catalyst for atherosclerosis, such as
diuretic antihypertensive agents, beta-blockers have that role. Angiotensin-converting
enzyme inhibitors, calcium antagonists on lipid metabolism have influenced it. The
coexistence of hypertension and hyperlipidemia patients, which were the best drug is of
Doxazosin, urapidil took a1-blockers, they can buck, and it helps lipid metabolism.
(5) the buck in treating hyperlipidemia showed no sign of improvement, but there
coronary heart disease risk factors, should Application Compatibility anti-hyperlipidemia
drugs.
Nephrotic syndrome and the relationship between hyperlipidemia
Patients with nephrotic syndrome in hyperlipidemia mechanism are still not clear. Often
patients with nephrotic syndrome resulting from the large number of urine protein plasma
protein decreased, hypoproteinemia may be compensatory to make the protein, in particular
lipoprotein such as very low density lipoprotein (VLDL) accelerated the synthesis, which
can be converted into low-density lipoprotein (LDL), thereby increasing LDL, it can be that
is the reasons for the formation of hyperlipidemia.
Therefore, the majority of patients with nephrotic syndrome increased plasma lipid, or even
a fasting plasma can emulsion. Although a variety of blood lipids can be increased, but the
largest increase in the neutral fat, cholesterol and triglycerides are increased, the
extent of its decline and plasma albumin was negatively correlated. Early blood cholesterol
greater than 7.15 cents mole / liter, serious increased to 25.86 cents mole / liter or so,
the proportion of cholesterol and phospholipids average increase to 1.28 (average normal
value of 0.95). Patients with yellow skin can be a tumor.
Nephrotic syndrome hyperlipidemia continued for too long, there may be atherosclerosis,
thrombosis and embolism. Researchers have observed that patients with chronic renal
insufficiency triglyceride synthesis of normal lipoprotein lipase activity decreased
triglyceride decomposition obstacles at the same time, because of chronic renal
insufficiency in patients with increased serum triglyceride levels, the incidence of
vascular lesions increased, therefore we have to seriously treating hyperlipidemia.
However, these patients with hyperlipidemia response to poor diet therapy should be used in
combination with the bile acid resins and nicotinic acid lipid-lowering treatment.
patients with nephrotic syndrome resulting from the large number of urine protein plasma
protein decreased, hypoproteinemia may be compensatory to make the protein, in particular
lipoprotein such as very low density lipoprotein (VLDL) accelerated the synthesis, which
can be converted into low-density lipoprotein (LDL), thereby increasing LDL, it can be that
is the reasons for the formation of hyperlipidemia.
Therefore, the majority of patients with nephrotic syndrome increased plasma lipid, or even
a fasting plasma can emulsion. Although a variety of blood lipids can be increased, but the
largest increase in the neutral fat, cholesterol and triglycerides are increased, the
extent of its decline and plasma albumin was negatively correlated. Early blood cholesterol
greater than 7.15 cents mole / liter, serious increased to 25.86 cents mole / liter or so,
the proportion of cholesterol and phospholipids average increase to 1.28 (average normal
value of 0.95). Patients with yellow skin can be a tumor.
Nephrotic syndrome hyperlipidemia continued for too long, there may be atherosclerosis,
thrombosis and embolism. Researchers have observed that patients with chronic renal
insufficiency triglyceride synthesis of normal lipoprotein lipase activity decreased
triglyceride decomposition obstacles at the same time, because of chronic renal
insufficiency in patients with increased serum triglyceride levels, the incidence of
vascular lesions increased, therefore we have to seriously treating hyperlipidemia.
However, these patients with hyperlipidemia response to poor diet therapy should be used in
combination with the bile acid resins and nicotinic acid lipid-lowering treatment.
Acute abdominal - hyperlipidemia syndrome
[Outlined]
Acute abdominal - high fat blood syndrome (Acute Abdomen - Hyperlipemia Syndrome),
also known as familial high blood group type I lipoprotein, high chylous particulate
familial hyperlipidemia, familial hyperlipidemia primary, hepatosplenomegaly of lipid
deposition disease, hypercholesterolemia Huang lipomatosis, idiopathic of lipid deposition,
Hypercholesterolemia Huang lipomatosis, idiopathic lipid deposition disease and acute
abdomen - hyperlipidemia syndrome. In 1932, Burger and Grutz first two reports, it is also
called Burger-Grutz syndrome. For familial autosomal recessive genetic disease. Clinical
rare.
[Diagnosis]
According to clinical manifestations in after-induced fat intake on the abdominal
pain, pancreatitis, and other symptoms and signs such as skin of yellow light can be
carried out with hyperlipidemia diagnosis.
[Treatment]
The main treatment for the low-fat diet. Request control fat intake in calories only
the 20% to 25%. The medium chain fatty acid compounds alternative glycerol ordinary fat.
When suffering from acute pancreatitis for the corresponding treatment.
【Pathological changes:
Visibility on the pathology of the skin yellow, rich in reticular cells (such as bone
marrow, liver, spleen) Visibility foam cells, inflammation of the pancreas have
pathological changes.
Clinical manifestations】 【
Chang began in early childhood morbidity. Gender may be suffering from. When fat
intake can be induced, expressed as upper abdominal discomfort, anorexia, abdominal pain,
no more nausea and vomiting. Febrile seizures can be accompanied by abdominal pain,
abdominal tenderness, pancreatitis and peritoneal irritation sign, hepatosplenomegaly,
spleen area have no tenderness. About 30% of the patients in the health ministries
(including the mucosa) of visible yellow, or on the basis of erythema in a yellow nodules.
After the attack of yellow faded in the last few weeks, or even disappear altogether.
【Auxiliary inspection --
Patients with static at 4 ° C in the upper deck were white environment for the type I
Hyperlipoproteinemia. Lipoprotein analysis showed that: very low density lipoprotein
(VLDL), low-density lipoprotein (LDL), high-density lipoprotein (HDL) normal or reduced.
Increased cholesterol, triglyceride increase. When increased leukocyte attack, liver
function and normal glucose tolerance test.
【Prognosis:
The prognosis of the disease with other types of hyperlipidemia, the difficulty seems
to be complicated by atherosclerosis. Danger is recurrent pancreatitis.
Acute abdominal - high fat blood syndrome (Acute Abdomen - Hyperlipemia Syndrome),
also known as familial high blood group type I lipoprotein, high chylous particulate
familial hyperlipidemia, familial hyperlipidemia primary, hepatosplenomegaly of lipid
deposition disease, hypercholesterolemia Huang lipomatosis, idiopathic of lipid deposition,
Hypercholesterolemia Huang lipomatosis, idiopathic lipid deposition disease and acute
abdomen - hyperlipidemia syndrome. In 1932, Burger and Grutz first two reports, it is also
called Burger-Grutz syndrome. For familial autosomal recessive genetic disease. Clinical
rare.
[Diagnosis]
According to clinical manifestations in after-induced fat intake on the abdominal
pain, pancreatitis, and other symptoms and signs such as skin of yellow light can be
carried out with hyperlipidemia diagnosis.
[Treatment]
The main treatment for the low-fat diet. Request control fat intake in calories only
the 20% to 25%. The medium chain fatty acid compounds alternative glycerol ordinary fat.
When suffering from acute pancreatitis for the corresponding treatment.
【Pathological changes:
Visibility on the pathology of the skin yellow, rich in reticular cells (such as bone
marrow, liver, spleen) Visibility foam cells, inflammation of the pancreas have
pathological changes.
Clinical manifestations】 【
Chang began in early childhood morbidity. Gender may be suffering from. When fat
intake can be induced, expressed as upper abdominal discomfort, anorexia, abdominal pain,
no more nausea and vomiting. Febrile seizures can be accompanied by abdominal pain,
abdominal tenderness, pancreatitis and peritoneal irritation sign, hepatosplenomegaly,
spleen area have no tenderness. About 30% of the patients in the health ministries
(including the mucosa) of visible yellow, or on the basis of erythema in a yellow nodules.
After the attack of yellow faded in the last few weeks, or even disappear altogether.
【Auxiliary inspection --
Patients with static at 4 ° C in the upper deck were white environment for the type I
Hyperlipoproteinemia. Lipoprotein analysis showed that: very low density lipoprotein
(VLDL), low-density lipoprotein (LDL), high-density lipoprotein (HDL) normal or reduced.
Increased cholesterol, triglyceride increase. When increased leukocyte attack, liver
function and normal glucose tolerance test.
【Prognosis:
The prognosis of the disease with other types of hyperlipidemia, the difficulty seems
to be complicated by atherosclerosis. Danger is recurrent pancreatitis.
Hyperlipidemia which endanger the patient?
(1) glomerulosclerosis, etc.: hyperlipidemia can cause vascular endothelial cell injury and
kitchen-off, resulting in increased vascular wall permeability, plasma lipoprotein was able
to get into the vessel wall and endometrial deposition was caused macrophage response and
the removal of vascular smooth muscle cell proliferation and form plaque, and I. caused by
arteriosclerosis, renal atherosclerosis, luminal stenosis can occur renal ischemia,
atrophy, interstitial fiber hyperplasia. If renal vascular occlusion is the corresponding
region infarction, infarction after formation of scar. This led glomerulosclerosis. In the
kidney, may accelerate the occurrence of coronary sclerosis, resulting in patients with
coronary heart disease and increase the risk of myocardial infarction. Similarly, while
other parts of arteriosclerosis caused by the corresponding diseases such as cerebral
arteriosclerosis, cerebral infarction, and so on.
(2) glomerular injury: hyperlipidemia may cause lipid deposition in the glomeruli, low-
density lipoprotein cycle can be activated monocytes and lead glomeruli infiltrating
mononuclear cells, and caused or exacerbated inflammatory response, while the glomerular
mesangial cells, endothelial cell activation can produce molecular oxygen, the promotion of
lipid peroxidation, oxidation of low-density lipoprotein (OX-LDL) are extremely cytotoxic
effects, leading to kidney damage. In addition, hyperlipidemia can arouse mesangial matrix
collagen, laminin and fibrin increase, and these components are directly related
glomerulosclerosis.
kitchen-off, resulting in increased vascular wall permeability, plasma lipoprotein was able
to get into the vessel wall and endometrial deposition was caused macrophage response and
the removal of vascular smooth muscle cell proliferation and form plaque, and I. caused by
arteriosclerosis, renal atherosclerosis, luminal stenosis can occur renal ischemia,
atrophy, interstitial fiber hyperplasia. If renal vascular occlusion is the corresponding
region infarction, infarction after formation of scar. This led glomerulosclerosis. In the
kidney, may accelerate the occurrence of coronary sclerosis, resulting in patients with
coronary heart disease and increase the risk of myocardial infarction. Similarly, while
other parts of arteriosclerosis caused by the corresponding diseases such as cerebral
arteriosclerosis, cerebral infarction, and so on.
(2) glomerular injury: hyperlipidemia may cause lipid deposition in the glomeruli, low-
density lipoprotein cycle can be activated monocytes and lead glomeruli infiltrating
mononuclear cells, and caused or exacerbated inflammatory response, while the glomerular
mesangial cells, endothelial cell activation can produce molecular oxygen, the promotion of
lipid peroxidation, oxidation of low-density lipoprotein (OX-LDL) are extremely cytotoxic
effects, leading to kidney damage. In addition, hyperlipidemia can arouse mesangial matrix
collagen, laminin and fibrin increase, and these components are directly related
glomerulosclerosis.
Hyperlipoproteinemia How did it happen?
Hyperlipoproteinemia according to the reasons for the onset usually divided into two
categories, namely primary and secondary Hyperlipoproteinemia of Hyperlipoproteinemia.
Primary Hyperlipoproteinemia also known as familial Hyperlipoproteinemia, mostly congenital
genetic disease, there are family history is the result of lipid and lipoprotein metabolism
congenital defects and certain environmental factors (such as diet, nutrition and drugs,
etc.), by unknown mechanisms arising. All five types of Hyperlipoproteinemia can for the
family, and may represent many different changes. In recent years, I think familial type
Hyperlipoproteinemia the cell surface in low density lipoprotein (LAL) receptor decreased
(found in different types of) or absent (seen at the same type of homozygous), and LDL can
not enter the cells with a normal rate and metabolism within the incidence.
Secondary Hyperlipoproteinemia incidence of the disease in some kind of pathology on the
basis of certain drugs or caused by the abnormal lipid metabolism, and clinical
manifestations of the characteristics of the primary disease or useful special drug
history, and with increased blood lipids. Failing to control diabetes, hypothyroidism and
myxedema, nephrotic syndrome, both inside and outside the liver bile duct obstruction,
pancreatitis, abnormal hypergammaglobulinemia, gout, alcoholism and use of contraceptives
and other women.
categories, namely primary and secondary Hyperlipoproteinemia of Hyperlipoproteinemia.
Primary Hyperlipoproteinemia also known as familial Hyperlipoproteinemia, mostly congenital
genetic disease, there are family history is the result of lipid and lipoprotein metabolism
congenital defects and certain environmental factors (such as diet, nutrition and drugs,
etc.), by unknown mechanisms arising. All five types of Hyperlipoproteinemia can for the
family, and may represent many different changes. In recent years, I think familial type
Hyperlipoproteinemia the cell surface in low density lipoprotein (LAL) receptor decreased
(found in different types of) or absent (seen at the same type of homozygous), and LDL can
not enter the cells with a normal rate and metabolism within the incidence.
Secondary Hyperlipoproteinemia incidence of the disease in some kind of pathology on the
basis of certain drugs or caused by the abnormal lipid metabolism, and clinical
manifestations of the characteristics of the primary disease or useful special drug
history, and with increased blood lipids. Failing to control diabetes, hypothyroidism and
myxedema, nephrotic syndrome, both inside and outside the liver bile duct obstruction,
pancreatitis, abnormal hypergammaglobulinemia, gout, alcoholism and use of contraceptives
and other women.
Wednesday, November 7, 2007
A summary of interstitial nephritis and classification
A tubular interstitial nephritis is a group of various reasons caused by the kidney disease. Major violations of tubular lesions and renal interstitial; clinical renal tubular dysfunction to its outstanding performance. According to the course, a tubular interstitial nephritis acute and chronic can be divided into two categories; there by infectious etiology, drugs, and genetic immune-mediated metabolism caused by obstacles such as interstitial nephritis. Clinical those caused by drugs for the most common, followed by urinary tract obstruction with the complexity of those caused chronic pyelonephritis. Its main diagnosis is based on: (1) patients with history of drug use or a history of chronic pyelonephritis. (2) In early disease glomerular diseases generally not the clinical features, such as, edema, hypertension, etc, and renal tubular dysfunction occurred in the earlier and glomerular dysfunction and disproportionate. In addition, renal dysfunction without hypertension, and the increase in mild proteinuria. Given the more than 90 percent of tubular interstitial nephritis one belonging to cure the cause, early diagnosis is crucial, even if the occurrence of renal dysfunction has been the patient, if discovered and promptly handle reversible factors (such as urinary obstruction, infection, etc.), can also suspend its development, and even improve kidney functional.
Drugs easily lead to the drug-induced liver disease?
Can cause liver damage in varying degrees of drugs, at least in 200 more, which in the central nervous medication (such as chlorpromazine, promethazine, halothane), chemotherapy drugs, sulfa drugs, isoniazid, rifampin, sodium ammonia Yang, antibiotics (tetracycline, erythromycin, bamboo Peach adriamycin , newborn Adriamycin), antipyretic analgesics (paracetamol, salicylic acid category, Bao, indomethacin, etc.), anti-cancer drugs (methotrexate, 6 - mercaptopurine), testicular ketones oral contraceptives, double vinegar small and methyl phenol Pakistan as the more common. Others such as hypoglycemic agents, anti-thyroid drugs, lipid-lowering drugs (clofibrate, blood-ling, aspartic acid amine enzyme), as well as some traditional Chinese medicine such as Cangerzi, xanthate son, Tong Tribulus terrestris, also can cause liver damage. According to statistics, cases of drug-induced liver damage, or about all drug reaction cases 10 percent to 15 percent, second only to the incidence of skin and mucosal damage drugs heat.
Drug-induced hepatitis clinical manifestations and prognosis
Clinical manifestations】 【 The clinical manifestations of liver medicine one drug with the type of liver damage caused liver disease and the different mechanism. According to clinical features of acute and chronic can be divided into two categories. Acute liver cell damage, acute hepatitis most common drugs, mainly to liver cell necrosis, the clinical manifestations of acute viral hepatitis resembles often fever, fatigue, lack of appetite, jaundice and elevated serum transaminase (normal 2 to 30 times), and albumin ALP affected smaller, hyperbilirubinemia and prothrombin time with the Director of the severity of liver damage associated. Less severe diseases, will be restored after stopping short-term (a few weeks to several months), who re-occurrence of liver failure, a progressive jaundice, bleeding tendencies and hepatic encephalopathy, and often death. Consisting mainly of acute allergic reaction to medicine liver, often fever, rash, jaundice, swollen lymph nodes, with serum aminotransferase, bilirubin and ALP moderately higher drug exposure history often shorter (four weeks within). To cholestasis based medicine liver, the clinical and laboratory manifestations and intrahepatic cholestasis, extrahepatic biliary obstruction, acute cholangitis similar, fever, jaundice, abdominal pain, itching, right upper quadrant tenderness and hepatomegaly with elevated serum transaminase more degrees, the ALP increased significantly (2 to 10 times) in light of bilirubin increased significantly (34 ~ 500 μ mol / L), bile salt, lipoprotein X, GGT and cholesterol increased, and anti-mitochondrial antibody negative. In general to stop after 3 months to 3 years resume, a few disappear with a chronic bile duct progress of the process. Occasionally the bile duct damage is not irreversible, progress liver cirrhosis. Drug-induced autoimmune chronic hepatitis and chronic hepatitis clinical manifestations similar to the light can be asymptomatic, and the re-occurrence of hepatic encephalopathy associated with liver failure. Biochemical same performance and chronic viral hepatitis, serum transaminase, G-GT increased, leading to cirrhosis of progress with hypoproteinemia and coagulation dysfunction. 【Prognosis: The vast majority of patients resume after the withdrawal, in clinical and histological improvement, only a few weeks faster, the slow take years. A small number of serious and extensive liver damage caused fulminant hepatic failure, or progress to cirrhosis, a liver transplant if they do not, death will occur.
Complications of alcoholic liver disease treatment
1, upper gastrointestinal bleeding: persons with chronic alcohol upper gastrointestinal bleeding, perhaps because of acute gastric erosion, canker or esophageal variceal bleeding (EVB), is subject to the bleeding site of the treatment decision. Ice water and a small amount of norepinephrine or other bleeding gastric lavage of the erosion caused by gastric bleeding may be effective. As for portal hypertension caused portal hypertensive gastropathy bleeding can be a good set, he Shi Ning effective. Sandostatin in the usage: 0.1 mg slow intravenous injection, then 3 mg intravenous continuous infusion for at least 48 hours, bleeding ulcer disease or ranitidine available treatment Losec. EVB treatment, the balloon is now available three cavity of oppression, plus a good set or he Shi Ning treatment, and applying Ibid. To better when hemostasis longer an option hardening agent therapy or ligation varicose vein therapy (EVL). AH (alcoholic hepatitis) portal hypertension caused by the treatment of portal pressure can return to normal, varicose veins can also disappear. 2, ascites: AH and AC (alcoholic cirrhosis) and ascites to improve liver function as the main treatment, when the portal pressure to normal, serum albumin levels increased, that is, to increase urine output. Sodium intake should be restricted, the use of diuretics is necessary to be careful because AH, AC patients often associated with hypokalemia, low magnesium, low calcium, hypophosphatemia. Should be banned single major role in proximal tubular chlorine Thiazide. Not because of the distal tubular aldosterone antagonist role, it not only with aldosteronism on the lack of diuretic effect in patients with liver cirrhosis, Japan _ will aggravate potassium, magnesium loss, evoked hypokalemic alkalosis and hepatic coma, it should be combined, such as spironolactone (50-100 mg) and the double urine Cypriot grams of hydrogen (50-100 mg / d) combined. Treatment should pay attention to during the regular reexamination blood and urine electrolyte, ECG and blood gas analysis to prevent the occurrence of high-K school. 3, hepatic coma patients such as AC and AH in hepatic encephalopathy should be induced to examine their reasons, such as gastrointestinal bleeding, electrolyte and acid-base disorders, secondary infection, preventive use glutamate as sodium, potassium misconduct, such as excessive protein intake. Its causes are sometimes complicated. Gastrointestinal bleeding and infection should be controlled, electrolyte and acid-base disorders should be promptly corrected. At the same time advised to reduce intestinal bacterial type of amino acid and urea decomposition. 4, infections due AH, AC patients with poor nutritional status, low immunity, as well as activities of daily living and health conditions affected by factors such as poor, vulnerable patients infected, especially lung infection and spontaneous bacterial peritonitis. The incidence of pneumonia in 3-4 times higher than that of the crowd, and an important cause of death for one, it should be in control of their attention. At the same time spontaneous bacterial peritonitis attention to the early diagnosis. In addition to conventional indicators, the current emphasis on ascites PH multinucleated cells and neutrophils (PMN) absolute count. Two of the three should consider the possible positive with spontaneous bacterial peritonitis, and appropriate timely treatment. 5, electrolyte and acid-base balance disorders due to less intake, excretion, gastrointestinal and renal tubular absorption due to bad acid-base disorders, as well as ethanol, AC, AH patients, electrolyte and acid-base often arise disorder, with hypokalemia, low magnesium, low calcium, hypophosphatemia and various acid-base balance. Its produce ethanol metabolism and the mechanism of lactic acid and other metabolic produce complications, such as anemia, muscle-ache, rhabdomyolysis, alcohol syndrome, hepatic coma, and so on. Low potassium, low magnesium, low calcium, phosphorus accompanied with the existence of clinical manifestations spasm, tremor, look difficult to distinguish the symptoms, ECG there is a lack of specific performance monitoring required blood and urine electrolyte. Metabolism produce ethanol, lactic acidosis, ketosis can lead AG (anion gap) metabolic acidosis, respiratory inhibition of ethanol excessive anesthesia can cause respiratory acidosis, excessive alcohol syndrome can be caused by breathing respiratory alkalosis, can be severe vomiting induced by low chlorine, hypokalemic metabolic alkalosis, latter-induced hepatic encephalopathy. If the merger of serious infections and improper medical treatment, the more complicated, you need to attach importance to monitoring electrolytes, blood gas analysis, ECG and check whether the proper treatment, combined with clinical timely adjust treatment.
Alcoholic fatty liver clinical performance
First, symptoms Fatty liver more asymptomatic mild, moderate and severe fatty liver in chronic hepatitis may show similar performance, such as systemic mild discomfort, burnout, easy fatigue, abdominal discomfort, nausea and vomiting, loss of appetite, abdominal distension, etc., a few patients have fever, diarrhea, limb numbness, sexual function diminish, such as male impotence. Second, signs Most good nutritional status, have obesity, and some patients have hepatomegaly, spleen little more. AFL (alcoholic fatty liver) patients with severe rarely cholestasis. ALD the United States a large-scale collaborative research shows that only 19% of patients with organized AFL performance of cholestasis, and the incidence of jaundice is as high as 31 percent, and the histological AFL cholestasis and whether there has been unrelated to liver cirrhosis. Sino-Japanese Friendship Hospital 15 cases of fatigue, abdominal distension, liver District pain each 67 percent; limbs, numbness, sexual dysfunction each 47 percent; impotence accounted for 40 percent hepatomegaly three cases Station 20%, of which one case of moderate liver fatty liver large 4 cm, the other one case of severe fatty liver big 9 cm. Third, laboratory examinations Laboratory examination of liver function abnormalities, depending on the degree of fatty invasion, the scope may be. The mild fatty liver can no significant laboratory abnormalities, severe fatty liver, there will be the ALT, AST and GGT, blood red bile quality (BiL), and triglyceride (TG) of mild to moderate increase. In the absence of alcohol in patients with TG increased significantly.
Cirrhosis of portal hypertension caused any harm?
Portal hypertension that is portal pressure increased. Portal is the liver of a larger population of vein from the superior mesenteric vein and splenic vein convergence from the hepatic portal divided into two into the human liver. The liver's blood 75 percent from the portal vein, 25 per cent from the hepatic artery. Primarily responsible for collecting the esophagus, stomach, intestine, pancreas, gallbladder and spleen of venous blood. Under normal circumstances, portal pressure 0.7-1.5 kPa, and more than 2.0 kPa that have clinical significance. Percutaneous puncture spleen measured the pressure within the spleen can often representative of portal pressure. When liver cirrhosis or liver, portal blood flow is obstructed, may enable portal hypertension, and, congenital dysplasia, malformation or tumor suppression, and other portal pressure also increased. Hepatic Lobules these lesions may cause substantial harm, such as liver cell degeneration and necrosis, capillary network damage, followed by liver nodules and connective tissue, fibrous tissue hyperplasia. So long it will intrahepatic vascular deformation, obstruction, disruption flow deposition. When severe hepatic venous outflow obstruction, liver cells ischemia and hypoxia, increased liver cell necrosis. Intrahepatic resistance to the increase. Under such circumstances, portacaval only to increase their systolic pressure by setting enlarged blood vessels to compensate. As time goes by the formation of portal hypertension. Long-term portal hypertension caused a series of complications, such as a congestive splenomegaly, gastrointestinal, and peritoneal chronic congestive establish collateral circulation, said portal hypertension. Portal hypertension will lead to esophageal varices, abdominal and rectal varices. When the esophageal varices and reach a certain level, in the role of external factors, could break down, cause upper gastrointestinal bleeding. Performance for the large number of hematemesis or tar-like stool; rectal bleeding caused when a large number hematochezia. Portal hypertension be enlarged spleen, abdominal distension, lack of appetite, abdominal multiple organ congestion, hypersplenism. Splenomegaly and hypersplenism to RBC, WBC and platelet destruction increased, from whole blood like anemia and decreased immune function low body resistance decreased. Portal hypertension is formed ascites, peritonitis, sepsis direct factor. The appearance of ascites, and often could easily lead to insufficient effective circulating blood volume, blood pressure drop, electrolyte imbalance, involving heart, brain, kidney and other organ functions. These serious complications, at any time endangering the lives of patients.
Why patients with liver cirrhosis often gastrointestinal discomfort?
In patients with liver cirrhosis gastrointestinal discomfort common symptoms are: anorexia, sometimes with nausea and vomiting, leading to more due to cirrhosis portal pressure, chronic congestive gastrointestinal tract, gastrointestinal secretion and absorption induced dysfunction. Diarrhea, very common, for the performance of stool or without and mucus. More from the bowel wall edema, fat malabsorption, and the lack of niacin parasitic infections, such as intestinal microflora imbalance caused. A small number of other symptoms of cirrhosis not obvious, and to diarrhea as the main performance. Abdominal distention, when more than gastric peristalsis cirrhosis due to dysfunction, hypokalemia, gastrointestinal Flatulence, ascites too much or hepatosplenomegaly, and other reasons. Abdominal pain, caused by inflammation around the reasons spleen, liver cell necrosis, inflammation around the liver, portal vein thrombosis formation and (or) portal vein inflammation. Abdominal pain can also result associated with peptic ulcer, biliary tract disease, such as intestinal infection caused.
Hepatitis cirrhosis and liver cancer relations
Hepatocellular carcinoma (HCC) is one of our common malignancy, or cancer mortality second place. Nearly a dozen years since the diagnosis and treatment of liver cancer in the original level on the basis of a greatly improved, and has made noteworthy achievements. First, the relationship between hepatitis and liver cancer Large epidemiological investigation and experimental study has proved B, hepatitis C and closely related to the occurrence of liver cancer. This has been recognized by the people, but so far its carcinogenic mechanism is not clear. HBV carcinogenic mechanism, in the past was that HBV genome contained oncogene views have long denied. After activation of HBV integration on the promoter or the mechanism of enhancer not be confirmed. In recent years that X gene and closely related to the occurrence of liver cancer; HCV is an RNA virus, according to recent study found that HCV core protein in vitro have the potential carcinogenic effect. The clinical findings, the majority of liver cancer patients have hepatitis and cirrhosis past history. Cirrhosis of liver cancer occur in those 15% -25%, generally around 20 percent, the majority of hepatocellular carcinoma in hepatitis cirrhosis basis happen. Second, how to evolve into liver cirrhosis liver cancer? Hepatitis is the main pathological changes in liver inflammation, necrosis and fibrosis, and some degree of necrosis heavier debris such as necrosis, bridging necrosis, followed by the Department of liver fibrosis district to enter into Hepatic Lobules, gradually forming false lobule, a renewable nodules. The occurrence of liver cancer nodules and regeneration closely related. Most scholars believe that adenomatous hyperplasia of liver cancer precancerous lesions, the multi-step evolution of liver cancer: large renewable nodules - adenomatous hyperplasia - atypical adenomatous hyperplasia - adenomatous hyperplasia deterioration of liver cells with a small number - well-differentiated (Level I) in the early liver cancer. Most of the incidence of liver cancer summarized as follows: HBV, HCV, alcohol, other - chronic hepatitis (inflammation, necrosis, fibrosis) - liver cirrhosis (nodule formation of different types of change, adenomatous hyperplasia) - HCC
Symptoms of cirrhosis causes complications
Cirrhosis is a common disease, can be part of the development of liver cancer. In China mainly caused by hepatitis, mainly abroad caused by excessive drinking. The types of hepatitis caused cirrhosis are hepatitis B, hepatitis C and hepatitis B co-infection with the hepatitis D. Clinical manifestations of liver dysfunction caused by burnout oil, jaundice, fatigue, loss of appetite, bleeding, hypoproteinemia and hepatic encephalopathy (abnormal liver function, can not effectively poison the central nervous system caused by the elimination of barriers), as well as portal hypertension caused by gastric - esophageal varices, abdominal water and hypersplenism. Light can be lifelong asymptomatic, can be life-threatening weight. Where patients with hepatitis B or hepatitis C, history in 3 to 5 years or more, reduced liver function in the performance of (lower serum albumin, bilirubin increased coagulation factor reduction, etc.) and ascites, hypersplenism, esophageal varices, liver ultrasound showed deformation, portal diagnosis can be widened cirrhosis. 【Symptoms: Symptoms fatigue, loss of appetite earlier by the end now 1, systemic symptoms: easy fatigue, physical and energy decreased significantly compared to the past, the ability to work also fell, the self-inductance and weak powerless. 2, loss of appetite, and even anorexia, often after eating flu epigastric discomfort, nausea or vomiting. 3, frequent nasal bleeding, bleeding gums, skin purpura and gastrointestinal bleeding tendency. In patients with liver cirrhosis, or in peacetime mouthwash, prone to dental bleeding, but also prone to nasal bleeding. Skin friction can be found the bleeding points, women can be found by the volume of excessive menstrual menstrual period or extension; traumatic time for the performance of some difficult to stop bleeding. Most patients with liver cirrhosis have different degrees of anemia. 4, estrogen and androgen increased reduction in estrogen increase was mainly due to liver dysfunction and reduced its inactivated attributable to the increase in the secretion of estrogen, these hormone changes often leads to the following endocrine disorders performance: male patients often loss of libido, hair loss, decreased beard and body hair Testicular increased shrinkage and breast; women have menstrual disorders, amenorrhea, infertility, and so on. 5, some patients may have jaundice. , In patients with advanced liver cirrhosis, there will be the ascites. 6, enlarged liver cirrhosis early can touch, texture hard. The late, liver narrow stiffen. About 80% to 90% of cirrhotic patients with enlarged spleen. 【Complications: First, upper gastrointestinal bleeding is the most common complication, suddenly more substantial hematemesis or black feces. Second, hepatic encephalopathy disease is the most serious complication is the most common cause of death. Third, the lower infection resistance in patients with liver cirrhosis, often complicated by bacterial infections, such as pneumonia, biliary tract infection, and E. coli sepsis, such as spontaneous bacterial peritonitis. 4. Primary Liver Cancer
Dietary fatty liver patients matters
Fatty liver is the body's lipid metabolism as obstacles to fat in liver cells over the content of the liver weight of more than 5%. In addition to fatty liver with some diseases such as endocrine obstacles, diabetes, hyperthyroidism, anemia and other reasons related to long-term, but also with the people's diet, nutrition has a close relationship. If the diet does not lead to obesity Festival, there are more than fatty liver exist, it was reported, 50 percent of the obese have different degrees of liver fatty infiltration, diet control this disease plays a vital role. Fatty liver patients need high-protein diet, adequate fat and sugar, if the intake of non-fat food, fatty acids and amino acids from some carbohydrate predecessor material synthesis, and the excessive intake of carbohydrates, can increase insulin secretion, glucose into fat. For obese and overweight patients, we should start with diet to reduce weight. If a height of 174 cm, weight 92 kg male, if in five months decreased by 25 kg weight, fatty liver can make disappear. Chronic hepatitis patients to normal intake of protein, carbohydrate and fat, and rich in fat should be unsaturated fatty acids vegetable oil-based.
Clinical acute fatty liver of pregnancy performance
There are two kinds of liver disease during pregnancy: a pregnancy and is a causal relationship between liver disease, liver disease that is caused by the pregnancy, such as gestational hypertension caused by secondary liver injury, intrahepatic cholestasis of pregnancy and acute fatty liver of pregnancy; Another situation is pregnant with liver disease, such as viral hepatitis, drug-induced liver disease, liver disease such can also occur in non-pregnant. More acute fatty liver of pregnancy occurred in the early young maternal morbidity time focused on pregnancy 28 ~ 40 weeks, an average of 36 weeks, then a few cases. Past statistics show that the acute fatty liver of pregnancy incidence rate of 1 in 10,000, maternal and child mortality rate as high as 85 percent. Recent trends in incidence rates have increased, the maternal and child mortality is down significantly. Acute fatty liver of pregnancy causes have not yet clear, pregnancy hormones may be related to metabolic disorder, malnutrition, and other relevant. Its clinical manifestations and liver function tests like severe hepatitis. Many anorexia, nausea, vomiting, general discomfort, right upper quadrant pain, decreased fetal movement, obviously bleeding tendency and awareness obstacles to its coma. Not normally associated with fever. Medical and para-examination can be found jaundice, high blood pressure, ascites, edema and renal failure, liver volume can be normal or reduced, ultrasonography showed fatty liver, liver biopsy showed acute diffuse alveolar small hepatic steatosis.
Why hepatitis patients with fatty liver
Acute hepatitis longer period of time due to the decreased appetite, can cause malnutrition, caloric, lack of protein, vitamins and choline, such as methionine to lipid substances can cause protein, caloric malnutrition fatty liver. The severely damaged liver cells, liver cells in fat decomposition and oxidation decreased, the result neutral fat accumulation in liver cells, is also the cause of fatty liver. Viral hepatitis, liver cell degeneration its smooth endoplasmic reticulum membrane degradation to network or mass, rough endoplasmic reticulum is reduced, such as expansion with threshing. The smooth endoplasmic reticulum function is complex, and lipoprotein synthesis, and free fatty acids were related to the activation. Intrahepatic often accompanied by inflammation of the liver microcirculation and cell proliferative changes in the liver cells to induce some hypoxia, ischemia, cells and blood oxygen-containing material exchange between insufficient to reduce hepatic fatty acid oxidation. These changes have meant that the intrahepatic more xylanase and ATP decreased hepatic lipoprotein synthesis decreased triglyceride and apolipoprotein a combination of obstacles, the output decline in triglyceride accumulation in the liver and fatty liver. The recovery in hepatitis, a significant increase in appetite, caloric surplus that is stored in the form of fat in case of obesity, followed fatty liver. This is a certain relationship between obesity. Obese "excessive intake of fatty liver" in the real mechanism of caloric food is not high, with a relative lack of protein and choline, if only to patients with high fever and additional cards protein dietary choline, does not make fatty liver removed and glucose metabolism and the mechanism of the disorder. Therefore fatty liver hepatitis merger also may be due to medical personnel in the course of treatment of hepatitis positive Hugan treatment, the large number of long-term intravenous glucose, excessive restrictions on activities, high-calorie diet for the results.
Hepatitis diagnosed with fatty liver
The first hepatitis history, symptoms and abnormal liver function, fatty liver, the merger no specific symptoms and therefore difficult to make an accurate from the clinical diagnosis. It was reported 19 cases of hepatitis fatty liver, triglyceride all of the high 2-3 times the normal serum cholesterol also increased 50%. But there are also reports of heavy only in the fatty liver can see lipids High, and has not exceeded the normal range. Therefore, the blood lipid indicators alone will be larger part of the merger of fatty liver hepatitis patients with missed diagnosis. It was reported that the type A simple fatty liver ultrasound on the clinical diagnosis was 95. Seven percent. And have reported only 44.4 percent of cases are Type A fatty liver ultrasound characteristics. The hepatitis B ultrasonic diagnosis of fatty liver seems no obvious advantages, particularly for light, medium patients with fatty liver. Therefore, a comprehensive inspection should continue, including CT, considered diagnosis. If clinical hepatitis deferred, especially appetite improved significantly after the rapid increase in weight, patients with hepatitis symptoms not overlapping, but not the liver retraction, such as ALT liver function continued to drop, should consider the possibility of fatty liver, and dynamic observation and, if necessary, liver biopsy or trial fatty liver treatment.
What are the common diseases of fatty liver due?
Fatty liver caused many reasons why common are: ① diet nutritional factors: chronic hunger or digestion and absorption barriers, lack of food protein and certain vitamins, or long-term intake of high-fat, high-cholesterol and high-precision diet. ② toxic fatty liver: Many chemicals, such as steroids, growth hormone, salicylic acid preparations, adenosine triphosphate, certain tranquilizers, epinephrine and norepinephrine, carbon tetrachloride, phosphorus, chloroform, benzene, alcohol, and so on. ③ infection: such as tuberculosis, streptococcal infection, pneumonia, typhoid fever, chronic cholecystitis, chronic bronchitis, chronic pancreatitis, and so on. ④ endocrine and metabolic diseases: such as diabetes, endocrine disorders and obesity. Hyperthyroidism, Cushing disease, hyperparathyroidism posterior lobe of pituitary such. ⑤ Iatrogenic: If in the course of treatment of hepatitis patients too much rest, coupled with the consumption of high-precision, high-calorie diet, weight gain or sustained long time, such as intravenous hypertonic glucose can cause fatty liver. ⑥ other: Pregnancy can cause fatty liver of pregnancy, congenital dementia syndrome, galactose hyperlipidemia, familial hyperlipidemia, non-β - Hyperlipoproteinemia, Crohn's disease and ulcerative colitis, and so can cause fatty liver.
Obese people Why should there be fatty liver?
Half of obese people may have mild fatty liver, but in severe obesity patients the incidence of fatty liver up to 61% -%%. Because obese adipose tissue in vivo increase in the free fatty acids and fatty acid release more energy into the main body of the material supply, and reduce the use of glucose. Under normal circumstances, the use of lower glucose, elevated blood glucose levels can stimulate insulin secretion to curb the release of free fatty acids, but at the substantial increase in body fat, even inhibited by insulin, free fatty acid release is the absolute quantity increased, making excessive fatty acids into large the synthesis of liver triglyceride, so formation of fatty liver. That is why obesity prone to the basic principles of fatty liver. In addition, the obese patient's diet aid high fever, fatty liver is also a factor. Fatty liver is proportional to the accumulation and body weight, weight control obese patients, the extent of its alleviate fatty liver. In contrast, weight gain, fatty liver also increased. This shows that obese patients fatty liver is the body part of the total fat. The assistance nutrient reduction, weight control, fatty liver can be improved.
Fatty liver awareness and prevention
Fatty liver is not a simple disease, which is caused by different causes. In recent years, with the continuous improvement of people's living standards, the incidence of fatty liver upward trend, the people should recognize that the harm of fatty liver, try to avoid the following major risk factors. One, the largest clinical see alcohol, or fatty liver disease due to the first. According to reports, daily alcohol consumption of 80 g, the long-term sustained 8-10 years drinkers in 90% fatty liver, cirrhosis until finally evolve into. Second, obesity improvement of living standards, nutrition, obesity caused by the growing surplus endanger people's health, exceed the weight 20 percent or more, it was reported that 53% fatty liver, especially women suffer from fatty liver disease patients more. Third, diabetic fatty liver were seen mainly in non-insulin-dependent diabetic adults, or about 50 percent, low-density lipoprotein in blood and free fatty acid increases, insulin-dependent diabetic patients suffering from fatty liver is rare. 4. Vein high nutritional fatty liver patients are unable to eat vein caused by the high nutritional importance has been attached to fatty liver. 5, fatty liver drug many drugs can cause liver fat content increased, a hormone which has the most. In addition, oral contraceptives, caused by anticancer drugs is particularly common chronic liver disease, we should also pay attention directed. How are we going to prevent fatty liver? ① Temperance: As the alcohol-induced fatty liver caused alcoholic hepatitis, cirrhosis final development, poor prognosis, liver detoxification function of poor people to quit drinking is particularly important. ② obese weight control: diet control and appropriate exercise. ③ of patients with diabetes and high blood: diet control, control blood sugar, but cautiously uses drugs (most drug will result in blood lipid deep plot in the liver). ④ avoid the use of harmful chemicals on the liver: such as contraceptives, hormones, which, to develop good eating habits, alcohol abuse, weight control, maintaining a healthy body, and on the health and lives of our work is necessary.
After suffering from the fatty liver how do?
Fatty liver in the elderly is a common liver disease, clinical about 50% of the patients in peacetime no uncomfortable feeling, usually in a body search, suddenly found suffering from a fatty liver. Many old people are worried about that end for fear of cancer in the future is disappointing. Well, suffer from fatty liver that how do? We think we should pay attention to the following aspects. (1) of fatty liver is not an independent clinical disease, but by all kinds of fatty liver caused by the excessive accumulation of a pathological state. Therefore, the search for treatment and the elimination of causes of the disease is a fundamental measure. Generally, the most common cause of fatty liver is the cause of obesity, diabetes, alcoholism and hepatitis, and other complications later from their fatty liver caused by about fatty liver more than half the total number. A small number of patients also can be caused by drugs or poison. (2) As we all know, people prone to obesity fatty liver. This is due to obesity are generally more food, less dynamic, and like eating sweet greasy of goods, it is prone to hyperlipidemia and fat accumulation in the liver, a fatty liver. Therefore, in order to remove unreasonable before eating habits, strict control of carbohydrate and fat intake, and gradually become "with more meat-less" diet. At the same time we must also strengthen sports, prompted in excessive fat consumption, body weight to efforts to the optimal level. (3) patients with diabetes accompanied fatty liver, the first such patients should be actively treated diabetes, in particular to carry out strict diet control, appropriate to participate in physical exercise. When some patients with weight loss, diabetes symptoms will reduce or disappear, too much fatty liver can be gradually reduced, and even returned to normal. In the course of treatment, but also the proper use of hypoglycemic, lipid-lowering, Baogan drugs. (4) caused by alcohol and fatty liver, the most common in developed Western countries, in recent years China has an increasing trend. Ethanol enters the human body, the liver following a series of biochemical processes, and ultimately into triglycerides. Long-term drinking will be a large number of substantial accumulation in the liver triglyceride, gradually forming fatty liver. Clearly, the most fundamental of this treatment is to quit drinking. Temperance alcoholic fatty liver would stop development, and is likely to return to normal; if continued drinking, a fatty liver may be turned to cirrhosis, liver cancer and even develop into. Drinkers When quit. (5) hepatitis treatment properly, can be complicated by the latter part of fatty liver. This is because in the acute phase of hepatitis, excessive emphasis on bed rest and added too much sugar, resulting in nutrient surplus into fatty liver. Therefore, people must pay attention to the prevention of hepatitis occurred; had hepatitis, should be under the guidance of specialists in comprehensive treatment, avoid one-sided emphasis on nutrition, leading to fatty liver.
Look at how Chinese medicine thromboangiitis obliterans
Thromboangiitis obliterans short Mai Guan Yan, the Chinese called the "delinking gangrene," "Ten scattered." Mai Guan Yan more complex reasons for the incidence, the general due to surplus arising from post-traumatic vascular and nerve injury;or the excessive labor, will enable heart, liver, kidney, spleen dysfunction, which led to Meridian, qi and blood dysfunction and disease. Mai Guan Yan-Deficiency - Cold Zheng type, hot and humid -, and thermal-induced toxicity type. Deficiency - Cold Zheng - yield initial leg of the cool, cold, numbness, pain, and fatigue associated with flu, local swelling or pressure plantar pad of a sense of intermittent claudication, leg walking by Shen storm, hold bulging, distance is shorter and shorter, temperature treatment to the cold-dispelling, Yiqihuoxue, Huayu Tongluo. Hygrothermal for-performance limb cold, pain, often migrans. Walking lower extremities acid storm, hold bulging, heavy fatigue; lower limb mass or nodule often arise, red hot pain; limb sometimes swelling. Treatment prefers Qingre Liangxue, then Huayu, Sanjie, Lishi. Limb - stasis performance for cold, inconsistent cool, and the pain was persistent, skin Purple,or green purple, a skin-foot deposition point. The temperature treatment to Tongluo, Huoxue Huayu. Thermal performance of the drug-limb pain, daytime light at night heavy limbs local redness, dry stool. Qingrejiedu Huayu treatment to Tongluo. Most of this type of muscle necrosis that the toe bones, the pain is just unbearable, and easily wound infections, bacterial toxins at this time, such as cold and heat wetlands violations threads, peripheral blood circulation serious obstacles, it is not appropriate at this time alone Naomaitong, weinaolutong expansion of vascular medicine, and so should combine western medicine with traditional Chinese medicine in Qingrejiedu, with Antibiotics prompted inflammation subsided, Huoxue Huayu give to the drug treatment. At this point the best hospitalization. Above all types of the third period there were toe-limb ulcers, gangrene possibility, it should be noted wound treatment, especially in summer, the hot weather, lesions easily breed bacteria and cause infection more opportunities, they should pay more attention to. Mai Guan Yan prevention: the cold season warm to the attention of the body, especially the limbs. Diet, personal,restraint, viscous eat less or eat food, such as the face, cakes, sesame sugar and so on. No smoking, drinking alcohol and feel happy, and, with passion, and abundant energy to live, study, work. Early patients found to the hospital to timely diagnosis and aggressive treatment. Do early discovery, early treatment.
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